ACLS Study Guide

 ACLS STUDY GUIDE

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 ACLS STUDY GUIDE Barbara Aehlert, MSEd, BSPA, RN

FIFTH EDITION

3251 Riverport Lane St. Louis, Missouri 63043  ACLS STUDY GUIDE, FIFTH EDITION

ISBN: 978-0-323-40114-2

Copyright  ©  2017, Elsevier Inc. All rights rights reserved. reserved. Previous editions copyrighted 2012, 2007, 2002. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or  mechanical, including photocopying, recording, or any information storage and retrieval system, without  permission permission in writing writing from the publisher. publisher. Details on how to seek permission, further further information about  the Publisher s permissions policies and our arrangements arrangements with organizations organizations such as the Copyright Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions website:  www.elsevier.com/permissions.. ’

 This book and the individual contributions contained in it are protected under copyright by the Publisher  (other than as may be noted herein). Notices

Knowledge Knowledge and best practice in this field are constantly constantly changing. changing. As new research and experience experience broaden our understanding, understanding, changes in research methods, professional practices, practices, or medical treatment treatment may become necessary. Practitioners Practitioners and researchers must always rely on their own experience experience and knowledge knowledge in evaluating evaluating and using any information, information, methods, compounds, compounds, or experiments experiments described herein. In using such information information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional professional responsibility. responsibility.  With respect to any drug or pharmaceutical products identified, readers are advised to check the most  current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, administered, to verify the recommended dose or formula, formula, the method and duration of administration, administration, and contraindicat contraindications. ions. It is the responsibility responsibility of practitioners practitioners,, relying relying on their own experience and knowledge knowledge of  their patients, patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, patient, and to take all appropriate safety precautions. precautions.  To the fullest extent of the law, neither ne ither the Publisher nor the authors, contributors, or editors, assume any  liability liability for any injury and/or damage to persons or property property as a matter of products liability, liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.

Content Strategist:  Sandra Clark  Content Development Specialist:  Melissa Kinsey/Melissa Rawe Content Development Manager:  Jean Sims Fornango Publishing Services Manager:  Hemamalini Rajendrababu Senior Project Manager:  Umarani Natarajan Design Direction:  Amy Buxton

Printed in Canada  Last digit is the print number: 9 8 7 6 5 4 3 2 1

PREFACE TO THE FIFTH EDITION

 As Stiggins has observed,  “ Many of us grew up in classrooms in which our teachers believed that the way   you maximize learning is i s by maximizing anxiety. Assessment was always the intimidator. Many of our  teachers believed that if a little intimidation doesn ’t work, turn up the heat —try a lot of intimidation.  This is why most adults today feel that being evaluated is a distin ctly dangerous enterprise. It always left  us feeling vulnerable”  (Stiggins, 2005, p. 18*  18* ). ). I took my first Advanced Cardiac Life Support (ACLS) class many years ago. I felt terrified and lost  through throughout out the entire entire course course.. Althou Although gh I had spent spent weeks weeks studyi studying ng before before the course course began, began, materi material al now  seemed to be written in a foreign language. I could find no resources to “translate” the information into something something that was useful useful to me. The course course consisted consisted of very long lectures lectures by by instructors instructors who read slides and offered little useful insight. The most memorable part of the course was the  “ Patient Management ” station, in which each course participant was evaluated one-on-one by an instructor. (Those of you who have have been been arou around nd a whileare whileare prob probab ably ly havi having ng flas flashb hbac acks ks of thos thosee days days.) .) I will will never forget forget that experience. experience. Despite my preparation, as soon as the door closed behind me I was a mental wreck. The instructor  proceeded to methodically strip away any self-confidence I might have had in treating patients with cardiac emergencie emergencies. s. I was able to answer answer the questions questions asked asked of me until I was presented presented with a patient patient who had symptomatic bradycardia. Atropine had not worked (transcutaneous pacing was not readily available back then), and the next drug recommended at that time was isoproterenol. I knew that. What I could not recall was whether isoproterenol was given in mcg/min (correct) or mg/min. I took a  “50/50” guess and said mg/min. Because that was the wrong decision, I was told I had failed and would need to attend another 2-day course. Before driving home, I sat outside for a few minutes contemplating what had happened and what I might have done to change the outcome. Then and there, promised myself I would become an ACLS instructor instructor someday someday and find a way to teach this information information in a more user-friend user-friendly ly way. I vowed to teach courses that were useful to practicing health care professionals and delivered in an environment in which the participants looked forward to the class —instead of dreading it.  As the years passed, I did become an ACLS instructor and I loved it. At the conclusion of each course, partic participa ipants nts often often wrote wrote on their their evalua evaluatio tion n forms forms that that a study study guide guide would would have have been been helpfu helpfull in prepar preparing  ing  for class. Those suggestions resulted in my writing a few pages of information that ultimately became a  book —this  book.   book.  The  ACLS Study Guide  is   is a course preparation tool designed for paramedic, nursing, and medical students, ECG monitor technicians, nurses, and other allied health personnel working in emergency  depart departmen ments, ts, critic critical al care care units, units, postan postanest esthes hesia ia care care units, units, operat operating ing rooms, rooms, and teleme telemetry try units. units. The fifth fifth edition of this book is based on the following scientific principles, treatment recommendations, and guidelines: • 2015 American Heart Association Guidelines for Cardiopulmonary Cardiopulmonary Resuscitation and Emergency  Cardiovascular Care International Consensus Consensus on Cardiopulmo Cardiopulmonary nary Resuscitation Resuscitation and Emergency Emergency Cardiovascular  Cardiovascular  • 2015 International Care Science with Treatment Recommendations Other evidence-based treatment recommendations or sources cited in the references section of rele•  vant chapters.

* 

introduction to student-involved student-involved assessment for learning (5th ed.).Upper Saddle Stiggin Stiggins, s, R. J. (2005) (2005).. An introduction Saddle River, River, NJ: Pearson Pearson Prentice Prentice Hall.

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Preface to the Fifth Edition

 This book is designed for use with the American Safety and Health Institute (ASHI) ACLS Course. It can also be used as supplementary material by those participating in ACLS courses offered by other  organizations. I have made every attempt to provide information consistent with the current literature, including the latest resuscitation guidelines; however, medicine is a dynamic field. Resuscitation guidelines change, new medications and technology are being developed, and medical research is ongoing. As a result, be sure to learn and follow local protocols as defined by your medical advisors. The author and publisher  assume no responsibility or liability for loss or damage resulting from the use of information contained  within. I genuinely hope the content of this book is helpful to you, and I wish you success in your ACLS course and clinical practice. Sincerely, Barbara Aehlert 

 ACKNOWLEDGMENTS

My sincerest thanks to Melissa Kinsey for her guidance throughout the development of this text. A special thanks to the manuscript reviewers who provided insightful comments and suggestions.  A special thanks to these instructors, who share my ACLS teaching philosophy: Robert Aiken, CEP;  Andrew Baird, CEP; Eileen Blackstone, CEP; Lynn Browne-Wagner, RN; Randy Budd, CEP; Joanna  Burgan, CEP; Thomas Cole, CEP; Mike Connor, CEP; Paul Honeywell, CEP; James Johnson, CEP; Stephen Knox, CEP; Bill Loughran, RN; Terence Mason, RN; Kevin McColm, CEP; Sean Newton, CEP; Anthony Pino, RN; Jan Post, RN; Gary Smith, MD; Ed Tirone, CEP; and Maryalice  Witzel, RN.

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REVIEWERS FOR THE FIFTH EDITION

N.K. Alexander, EMT-P Instructor/Chief Operating Officer   Wilton Emergency Squad, Inc Saratoga Springs, New York 

J.A. Nelson, DO, MS, FACOEP, FACEP State EMS Medical Director  Florida Department of Health  Tallahassee, Florida 

B. Cetanyan, RN Eastern Iowa Community College Davenport, Iowa 

S.L. Pinski, MD Head, Section of Cardiac Pacing and Electrophysiology  Robert and Suzanne Tomsich Department of  Cardiology  Cleveland Clinic Florida   Weston, Florida 

F.O. Garcia, EMT-P President  Professional EMS Education, LLC Grand Junction, Colorado C. Horsfield, BA Paramedic Teaching Fellow  School of Health Sciences University of Surrey  Guildford, Surrey, UK 

B.R. Shade, EMT-P, EMS-I, AAS  AHA Program Instructor, Adjunct Faculty, Firefighter  Paramedic, retired Assistant Safety Director  Cleveland Clinic, Cuyahoga Community College,  Willoughby Fire Department, City of  Cleveland Cleveland, Ohio

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 ABOUT THE AUTHOR

Barbara Aehlert, MSEd, BSPA, RN, has been a registered nurse for more than 40 years, with clinical experience in medical/surgical nursing, critical care nursing, prehospital education, and nursing education. Barbara is an active CPR and ACLS instructor with a special interest in teaching basic dysrhythmia  recognition and ACLS to nurses and paramedics.

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CONTENTS

1

2

Emergency Cardiovascular Care

1

Introduction Sudden Cardiac Death Out-of-Hospital Cardiac Arrest In-Hospital Cardiac Arrest Chain of Survival Out-of-Hospital Chain of Survival In-Hospital Chain of Survival Cardiopulmonary Resuscitation Physiology of Chest Compressions Barriers to Effective Cardiopulmonary Resuscitation Feedback during Cardiopulmonary Resuscitation Mechanical Chest Compression Devices Patient Assessment Primary Survey Secondary Survey Putting It All Together Chapter Quiz Chapter Quiz Answers References

1 2 4 5 5 5 8 10 10 10 11 12 14 15 17   18 18 19 20

Airway Management

Introduction  Anatomy Review Upper Airway Lower Airway The Patient with Respiratory Compromise Patient Assessment Oxygen Delivery Devices Nasal Cannula Simple Face Mask Partial Rebreather Mask Nonrebreather Mask Manual Airway Maneuvers Head Tilt  –Chin Lift  Jaw Thrust Suctioning  Airway Adjuncts Oral Airway Nasal Airway

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23 25 25 27 28 29 32 33 34 35 36 37 37 38 39 40 40 42

 

 

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Contents

Positive Pressure Ventilation Noninvasive Positive Pressure Ventilation Mouth-to-Mask Ventilation Bag-Mask Ventilation  Advanced Airways Confirming Endotracheal Tube Placement Putting It All Together Chapter Quiz Chapter Quiz Answers References 3

4

Cardiac Anatomy and Electrophysiology

44 44 45 47   49 51 53 53 57   60 63

Introduction Coronary Arteries Cardiac Cells Cardiac Action Potential Depolarization Repolarization Phases of the Cardiac Action Potential Refractory Periods Conduction System Sinoatrial Node  Atrioventricular Node and Bundle Right and Left Bundle Branches Purkinje Fibers The Electrocardiogram Electrodes Leads Electrocardiography Paper Waveforms and Complexes Segments and Intervals  Acute Coronary Syndromes Putting It All Together Chapter Quiz Chapter Quiz Answers References

63 65 66 66 67   67   67   68 69 69 70 70 70 71 72 72 76 76 77   78 79 79 80 81

Cardiac Arrest Rhythms

83

Introduction Cardiac Arrest Rhythms Ventricular Tachycardia Ventricular Fibrillation  Asystole Pulseless Electrical Activity Defibrillation Monophasic versus Biphasic Defibrillation Transthoracic Impedance Defibrillation Procedure  Automated External Defibrillation  Automated External Cardioverter-Defibrillators Possible Complications The Resuscitation Team Team Leader Responsibilities Team Member Responsibilities Resuscitation Efforts Helping the Caregivers

83 84 85 85 88 90 91 93 94 97   99 100 100 100 101 102 104 112

Contents

Putting It All Together Chapter Quiz Chapter Quiz Answers References

5

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113 113 120 125

Tachycardias

129

Introduction Narrow-QRS Tachycardias Sinus Tachycardia Supraventricular Tachycardia Wide-QRS Tachycardias Ventricular Tachycardia Irregular Tachycardias Multifocal Atrial Tachycardia  Atrial Flutter  Atrial Fibrillation Polymorphic Ventricular Tachycardia Synchronized Cardioversion Procedure Putting It All Together Chapter Quiz Chapter Quiz Answers References

129 131 131 132 140 142 143 143 144 145 148 150 150 153 153 160 165

Bradycardias

167

Introduction Sinus Bradycardia Junctional Escape Rhythm  Ventricular Escape Rhythm  Atrioventricular Blocks First-Degree Atrioventricular Block Second-Degree Atrioventricular Blocks Third-Degree Atrioventricular Block Transcutaneous Pacing Indications Procedure Limitations Possible Complications Putting It All Together Chapter Quiz Chapter Quiz Answers References

167 169 169 171 172 172 173 176 176 177   178 179 180 181 181 187   191

Acute Coronary Syndromes

193

Introduction Pathophysiology of Acute Coronary Syndromes Myocardial Ischemia, Injury, and Infarction Myocardial Ischemia Myocardial Injury Myocardial Infarction

193 194 196 196 199 200

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Contents

Patient Evaluation Patient History  Atypical Presentation Physical Examination Electrocardiogram Findings Cardiac Biomarkers Imaging Studies Initial Management of Acute Coronary Syndromes Prehospital Management Emergency Department Management Pharmacologic Therapies Reperfusion Therapies Putting It All Together Chapter Quiz Chapter Quiz Answers References 8

9

Acute Ischemic Stroke

201 201 202 203 204 214 215 215 215 216 217   224 227 227   232 235 237

Introduction Definition of Stroke  Anatomy Review Stroke Types Subarachnoid Hemorrhage Intracerebral Hemorrhage Ischemic Stroke Transient Ischemic Attack Stroke Systems of Care Public Education Emergency Medical Services Stroke Centers Putting It All Together Chapter Quiz Chapter Quiz Answers References

237 239 239 240 240 241 242 243 243 244 244 246 251 251 254 256

Post Test

259

Post test Answers References

269 276

Glossary 

277

Index 

281

CHAPTER

1

Emergency Cardiovascular Care INTRODUCTION Heart disease is a broad term that refers to conditions that affect the heart, and it is a leading cause of  death forboth men and women in the United States. Because someonein the United States experiences a  coronary event every 25 seconds, the likelihood of encountering a patient who requires basic life support  (BLS) or advanced cardiac life support (ACLS) care is high ( Roger, et al., 2012).  Just as BLS is a systematic way of providing care to a choking victim or to someone who needs cardiopulmonary resuscitation (CPR), ACLS is an orderly approach to providing advanced emergency care to a patient who is experiencing a cardiac-related problem. This chapter discusses risk factors for coronary  artery disease (CAD), sudden cardiac death (SCD), the Chain of Survival, and a systematic approach to patient assessment.

DESIRED RESULTS

G O A L Given a patient situation, and working in a team setting, direct or perform an initial patient   assessment, identify common barriers to effective CPR, and identify actions that can be taken to overcome them.

LEARNING OBJECTIVES

 After completing this chapter, you should be able to: 1. Define cardiovascular collapse, cardiac arrest, sudden cardiac death, and sudden cardiac arrest. 2.  Discuss the phases of a cardiac arrest. 3.  Discuss the prearrest factors that influence survival in out-of-hospital cardiac arrest (OHCA). 4. Identify the initial cardiac rhythms that are typically recorded in OHCA. 5.  Discuss the prearrest factors that influence survival in in-hospital cardiac arrest (IHCA). 6. Identify the initial cardiac rhythms that are typically recorded in IHCA. 7.  Describe the links in the Chain of Survival. 8.  Discuss the requirements for performing high-quality CPR. 9. Discuss common barriers to effective CPR and possible actions that can be taken to overcome them. 10.  Explore the use of feedback devices during CPR.

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CHAPTER 1   Emergency Cardiovascular Care 11.  Discuss the use of continuous end-tidal carbon dioxide (EtCO2 ) monitoring during

resuscitation efforts. 12.  Discuss the use of mechanical chest compression devices during resuscitation efforts. 13. State three areas to assess when forming a general impression of a patient. 14.  Differentiate between the purposes and components of the primary and secondary surveys. 15.  Discuss a systematic approach to the initial emergency care of an unresponsive patient.

LEARNING PLAN •

• •

•

Whether you are preparing for your first ACLS course or your tenth, schedule time to study and review before the course. Studying in half-hour intervals with 10-minute breaks allows a reasonable period for both learning and relaxation. Read this chapter before class. Take the time to highlight important concepts as you read. Develop and use flashcards, flowcharts, and mnemonics to help enhance your retention of  the information presented. Complete the chapter quiz and review the quiz answers provided.

KEY TERMS

 Automated external defibrillator (AED)  A machine with a sophisticated computer system that analyzes a patient’s heart rhythm using an algorithm to distinguish shockable rhythms from nonshockable rhythms and provides visual and auditory instructions to the rescuer to deliver an electrical shock if a shock is indicated. Cardiopulmonary (cardiac) arrest  The absence of cardiac mechanical activity, which is confirmed by the absence of a detectable pulse, unresponsiveness, and apnea or agonal, gasping breathing. Cardiovascular collapse A sudden loss of effective blood flow that is caused by cardiac and/  or peripheral vascular factors that may reverse spontaneously (eg, syncope) or only with interventions (eg, cardiac arrest). Cardiovascular disease (CVD)  A collection of conditions that involve the circulatory system, which contains the heart (cardio) and blood vessels (vascular), including congenital cardiovascular diseases. Chain of Survival  The essential elements of a system of care that are necessary to link the victim of sudden cardiac arrest with survival. Coronary artery disease (CAD) Disease affecting the arteries that supply the heart muscle with blood. Coronary heart disease (CHD) Disease of the coronary arteries and resulting complications, such as angina pectoris and acute myocardial infarction. Heart disease A broad term that refers to conditions affecting the heart. Risk factors  Traits and lifestyle habits that may increase a person’s chance of developing a disease. Sudden cardiac death (SCD) A natural death of cardiac cause that is preceded by an abrupt loss of consciousness within 1 hour of the onset of an acute change in cardiovascular  status; sudden cardiac arrest is a term commonly applied to such an event when the patient survives.

SUDDEN CARDIAC DEATH [Objectives 1, 2] Cardiovascular disease (CVD) is a collection of conditions that involve the circulatory system, which contains the heart (cardio) and blood vessels (vascular), including congenital CVD. More than one in three American adults has one or more types of cardiovascular disease (Roger, et al., 2012). The prevention of CVD requires the management of risk factors. Risk factors are traits and lifestyle habits that may  increase a person ’s chance of developing a disease. Some risk factors can be modified by specific,

CHAPTER 1   Emergency Cardiovascular Care

preventable measures. Risk factors that cannot be modified are called  nonmodifiable  or  fixed  risk factors. Contributing risk factors are thought to lead to an increased risk of heart disease, but their exact role has not been defined ( Table 1.1). Coronary heart disease (CHD) refers to disease of the coronary arteries and resulting complications, such as angina pectoris and acute myocardial infarction. Approximately one of every six deaths in the United States was caused by CHD in 2008 (Roger, et al., 2012). Coronary artery disease (CAD) affects the arteries that supply the heart muscle with blood. More than 90% of CAD events occur in individuals  who have at least one risk factor (Mack & Gopal, 2014). The relationships among CAD and its major  sequelae are shown in Fig. 1.1. Cardiovascular collapse is a sudden loss of effective blood flow caused by cardiac factors, peripheral  vascular factors, or both, that may reverse spontaneously (eg, syncope) or only with interventions (eg, cardiac arrest) (Myerburg & Castellanos, 2012). Cardiopulmonary (cardiac) arrest   is the absence of cardiac mechanical activity, which is confirmed by the absence of a detectable pulse, unresponsiveness, and apnea or agonal, gasping breathing. Gasping is abnormal breathing, is common during the first few  minutes of primary cardiac arrest, and is a sign of adequate blood flow to the brainstem (Ewy, 2012). Respiratory efforts can persist for 1 minute or longer after the onset of a cardiac arrest (Myerburg &  Castellanos, 2012). TABLE 1.1

Cardiovascular Disease Risk Factors

Nonmodifiable (Fixed) Factors • • • •

Age Family history of cardiovascular disease   Gender   Race

Modifiable Factors

Contributing Factors

•

  Diabetes mellitus Elevated serum cholesterol levels •   Hypertension •   Metabolic syndrome •   Obesity •   Physical inactivity •   Tobacco exposure • Unhealthy dietary habits

•

•

•

  Alcohol intake   Inflammatory markers •   Psychosocial factors •   Sleep apnea •   Stress

CORONARY ARTERY DISEASE

Myocardial ischemia

Acute plaque change; coronary artery thrombosis

Myocardial ischemia of increased severity and duration

MYOCARDIAL INFARCTION

with muscle loss and arrhythmias

Infarct healing

Ventricular remodeling

Hypertrophy, dilation of viable muscle

Chronic ischemic heart disease

Congestive heart failure

SUDDEN CARDIAC DEATH

Fig. 1.1 The relationships among coronary artery disease and its major sequelae. (From Kumar V, Abbas AK, Aster JC: Rob-  bins basic pathology , ed 9, Philadelphia, 2013, Saunders.)

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TABLE 1.2

Phases of Cardiac Arrest

Phase

Interval

Focus of Care

Prearrest

Period before the arrest

No flow

Untreated cardiac arrest

Low flow

Onset of cardiopulmonary resuscitation Return of spontaneous circulation

Identify, anticipate, and manage factors that may result in cardiac arrest (eg, use of rapid response teams to recognize and treat patients at risk of deterioration) Prompt initiation of basic life support upon recognition of the arrest by a bystander or health care professional Delivery of high-quality chest compressions to optimize myocardial and cerebral perfusion Identify and treat the cause of the arrest, preserve neurologic function, and support end organ perfusion and function

Postresuscitation

Sudden cardiac death (SCD) is a natural death of cardiac cause that is preceded by an abrupt loss of  consciousness within 1 hour of the onset of an acute change in cardiovascular status ( Myerburg &  Castellanos, 2012). SCD is often the patient ’s first and only symptom of heart disease (O’Connor, et al., 2010). For others, warning signs may be present up to 1 hour before the actual arrest. Sudden cardiac  arrest   is a term commonly applied to such an event when the patient survives ( Taniguchi, et al., 2012). Four phases of cardiac arrest have been described, each with unique physiology and treatment strategies ( Topjian, et al., 2013) ( Table 1.2). Heart rhythms that may be observed in a cardiac arrest include the following: 1. Pulseless ventricular tachycardia (pVT), in which the electrocardiogram (ECG) displays a wide, regular QRS complex at a rate faster than 120 beats per minute (beats/min). 2. Ventricular fibrillation (VF), in which irregular chaotic deflections that vary in shape and height are observed on the ECG but there is no coordinated ventricular contraction. 3. Asystole, in which no cardiac electrical activity is present. 4. Pulseless electrical activity (PEA), in which electrical activity is visible on the ECG but central pulses are absent. pVT and VF are shockable rhythms. This means that delivering a shock to the heart by means of a  defibrillator may result in termination of the rhythm. Asystole and PEA are nonshockable rhythms.

Out-of-Hospital Cardiac Arrest [Objectives 3, 4] Most nontraumatic OHCAs in the United States are the result of a primary cardiac arrest, rather than secondary to respiratory arrest (Ewy & Bobrow, 2016). A  primary cardiac arrest  is an unexpected witnessed (ie, seen or heard) collapse in an individual who is not responsive (Ewy, 2012). Seventy percent  of nontraumatic OHCAs occur in the home (Centers for Disease Control and Prevention, 2014). Of  these arrests, 50.3% are unwitnessed, 37.7% are witnessed by a bystander, and 12.1% are witnessed by a 9-1-1 responder (Centers for Disease Control and Prevention, 2014). Prearrest factors that influence survival in OHCA include the following (Boyd & Perina, 2012; Martinez, 2012): Performance of bystander CPR  • • Mode of arrest (ie, respiratory versus cardiac) •   Witnessed arrest  • Age (older age associated with worsened survival) Initial presenting rhythm of VF  • Short response times to defibrillation • Location of the arrest (survival is 3 to 4 times more likely if an arrest occurs in a public place; survival is • 6 times more likely if the arrest occurs in the workplace) Time of day (peak incidence occurs between 8 am and 10 am; survival to hospital discharge lowest for  • arrests between midnight and 6 am)  When an OHCA occurs, the initial rhythm recorded by emergency personnel is generally considered the electrical mechanism of the arrest (Myerburg & Castellanos, 2012). This information is important  because it affects patient outcome. Patients who are in sustained VT at the time of initial contact have the

CHAPTER 1   Emergency Cardiovascular Care

best outcome, whereas those who present with a bradyarrhythmia or asystole at initial contact have the  worst prognosis (Myerburg & Castellanos, 2012). When the initial rhythm recorded is VF, the patient ’s outcome is intermediate between the outcomes associated with sustained VT and those of bradyarrhythmia and asystole (Myerburg & Castellanos, 2012). Data from nontraumatic OHCAs in 2014 indicate that asystole was the most common initial cardiac arrest rhythm (45.6%), followed by an idioventricular  rhythm/PEA (21.4%), VF/pVT/unknown shockable rhythm (20.4%), and an unknown nonshockable rhythm (12.5%) (Centers for Disease Control and Prevention, 2014). Overall survival from nontraumatic OHCA to hospital admission was 28.3%, and overall survival to hospital discharge was 10.8% ( Centers for Disease Control and Prevention, 2014).

In-Hospital Cardiac Arrest [Objectives 5, 6]  The most common causes of IHCA include cardiac arrhythmia, acute respiratory insufficiency, and hypotension (Morrison, et al., 2013) with predictable deterioration before the event (eg, tachypnea, tachycardia) (Kronick, et al., 2015). Prearrest factors that influence survival in IHCA include the following (Martinez, 2012): Initial presenting rhythm of VF  • Time to CPR and defibrillation (survival is 33% when CPR is started within 1 minute of arrest versus • 14% if the time interval is greater than 1 minute; survival is 38% in pVT/VF arrests when defibrillation is performed within 3 minutes versus 21% if the time interval is greater than 3 minutes) Location (survival is highest if an arrest occurs in an intensive care unit [ICU; witnessed and mon• itored arrest, advanced life support {ALS} immediately available], better survival rates for wards that  have more than 5 cardiac arrests per year) Time of day (arrests that occur at night on general hospital wards have one-half the likelihood of  • survival) •   AED use  With regard to adult IHCA, asystole and PEA are more common than VF or pVT as the initial rhythm (Morrison, et al., 2013). In a largestudy of adult IHCA patients, only 23% presented with shockable rhythms ( Wallace, et al., 2013). An analysis of multicenter IHCAs published in 2010 observed that  the onset of the IHCA was witnessed in 79.2% of instances and approximately 32% of IHCAs occurred  within 24 hours of admission, 34% occurred within 1 week of admission, and 23% occurred more than 1 week after admission (Larkin, et al., 2010). Generally, IHCA has a better outcome than OHCA with 22.3% to 25.5% of adult patients surviving to discharge (Kleinman, et al., 2015).  The terms code  and code blue  are often used in hospitals when a patient experiences a respiratory arrest, a cardiac arrest, or a cardiac dysrhythmia that is associated with unresponsiveness. When a code blue is called, usually by means of an overhead paging system, a predesignated team of health care professionals is deployed to the patient ’s bedside to provide lifesaving interventions. The configuration of the resuscitation team and the responsibilities of each team member are discussed in  Chapter 4.

CHAIN OF SURVIVAL [Objective 7]  The Chain of Survival represents the essential elements of a system of care that are necessary to link the  victim of sudden cardiac arrest with survival. Although links of the Chain have been used for almost  25 years to depict the interrelated steps necessary with regard to an adult cardiac arrest both outside and inside the hospital setting, the 2015 resuscitation guidelines depict two separate chains because there are differences in these systems of care. Time is critical when dealing with a victim of sudden cardiac arrest; a weak or missing link in either Chain of Survival can reduce the likelihood of a positive outcome.

Out-of-Hospital Chain of Survival [Objective 7]  The links in the out-of-hospital Chain of Survival for adults include early recognition and activation, early CPR, rapid defibrillation, effective ALS, and integrated post  – cardiac arrest care.

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Early Recognition and Activation  The first link in the out-of-hospital Chain of Survival is early recognition and activation of the emergency  medical services system (EMSS). When a cardiac emergency occurs, the patient (or a family member or  bystander) must identify his or her signs and symptoms, recognize that they are related to a heart condition, and seek medical assistance in the hope of preventing cardiac arrest. Delays in seeking assistance and delays in the arrival of assistance ultimately affect patient outcome. Emergency dispatchers, who are located at public service access points, are the link between the call for help and the arrival of medical assistance (Kronick, et al., 2015). Dispatchers are trained to recognize the caller ’s description of a potential heart attack or cardiac arrest and to provide real-time CPR instructions over the phone if necessary while quickly sending appropriately trained and equipped emergency medical services (EMS) personnel to the scene. Some emergency medical dispatch protocols include telephone instructions for guiding an untrained rescuer in performing  compression-only CPR. In some areas, emergency dispatchers have used social media to summon  volunteer rescuers to the scene to provide bystander CPR until the arrival of EMS professionals (Kronick, et al., 2015). Early Cardiopulmonary Resuscitation  After recognizing that an emergency exists, the scene must be assessed to ensure that it is safe to enter. If  the scene is safe, the patient must be quickly assessed for life-threatening conditions and the nature of the emergency determined. CPR is a part of BLS. BLS includes the recognition of signs of cardiac arrest, heart attack, stroke, and foreign body airway obstruction (FBAO); the relief of FBAO; CPR; and defibrillation with an AED. BLS must be provided until advanced medical help arrives and assumes responsibility for the patient ’s care. Necessary care may include the following: •   Patient positioning  CPR for victims of cardiac arrest  • Defibrillation with an AED • • Rescue breathing for victims of respiratory arrest  Recognition and relief of FBAO • If CPR is necessary, compressions on adult victims of cardiac arrest should be performed at a rate of  100 to 120 compressions/minute with a compression depth of at least 2 inches (5 cm) but no more than 2.4 inches (6 cm) (Kleinman, et al., 2015). Rapid Defibrillation  When an individual experiences a cardiac arrest, the likelihood of successful resuscitation is affected by the speed with which CPR and defibrillation are performed. The goal for providing the first  shock for sudden cardiac arrest resulting from VF or pVT is within 3 minutes of collapse ( Link, et al., 2010).  The American Heart Association has promoted the development of AED programs to improve sur vival from sudden cardiac arrest since 1995. An automated external defibrillator (AED)  is a machine  with a sophisticated computer system that analyzes the patient ’s heart rhythm (Figs. 1.2 to 1.4).The AED uses an algorithm to distinguish shockable rhythms from nonshockable rhythms. If the AED detects a  shockable rhythm, it provides visual and auditory instructions to the rescuer to deliver an electrical shock. Defibrillation performed by citizens (such as flight attendants, casino security officers, athletic or golf club employees, and ushers at sporting events) at the scene is called  public access defibrillation. Some AEDs: Have CPR pads available that are equipped with a sensor that detects the rate and depth of chest  • compressions. If the rate or depth of compressions is inadequate, the machine provides voice prompts to the rescuer. Provide voice instructions in adult and infant/child CPR at the user ’s option. A metronome function • encourages rescuers to perform chest compressions at the recommended rate per minute. Are programmed to detect spontaneous movement by the patient or others. • Have adapters available for many popular manual defibrillators, enabling the AED pads to remain on • the patient when patient care is transferred. Can be configured to allow ALS personnel to switch to a manual mode, allowing more decision• making control. Are equipped with a small screen that allows the rescuer to view the patient ’s cardiac rhythm, assisting  • in identification of shockable versus nonshockable rhythms.

CHAPTER 1   Emergency Cardiovascular Care

Fig. 1.2 The Philips HeartStart FR3 AED. (Courtesy of Philips Healthcare. All rights reserved.)

Fig. 1.3 The Cardiac Science Powerheart G3 Plus automated external defibrillator. (Courtesy Cardiac Science Corporation, Waukesha, WI)

Fig. 1.4   The LIFEPAK ® 1000 Defibrillator. (Courtesy Physio-Control, Inc., Redmond, WA)

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CHAPTER 1   Emergency Cardiovascular Care •

•

Can detect the patient ’s transthoracic resistance through the adhesive pads applied to the patient ’s chest. The AED automatically adjusts the voltage and length of the shock, thus customizing how  the energy is delivered to that patient. Are equipped with a pediatric attenuator (ie, a pad-cable system or key). When the attenuator is attached to the AED, the machine recognizes the pediatric cable connection and automatically adjusts its defibrillation energy accordingly. Defibrillation is discussed in more detail in Chapter 4.

Effective Advanced Life Support Outside the hospital, early advanced care is provided by paramedics (and/or nurses) arriving on the scene. Prehospital professionals work quickly to stabilize the patient by providing ventilation support, vascular  access, and giving emergency medications, among other interventions. Integration of Post–Cardiac Arrest Care Prehospital professionals transportand then transfer the patient to the closest most appropriate emergency  department (ED) or directly to a specialized cardiac arrest center where definitive care can be provided.

In-Hospital Chain of Survival [Objective 7]  The links in the in-hospital Chain of Survival for adults include surveillance and prevention of cardiac arrest, prompt notification and response when a cardiac arrest occurs, the performance of high-quality  CPR, prompt defibrillation, and intra-arrest and post  – cardiac arrest care (Kronick, et al., 2015). Surveillance and Prevention  A cardiac arrest experienced by a hospitalized adult is often preceded by warning signs and symptoms that suggest physiologic deterioration such as tachypnea, tachycardia, and hypotension ( Tibballs & van der Jagt, 2008). Recognizing that early detection and treatment of the patient who demonstrates signs of  clinical deterioration may prevent cardiac arrest and improve patient outcome, the concept of a Rapid Response System (RRS) emerged. The RRS is mobilized by other hospital staff based on predetermined criteria for activation of the team. The Joint Commission National Patient Safety Goals   require hospitals to implement systems that enable health care workers to directly request additional assistance from specially trained individuals when the patient ’s condition appears to be worsening ( Joint Commission on  Accreditation of Healthcare Organizations, 2007). Several types of responding teams exist, and large hospitals may require more than one response team. It has been suggested that the term medical emergency team (MET) be used for teams that are generally led by physicians and have the ability to: (1) prescribe therapy; (2) place central vascular lines; (3) initiate ICU-level care at the bedside; and (4) perform advanced airway management (Devita, et al., 2006; McCurdy & Wood, 2012). It is recommended that the term  rapid response team (RRT)  be used to describe a team without all four of those abilities that performs a preliminary evaluation of a patient  and summons additional help or facilitates patient transfer to a higher level of care if warranted (McCurdy & Wood, 2012). RRTs typically consist of multidisciplinary members such as a physician (eg, critical care or hospitalist), a critical care nurse, and a respiratory therapist who respond to emergencies, proactively identify and evaluate patients at risk for decompensation, educate and act as a liaison to  ward staff, and follow up on patients who have been discharged from the ICU. In addition to their role in identifying prearrest conditions, studies have shown that MET and RRT services have also contributed to the detection and management of medical errors, surgical postoperative morbidity, and clarification of  do not resuscitate status ( Tibballs & van der Jagt, 2008). Several scoring systems for detecting warning signs of patient deterioration exist, and they are used as tools to assist in determining when the RRT should be activated. For example, with one type of scoring  system, the RRT is activated when a single vital sign or clinical abnormality is outside a predetermined range (Box 1.1). With the Modified Early Warning Score (MEWS) points are assigned based on the degree of derangement of ventilatory rate, heart rate, systolic blood pressure (BP), mental status, temperature, and hourly urine output. Regardless of the type of scoring system used, the decision to activate the RRT based on a score is ultimately the responsibility of the bedside clinician (McCurdy & Wood, 2012).  Adoption of an RRT necessitates teaching and staff empowerment because it usually  “involves substituting a traditional response reserved for cardiac or respiratory arrest (eg, Code Blue) with a system that responds to the early onset of signs and symptoms that may lead to these conditions” ( Tibballs & van

CHAPTER 1   Emergency Cardiovascular Care

BOX 1.1 • • •

•

•

Rapid Response System Calling Criteria

Abnormalor worseningrespiratorysymptoms Acute change in mental status   Chest pain or discomfort unrelieved by nitroglycerin Heart rate greater than 140 beats/minute or  less than 40 beats/minute Oxygen saturation less than 90% despite supplemental oxygen

• • •

• • •

Progressive lethargy Staff concern about the patient’s condition Systolic blood pressure greater than 180 mm Hg or less than 90 mm Hg Threatened airway Urine output less than 50 mL over 4 hours   Ventilatory rate greater than 28 breaths/  minute or less than 8 breaths/minute

der Jagt, 2008). Barriers to activation of the RRT by nurses have been identified and include the following (McCurdy & Wood, 2012): • The nurse may not know whom to contact when a patient ’s condition deteriorates. The nurse may fear blame if activation of the RRS is later deemed unnecessary. • Nurses often observe patients who briefly exhibit abnormal vital signs that spontaneously normalize. • Even when a dedicated response team exists within an institution, such teams are usually not immediately available and most medical emergencies must be managed by ad-hoc teams (Monteleone & Lin, 2012). After-hours cardiac arrests (ie, evening and weekend) are associated with twice the mortality of  office-hour arrests, which is thought to be a result of both the availability and the experience of staff  (Herlitz, et al., 2002; Monteleone & Lin, 2012). Studies show considerable variation in patient outcome data with regard to the use of RRTs. In adults, some studies demonstrate reductions in both IHCA and mortality, others demonstrate reductions in IHCA without a significant change in mortality, and still others show no significant differences in either  IHCA or mortality (McCurdy & Wood, 2012). The 2015 resuscitation guidelines note that for adult  patients, RRTs or MET systems can be effective in reducing the incidence of cardiac arrest, particularly  in general care wards; pediatric MET/RRT systems may be considered in facilities where children with high-risk illnesses are cared for on general in-patient units; and the use of early warning sign systems may  be considered for adults and children (Kronick, et al., 2015). Notification and Response Every member of the hospital staff should know how to recognize a cardiac arrest and know how to summon assistance when such an event occurs. Prompt notification and activation of the code team may  include pressing a  “code button”  at the patient ’s bedside, calling a specific phone extension, or use of a  “quick dial button”  located on telephones within the facility. When the operator is reached, the type of emergency and its location are stated. Once the operator is notified of the emergency, members of  the code team typically are activated by means of cell phones and/or a hospital-wide public address system. Cardiopulmonary Resuscitation  Although cardiac arrests and the performance of CPR are relatively uncommon in in-hospital environments (Kronick, et al., 2015), it is essential that hospital staff be able to perform high-quality CPR. Because training may not be adequate to ensure optimal performance, strategies such as timely access to equipment, visual reminders, regular testing, and point-of-care feedback have been suggested as methods to improve the translation of resuscitation guidelines into practice during cardiac arrest  (Morrison, et al., 2013). Prompt Defibrillation It has been estimated that about half of all IHCAs occur outside the ICU ( Morrison, et al., 2013). Because it can take several minutes for code team members to arrive with a defibrillator, the strategic deployment of AEDs throughout the facility can aid in achieving prompt defibrillation, with the goal being the delivery of the first shock within 3 minutes of collapse (Link, et al., 2010). Intra-Arrest and Post–Cardiac Arrest Care During the arrest, and underthe direction of a team leader, the code team works to stabilize the patient by  continuing high-quality CPR, performing defibrillation for pVT/VF, obtaining vascular access and giving medications, performing advanced airway management procedures when warranted, and providing 

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 ventilation support, among other interventions. If a return of spontaneous circulation (ROSC) is achieved, post  – cardiac arrest care, including advanced monitoring and targeted temperature management, is provided by a multidisciplinary team in an ICU. Post  – cardiac arrest care is discussed in more detail in Chapter 4. After the resuscitation, a debriefing of the resuscitation team is recommended to discuss areas such as psychomotor skill issues, cognitive issues, team issues, family emotional issues, and professional staff emotional issues (Kronick, et al., 2015).

CARDIOPULMONARY RESUSCITATION [Objective 8]  When an adult develops VF and suddenly collapses, his or her lungs, pulmonary veins, left heart, aorta, and arteries contain oxygenated blood (Ewy, 2005; Meursing, et al., 2005). After recognizing that CPR  is indicated, chest compressions should be the initial action performed (instead of opening the airway or  giving ventilations) when starting CPR in victims of sudden cardiac arrest. Performing chest compressions before ventilations enables better delivery of the oxygen that is already present in the lungs and arterial circulation to the heart and brain (Kern & Mostafizi, 2009).

Physiology of Chest Compressions [Objective 8] During CPR, myocardial blood flow is dependent on coronary perfusion pressure, which is generated  when performing chest compressions. Coronary perfusion pressure is a key determinant of the success of resuscitation, and adequate cerebral and coronary perfusion pressures are critical to neurologically normal survival (Ewy, 2005). During the low-flow phase of cardiac arrest, the only   source of coronary and cerebral perfusion pressures comes from the BP generated by high-quality chest compressions ( Berg, et al., 2010). High-quality chest compressions require compressing the chest at an adequate rate and depth, allowing full chest recoil after each compression (enabling the heart to refill with blood), minimizing interruptions in chest compressions, and avoiding excessive ventilation (Kleinman, et al., 2015). Cardiac output is the product of stroke volume and heart rate. During CPR, the force of compressions is a major determinant of stroke volume and the rate of compressions is the determinant of heart rate (Berg, et al., 2010). Current resuscitation guidelines recommend a compression rate for adults of 100 to 120 per minute (Kleinman, et al., 2015). Because stroke volume also depends on preload, an adequate blood volume is necessary for adequate perfusion. An adequate perfusion pressure cannot be obtained if  the patient ’s blood volume is low, such as that caused by blood loss or significant venous dilation (eg, hypovolemic shock, septic shock). These patients may require additional intravascular fluid volume to generate an adequate stroke volume with chest compressions (Berg, et al., 2010). During the compression (systolic) phase of chest compression, it is essential that the compressions delivered be of sufficient depth to deliver adequate stroke volume and cerebral perfusion pressure (Benner, et al., 2011). Current resuscitation guidelines recommend a compression depth for adults of  at least 2 inches (5 cm), not to exceed 2.4 inches (6 cm) (Kleinman, et al., 2015). During the release (diastolic) phase of chest compression, intrathoracic pressure is low. This helps increase the return of   venous blood into the chest. If intrathoracic pressure is too high, venous return is inhibited.

ACLS Pearl Hyperventilation is a common cause of excessive intrathoracic pressure during CPR. It is important to ventilate a patient in cardiac arrest at an age-appropriate rate and with just enough volume to see the patient’s chest rise gently. Ventilating a cardiac arrest patient too fast or with too much volume results in excessive intrathoracic pressure, which results in decreased venous return into the chest, decreased coronary and cerebral perfusion pressures, diminished cardiac output, and decreased rates of survival.

Barriers to Effective Cardiopulmonary Resuscitation [Objective 9] Numerous studies have shown that the quality of CPR during actual resuscitation often falls short of  established resuscitation guidelines in both out-of-hospital and in-hospital settings. Possible factors

CHAPTER 1   Emergency Cardiovascular Care

influencing these deficiencies include infrequent training, lack of awareness of the quality of CPR during  resuscitation, and inadequate team leadership during resuscitation efforts ( Abella, et al., 2014). Rescuer fatigue has been identified as an important potential contributor to poor CPR quality  (Brooks, et al., 2014). Rescuer fatigue contributes to an inadequate depth of compressions, compromises coronary perfusion pressure, and also leads to inadequate chest recoil ( Reynolds, et al., 2012). Research has shown that the depth of compressions is compromised after just 1 minute of performing CPR  (Hightower, et al., 1995; Zhang, et al., 2013) and rescuers tend not to recognize their own fatigue until after approximately 5 minutes of CPR (Reynolds, et al., 2012). To minimize fatigue, rescuers delivering  chest compressions should rotate every 2 minutes. Ideally, the switch should be accomplished in less than 5 seconds and should be done while another intervention is being performed (eg, defibrillation).  The brain and heart are sensitive to ischemic injury. Because it takes time to build up cerebral and coronary perfusion pressures, even short pauses (4 to 5 seconds) in chest compressions have resulted in a dramatic drop-off in cerebral and coronary perfusion pressures, thereby reducing blood flow to the brain and heart (Ewy, 2005; Wik, et al., 2005). When chest compressions are stopped during cardiac arrest, no blood flow is generated. Even after compressions are resumed, several chest compressions are needed to restore coronary perfusion pressure.

ACLS Pearl When caring for a patient in cardiac arrest it is  essential  that interruptions in chest compressions for  cardiac rhythm analysis, vascular access, airway management, and other interventions be kept to a minimum. For example, charging the defibrillator  before the end of a compression cycle in anticipation of delivering a shock is one technique that is often used to minimize compression interruptions.

It is important to allow the chest wall to rebound to its normal position after each compression. Incomplete chest wall recoil is common when performing CPR, particularly when rescuers are fatigued, and can occur when a rescuer leans over the patient ’s chest (Meaney, et al., 2013). Incomplete recoil results in higher intrathoracic pressure, decreased coronary perfusion pressure, decreased myocardial blood flow, decreased cerebral perfusion, and decreased cardiac output (Rajab, et al., 2011; Reynolds, et al., 2012).

Feedback during Cardiopulmonary Resuscitation [Objectives 10, 11] Feedback devices provide voice or visual cues about the quality of CPR that are measured and reported by a defibrillator, a handheld device, or alternative technology (Morrison, et al., 2013). For example, a  metronome can be used to guide the rate and rhythm of chest compressions using auditory or visual prompting at regular intervals. Timing lights may be used to prompt or time ventilations. Some feedback devices enable information about CPR quality (eg, chest compression rate, depth, chest   wall recoil) to be fed back to the rescuer using a sternal force detector or accelerometer (or both) through an external device placed between the rescuer ’s hands and the patient ’s sternum (Sutton, et al., 2012). With some feedback-enabled defibrillators, audible voiceprompts and visual messages on the monitor screen are triggered when measured chest compressions or ventilations are interrupted or when they deviate from preprogrammed resuscitation guideline parameters (Fig. 1.5). It is important that the chest compressor  have an unobstructed view of the monitor screen throughout a resuscitation effort to enhance the effectiveness of audiovisual feedback (Bobrow, et al., 2013). Some defibrillators also possess technology that  filters CPR artifact, allowing the rescuer to analyze a patient ’s cardiac rhythm without interrupting CPR  (Fig. 1.6). Although studies to date have not demonstrated a significant improvement in favorable neurologic outcome or survival to hospital discharge with the use of CPR feedback devices during actual cardiac arrest events, current resuscitation guidelines reflect that it may be reasonable to use audiovisual feedback devices during CPR for real-time optimization of CPR performance ( Kleinman, et al., 2015). For intubated patients, continuous EtCO2 monitoring should be used to monitor the quality of compressions during resuscitation efforts. When ventilation is constant, EtCO 2 reflects lung perfusion and therefore cardiac output (McGlinch & White, 2009). EtCO2  falls sharply with the onset of cardiac arrest, increases when effective CPR is delivered (generally 10 to 20 millimeters of mercury [mm Hg]), and returns to physiologic levels (35 to 40 mm Hg) with the ROSC ( Abella, et al., 2014). Low EtCO2  values (ie, less than 10 mm Hg) during resuscitation efforts indicate the need to explore factors that are hindering effective CPR (eg, rescuer fatigue, cardiac tamponade, pneumothorax, bronchospasm, mucus plugging of the endotracheal tube (ETT), kinking of the ETT, alveolar fluid in the

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Fig. 1.5 Several defibrillators, such as the MRx-QCPR shown here, are equipped with a chest compression pad that enables monitoring of the quality of chest compressions and provides corrective feedback to rescuers. (Courtesy of Philips Healthcare.  All rights reserved.)

Fig. 1.6 This Zoll R Series Monitor defibrillator filters cardiopulmonary resuscitation artifact, enabling the rescuer to analyze a patient ’s cardiac rhythm without interrupting chest compressions. (Courtesy Zoll Medical Corporation, Chelmsford, MA)

ETT, an airway with an air leak, hyperventilation) (Kodali & Urman, 2014; Link, et al., 2015). As the rescuer performing chest compressions tires, a gradual decrease in waveform height can be observed on the monitor screen, indicating the need to change rescuer positions. A sudden sustained increase in EtCO2  during CPR is an indicator of ROSC. In addition to improving the quality of CPR delivered, EtCO2  monitoring allows clinicians to perform chest compressions without pausing for pulse checks unless a sudden increase in EtCO 2  is observed, at which time ROSC can be verified (Cunningham, et al., 2012). When feasible, additional physiologic parameters that may be used to monitor and optimize CPR quality, guide vasopressor therapy, and detect ROSC include arterial relaxation diastolic pressure, arterial pressure monitoring, and central venous oxygen saturation (Link, et al., 2015).

Mechanical Chest Compression Devices [Objectives 12]  The use of mechanical chest compression devices has been proposed as an alternative to manual compressions to improve compression depth, rate, and consistency. When mechanical devices are used, training should be provided to reduce the time needed for device deployment ( Brooks, et al., 2014).  Training should also stress the importance of minimizing interruptions in chest compressions while the device is in use (Morrison, et al., 2013).

CHAPTER 1   Emergency Cardiovascular Care

Fig. 1.7 The AutoPulse uses a load-distributing band to compress the chest at a rate and depth consistent with resuscitation guidelines. (Courtesy Zoll Medical Corporation, Chelmsford, MA)

Several mechanical chest compression devices are available. The AutoPulse (Zoll Medical Corporation, Chelmsford, MA) uses a load-distributing band that is attached to a backboard and batterypowered motor (Fig. 1.7). The band encircles the patient ’s chest and mechanically and rhythmically  shortens and lengthens to compress the chest at a rate and depth consistent with resuscitation guidelines.  The LUCAS Chest Compression System (Physio-Control, Jolife AB, Redmond, WA) uses a back  plate that is positioned underneath the patient as a support and a piston/suction cup to compress the patient ’s anterior chest. The LUCAS 1 is powered by compressed air from a wall outlet or cylinder  (Fig. 1.8). The LUCAS 2 is electrically powered (Fig. 1.9). A UK trial studied whether the introduction of the LUCAS 2 device into front-line emergency response vehicles would improve survival from OHCA (Perkins, et al., 2015). Results showed no evidence of improvement in 30-day survival with the LUCAS 2 compared with manual compressions. The Life-Stat, formerly the Thumper (Michigan Instruments, Grand Rapids, MI), is a gas-powered piston device that is equipped with an automatic transport ventilator (Fig. 1.10). Current resuscitation guidelines state that although manual chest compressions remain the standard of care for the treatment of cardiac arrest, the use of mechanical chest compression devices may be a  reasonable alternative for use by properly trained personnel and “may be considered in specific settings  where the delivery of high-quality manual compressions may be challenging or dangerous for the pro vider (eg, limited rescuers available, prolonged CPR, during hypothermic cardiac arrest, in a moving  ambulance, in the angiography suite, during preparation for extracorporeal CPR), provided that rescuers strictly limit interruptions in CPR during deployment and removal of the devices ” (Brooks, et al., 2015).

Fig. 1.8   The LUCAS® 1 Chest Compression System is powered by compressed air from a wall outlet or cylinder. (Courtesy Physio-Control, Inc., Redmond, WA; Jolife AB, Lund, Sweden)

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Fig. 1.9   The LUCAS® 2 Chest Compression System is electrically powered. (Courtesy Physio-Control, Inc., Redmond, WA; Jolife AB, Lund, Sweden)

Fig. 1.10  The Life-Stat is a gas-powered piston device that is equipped with an automatic transport ventilator. (Courtesy Michigan Instruments, Grand Rapids, MI)

PATIENT ASSESSMENT  [Objectives 13] Patient assessment is a systematic method of evaluating a patient ’s condition and is the foundation of medical care. The information obtained by the clinician when performing a patient assessment helps guide treatment decisions. Recognizing when a patient ’s condition becomes unstable requires good patient  assessment skills and is essential for improved patient outcomes. Before approaching the patient, make sure that the scene is safe. Note any hazards or potential hazards and any visible mechanism of injury or illness. Always use appropriate personal protective equipment. Once you come into view of the patient, immediately begin to form a general impression, which is an “across-the-room” or  “ from-the-doorway ” assessment of the severity of the patient ’s condition. Your  general impression should focus on three main areas that can be remembered by the mnemonic ABC:  A ppearance, (work of) Breathing, and Circulation. As you finish forming your general impression, you  will have a good idea if the patient is sick (unstable) or not sick (stable).

CHAPTER 1   Emergency Cardiovascular Care

  Appearance.   The patient ’s appearance reflects the adequacy of oxygenation, ventilation, and central nervous system function. When forming a general impression, normal findings include a  patient who is aware of your approach and has normal muscle tone and equal movement of all extremities. •   Breathing. Breathing reflects the adequacy of the patient ’s oxygenation and ventilation. Normal findings include breathing without excessive respiratory muscle effort that is quiet and regular with equal rise and fall of the chest. Abnormal findings include use of accessory muscles to breathe, the presence of retractions, and audible respiratory sounds that can be heard without a stethoscope such as stridor, gasping, wheezing, snoring, or gurgling. •   Circulation. Circulation reflects the adequacy of cardiac output and perfusion of vital organs. When forming a general impression, circulation refers to skin color. Skin color normally is some shade of  pink. Even patients who have heavy pigmentation have an underlying pink color to the skin. Abnormal findings include pallor, mottling, and cyanosis.  An abnormal finding that is observed when assessing any of these areas suggests that the patient is sick  (unstable); move quickly and proceed immediately   to the primary survey. If the patient ’s condition does not appear to be urgent, proceed systematically starting with the primary survey and then the secondary  survey. •

Primary Survey  [Objectives 14]  The primary survey is a rapid hands-on patient assessment that focuses on basic  life support interventions and management. The purposes of the primary survey are to detect the presence of life-threatening problems and to immediately correct them. During this phase of patient assessment, assessment and management occur at the same time.  The ABCDE sequence of the primary survey is taught to physicians, nurses, and prehospital personnel in many types of educational courses. In programs other than cardiac-related courses, the primary  survey sequence stands for  A irway, Breathing, Circulation, Disability (referring to a brief neurologic exam), and E xposure. In cardiac-related courses, the “D”  also stands for  Defibrillation. Repeat the primary survey: With any sudden change in the patient ’s condition • When interventions do not appear to be working  • When vital signs are unstable • Before any procedures are performed • When a change in rhythm is observed on the cardiac monitor  • Begin the primary survey by assessing responsiveness. Start by asking, “ Are you all right?” or  “ Can you hear me? ” If there is no response, then gently tap or squeeze the victim ’s shoulder while repeating verbal cues. Look at the chest for movement for 5 to 10 seconds. Call for help and ask someone to get an AED or defibrillator.

ACLS Pearl Use the AVPU acronym when evaluating level of responsiveness: • A   A lert Responds to  v erbal stimuli • V  • P Responds to  p ainful stimuli • U Unresponsive ¼

¼

¼

¼

Responsive Patient  Ask the patient questions to determine his or her level of responsiveness and the adequacy of his or her  airway and breathing. Airway  If the airway is not clear, clear it with suctioning or positioning as indicated. If the airway is open, move on and assess the patient ’s breathing.

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Breathing   An open airway does not ensure adequate breathing. Evaluate the depth (tidal volume) and symmetry of  movement with each breath. Chest expansion should be adequate, with sufficient tidal volume to make the chest rise, and equal, with no excessive use of accessory muscles during inspiration or expiration.  Assess the patient ’s breathing with regard to rate, quality, and regularity. A patient who has breathing  difficulty often has a ventilatory rate outside the normal limits for his or her age.  Normal, noisy, labored, or   shallow are terms used to describe the quality of ventilations. Note if breathing is quiet, absent, or  noisy (eg, stridor, gasping, wheezing, snoring, gurgling). Labored breathing is evident when a patient is  working hard to breathe. It is often evidenced by the use of accessory muscles to breathe, pursed-lip breathing, retractions, leaning forward to inhale, or the patient ’s inability to speak in full sentences without pausing to take a breath. Shallow breathing may result in ineffective delivery of oxygen to the body ’s tissues and ineffective elimination of carbon dioxide, even when the ventilatory rate is normal. A bagmask device (BMD) is often used to provide assisted ventilation for the patient who has an inadequate rate or depth of breathing (see  Chapter 2). If the patient ’s breathing is adequate, move on to assessment  of circulation. Circulation  Quickly estimate the patient ’s heart rate and determine the quality of the pulse (ie, fast or slow, regular or  irregular, weak or strong). Evaluate the patient ’s skin temperature, color, and moisture to assess perfusion. Disability/Defibrillation  Perform a brief neurologic evaluation (ie, obtain a Glasgow Coma Scale score) and assess the need for a  defibrillator. Exposure  Expose the patient for further evaluation.

Unresponsive Patient [Objective 15] If your assessment of responsiveness indicated that the patient is unresponsive, call for help and ask  someone to get an AED or defibrillator. Look at the chest for movement while simultaneously feeling  for a carotid pulse for no more than 10 seconds.

ACLS Pearl If the patient is unresponsive buthas normal breathing, CPR is not needed. Perform a primary survey as you would for a responsive patient.

If a pulse is present, open the airway and begin rescue breathing, providing one breath every 5 to 6 seconds, or about 10 to 12 breaths/min (Kleinman, et al., 2015). Recheck a pulse every 2 minutes for up to 10 seconds. If there is no pulse or if you are unsure if there is a pulse and the patient is an adult, begin chest compressions, remembering to allow the chest wall to rebound after each compression. Minimize interruptions of chest compressions. Rotate chest compressors at 2-minute intervals (ideally in less than 5 seconds) to avoid tiring. If an opioid overdose is suspected, administer naloxone if it is available (check   your agency ’s protocol). If there is no pulse, check for a shockable rhythm using a monitor-defibrillator or AED. Provide shocks as indicated. Refer to the specific operating instructions of the AED model being used as models may vary. After each shock, immediately resume CPR beginning with chest compressions for  2 minutes.  After 30 compressions, open the airway using a head tilt  – chin lift (see Chapter 2). If head or neck  trauma is suspected, open the airway using the jaw thrust without neck extension maneuver. Next, use a pocket mask or BMD and deliver 2 breaths, ensuring that the delivery of each breath takes about  1 second. Make sure the breaths are effective (the chest rises). If the chest does not rise, reposition the head, make a better seal, and try again. Avoid excessive ventilation (ie, too many breaths, too large a volume).

CHAPTER 1   Emergency Cardiovascular Care

BOX 1.2 • • • •

Secondary Survey Components

  Airway   Breathing   Circulation Differential diagnosis and diagnostic procedures

• •

Evaluate interventions and pain management Facilitate family presence for invasive and resuscitative procedures

Secondary Survey  [Objectives 14]  The purpose of the physical examination during the secondary survey is to detect potentially lifethreatening conditions and to provide care for those conditions (Box 1.2). The secondary survey focuses on advanced  life support interventions and management. If the patient is responsive, obtain the patient ’s  vital signs; attach a pulse oximeter, ECG, and BP monitor; and obtain a focused history. The history is often obtained while the physical examination is being performed and emergency care is being given. Reassess the effectiveness of initial airway maneuvers and interventions. If needed, insert an advanced airway. If an advanced airway has been inserted, confirm proper placement using clinical assessment and  waveform capnography. Make sure the tube is adequately secured. Obtain a chest radiograph to confirm proper placement. If bag-mask ventilation is adequate, advanced airway insertion may be deferred until spontaneous circulation returns or the patient fails to respond to initial resuscitation efforts. Reassess the adequacy of oxygenation (using pulse oximetry) and ventilation (using capnography). Reassess chest rise. If oxygenation is inadequate, administer supplemental oxygen to achieve an oxygen saturation of 94% or greater. If breathing is inadequate, assist ventilations with a BMD at an ageappropriate rate. If the patient has a pulse, check its rate and quality often. If not already done, attach ECG electrodes and connect the patient to an ECG monitor. ECG monitoring allows continuous recording and reassessment of the cardiac rhythm. Obtain a 12-lead ECG if appropriate. Perform defibrillation or cardio version as indicated. Establish vascular access and give medications appropriate for the cardiac rhythm/  clinical situation. Vascular access is usually established via a peripheral IV; however, intraosseous (IO) access in cardiac arrest is safe, effective, and appropriate for patients of all ages. Consider limiting peripheral IV attempts to no more than two unsuccessful attempts before initiating IO access. During cardiac arrest, establishing vascular access is important, but it should not interfere with CPR and the delivery of  shocks. Each medication given during a cardiac arrest should be followed with a 20 mL IV fluid bolus and elevation of the extremity. These techniques help speed delivery of the medication to the central circulation. During a cardiac arrest, medications should be given without interrupting CPR. Search for, find, and treat reversible causes of the cardiac arrest, rhythm, or clinical situation. Reassess the effectiveness of the care given thus far and troubleshoot as needed. If the patient is responsive and complaining of discomfort, begin appropriate pain management if his or her BP and other vital signs will tolerate it. Facilitate family presence for invasive and resuscitative procedures. Explain what is being done for the patient to family members who are present.

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PUTTING IT ALL TOGETHER CHAPTER QUIZ

 Multiple Choice  Identify the choice that best completes the statement or answers the question.

____

1.

Which of the following memory aids may be used when evaluating a patient ’s level of  responsiveness?  A. CAB B. AVPU C. ABCDE D. OPQRST

____

2.

Upon finding an unresponsive adult patient, you called for help and asked that  someone get an AED or defibrillator. Your next action should be to:  A. Begin chest compressions. B. Reposition the patient ’s head. C. Open the airway and begin rescue breathing. D. Simultaneously look for breathing and feel for a pulse.

____

3.

During which phase of a cardiac arrest is CPR performed?  A. No-flow phase B. Prearrest phase C. Low-flow phase D. Postresuscitation phase

____

4.

The purpose of the primary survey is to:  A. Perform a detailed head-to-toe physical examination. B. Determine the number of personnel needed to assist in the patient ’s care. C. Focus on the patient ’s chief complaint/reason for seeking medical assistance. D. Detect the presence of life-threatening problems that require rapid intervention.

____

5.

Shockable cardiac arrest rhythms include:  A. Asystole and PEA. B. pVT and asystole. C. PEA and VF. D. VF and pVT.

____

6.

Which of the following is (are) the initial cardiac rhythm(s) typically recorded in an out-of-hospital cardiac arrest?  A. Asystole B. Idioventricular rhythm, PEA C. VF, pVT D. pVT, PEA

____

7.

During the primary survey, for what length of time should you assess for the presence of a pulse?  A. Check for a pulse for no more than 3 seconds. B. Check for a pulse for no more than 5 seconds. C. Check for a pulse for at least 5 seconds but no more than 10 seconds. D. Check for a pulse for at least 10 seconds but no more than 30 seconds.

____

8.

Which of the following is a common cause of excessive intrathoracic pressure during  CPR?  A. Hyperventilation B. Inability to open the victim’s airway  C. Inadequate rate of chest compressions D. Frequent interruptions for rhythm/pulse checks

CHAPTER 1   Emergency Cardiovascular Care

 Matching  Match the components of patient assessment with their descriptions .

 A. General impression B. Primary survey  C. Secondary survey  ____

9.

Establish vascular access

____

10.

From a distance, assess the patient ’s breathing effort 

____

11.

Insert an advanced airway, if needed

____

12.

Open the airway if the patient is unresponsive

____

13.

From a distance, assess skin color 

____

14.

Obtain a 12-lead ECG if appropriate

____

15.

Apply pads to the patient ’s bare chest and defibrillate if indicated

____

16.

Obtain vital signs; attach a pulse oximeter, cardiac monitor, and BP monitor 

CHAPTER QUIZ ANSWERS

 Multiple Choice

1. B. The AVPU acronym is used to quickly assess a patient ’s level of responsiveness. AVPU  –  Alert, responds to verbal stimuli, responds to painful stimuli, unresponsive. ABCDE is an acronym that  reflects the components of the primary survey. OPQRST is an acronym that is used when evaluating  a patient ’s complaint of pain. CAB is an acronym that emphasizes the importance of performing  chest compressions first, followed by opening the airway and assessing breathing, in victims of cardiac arrest. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 2. D. If you find an unresponsive patient, call for help and ask someone to get an AED or defibrillator. Look at the chest for movement while simultaneously feeling for a carotid pulse for up to 10 seconds. Gasping, if present, is abnormal breathing and should not be interpreted as a sign of effective breathing. If the patient has no pulse, begin chest compressions. If the patient is breathing normally, continue monitoring until additional help arrives. If the patient is not breathing normally but a pulse is present, provide rescue breathing and recheck for a pulse about every 2 minutes. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient. 3. C. Four phases of cardiac arrest have been described: (1) the prearrest phase, (2) the no-flow phase, (3) the low-flow phase, and (4) the postresuscitation phase ( Berg, et al., 2010). The prearrest phase is the period that precedes cardiac arrest. The no-flow phase reflects untreated cardiac arrest. The lowflow phase begins with the onset of CPR. During this phase of cardiac arrest, the  only  source of coronary and cerebral perfusion pressures comes from the BP generated by high-quality chest compressions. The postresuscitation phase begins with the ROSC. OBJ: Discuss the phases of a cardiac arrest. 4. D. The primary survey is a rapid hands-on assessment to detect the presence of life-threatening  problems and immediately correct them. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 5. D. The four cardiac arrest rhythms are pVT, VF, asystole, and PEA. pVT and VF are shockable rhythms. Defibrillation is not indicated for asystole or PEA. OBJ: Differentiate between shockable and nonshockable cardiac arrest rhythms.

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CHAPTER 1   Emergency Cardiovascular Care

6. A. Data from nontraumatic OHCAs in 2014 indicate that asystole was the most common (45.6%) initial cardiac arrest rhythm, followed by an idioventricular rhythm/PEA (21.4%), VF/pVT/  unknown shockable rhythm (20.4%), and an unknown nonshockable rhythm (12.5%) (Centers for  Disease Control and Prevention, 2014). OBJ: Recognize the initial cardiac rhythms that are typically recorded in OHCA. 7. C. Check for a pulse for at least 5 seconds but no more than 10 seconds. If the patient has no pulse, begin chest compressions. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 8. A. Hyperventilation is a common cause of excessive intrathoracic pressure during CPR. It is important to ventilate a patient in cardiac arrest at an age-appropriate rate and with just enough volume to see the patient ’s chest rise gently. Ventilating a cardiac arrest patient too fast or with too much volume results in excessive intrathoracic pressure, which results in decreased venous return into the chest, decreased coronary and cerebral perfusion pressures, diminished cardiac output, and decreased rates of survival. OBJ: Discuss common barriers to effective CPR and possible actions that can be taken to overcome them.  Matching

9. C 10. A 11. C 12. B 13. A 14. C 15. B 16. C

REFERENCES  Abella, B. S., Gonzalez, M. R., & Becker, L. B. (2014). Artificial perfusion during cardiac arrest. In J. R. Roberts, C. B. Custalow, T. W. Thomsen, & J. R. Hedges (Eds.), Roberts and Hedges   clinical procedures in emergency medicine  (6th ed., pp. 319 – 324). Philadelphia: Saunders. Benner, J. P., Morris, S., & Brady, W. J. (2011). A phased approach to cardiac arrest resuscitation involving ventricular fibrillation and pulseless ventricular tachycardia. Emerg Med Clin North Am, 29(4), 711 – 719. Berg, M. D., Nadkarni, V. M., Gausche-Hill, M., Kaji, A. H., & Berg, R. A. (2010). Pediatric resuscitation. In J. A. Marx, R. S. Hockberger, & R. M. Walls (Eds.), Rosen s emergency medicine: Concepts and clinical practice  (7th ed., pp. 64 – 76). Philadelphia: Saunders. Bobrow, B. J., Vadeboncoeur, T. F., Stolz, U., Silver, A. E., Tobin, J. M., Crawford, S. A., et al. (2013). The influence of scenario-based training and real-time audiovisual feedback on out-of-hospital cardiopulmonary resuscitation quality and survival from out-of-hospital cardiac arrest. Ann Emerg Med ,  62(1), 47 – 56. Boyd, T. S., & Perina, D. G. (2012). Out-of-hospital cardiac arrest. Emerg Med Clin North Am, 30 (1), 13 – 23. Brooks, S. C., Anderson, M. L., Bruder, E., Daya, M. R., Gaffney, A., Otto, C. W., et al. (2015, Oct). 2015 American Heart Association guidelines for CPR & ECC.  Retrieved Oct 30, 2015, from American Heart Association. In  web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care—part 6:  Alternative techniques and ancillary devices for cardiopulmonary resuscitation:  Eccguidelines.heart.org . ’  

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Brooks, S. C., Hassan, N., Bigham, B. L., & Morrison, L. J. (2014). Mechanical versus manual chest compressions for cardiac arrest. Cochrane Database of Systematic Reviews , 2014 (2), 1 – 49. Centers for Disease Control and Prevention. (2014). Cardiac Arrest Registry to Enhance Survival (CARES). Retrieved Oct 31, 2015, from   CARES 2014 non-traumatic national summary report:   https://mycares.net/  sitepages/reports2014.jsp. Cunningham, L. M., Mattu, A., O ’Connor, R. E., & Brady, W. J. (2012). Cardiopulmonary resuscitation for cardiac arrest: The importance of uninterrupted chest compressions in cardiac arrest resuscitation. Am J Emerg Med , 30 (8), 1630 – 1638. Devita, M. A., Bellomo, R., Hillman, K., Kellum, J., Rotondi, A., Teres, D., et al. (2006). Findings of the first  consensus conference on medical emergency teams. Crit Care Med ,  34 (9), 2463 – 2478. Ewy, G. A. (2005). Cardiocerebral resuscitation: The new cardiopulmonary resuscitation.  Circulation, 111(16), 2134 – 2142. Ewy, G. A. (2012). The cardiocerebral resuscitation protocol for treatment of out-of-hospital primary cardiac arrest. Scand J Trauma Resusc Emerg Med ,  20 (65), 1 – 6. Ewy, G. A., & Bobrow, B. J. (2016). Cardiocerebral resuscitation: An approach to improving survival of patients  with primary cardiac arrest. J Intensive Care Med ,  31(1), 24 – 33. Herlitz, B., Bång, A., Alsen, B., & Aune, S. (2002). Characteristics and outcome among patients suffering from in hospital cardiac arrest in relation to whether the arrest took place during office hours.  Resuscitation, 53(2), 127 – 133. Hightower, D., Thomas, S. H., Stone, C. K., Dunn, K., & March, J. A. (1995). Decay in quality of closed-chest  compressions over time. Ann Emerg Med ,  26(3), 300 – 303.  Joint Commission on Accreditation of Healthcare Organizations. (2007). 2008 national patient safety goals. Joint  Commission Perspectives ,  27 (7), 1 – 12. Kern, K. B., & Mostafizi, K. (2009). A hands-on approach. What compression-only CPR means for EMS. JEMS , Suppl , 8 – 11. Kleinman, M. E., Brennan, E. E., Goldberger, Z. D., Swor, R. A., Terry, M., Bobrow, B. J., et al. (2015, Oct).  2015 American Heart Association guidelines for CPR & ECC . Retrieved Jan 11, 2016, from American Heart   Association. In web-based integrated guidelines for cardiopulmonary resuscitation and emergency  cardiovascular care—part 5: Adult basic life support and cardiopulmonary resuscitation quality: Eccguidelines. heart.org . Kodali, B. S., & Urman, R. D. (2014). Capnography during cardiopulmonary resuscitation: Current evidence and future directions. J Emerg Trauma Shock, 7 (4), 332 – 340. Kronick, S.L., Kurz, M.C., Lin,S., Edelson,D. P., Berg, R. A., Billi,J. E., etal. (2015). Part4: Systems of careand continuous quality improvement: 2015 American Heart Association guidelines update for cardiopulmonary  resuscitation and emergency cardiovascular care. Circulation, 132(suppl 2), S397 – S413. Larkin, G. L., Copes, W. S., Nathanson, B. H., & Kaye, W. (2010). Pre-resuscitation factors associated with mortality in 49,130 cases of in-hospital cardiac arrest: A report from the National Registry for Cardiopulmonary  Resuscitation. Resuscitation, 81(3), 302 – 311. Link, M. S., Atkins, D. L., Passman, R. S., Halperin, H. R., Samson, R. A., White, R. D., et al. (2010). Part 6: Electrical therapies: Automated external defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 122(suppl 3), S706 – S719. Link, M. S., Berkow, L. C., Kudenchuk, P. J., Halperin, H. R., Hess, E. P., Moitra, V. K., et al. (2015, Oct). 2015   American Heart Association guidelines for CPR & ECC . Retrieved Jan 11, 2016, from American Heart   Association. In web-based integrated guide lines for cardiopulmonary resuscitation a nd emergency cardiovascular  care—part 7: Adult advanced cardiovascular life support:  Eccguidelines.heart.org . Mack, M., & Gopal, A. (2014). Epidemiology, traditional and novel risk factors in coronary artery disease.  Cardiol  Clin, 32(3), 323 – 332. Martinez, J. P. (2012). Prognosis in cardiac arrest. Emerg Med Clin North Am, 30 (1), 91 – 103. McCurdy, M. T., & Wood, S. L. (2012). Rapid response systems: Identification and management of the  “ prearrest  state.”  Emerg Med Clin North Am, 30 (1), 141 – 152. McGlinch, B. P., & White, R. D. (2009). Cardiopulmonary resuscitation: Basic and advanced life support. In R. D. Miller, L. I. Eriksson, L. Fleisher, J. P. Wiener-Kronish, & W. L. Young (Eds.), Miller s anesthesia  (7th ed., pp. 2971 – 3001). Philadelphia: Churchill Livingstone. Meaney, P. A., Bobrow, B. J., Mancini, M. E., Christenson, J., de Caen, A. R., Bhanji, F., et al. (2013). Cardiopulmonary resuscitation quality: [Corrected] improving cardiac resuscitation outcomes both inside andoutsidethehospital:AconsensusstatementfromtheAmericanHeartAssociation.Circulation, 128 (4),417 – 435. Meursing, B. T., Wulterkens, D. W., & van Kesteren, R. G. (2005). The ABC of resuscitation and the Dutch (re) treat. Resuscitation, 64 (3), 279 – 286. Monteleone, P. P., & Lin, C. M. (2012). In-hospital cardiac arrest. Emerg Med Clin North Am, 30 (1), 25 – 34. 

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Morrison, L. J., Neumar, R. W., Zimmerman, J. L., Link, M. S., Newby, L. K., McMullan Jr., P. W., et al. (2013). Strategies for improving survival after in-hospital cardiac arrest in the United States: 2013 consensus recommendations. Circulation, 127 , 1538 – 1563. Myerburg, R. J., & Castellanos, A. (2012). Cardiac arrest and sudden cardiac death. In R. W. Bonow, D. L. Mann, D. P. Zipes, & P. Libby (Eds.), Braunwald s heart disease: A textbook of cardiovascular medicine  (9th ed., pp. 845 – 881). Philadelphia: Saunders. O’Connor, R. E., Brady, W., Brooks, S. C., Diercks, D., Egan, J., Ghaemmaghami, C., et al. (2010). Part 10: Acute coronary syndromes: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 122(suppl 3), S787 – S817. Perkins, G. D., Lall, R., Quinn, T., Deakin, C. D., Cooke, M. W., Horton, J., et al. (2015). Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): A pragmatic, cluster randomised controlled trial. Lancet ,  385 (9972), 947 – 955. Rajab, T. K., Pozner, C. N., Conrad, C., Cohn, L. H., & Schmitto, J. D. (2011). Technique for chest compressions in adult CPR. World J Emerg Surg ,  6(41), 1 – 5. Reynolds, J. C., Bond, M. C., & Shaikh, S. (2012). Cardiopulmonary resuscitation update. Emerg Med Clin North  Am, 30 (1), 35 – 49. Roger, V. L., Go, A. S., Lloyd-Jones, D. M., Benjamin, E. J., Berry, J. D., Borden, W. B., et al. (2012). Heart  disease and stroke statistics—2012 update: A report from the American Heart Association.  Circulation, 125 , e2 – e220. Sutton, R. M., Nadkarni, V., & Abella, B. S. (2012). “ Putting it all together ” to improve resuscitation quality. Emerg   Med Clin North Am, 30 (1), 105 – 122.  Taniguchi, D., Baernstein, A., & Nichol, G. (2012). Cardiac arrest: A public health perspective. Emerg Med Clin  North Am, 30 (1), 1 – 12.  Tibballs, J., & van der Jagt, E. W. (2008). Medical emergency and rapid response teams. Pediatr Clin North Am, 55 (4), 989 – 1010.  Topjian, A. A., Berg, R. A., & Nadkarni, V. M. (2013). Advances in recognition, resuscitation, and stabilization of  the critically ill child. Pediatr Clin North Am, 60 (3), 605 – 620.  Wallace, S. K., Abella, B. S., & Becker, L. B. (2013). Quantifying the effect of cardiopulmonary resuscitation quality  on cardiac arrest outcome: A systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes , 6(2), 148 – 156.  Wik, L., Kramer-Johansen, J., Myklebust, H., Sørebø, H., Svensson, L., Fellows, B., et al. (2005). Quality of  cardiopulmonary resuscitation during out-of-hospital cardiac arrest. JAMA ,  293(3), 299 – 304. Zhang, F. L., Yan, L., Huang, S. F., & Bai, X. J. (2013). Correlations between quality indexes of chest compression. World J Emerg Med ,  4 (1), 54 – 58. ’  

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2

Airway Management INTRODUCTION  As a health care professional, it is essential that you be able to recognize if a patient has clinical signs and symptoms of inadequate oxygenation, inadequate ventilation, or both, and know how to confidently pro vide appropriate emergency care in such situations. This chapter briefly describes respiratory system anatomy, reviews the devices used to deliver supplemental oxygen, discusses the techniques used for opening  the airway of an unresponsive patient, discusses the devices used for delivering positive pressure ventilation, and discusses methods used to confirm proper positioning of an endotracheal tube (ETT).

DESIRED RESULTS

G O A L Given a patient situation, and working in a team setting, competently direct the initial emer gency care for a patient experiencing a respiratory arrest.

LEARNING OBJECTIVES

 After completing this chapter, you should be able to: 1.  Differentiate among respiratory distress, respiratory failure, and respiratory arrest and implement a treatment plan based on the severity of the patient’s respiratory compromise. 2.  Discuss the evaluation of oxygenation and ventilation with the use of pulse oximetry and capnography. 3.  Describe the advantages, disadvantages, oxygen liter flow per minute, and estimated oxygen percentage delivered with each of the following devices: nasal cannula, simple face mask, partial nonrebreather mask, and nonrebreather mask. 4.  Describe and demonstrate the steps needed to perform the head tilt–chin lift and the jaw thrust without neck extension maneuvers and relate the mechanism of injury to the opening of the airway. 5.  Describe and demonstrate the procedure for suctioning the upper airway, and discuss possible complications associated with this procedure. 6.  Discuss the indications, contraindications, advantages, and disadvantages of oral and nasal airways, and demonstrate how to correctly size and insert each of these airway adjuncts. 7.  Describe methods by which positive pressure ventilation is delivered. 8.  Differentiate between continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP). 9.  Describe the oxygen liter flow per minute and the estimated inspired oxygen concentration delivered with a pocket face mask and a bag-mask device (BMD).

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CHAPTER 2   Airway Management  10. Describe and demonstrate how to ventilate a patient with a BMD and two rescuers. 11.  Recognize the signs of adequate and inadequate bag-mask ventilation (BMV). 12.  Differentiate between extraglottic airways and intraglottic airways. 13.  Describe methods that are used to confirm correct ETT placement.

LEARNING PLAN • • •

Read this chapter before class. Take the time to highlight important concepts as you read. Master the following medications: O2. Master the following skills: Ensure scene safety and the use of personal protective equipment. Assign team member roles or perform as a team member in a simulated patient situation. Direct or perform an initial patient assessment. Recognize signs and symptoms of respiratory compromise. Develop and implement a treatment plan on the basis of the severity of the patient’s respiratory compromise, history, physical examination, and diagnostic test results. Obtain vital signs, establish vascular access, attach a pulse oximeter and blood pressure and cardiac monitor, and give supplemental O2  if indicated. Demonstrate manual methods for opening the airway. Demonstrate the procedure for suctioning the upper airway. Demonstrate how to properly size and insert an oral airway and a nasal airway. Perform two-rescuer BMV when indicated. Demonstrate how to troubleshoot inadequate BMV. Demonstrate how to confirm the correct positioning of an ETT. Review your performance as a team leader or team member during a postevent debriefing. Develop and use flashcards, flowcharts, and mnemonics to help enhance your retention of  the information presented. Complete the chapter quiz and review the quiz answers provided. Read the case study at the end of this chapter and answer each question that follows it. Compare your answers with the answers provided at the end of the case study. • •

• • •

•

• • • • • • •

•

• •

KEY TERMS

Capnography  The continuous analysis and recording of carbon dioxide concentrations in respiratory gases. Carina The point where the trachea divides into the right and left primary bronchi. Cricothyroid membrane  A fibrous membrane located between the cricoid and thyroid cartilages. Epiglottis  A small piece of cartilage located at the top of the larynx that prevents foreign material from entering the trachea during swallowing. Glottis  The true vocal cords and the space between them. Hard palate  Bony portion of the roof of the mouth that forms the floor of the nasal cavity. Nasal cannula A piece of plastic tubing with two soft prongs that project from the tubing; used to deliver supplemental oxygen to a spontaneously breathing patient. Oxygenation  The process of getting oxygen into the body and to its tissues for metabolism. Pulse oximeter  A small instrument with a light sensor that quickly calculates the percentage of hemoglobin that is saturated with oxygen in a pulsating capillary bed. Respiration  The exchange of oxygen and carbon dioxide during cellular metabolism. Simple face mask  An oxygen delivery device that consists of a plastic reservoir that fits over  a patient’s nose and mouth and a small diameter tube connected to the base of the mask  through which oxygen is delivered; also called a standard mask. Soft palate  The back part of the roof of the mouth that is made up of mucous membrane, muscular fibers, and mucous glands.

CHAPTER 2   Airway Management 

Uvula Fleshy tissue that hangs down from the soft palate and into the posterior portion of the oral cavity.  Vallecula  The space or  “pocket”  between the base of the tongue and the epiglottis.  Ventilation  The mechanical movement of gas or air into and out of the lungs.

 ANATOMY REVIEW  Upper Airway   The upper airway extends from the mouth and nose to the upper trachea. The upper airway functions as a  passageway for gas flow; for filtering, warming, and humidifying the air; and for protecting the surfaces of  the lower respiratory tract (Fig. 2.1). The upper airway also functions in phonation and in the senses of  smell and taste.  The nasal cavity and the mouth meet at the pharynx (ie, the throat). The pharynx extends from the nasal cavities to the larynx, and it includes three parts: the nasopharynx, the oropharynx, and the laryngopharynx or hypopharynx. The pharynx is a passageway that is common to both the respiratory and digestive systems. The separation of the respiratory and digestive tracts occurs immediately below the laryngopharynx.  The nasopharynx is located at the posterior end of the nasal cavity, and it extends to the tip of the uvula. The mucous lining of the nasopharynx filters, warms, and moistens the air. The nasopharynx contains two pharyngeal tonsils (also called adenoids ) and the eustachian tube openings. Tissues of the nasopharynx are extremely delicate and vascular. The improper or overly aggressive placement of tubes or  airways may result in significant bleeding.  The oropharynx begins at the uvula , which is fleshy tissue that hangs down from the soft palate and into the posterior portion of the oral cavity. The posterior portion of the oral cavity opens into the oropharynx. The oropharynx extends to the upper rim of the epiglottis. The epiglottis is a small piece of  cartilage located at the top of the larynx that prevents foreign material from entering the trachea during  swallowing. The oropharynx functions in respiration and digestion. The anterior oropharynx opens into the oral cavity, which comprises the lips, cheeks, teeth, tongue, and hard and soft palates ( Fig. 2.2). The

Frontal sinus Nasal bone Nasal cartilage Superior nasal concha

Sphenoidal sinus Internal naris

Middle nasal concha

Pharyngeal tonsil Opening for auditory tube

External naris

Nasopharynx

Inferior nasal concha

Soft palate

Hard palate

Uvula Palatine tonsil

Oral cavity

Oropharynx

Tongue Mandible Fauces

Epiglottis Hyoid bone

Laryngopharynx Larynx

Lingual tonsil Thyroid cartilage

Vestibular folds

Cricoid cartilage Trachea

True vocal folds Esophagus

Fig. 2.1  Structures of the upper airway. (From Applegate:  The anatomy and physiology learning system , ed 4, 2011, Saunders.)

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CHAPTER 2   Airway Management 

Philtrum Upper lip

Hard palate

Soft palate Uvula Palatine tonsil Tongue Fauces (opening)

Lower lip

Fig. 2.2  Frontal view into the open mouth showing the major structures within. (From Patton K, Thibodeau G:  Anatomy &  physiology , ed 7, St. Louis, 2013, Mosby.)

anterior roof of the oral cavity is formed by the maxillary bone and is called the hard palate. The posterior  portion of the roof of the mouth is called the soft palate because it is made up of mucous membrane, muscular fibers, and mucous glands. The cheeks form the walls, and the tongue dominates the floor of  the oral cavity. Located on the lateral walls of the oropharynx are a pair of palatine tonsils that can cause a  partial airway obstruction if they become excessively swollen. The space (or  “ pocket ”) between the base of  the tongue and the epiglottis is called the vallecula . When performing orotracheal intubation, the epiglottis is lifted out of the way to visualize the area during the passage of the tracheal tube between the  vocal cords. The vallecula is an important anatomic landmark to identify when intubating a patient with the use of a curved laryngoscope blade.  The laryngopharynx extends from the upper rim of the epiglottis to the glottis, which encompasses the true vocal cords and the space between them (ie, the glottic opening). Theglottis is the narrowest part  of the adult larynx. The laryngopharynx is connected to the esophagus, and the laryngopharynx functions in respiration and digestion.

ACLS Pearl In the unresponsive patient, a partial or complete airway obstruction can result when the muscles of  the tongue and laryngopharynx relax, thus allowing the tongue and other soft tissues to block the opening of the laryngopharynx.

 The larynx (ie, voice box) connects the pharynx to the trachea at the level of the cervical vertebrae. It  conducts air between the pharynx and the lungs; it prevents food and foreign substances from entering  the trachea; and it houses the vocal cords, which are involved in speech production. The larynx is a tubular  structure made up of muscles, ligaments, and nine cartilages (see  Fig. 2.1). The thyroid cartilage (ie,  Adam’s apple) is the largest and most superior cartilage of the larynx. It is more pronounced in adult  males than adult females. The thyroid gland lies over the outer surface of the thyroid cartilage. The pyramid-shaped arytenoid cartilages of the larynx serve as a point of attachment for the vocal cords.  The arytenoid cartilages often serve as an important landmark during intubation.  The cricoid cartilage is inferior to the thyroid cartilage. It is considered the first tracheal ring, and it  is the only complete ring of cartilage in the larynx. The other cartilages of the larynx are incomplete

CHAPTER 2   Airway Management 

C-shaped rings on the posterior surface. The C-shaped rings are open to permit the esophagus, which lies behind the trachea, to bulge forward as food moves to the stomach. The narrowest diameter of the airway in infants and children who are younger than age 10 is at the cricoid cartilage. The  cricothyroid membrane is a fibrous membrane that is located between the cricoid and thyroid cartilages. This site may  be used for surgical and alternative airway placement.

ACLS Pearl Stimulation of the larynx by a laryngoscope blade, tracheal tube, or suction catheter can result in bradycardia, hypotension, and a decreased ventilatory rate because the larynx is innervated with nerve endings from the vagus nerves. Monitor the patient closely for these effects and discontinue the treatment that is causing them if they appear.

Lower Airway   The lower airway extends from the lower trachea to the alveoli, and it functions in the exchange of oxygen and carbon dioxide. Air moves from the larynx through the glottic opening and into the trachea. The adult trachea is about twelve centimeters (cm) in length and has an inner diameter of about 2 cm. It  divides or bifurcates into two separate tubes called the  left  and right primary bronchi  (Fig. 2.3). The point   where the trachea divides into the right and left primary bronchi is called the carina . The right bronchus serves three lobes of the lung and the left bronchus serves two. The right primary bronchus is shorter,  wider, and straighter or less angled than the left, because the heart occupies space in the left chest cavity.

Fig. 2.3 An adult and infant trachea showing the different angles of primary bronchi bifurcation. (From Kacmarek R, Stoller J, Heuer A: Egan  s fundamentals of respiratory care , ed 11, Elsevier, 2017.) ’  

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 Therefore a tracheal tube that is inserted too far or foreign material that is aspirated is more likely to enter  the right primary bronchus than the left.  The walls of the trachea are supported and held open by a series of 16 to 20 C-shaped cartilaginous rings. The area between the tracheal cartilages is composed of connective tissue and smooth muscle,  which allow for changes in the diameter of the trachea. Tracheal smooth muscle is innervated by the parasympathetic division of the autonomic nervous system. Internally, the trachea is lined with a mucous membrane that contains cilia as well as mucusproducing cells. The cilia sweep foreign materials out of the airway and the mucus can also trap particulate matter that is then expelled during coughing. Obstruction of the trachea will result in death if not  corrected within minutes.  The primary bronchi branch into narrowing secondary and tertiary bronchi, which then branch into bronchioles. As the bronchi continue to divide into the lung tissue and become smaller passageways, they  become bronchioles. Bronchioles are composed entirely of smooth muscle that is supported by connective tissue. Bronchioles are responsible for regulating the flow of air to the alveoli. The stimulation of  beta 2  receptor sites in the bronchioles results in relaxation of bronchial smooth muscle. After multiple subdivisions, the bronchioles divide into tiny tubes calledalveolar ducts , where gas exchange first becomes possible. These ducts end in alveoli, which are tiny, hollow air sacs. Each lung of an average adult contains about 300 million alveoli, and each alveolus is surrounded by a pulmonary capillary. Oxygen diffuses through the thin walls of the alveoli to the capillaries, and carbon dioxide diffuses from the capillaries to the alveoli.

 THE PATIENT WITH RESPIRATORY COMPROMISE [Objective 1] Respiratory complaints are common in patients of all ages. Respiratory distress, respiratory failure, and respiratory arrest reflect increasing levels of severity of respiratory compromise. Signs of adequate ventilation include the ability to breathe at a regular rate and within normal limits for the patient ’s age, an equal rise and fall of the chest with each breath, an adequate depth of breathing (ie, tidal volume), and the ability to speak in full sentences without pausing. Signs of inadequate ventilation include the following: A breathing rate that is too fast or slow for the patient ’s age • Abnormal breath sounds (stridor, wheezing, crackles, silent chest, unequal) • Abnormal work (effort) of breathing (retractions, accessory muscle use, sweating, tripod position, • flared nostrils, pursed lips) An irregular breathing pattern • • Anxious appearance, concentration on breathing  •   Confusion, restlessness Depth of breathing that is unusually deep or shallow  • Inability to speak in complete sentences • Inadequate chest wall movement (paradoxical, splinting, asymmetric) • Pain with breathing  • Signs of respiratory distress reflect an attempt to compensate for hypoxia and may include mental status changes (eg, anxiety, restlessness, decreased ability to concentrate), nasal flaring, pallor or mottling, retractions, stridor, tachypnea, wheezing, and the use of accessory muscles of breathing. Because the causes of respiratory distress are many, possible therapeutic interventions include allowing the patient  to assume a position of comfort, the administration of supplemental oxygen if indicated, and pharmacologic therapy (eg, bronchodilators). Uncorrected respiratory distress may lead to respiratory failure.  Acute respiratory failure develops when the exchange of oxygen and carbon dioxide within the lungs is inadequate. Hypoxemic respiratory failure  refers to respiratory failure associated with failure to oxygenate,  whereas  hypercarbic respiratory failure  is the failure to ventilate (Casserly & Rounds, 2010). Signs of  impending respiratory failure include agitation, irritability, confusion, lethargy, accessory muscle use, nasal flaring, pursed-lip breathing, retractions, tachypnea, and pallor, mottling, or cyanosis despite oxygen therapy. Although tachycardia is often seen with early respiratory failure, the patient may become bradycardic with impending respiratory arrest. Depending on its cause and severity, possible therapeutic interventions for respiratory failure may include suctioning, administration of supplemental oxygen, noninvasive positive pressure ventilation (NPPV), BMV, and treatment of specific contributing or causative factors.

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 With respiratory arrest, the patient is unresponsive with no visible chest rise, no ventilatory effort, and limp muscle tone. Therapeutic interventions include the use of manual maneuvers to open the airway, the removal of a foreign body if present, insertion of an oral or nasal airway, suctioning, BMV with supplemental oxygen, possible insertion of an advanced airway by an appropriately trained clinician, and treatment of specific contributing or causative factors.

Patient Assessment [Objective 2]  As you approach the patient with a respiratory complaint, form a general impression to determine  whether the patient is sick (ie, unstable) or not sick (ie, stable) and to determine the urgency of further  assessment and care. When forming a general impression, an altered mental status, an inability to maintain ventilatory effort, and/or the presence of mottling or cyanosis are red flags that suggest imminent  respiratory arrest and warrant  immediate   intervention (McEvoy, 2013). Flaring nostrils and the use of  accessory muscles are signs that suggest the patient is struggling to breathe. Noting the patient ’s position may be helpful in assessing the severity of the patient ’s respiratory problem. For example, a patient who is sitting upright with his elbows braced on a table or with his hands on his knees and elbows out while leaning forward is said to be tripoding   or assuming a   tripod position. If abnormal findings are present, move quickly and proceed immediately to the primary survey and begin emergency care. If the patient ’s condition does not appear to be urgent, work at a reasonable pace and proceed systematically with your  patient assessment. Because his or her condition can quickly change, it is important to reassess the patient often. If the patient is responsive, ask the patient questions to determine his or her level of responsiveness and the adequacy of his or her airway and breathing. Observe for agitation, confusion, restlessness, or  combativeness, which may be the result of hypoxia. Also observe if the patient is able to speak in sentences before requiring a breath or if he or she experiences shortness of breath after speaking only a few   words. If the patient is unresponsive, manual maneuvers may be needed to open the patient ’s airway. Manual airway maneuvers are discussed later in this chapter.  The evaluation of a patient ’s breathing should include an assessment of the patient ’s tidal volume (ie, depth of breathing), ventilation rate, and symmetry of movement with each breath. Ventilation (which is often misnamed respiration) is the mechanical movement of air into and out of the lungs. Respiration is the exchange of oxygen and carbon dioxide during cellular metabolism. During normal, quiet breathing, an adult male moves an average of 500 mL (5 to 7 mL/kg) of air into and out of the respiratory tract with each breath (Douce, 2009); this amount is called the tidal volume. Chest expansion should be adequate  with sufficient tidal volume to make the chest rise equally with no excessive use of accessory muscles during inspiration or expiration. Look for signs of increased work of breathing such as pursed-lip breathing, use of accessory muscles, leaning forward to inhale, or retractions. Frequently auscultate breath sounds to detect decreased ventilation, crackles, wheezes, or rhonchi. If breathing is inadequate, provide supplemental oxygen if indicated and, if necessary, provide positive pressure ventilation. Oxygen delivery  devices and techniques of positive pressure ventilation are discussed later in this chapter.  Assess the patient ’s heart rate, pulse quality, and skin temperature, color, and moisture. Obtain a  Glasgow Coma Scale score, assess the need for a defibrillator, and expose pertinent areas of the patient  for further examination as necessary. Obtain the patient ’s vital signs, attach a pulse oximeter, cardiac monitor, and blood pressure monitor, and obtain a focused history. Pulse Oximetry  [Objective 2] Oxygenation is the process of getting oxygen into the body and to its tissues for metabolism. A pulse oximeter , which is commonly called a   pulse ox, is a small instrument with a light sensor that quickly  calculates the percentage of hemoglobin that is saturated with oxygen in a pulsating capillary bed. This calculation is called the saturation of peripheral oxygen or  SpO  2. The oximeter displays this value as a percentage and the patient ’s pulse rate on its screen. The oximeter ’s sensor is typically applied to a finger  (Fig. 2.4), but the forehead, an earlobe, or a toe can also be used with the selection of a sensor that is appropriate for the chosen site. For example, an adhesive or clip-on sensor can be used for a finger, but a forehead sensor is usually adhesive. Pulse oximetry sensors may be disposable or reusable. When using a disposable sensor, assess the site every 2 to 4 hours and replace the sensor every 24 hours ( Schutz, 2011). Assess the site for decreased

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Fig. 2.4  Finger application of a pulse oximeter sensor. (From Bonewit-West K: Clinical procedures for medical assistants , ed 9, St. Louis, 2015, Saunders.)

temperature, decreased peripheral pulse, cyanosis, and tissue integrity. Reusable clip-on sensors are generally used when spot-checking oximetry values, when monitoring continuously for less than 10 minutes, and when monitoring patients who are immobile. When a reusable sensor is applied, assess the site every  2 hours and change the site every 4 hours (Schutz, 2011). Possible indications for continuous pulse oximetry monitoring include the following: A patient with a critical or unstable airway  • A patient who requires oxygen therapy  • During the intrahospital and interhospital transfer of a critically ill patient  • •   During hemodialysis A patient who has a condition or who is undergoing a procedure that alters oxygen saturation or a  • patient who has a condition or history that suggests a risk for significant desaturation Pulse oximetry may be inaccurate in situations that involve poor capillary blood flow, an abnormal hemoglobin concentration, or an abnormal shape of the hemoglobin molecule. Examples of conditions that may give misleading results are listed in Box 2.1.

ACLS Pearl  A pulse oximeter is an adjunct to—not a replacement of —vigilant patient assessment. You must correlate your assessment findings with pulse oximeter readings to determine appropriate treatment interventions for the patient.

BOX 2.1 • • •

•

Factors Affecting the Accuracy of Pulse Oximetry Readings

Anemia (conflicting evidence) Artificial acrylic nails (conflicting evidence) Bright ambient light such as sunlight, or surgical, fluorescent, or heating lamps (conflicting evidence) Carbon monoxide or cyanide poisoning or  presence of other molecules that bind to hemoglobin

• • • • •

Darkor metallicnail polish (conflictingevidence) Dark skin pigmentation Medications (eg, vasoconstrictors) Motion artifact Poorperipheralperfusionas a result of cardiac arrest, shock, hypotension, or hypothermia

Carbon Dioxide Monitoring [Objective 2] Carbon dioxide is produced during cellular metabolism, carried to the lungs by the circulatory system, and excreted by the lungs during ventilation. Capnography   is the continuous analysis and recording of  CO2 concentrations in respiratory gases. Capnography provides health care professionals with breath-tobreath patient information, thereby enabling the early recognition of hypoventilation, apnea, or airway  obstruction and thus preventing hypoxic episodes. The monitoring of exhaled carbon dioxide with either  capnometry or capnography can detect changes in metabolism, circulation, respiration, the airway, or the respiratory system. Exhaled carbon dioxide detection devices are used in conjunction with the history and clinical assessment of the patient, which may include mental status, lung sounds, pulse rate, and skin color. Examples of situations in which exhaled CO 2  monitoring is commonly used include the following:

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Assessment of the adequacy of ventilation in patients with altered mental status, bronchospasm, asthma, chronic obstructive pulmonary disease (COPD), anaphylaxis, heart failure, drug overdose, stroke, shock, or circulatory compromise Confirmation of correct tracheal tube placement (capnography should not be used as the only means of  • assessing tracheal tube placement) and continuous monitoring of tracheal tube position (including  during patient transport) Evaluation of the effectiveness of chest compressions during resuscitation efforts and the detection of  • the return of spontaneous circulation Monitoring of exhaled CO2  levels in patients with suspected increased intracranial pressure • Procedural sedation and analgesia  •  Alveolar CO 2 and arterial CO 2  (Pa CO2) values are closely related in patients with normal cardiopulmonary function, and they usually range between 35 and 45 millimeters of mercury (mm Hg). In patients  with normal lung and cardiac function, normal values for end-tidal carbon dioxide (EtCO2) range between 33 mm Hg and 43 mm Hg. This is dependent on adequate ventilation and adequate perfusion: a change in either factor will increase or decrease the amount of exhaled CO 2. Digital capnometers use infrared technology to analyze exhaled gas. These devices provide a quantitative measurement of the exhaled CO 2, in that they provide the exact amount of CO 2   exhaled (Fig. 2.5). This is beneficial as trends in CO2 levels can be monitored and the effectiveness of treatment  can be determined. In conjunction with clinical assessment, continuous waveform capnography is the preferred method for confirming tracheal tube placement, for the continuous monitoring of tracheal tube position (including during patient transport), and for the evaluation of chest compressions during resuscitative efforts and detection of the return of spontaneous circulation. •

ACLS Pearl Interpreting capnograms should be done with the use of a systematic approach that includes the evaluation of height, contour, baseline, frequency, and rhythm. Capnogram interpretation is beyond the scope of this text and the Advanced Cardiac Life Support course.

 A colorimetric capnometer functions through a pH change that occurs with the breath of a patient.  The patient ’s breath causes a chemical reaction on pH-sensitive litmus paper housed in the detector.  The capnometer is placed between a tracheal tube or advanced airway device and a ventilation

Fig. 2.5  A combination handheld capnograph and pulse oximeter. (Copyright ©2016 Medtronic. All rights reserved. Used with the permission of Medtronic.)

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Fig. 2.6 Colorimetric exhaled carbon dioxide detector. (Copyright ©2016 Medtronic. All rights reserved. Used with the permission of Medtronic.)

device (Fig. 2.6). The presence of CO2, which is evidenced by a color change on the colorimetric device, suggests placement of the tube in the trachea. A colorimetric capnometer is qualitative in that it simply  shows the presence of CO2. It has no ability to provide an actual CO2 reading or to indicate the presence of hypercarbia, and it provides no opportunity for ongoing monitoring to ensure that the tube remains in the trachea. A lack of CO2 (ie, no color change) suggests tube placement in the esophagus, particularly in patients with a perfusing rhythm (ie, not in cardiac arrest). Some manufacturers of colorimetric capnometers recommend ventilating the patient at least six times before attempting to use an exhaled CO2  detector to assess tracheal tube placement. The rationale for this action is to quickly wash out  any retained CO2  that is present in the stomach or esophagus as a result of BMV. Any CO 2  that is detected after six positive pressure ventilations can be presumed to be from the lungs ( Ornato, et al., 1992; Sum Ping, et al., 1992). Colorimetric capnometers are susceptible to inaccurate results as a result  of the age of the paper and exposure of the paper to the environment. A colorimetric capnometer may not  change color if the paper is contaminated with patient secretions (eg, vomitus) or acidic drugs (eg, tracheally administered epinephrine) (Cantineau, et al., 1994). When CO2  is not detected, an alternative method should be used to confirm tracheal tube placement, such as direct visualization or the use of an esophageal detector device (EDD).

ACLS Pearl Pulse oximetry provides important information about oxygenation, but does not provide information about theeffectiveness of a patient’s ventilation. Capnography provides information about the effectiveness of ventilation, but does not measure oxygenation.

OXYGEN DELIVERY DEVICES  The fraction of inspired gas that is oxygen is abbreviated as FiO2 and is often expressed as a percentage. Research has shown that routine use of supplemental oxygen in cardiac patients may have unto ward effects, including increased coronary vascular resistance, reduced coronary blood flow, and increased risk of mortality ( Amsterdam, et al., 2014). Indications for supplemental oxygen administration include clinically significant hypoxemia (ie, oxygen saturation less than 90%), heart failure, dyspnea, cyanosis, or when other high-risk features of hypoxemia are present ( Amsterdam, et al., 2014; O’Gara, et al., 2013).

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Nasal Cannula [Objective 3]  A nasal cannula , which is also called nasal prongs, is a piece of plastic tubing with two soft prongs that  project from the tubing. The prongs are inserted into the patient ’s nostrils, and the tubing is then secured to the patient ’s face (Fig. 2.7). Oxygen flows from the cannula into the patient ’s nasopharynx, which acts as an anatomic reservoir. Factors that influence the Fi O2 delivered by a nasal cannula include the oxygen flow rate, the patient ’s ventilatory rate and tidal volume, and the anatomy and geometry of the patient ’s nasal cavity, nasopharynx, and oropharynx ( Ward, 2013). For many years it was thought that for every liter-per-minute (L/min) increase in oxygen flow when using a nasal cannula, the effective FiO2  increased by about 4 percentage points. For example, giving  supplemental O2  at 1 L/min by cannula would raise the Fi O2  to about 24%, 2 L/min would raise it  to 28%, and up to 6 L/min would raise it to 44% (Markovitz, et al., 2010). Research has shown these estimates of cannula performance to be overly optimistic ( Ward, 2013). In a 2010 study, the FiO2 levels produced in the trachea at oxygen flow rates of 1, 3, and 5 L/min were measured while subjects breathed at a normal rate and pattern. Researchers found the delivered Fi O2  to be about 23% at 1 L/min, about  28% at 3 L/min, and about 32% at 5 L/min (Markovitz, et al., 2010). Delivered FiO2 decreases considerably during conditions associated with dyspnea ( Ward, 2013). Advantages and disadvantages of using a  nasal cannula are shown in Box 2.2.

Fig. 2.7  Low-flow nasal cannula. (From Potter PA & Perry AG:  Fundamentals of nursing: Concepts, process, and practice, ed 8, St. Louis, 2013, Mosby.)

BOX 2.2

Low-Flow Nasal Cannula—Advantages and Disadvantages

 ADVANTAGES • • • • • • •

Comfortable and well tolerated by most  patients Does not interfere with patient assessment or impede patient communication with health care personnel Allows for talking and eating No rebreathing of expired air Can be used with mouth breathers Useful for patients who are predisposed to carbon dioxide retention Can be used for patients who require oxygen but who cannot tolerate a nonrebreather mask 

DISADVANTAGES • • • • • • •

Can only be used in a spontaneously breathing patient    Easily displaced Nasal passages must be open Drying to mucous membranes; may cause sinus pain Tubing may cause skin breakdown or irritation Deviated septum and mouth breathing may reduce FiO2 Oxygen flow rates of more than 6 L/min do not enhance delivered oxygen concentration

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High-flow nasal cannula (HFNC) systems are being used with increasing frequency for some critically  ill patients. Components needed to provide HFNC oxygen include a nasal cannula that can accommodate high inlet flow, a high-flow oxygen flowmeter, and a humdifier ( Ward, 2013). Commercially available humidified HFNC systems use flow rates of 5 to 40 L/min and deliver an Fi O2  of close to 100% (Reardon, et al., 2014a).

Simple Face Mask  [Objective 3]  A simple face mask , which is also called a  standard mask, is a plastic reservoir that has been designed to fit over the nose and mouth of a spontaneously breathing patient. The mask is secured around the patient ’s head by means of an elastic strap. The internal capacity of the mask produces a reservoir  effect. Small holes on each side of the mask allow for the passage of inspired and expired air. Supplemental oxygen is delivered through a small-diameter tube connected to the base of the mask  (Fig. 2.8).  When using a simple face mask, the oxygen flow rate must be higher than 5 L/min to flush the buildup of the patient ’s exhaled carbon dioxide from the mask. At 5 to 10 L/min, the simple face mask  can deliver an inspired oxygen concentration of approximately 35% to 60%. The patient ’s actual inspired oxygen concentration will vary, because the amount of air that mixes with supplemental oxygen is dependent on the patient ’s inspiratory flow rate. Advantages and disadvantages of using a simple face mask are shown in Box 2.3.

Exhalation ports

Oxygen inlet

Fig. 2.8 Simple face mask. (From Kacmarek, Stoller, Heuer: Egan's fundamentals of respiratory care , ed 10, St. Louis, 2013, Mosby.)

BOX 2.3

Simple Face Mask —Advantages and Disadvantages

 ADVANTAGES •

Higher oxygen concentration delivered than by nasal cannula

DISADVANTAGES • • • • • • • •

Can only be used in a spontaneously breathing patient  Not tolerated well by severely dyspneic patients Can be uncomfortable Difficult to hear the patient speaking when the device is in place Must be removed at meals Requires a tight face seal to prevent the leakage of oxygen Side holes in the mask permit inhalation of room air Oxygen flow rates of more than 10 L/min do not enhance delivered oxygen concentration

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Partial Rebreather Mask  [Objective 3]  A partial rebreather mask is similar to a simple face mask, but it has an attached oxygen-collecting device (ie, reservoir) at the base of the mask that is filled before patient use (Fig. 2.9A). When the patient  breathes in, 100% oxygen is drawn into the mask from the reservoir (bag). When the patient breathes out, oxygen enters the bag from the oxygen source and some of the patient ’s exhaled air enters the bag (ie, an amount that is approximately equal to the volume of the patient ’s anatomic dead space). The amount  ofCO2 that is rebreathed is negligible as long as the oxygen flow keeps the bag from collapsing more than about one-third during inhalation (Heuer, 2013).

Valves

Reservoir bag

A

Reservoir bag

B

Fig. 2.9 A, Partial rebreather mask. B, Nonrebreather mask. (From Kacmarek, Stoller, Heuer: Egan's fundamentals of respi-  ratory care , ed 10, St. Louis, 2013, Mosby.)

BOX 2.4

Partial Rebreather Mask —Advantages and Disadvantages

 ADVANTAGES •

Higher oxygen concentration delivered than by nasal cannula

DISADVANTAGES • • • • • • • •

Can only be used in a spontaneously breathing patient  Not tolerated well in severely dyspneic patients Can be uncomfortable Difficult to hear the patient speaking when the device is in place Must be removed at meals Requires a tight face seal to prevent the leakage of  oxygen May cause skin irritation Lacks inspiratory valve; thus exhaled air mixes with inspired air

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 The oxygen concentration of the patient ’s exhaled air, in combination with the supply of 100% oxygen, allows for the use of oxygen flow rates that are lower than those that are necessary for a nonrebreather  mask. Depending on the patient ’s breathing pattern, the mask fit, and the oxygen flowmeter setting, oxygen concentrations of 35% to 60% can be delivered when an oxygen flow rate is used that prevents the reservoir bag from completely collapsing on inspiration (ie, typically 6 to 10 L/min). Advantages and disadvantages of using a partial rebreather mask are shown in  Box 2.4.

Nonrebreather Mask  [Objective 3]  A nonrebreather mask, also called a nonrebreathing mask, is similar to a partial rebreather mask, but it does not permit the mixing of the patient ’s exhaled air with 100% oxygen. A one-way valve between the mask  and the reservoir bag and a flap over one of the exhalation ports on the side of the mask prevent the inhalation of room air (Fig. 2.9B). When the patient breathes in, oxygen is drawn into the mask from the reservoir (ie, bag) through the one-way valve that separates the bag from the mask. When the patient  breathes out, the exhaled air exits through the open side port on the mask. The one-way valve prevents the patient ’s exhaled air from returning to the reservoir bag (thus the name nonrebreather ). This ensures a  supply of 100% oxygen to the patient, with minimal dilution from room air.  A nonrebreather mask is the delivery device of choice when high concentrations of oxygen are needed for the spontaneously breathing patient. Depending on the patient ’s breathing pattern, the fit of the mask, and the oxygen flowmeter setting, oxygen concentrations of 60% to 80% can be delivered when an oxygen flow rate (typically a minimum of 10 L/min) is used that prevents the reservoir bag from collapsing completely on inspiration (Heuer, 2013). Inflate the reservoir bag with oxygen before  placing the nonrebreather mask on the patient. Advantages and disadvantages of using a nonrebreather mask are shown in Box 2.5. A summary of oxygen percentages by device is shown in Table 2.1.

ACLS Pearl When using a partial rebreather or nonrebreather mask, make sure that the bag does not collapse when the patient inhales. Should the bag collapse, increase the delivered oxygen by 2 L increments until the bag remains inflated during inhalation. The reservoir bag must remain at least two-thirds full so that sufficient supplemental oxygen is available for each breath.

BOX 2.5

Nonrebreather Mask —Advantages and Disadvantages

 ADVANTAGES •

•

Higher oxygen concentration delivered than by nasal cannula, simple face mask, and partial rebreather mask  Inspired oxygen is not mixed with room air

DISADVANTAGES • • • • • •

•

Can only be used with a spontaneously breathing patient  Not tolerated well in severely dyspneic patients Can be uncomfortable Difficult to hear the patient speaking when the device is in place Must be removed at meals Mask must fit snugly on the patient ’s face to prevent room air from mixing with oxygen inhaled from the reservoir bag May cause skin irritation

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TABLE 2.1

Oxygen Percentage Delivery by Device

Device

Approximate Inspired Oxygen Concentration

Nasal cannula Simple face mask Partial rebreather mask

23% to 32% 35% to 60% 35% to 60%

Nonrebreather mask

60% to 80%

Liter Flow (Liters/Minute) 1 to 5 5 to 10 Typically, 6 to 10 to prevent bag collapse on inspiration Typically, a minimum of 10 to prevent bag collapse on inspiration

MANUAL AIRWAY MANEUVERS  The most common cause of a partial airway obstruction in an unresponsive patient is the result of a loss of  muscle tone, which causes the tongue to fall back into the pharynx and block airflow. Manual airway  maneuvers are performed to lift the tongue off the back of the throat and open the airway. If the unresponsive patient is breathing, snoring sounds are a sign of airway obstruction from displacement of the tongue. If the patient is not breathing, airway obstruction from the tongue may go undetected until positive pressure ventilation is attempted. Ventilating a nonbreathing patient with an airway  obstruction is difficult. If the airway obstruction is caused by the tongue, repositioning the patient ’s head and jaw may be all that is needed to open the airway.

Head Tilt–Chin Lift [Objective 4]  The head tilt  – chin lift is the preferred technique for opening the airway of an unresponsive patient without suspected cervical spine injury (Kleinman, et al., 2015). Follow these steps to perform a head tilt  – chin lift: 1. Place the patient in a supine position. 2. Place one hand on the patient ’s forehead, and apply downward pressure with your palm to gently tilt  the patient ’s head back (Fig. 2.10). 3. Place the tips of the fingers of your other hand under the bony part of the patient ’s chin, and gently lift  up and pull the jaw forward. Positioning your fingers under the bony part of the patient ’s chin is important because compression of the soft tissue under the patient ’s chin can obstruct the airway. 4. If needed, open the patient ’s mouth by pulling down on the patient ’s lower lip using the thumb of the same hand used to lift the chin.

Fig. 2.10 Opening the airway with a head tilt –chin lift maneuver. (From Kacmarek, Stoller, Heuer: Egan's fundamentals of  respiratory care , ed 10, St. Louis, 2013, Mosby.)

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Jaw Thrust [Objective 4]  A jaw thrust maneuver may be performed with or without an accompanying head tilt. For patients who are unresponsive without  any risk of spinal injury, perform the following technique: 1. With the patient supine, position yourself above the patient ’s head or at his or her side, looking at  the face. 2. Place your fingers on each side of the lower jaw at the angle of the jaw near the bottom of the patient ’s ears. 3. Lift the jaw forward toward the patient ’s face and gently open the mouth. 4. Gently tilt the patient ’s head while maintaining displacement of the lower jaw.  The jaw thrust without neck extension maneuver (also called the modified jaw thrust ) is the technique that is recommended for opening the airway when cervical spine injury is suspected. Perform the following for a jaw thrust without neck extension maneuver: 1. Ensure that the patient is in a supine position. 2. While stabilizing the patient ’s head in a neutral position, grasp the angles of the patient ’s lower jaw   with your fingertips (Fig. 2.11). 3. Displace the lower jaw forward.  The jaw thrust without neck extension maneuver is a difficult technique for one person to manage. In most cases, one rescuer is needed to displace the patient ’s lower jaw forward while a second rescuer ventilates the patient. Health care professionals should use the head tilt  – chin lift maneuver to open the air way if use of the jaw thrust without neck extension maneuver is unsuccessful (Kleinman, et al., 2015). Manual airway maneuvers are summarized in Table 2.2.

Fig. 2.11 The jaw thrust without neck extension maneuver is used to open the airway when cervical spine injury is suspected. (From Kacmarek, Stoller, Heuer: Egan's fundamentals of respiratory care , ed 10, St. Louis, 2013, Mosby.)

TABLE 2.2

Manual Airway Maneuvers

Considerations

Head Tilt –Chin Lift

Indications

•

 Advantages

• • •

Disadvantages

• •

Unresponsive patient with no mechanism for cervical spine injury Simple to perform No equipment required   Noninvasive Does not protect the lower airway from aspiration May cause spinal movement 

Jaw Thrust without Neck Extension Unresponsive patient with possible cervical spine injury • No equipment required •   Noninvasive •

• • • •

Difficult to maintain Second rescuer needed for bag-mask  ventilation Does not protect the lower airway from aspiration May cause spinal movement 

CHAPTER 2   Airway Management 

SUCTIONING [Objective 5] Suctioning is performed for the following reasons: To remove vomitus, saliva, blood, or foreign material from the patient ’s airway  • To maintain patency of an artificial airway (eg, ETT, tracheostomy tube) • To improve gas exchange by allowing air to pass through to the lower airway  • To obtain secretions for diagnosis • Rigid suction catheters, also called tonsil tip  or  Yankauer  catheters, are made of hard plastic and angled to help with the removal of secretions from the mouth and throat (Fig. 2.12). Because of its size, a rigid suction catheter is not used to suction the nares, except externally. The catheter typically has one large and several small holes at the distal end through which particles may be suctioned. The HI-D Big Stick suction tip (SSCOR, Inc., Sun Valley, CA) is a large-bore suction tip that is effective in clearing vomitus and secretions from the upper airway (Fig. 2.13). Soft suction catheters are also called whistle tip, flexible, or   French catheters. They are long, narrow, flexible pieces of plastic that are used to clear blood or mucus from the oropharynx or nasopharynx, an ETT, or a tracheostomy tube (Fig. 2.14). When suctioning the lower airway, the outer diameter of the suction catheter should be no more than half the internal diameter of the tracheal or tracheostomy tube to minimize the risk of atelectasis and hypoxemia when suction is applied ( Tiffin, et al., 1990).

Fig. 2.12 A rigid suction catheter is used to remove secretions from the mouth and throat. (From Perry, Potter: Clinical  nursing skills & techniques , ed 8, St. Louis, 2013, Mosby.)

HI-D Big Stick suction tip

5/16” suction tubing

Fig. 2.13 TheHI-D BigSticksuction tipis effective in clearing vomitus andsecretions from the upperairway. (From Roberts J: Roberts and Hedges    clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.) ’  

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CHAPTER 2   Airway Management 

Fig. 2.14 A soft suction catheter is used to remove secretions from the lower airway. (From Perry, Potter: Clinical nursing  skills & techniques , ed 8, St. Louis, 2013, Mosby.)

 A suction catheter is inserted without applying suction. Suction is applied as the catheter is withdrawn and should not be applied for more than 10 seconds to avoid hypoxia. After suctioning, reevaluate airway  patency and auscultate lung sounds. Document the amount, color, and consistency of any secretions that  are obtained. Possible complications of suctioning are shown in Box 2.6.

ACLS Pearl  Although microorganisms are present throughout the airway, the mouth and throat are considered “clean”  areas and the portion of the airway below the glottis is considered “sterile”   because the upper airway contains more microorganisms than the lower airway. When a patient requires both upper and lower airway suctioning, change catheters after suctioning the upper airway and before suctioning the lower airway. Alternately, the same suction catheter may be used if lower airway suctioning is performed   before upper airway suctioning. Suctioning the lower airway first leads to less potential for transmission of microorganisms to the lungs.

BOX 2.6 • •

• • •

  Suctioning—Possible Complications

  Arrhythmias   Bradycardia and hypotension from vagal stimulation   Bronchospasm   Hemorrhage   Hypertension

• • • • • •

  Hypoxia Increased intracranial pressure Local swelling   Tachycardia Tracheal infection Tracheal trauma

 AIRWAY ADJUNCTS Manualmaneuversfacilitatetheopeningofanairway.Airwayadjuncts,suchaspharyngealairways,aredevices that assist in keeping the airway open by keeping the tongue away from the posterior wall of the pharynx.

Oral Airway  [Objective 6]  An oral airway, also called an oropharyngeal airway  or   OPA, is a J-shaped plastic device that is used to create an air passage between the patient ’s mouth and the posterior wall of the pharynx. Because oral airway insertion may provoke vomiting and thus increase the risk of aspiration in a patient with an intact  gag reflex, indications for insertion include patients who are unresponsive and have no gag reflex. An oral airway may be used as a bite block after the insertion of a tracheal tube or an orogastric tube. Oral airways are available in a variety of sizes that range from 0 for neonates up to 6 for large adults.  The size of the airway is based on the distance, in millimeters, from the flange to the distal tip.  Thereare two main oral airwaydesigns.The Guedelairwayhas a tubulardesign with a single centerchannelthat allowsfor ventilation and thepassageof a suction catheter (Fig.2.15A). TheBerman airway has two

CHAPTER 2   Airway Management 

Oropharyngeal tube in place Flange (1)

A

Body (2)

Channel (3) Flange (1) Body (2)

Channel (3)

B

C

Fig. 2.15 A, Guedel oral airway. B, Berman oral airway. C, Oral airway in place. (From Kacmarek, Stoller, Heuer:  Egan's  fundamentals of respiratory care , ed 10, St. Louis, 2013, Mosby.)

airway channelsalong each sideof thedevice through which a suctioncatheter canbe passed to removesecretionsfromthebackofthethroat(Fig.2.15B).Whencorrectlypositioned,theflangeofthedevicerestsonthe patient ’s lips or teeth. The distal tip lies between the base of the tongue and the back of the throat, thereby  preventing the tongue from blocking the airway (Fig. 2.15C). Air passes around and through the device. Proper oral airway size is determined by holding the device against the side of the patient ’s face and selecting an airway that extends from the corner of the mouth to the tip of the earlobe or to the angle of  the jaw (Fig. 2.16). To prevent inaccurate measurements for patients who experience facial drooping after  a stroke, some experts recommend measuring from the first incisor or from the center of the lips to the tip of the earlobe or to the angle of the jaw. If an oral airway is too long, it may press the epiglottis against the entrance of the larynx, which may result in a complete airway obstruction (Fig. 2.17). If the airway is too short, it will not displace the tongue, and it may advance out of the mouth ( Fig. 2.18).  When inserting an oral airway into a patient ’s mouth, hold the device at its flange end and insert it   with the tip pointing toward the roof of the mouth (Fig. 2.19). As the distal end nears the back of the throat, rotate the airway 180 degrees so that it is positioned over the tongue. Alternatively, the airway can be inserted sideways and rotated 90 degrees into position. When the oral airway is inserted properly, the flange should rest comfortably on the patient ’s lips or teeth. The proper placement of the device is confirmed by ventilating the patient. If the airway is placed correctly, chest rise should be visible and breath sounds should be present on auscultation of the lungs during ventilation. If the patient is not breathing or  if his or her breathing is inadequate, begin positive pressure ventilation.  Another method of oral airway insertion requires the use of a tongue blade to depress the tongue. If  this method is used, the airway is inserted with its tip facing the floor of the patient ’s mouth (ie, curved side down). With the use of the tongue blade to depress the tongue, the oral airway is advanced gently  into place over the tongue. If the patient ’s gag reflex returns or if he or she spontaneously attempts to displace the airway, remove the airway to minimize the risk of aspiration.

Fig. 2.16 Select an oral airway of appropriate size. (From Roberts J: Roberts and Hedges   clinical procedures in emergency  ’  

medicine , ed 6, Philadelphia, 2014, Saunders.)

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CHAPTER 2   Airway Management 

Fig. 2.17 An oral airway that is too long may press the epiglottis against the entrance of the larynx, which may result in a complete airway obstruction. (From McSwain N, Paturas J: The basic EMT , ed 2, 2003, Mosby.)

Fig. 2.18 An oral airway that is too short will not displace the tongue, and it may advance out of the mouth. (From McSwain N, Paturas J: The basic EMT , ed 2, 2003, Mosby.)

Fig. 2.19   Open the patient ’s mouth and insert the oral airway with the tip pointing toward the roof of the mouth. (From Roberts J: Roberts and Hedges    clinical procedures in emergency medicine , ed 6, Philadelphia, 2014, Saunders.) ’  

Nasal Airway  [Objective 6]  A nasal airway (also called a  nasopharyngeal airway, NPA, or  nasal trumpet ) is a soft, uncuffed tube made from rubber or plastic polymers that is designed to keep the tongue away from the back of the throat. Indications for the use of a nasal airway include unresponsive patients or those with an altered level of  consciousness who continue to have an intact gag reflex but who need assistance with maintaining an

CHAPTER 2   Airway Management 

Fig. 2.20 Nasal airways. (From Harkreader, Hogan, Thobaben: Fundamentals of nursing: caring and clinical judgment , ed 3, St. Louis, 2007, Saunders.)

open airway. A nasal airway should not be used with patients who have sustained trauma to the nasal area  or when space-occupying lesions or foreign objects block the nasal passages ( Barnes, 2013). Nasal airways are available in many sizes varying in length and internal diameter (Fig. 2.20). Proper  airway size is determined by holding the device against the side of the patient ’s face and selecting an airway that extends from the tip of the nose to the angle of the jaw or to the earlobe ( Fig. 2.21). A nasal airway that is too long may stimulate the gag reflex; one that is too short may not be inserted far enough to keep the tongue away from the back of the throat. Before inserting a nasal airway, lubricate the distal tip of the device liberally with a water-soluble lubricant to minimize resistance and to decrease the irritation of the nasal passage. Hold the nasal airway at its flange end like a pencil, and slowly insert it into the larger of the patient ’s two nares, with the bevel facing  the nasal septum (Fig. 2.22). During insertion, do not force the airway, because it may cut or scrape the nasal mucosa; this may result in significant bleeding, which increases the risk of aspiration. Bleeding can occur in up to 30% of patients after nasal airway insertion (Link, et al., 2015). If resistance is encountered, a gentle back-and-forth rotation of the device between your fingers may ease insertion. If resistance continues, withdraw the nasal airway, reapply lubricant, and attempt insertion in the patient ’s other nostril.  Advance the airway along the floor of the nostril, following the natural curvature of the nasal passage until the flange is flush with the nostril. If blanching of the nostril is observed after placement of the

Fig. 2.21 A nasal airway of proper size extends from the tip of the patient ’s nose to the angle of the jaw or to the earlobe. (From Roberts J: Roberts and Hedges    clinical procedures in emergency medicine , ed 6, Philadelphia, 2014, Saunders.) ’  

Fig. 2.22 Nasal airway insertion. (From Roberts J: Roberts and Hedges    clinical procedures in emergency medicine , ed 6, ’  

Philadelphia, 2014, Saunders.)

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CHAPTER 2   Airway Management 

TABLE 2.3

Oral and Nasal Airways

Considerations

Oral Airway

Nasal Airway

Indications

Helps maintain an open airway in an unresponsive patient with no gag reflex  who is not intubated • Helps maintain an open airway in an unresponsive patient with no gag reflex  who is being ventilated with a bag-mask  or other positive pressure device • May be used as a bite block after insertion of a tracheal tube or orogastric tube • Responsive patient with an intact gag reflex  • Corner of the mouth to the tip of the earlobe or the angle of the jaw • Positions the tongue forward and away from the back of the throat    Easily placed • • Does not protect the lower airway from aspiration • May produce vomiting if used in a responsive or semiresponsive patient  with a gag reflex 

•

To aid in maintaining an airway when use of an oral airway is contraindicated or difficult to place such as when the patient ’s jaw is clenched during a seizure or if oral trauma is present 

•

Severe craniofacial trauma   Patient intolerance Tip of nose to the angle of the jaw or the earlobe Provides a patent airway Tolerated by responsive patients Does not require the mouth to be open Does not protect the lower airway from aspiration Improper technique may result in severe bleeding; resulting epistaxis may be difficult to control Suctioning through the device is difficult  Although tolerated by most responsive and semiresponsive patients, can stimulate the gag reflex in sensitive patients, precipitating vomiting, gagging, or laryngospasm Use of the device does not eliminate the need for maintaining proper head position

Contraindications Sizing  Advantages

Disadvantages

•

• • • • • • •

• •

Precautions

•

Use of the device does not eliminate the need for maintaining proper head position

•

adjunct, the diameter of the nasal airway is too big. The nasal airway should be removed and a smaller  airway should be inserted.  The proper placement of the device is confirmed by ventilating the patient. If the nasal airway is correctly placed, chest rise should be visible, and breath sounds should be present on auscultation of the lungs during ventilation. If the patient is not breathing or if breathing is inadequate, begin positive pressure ventilation. Indications, contraindications, advantages, and disadvantages of oral and nasal airways are shown in Table 2.3.

POSITIVE PRESSURE VENTILATION [Objective 7]  Adequate oxygenation requires an open airway  and  adequate air exchange. After the airway has been opened, determine whether the patient ’s breathing is adequate or inadequate. If ventilatory efforts are inadequate, the patient ’s breathing may be assisted by forcing air into the lungs (ie, delivering positive pressure ventilations). NPPV, mouth-to-mask ventilation, and BMV are examples of methods that may  be used to deliver positive pressure ventilation.

Noninvasive Positive Pressure Ventilation [Objectives 7, 8] NPPV, also called noninvasive ventilation (NIV), is the delivery of ventilatory support to a spontaneously  breathing patient without using an invasive artificial airway (eg, ETT, tracheostomy tube). NPPV has

CHAPTER 2   Airway Management 

been effectively used to avoid or decrease the rates of endotracheal intubation and to improve outcomes (eg, reduce rates of mortality, decrease duration of hospital stays) in patients with severe exacerbations of  COPD or acute cardiogenic pulmonary edema, in immunosuppressed patients with acute respiratory  distress or failure, and as an adjunct to early liberation from mechanical ventilation in patients who have COPD (Keenan, et al., 2011). In general, the best candidates for NPPV are cooperative, able to protect  their airway, and are hemodynamically stable (Liesching, et al., 2003).  Although a number of interfaces are available, the patient typically wears a nasal mask, oronasal mask, or full face mask equipped with straps to hold the mask firmly in place. Ventilatory support is provided by  means of a portable or standard ventilator.  The term noninvasive positive pressure ventilation encompasses various modes of positive pressure ventilation including CPAP and BPAP, but these modes of NPPV are distinctly different. With noninvasive CPAP, a continuous pressure that is greater than atmospheric pressure is delivered throughout the respiratory cycle. CPAP provides airway support by splinting open the upper airway, increasing lung   volume, and increasing intrathoracic pressure, but it does not decrease the workload of the patient ’s inspiratory muscles during breathing (Hess, 2013). Because CPAP is helpful in improving alveolar oxygenation, it is more effective in hypoxemic conditions (eg, heart failure) than in hypercapnic states. When BPAP is administered, two levels of pressure are applied; a higher pressure is used during inspiration (ie, inspiratory positive airway pressure) and a lower pressure is used during expiration (expiratory positive airway pressure), thus decreasing the patient ’s inspiratory muscle workload. BPAP is useful in hypercapnic failure (eg, exacerbations of COPD) as well as in mixed hypoxic and hypercapnic failure. Contraindications for NPPV are shown in Box 2.7.

ACLS Pearl Because BPAP is themost commonmode used with NPPV, some clinicians usethe terms BPAP and NPPV synonymously.

BOX 2.7 • • • • • •

Noninvasive Positive Pressure Ventilation—Contraindications

Cardiac arrest Complete upper airway obstruction Excessive secretions Facial trauma or deformity Hemodynamic instability High risk for aspiration

• • • • • •

Inability to fit mask  Inability to protect airway Recent facial, esophageal, or gastric surgery Respiratory arrest Uncontrolled vomiting Uncooperative patient

Mouth-to-Mask Ventilation [Objectives 7, 9]  The device used for mouth-to-mask ventilation is commonly called a  pocket mask, pocket face mask, ventilation face mask, or  resuscitation mask. A pocket face mask is a clear, semirigid mask that is sealed around

Fig. 2.23   Pocket mask. (Courtesy Laerdal Medical.)

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CHAPTER 2   Airway Management 

the patient ’s mouth and nose (Fig. 2.23). Masks used for ventilation should be made of transparent material to allow assessment of the patient ’s lip color and detection of vomitus, secretions, or other substances and they should be equipped with an oxygen inlet and a standard connector that enables connection to a  bag-mask (or other ventilation) device.  When ventilating with a patient using a pocket mask, connect a one-way valve to the ventilation port  on the mask. If an oxygen inlet is present on the mask and oxygen is available, connect oxygen tubing to the oxygen inlet, and set the flow rate at 10 to 12 L/min. Position yourself at the patient ’s head or side. Positioning yourself directly above the patient ’s head allows you to watch the patient ’s chest while delivering ventilations. This position is used if the patient is in respiratory arrest (but not cardiac arrest) or when two-rescuer cardiopulmonary resuscitation (CPR) is being performed. If you are by yourself, positioning yourself at the patient ’s side allows you to maintain the same position for both rescue breathing and chest compressions. Open the patient ’s airway. If needed, clear the patient ’s airway of secretions or vomitus. If the patient is unresponsive and has no gag reflex, insert an oral airway. Select a mask of appropriate size and place it on the patient ’s face. A mask of correct size should extend from the bridge of the nose to the groove between the lower lip and chin. If the mask is not properly positioned and a tight seal maintained, air will leak from between the mask and the patient ’s face, thereby resulting in the delivery of  less tidal volume to the patient. Less tidal volume results in less lung inflation, which means less oxygenation.  The E-C clamp technique, also called the E-C grip, can be used to create a good face-to-mask seal and provide effective ventilation (Fig. 2.24). Apply the narrow portion (ie, apex) of the mask over the bridge of  the patient ’s nose and stabilize it in place with your thumbs. Lower the mask over the patient ’s face and mouth. Use your index fingers to stabilize the wide end (ie, base) of the mask over the groove between the patient ’s lower lip and chin. When properly positioned, your thumb and index finger will create a  “C.”  Gently push down on the mask to establish an adequate mask seal. Position your remaining fingers along the angle of the jaw to form an “E.” Use these fingers to lift the jaw and pull the patient ’s chin into the mask.Ventilate thelungs through theone-way valveon thetop of themaskat a rate of onebreath every 5 to 6 seconds, or about 10 to 12 breaths/min. Deliver each breath over 1 second and stop ventilation when gentle chest rise is observed.

Fig. 2.24 The E-C clamp technique for mouth-to-mask or BMV. (From Roberts J: Roberts and Hedges   clinical procedures in  ’  

emergency medicine , ed 6, Philadelphia, 2014, Saunders.)

ACLS Pearl Gastric distention is a complication of positive pressure ventilation that can lead to vomiting and subsequent aspiration. Gastric distention also restricts movement of the diaphragm, impeding ventilation, and decreases the effectiveness of CPR if the patient is in cardiac arrest.

 Another method used for ventilation is the thenar eminence (TE) technique, also called the TE grip.  When the TE method is used, the TEs of both hands are used to hold the mask in place (Fig. 2.25). The rescuer ’s fingers are positioned under the angle of the patient ’s mandible to perform a jaw lift (Fig. 2.26). Research has shown that use of the TE technique is easier for inexperienced providers and results in improved ventilation compared with the E-C clamp technique (Gerstein, et al., 2013). Indications, advantages, and disadvantages of mouth-to-mask ventilation are shown in Table 2.4.

CHAPTER 2   Airway Management 

Fig. 2.25   The thenareminences of both hands of there-

Fig. 2.26   The rescuer’s fingers are positioned under the angle

scuer hold the face mask firmly in place. (From Roberts J: Roberts and Hedges    clinical procedures in emergency  medicine , ed 6, Philadelphia, 2014, Saunders.)

of the patient ’s mandible to perform a jaw lift. (From Roberts J: Roberts and Hedges   clinical procedures in emergency medicine , ed 6, Philadelphia, 2014, Saunders.)

’  

’  

TABLE 2.4

Mouth-to-Mask Ventilation

Inspired Oxygen Concentration

Without supplemental oxygen equals about 16% to 17% (exhaled air) Mouth-to-mask breathing combined with supplemental oxygen at a minimum flow rate of  10 L/min equals about 50% • Esthetically more acceptable than mouth-to-mouth ventilation • Easy to teach and learn • Physical barrier between the rescuer and the patient ’s nose, mouth, and secretions • Reduces (but does not prevent) the risk of exposure to infectious diseases • Use of a one-way valve at the ventilation port decreases exposure to the patient  ’s exhaled air • If the patient resumes spontaneous breathing, the mask can be used as a simple face mask to deliver 40% to 60% oxygen by giving supplemental oxygen through the oxygen inlet on the mask (if so equipped) • Can deliver a greater tidal volume compared with a BMD • Rescuer can feel the compliance of the patient ’s lungs (compliance refers to the resistance of the patient ’s lung tissue to ventilation) •   Rescuer fatigue • Possible gastric distention

 Advantages

Disadvantages

• •

Bag-Mask Ventilation [Objective 7]  A BMDis a self-inflatingbag witha nonrebreathing valvemechanism(Fig.2.27).ABMDmayalsobereferred toasa bag-mask, bag-valve-mask device or bag-maskresuscitator (whenthemaskisused),orasa bag-valvedevice  (when the mask is notused [ie, when ventilating a patient with a tracheal tube or tracheostomy tube in place]).  The BMD should be equipped with a transparent disposable plastic mask with a high-volume, low-pressure cuff; standard fittings to allow forattachment of the device to a standard mask, advanced airway, or other ventilationdevice; andan oxygen-collectingdevice (ie,reservoir)to allowdeliveryof highconcentrations of oxygen. Oxygen Delivery  [Objective 9]  When using a BMD, the amount of delivered O2 is dependent on the ventilatory rate, the volume delivered during each breath, the O 2  flow rate into the ventilating bag, the filling time for the reservoir bag,

Fig. 2.27   Bag-mask devices. (Courtesy Laerdal Medical.)

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CHAPTER 2   Airway Management 

and the type of reservoir used (Reardon, et al., 2014a). Delivered tidal volumes vary with bag type, hand size, and patient body characteristics (Rouse & Frakes, 2010).  A BMD that is used without supplemental oxygen will deliver 21% oxygen (ie, room air) to the patient. The BMD should be connected to an oxygen source. To do this, attach one end of a piece of oxygen connecting tubing to the oxygen inlet on the BMD and the other end to an oxygen regulator.  A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min delivers approximately  40% to 60% oxygen to the patient when a reservoir is not used. Ideally, an oxygen reservoir should be attached to the bag-mask to deliver a high concentration of oxygen. The reservoir collects a volume of 100% oxygen that is equal to the capacity of the bag.  After squeezing the bag, it reexpands and draws 100% oxygen from the reservoir into the bag.  A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min and with an attached reservoir delivers approximately 90% to 100% oxygen to the patient. Advantages and disadvantages of  BMV are shown in Box 2.8.  Ventilating with a Bag-Mask Device [Objectives 7, 10] Performing positive pressure ventilation with a BMD can be difficult. Several reasons contribute to this, but none as much as the inability to create a good seal with the mask while simultaneously generating an adequate tidal volume by squeezing the bag. BMV should be a two-rescuer operation. With two people, one is assigned the responsibility of opening and maintaining the airway while creating a good seal with the mask. That frees a second person to squeeze the bag.  To ventilate a patient with a BMD, position yourself at the top of the supine patient ’s head and open the patient ’s airway. If needed, clear the patient ’s airway of secretions or vomitus. If the patient  is unresponsive, insert an oral airway. Next, select a bag and mask of appropriate size for the patient. Connect the bag to the mask if this has not already been done. Connect the bag to oxygen at a flow rate of 15 L/min, and attach a reservoir. Place the mask on the patient ’s face. Create a good face-to-mask seal  with the mask positioned over the patient ’s mouth and nose.  Although single-rescuer BMV is not recommended during CPR (Link, et al., 2015), if you find yourself in this situation, press the mask firmly against the patient ’s face with one hand using the E-C clamp technique previously described (and simultaneously use it to maintain the patient ’s proper head position), and then squeeze the bag with the other hand (Fig. 2.28). If a second rescuer is present, the E-C clamp technique or the TE technique can be used. If an assistant is available, ask him or her to squeeze the bag until the patient ’s chest rises while you press the mask firmly against the patient ’s face with both hands and simultaneously maintain the patient ’s proper head position (see Fig. 2.26). Observe the rise and fall of the patient ’s chest with each ventilation. Deliver each breath over 1 second and stop ventilation when gentle chest rise is observed. Ventilate the adult patient at a rate of one breath every 5 to 6 seconds, or about 10 to 12 breaths/min.

ACLS Pearl  Assessment of chest rise, breath sounds, oxygen saturation, and capnography should be used to evaluate the effectiveness of oxygenation and ventilation ( Reardon, et al., 2014a).

 A reliable indicator of adequate ventilation is the rise and fall of the patient ’s chest wall with each  ventilation at an age-appropriate rate. Another indication that the patient is being well ventilated is

BOX 2.8

Bag-Mask Ventilation

 Advantages

• • • •

Disadvantages

• • • •

Provides a means for delivery of an oxygen-enriched mixture to the patient Can be used with the spontaneously breathing patient as well as with the nonbreathing patient Conveys a sense of compliance of the patient’s lungs to the BMD operator  Provides a means for immediate ventilatory support Requires practice to be used effectively Delivery of inadequate tidal volumes Causes rescuer fatigue Can lead to possible gastric distention

CHAPTER 2   Airway Management 

Fig. 2.28 Single-rescuer bag-mask ventilation using the E-C clamp. (From Sole ML, Klein DG, Moseley MJ: Introduction MJ:  Introduction to  critical care nursing , ed 6, St Louis, 2013, Saunders.)

an improvement of the patient ’s condition as evidenced by improvements in color, pulse oximeter readings, heart rate, and responsiveness. During BMV, avoid excessive ventilation (either by rate or volume) and allow adequate time for  exhala exhalatio tion n to occur.Exces occur.Excessiveventi siveventilat lation ion decrea decreases ses corona coronary ry perfus perfusion ion pressu pressure re and may decrea decrease se thelikelihood for return of spontaneous circulation in patients in cardiopulmonary arrest ( Aufderheide, ( Aufderheide, et al., compliance  refers to 2004). 2004 ). Also, feel for compliance when ventilating the patient ’s lungs. Pulmonary lungs.  Pulmonary compliance  refers the resistance of the patient ’s lung tissue to ventilation. The lungs are normally pliable and expand easily. If thelungsfeelstiffor inflex inflexibl ible, e, lung lung complia complianceis nceis said said to bepoor.Upper bepoor.Upper airwayobstr airwayobstruct uction,lowerairw ion,lowerairway  ay  obstruction, severe bronchospasm, and tension pneumothorax are examples of conditions that can cause poor lung compliance and an inability to ventilate. If at any time you sense poor compliance, reassess the patient to ensure that the airway remains unobstructed and that lung sounds are clear and equal. Troubleshooting Bag-Mask Ventilation [Objective 11]  The most frequent problems with BMV are the inability to deliver adequate ventilatory volumes and gastric inflation (Reardon, (Reardon, et al., 2014a). 2014a). The delivery of an inadequate ventilatory volume may be the result of difficulty with providing a leak-proof seal to the face while simultaneously maintaining  an open airway, incomplete bag compression, or both. Gastric inflation may result if excessive force and volume are used during ventilation. If the chest does not rise and fall with BMV, reassess the patient in the following manner: •   Begin by reassessing the patient ’ s head position. Reposition the airway, and try to ventilate again. Inadequate tidal volume delivery may be the result of an improper mask seal or incomplete bag com• pression. If air is escaping from under the mask, reposition your fingers and the mask, and reevaluate the effectiveness of bag compression. obstruction. Lift the jaw, and suction the airway airway as needed. If the chest still does • Check for an airway obstruction. not rise, select an alternative method of positive pressure ventilation.

 ADVANCED AIRWAYS [Objective 12] called  supraglottic airways,  are advanced airways that are blindly   Extraglottic airway devices,  devices,   formerly called supraglottic inserted. They may be used in areas where tracheal intubation is not permitted, or in communities in  which health care providers have little opportunity to obtain experience with the technique of orotracheal orotracheal intuba intubatio tion n as a result result of having having few patien patients. ts. They They may also also be used used by anesth anesthesi esiolog ologist istss for short, short, low-ri low-risk  sk  procedures. Extraglottic airways are available in a range of sizes and can be placed while CPR is in progress, thereby minimizing interruptions when performing chest compressions ( Anders, ( Anders, et al., 2014 2014). ). Examples Examples of extraglottic extraglottic airway airway devices include include the esophagealesophageal-trac tracheal heal Combitube Combitube (Nellcor, (Nellcor, Pleasanton, Pleasanton, CA), CA), larynge laryngeal al mask mask airway airway (LMA) (LMA) (Laryn (Laryngea geall Mask Mask Compan Company, y, Singap Singapore ore)) (Fig Fig.. 2.2 2.299), air-Q air-Q (Cookg (Cookgas, as,

49

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CHAPTER 2   Airway Management 

St. Louis, MO), i-gel (Intersurgical LTD, Wokingham, Berkshire, UK), laryngeal tube (King AirwayLTS-D, King Systems, Noblesville, Noblesville, IN), and R usch u€sch EasyTube (Teleflex Medical, Limerick, PA). Endotracheal intubation is an example of an intraglottic  an  intraglottic  airway  airway procedure in which a tube is placed directly into the trachea (Fig. ( Fig. 2.30). 2.30). This procedure requires special training, equipment, and supplies and may be performed for a variety of reasons including for the delivery of anesthesia, to assist a patient ’s breathing with positive pressure ventilation, and to protect the patient ’s airway from aspiration.

Fig. 2.29 The laryngeal mask airway is an example of an extraglottic extraglottic airway. (From Rothrock: Alexander's Rothrock: Alexander's care of the patient  in surgery , ed 15, St. Louis, 2015.)

Fig. 2.30 Endotracheal intubation is an example of an intraglottic airway procedure. (From Pfenninger JL, Fowler GC: Pfen-  GC: Pfen-  ninger and Fowler's Procedures for Primary Care , ed 3, Philadelphia, 2011, Saunders.)

ACLS Pearl  Advanced airway insertion requires a high degree of skill and knowledge as well as regular practice to maintain proficiency. Regular practice, continuing education programs, and an effective quality management program to monitor skill performance are essential for all health care professionals who perform this skill.

Current resuscitation guidelines reflect that there is inadequate evidence to show a difference in sur vival or favorable neurologic outcome with the use of BMV compared with endotracheal intubation or  other advanced airway devices; further, the ideal timing of advanced airway placement to maximize outcome has not been adequately studied (Link, ( Link, et al., 2015). 2015). Therefore either a BMD or an advanced air way may be used for oxygenation and ventilation during CPR in both the in-hospital and out-of-hospital setting (Link, (Link, et al., 2015). 2015). For health care providers trained in their use, either an extraglottic airway or  an ETT may be used as the initial advanced airway during CPR ( Link, et al., 2015). 2015). In cardiac arrest situations, members of the resuscitation team may opt to delay insertion of an advanced airway until after several minutes of cardiac arrest management or until there is a return of  spontaneous circulation. If an advanced airway is not  is  not  inserted,   inserted, the patient should be ventilated at a rate of 10 to 12 breaths per minute. If the decision is made to insert an advanced airway during the

CHAPTER 2   Airway Management 

resuscitati resuscitation on effort, effort, ventilation ventilation does not require require interrupti interruption on (or even pausing) of chest compressions compressions once the advanced airway is in place —unless ventilation is inadequate when compressions are not paused (Li Link nk,, et al al., ., 20 2015 15). ). Afte Afterr inse insert rtion ion of an adva advance nced d airw airway ay,, the the pati patien entt shou should ld be vent ventil ilat ated ed at a rate rate of one one breath every 6 seconds (10 breaths/min) (Link, ( Link, et al., 2015). 2015). Avoid delivering an excessive number or   volume of ventilations.

ACLS Pearl Rememb Remember er that that ventil ventilati ating ng a cardia cardiac c arrest arrest patien patientt too fastor with with too much much volume volume result results s in excesexcessive intrathoracic pressure, which results in decreased venous return into the chest, decreased coronary and cerebral perfusion pressures, diminished diminished cardiac output, and decreased rates of survival.

Confirm Conf irming ing End Endotr otrachea acheall Tub Tube e Plac Placemen ementt [Objective 13] Methods that are used to verify the proper placement of an ETT include the following: Visualizing Visualizing the passage of the tracheal tracheal tube between between the vocal cords • Auscultating the presence of bilateral breath sounds • • Confirming the absence of sounds over over the epigastrium during ventilation ventilation Observing adequate chest rise with each ventilation • Determining Determining the absence absence of vocal sounds after after the placement placement of the tracheal tracheal tube • • Measuring Measuring the level level of EtCO2  (continuous waveform capnography is preferred) Verifying Verifying tube placement placement with the use of an EDD • • Obtaining a chest radiograph In addition to these methods, some institutions use ultrasound imaging as an adjunct to monitor  proper ETT position. Do position.  Do not rely exclusively on one method or device to detect and monitor for inadvertent  esophageal intubation. Current Current resuscitat resuscitation ion guidelines guidelines recommend the use of continuous continuous waveform waveform capnograph capnographyy in addition to clinical assessment as the most reliable method of confirming and monitoring correct  placement of an ETT (Link, (Link, et al., 2015). 2015). A nonwaveform CO 2 detector, EDD, or ultrasound used by  an experienced operator are reasonable alternatives if continuous waveform capnometry is not available (Link, et al., 2015). 2015).

ACLS Pearl  An advanced airway that is misplaced or that becomes dislodged can be fatal. Make it a habit to recheck the placement of an advanced airway immediately after insertion, after securing the tube, during intrafacility or interfacility transport, and whenever the patient is moved. Be certain to documentthe mentthe cm posi positi tion on of the the tube tube at the the pati patien entt’s teeth/ teeth/lip lips. s. Capnog Capnograp raphy hy can be used used to immedi immediate ately ly alert you to a misplaced or dislodged tube.

Esophageal Detector Devices [Objective 13] EDDs, also called esophageal called esophageal intubation detectors, are detectors, are used to help determine whether a tracheal tube is in the trachea or the esophagus. There are two types of esophageal detectors: syringes and bulbs.  The syringe device is connected to a tracheal tube with the plunger fully inserted into the barrel of the syringe. If the tube is in the trachea, the plunger can be easily withdrawn from the syringe barrel. If the tracheal tube is in the esophagus, resistance will be felt when the plunger is withdrawn because the walls of the esophagus will collapse when negative pressure is applied to the syringe. The EDD should be checked for air leaks before use. If any connections are loose, the leak may allow the syringe to be easily   withdrawn, thus mimicking tracheal location of the tube (Reardon, et al., 2014b). 2014b).  The bulb device is compressed before it is connected to a tracheal tube (Fig Fig.. 2.3 2.311). A vacu vacuum um is crea create ted d as the pressure on the bulb is released. If the tube is in the trachea, trachea, the bulb will refill easily when pressure is released, thereby indicating proper tube placement. If the tracheal tube is in the esophagus, the bulb  will remain collapsed, which indicates ind icates improper tube placement. Conditions in which the trachea tends to collapse can result in misleading findings. Examples of these conditions include morbid obesity, late pregnancy, status asthmaticus, and the presence of profuse tracheal secretions.

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Fig. 2.31 Bulb-type esophageal detector detector device. (From Sandberg, Urman, Ehrenfeld: The Ehrenfeld: The MGH textbook of anesthetic equip-  ment , Philadelphia, 2011, Saunders.)

If an EDD is used to confirm the placement of the tube, apply the device to the tube before the inflation of the distal cuff. Inflating the cuff moves the distal end of the tracheal tube away from the walls of  the esophagus. If the tube was inadvertently inserted into the esophagus, this movement will cause the detector bulb to reexpand, which falsely suggests that the tube is in the trachea.

CHAPTER 2   Airway Management 

PUTTING IT ALL TOGETHER  The chapter quiz and case study that follow are provided to help you i ntegrate the information presented in this chapter. As you work through the case study, remember that there may be alternative actions that  are perfectly perfectly acceptable acceptable,, yet not presented presented in the case study. CHAPTER QUIZ

 Multiple Choice  Identify the choice that best completes the statement or answers the question. question.

____ _____

1.

If no head head or neck neck trauma trauma is suspec suspected ted,, which which of the followi following ng techni technique quess should should health care professionals use to open the airway?  A. Tongue –  jaw lift  l ift  B. Head tilt  – chin chin lift  C. Head tilt  – neck neck lift  D. Jaw thrust without without neck extension extension

_____

2.

An oral airway:  A. May result in an airway obstruction if improperly inserted. B. Is usually well tolerated tolerated in the responsive responsive or semiresponsive semiresponsive patient. patient. C. Should be lubricated lubricated with a petroleum-based petroleum-based lubricant lubricant before before insertion. D. May inadve inadverte rtentl ntlyy enter enter the crani cranial al vault vault ifif used used in a patie patient nt with with a crani craniofa ofacia ciall injur injury. y.

____ _____

3.

Which Which of the follow following ing device devicess may be used used to delive deliverr positi positive ve pressur pressuree ventil ventilati ation? on?  A. Nasal cannula  B. Pocket face mask  C. Simple face mask  D. Nonrebreat Nonrebreather her mask 

____ _____

4.

Whic Which h of the the foll follow owing ing stat statem emen ents ts is true true about about a nasa nasall airw airway ay??  A. A nasal airway can be placed in either nostril to help maintain an open airway. B. A nasal airway should only be used in unresponsive patients who do not have a gag  reflex. C. A corr correc ectl tlyy size sized d nasa nasall airwa airwayy exte extend ndss from from the the corn corner er of the the pati patien ent  t ’s mout mouth h to the the tip of the ear lobe. D. When properly properly positioned, positioned, the distal tip of the nasal airway rests rests in the patient  patient ’s trachea.

____ _____

5.

Pulm Pulmon onar aryy comp compli lian ance ce refe refers rs to: to:  A. The resistance of the patient ’s lung tissue to ventilation. B. The amount of gas inhaled or exhaled exhaled during a normal breath. breath. C. The exchange of oxygen and carbon dioxide during cellular cellular metabolism. metabolism. D. The amount of air moved in and out of the respirator respiratoryy tract in 1 minute. minute.

____ _____

6.

You and a cowork coworker er arrive arrive to find a 78-yea 78-year-o r-old ld woman woman unresp unrespons onsive ive in bed. bed. She is not breathing but does have a pulse. You have a pocket face mask on hand that is equipped with an oxygen inlet. After quickly connecting oxygen tubing to the inlet on the mask, you should set the oxygen flow rate at:  A. 1 to 2 L/min. B. 4 to 6 L/min. C. 8 to 10 L/min. L/min. D. 10 to 12 L/min.

____ _____

7.

Which Which of the follow following ing will will delive deliverr the highes highestt oxygen oxygen concen concentra tratio tion? n?  A. A nasal cannula with an oxygen flow rate of 4 L/min B. A pocket mask mask with an oxygen flow rate rate of 10 L/min C. A simple face mask mask with an oxygen flow rate of 8 L/min L/min D. A nonrebreathe nonrebreatherr mask with an oxygen flow rate of 10 L/min

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____ ____

8.

Signs Signs of adequa adequate te ventil ventilati ation on when when delive deliverin ringg ventila ventilatio tions ns with with a BMD includ include: e:  A. The presence of gurgling sounds during ventilation. B. The rise and fall of the patient ’s chest wall with each ventilation. C. The collapse collapse of the oxygen reservoir reservoir on the BMD with each ventilation. ventilation. D. The BMD become becomess progre progressi ssively vely more more diffic difficult ult to compre compress ss with with each each ventil ventilatio ation. n.

____ _____

9.

Which hich of the the foll follow owin ingg is not  is not  an   an example of an extraglottic airway device?  A. Laryngeal tube B. ETT C. LMA D. Esophageal-tracheal Combitube

______ 10.

A 19-year-old 19-year-old man is unresponsiv unresponsivee and not breathing. breathing. A slow, weak pulse is present. present.  Your best course of action will be to:  A. Begin chest compressions. B. Insert Insert an advanced airway. airway. C. Administer Administer oxygen oxygen by nasal cannula. cannula. D. Insert Insert an oral airway and begin begin BMV.

____ _____

11. 11.

Trac Trache heal al intu intuba bati tion on::  A. Is contraindicated in unresponsive patients. B. Eliminates Eliminates the risk of aspiration aspiration of gastric contents. contents. C. Should be preceded preceded by efforts efforts to ventilate ventilate by another another method. D. When attempted, attempted, should should be performed in less than 60 seconds.

____ ____

12. 12.

Whenven Whenventi tila lati ting ng a pati patien entt by mean meanss of a BMD, BMD, resc rescue uers rs can can succ succes essf sful ully ly deli delive verr abou about  t  __ oxygen without the use of supplemental oxygen.  A. 16% B. 21% C. 50% D. 80%

CHAPTER 2   Airway Management 

CASE STUDY 2-1  Your patient is an 85-year-old woman who presents with difficulty breathing. She has a long history of  COPD and has experienced increasing shortness of breath since yesterday. You have a sufficient number  of advanced life support personnel available to assist you and carry out your instructions. Emergency  equipment is available. 1. As you approach the patient, you observe that she is supine on a stretcher. Her eyes are closed, her lips are blue, and her skin is pale. You see no signs of breathing. What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 2. The patient is unresponsive. What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 3. The patient is not breathing but a carotid pulse is present. The rate is slow, weak, and regular. What  should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 4. How will you open the patient ’s airway? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 5. A significant amount of mucus is observed in the patient ’s mouth. How will you remedy this problem? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 6. The patient ’s airway is clear. You have asked a team member to insert an oral airway. How is proper  oral airway size determined? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 7. When is the use of an oral airway contraindicated? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

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8. An oral airway has been inserted. The patient is still not breathing. What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 9. Differentiate between the E-C clamp technique and the TE technique when performing BMV. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 10. What are the most common problems associated with the use of BMV? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 11. The patient ’s chest does not rise despite attempts to ventilate the patient with a BMD. What is the first thing you should do to remedy this problem? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 12. Equal chest rise is now present with BMV. Breath sounds reveal clear upper lobes and diminished sounds in the lower lobes bilaterally. The patient ’s blood pressure is 108/74 mm Hg. She has been placed on the cardiac monitor, which reveals the rhythm shown. What is the rhythm on the monitor?  What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

(From Aehlert: ECGs made easy , ed 4, St. Louis, 2011, Mosby.)

13. Vascular access has been established with normal saline. An ETT has been inserted and the cuff  inflated. How will you confirm placement of the ETT? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 14. Waveform capnography confirms the presence of CO2. The ETT has been secured. What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

CHAPTER 2   Airway Management  CHAPTER QUIZ ANSWERS

1. B. The head tilt  – chin lift is the preferred technique for opening the airway of an unresponsive patient   without suspected cervical spine injury. If trauma is suspected, the jaw thrust without neck extension maneuver should be used. Health care professionals should use the head tilt  – chin lift maneuver to open the airway if use of the jaw thrust without neck extension maneuver is unsuccessful. OBJ: Describe and demonstrate the steps needed to perform the head tilt  – chin lift and jaw thrust   without neck extension maneuvers and relate the mechanism of injury to the opening of the airway. 2. A. An oral airway should only be used in unresponsive patients who have no cough or gag reflex because it may stimulate vomiting or laryngospasm in responsive or semiresponsive patients. If  the airway is too long, it may press the epiglottis against the entrance of the larynx resulting in a  complete airway obstruction. If the airway is too short, it will not displace the tongue and may  advance out of the mouth. A petroleum-based lubricant should never be used because it may damage the airway device and cause tissue inflammation. A nasal airway (not an oral airway) may inadvertently enter the cranial vault if it is inserted into the nose of a patient who has sustained a craniofacial injury. OBJ: Discuss the indications, contraindications, advantages, and disadvantages of oral and nasal airways, and demonstrate how to correctly size and insert each of these airway adjuncts. 3. B. NPPV, mouth-to-mask ventilation, and BMV are examples of methods that may be used to deliver positive pressure ventilation. The remaining devices listed (nasal cannula, simple face mask, and nonrebreather mask) do not deliver a tidal volume; they are oxygen delivery devices and require a  spontaneously breathing patient. OBJ: Describe methods by which positive pressure ventilation is delivered. 4. A. A nasal airway can be used in an unresponsive patient and may be useful in semiresponsive patients who have a gag reflex. It can be placed in either nostril to help maintain an open airway.  To select a nasal airway of proper size, hold the device against the side of the patient ’s face. Select an airway that extends from the tip of the patient ’s nose to the angle of the jaw or the earlobe. When a  nasal airway of the proper size is correctly positioned, the tip rests in the back of the throat. OBJ: Discuss the indications, contraindications, advantages, and disadvantages of oral and nasal airways, and demonstrate how to correctly size and insert each of these airway adjuncts. 5. A. Pulmonary compliance refers to the resistance of the patient ’s lung tissue to ventilation. The lungs are normally pliable and expand easily. If the lungs feel stiff or inflexible during positive pressure  ventilation, lung compliance is said to be poor. Upper airway obstruction, lower airway obstruction, severe bronchospasm, and tension pneumothorax are examples of conditions that can cause poor  lung compliance and an inability to ventilate. If at any time you sense poor compliance, reassess the patient to ensure that the airway remains unobstructed and that lung sounds are clear and equal.  Tidal volume is the amount of gas inhaled or exhaled during a normal breath. Respiration is the exchange of oxygen and carbon dioxide during cellular metabolism. Minute volume is the amount  of air moved in and out of the respiratory tract in 1 minute. OBJ: Recognize the signs of adequate and inadequate BMV. 6. D. If not already attached, connect a one-way valve to the ventilation port on the pocket face mask  and connect oxygen tubing to the oxygen inlet on the mask. Set the oxygen flow rate at 10 to 12 L/min. OBJ: Describe the oxygen liter flow per minute and the estimated inspired oxygen concentration delivered with a pocket face mask and a BMD. 7. D. Of the oxygen delivery devices listed, a nonrebreather mask with an oxygen flow rate of 10 L/min  will deliver the highest oxygen concentration. OBJ: Describe the advantages, disadvantages, oxygen liter flow per minute, and estimated oxygen percentage delivered with each of the following devices: nasal cannula, simple face mask, partial nonrebreather mask, and nonrebreather mask.

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8. B. A reliable indicator of ventilation adequacy is the rise and fall of the patient ’s chest wall. Gurgling  sounds are abnormal and indicate the need for suctioning. If the oxygen reservoir on the BMD collapses with each ventilation, it may indicate that the oxygen flow is too low or the ventilation rate is too rapid. If the BMD becomes progressively more difficult to squeeze when ventilating a patient, assess the need to suction, ensure that proper airway opening procedures are in use, suspect that there may be excessive air in the stomach (anticipate vomiting), and suspect a possible pneumothorax. OBJ: Recognize the signs of adequate and inadequate BMV. 9. B. An ETT is an intraglottic airway device that is placed directly into the trachea. Extraglottic airway  devices, formerly called supraglottic airways, are advanced airways that are blindly inserted. Examples of extraglottic airway devices include the esophageal-tracheal Combitube, LMA, air-Q, i-gel, laryngeal tube, and R €usch EasyTube. OBJ: Differentiate between extraglottic airways and intraglottic airways. 10. D. The patient has experienced a respiratory arrest. Your best course of action will be to insert an oral airway and begin positive pressure ventilation with a BMD. Chest compressions are not indicated because the patient has a pulse. Although insertion of an advanced airway is appropriate, it must be preceded by another form of ventilation (such as BMV) while preparations are made to insert the airway. Use of a nasal cannula is inappropriate because it can only be used in a spontaneously breathing patient. OBJ: Differentiate among respiratory distress, respiratory failure, and respiratory arrest and implement a treatment plan based on the severity of the patient ’s respiratory compromise. 11. C. Tracheal intubation should be preceded by attempts to ventilate by another method. Tracheal intubation is indicated in situations where the patient is unable to protect his/her own airway. Tracheal intubation reduces (but does not eliminate) the risk of aspiration of gastric contents and, when attempted, should be performed in less than 30 seconds. OBJ: Describe methods that are used to confirm correct ETT placement. 12. B. A BMD that is used without supplemental oxygen will deliver 21% oxygen (ie, room air, not  expired air) to the patient. A BMD that is used with supplemental oxygen set at a flow rate of  10 to 15 L/min delivers approximately 40% to 60% oxygen to the patient when a reservoir is not  used. A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min and with an attached reservoir delivers approximately 90% to 100% oxygen to the patient. OBJ: Describe the oxygen liter flow per minute and the estimated inspired oxygen concentration delivered with a pocket face mask and a BMD.

CASE STUDY 2-1 ANSWERS 1. Your general impression should focus on three main areas that can be remembered by the mnemonic  ABC: A ppearance, (work of) Breathing, and Circulation. As you finish forming your general impression, you will have a good idea if the patient is sick (ie, unstable) or not sick (ie, stable). Begin the primary survey by assessing responsiveness. Start by asking,  “ Are you all right?” or  “ Can you hear  me?”   If there is no response, then gently tap or squeeze the patient ’s shoulder while repeating   verbal cues. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient. 2. Call for help and ask someone to get an automated external defibrillator (AED) or defibrillator. Look at the chest for movement while simultaneously feeling for a pulse for 5 to 10 seconds. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient. 3. If the patient had no pulse, you would direct your team to start chest compressions and attach an  AED to the patient. In this situation, chest compressions are not indicated because a pulse is present. Open the airway and begin rescue breathing. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient.

CHAPTER 2   Airway Management 

4. Because there is no evidence of trauma, open the patient ’s airway using a head tilt  – chin lift. If there  was anything that suggested trauma in this situation, you would open the airway with a jaw thrust   without neck extension maneuver. Look in the mouth for blood, broken teeth or loose dentures, gastric contents, and foreign objects. OBJ: Describe and demonstrate the steps needed to perform the head tilt  – chin lift and jaw thrust   without neck extension maneuvers and relate the mechanism of injury to the opening of the airway. 5. Ask a team memberto suction the patient ’s upper airway. Suction should be applied as the catheter is  withdrawn and should not be applied for more than 10 seconds to avoid hypoxia. OBJ: Describe and demonstrate the procedure for suctioning the upper airway, and discuss possible complications associated with this procedure. 6. Proper oral airway size is determined by holding the device against the side of the patient ’s face and selecting an airway that extends from the corner of the mouth to the tip of the earlobe or to the angle of the jaw. To prevent inaccurate measurements for patients who experience facial drooping after a  stroke, some experts recommend measuring from the first incisor or from the center of the lips to the tip of the earlobe or to the angle of the jaw. OBJ: Discuss the indications, contraindications, advantages, and disadvantages of oral and nasal airways, and demonstrate how to correctly size and insert each of these airway adjuncts. 7. The use of an oral airway is contraindicated in responsive patients who have an intact gag reflex. An oral airway should only be used in unresponsive patients who have no gag reflex because it may stimulate vomiting or laryngospasm in responsive or semiresponsive patients. OBJ: Discuss the indications, contraindications, advantages, and disadvantages of oral and nasal airways, and demonstrate how to correctly size and insert each of these airway adjuncts. 8. Begin positive pressure ventilation with a BMD connected to 100% oxygen. Ideally, two team members should be assigned this task. Ask one team member to open and maintain the airway while creating a good seal with the mask. Ask the other team member to squeeze the bag at an ageappropriate rate. Ask a team member to assess baseline breath sounds while the patient is being   ventilated. OBJ: Describe and demonstrate how to ventilate a patient with a BMD and two rescuers. 9. The E-C clamp technique can be used when performing mouth-to-mask or BMV. The rescuer ’s thumb and index finger form a  “C”  around the mask and the remaining fingers form an “E”  on the inferior portion of the patient ’s mandible. If the rescuer is alone, one hand is used to form the E-C clamp while the other is used to squeeze the bag. If a second rescuer is present, the first  rescuer uses both hands to form the E-C clamp while the second rescuer squeezes the bag. When the TE method of ventilation is used, the TEs of both hands are used to hold the mask in place and the rescuer ’s fingers are positioned under the angle of the patient ’s mandible to pull the jaw upward toward the mask. A second rescuer is needed to squeeze the BMD. OBJ: Describe and demonstrate how to ventilate a patient with a BMD and two rescuers. 10. The most frequent problems with BMV are the inability to deliver adequate ventilatory volumes and gastric inflation. The delivery of an inadequate ventilatory volume may be the result of difficulty with providing a leak-proof seal to the face while simultaneously maintaining an open airway, incomplete bag compression, or both. Gastric inflation may result if excessive force and volume are used during   ventilation. OBJ: Recognize the signs of adequate and inadequate BMV. 11. If the chest does not rise and fall with BMV, your first action should be to reposition the patient ’s head and try to ventilate again. OBJ: Recognize the signs of adequate and inadequate BMV.

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12. The rhythm is a sinus bradycardia. Ask a qualified team member to prepare to intubate the patient.  Ask another team member to start an IV with normal saline. Order a 12-lead electrocardiogram (ECG) and portable chest radiograph and perform a focused physical examination. Resist the temptation to treat the patient ’s bradycardia with atropine. The most likely cause of the patient ’s bradycardia is hypoxia. Make sure the patient is adequately oxygenated and ventilated before considering  other possible causes of the patient ’s respiratory arrest or the use of atropine. OBJ: Differentiate among respiratory distress, respiratory failure, and respiratory arrest and implement a treatment plan based on the severity of the patient ’s respiratory compromise. 13. Attach a ventilation device to the ETT and ventilate the patient. Confirm proper placement of the tube by visualizing the passage of the tracheal tube between the vocal cords. Next, auscultate over the epigastrium (should be silent) and then in the midaxillary and anterior chest line on the right and left  sides of the patient ’s chest. Observe the patient ’s chest for adequate chest rise with ventilation. After  confirming proper tube position with the use of capnography, note the cm markings on the tracheal tube and then secure the tube in place with a commercial tube holder or tape. Waveform capnography is recommended for the continuous monitoring of proper tube placement. After securing the tube, recheck and record the tube depth at the patient ’s teeth. This value is typically between the 19 and 23 cm marks on the tube at the front teeth. Average tube depth in men is 23 cm at  the lips, 22 cm at the teeth; average tube depth in women is 22 cm at the lips, 21 cm at the teeth. OBJ: Describe methods that are used to confirm correct ETT placement. 14. Repeat the primary survey and obtain another set of vital signs. Order laboratory studies, evaluate the patient ’s 12-lead ECG and chest radiograph results, and attempt to determine possible causes of the patient ’s respiratory arrest. Transfer the patient for continued monitoring and care. OBJ: Differentiate among respiratory distress, respiratory failure, and respiratory arrest and implement a treatment plan based on the severity of the patient ’s respiratory compromise.

REFERENCES  Amsterdam, E. A., Wenger, N. K., Brindis, R. G., Casey, D. E., Jr., Ganiats, T. G., Holmes, D. ,R.Jr., et al. (2014). 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes.  J   Am Coll Cardiol ,  64 (24), e139 – e228.  Anders, J., Brown, K., Simpso n, J., & Gausche-Hill, M. (2014). Evidence and controversies in pe diatric prehospital airway management. Clin Pediatr Emerg Med ,  15 (1), 28 – 37.  Aufderheide, T. P., Sigurdsson, G., Pirrallo, R. G., Yannopoulos, D., McKnite, S., von Briesen, C,.et al. (2004). Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation, 109(16), 1960 – 1965. Barnes, T. A. (2013). Emergency cardiovascular life support. In R. M. Kacmarek, J. K. Stoller, & A. J. Heuer (Eds.),  Egan s fundamentals of respiratory care  (10th ed., pp. 787 – 817). St. Louis: Mosby. Cantineau, J. P., Merckx, P., Lambert, Y., Sorkine, M., Bertrand, C., & Duvaldestin, P. (1994). Effect of epinephrine on end-tidal carbon dioxide pressure during prehospital cardiopulmonary resuscitation. Am J Emerg Med , 12 (3), 267 – 270. Casserly, B., & Rounds, S. (2010). Essentials in critical care medicine. In T. E. Andreoli, I. J. Benjamin, R. C. Griggs, & E. J. Wing (Eds.),  Andreoli and Carpenter  s Cecil essentials of medicine  (8th ed., pp. 259 – 265). Philadelphia: Saunders. Douce, H. F. (2009). Pulmonary function testing. In R. L. Wilkins, J. K. Stoller, & R. M. Kacmarek  Egan s fundamentals of respiratory care  (9th ed., pp. 415 – 418). St. Louis: Mosby. Gerstein, N. S., Carey, M. C., Braude, D. A., Tawil, I., Petersen, T. R., Deriy, L,.et al. (2013). Efficacy of facemask   ventilation techniques in novice providers. J Clin Anesth, 25 (3), 193 – 197. Hess, D. R. (2013). Noninvasive ventilation for acute respiratory failure. Respir Care ,  58 (6), 950 – 972. Heuer, A. J. (2013). Medical gas therapy. In R. M. Kacmarek, J. K. Stoller, & A. J. Heuer (Eds.),  Egan s fundamentals of respiratory care  (10th ed., pp. 909 – 944). St. Louis: Mosby. Keenan, S. P., Sinuff, T., Burns, K. E., Muscedere, J., Kutsogiannis, J., Mehta, S,.et al. (2011). Clinical practice guidelines for the use of noninvasive positive-pressure ventilation and noninvasive continuous positive airway  pressure in the acute care setting. CMAJ ,  183(3), e195 – e214. Kleinman, M. E., Brennan, E. E., Goldberger, Z. D., Swor, R. A., Terry, M., Bobrow, B. J.,et al. (2015, Oct). 2015   American Heart Association guidelines for CPR & ECC . In Web-based integrated guidelines for cardiopulmonary  ’  

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resuscitation and emergency cardiovascular care—part 5: Adult basic life support and cardiopulmonary resuscitation quality:  Eccguidelines.heart.org . Liesching, T., Kwok, H., & Hill, N. S. (2003). Acute applications of noninvasive positive pressure ventilation.Chest , 124 (2), 699 – 713. Link, M. S., Berkow, L. C., Kudenchuk, P. J., Halperin, H. R., Hess, E. P., Moitra, V. K,.et al. (2015, Oct). 2015   American Heart Association guidelines for CPR & ECC . In Web-based integrated guidelines for cardiopulmonary  resuscitation and emergency cardiovascular care—part 7: Adult advanced cardiovascular life support: Eccguidelines.heart.org . Markovitz, G. H., Colthurst, J., Storer, T. W., & Cooper, C. B. (2010). Effective inspired oxygen concentration measured via transtracheal and oral gas analysis. Respir Care ,  55 (4), 453 – 459. McEvoy, M. (2013). How to assess and treat acute respiratory distress. JEMS ,  38 (8). O’Gara, P. T., Kushner, F. G., Ascheim, D. D., Casey, D. E., Jr., Chung, M. K., de Lemos, J. ,A.et al. (2013). 2013  ACCF/AHA guideline for the management of ST-elevation myocardial infarction. J Am Coll Cardiol ,  61(4), e78 – e140. Ornato, J. P., Shipley, J. B., Racht, E. M., Slovis, C. M., Wrenn, K. D., Pepe, P. ,E.et al. (1992). Multicenter  study of a portable, hand-size, colorimetric end-tidal carbon dioxide detection device. Ann Emerg Med ,  21(5), 518 – 523. Reardon, R. F., Mason, P. E., & Clinton, J. E. (2014a). Basic airway management and decision making. In J. R. Roberts, C. B. Custalow, T. W. Thomsen, & J. R. Hedges (Eds.),Roberts and Hedges  clinical procedures  in emergency medicine   (6th ed., pp. 39 – 61). Philadelphia: Saunders. Reardon, R. F., McGill, J. W., & Clinton, J. E. (2014b). Tracheal intubation. In J. R. Roberts, C. B. Custalow,  T. W. Thomsen, & J. R. Hedges (Eds.), Roberts and Hedges    clinical procedures in emergency medicine  (6th ed., pp. 62 – 106). Philadelphia: Saunders. Rouse, M., & Frakes, M. (2010). Airway management. In R. S. Holleran (Ed.), ASTNA patient transport: Principles  and practice  (4th ed., pp. 181 – 233). St. Louis: Mosby. Schutz, S. L. (2011). Oxygen saturation monitoring with pulse oximetry. In D. L.-M. Wiegand (Ed.),  AACN   procedure manual for critical care  (6th ed., pp. 121 – 128). St. Louis: Saunders. Sum Ping, S. T., Mehta, M. P., & Symreng, T. (1992). Accuracy of the FEF CO2 detector in the assessment of  endotracheal tube placement. Anesth Analg ,  74 (3), 415 – 419.  Tiffin, N. H., Keim, M. R., & Frewen, T. C. (1990). The effects of variations in flow through an insufflating  catheter and endotracheal tube and suction catheter size on test lung pressures. Respir Care ,  35 (9), 889 – 897.  Ward, J. J. (2013). High-flow oxygen administration by nasal cannula for adult and perinatal patients. Respir Care , 58 (1), 98 – 122. ’  

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CHAPTER

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Cardiac Anatomy and Electrophysiology INTRODUCTION  A prerequisite to participation in most Advanced Cardiac Life Support (ACLS) courses is completion of  a basic electrocardiogram (ECG) recognition course. This requirement exists because there simply is not  time in an ACLS course to cover detailed information about rhythm recognition. A basic ECG course teaches you how to identify cardiac rhythms. An ACLS course quickly reviews cardiac rhythms, but  focuses on teaching how to recognize serious signs and symptoms related to those rhythms and how  to manage them. Normally, the heart beats at a very regular rate and rhythm. If this pattern is interrupted, an abnormal heart rhythm can result. Although arrhythmia   technically means absence of rhythm  and dysrhythmia  means abnormal heart rhythm,  these terms are used interchangeably by health care professionals to refer to disturbances in cardiac rhythm. To help you understand and recognize cardiac dysrhythmias, this chapter reviews the heart  s blood supply and normal conduction pathways; normal waveforms and intervals; lead systems; and ECG changes associated with myocardial ischemia, injury, and infarction. “

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DESIRED RESULTS

G O A L Given a patient situation, correlate electrophysiologic, physiologic, and pathophysiologic cardiac events with the patient  s presentation; direct or perform accurate placement for monitoring  leads and a standard 12-lead ECG; and associate coronary artery blood flow with areas of myocardial ischemia, injury, and infarction. ’

LEARNING OBJECTIVES

 After completing this chapter, you should be able to: 1.  Name the primary branches and areas of the heart supplied by the right and left coronary arteries. 2. Define the events of the cardiac action potential and correlate them with the waveforms produced on the ECG. 3.  Define the absolute, effective, relative refractory, and supernormal periods and their  locations in the cardiac cycle. 4.  Describe the normal sequence of electrical conduction through the heart.

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CHAPTER 3   Cardiac Anatomy and Electrophysiology 5.  Describe the location, function, and, where appropriate, intrinsic rate of the following

structures: the sinoatrial (SA) node, the atrioventricular (AV) bundle, and the Purkinje fibers. 6.  Differentiate between the frontal plane and the horizontal plane leads. 7. Relate the cardiac surfaces or areas represented by the ECG leads. 8.  Define and describe the significance of each of the following as they relate to cardiac electrical activity: the P wave, the QRS complex, the T wave, the U wave, the PR segment, the TP segment, the ST segment, the PR interval, the QRS duration, and the QT interval. 9.  Recognize the changes on the ECG that may reflect evidence of myocardial ischemia, injury, and infarction.

LEARNING PLAN • •

Read this chapter before class. Master the following skills: Application of ECG monitoring leads. Recognition of myocardial ischemia, injury, and infarction on an ECG. Complete the chapter quiz and review the quiz answers provided. • •

•

KEY TERMS

 Absolute refractory period (ARP) Corresponds with the onset of the QRS complex to approximately the peak of the T wave on the ECG; cardiac cells cannot be stimulated to conduct an electrical impulse, no matter how strong the stimulus.  Accessory pathway  An extra bundle of working myocardial tissue that forms a connection between the atria and ventricles outside the normal conduction system.  Action potential  A five-phase cycle that reflects the difference in the concentration of  charged particles across the cell membrane at any given time.  Acute coronary syndromes (ACSs)  A group of conditions that are caused by an abrupt reduction in coronary artery blood flow; ACSs consist of three major syndromes: unstable angina, non–ST segment elevation myocardial infarction (NSTEMI), and ST segment – elevation myocardial infarction (STEMI).  Atrioventricular (AV) junction  AV node and the bundle of His.  AV node   Specialized cells located in the lower portion of the right atrium; delays the electrical impulse to allow the atria to contract and complete filling of the ventricles. Bundle of His  Fibers located in the upper portion of the interventricular septum that conduct an electrical impulse through the heart. Conduction system A system of pathways in the heart composed of specialized electrical (ie, pacemaker) cells. Depolarization Movement of ions across a cell membrane, causing the inside of the cell to become more positive; an electrical event expected to result in contraction. Effective refractory period (ERP) Period of the cardiac action potential that includes the  ARP and the first half of the relative refractory period. Electrocardiogram (ECG)  A recording of the heart ’s electrical activity from the body surface that appears on ECG paper as specific waveforms and complexes. Electrode Adhesive pad that contains a conductive gel and is applied at a specific location on the patient’s chest wall or extremities and is connected by cables to an ECG machine. His-Purkinje system  Portion of the conduction system consisting of the bundle of His, bundle branches, and Purkinje fibers. Interval  On the ECG, a waveform and a segment. Lead  A record (ie, tracing) of electrical activity between two electrodes. Myocardial cells  Working cells of the myocardium that contain contractile filaments and form the muscular layer of the atrial walls and the thicker muscular layer of the ventricular walls. Pacemaker cells  Specialized cells of the heart’s electrical conduction system capable of  spontaneously generating and conducting electrical impulses.

CHAPTER 3   Cardiac Anatomy and Electrophysiology

Refractoriness  A term used to describe the period of recovery that cells need after being discharged before they are able to respond to a stimulus. Relative refractory period (RRP) Corresponds with the downslope of the T wave on the ECG; cardiac cells can be stimulated to depolarize if the stimulus is strong enough. Repolarization  Movement of ions across a cell membrane in which the inside of the cell is restored to its negative charge. Segment  On the ECG, a line between waveforms that is named by the waveform that precedes or follows it. Supernormal period (SNP) Period during the cardiac cycle when a weaker than normal stimulus can cause cardiac cells to depolarize.

CORONARY ARTERIES [Objective 1]  The right coronary artery (RCA) originates from the right side of the aorta. It travels along the groove between the right atrium and right ventricle (Fig. 3.1). Blockage of the RCA can result in inferior wall myocardial infarction (MI), disturbances in AV conduction, or both.  The left coronary artery (LCA) originates from the left side of the aorta. The first segment of the LCA is called the left main coronary artery (LMCA). The LMCA supplies oxygenated blood to its two primary  branches: the left anterior descending artery (LAD), which is also called the  anterior interventricular  artery, and the circumflex (CX) artery. Blockage of the proximal LAD coronary artery has been referred to as the widow maker  because of its association with sudden cardiac arrest when it is blocked.  The major branches of the LAD are the septal and diagonal arteries. Blockage of the septal branch of  the LAD can result in a septal MI. Blockage of the diagonal branch of the LAD can result in an anterior   wall MI. Blockage of the LAD can also result in pump failure, intraventricular conduction delays, or both.  The CX coronary artery circles around the left side of the heart. Blockage of the CX artery can result in a lateral wall MI. In some patients, the CX artery may also supply the inferior portion of the left ventricle.  A posterior wall MI may occur because of blockage of the RCA or the CX artery.

Superior vena cava Aortic arch

Superior vena cava

Pulmonary artery Left atrium

Left main coronary artery Left circumflex coronary artery Left anterior descending coronary artery (LAD) Diagonal branch of LAD Right ventricle Left ventricle Right coronary artery

Right coronary artery

Fig. 3.1  Major coronary arteries and some of their branches. (From Benjamin I, Griggs RC, Wing EJ, Fitz JG, Andreoli TE:  Andreoli and Carpenter's Cecil essentials of medicine , ed 8, Philadelphia, 2011, Saunders.)

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ACLS Pearl  A common cause of MI is an obstructed coronary artery. When viewing the patient’s 12-lead ECG, an understanding of the coronary artery anatomy makes it possible to predict which coronary artery is blocked.

CARDIAC CELLS In general, cardiac cells have either a mechanical (ie, contractile) or an electrical (ie, pacemaker) function. Myocardial cells are also called working cells  or   mechanical cells, and they contain contractile filaments.  When these cells are electrically stimulated, these filaments slide together and cause the myocardial cell to contract. These myocardial cells form the thin muscular layer of the atrial walls and the thicker muscular  layer of the ventricular walls (ie, the myocardium). These cells do not normally generate electrical impulses, and they rely on pacemaker cells for this function. Pacemaker cells are specialized cells of the electrical conduction system. Pacemaker cells also may  be referred to as conducting cells  or   automatic cells. They are responsible for the spontaneous generation and conduction of electrical impulses. The heart  s pacemaker cells can generate an electrical impulse  without being stimulated by a nerve. The ability of cardiac pacemaker cells to create an electrical impulse  without being stimulated by another source is called automaticity. Increased blood concentrations of calcium (Ca ++) increase automaticity. Decreased concentrations of potassium (K +) in the blood decrease automaticity. The heart s normal pacemaker (ie, the SA node) usually prevents other areas of the heart  from assuming this function because its cells depolarize more rapidly than other pacemaker cells. ’

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CARDIAC ACTION POTENTIAL [Objective 2] Human body fluids contain electrolytes, which are elements or compounds that break into charged particles (ie, ions) when melted or dissolved in water or another solvent. Cell membranes contain poresorchannelsthroughwhichspecificelectrolytesandothersmall,water-solublemoleculescancrossthe cellmembranefromtheoutsidetotheinside( Fig.3.2).Aslightdifferenceintheconcentrationsofcharged particles across the membranes of cells is normal. Potential energy (ie, voltage) exists because of the imbalance of charged particles. This imbalance makes the cells excitable. The energy expended by the cells to moveelectrolytesacrossthemembranesofcellscreatesaflowofcurrent.Thisflowofcurrentismeasuredin  volts or millivolts (mV). Voltage appears on an ECG as spikes or waveforms.

ACLS Pearl Differences in the composition of ions between the body ’s intracellular and extracellular fluid compartments are important for normal function. The main electrolytes that affect the function of the heart are Na +, K +, Ca++, and chloride (Cl  ).

Membrane channels

Open

Closed

Fig. 3.2 Cell membranes contain membrane channels. These channels are pores through which specific ions or other small, water-soluble molecules can cross the cell membrane from outside to inside. (From Patton KT, Thibodeau GA:  Anatomy &  physiology, ed 8, St. Louis, 2013, Mosby.)

CHAPTER 3   Cardiac Anatomy and Electrophysiology

Depolarization [Objective 2]  When a cell is stimulated, the cell membrane changes and becomes permeable to sodium (Na +) and K +, allowing the passage of electrolytes once it is open. Na + rushes into the cell through Na + channels. This causes the inside of the cell to become more positive relative to the outside. A spike (ie, a waveform) is then recorded on the ECG. The stimulus that alters the electrical charges across the cell membrane may  be electrical, mechanical, or chemical.  When opposite charges come together, energy is released. When the movement of electrolytes changes the electrical charge of the inside of the cell from negative to positive, an impulse is generated.  The impulse causes channels to open in the next cell membrane and then the next. The movement of  charged particles across a cell membrane that causes the inside of the cell to become positive is called depolarization. Depolarization, which is an electrical event, must take place before the heart can contract  and pump blood, which is a mechanical event.  An impulse normally begins in the pacemaker cells found in the SA node of the heart. A chain reaction occurs from cell to cell in the heart  s electrical conduction system until all the cells have been stimulated and depolarized. This chain reaction is a  wave of depolarization that proceeds from the innermost  layer of the heart (ie, endocardium) to the outermost layer (ie, epicardium). Eventually the impulse is spread from the pacemaker cells to the working myocardial cells, which contract when they are stimulated. When the atria are stimulated, a P wave is recorded on the ECG; thus the P wave represents atrial depolarization. When the ventricles are stimulated, a QRS complex is recorded on the ECG; thus the QRS complex represents ventricular depolarization. ’

ACLS Pearl Depolarization is notthe same as contraction. Depolarization is an electrical event that is expected to result in contraction, which is a mechanical event. It is possible to see organized electrical activity on the cardiac monitor, even when the assessment of the patient reveals no palpable pulse. This clinical situation is called pulseless electrical activity (PEA).

Repolarization [Objective 2]  After the cell depolarizes, it quickly begins to recover and restore its electrical charges to normal. The movement of charged particles across a cell membrane in which the inside of the cell is restored to its negative charge is called repolarization.  The cell membrane stops the flow of Na + into the cell and allows K + to leave it. Negatively charged particles are left inside the cell; thus the cell is returned to its resting state. This causes contractile proteins in the working myocardial cells to separate (ie, relax).  The cell can be stimulated again if another electrical impulse arrives at the cell membrane. Repolarization proceeds from the epicardium to the endocardium. On the ECG, the ST segment and T wave represent   ventricular repolarization.

Phases of the Cardiac Action Potential [Objective 2]  The action potential of a cardiac cell reflects the rapid sequence of voltage changes that occur across the cell membrane during the electrical cardiac cycle. The configuration of the action potential varies depending on the location, size, and function of the cardiac cell (Fig. 3.3).  There are two main types of action potentials in the heart. The first type, the fast response action potential, occurs in normal atrial and ventricular myocardial cells and in the Purkinje fibers, which are specialized conducting fibers found in both ventricles that conduct an electrical impulse through the heart. The second type of cardiac action potential, the slow response action potential, occurs in the heart s normal pacemaker (ie, the SA node) and in the AV node, which is the specialized conducting tissue that  carries an electrical impulse from the atria to the ventricles. ’

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CARDIAC ACTION POTENTIALS Ventricle    )    V   m    (    l   a    i    t   n   e    t   o   p   e   n   a   r    b   m   e    M

+20

1

Atrium

Sinoatrial node

1

2

2

0 –20

0 0

3

0

–40

3

4

–60 –80

3

4

4

–100

A

100 msec

B

C

100 msec

100 msec

Fig. 3.3 Cardiac action potentials in the ventricle, atrium, and sinoatrial (SA) node. The numbers correspond to the phases of theaction potentials. A, Ventricle. B, Atrium. C, SA node. (From Costanzo LS:Physiology , ed 5, Philadelphia, 2014,Saunders.)

ACLS Pearl  Although there is no universally accepted classification scheme for antiarrhythmic agents, a commonly used system is to classify the medications by their effects on the cardiac action potential. For example, Class I antiarrhythmic medications such as procainamide and lidocaine block sodium channels, interfering with phase 0 depolarization. Class IV antiarrhythmics (ie, Ca ++ channel blockers) such as verapamil and diltiazem slow the rate at which calcium passes through the cells, interfering with phase 2 in the cells of the atria, ventricles, and Purkinje fibers.

Refractory Periods [Objective 3] Refractoriness is a term that is used to describe the period of recovery that cells need after being discharged before they are able to respond to a stimulus. During the ventricular  absolute refractory period (ARP), the cell will not respond to further stimulation within itself ( Fig. 3.4). This means that the myocardial working cells cannot contract and that the pacemaker cells cannot conduct an electrical impulse, no matter how strong the internal electrical stimulus.

+20

0    )    V   m    (    l   a    i    t   n   e    t   o   p   e   n   a   r    b   m   e    M

–20

RRP ARP

–40 SNP –60

ERP

–80

–100

Fig. 3.4   Refractory periods of the ventricular action potential. The effective refractory period (ERP) includes the absolute refractory period (ARP) and the first half of the relative refractory period (RRP). The RRP begins when the ARP ends and includes the last portion of the ERP. The supernormal period (SNP) begins when the RRP ends. (From Costanzo LS:  Physiology , ed 5, Philadelphia, 2014, Saunders.)

CHAPTER 3   Cardiac Anatomy and Electrophysiology

 The effective refractory period (ERP) includes the ARP and the first half of the RRP (see  Fig. 3.4).  The distinction between the absolute and effective refractory periods is that  absolute  means absolutely  no stimulus is large enough to generate another action potential;  effective   means that a   conducted   action potential cannot be generated (ie, there is not enough inward current to conduct to the next site). (Costanzo, 2014, p. 135)  The relative refractory period (RRP) begins at the end of the ARP and ends when the cell membrane is almost fully repolarized. During the RRP, some cardiac cells have repolarized to their threshold potential and thus can be stimulated to respond (ie, depolarize) to a stronger-than-normal stimulus.  After the RRP is a  supernormal period (SNP). Because the cell is more excitable than normal during  this period, a weaker-than-normal stimulus can cause cardiac cells to depolarize and cause the development of dysrhythmias (see Fig. 3.4). “

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CONDUCTION SYSTEM  The heart  s pacemaker cells are arranged in a system of interconnected pathways called the  conduction system. The conduction system makes sure that the chambers of the heart contract in a coordinated fashion. ’

Sinoatrial Node [Objectives 4, 5]  The normal heartbeat is the result of an electrical impulse (ie, an action potential) that begins in the SA node. The SA node is normally the primary pacemaker of the heart because it has the fastest firing rate of  all of the heart s normal pacemaker sites (Fig. 3.5). The built-in (ie, intrinsic) rate of the SA node is 60 to 100 beats per minute (beats/min).  The SA node is richly supplied by sympathetic and parasympathetic nerve fibers. Although the SA node normally fires at a rate of 60 to 100 beats/min, this rate can increase to about 180 beats/min, primarily through sympathetic stimulation. Heart rates faster than 150 beats/min can be problematic ’

Sinoatrial node

Atrioventricular node

Right atrium

Left atrium

Bundle of His (common bundle) Right bundle branch

Right ventricle

Left ventricle

Left bundle branch

Purkinje fibers

Fig. 3.5   Conduction pathways through the normal heart. (From Costanzo LS:   Physiology , ed 5, Philadelphia, 2014, Saunders.)

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because: (1) the duration of diastole shortens as heart rate increases, reducing ventricular filling time and, potentially, stroke volume, and (2) the heart  s workload and oxygen requirements are increased, but the time for coronary artery filling, which occurs during diastole, is decreased (DeBeasi, 2003).  Areas of the heart other than the SA node can initiate beats and assume pacemaker responsibility  under special circumstances. The term ectopic, which means out of place, or   latent   is used to describe an impulse that originates from a source other than the SA node. Ectopic pacemaker sites include the cells of the AV bundle and Purkinje fibers, although their intrinsic rates are slower than that of  the SA node. ’

ACLS Pearl  Although the presence of ectopic pacemakers provides a backup or safety mechanism in the e vent of SA node failure, ectopic pacemaker sites can be problematic if they fire while the SA node is still functioning. For example, ectopic sites may cause early (ie, premature) beats or sustained rhythm disturbances.

 Atrioventricular Node and Bundle [Objectives 4, 5] Conduction through the AV node begins before atrial depolarization is completed. The AV node is supplied by both sympathetic and parasympathetic nerve fibers.  The bundle of His, also called the common bundle  or the AV bundle, is located in the upper portion of the interventricular septum and connects the AV node with the bundle branches. When the AV  node and bundle are bypassed by an abnormal pathway, the abnormal route is called an  accessory  pathway.  The AV bundle has pacemaker cells that have an intrinsic rate of 40 to 60 beats/min. The AV node and the AV bundle are called the AV junction. The term His-Purkinje system or  His-Purkinje network refers to the bundle of His, bundle branches, and Purkinje fibers.

ACLS Pearl  Abnormal cardiac rhythms that develop near or within the AV node are called junctional dysrhyth mias. Those that develop above the bundle of His or activate the ventricles through an accessory pathway are called  supraventricular dysrhythmias.  Dysrhythmias that develop below the bundle of His are called ventricular dysrhythmias.

Right and Left Bundle Branches [Objective 4]  The right bundle branch innervates the right ventricle. The left bundle branch spreads the electrical impulse to the interventricular septum and left ventricle. The left bundle branch divides into  fascicles,  which are small bundles of nerve fibers that allow electrical innervation of the larger, more muscular left   ventricle.

Purkinje Fibers [Objectives 4, 5]  The right and left bundle branches divide into smaller and smaller branches and then into a special net work of fibers called the Purkinje fibers. The Purkinje fibers have pacemaker cells that have an intrinsic rate of 20 to 40 beats/min. The electrical impulse spreads rapidly through the right and left bundle branches and the Purkinje fibers to reach the ventricular muscle. The electrical impulse spreads from the endocardium to the myocardium, finally reaching the epicardial surface. The conduction system is summarized in Table 3.1.

CHAPTER 3   Cardiac Anatomy and Electrophysiology

TABLE 3.1

Summary of the Conduction System Intrinsic Pacemaker Rate (beats/min)

Structure

Function

Sinoatrial (SA) node

Primary pacemaker; initiates impulse that is normally 60 to 100 conducted throughout the left and right atria Receives impulse from SA node and delays relay of  the impulse to the bundle of His, allowing time for the atria to empty their contents into the ventricles before the onset of ventricular contraction. Receives impulse from AV node and relays it to right  40 to 60 and left bundle branches Receives impulse from bundle of His and relays it to Purkinje fibers Receives impulse from bundle branches and relays it  20 to 40 to ventricular myocardium

 Atrioventricular (AV) node

Bundle of His (AV bundle) Right and left bundle branches Purkinje fibers

 THE ELECTROCARDIOGRAM  The  electrocardiogram (ECG) is a graphic display of the heart s electrical activity. When electrodes are attached to the patient  s limbs or chest and connected by cables to an ECG machine, the ECG machine functions as a voltmeter, detecting and recording the changes in voltage (ie, action potentials) generated by depolarization and repolarization of the heart  s cells. The voltage changes are displayed as specific waveforms and complexes (Fig. 3.6). Practice standards for ECG monitoring  are shown in  Box 3.1. ’

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Sinoatrial (SA) node

Atrial excitation Excitation of ventricles begins (initial downward deflection is a Q wave) Pulmonary artery R

Left atrium Right atrium Internodal pathways

T Septum Left ventricle

Atrioventricular (AV) node

AV bundle (bundle of His)

P

Q S

Right ventricle

Fig. 3.6 Schematic drawing of the conducting system of the heart. An impulse normally is generated in the SA node and travels through the atria to the atrioventricular (AV) node, down the bundle of His and Purkinje fibers, and to the ventricular myocardium. Recording of the depolarizing and repolarizing currents in the heart with electrodes on the surface of the body produces characteristic waveforms. (From Copstead-Kirkhorn LE, Banasik JL: Pathophysiology , ed 5, St Louis, 2013, Saunders.)

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Practice Standards for Cardiac Monitoring

BOX 3.1

Cardiac monitoring is indicated in most, if not all, of the following: • Patients resuscitated from sudden cardiac death • Patients in the early phase of ACSs • Patients with unstable coronary syndromes and newly diagnosed high-risk coronary lesions • Adults and children who have undergone cardiac surgery • Patients who have undergone nonurgent percutaneous coronary intervention with complications • Patients who have undergone implantation of an automated defibrillator lead or 

•

• •

•

• • • • • •

a pacemaker lead and who are considered pacemaker dependent Patients with a temporary pacemaker or  transcutaneous pacing pads Patients with AV block  Patients with arrhythmias and WolffParkinson-White syndrome Patients with long-QT syndrome and arrhythmias Patients with intra-aortic balloon pumps Patients with acute heart failure Patients with indications for intensive care Patients undergoing conscious sedation Patients with unstable arrhythmias Pediatric patients with symptoms of  arrhythmia

(Drew, et al., 2004)

Fig. 3.7 Electrodes are adhesive pads applied at specific locations on the patient s chest wall and limbs. (Courtesy Bruce R. ’

Shade, EMT-P, EMS-I, AAS.)

Electrodes Electrode refers to an adhesive pad containing a conductive substance in the center that is applied to the patient s skin (Fig. 3.7). The conductive media of the electrode conducts skin surface voltage changes through wires to a cardiac monitor (ie, electrocardiograph). Electrodes are applied at specific locations on the patient s chest wall and extremities to view the heart  s electrical activity from different angles and planes. One end of a monitoring cable, which is also called a   lead wire, is attached to the electrode and the other end to an ECG machine. The cable conducts current back to the cardiac monitor. Three-lead wire systems are often used with portable monitor defibrillators. Five-lead wire systems allow viewing of the six limb leads (ie, I, II, III, aVR, aVL, and aVF) and one chest lead. ’

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Leads [Objective 6]  A lead is a record (ie, tracing) of electrical activity between two electrodes. Each lead records the  average  current flow at a specific time in a portion of the heart. A 12-lead ECG provides views of the heart in both the frontal and horizontal planes and views the surfaces of the left ventricle from 12 different angles. From this, ischemia, injury, and infarction affecting areas of the heart can be identified. The 12-lead ECG is an essential part of the diagnostic workup of patients with a suspected ACS.

CHAPTER 3   Cardiac Anatomy and Electrophysiology

Frontal Plane Leads [Objectives 6, 7] Six leads view the heart in the frontal plane. Leads I, II, and III are called standard limb leads. Leads aVR, aVL, and aVF are called augmented limb leads.  A bipolar lead  is an ECG lead that has a positive and negative electrode. Each lead records the difference in electrical potential (ie, voltage) between two selected electrodes. Although all ECG leads are technically bipolar, leads I, II, and III use two distinct electrodes, one of which is connected to the positive input of the ECG machine and the other to the negative input ( Wagner, et al., 2009). Leads I, II, and III make up the standard limb leads. If an electrode is placed on the right arm, left arm, and left leg, three leads are formed (Fig. 3.8). The positive electrode is located at the left wrist in lead I,  while leads II and III both have the positive electrode located at the left foot. The difference in electrical potential between the positive pole and its corresponding negative pole is measured by each lead. Leads aVR, aVL, and aVF are limb leads that record measurements at a specific electrode with respect  to a reference electrode (see Fig. 3.8). The a  in aVR, aVL, and aVF refers to augmented. The V   refers to voltage, and the last letter refers to the position of the positive electrode. The R  refers to the rightarm, the L  to left arm, and the F   to left foot (ie, leg). A summary of the limb leads appears in Table 3.2. “

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Horizontal Plane Leads [Objectives 6, 7] Six chest (ie, precordial or  V  ) leadsview the heart in the horizontal plane. This allows a view of the front  and left side of the heart. The chest leads are identified as V 1, V 2, V 3, V 4, V 5, and V 6. Each electrode placed in a  V   position is a positive electrode (Fig. 3.9). A summary of the chest leads can be found in  Table 3.3. “

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”

ACLS Pearl Lead V 1  is particularly useful for analyzing dysrhythmias that have a wide QRS complex (eg, bundle branch blocks, ventricular pacemaker rhythms, wide-QRS tachycardias).

Fig. 3.8 View of the standard limb leads and augmented leads. LA, left arm; LL, left leg; RA, right arm. (From Boron WF: Medical physiology, ed 2 updated edition, Philadelphia, 2011, Saunders.)

TABLE 3.2

Limb Leads

Lead

Positive Electrode Position

Negative Electrode Position

Heart Surface Viewed

I II III aVR aVL aVF

Left arm Left leg Left leg Right arm Left arm Left foot (ie, leg)

Right arm Right arm Left arm Reference electrode Reference electrode Reference electrode

Lateral Inferior Inferior None Lateral Inferior

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CHAPTER 3   Cardiac Anatomy and Electrophysiology

Midclavicular line

Anterior axillary line Midaxillary line

X

X X

V1

X

V3 V2

X

X

V5 V4

V6

Fig. 3.9 Chest (ie, precordial) leads V 1 through V 6. (From Copstead-Kirkhorn LE, Banasik JL: Pathophysiology , ed 5, St Louis, 2013, Saunders.)

TABLE 3.3

Chest Leads

Lead

Positive Electrode Position

Heart Area Viewed

 V 1  V 2  V 3  V 4  V 5  V 6

Right side of sternum, fourth intercostal space Left side of sternum, fourth intercostal space Midway between V 2  and V 4 Left midclavicular line, fifth intercostal space Left anterior axillary line; same level as V 4 Left midaxillary line, fifth intercostal space

Interventricular septum Interventricular septum Anterior surface Anterior surface Lateral surface Lateral surface

Right chest leads are used to evaluate the right ventricle(Fig. 3.10). The placement of right chest leads is identical to the placement of the standard chestleads except that it is done on the rightside of the chest. If time does not permit obtaining all of the right chest leads, the lead of choice is V 4R. A summary of the right chest leads can be found in Table 3.4. Leads V 7, V 8, and V 9 permit viewing of the posterior surface of the heart ( Fig. 3.11). All of the leads are placed on the same horizontal line as V 4 to V 6.LeadV 7 is placed at the posterior axillary line. Lead V 8 is placed at the angle of the scapula (ie, the posterior scapular line), and lead V 9  is placed over the left  border of the spine.

ACLS Pearl Multiple-lead ECGs are used to help spot infarctions of the right ventricle and the posterior wall of  the left ventricle. The 15-lead ECG uses all of the leads of a standard 12-leadECG plus leads V 4R, V 8, and V 9  or a standard 12-lead plus posterior leads V 7, V 8, and V 9. A 16-lead ECG machine allows recording of a standard 12-lead plus leads V 3R, V 4R, V 5R, and V 6R. An 18-lead ECG uses all of  the leads of a standard 12-lead ECG plus leads V 4R, V 5R, V 6R, V 7. V 8, and V 9.

CHAPTER 3   Cardiac Anatomy and Electrophysiology

Midclavicular line Anterior axillary line Angle of Louis

Midaxillary line

RIGHT CHEST LEADS V1R: Fourth intercostal space (ICS) at left sternal border (same as V 2)

1 2 3

V2R: Fourth ICS at right sternal border (same as V 1)

4 5

V3R: Halfway between V 2R and V4R

6 V4R: Right midclavicular line in the fifth ICS

7 8

V5R: Right anterior axillary line at the fifth ICS

9 V6R: Right midaxillary line at the fifth ICS V6R V5R

V4R V3R V2R V1R

Fig. 3.10 Electrode locations for recording a right chest electrocardiogram (ECG). Right chest leads are not part of a standard 12-lead ECG but are used when a right ventricular infarction is suspected. (From Drew BJ, Ide B: Right ventricular infarction, Prog Cardiovascular Nurs   10:46, 1195.)

TABLE 3.4

Right Chest Leads and Their Placement

Lead

Placement

 V 1R  V 2R  V 3R  V 4R  V 5R  V 6R

Left side of sternum, fourth intercostal space Right side of sternum, fourth intercostal space Midway between V2R   and V 4R Right midclavicular line, fifth intercostal space Right anterior axillary line; same level as V4 R Right midaxillary line, fifth intercostal space

Posterior axillary line

Left paraspinal

Midaxillary line 1 2 3

LEFT POSTERIOR LEADS V7: Posterior axillary line at the same level as V 4 to V6

4 5 6

V8: Halfway between V 7 and V9

7 8

V9: Left paraspinal line at the same level as V 4 to V6

9

V6

V7

V8

V9

Fig. 3.11 Posterior chest lead placement. (From Drew BJ, Ide B: Right ventricular infarction, Prog Cardiovascular Nurs  10:46, 1195.)

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   V   m    1  .    0   =   m   m    1

5 mm = 0.20 s

   )   e   g   a    t    l   o   v    (

   V   m    5  .    0   =   m   m    5

  e    d   u    t    i    l   p   m    A

1 mm = 0.04 s

Duration (time)

Fig. 3.12 ECG strip showing the markings for measuring amplitude and duration of waveforms, using a standard recording speed of 25 mm/sec. (From Copstead-Kirkhorn LE, Banasik JL:  Pathophysiology , ed 5, St Louis, 2013, Saunders.)

Electrocardiography Paper ECG paper is graph paper made up of small and large boxes measured in millimeters (mms). The smallest boxes are 1 mm wide and 1 mm high (Fig. 3.12). The horizontal axis of the paper corresponds  with time, which is stated in seconds. ECG paper normally records at a constant speed of 25 mm/second.  Thus each horizontal 1 mm box represents 0.04 second (25 mm/sec  0.04 second ¼ 1 mm). The lines after every five small boxes on the paper are heavier. The heavier lines indicate one large box, which represents 0.20 second.  The vertical axis of the graph paper represents the voltage or amplitude of theECG waveformsor deflections. Voltage is measured in mV. Amplitude is measured in mm. When properly calibrated, a small box is 1 mm high (ie, 0.1 mV), and a large box, which is equal to five small boxes, is 5 mm high (ie, 0.5 mV).

 Waveforms and Complexes [Objective 8]  An ECG waveform (ie, a deflection) is movement away from the baseline (ie, isoelectric line) in either a  positive (ie, upward) or negative (ie, downward) direction. Waveforms are named alphabetically, beginning with P, QRS, and T (Fig. 3.13).  The P wave is the first waveform in the cardiac cycle and represents atrial depolarization and the spread of the electrical impulse throughout the right and left atria. A P wave is normally positive (ie, upright) in standard leads and precedes each QRS complex. Atria

Ventricles

+1

RR interval R wave

PR interval

T wave

ST segment

P wave Voltage (mV)

0

SA AV node node

S wave Q wave

QRS duration

The ECG cannot show the electrical activity of these five structures.

Bundle of His Bundle branches Purkinje network

QT interval

–1 0

0.2

0.4

0.6

0.8

1.0 Time (sec)

1.2

1.4

1.6

1.8

2.0

Fig. 3.13 Components of the ECG recording. AV, atrioventricular; SA, sinoatrial. (From Boron WF: Medical physiology , ed 2 updated edition, Philadelphia, 2011, Saunders.)

CHAPTER 3   Cardiac Anatomy and Electrophysiology

 The QRS complex consists of the Q wave, R wave, and S wave. It represents the spread of the electrical impulse through the ventricles (ie, ventricular depolarization). A QRS complex normally follows each P wave. In adults, the normal duration of the QRS complex is 0.11 second or less (Surawicz, et al., 2009). When viewing the chest leads in a normal heart, the R wave becomes taller (ie, increases in amplitude) and the S wave becomes smaller as the electrode is moved from right to left. This pattern is called R-wave progression. The transition zone   is the area at which the amplitude of the R wave begins to exceed the amplitude of the S wave (Ganz, 2012). This usually occurs in the area of leads V 3  and V 4. Poor R-wave progression is a phrase used to describe R waves that decrease in size from V 1 to V 4. Possible causes include right or left ventricular hypertrophy and left bundle branch block, among other causes. Poor R-wave progression may also be a nonspecific indicator of anterior wall infarction. Electrode placement in the correct intercostal space is critical when evaluating R-wave progression. Ventricular repolarization is represented on the ECG by the ST segment (discussed later) and the  T wave. The direction of the T wave is normally the same as the QRS complex that precedes it.  A U wave is a small waveform that, when seen, follows the T wave. The U wave is thought to represent  repolarization of the Purkinje fibers in the papillary muscle of the ventricular myocardium.

Segments and Intervals [Objectives 8, 9]  A segment   is a line between waveforms. It is named by the waveform that precedes or follows it. An interval is made up of a waveform and a segment.  The PR segment is the horizontal line between the end of the P wave and the beginning of the QRS complex. The P wave plus the PR segment equals the PR interval. The PR interval normally measures 0.12 to 0.20 second in adults.  The TP segment is the portion of the ECG tracing between the end of the T wave and the beginning  of the next P wave, during which there is no electrical activity (Fig. 3.14). When the heart rate is within normal limits, the TP segment is usually isoelectric and is used as the reference point from which to estimate the position of the isoelectric line and determine ST segment displacement. With rapid heart  rates, the TP segment is often unrecognizable because the P wave encroaches on the preceding T wave.  When the TP segment is unrecognizable, the PR segment is used as the reference point from which to estimate the position of the isoelectric line.  The portion of the ECG tracing between the QRS complex and the T wave is the ST segment (see Fig. 3.13). The ST segment represents the early part of repolarization of the right and left ventricles. In the limb leads, the normal ST segment is isoelectric (ie, flat) but may normally be slightly elevated or depressed. The point where the QRS complex and the ST segment meet is called the  ST junction or the J point. The ST segment is considered elevated if the segment is deviated above the baseline and is considered depressed if the segment deviates below it. Various conditions may cause the displacement of the ST segment from the isoelectric line in either a positive or a negative direction. Some displacement of the ST segment from the isoelectric line is normal and dependent on age, gender, and ECG lead.  When looking for ST segment elevation or depression, first locate the J point. Next use the TP segment to estimate the position of the isoelectric line. Then compare the level of the ST segment to the isoelectric line. Deviation is measured as the number of mm of vertical ST segment displacement from the isoelectric line or from the patient s baseline at the J point ( Thygesen, et al., 2012). Proper machine ’

R T

P QS

P

TP-segment

PR-segment

Fig. 3.14 The TP segment is used as the reference point for the isoelectric line. (From Aehlert B: ECGs made easy, ed 3, St. Louis, 2006, Mosby.)

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BOX 3.2

Systematic Rhythm Interpretation

1. Assess regularity (atrial and ventricular). 2. Assess rate (atrial and ventricular). 3. Identify and examine waveforms.

4. Assess intervals (eg, PR, QRS, QT) and examine ST segments. 5. Interpret the rhythm and assess its clinical significance.

calibration is critical when analyzing ST segments. The ST segment criteria described here apply  only   when the monitor is adjusted to standard calibration.  The QT interval is the period from the beginning of the QRS complex to the end of the T wave (see Fig. 3.13). It represents total ventricular activity; this is the time from ventricular depolarization (ie, acti vation) to repolarization (ie, recovery). The QT interval is measured from the beginning of the QRS complex to the end of the T wave. In the absence of a Q wave, the QT interval is measured from the beginning ofthe R wave to the end of the T wave. The term QT interval   is used regardless of whether  the QRS complex begins with a Q wave or an R wave.  The duration of the QT interval varies in accordance with age, gender, and heart rate. As the heart  rate increases, the QT interval shortens (ie, decreases). As the heart rate decreases, the QT interval lengthens (ie, increases). Because of the variability of the QT interval with the heart rate, it can be measured more accurately if it is corrected (ie, adjusted) for the patient  s heart rate. The corrected QT interval is noted as QTc.  The QT interval is considered short if it is 0.39 second or less and prolonged if it is 0.46 second or longer in women or 0.45 second or longer in men (Rautaharju, et al., 2009). A prolonged QT interval may be congenital or acquired and indicates a lengthened RRP. A QTc of more than 0.50 second in either gender has been correlated with a higher risk for  life-threatening dysrhythmias (eg, torsades de pointes [TdP]). A systematic approach to rhythm analysis appears in Box 3.2. ’

 ACUTE CORONARY SYNDROMES  Acute coronary syndromes (ACSs) are a group of conditions that are caused by an abrupt reduction in coronary artery blood flow ( Amsterdam, et al., 2014). Myocardial ischemia, injury, and infarction are among the causes of ST segment deviation. When ECG changes of myocardial ischemia, injury, or infarction occur, they are not found in every lead of the ECG.  Indicative changes   are ECG findings that are seen in leads that look directly at the area fed by the blocked vessel.  Reciprocal changes, also called mirror image changes,  are ECG findings that are seen in leads opposite the affected area. Indicative changes are significant when they are seen in two anatomically contiguous  leads. Two leads are contiguous if they look at the same or adjacent areas of the heart or if they are numerically consecutive chest leads. ST segment depression of 0.5 mm or more in a patient who is experiencing an ACS is suggestive of myocardial ischemia when it is viewed in two or more anatomically contiguous leads ( Amsterdam, et al., 2014). Evidence of myocardial injury can be seen on the ECG as ST segment elevation (see Chapter 7).

ACLS Pearl The LMCA perfuses a large area of the anterior wall of the heart. Research has shown that ST segment elevation in lead aVR can predict occlusion of the LMCA ( Lawner, et al., 2012 ).

CHAPTER 3   Cardiac Anatomy and Electrophysiology

PUTTING IT ALL TOGETHER CHAPTER QUIZ

 Multiple Choice  Identify the choice that best completes the statement or answers the question.

____

1.

In the heart  s conduction system, the ___ receive(s) an electrical impulse from the right  and left bundle branches and relay(s) it to the ventricular myocardium.  A. Purkinje fibers B. SA node C. AV node D. Atrial pacemaker cells

____

2.

When the heart rate is within normal limits, which of the following is used as the reference point from which to estimate the position of the isoelectric line and determine ST segment displacement?  A. PR segment  B. TP segment  C. QT interval D. QRS complex

____

3.

Which of the following represent ventricular repolarization on the ECG?  A. P wave and PR interval B. ST segment and T wave C. PR interval and ST segment  D. QRS complex and ST segment 

____

4.

The period during the cardiac cycle when cells cannot respond to a stimulus, no matter  how strong, is called the:  A. Supernormal period. B. Depolarized period. C. Relative refractory period. D. Absolute refractory period.

____

5.

Which of the following are the main branches of the left coronary artery?  A. Marginal and oblique arteries B. CX and marginal arteries C. Anterior descending and oblique arteries D. CX and anterior descending arteries

____

6.

Which of the following leads view the heart in the frontal plane?  A. I, II, III, V 1, V 2, and V 3 B. V 1, V 2, V 3, V 4, V 5, and V 6 C. I, II, III, aVR, aVL, and aVF  D. aVR, aVL, aVF, V 4, V 5, and V 6

____

7.

What does the QRS complex represent?  A. Atrial depolarization B. Ventricular contraction C. Ventricular depolarization D. Ventricular repolarization

’

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 Matching  Match each description with its corresponding answer .

 A. B. C. D.

TP segment PR segment QT interval ST segment

E. F. G. H.

P wave Interval QRS complex PR interval

____

8.

Represents atrial depolarization

____

9.

A waveform and a segment 

____

10.

Normally measures 0.11 second or less in adults

____

11.

Horizontal line between the end of the P wave and the beginning of the QRS complex

____

12.

Portion of the ECG tracing between the end of the T wave and the beginning of the next P wave

____

13.

Normally measures 0.12 to 0.20 second in adults

____

14.

Portion of the ECG tracing between the QRS complex and the T wave

____

15.

Represents total ventricular activity: the time from ventricular depolarization (ie, stimulation) to repolarization (ie, recovery)

CHAPTER QUIZ ANSWERS

 Multiple Choice

1. A. The right and left bundle branches divide into smaller and smaller branches and then into a special network of fibers called the Purkinje fibers. These fibers spread from the interventricular septum into the papillary muscles. They continue downward to the apex of the heart, making up an elaborate web that penetrates about one-third of the way into the ventricular muscle mass. The fibers then become continuous with the muscle cells of the right and left ventricles. The Purkinje fibers have pacemaker  cells that have an intrinsic rate of 20 to 40 beats/min. OBJ: Describe the normal sequence of electrical conduction through the heart. 2. B. When the heart rate is within normal limits, the TP segment is usually isoelectric and used as the reference point from which to estimate the position of the isoelectric line and determine ST segment  displacement. With rapid heart rates, the TP segment is often unrecognizable because the P wave encroaches on the preceding T wave. When the TP segment is unrecognizable, the PR segment  is used as the reference point from which to estimate the position of the isoelectric line. OBJ: Define and describe the significance of each of the following as they relate to cardiac electrical activity: the P wave, the QRS complex, the T wave, the U wave, the PR segment, the TP segment, the ST segment, the PR interval, the QRS duration, and the QT interval. 3. B. On the ECG, the ST segment and T wave represent ventricular repolarization. OBJ: Define and describe the significance of each of the following as they relate to cardiac electrical activity: the P wave, the QRS complex, the T wave, the U wave, the PR segment, the TP segment, the ST segment, the PR interval, the QRS duration, and the QT interval. 4. D. During the ARP, the cell will not respond to further stimulation within itself. This means that the myocardial working cells cannot contract and the cells of the electrical conduction system cannot conduct an electrical impulse, no matter how strong the internal electrical stimulus. As a result, tetanic (ie, sustained) contractions cannot be provoked in cardiac muscle. OBJ: Define the absolute, effective, relative refractory, and supernormal periods and their locations in the cardiac cycle.

CHAPTER 3   Cardiac Anatomy and Electrophysiology

5. D. The CX and anterior descending arteries are the main branches of the LCA. OBJ: Name the primary branches and areas of the heart supplied by the right and left coronary  arteries. 6. C. Frontal plane leads view the heart from the front of the body as if it were flat. Directions in the frontal plane are superior, inferior, right, and left. Six leads view the heart in the frontal plane. Leads I, II, and III are called standard limb leads. Leads aVR, aVL, and aVF are called augmented limb leads. Six chest (ie, precordial or  V  ) leads view the heart in the horizontal plane. The chest leads are identified as V 1, V 2, V 3, V 4, V 5, and V 6. OBJ: Differentiate between the frontal plane and the horizontal plane leads. “

”

7. C. When the ventricles are stimulated, a QRS complex is recorded on the ECG. Thus the QRS complex represents ventricular depolarization. OBJ: Define and describe the significance of each of the following as they relate to cardiac electrical activity: the P wave, the QRS complex, the T wave, the U wave, the PR segment, the TP segment, the ST segment, the PR interval, the QRS duration, and the QT interval.  Matching

8. E 9. F  10. G 11. B 12. A 13. H 14. D 15. C

REFERENCES  Amsterdam, E. A., We nger, N. K., Brindis, R. G., Casey, D. E., Ganiats, T. G., Holmes, D. R.,et al. (2014). 2014  AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes. J Am Coll Cardiol , 1 – 150. Costanzo, L. S. (2014). Cardiovascular physiology. In Physiology  (5th ed., pp. 113 – 184). Philadelphia: Saunders. DeBeasi, L. C. (2003). Physiology of the cardiovascular system. In S. A. Price, & L. M. Wilson (Eds.), Pathophysiology: Clinical concepts of disease processes  (6th ed., pp. 416 – 428). St. Louis: Mosby. Drew, B. J., Califf, R. M., Funk, M., Kaufman, E. S., Krucoff, M. W., Laks, M. M.,et al. (2004). Practice standards for electrocardiographic monitoring in hospital settings: An American Heart Association scientific statement  from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young. Circulation, 110 , 2721 – 2746. Ganz, L. (2012). Electrocardiography. In L. Goldman, & A. I. Schafer (Eds.), Goldman s Cecil medicine  (24th ed., pp. 272 – 278). Philadelphia: Saunders. Lawner, B. J.,Nable, J. V., & Mattu, A. (2012). Novel patterns of ischemiaand STEMI equivalents.Cardiol Clin, 30  (4), 591 – 599. Surawicz, B., Childers, R., Deal, B. J., & Gettes, L. S. (2009). AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part III: Intraventricular conduction disturbances:  A scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee.  J Am Coll Cardiol , 53(11), 976 – 981.  Thygesen, K., Alpert, J. S., Jaffe, A. S., Simoons, M. L., Chaitman, B. R., & White, H. D. (2012). Third universal definition of myocardial infarction. Circulation, 126(16), 2020 – 2035.  Wagner, G. S., Macfarlane, P., Wellens, H., Josephson, M., Gorgels, A., Mirvis, D. M.,et al. (2009). AHA/ACCF/  HRS recommendations for the standardization and interpretation of the electrocardiogram:Part VI: Acute ischemia/infarction: A scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee. J Am Coll Cardiol ,  53, 1003 – 1011. ’  

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CHAPTER

4

Cardiac Arrest Rhythms INTRODUCTION Evaluation of your ability to manage a patient who is experiencing a cardiac arrest and your ability to manage the team who will assist you in providing patient care is part of the Advanced Cardiac Life Support (ACLS) course. This chapter discusses the cardiac arrest rhythms and their management; defibrillation; and the roles and responsibilities of each member of the resuscitation team.

DESIRED RESULTS

G O A L Given a patient situation, and working in a team setting, competently direct the initial emer gency care (including mechanical, pharmacologic, and electrical therapy where applicable) for a  patient experiencing a cardiac arrest.

LEARNING OBJECTIVES

 After completing this chapter, you should be able to: 1.  Identify four cardiac rhythms that are associated with cardiac arrest. 2.  Differentiate between shockable and nonshockable cardiac arrest rhythms. 3.  Given a patient situation, describe the electrocardiogram (ECG) characteristics and initial emergency care for cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 4.  Explain defibrillation, its indications, proper pad or paddle placement, relevant precautions, and the steps required to perform this procedure with a manual defibrillator  and an automated external defibrillator (AED). 5.  Differentiate between monophasic and biphasic defibrillation. 6. Identify the energy levels that are currently recommended, and indicate if the shock  delivered should be a synchronized or unsynchronized countershock, for pulseless monomorphic ventricular tachycardia (VT), polymorphic VT (PMVT), and ventricular  fibrillation (VF). 7. Describe the role of each member of the resuscitation team. 8.  Discuss the events of a typical resuscitation effort. 9.  Discuss immediate post–cardiac arrest care upon return of spontaneous circulation (ROSC). 10.  Recognize the opportunities provided when a postevent debriefing is held. 11.  Discuss the use of the SPIKES protocol when conveying bad news.

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LEARNING PLAN • •

• •

Read this chapter before class. Master identification of the following rhythms: VF, monomorphic VT, PMVT, asystole, and pulseless electrical activity (PEA). Master the following medications: O2, epinephrine, amiodarone, and lidocaine. Master the following skills: Ensure scene safety and the use of personal protective equipment. Assign team member roles or perform as a team member in a simulated patient situation. Direct or perform an initial patient assessment. Quickly recognize cardiopulmonary arrest. Demonstrate familiarity with the cardiac arrest algorithm. Ensure the performance of high-quality cardiopulmonary resuscitation (CPR) when indicated. Demonstrate safe operation of a manual defibrillator and an AED if electrical therapy is indicated. Demonstrate an understanding of the actions, indications, dosages, adverse effects, and contraindications for the medications used in the treatment of cardiac arrest. Consider the possible reversible causes of a cardiac emergency. Direct the performance of appropriate airway management throughout a resuscitation effort. Recognize the ROSC and direct the performance of immediate post–cardiac arrest care. Review your performance as a team leader or team member during a postevent debriefing. Develop and use flashcards, flowcharts, and mnemonics to help enhance your retention of  the information presented. Complete the chapter quiz and review the quiz answers provided. Read the case studies at the end of this chapter and compare your answers with the answers provided. • • • • • •

•

•

• •

•

•

•

• •

KEY TERMS

 Automated external defibrillation  The placement of paddles or pads on a patient ’s chest and interpretation of the patient’s cardiac rhythm by the defibrillator ’s computerized analysis system. Depending on the type of AED used, the machine will deliver a shock (if a shockable rhythm is detected) or instruct the operator to deliver a shock. Defibrillation Delivery of an electrical current across the heart muscle over a very brief period to terminatean abnormal heart rhythm;also calledunsynchronizedcountershock or  asynchronous countershock because the delivery of current has no relationship to the cardiac cycle. Defibrillator  A device used to administer an electrical shock at a preset energy level to terminate a cardiac dysrhythmia. Manual defibrillation The placementof paddles or pads on a patient’s chest, interpretation of  the patient’s cardiac rhythm by a trained health care professional, and the health care professional’s decision to deliver a shock (if indicated). Transthoracic impedance (resistance)  The resistance of the chest wall to current.

CARDIAC ARREST RHYTHMS [Objectives 1, 2]  The initial rhythms that may be observed in a cardiac arrest include the following: 1. Pulseless VT (pVT), in which the ECG displays a wide, regular QRS complex at a rate faster than 120 beats per minute (beats/min) 2. VF, in which irregular chaotic deflections that vary in shape and height are observed on the ECG but  there is no coordinated ventricular contraction

CHAPTER 4  Cardiac Arrest Rhythms

3. Asystole, in which no cardiac electrical activity is present  4. PEA, in which electrical activity is visible on the ECG but central pulses are absent  VF and pVT are shockable rhythms. This means that delivering a shock to the heart by means of a  defibrillator may result in termination of the rhythm. Asystole and PEA are nonshockable rhythms. Survival when a patient presents in a shockable rhythm is up to 6 times as high as when they have a  nonshockable rhythm (Herlitz, et al., 2002; Martinez, 2012).

 Ventricular Tachycardia VT exists when three or more ventricular complexes occur in immediate succession at a rate greater than 100 beats/min. VT may occur with or without pulses, and the patient may be stable or unstable with this rhythm.  When the QRS complexes of VT are of the same shape and amplitude, the rhythm is called monomorphic VT ( Table 4.1, Fig. 4.1). When the QRS complexes of VT vary in shape and amplitude from beat  to beat, the rhythm is called polymorphic VT (PMVT). In PMVT, the QRS complexes appear to twist  from upright to negative, or negative to upright, and back. PMVT is a dysrhythmia of intermediate severity between monomorphic VT and VF. If monomorphic VT or PMVT is present without a pulse, the rhythm is treated as VF (discussed later). Monomorphic VT is discussed in more detail in Chapter 5 with  wide-QRS tachycardias. PMVT is discussed in Chapter 5 with irregular tachycardias.

TABLE 4.1

Rhythm Rate P waves PR interval QRS duration

Characteristics of Monomorphic Ventricular Tachycardia Ventricular rhythm essentially regular 101 to 250 (121 to 250 per some cardiologists) beats/min Usually not seen; if present, they have no set relationship with the QRS complexes that appear between them at a rate different from that of the VT None 0.12 sec or greater; often difficult to differentiate between the QRS and the T wave

Fig. 4.1 When the QRS complexes of ventricular tachycardia (VT) are of the same shape and amplitude, the rhythm is called monomorphic VT. (From Aehlert B: ECG study cards,  St. Louis, 2004, Mosby.)

 Ventricular Fibrillation [Objective 3] VF is a chaotic rhythm that begins in the ventricles ( Table 4.2). With VF, there is no organized depolarization of the ventricles. The ventricular muscle quivers, and as a result, there is no effective myocardial contraction and no pulse. The resulting rhythm looks chaotic with deflections that vary in shape and amplitude; no normal-looking waveforms are visible. The amplitude of VF waveforms decreases over  TABLE 4.2

Characteristics of Ventricular Fibrillation

Rhythm Rate P waves PR interval QRS duration

Rapid and chaotic with no pattern or regularity Cannot be determined because there are no discernible waves or complexes to measure Not discernible Not discernible Not discernible

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A

B

C 1 sec

Fig. 4.2 Ventricular tachydysrhythmias. A, Rhythm strip showing monomorphic VT. B, Example of polymorphic VT (PMVT). C, Example of ventricular fibrillation (VF). All tracings are from lead V 1. (From Goldman L, Ausiello DA, Arend W, et al.:  Cecil  medicine, ed 23, Philadelphia, 2007, Saunders.)

time as myocardial blood flow and energy metabolism diminishes (Li & Tang, 2012). VF with waves that  are 3 or more millimeters (mm) high is called  coarse   VF. VF with low amplitude waves (ie, less than 3 mm) is called fine   VF. Survival to hospital discharge increases with VF waveforms of 3 to 4 mm and is best for VF of 5 mm or greater ( Li & Tang, 2012). Fig. 4.2 illustrates a comparison of ventricular  dysrhythmias. Factors that increase the susceptibility of the myocardium to fibrillate include the following: Acute coronary syndromes • •   Dysrhythmias •   Electrolyte imbalance Environmental factors (eg, electrocution) • •   Hypertrophy  Increased sympathetic nervous system activity  • Proarrhythmic effect of antiarrhythmics and other medications • Severe heart failure • •   Vagal stimulation  The patient in VF is unresponsive, apneic, and pulseless. The priorities of care in cardiac arrest  because of pVT or VF are high-quality CPR and defibrillation. When pVT or VF persists or recurs after one or more shocks it is called   refractory pVT/VF  (Link, et al., 2015). Use the memory aids PATCH-4-MD and the Five Hs and Five Ts to recall possible reversible causes of cardiac emergencies (Boxes 4.1, 4.2). Medications that may be used in the treatment of pVT/VF includeepinephrine ( Table 4.3) and amiodarone. Epinephrine is a vasopressor. A vasopressor is administered during cardiac arrest to increase the perfusion pressure of (1) the myocardium, for increased chance of ROSC; and (2) the brain, for increased chance of neurologically intact survival (Sunde & Steen, 2012). Epinephrine is a potent medication that  stimulates both alpha- and beta-adrenergic receptors. It should be given by the intravenous (IV) or  intraosseous (IO) route in cardiac arrest. Because the effects of epinephrine do not last long, epinephrine should be repeated every 3 to 5 minutes as long as the patient is in cardiac arrest. Although epinephrine has been used in the management of cardiac arrest for more than 40 years, there is some concern that  BOX 4.1

  PATCH-4-MD

Pulmonary embolism—anticoagulants? Fibrinolytics? Surgery?  A cidosis—ventilation, correct acid-base disturbances Tension pneumothorax—needle decompression Cardiac tamponade—pericardiocentesis Hypovolemia—replace intravascular volume Hypoxia—ensure adequate oxygenation and ventilation

Heat/cold (hyperthermia/hypothermia)—cooling/warming methods Hypokalemia/hyperkalemia (and other electrolytes)—monitor serum glucose levels closely in concert with correcting electrolyte disturbances Myocardial infarction—reperfusion therapy Drug overdose/accidents—antidote/specific therapy

CHAPTER 4  Cardiac Arrest Rhythms

BOX 4.2

Five Hs and Five Ts

Hypovolemia Hypoxia Hypothermia Hypokalemia/Hyperkalemia Hydrogen ion (acidosis)

TABLE 4.3

Class Mechanism of   Action Indications

Dosage

Considerations

Tamponade, cardiac Tension pneumothorax Thrombosis: lungs (ie, massive pulmonary embolism) Thrombosis: heart (ie, acute coronary syndromes) Tablets/toxins: drug overdose

Epinephrine (Adrenalin) Natural catecholamine; sympathomimetic; adrenergic agonist  Binds with alpha- and beta-adrenergic receptors, increasing heart rate and force of  contraction, causing vasoconstriction, and relaxing bronchial smooth muscle • Cardiac arrest: VF, pVT, asystole, PEA  •   Symptomatic bradycardia •   Hypotension Cardiac arrest   • IV/IO: 1 mg (10 mL) of 1:10,000 solution IV push, follow with 20 mL fluid flush; may repeat 1 mg dose every 3 to 5 min (Link, et al., 2015) • Tracheal: 2 to 2.5 mg diluted in 5 to 10 mL of sterile water or normal saline Post –cardiac arrest care: Continuous IV infusion of 0.1 to 0.5 mcg/kg/min (Callaway, et al., 2015) Symptomatic bradycardia or hypotension: Continuous infusion at 2 to 10 mcg/min (Link, et al., 2015) • Epinephrine is available in different concentrations and in different medication containers. Read the label carefully before giving epinephrine to ensure that you are giving the right dose and using the right concentration of the drug. • Increases myocardial oxygen demand; may cause postresuscitation myocardial dysfunction and ventricular dysrhythmias ( Attaran & Ewy, 2010). • Administer an epinephrine infusion via an infusion pump. • Check IV site frequently for evidence of tissue sloughing. • Should not be administered in the same IV line as alkaline solutions: this inactivates epinephrine. • According to the Institute for Safe Medication Practices, ratio expressions no longer appear on single entity drug products as of May 1, 2016. Epinephrine 1:1000 is displayed as 1 mg/mL and epinephrine 1:10,000 is displayed as 0.1 mg/mL.

ECG, electrocardiogram; IO, intraosseous; IV, intravenous; PEA, pulseless electrical activity; pVT, pulseless ventricular tachycardia; VF, ventricular fibrillation

epinephrine administration during cardiac arrest may negatively affect patient outcomes. In a study that  compared patients given epinephrine versus no epinephrine, the investigators concluded that although patients receiving epinephrine experienced ROSC more frequently and had a statistically significant  improvement for survival to hospital admission, the final outcome was not significantly affected (Herlitz, et al., 1995). A more recent study found that although the rate of ROSC increased with epinephrine, there was no statistically significant difference in hospital discharge rate ( Jacobs, et al., 2011).  After its administration, epinephrine can have unwanted effects including increased myocardial oxygen consumption and postdefibrillation ventricular dysrhythmias ( Attaran & Ewy, 2010). Noting that the  value and safety of its beta-adrenergic effects are controversial because they may increase myocardial work  and reduce subendocardial perfusion, current resuscitation guidelines reflect that standard-dose epinephrine (ie, 1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest ( Link, et al., 2015).  With regard to the timing of epinephrine administration during cardiac arrest, current guidelines state that it may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest  associated with an initial nonshockable  rhythm (Link, et al., 2015). However, because optimal timing may   vary based on patient factors and resuscitation conditions, there is insufficient evidence to make a recommendation as to the optimal timing of epinephrine, particularly in relation to defibrillation, when cardiac arrest is associated with a  shockable  rhythm (Link, et al., 2015).

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CHAPTER 4   Cardiac Arrest Rhythms

ACLS Pearl  An agonist   An  agonist  is   is a drug or substance that produces a predictable response (ie, stimulates action). An  antagonist is  antagonist is an agent agent that that exerts exerts an action action opposi opposite te to anothe anotherr (ie, (ie, blocks blocks action action). ). A chronotrope chronotrope is a substance that affects the heart rate: positive chronotrope ¼ "  heart rate; negative chronotrope ¼ # heart heart rate. rate. A dromotrope A dromotrope is a substa substance nce that that affect affects s AV conduc conductio tion n veloci velocity: ty: positi positive ve dromot dromotrop rope e¼ "  AV conduction velocity; negative dromotrope¼ # AV conduction velocity. An inotrope An inotrope is a substa substance nce that affects myocardial contractility: positive inotrope ¼ " force of contraction; negative inotrope ¼ # force of contraction.

ACLS Pearl Sympathetic (ie, adrenergic) receptors are located in different organs and have different physiologic action actions s when when stimul stimulate ated. d. Adrene Adrenergi rgic c recept receptors ors have have been been catego categori rized zed into into the follow followin ing g main main types: types: alpha1, alpha alpha2, beta beta1, beta beta2, and and beta beta3. Alpha Alpha1 recept receptors ors are found found in theeyes, periph periphera erall small small arterarteries and arterioles arterioles,, bladder, bladder, gastrointe gastrointestin stinal al sphincter sphincters, s, and male reproduct reproductive ive organs. organs. Stimulati Stimulation on of  alpha1 receptor receptor sites primaril primarily y causes constrict constriction ion of vascular vascular smooth smooth muscle. muscle. Alpha Alpha2 receptor receptor sites are found on platelets, blood vessels, and both presynaptically and postsynaptically on neurons in the brain ( Wecker, Wecker, et al., 2010 ). 2010 ). Stimulation results in suppression of further norepinephrine release. Both Both alpha alpha1 and alpha2 receptors have been found in the myocardium but their physiologic function remains more clearly defined in the peripheral blood vessels than in the heart ( Opie ( Opie & Hasenfuss, 2012 ). 2012  ). Beta receptor sites are divided into beta1,  beta2, and beta3. Beta1  receptors are found in the heart and kidneys. In the heart, stimulation of beta 1 receptor sites results in an increase in heart rate (ie, positive positive chronotrop chronotropy), y), an increase increase in the strength strength of cardiac cardiac contractio contraction n (ie, positive positive inotropy), inotropy), and, ultimately, irritability of cardiac cells. Beta 2  receptor sites are found in several locations in the body. In the lungs, stimulation of these receptors causes bronchodilation. Beta 2 receptors have also been found in the heart and account for about 20% of beta receptors in the left ventricle and about 40% in the atria ( Opie Opie & Hasenfuss, 2012 ). Beta 3  receptors are localized in fat cells.

Consider administration of an antiarrhythmic if pVT/VF continues despite CPR, defibrillation, and giving a vasopressor vasopressor.. Although some antiarrhythm antiarrhythmics ics have been associated associated with increased increased rates of ROSC and hospit hospital al admis admissio sion, n, none none has proved proved to increa increase se long-t long-term erm surviva survivall or surviva survivall with with a good good neurolo neurologic gic outcome (Link, (Link, et al., 2015). 2015). Further, the ideal sequence and timing of antiarrhythmic administration during cardia cardiacc arrest arrest in relation relation to the delivery delivery of shocks shocks is not known (Link, (Link, et et al., 2015 2015). ). Amiodaro Amiodarone ne is an antiarrhythmic that blocks sodium channels, inhibits sympathetic stimulation, and blocks potassium chan channe nels ls as well well as calci calcium um chan channel nelss ( Table 4.4 4.4). ). The The admi adminis nistr trat atio ion n of lidoc lidocain ainee may may be cons consid ider ered ed as an alternative to amiodarone for pVT/VF that is unresponsive to CPR, defibrillation, and vasopressor therapy(Li apy(Link nk,, et al al., ., 20 2015 15). ). Lido Lidoca caine ine is a Clas Classs 1B anti antiar arrh rhyt ythm hmic ic that that inhi inhibi bits ts the the influ influxx of sodi sodium um thro throug ugh h the fast channels of the myocardial cell membrane and decreases conduction in ischemic cardiac tissue  without adversely affecting normal conduction ( Table  Table 4.5). 4.5 ). Although the routine use of lidocaine after  cardiac arrest is not supported by current resuscitation guidelines, the initiation or continuation of lidocaine may be considered immediately after ROSC from cardiac arrest associated with pVT/VF ( Link, et al., 2015). 2015).

 Asystole [Objective 3]  Asystole, which is also called  called   ventricular asystole,   is a total absence of ventricular electrical activity  ( Table 4.6, 4.6, Fig. 4.3). 4.3). There is no ventricular rate or rhythm, no pulse, and no cardiac output. Some atrial electrical activity may be evident. If atrial electrical activity is present, the rhythm is called P-wave  asystole  or    ventricular standstill  (Fig.  or  ventricular  ( Fig. 4.4). 4.4).  The memory aids PATCH-4-MD and the Five Hs and Five Ts may be used to recall possible reversible causes of asystole. In addition, ventricular asystole may occur temporarily after termination of a  tachycardia with medications, defibrillation, or synchronized cardioversion.  When asystole is observed on a cardiac monitor, confirm that the patient is i s unresponsive and has no pulse, and then begin high-quality CPR. Additional care includes establishing vascular access, considering possible reversible causes of the arrest, administering epinephrine, and possibly inserting an advanced airway. For intubated patients, use continuous end-tidal carbon dioxide (EtCO 2) monitoring  to assess the quality of compressions during the resuscitation effort and to monitor the ROSC. “   

”   ”  

TABLE 4.4

Class Mechanism of   Action

Indications

Dosage

Considerations

Amiodarone (Cordarone) Class III antiarrhythmic Directly Directly depresses the automaticity automaticity of the SA and AV nodes conduction through the AV node and in the accessory accessory pathway of patients patients with • Slows conduction Wolff-Parkinson-White preexcitation pattern Inhibits alpha- and beta-adrenergic beta-adrenergic receptors • Inhibits Possesses Posses ses both vagolytic and calcium channel channel blocking properties • peripheral vasodilator vasodilator • Coronary and peripheral cardiac output may actually increase increase • Mild decrease in myocardial contractility; however, cardiac because because of decreased decreased afterload pVT/VF (after CPR, defibrillation, defibrillation, and a vasopressor) • pVT/VF narrow-QRS tachycardias tachycardias if the rhythm persists despite despite vagal maneuvers or • Stable narrow-QRS adenosine, or the tachycardia is recurrent  ventricular rate in atrial fibrillation fibrillation • To control ventricular ventricular rate in preexcited atrial dysrhythmias dysrhythmias with conduction conduction over an • To control ventricular accessory pathway monomorphicc VT • Stable monomorphi normal QT interval interval • PMVT with normal (Link, et al., • pVT/VF: Initial bolus of 300 mg IV/IO; can be followed by 1 dose of 150 mg (Link, 2015). 2015 ). If ROSC, can consider continuous IV infusion (1 mg/min infusion for 6 hours and then a 0.5 mg/min maintenance maintenance infusion infusion over 18 hours). hours). Maximum daily dose 2.2 g IV  per 24 hours. indications: Loading Loading dose of 150 mg IV over 10 min. May repeat every 10 min if  • Other indications: needed. needed. After conversion, conversion, follow with with a 1 mg/min infusion infusion for 6 hours hours and then then a 0.5 mg/  min maintenance infusion over 18 hours. Maximum cumulative dose 2.2 g IV per 24 hours (Link, (Link, et al., 2015). 2015 ). amiodarone is available in two formulations. formulations. One formulation formulation • In the United States, amiodarone contains polysorbate 80, which is a vasoactive solvent that can produce hypotension. The other contains cyclodextrin (Captisol), which possesses no vasoactive effects (Link, ( Link, et al., 2015). 2015). Hypotension, bradycardia, bradycardia, and AV block are adverse effects effects of amiodarone amiodarone • Hypotension, administration. Slow the infusion rate or discontinue if seen. Prolongs the PR, QRS, and QT intervals, intervals, and has an additive additive effect with other • Prolongs medications medications that prolong the QT interval (eg, procainamide, procainamide, phenothiazines, phenothiazines, some tricyclic tricyclic antidepressan antidepressants, ts, thiazide diuretics, diuretics, sotalol). sotalol). Although Although prolongation prolongation of the QRS duration and QT interval may be beneficial in some patients, it may also increase the risk  for TdP. •

 AV, atrioventricular; CPR, cardiopulmonary resuscitation; IV, intravenous; PMVT, polymorphic ventricular tachycardia; pVT, pulseless ventricular tachycardia; ROSC, return of spontaneous circulation; SA, sinoatrial; TdP, torsades de pointes; VF, ventricular fibrillation; VT, ventricular tachycardia

TABLE 4.5

Class Mechanism of   Action Indications

Dosage

Considerations

Lidocaine (Xylocaine) Class 1B antiarrhythmic Decreases Decreases conduction in ischemic ischemic cardiac tissue without adversely adversely affecting affecting normal conduction monomorphicc VT • Stable monomorphi amiodarone for pVT/VF that is unresponsive unresponsive to • May be considered as an alternative to amiodarone CPR, defibrillation, and vasopressor therapy (Link, (Link, et al., 2015) 2015 ) • Initial dose: 1 to 1.5 mg/kg IV/IO bolus; consider repeat dose (0.5 to 0.75 mg/kg) at 5 to 10 min intervals Cumulative IV/IO bolus dose should not exceed 3 mg/kg mg/kg • Cumulative Maintenance infusion: infusion: 1 to 4 mg/min mg/min • Maintenance Tracheal dose: 2 to 3 mg/kg (2 to 2.5 times IV dose) • Tracheal Lidocaine may be lethal for a patient with a bradycardia bradycardia with a ventricular escape escape • Lidocaine rhythm. continuation of lidocaine may be considered considered immediately immediately after a ROSC • The initiation or continuation from cardiac arrest associated with pVT or VF (Link, ( Link, et al., 2015). 2015).

IO, intraosseo intraosseous; us; IV, intravenou intravenous; s; pVT, pulseless ventricular ventricular tachycardi tachycardia; a; ROSC, return of spontaneou spontaneouss circulatio circulation; n; VF, ventricular fibrillation; VT, ventricular tachycardia

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CHAPTER 4   Cardiac Arrest Rhythms

TABLE 4.6

Rhyt Rhythm hm Rate Rate P waves PR interval QRS duration

Characteristics of Asystole Asystole Ventr entric icul ular ar not not disce iscern rnib ible le;; atri atrial al may may be disce iscern rnib ible le Ventr entric icul ular ar not not disce iscern rnib ible le but but atri atrial al acti activi vity ty may may be obse observ rved ed (ie, ie, “P-wave”  asystole) Usually not discernible Not measurable Absent  

Fig. 4.3   Asystole. (From Aehlert B: ECG B:  ECG study cards,  St. Louis, 2004, Mosby.)

Fig. 4.4 “P-wave”  asystole. (From Aehlert B: ECG B: ECG study cards,  St. Louis, 2004, Mosby.)

Pulseless Pulseles s Electr Electrical ical Activit Activity  y  [Objective 3] PEA is a clinical situation, not a specific dysrhythmia. PEA exists when organized electrical activity  (other than VT) is observed on the cardiac monitor but the patient is unresponsive and not breathing, and a pulse cannot be felt (Fig. (Fig. 4.5). 4.5). PEA was formerly called electromechanical called  electromechanical dissociation. The dissociation.  The term was changed because research using ultrasonography and indwelling pressure catheters revealed that the electrical trical activit activityy seen seen in some some of these these situat situation ionss is indeed indeed associ associate ated d with with mechan mechanical ical contra contracti ctions ons;; howeve however, r, the contractions are simply too weak to produce a palpable pulse or measurable blood pressure. PEA has a poor prognosis unless the underlying cause can be rapidly identified and appropriately  managed. Emergency care includes high-quality CPR, establishing vascular access, an aggressive search for possible reversible causes of the arrest, the administration of epinephrine, and considering the insertion of an advanced airway. Point of care ultrasound (POCUS) can be useful in identifying mechanical causes of PEA. The cardiac arrest algorithm is shown in  Fig. 4.6. 4.6.

ACLS Pearl  Although memory aids can be used to recall possible reversible causes of PEA, an approach that focuses on differentiation between narrow- or wide-QRS complexes on the cardiac monitor has been suggested ( Littmann, Littmann, et al., 2014 ). 2014 ). This approach requires study, and it does not apply to trauma settings. Narrow-QRS PEA is often the result of a mechanical problem caused by right ventricular inflow or outflow obstruction (eg, cardiac tamponade, tension pneumothorax, mechanical hyperinflation, pulmonary embolism). The presence of wide-QRS PEA suggests a metabolic (ie, left ventricular) problem such as severe hyperkalemia with or without metabolic acidosis, or sodium channel blocker toxicity. When used in conjunction with POCUS, this approach could help guide initial treatment decisions when managing PEA.

CHAPTER 4  Cardiac Arrest Rhythms

A

F

II

B

G

C

H

II

II

D

I II

E

J

Fig. 4.5 Pulseless electrical activity (PEA) requires the the absence of detectable mechanical mechanical activity in the heart (ie, absence absence of a pulse) with some form of organized electrical activity in the heart (ie, a rhythm). The most typical dysrhythmias seen in patients with PEA include both narrow- and wide-QRS complex rhythms. A, Sinus bradycardia. B, Junctional rhythm. C, Atrial fibrillation with slow ventricular response. D, Third-degree AV block. E, Idioventricular bradycardia. F, Idioventricular rhythm. G, Accelerated idioventricular rhythm. H, Accelerated idioventricular rhythm. I, Atrial tachycardia. J, Sinus tachycardia with bundle branch block morphology. (From Adams JG:  Emergency Medicine , ed 2, Philadelphia, 2013, Saunders.)

DEFIBRILLATION [Objective 4] Defibrillation is Defibrillation  is the delivery of an electrical current across the heart muscle over a very brief period to terminate an abnormal heart rhythm. Defibrillation is also called unsynchronized called  unsynchronized countershock or  countershock or  asynchro asynchronous countershock, because countershock,  because the delivery of current has no relationship to the cardiac cycle. Indications for  defibrillatio defibrillation n include include pulseless pulseless monomorphic monomorphic VT, sustained sustained PMVT, and VF. Recall Recall that the goal for  providing the first shock for sudden cardiac arrest resulting from VF or pVT is within 3 minutes of  patient collapse (Link, (Link, et al., 2010). 2010). Manual defibrillation  refers to the following: placement of paddles or pads on a patient ’s chest, the interpretation of the patient ’s cardiac rhythm by a trained health care professional, and the health care professional ’s decision to deliver a shock, if indicated. Automated indicated.  Automated external defibrillation refers tion  refers to the following: placement of pads on a patient ’s chest and the interpretation of the patient ’s cardiac rhythm by the defibrillator ’s computerized analysis system. Depending on the type of AED used, the machine will deliver a shock (if a shockable rhythm is detected) or instruct the operator to deliver a shock. AEDs are discussed in more detail later in this chapter. In the hospital setting, it is recommended that manual defibrillators or AEDs should be readily accessible in any  patient area and that all staff should know the location of this equipment and how to use it  (Morrison, et al., 2013). 2013). Defibrillation does not  “ “ jump start ” the heart. The shock attempts to deliver a uniform electrical current of sufficient intensity to depolarize myocardial cells (including fibrillating cells) at the same time, thereby briefly  “stunning ”  the heart. This provides an opportunity for the heart ’s natural pacemakers to resume normal activity. When the cells repolarize, the pacemaker with the highest degree of automaticity should assume responsibility for pacing the heart.

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Fig. 4.6 Cardiac Cardiac arrest algorithm. algorithm. (Reprinted (Reprinted with permission permission.. 2015 American Heart Association Association Guidelines Guidelines for CardioCardiopulmonary pulmonary Resuscita Resuscitation tion and Emergenc Emergencyy Cardiovascu Cardiovascular lar Care—Part 7: Adult Adult Advanced Advanced Cardiovascular Cardiovascular Life Support. ECCguidelines.heart.org. © 2015 American Heart Association, Inc.)

 A defibrillator   A  defibrillator  is   is a device that is used to deliver a shock to eliminate an abnormal heart rhythm (Fig. 4.7). 4.7). It consists of the following: A  capacitor  that  that stores stores energy energy (ie, electrons) electrons) at a particular particular voltage: voltage: think of voltage voltage as the electrical electrical • pressure that drives a flow of electrons (ie, current) through a defibrillator circuit (eg, the chest). An energy select button or dial: The shocks that are used for defibrillation defibrillation and cardioversion cardioversion are • expressed in joules (J) of energy. A charge switch/button that allows allows the capacitor to charge. charge. • Discharge buttons that allow the capacitor to discharge. •

CHAPTER 4  Cardiac Arrest Rhythms

Fig. 4.7 A defibrillator is used to deliver an electrical shock to terminate terminate an abnormal heart rhythm. rhythm. (Courtesy Physio-Control, Physio-Control, Redmond, Redmond, WA.) •

  Handheld paddles, which require the use of conductive media, or combination pads through  which current is delivered delive red from the defibrillator defibril lator to the patient. Combination Combinati on pads consist of a  flexible metal “paddle,”  a layer of conductive gel, and an adhesive ring that holds them in place on the patient ’s chest. They are disposable and have multiple functions. Combination pads are applied to a patient ’s bare chest for ECG monitoring and then used for defibrillation, synchronized cardioversion, and, in some cases, pacing. Combination pads physically separate the operator from the patient. Instead of leaning over the patient with handheld paddles, the operator  delivers a shock to the patient by means of a discharge button that is located on a remote cable, an adapter, or on the defibrillator itself.

ACLS Pearl Combinat Combination ion pads pads have multip multiple le names names includ including ingcombo combo pads, multipurpos multipurpose e pads, multifunction multifunction electrode pads, combination electrodes, therapy electrodes, and  and   self-adhesive monitoring/defibrillation  pads.  pads. Not all combination pads are alike. Some pads can be used for defibrillation, synchronized cardioversion, ECG monitoring, and pacing. Others can be used for defibrillation, synchronized cardioversion, and ECG monitoring, but not for pacing. Some pads have a built-in sensor that provides feedback with regard to the proper proper rate and depth of compressions compressions during CPR. Be sure that you are familiar with the capabilities of the pads that you are using.

 When the charge button on the defibrillator is pushed, the capacitor charges. Once the capacitor is charged and the shock control is pressed, voltage pushes a flow of electrons (ie, current) to the patient by  means of handheld paddles or combination pads. Current passes through the heart in “ waveforms” that  travel from one paddle/pad, through the chest, and to the other paddle/pad over a brief period.

Monopha Mon ophasic sic vers versus us Bip Biphasi hasic c Defi Defibri brilla llatio tion n [Objective 5] Different types of defibrillation waveforms exist. Waveforms are classified by whether the current flow  delivered delivered is in one direction, direction, two directions, directions, or multiple directions. directions.  When a monophasic waveform is used, current passes through the heart in one (ie, mono) direction (Fig. 4.8). 4.8). Although few monophasic waveform defibrillators are manufactured today, many are still in use. With biphasic waveforms, energy is delivered in two (ie, bi) phases. The current moves in one direction for a specified period, stops, and then passes through the heart a second time in the opposite

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Fig. 4.8   When a monophasic waveform is used, current 

Fig. 4.9   With biphasic waveforms, energy is delivered in

passes through the heart in one direction.

two phases. The current moves in one direction for a specified period, stops, and then passes through the heart a second time in the opposite direction.

direction during a very short period (ie, milliseconds) (Fig. 4.9). Today ’s manual defibrillators and AEDs use biphasic truncated exponential (BTE), rectilinear biphasic (RLB), or pulsed biphasic waveforms.  These waveforms deliver different peak currents at the same programmed energy setting and may adjust  their energy output with regard to patient impedance (discussed later) in differing ways (Link, et al., 2015). Defibrillators using biphasic waveforms (ie, BTE or RLB) are preferred to monophasic defibrillators for treatment of both atrial and ventricular dysrhythmias because of their greater success with dysrhythmia termination (Link, et al., 2015). Both escalating (ie, increasing energy levels) and nonescalating (ie, no increase in energy level) biphasic waveform defibrillators are available.  When preparing to deliver electrical therapy to a patient, knowledge of the type of device that you are using (ie, monophasic versus biphasic) and the manufacturer s recommended energy levels for the dysrhythmia you are treating is essential. ’  

 Transthoracic Impedance  Although the energy selected for defibrill ation or cardioversion is expressed in J, it is current  that delivers energy to the patient and that depolarizes the myocardium. Transthoracic impedance (resistance) refers to the resistance of the chest wall to the flow of current at the interface between the patient  ’s chest wall and combination pads or defibrillation paddles. If transthoracic resistance is high, the amount of current  that is actually delivered to the myocardium can be compromised, leading to failed shocks. Transthoracic impedance varies greatly among individuals. Some of the factors known to affect transthoracic impedance are discussed below.

ACLS Pearl When a biphasic defibrillator is used, the patient’s transthoracic impedance is measured through the paddles or combination pads in contact with the patient ’s chest. The biphasic defibrillator compensates for transthoracic impedance before the delivery of the shock, allowing the defibrillator to deliver the actual amount of energy selected by the clinician.

Chest Hair Chest hair can cause significant increases in transthoracic resistance ( Sado, et al., 2004). It may be difficult to ensure good electrode-to-skin contact in a patient who has a hairy chest. However, if good contact is not ensured, transthoracic impedance will be high and the effectiveness of the shocks delivered will be reduced. (Bissing & Kerber, 2000; Sado, et al., 2004). There is an increased risk of burns from arcing  (ie, sparks) from electrode to skin and from electrode to electrode; ECG identification and analysis can also be inhibited.

CHAPTER 4  Cardiac Arrest Rhythms

ACLS Pearl If excessive chest hair is present and if time permits, quickly clip or shave the hair in the areas of  intended electrode placement to ensure the proper adhesion of the pads. If this is not feasible (or  if a razor is not available), check to see if an extra set of electrodes is available. If so, apply one set to the patient’s chest and then quickly remove them. This should remove some hair and improve electrode-to-skin contact when you apply a second set of pads.

Paddle/Pad Size Studies have shown that adult paddles or pads should be used for patients weighing more than 10 kg  (22 lb.) (ie, generally older than age 1) (de Caen, et al., 2015). Avoid using pediatric electrodes for adult  defibrillation because myocardial injury can occur (Dahl, et al., 1974). Because the optimum pad sizes for  defibrillation and pacing on the basis of patient age and weight vary by manufacturer, it is important to carefully follow all manufacturer instructions.  When applying paddles or pads, remove the patient ’s clothing and expose his or her chest. Do not use alcohol, tincture of benzoin, or antiperspirant when preparing the skin for paddle or pad placement. Look  at the patient ’s chest for transdermal patches or disks, which may be used to deliver medications such as nitroglycerin,nicotine, analgesics,hormones,or antihypertensives.Do notapplypaddlesor padsdirectlyover  the medication patch or disk, because the patch may prevent good electrode contact, thereby hindering  thedeliveryofenergyfromthedefibrillationpaddleorpadtotheheart(  Wrenn,1990).Alackofgoodcontact  can cause arcing and may cause skin burns (Panacek, et al., 1992). If a medication patch, disk, or ointment  is located at or near the site of paddle or pad placement, remove it and wipe the area clean (do not use alcohol or alcohol-based cleansers) before applying the defibrillation paddles or pads ( Wrenn, 1990). Because some patients wear jewelry in various body locations, take a moment to look for metal body  piercings after the patient ’s chest is exposed. Although the presence of these materials is not a contraindication to defibrillation, it is possible that their presence can divert the defibrillating current from the myocardium and decrease defibrillation effectiveness. If feasible and if time permits, the metal object  should be removed to minimize the potential for burn injuries across the chest. Paddle/Pad Position Handheld paddles or combination pads should be placed on the patient ’s bare chest in accordance with the manufacturer ’s instructions. Paddles or pads may be labeled according to their intended position on the chest (eg, sternum/apex, front/back) or according to their polarity (eg, positive, negative).  The typical paddle or pad position that is used during resuscitation is the sternum – apex position,  which is also called the anterolateral  or   apex  – anterior  position. This position is often used because the anterior chest is usually easy to get to and placement of the paddles or pads in this position approximates ECG electrode positioning in lead II. Place the sternum paddle or pad lateral to the right side of the patient ’s sternum, just below the clavicle. Place the center of the left (ie, apex) paddle or pad in the midaxillary line, lateral to the patient ’s left nipple (Fig. 4.10). If the patient is a woman, elevate the left breast  and place the apex paddle or pad lateral to or underneath the breast. Placing defibrillation paddles or pads directly on breast tissue results in higher transthoracic impedance, thereby reducing current flow ( PaganCarlo, et al., 1996).

Anterior

Sternum

Sternum

Lateral

Quick-combo electrodes

Apex

Fast-patch electrodes

Fig. 4.10  Combination pads and standard paddles in a sternum –apex position.

Apex

Standard paddles

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 Another common position used for paddle or pad placement is the anterior  – posterior position. In this position, one paddle or pad is placed over the patient ’s the left chest with the upper edge of the pad below  the nipple. The other is placed on the back, just below his or her left scapula (Fig. 4.11). Alternative positions (eg, anterior  – left infrascapular, anterior  – right infrascapular) may be considered based on indi vidual patient characteristics (Link, et al., 2015). Use of Conductive Material  When using handheld paddles, the use of gels, pastes, or pre-gelled defibrillation pads aids the passage of  current at the interface between the defibrillator paddles/electrodes and the body surface (Fig. 4.12). Failure to use conductive material results in increased transthoracic impedance, a lack of penetration of current, and burns to the skin surface. Combination pads are pre-gelled and do not require the application of  additional gel to the patient ’s chest.  When applying adhesive pads to the patient ’s bare chest, press from one edge of the pad across the entire surface to remove all air and to avoid the development of air pockets. A hands-free defibrillation cable is used to attach the pads to the monitor/defibrillator.  When using pre-gelled pads with handheld paddles, make sure that the pads cover the entire paddle surface to avoid arcing current and potential burns. Do not use saline-soaked gauze or alcohol-soaked pads for defibrillation. Excess saline on the chest may cause arcing and burns. Alcohol-soaked pads may ignite. Do not use gels or pastes that are not specifically made for defibrillation (eg, ultrasound gel). The use of improper pastes, creams, gels, or pads can cause burns or sparks and may pose a risk of  fire in an oxygen-enriched environment (Hummel III, et al., 1988). If too much gel is used, the

Anterior

Posterior

Fig. 4.11   Combination pads in an anterior–posterior position.

A

B

Fig. 4.12 Use of conductive material is essential when performing defibrillation or cardioversion to lower the impedance to flow of current at the electrode-chest interface. A, If standard paddles are being used, electrode gel must be applied before the procedure. B, Self-adhesive pads have conductive material incorporated into the adhesive. Use of gel with these pads is unnecessary. (From Roberts and Hedges    clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.) ’  

CHAPTER 4  Cardiac Arrest Rhythms

material may spread across the chest wall during resuscitation. This can lead to the arcing of the current  from one paddle to another and away from the heart, and this can also produce a potentially dangerous spark or burn. Paddle Pressure  When using handheld paddles for adult defibrillation, apply firm pressure (ie, about 25 lbs.) to each paddle. This lowers transthoracic impedance by improving contact between the skin surface and the paddles and by decreasing the amount of air in the lungs. No pressure is applied when combination pads are used. Selected Energy   When electrical therapy is used to treat an abnormal heart rhythm, it is important to select the appropriate energy level (ie, the right amount of J). If the energy level selected and the current delivered are too low, the shock will not eliminate the abnormal rhythm. During adult cardiac arrest, use 360 J for all shocks when using a monophasic defibrillator (Link, et al., 2015). When using a biphasic defibrillator, use the energy level recommended by the manufacturer for the initial shock (eg, 120 to 200 J). If you do not know what the recommended energy level is, consider defibrillation at the maximal dose (Link, et al., 2015). The second and subsequent energy doses should be equivalent and higher doses may be considered (Link, et al., 2015).

Defibrillation Procedure [Objectives 4, 6]  The procedure described next assumes that the patient is an adult and confirmed to be unresponsive, apneic, and pulseless. It also assumes that the patient ’s cardiac rhythm is pVT or VF and that team members are available to assist with procedures during the resuscitation effort. Be sure that high-quality CPR is continued as the defibrillator is readied for use ( Fig. 4.13). While CPR continues, instruct a team member to expose the patient ’s chest and to remove any transdermal medication patches or ointment from the patient ’s chest, if present. If handheld paddles are used, apply  conductive material (eg, gel) to the defibrillator paddles or apply disposable pre-gelled defibrillator pads to the patient ’s bare chest. If combination pads are used, remove the pads from their sealed package. Check the pads for the presence of adequate gel. Attach the pads to the hands-free defibrillation cable, and then attach the combination pads to the patient ’s chest in the position recommended by the manufacturer (Fig. 4.14).  Turn the power to the monitor/defibrillator on and verify the presence of a shockable rhythm on the monitor (Fig. 4.15). Select an appropriate energy level (Fig. 4.16). Charge the defibrillator (Fig. 4.17). If handheld paddles are used, press the “Charge” button on the machine or the button located on the apex paddle. If combination pads are used, press the “Charge”  button on the machine.

ACLS Pearl When a shockable rhythm is present in cardiac arrest, give  one shock and then immediately resume CPR, starting with chest compressions. Thereasonfor this is that lengthy interruptions in chest compressions are associated with a decreased probability of conversion of a shockable rhythm to a perfusing rhythm. Resuming CPR immediately after a shock is more likely to be beneficial than another shock.

 All team members, with the exception of the chest compressor, should immediately clear the patient as the machine charges. Listen as the machine charges. The sound usually changes when it reaches its full charge. To help minimize interruptions in chest compressions, the person who is performing chest  compressions should continue CPR while the machine is charging. When the defibrillator is charged, the chest compressor should immediately   clear the patient. If a shockable rhythm is still present, call “Clear!” Look around you (360 degrees) to be sure that everyone —including you—is clear of the patient, the bed, and any equipment that is connected to the patient. Be sure oxygen is not flowing over the patient ’s chest.

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ACLS Pearl Remove supplemental oxygen sources from the area of the patient’s bed before defibrillation attempts are made, and place them at least 3.5 to 4 feet away from the patient ’s chest. Examples of supplemental oxygen sources include masks, nasal cannulae, resuscitation bags, and ventilator  tubing.

Press the “Shock ”  control to defibrillate the patient (Fig. 4.18). Release the shock control after the shock has been delivered. Instruct the team to resume chest compressions immediately without pausing  for a rhythm or pulse check.

Fig. 4.13 Continue CPR while the defibrillator is read-

Fig. 4.14   Attach the combination pads to the

ied for use. (From Roberts and Hedges    clinical proce-  dures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

patient ’s chest. (From  Roberts and Hedges   clinical  procedures in emergency medicine,  ed 6, Philadelphia, 2014, Saunders.)

’  

’  

Fig. 4.15 Verify the presence of a shockable rhythm on

Fig. 4.16 Select an appropriate energy level using the

the cardiac monitor. (From Roberts and Hedges    clinical  procedures in emergency medicine,   ed 6, Philadelphia, 2014, Saunders.)

manufacturer’s recommended energy dose. (From Rob-  erts and Hedges   clinical procedures in emergency med-  icine, ed 6, Philadelphia, 2014, Saunders.)

’  

’  

Fig. 4.17 Charge the defibrillator and clear everyone

Fig. 4.18   After ensuring that everyone is clear of the

from the patient. (From   Roberts and Hedges   clinical  procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

patient, press the “Shock ” control to defibrillate. (From Rob-  erts and Hedges   clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

’  

’  

CHAPTER 4  Cardiac Arrest Rhythms

ACLS Pearl When defibrillating or cardioverting a patient with a permanent pacemaker or an implantable cardioverter-defibrillator (ICD), be careful to not place the defibrillator paddles or combination pads directly over the pulse generator (there will be a bulge under the patient ’s skin). The anterior – posterior and anterolateral paddle or pad positions are considered acceptable in these patients. Depending on the manufacturer, the ICD may deliver a maximum of six shocks for VF. A shock  of about 2 J is delivered at the body surface when the ICD discharges internally. Rescuers who are in contact with the patient may feel a tingling sensation when the ICD delivers a shock. Although the energy is enough to be felt by the rescuer, it is not enough to cause physiologic harm. Because some of the defibrillation current flows down the pacemaker leads, a patient who has a permanent pacemaker or ICD should have the device checked to ensure proper function after defibrillation.

 Automated External Defibrillation  An AED is an external defibrillator that has a computerized cardiac rhythm analysis system. AEDs are easy to use. Voice prompts and visual indicators guide the user through a series of steps that may include defibrillation. When the adhesive electrodes are attached to the patient ’s chest, the AED examines the patient ’s cardiac rhythm and analyzes it. Some AEDs require the operator to press an “ Analyze” control to initiate rhythm analysis, whereas others automatically begin analyzing the patient ’s cardiac rhythm  when the electrode pads are attached to the patient ’s chest. Safety filters check for false signals (eg, radio transmissions, poor electrode contact, 60-cycle interference, loose electrodes).  When the AED analyzes the patient ’s cardiac rhythm, it  “looks” at multiple features of the rhythm, including the QRS width, rate, and amplitude. If the AED detects a shockable rhythm, it then charges its capacitors. If the machine is a fully automated AED and a shockable rhythm is detected, it will signal everyone to stand clear of the patient and then deliver a shock by means of the adhesive pads that were applied to the patient ’s chest. If the machine is a semiautomated AED and a shockable rhythm is detected, it will instruct the AED operator (by means of voice prompts and visual signals) to press the shock control to deliver a shock. Use a standard AED for a patient who is unresponsive, apneic, pulseless, and age 8 or older. If the patient is between age 1 and 8 and a pediatric attenuator is unavailable for the AED, use a standard AED ( Atkins, et al., 2015). For infants, defibrillation with a manual defibrillator is preferred ( Atkins, et al., 2015). If a manual defibrillator is not available, an AED equipped with a pediatric attenuator is desirable. If neither is available, use a standard AED. Operation [Objective 4] Assess responsiveness. If the patient is unresponsive, quickly check for breathing while simultaneously  • checking for a pulse for no more than 10 seconds. If a pulse is absent or if you are not certain that a  pulse is present, begin chest compressions. Turn on the power to the AED. Depending on the brand of AED, this is achieved by either pressing  • the “On”  button or lifting up the monitor screen or lid. • Open the package containing the adhesive pads. If the gel in the pads is dried out, use a new set of  pads. Connect the pads to the AED cables (if not preconnected), and then apply the pads to the patient ’s chest in the locations specified by the AED manufacturer. Most models require connection of the AED cable to the AED before use. Analyze the ECG rhythm. If several “looks” confirm the presence of a shockable rhythm, the AED •  will signal that a shock is indicated. Listen for the voice prompts. The chest compressor and ventilator  should switch positions during rhythm analysis. Clear the area surrounding the patient. Be sure to look around you. Ensure that everyone is clear of the • patient, the bed, and any equipment that is connected to the patient. Make sure that oxygen is not  flowing over the patient ’s chest. If the area is clear and the AED advisesa shock, confirm that all team members are clear and then press • the shock control to deliver the energy to the patient when prompted to do so by the AED. After  delivering the shock, immediately resume CPR, beginning with chest compressions. After about  2 minutes of CPR, reanalyze the rhythm. Continue to provide care as indicated by the AED ’s voice and screen prompts.

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 Automated External Cardioverter-Defibrillators  Automated external cardioverter-defibrillators (AECDs), such as the Powerheart Cardiac Rhythm Module (CRM) (Cardiac Science Inc., Irvine, CA), differ from AEDs. AECDs are being used with increased frequency in hospitals to reduce the interval between the onset of sustained pVT/VF and the first  defibrillation.  The Powerheart CRM combines biphasic defibrillation technology, noninvasive external pacing, and ECG monitoring technology. Dysrhythmia detection criteria and therapy protocols are programmed and customized for individual patients by hospital staff. Once programmed and attached to the patient by  means of its disposable adhesive pads, the CRM can continuously monitor the patient ’s cardiac rhythm, detect the onset of life-threatening dysrhythmias using rhythm analysis software, and advise or automatically deliver defibrillation therapy to patients upon detection of a shockable rhythm. The CRM can also be used as a manual defibrillator or cardioverter.

Possible Complications Possible complications of electrical therapy include the following: • Injury to the operator or other team members if improper technique is used Risk of fire from the combination of electrical and oxygen sources • Myocardial damage or dysfunction • •   Embolic episodes Dysrhythmias including asystole, atrioventricular (AV) block, bradycardia, or VF after cardioversion • Skin burns to the patient as a result of a lack of conductive material or of gel “bridging ”  (ie, the gel • forms a  “bridge”  on the skin) when using handheld paddles

 THE RESUSCITATION TEAM [Objective 7] During a resuscitation effort, an interdisciplinary team works together to provide coordinated patient  care. Teamwork helps to ensure that the patient ’s many needs are met throughout the resuscitation effort. Regardless of where a cardiac arrest occurs, the primary goals of resuscitation are to restore spontaneous circulation and meaningful neurologic recovery and to preserve vital organ function.  The size of a resuscitation team, also called a   code team,   and the skills of each team member   vary. Essential tasks that must be coordinated during a resuscitation effort include chest compressions, ECG monitoring and defibrillation, airway management, vascular access and medication administration, and documentation of the events of the code. The American College of Critical Care Medicine recommends that a family support person be a recognized member of the code team (Davidson, et al., 2007). In the prehospital setting, emergency medical technicians (EMTs) and paramedics often work in teams of two to four. The number varies depending on the environment in which the EMT or paramedic  works. For example, a fire department crew that responds to an emergency medical services (EMS) call may be staffed with two EMTs and two paramedics on the vehicle. Although staffing may differ, the ambulance that arrives on the scene is typically staffed with two EMTs, an EMT and a paramedic, or an EMT and a registered nurse. A helicopter flight crew is typically staffed with a registered nurse and a paramedic. In the hospital setting, a predesignated resuscitation team should be available 24 hours a day, 7 days a week. It is estimated that 77% of U.S. hospitals have a predesignated resuscitation team, but nearly  one-quarter do not (Kronick, et al., 2015). It is essential that health care facilities have policies and procedures in place for activating the code team. Just as it is important to know how to use a piece of equipment before using it in an emergency, you must know your facility ’s procedure for activating the team. It is important to know, learn, and practice your facility ’s code procedure and to learn what is expected of you as a member of the resuscitation team. Frequent (eg, monthly) practice using methods such as simulation-based mock codes is needed to minimize errors, maintain skills, and optimize patient  outcome (Morrison, et al., 2013).

CHAPTER 4  Cardiac Arrest Rhythms

ACLS Pearl Knowledge of the algorithms is essential to successful completion of an ACLS course. During an  ACLS course, your knowledge of the ACLS algorithms is evaluated in simulated situations and on the course posttest. The simulations (also called cases ) are evaluated by an ACLS instructor. The cardiac arrest algorithms are evaluated in the Cardiac Arrest Management (also called the Mega Code) station. In this station, you work in teams of four or five persons. Each person takes a turn as the team leader and as individual resuscitation team members, performing each of the critical tasks of resuscitation. The team leader is evaluated on his or herknowledge of the ACLS algorithms, ability to manage the resuscitation team, and his or her decisions regarding patient management. Although the team leader is responsible for directing the overall actions of the team, a resuscitation effort requires teamwork.  Each member of the team must know his or her responsibilities and should be able to anticipate the team leader ’s instructions. This is true in real life, as well as in simulated situations.

 Team Leader Responsibilities [Objective 7] Every resuscitation effort must have someone who assumes responsibility for overseeing the actions of the code team. If more than one person attempts to make decisions regarding the patient ’s care, confusion reigns and chaos will most likely result. The person in charge of the resuscitation effort is typically called the code director  or   team leader. In the prehospital setting, resuscitation efforts are usually led by a paramedic or nurse who operates under standing physician orders, local protocols, or both. In the hospital setting, the team leader is usually  a physician who is experienced in cardiac arrest management. In most institutions, ACLS is considered the standard of care in a cardiac arrest situation and, in the absence of a physician, emergency care may be initiated by appropriately trained nurses per that institution ’s policy.  The team leader guides the members of the code team and uses rapid, dynamic reasoning that considers several things at once. Because research has shown that team leaders who perform hands-on tasks in an emergency are less likely to be efficient leaders, the team leader should be in a position to “stand back ”  to view and direct the resuscitation effort (Hunziker, et al., 2011). It is likely that anyone who has been involved in, or simply observed, a resuscitation effort can recall at  least one chaotic event where the team leader shouted at everyone and the team members became flustered, not knowing what to anticipate next. As the team leader, it is essential that your manner, attitude,  words, and skills be professional throughout the resuscitation effort. A modified autocratic leadership style that allows for team feedback and knowledge sharing is necessary during a code. It is best to speak  in a calm and confident tone to the members of your team using terms that are known and shared by all team members. Generally, speaking in a normal, composed tone has a calming effect on those present. A good team leader values his or her team members, fosters an environment in which team members feel comfortable speaking up, and encourages a respectful exchange of ideas. During the resuscitation effort, the team leader: Instructs a team member to perform the primary and secondary surveys and to relay his or her findings • to the team leader. Receives a concise history of the event and care given, when applicable. For example, a first responder  • relays information to arriving paramedics. Paramedics relay information to the emergency department  nurse or physician. In the hospital, the nurse who was providing patient care relays important prearrest  information to the team leader. Instructs the team to perform high-quality chest compressions and evaluates the adequacy of chest  • compressions including hand position, depth of cardiac compressions, proper rate, and ratio of compressions to ventilations. Directstheteamto administerappropriate oxygen therapyto thepatientthroughout theresuscitationeffort. • Instructs the team to perform defibrillation, when indicated, and ensures that it is performed safely  • and correctly. Instructs the team to establish vascular access (IV or IO). • • Orders the administration of the correct medications, doses, and routes for the dysrhythmia.

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Considers placement of an advanced airway; if the decision is made to insert an advanced airway, directs a qualified team member to insert it and instructs the team to confirm proper positioning  of the device. Considers baseline laboratory values and other relevant data if necessary. • Directs reassessment of the patient ’s response to interventions. • • Monitors the performance of team members. Ensures family notification of resuscitation events. • Problem-solves (including evaluating possible causes of the arrest and recognizing malfunctioning  • equipment and misplaced or displaced tubes or lines). Considers special resuscitation protocols (eg, asthma, anaphylaxis, pregnancy, toxic ingestion, trauma, • accidental hypothermia, submersion incident, electric shock or lightning strike), when appropriate. •   Directs post   – cardiac arrest care when there is a ROSC. Decides when to terminate resuscitation efforts (in consultation with team members), when there is no • response to resuscitation efforts after a reasonable period. • Provides an opportunity for team members to be involved in a team debriefing or reflection on the resuscitation effort after the event. Remember that during a cardiacarrest,the most important priorities arethe performance of high-quality  CPRand, if a shockable rhythm is present, defibrillation. Obtaining vascular access,giving medications,and inserting an advanced airway are of secondary importance. The rhythm present on the cardiac monitor will guide the sequence of procedures that need to be done next. For example, if the patient is in cardiac arrest  and the cardiac monitor shows no electrical activity, asystole is present. If the monitor shows an organized rhythm despite no central pulse when you assess the patient, PEA is present. Defibrillation is not indicated for asystole or PEA. If the monitor shows VF or pVT, defibrillation is indicated.  Throughout the resuscitation effort, keep in mind that a change in the patient ’s cardiac rhythm or  pulse status (eg, pulseless to pulse present) usually results in a change in the recommended treatment  sequence (ie, algorithm). For instance, if defibrillation of pVT/VF results in the observation of an organized rhythm on the monitor, a pulse check should be performed (Link, et al., 2015). If the patient has a  pulse, the algorithm changes because of the rhythm change as well as the presence of a pulse. If the organized rhythm on the monitor   does not  produce a pulse, PEA exists and treatment continues using the cardiac arrest algorithm; however, the treatment sequence changes from the shockable rhythm segment  of the algorithm to the nonshockable rhythm segment. If the organized rhythm on the monitor  does  produce a pulse, supportive measures must be taken to maintain the perfusing rhythm. This is called  postresuscitation support  or  post  – cardiac arrest care. Assess the patient ’s vital signs upon the return of a pulse. If  defibrillation of pVT results in VF (or vice versa), there is no change in the algorithm because pVT and VF are treated in the same way. •

 Team Member Responsibilities [Objective 7] Each member of the resuscitation team must have clear roles and responsibilities, must know his or her  limitations, must be knowledgeable about current resuscitation algorithms, must be practiced in resuscitation skills, and must be prepared to question other team members if an action is about to occur that  may be inappropriate. Nurses who respond to a cardiac arrest must be familiar with the layout of the code cart, which is also called a   crash cart, and the location of all items contained therein. In the prehospital setting, paramedics must be familiar with the location of all medications in their drug box and the resuscitation-related equipment in their emergency bags and vehicles, if applicable.  The team member responsible for CPR must be able to properly perform CPR and provide chest  compressions of adequate rate, force, and depth in the correct location.  The team member responsible for ECG monitoring and defibrillation should know how to do the following: Operate an AED and a manual defibrillator. • Properly place handheld defibrillator paddles and combination adhesive pads. • Consider the necessary safety precautions when performing electrical therapy. • Solve problems with regard to equipment failure. •  The team member responsible for airway management should know how to do the following: Perform the head tilt  – chin lift maneuver and the jaw thrust without neck extension maneuver. • Correctly size and insert an oral airway and a nasal airway. •

CHAPTER 4  Cardiac Arrest Rhythms •

•

•

• •

•

Correctly apply and understand the indications, contraindications, advantages, disadvantages, complications, liter flow ranges, and concentrations of delivered oxygen for oxygen delivery devices, including the nasal cannula, the simple face mask, the pocket mask, the nonrebreathing mask, and the bag-mask device (BMD). Suction the upper airway by selecting an appropriate suction device and catheter and by using correct  technique. Know the indications, contraindications, advantages, disadvantages, complications, equipment, and techniques for the insertion of an advanced airway, if this is within his or her scope of practice. Know how to confirm the placement of an advanced airway. Know how to use waveform capnography, an exhaled carbon dioxide detector, and an esophageal detector device. Know how to properly secure an advanced airway.

ACLS Pearl In the hospital, an anesthesiologist or nurse anesthetist typically assumes responsibility for the patient’s oxygenation and ventilation and is aided by a respiratory therapist who assists with suctioning, equipment set up, and manual ventilation of the patient. In some institutions, the respiratory therapist performs tracheal intubation.

 The team member responsible for vascular access and medication administration must be familiar   with the location of the emergency medications, IV fluids, and related supplies that may be used during  a resuscitation effort. This team member prepares and labels the medications and IV fluids used during  the code as directed by the team leader. During circulatory collapse or cardiac arrest, the preferred vascular access site is the largest, most  accessible vein that does not require the interruption of resuscitation efforts. If no IV is in place before the arrest, establish IV access using a peripheral vein —preferably the antecubital or external jugular   vein. Normal saline is the preferred IV fluid because it expands intravascular volume better than dextrose. During cardiac arrest, give IV drugs rapidly by bolus injection. Follow each drug with a 20 mL bolus of IV fluid and briefly raise the extremity during and after drug administration to aid delivery of  the drug(s) to the central circulation (Link, et al., 2015). If peripheral IV access is unsuccessful during  cardiac arrest, consider an IO infusion before considering placement of a central line. To improve flow  rates during an IO infusion, the use of a pressure bag or infusion pump may be necessary. Current  resuscitation guidelines note that an appropriately trained provider can consider placement of an internal jugular or subclavian central line during cardiac arrest, unless there are contraindications ( Link, et al., 2015).  The vascular access and medication administration team member should know the following: The antecubital fossa is the site of first choice for vascular access if no IV catheter is in place at the time • of cardiac arrest. The procedure for performing IO access in an adult. • The importance of following each medication given during a cardiac arrest with a 20 mL IV fluid • bolus and brief elevation of the extremity. The routes of administration and appropriate dosages for IV, IO, and tracheal resuscitation • medications.

ACLS Pearl The tracheal route of drug administration is not preferred because multiple studies have shown that giving drugs (eg, lidocaine, epinephrine, atropine, naloxone, vasopressin) tracheally results in lower  blood concentrations than the same dose given intravascularly ( Link, et al., 2015 ). Intravascular drug administration provides more predictable drug delivery and pharmacologic effect ( Link, et al., 2015 ). The recommended dose of some medications that can be given via the tracheal route is generally 2 to 2.5 times the intravascular dose, although the optimal tracheal dose of most drugs is unknown.

Support Roles [Objective 7]  There are many support roles in a resuscitation effort. In the hospital, a nursing supervisor often assumes responsibility for contacting the patient ’s attending physician, limiting the number of people present to

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those necessary (ie, crowd control), ensuring that a critical care bed is available, and coordinating the transfer of the patient to the intensive care unit (ICU). Another nurse typically assumes responsibility  for bringing the patient ’s chart to the bedside or referring to the patient ’s electronic chart for pertinent  patient information (eg, code status, allergies, most recent laboratory results) and relaying that information to the team leader. Support staff is needed to remove excess furniture or equipment from the room (eg, overbed table,  wheelchair), to assist the patient ’s roommate (if applicable), and to provide ongoing care to other patients on the ward. Pastoral care, social workers, or other nursing staff are needed for family support. The use of  a professional language interpreter may be needed to explain the patient ’s condition to the family.

Resuscitation Efforts [Objective 8] It is important that resuscitation efforts be performed with the patient on a firm surface. In the field, care should begin where the patient is found unless EMS personnel do not have enough space in which to resuscitate the patient or conditions exist that may be hazardous to them or to the patient. In the hospital, a team member must ensure that a code board is placed under the patient. Most hospital beds have a  “code”  feature that quickly places the bed flat and deflates cushioning devices at the same time. Simulation studies have demonstrated that even with the use of a backboard, mattress compression can account for as much as 40% of measured compression depth in patients with in-hospital cardiac arrest  (IHCA); thus deeper chest compressions in the IHCA setting may be needed to compensate for mattress movement if it cannot be neutralized by the use of a backboard (Morrison, et al., 2013).

ACLS Pearl  Although not always available, information related to the arrest should be sought, including the following: • When and where did the arrest occur? • Was the arrest witnessed? • Was CPR performed? If yes, how long was the patient down before CPR was started? • What was the patient’s initial cardiac rhythm? If VF or pVT, when was the first shock delivered? •   Are there any special circumstances to consider such as hypothermia, trauma, drug overdose, or  do-not-attempt-resuscitation (DNAR) orders? • What treatment has been given? • What information is available regarding the patient’s past medical history?

CPR should be continued by the caregivers who recognized the patient ’s arrest. The team leader  assigns team member roles as the team members are assembled, if the roles of each member of the team have not been preassigned. Several tasks are performed simultaneously as the members of the code team converge and position themselves around the patient to begin or continue resuscitation efforts. For example, the code cart is positioned at the patient ’s bedside for easy access to the defibrillator, oxygen, suction equipment, medications, and supplies, as well as for viewing the ECG monitor. The patient is attached to a cardiac monitor and to a continuous EtCO 2 monitor (if available), combination pads are applied to the patient ’s bare chest, an oxygen source is attached to a BMD, and suction is set up. Pertinent information from the patient ’s caregiver should be quickly obtained such as patient age, weight (this allows rescuers to anticipate weight-based drug dosages), estimated time of arrest, the circumstances surrounding the arrest, and the presence of a DNAR order.

ACLS Pearl Originally developed as a communication technique by the U.S. Navy, SBAR is an acronym for  Situation, Background, A ssessment, and Recommendation that is often used by healthcare personnel as a tool to ensure rapid, effective communication when transferring patient care. The  Reason, Story, V ital Signs,  Plan (RSVP) system is another communication tool that is used to convey patient information.

CHAPTER 4  Cardiac Arrest Rhythms

Closed-Loop Communication It is important that the team leader, team members, and the event recorder communicate clearly throughout the resuscitation effort. Because there are often a large number of persons present during a code, sidebar conversations among team members that can be distracting to other team members must be avoided. To avoid information overload and to help ensure that what is  said   by the team leader is what  is heard  by the team members, the team leader should state his or her instructions one at a time using  terms that are known and shared by all team members. The team member ’s name should be used, if  known. For example, “ Aubree, please charge the defibrillator to 150 joules ”  or  “ Andrew, please insert  an oral airway.”  To avoid the need for repetitious instructions, team members must clearly acknowledge when procedures and medications are complete. For example, if a team member was directed to establish an IV or  give a medication, he or she should respond by saying something like, “IV started, left antecubital vein” or  “epinephrine 1 mg of 1:10,000 solution given IV ” when the task is completed. This practice allows those sending and receiving messages an opportunity to recognize and correct errors and helps to ensure accurate documentation of the interventions performed, the timing of those interventions, and the patient ’s response to them by the designated event recorder. Because safe practice includes the verification of orders, it is important that team members request  clarification of any orders that are unclear. Team members must also verbalize any change in the status of the patient ’s pulse, cardiac rhythm, oxygenation, or ventilation to the team leader. For example, “Dr. __, the rhythm on the monitor has changed ” or  “ Dr. __, bag-mask ventilation is becoming increasingly difficult.”

ACLS Pearl Regardless of your role in a resuscitation effort or your level of certification or licensure, it is important to tactfully voice your concerns and question an intervention if you know a mistake is being made or  is about to occur.

Shockable Rhythms [Objectives 2, 7, 8]  When pVT/VF is present, defibrillation is indicated. Be sure that the CPR team member continues chest compressions as the defibrillator is readied for use. The airway team member should coordinate ventilations with the CPR team member until an advanced airway is placed and its position confirmed.  While high-quality CPR continues, instruct the defibrillation team member to expose the patient ’s chest and to attach the combination pads to the patient ’s chest, if not already done. Verify the presence of  a shockable rhythm on the monitor and select an appropriate energy level. While the defibrillator is readied, instruct the IV/medication team member to prepare the initial medications that will be used and to establish vascular access after the first shock is delivered.  When it is time to deliver a shock, instruct all team members with the exception of the person performing chest compressions to immediately   clear the patient. The airway team member must make sure that oxygen is not flowing over the patient ’s chest. Once the defibrillator is charged, the chest compressor  should clear the patient. In this way, chest compressions are interrupted for the least amount of time possible during the resuscitation effort. Check to be certain that everyone is clear and then instruct  the defibrillation team member to defibrillate the patient. Once the shock is delivered, instruct the team to resume chest compressions immediately without  pausing for a rhythm or pulse check. Instruct the airway team member to coordinate ventilations with the chest compressor. Assuming that vascular access has been established, instruct the IV/medications team member to give the patient a vasopressor during CPR.  After five cycles of CPR (about 2 minutes), recheck the rhythm. Pauses in chest compressions for  rhythm checks should not exceed 10 seconds. If a shockable rhythm is present, charge the defibrillator  and then call “Clear!” Check to be certain that everyone is clear, and then defibrillate. Resume chest compressions immediately. While continuing CPR, consider giving an antiarrhythmic (eg, amiodarone).

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Consider placement of an advanced airway. After intubation, initiate capnography to determine the adequacy of CPR. Use the memory aids PATCH-4-MD or the Five Hs and Five Ts to help identify  possible reversible causes of the arrest or factors that may be complicating the resuscitation effort.

ACLS Pearl Current resuscitation guidelines note that although there is insufficient evidence to recommend the use of extracorporeal CPR (ECPR) for patients with cardiac arrest, in settings where it can be rapidly implemented, ECPR may be considered for select cardiac arrest patients for whom the suspected cause of the arrest is potentially reversible. Examples given include acute coronary artery occlusion, pulmonary embolism, refractory VF, profound hypothermia, cardiac injury, myocarditis, cardiomyopathy, heart failure, and drug intoxication. ECPR can serve as a bridge for left ventricular assist device implantation or cardiac transplantation during a limited period of mechanical cardiorespiratory support ( Link, et al., 2015 ).

If defibrillation restores an organized rhythm, check for a pulse (Link, et al., 2015). If you are not sure if a pulse is present, resume CPR. If a pulse is present, repeat the primary survey, ask a team member to obtain the patient ’s vital signs, and begin post  – cardiac arrest care. If a spontaneous pulse has returned, efforts of the code team should be focused on the following: • Repeating the primary and secondary surveys Anticipating changes in the patient ’s condition (and preventing deterioration) • Stabilizing vital signs • • Securing tubes and lines Troubleshooting any problem areas • Preparing the patient for transport or transfer  • Accurately documenting the events that took place during the resuscitation effort  • Drawing blood for laboratory tests and treating the patient as needed on the basis of results • If defibrillation successfully terminated pVT/VF but the rhythm recurs, begin defibrillation at the last  energy level used that resulted in successful defibrillation. Nonshockable Rhythms [Objectives 2, 7, 8] If a rhythm check reveals a nonshockable rhythm, continue high-quality CPR. Establish vascular access and give epinephrine every 3 to 5 minutes. Consider placement of an advanced airway and the use of capnography after intubation. Because hypoxemia is a possible reversible cause of cardiac arrest, advanced air way placement is theoretically more important during a cardiac arrest associated with PEA or asystole than  with pVT/VF and may be necessary to achieve adequate oxygenation or ventilation (Link, et al., 2015). Reassess the patient ’s cardiac rhythm. If an organized rhythm is present, perform a pulse check. If a  pulse is present, begin post  – cardiac arrest care. If a nonshockable rhythm persists, resume high-quality  CPR. Search for and treat reversible causes of the arrest or factors that may be complicating the resuscitation effort during each 2-minute period of CPR (Link, et al., 2015). If PEA is present and ultrasound equipment and a qualified sonographer are available, this technology can be useful in identifying potentially treatable causes of cardiac arrest and guiding patient management decisions. For example, ultrasound can be used to recognize cardiac tamponade and pneumothorax, to identify the presence of  tumors or clots, to assess myocardial contractility during CPR, and to assess ventricular volume. The use of cardiac or noncardiac ultrasound should not interfere with standard cardiac arrest treatment protocols (Link, et al., 2015). Continue CPR for 2 minutes before performing another rhythm check. Remember to switch chest  compressors every 2 minutes to avoid rescuer fatigue. If there is no response to appropriately performed interventions after a reasonable period, consider termination of efforts after consultation with the members of the resuscitation team. Examples of factors that are considered when deciding to terminate inhospital resuscitative efforts include the following: The time from patient collapse to CPR  • •   The patient ’s initial cardiac rhythm at the time of the arrest  The time from collapse to the first defibrillation attempt (if a shockable rhythm was present) • The existence of special circumstances (eg, traumatic injury, asthma, pregnancy, poisoning, hypother• mia, submersion injury, electrical/lightning injury) The presence of comorbid disease •

CHAPTER 4  Cardiac Arrest Rhythms •

  The patient ’s response to resuscitative measures, including physiologic parameters such as quantitative  waveform capnography, arterial relaxation diastolic pressure, arterial pressure monitoring, and central  venous oxygen saturation (Link, et al., 2015)

ACLS Pearl For intubated patients, continuous EtCO 2 monitoring should be used to monitor the quality of compressions during resuscitation efforts. Failure to achieve an EtCO 2 of greater than 10 mm Hg immediately after intubation and after 20 minutes of CPR is associated with extremely poor chances for  ROSC and survival ( Link, et al., 2015 ). This finding, in combination with other factors, may be considered when deciding when to terminate resuscitation ( Link, et al., 2015 ).

Special Resuscitation Situations Some situations require basic life support (BLS) or advanced life support modifications during resuscitative efforts. Cardiac arrest in patients with known or suspected opioid overdose and cardiac arrest in pregnancy are discussed below. Known or Suspected Opioid Overdose  Recognizing that opioid overdose became the leading cause of unintentional injurious death in people aged 25 to 60 years in the United States in 2012 (Lavonas, et al., 2015), the 2015 resuscitation guidelines address cardiac or respiratory arrest associated with known or suspected opioid overdose. It is reasonable for appropriately trained lay rescuers and BLS providers to administer intramuscular (IM) or intranasal (IN) naloxone in addition to providing standard BLS care for the patient who is unresponsive, is not  breathing normally or is only gasping, who has a clearly palpable pulse, and who is suspected of having  an opioid overdose (Lavonas, et al., 2015). Naloxone should be given as soon as it is available and may be repeated after 4 minutes.  The unresponsive patient who is not breathing and who has no pulse may be in cardiac arrest or may  have a pulse that is too weak or too slow to be detected (Lavonas, et al., 2015). Standard resuscitative measures, including high-quality CPR, should be used to manage these patients. Naloxone administration may be considered after CPR is begun if opioid overdose is suspected (Kleinman, et al., 2015). Cardiac Arrest and Pregnancy  Common causes of common maternal cardiac arrest include hemorrhage, cardiovascular diseases, amniotic fluid embolism, sepsis, aspiration pneumonitis, pulmonary embolism, and eclampsia (Lavonas, et al., 2015). In the latter half of pregnancy, cesarean delivery may be considered part of maternal resuscitation, regardless of fetal viability (Lavonas, et al., 2015).  At 20 weeks’ gestation, the fundal height is typically at the level of the umbilicus. The weight of the pregnant uterus on the inferior vena cava and aorta can hinder venous return and cardiac output when the patient is supine. During cardiac arrest, the uterus should be manually displaced to the left when the fundal height is at or above the level of the umbilicus to shift the weight of the uterus off these major  blood vessels and improve cardiac output. High-quality CPR should be performed with the patient in this position. If manual uterine displacement is unsuccessful and a firm wedge is immediately available, consider placing the patient in a left lateral tilt of 27 to 30 degrees, using the wedge to support the patient ’s thorax and pelvis (Lavonas, et al., 2015). Cesarean delivery should be considered at 4 minutes after the onset of maternal cardiac arrest or resuscitative efforts (for the unwitnessed arrest) if there is no ROSC ( Lavonas, et al., 2015). Factors to consider   with regardto the decision to perform a cesarean deliveryincludethe availability of appropriately trained personnel, gestational age, etiology of the arrest, and available equipment and resources (Lavonas, et al., 2015).

Patient Transfer  The resuscitation team’s responsibility to the patient continues until patient care is transferred to a health care team with equal or greater expertise. Transfer the patient with oxygen, ECG monitoring, and resuscitation equipment and ensure that trained personnel accompany the patient. When transferring care, provide information that is well organized, concise, and complete. Make certain that the family has been updated regarding events.

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Post–Cardiac Arrest Care [Objective 9] Care of the patient with ROSC after cardiac arrest has a strong impact on patient morbidity and mortality (Boutsikaris & Winters, 2012). Best practices include a multidisciplinary team approach that  includes personnel from cardiology, interventional cardiology, cardiac electrophysiology, intensive care, and neurology (Morrison, et al., 2013). The components of post  – cardiac arrest syndrome are shown in  Table 4.7. The post  – cardiac arrest algorithm is shown in Fig. 4.19. Oxygenation and Ventilation  Immediately after the ROSC, repeat the primary survey, and then perform a thorough physical examination and assess vital signs. Reassess the effectiveness of initial airway maneuvers and interventions. Apply a pulse oximeter and assess oxygen saturation. To avoid hypoxia during the period immediately after ROSC, the highest available oxygen concentration may be used until the arterial oxyhemoglobin saturation or the partial pressure of arterial oxygen can be measured (Callaway, et al., 2015). When resources are available to titrate the fraction of inspired gas that is oxygen (FiO2) and to monitor oxyhemoglobin saturation, it is reasonable to decrease the Fi O2 when the oxyhemoglobin saturation is 100%, provided that a blood oxygen saturation level (SpO2) of 94% or greater can be maintained ( Callaway, et al., 2015).  Assess and monitor the effectiveness of ventilations with capnography. Mechanical ventilation may be necessary for absent or inadequate spontaneous breathing and to minimize acute lung injury and potential oxygen toxicity (Callaway, et al., 2015). Avoid hyperventilation, which increases intrathoracic pressure and can potentially worsen hemodynamic instability (Boutsikaris & Winters, 2012). Avoid hypoventilation, which can contribute to hypoxia and hypercarbia. The 2015 resuscitation guidelines state that it is reasonable to maintain the partial pressure of carbon dioxide(Pa CO2) within a normal physiologic range, taking into account any temperature correction, unless patient factors prompt more indi vidualized treatment (Callaway, et al., 2015). If tolerated, elevate the head of the bed 30 degrees to reduce the incidence of cerebral edema, aspiration, and ventilatory-associated pneumonia (Peberdy, et al., 2010). Obtain a chest radiograph to confirm advanced airway placement and identify potential breathing causes or complications of resuscitation such as pneumothorax, rib fractures, sternal fractures, pneumonitis, pneumonia, or pulmonary edema (Callaway, et al., 2015). The administration of fibrinolytics may be considered for the post ‒cardiac arrest patient with arrest resulting from presumed or known pulmonary  embolism (Callaway, et al., 2015). TABLE 4.7

Components of Post–Cardiac Arrest Syndrome

Component

Clinical Manifestations

Possible Interventions

Brain injury

Coma Seizures Myoclonus  Varying degrees of neurocognitive dysfunction (ranging from memory deficits to a persistent  vegetative state) Stroke Brain death Circulatory collapse Dysrhythmias Hypotension

TTM Seizure control

Myocardial dysfunction

Systemic ischemia/  reperfusion response Persistent  precipitating cause

Circulatory collapse Hypotension Hypovolemia Multiorgan failure Cause-specific (eg, acute coronary syndrome, asthma, hemorrhage, hypovolemia, overdose, pulmonary embolism, sepsis, stroke)

TTM, Targeted temperature management 

Coronary reperfusion Hemodynamic support  Mechanical support (eg, left  ventricular assist device, intraaortic balloon pump) Hemodynamic support  Temperature control

Disease-specific interventions

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Fig. 4.19   The post –cardiac arrest algorithm. (Reprinted with permission. 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care—Part 8: Post –Cardiac Arrest Care. ECCguidelines. heart.org. © 2015 American Heart Association, Inc.)

Cardiovascular Care  Heart rate and blood pressure are extremely variable immediately after ROSC. After ROSC, all patients should receive continuous ECG monitoring and a 12-lead ECG should be obtained as soon as possible to determine whether acute ST segment elevation is present (Callaway, et al., 2015). Emergent coronary angiography is recommended for out-of-hospital cardiac arrest (OHCA) patients  with a presumed cardiac cause of arrest and with ST segment elevation (Callaway, et al., 2015). Emergent  coronary angiography is considered reasonable for electrically or hemodynamicallyunstablepatients who are comatoseafterOHCA of suspected cardiacoriginbut withoutST segmentelevation(Callaway,etal.,2015). Coronary angiography is reasonable in post  – cardiac arrest patients for whom coronary angiography is indicated regardless of whether the patient is comatose or awake (Callaway, et al., 2015). Establish IV access with normal saline or lactated Ringer ’s solution if not already done. Hypotonic fluids should be avoided because they may increase edema, including cerebral edema ( Peberdy, et al., 2010). If IO access was used during the arrest, establish an IV line to replace it when time permits. Insert  a nasogastric tube and urinary catheter to monitor intake and output. Dysrhythmias that occur during the post ‒cardiac arrest period should be treated in the same way as that for a patient who has not had a cardiac arrest ( Boutsikaris & Winters, 2012). Current guidelines consider it reasonable to avoid and to immediately correct hypotension (ie, systolic blood pressure less than 90 millimeters of mercury [mm Hg], mean arterial pressure less than 65 mm Hg) during  post ‒cardiac arrest care (Callaway, et al., 2015). Administration of IV/IO fluid boluses, about 1 to 2 liters

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of normal saline or lactated Ringer ’s solution, may be necessary to restore intravascular volume, and the administration of vasoactive medications may be necessary to maintain perfusion if hypotension persists (Callaway, et al., 2015). For example, chronotropic agents may be needed to improve heart rate, inotropic agents may be necessary to enhance myocardial contractility, vasoconstrictive medications may be needed to increase arterial pressure, or vasodilators may be necessary to reduce afterload (Callaway, et al., 2015). Neurologic Care   Targeted temperature management (TTM), formerly known as therapeutic hypothermia, is recommended for adult patients who lack a meaningful response to verbal commands after ROSC (Callaway, et al., 2015). Selecting and maintaining a constant temperature between 32 C and 36 C is recommended and it is reasonable that TTM be maintained for at least 24 hours after cardiac arrest  after achieving target temperature (Callaway, et al., 2015). The routine prehospital cooling of patients after ROSC with rapid infusion of cold intravascular fluids is not recommended ( Callaway, et al., 2015). Clinical manifestations of post  – cardiac arrest brain injury include coma, seizures, myoclonus, various degrees of neurocognitive dysfunction (ranging from memory deficits to a persistent vegetative state), and brain death (Callaway, et al., 2015). Because seizures after a cardiac arrest may be caused by, as well as  worsen, post  – cardiac arrest brain injury, an electroencephalogram should be promptly performed and interpreted and then should be monitored frequently or continuously in comatose survivors of cardiac arrest (Callaway, et al., 2015). Current evidence does not support the routine administration of anticon vulsant medications for patients after cardiac arrest without seizure activity. If seizures are present, the same anticonvulsant regimens for the treatment of status epilepticus associated with other etiologies may  be considered after cardiac arrest (Callaway, et al., 2015). º

º

Debriefing [Objective 10] Regardless of the outcome of a resuscitation effort or its length, the team leader is responsible for making  sure that a postevent debriefing takes place. Data from the defibrillator, the code sheet, feedback devices, and other sources that captured data during the resuscitation effort should be collected and provided for  feedback to the code team. During a debriefing, each member of the code team has an opportunity to engage in honest dialogue to gain understanding and to identify lessons learned in a nonpunitive environment. Ideally, the indi vidual who leads the debriefing should have training and experience as a facilitator. A debriefing provides the following: • An opportunity for each team member to reflect on what   they did, when they did it, how they did it, why   they did it, and how they can improve (Phrampus & O ’Donnell, 2013) • An opportunity to identify and address performance gaps (ie, the gap between desired and actual performance) and perception gaps (ie, the difference between the team member ’s perception of their performance and actual performance as defined by objective measures) ( Phrampus & O'Donnell, 2013) An opportunity to review the clinical judgments made and actions performed during the event and • compare them with current resuscitation algorithms, professional standards, institution policies, and local protocols An opportunity to address emotional responses related to the event  • An opportunity for self-reflection that can be translated to actionable knowledge to guide future deci• sions and actions, and ultimately improve patient care An opportunity to identify and discuss the elements of the resuscitation that went well, those areas that  • could be improved, and recommendations for future resuscitation efforts  Although there are many debriefing techniques, the structured and supported debriefing model is a  method that is commonly used in advanced life support courses. This model consists of the following  phases: (Phrampus & O’Donnell, 2013) 1.   Gather phase. This phase is used for gauging the reaction of the team to the event, clarifying facts, describing what happened, and creating an environment for reflective learning. During this phase of the debriefing, the team leader is asked to provide a synopsis of what occurred and supplemental information is requested from team members. Using open-ended questions, the facilitator listens to the team members describe their perceptions of their behaviors. 2.  Analysis phase. During this phase, the record of the event (eg, code sheet, data from feedback-enabled devices) is reviewed and the observations of team members are reported. The facilitator asks questions to assist with self-reflection and analysis of each team member ’s actions, changes in the patient ’s

CHAPTER 4  Cardiac Arrest Rhythms

condition that may have occurred during the event, and how individual and team actions may have influenced the outcome of the event. The actions of the team can be compared with current resuscitation algorithms, professional standards, institution policies, best evidence, and local protocols to enhance understanding. 3.  Summary phase. The debriefing concludes with a review of the lessons learned and a summary of the main take-home messages and needed performance improvements. Family Notification Several surveys have revealed that most relatives of patients who require CPR would like to be offered the possibility of being present during a resuscitation attempt. According to follow-up surveys with family  members who had witnessed a resuscitation effort, most felt that their adjustment to the death or grieving   was facilitated by their witnessing the resuscitation and that their being present was beneficial to the dying family member. If family members are not present during the resuscitation effort, they should be told that resuscitation efforts have begun and they should be periodically updated. The result of the resuscitation effort, whether  successful or unsuccessful, should be relayed to the family promptly with honesty and compassion.  When speaking with the family, speak slowly and in a quiet, calm voice. Use simple terms rather than medical terms. Pause every few seconds to ask if they understand what is being said. You may need to repeat information several times. Generally, you should make eye contact with the family members, except where cultural differences may exist. Enlist the assistance of a social worker, a clergy member, or grief support personnel, as needed. Conveying Bad News  [Objective 11] Health care professionals may not receive sufficient training regarding how the death of a loved one should be conveyed to survivors. Family members often do not remember what was said to them when the news of a death was relayed as much as they remember the attitude and empathy of the person who spoke to them (Schmid, et al., 2005). SPIKES is an acronym for a six-step protocol that is used for conveying distressing information to patients and families (Box 4.3) (Baile, et al., 2000). Using the SPIKES protocol can help ease the distress felt by the patient or family who is receiving the news and the health care professional who is breaking the news (Kaplan, 2010). 1.   Setting. Organize your thoughts about the information that you will need to convey and anticipate questions that family members will ask. Select a location that provides for privacy with all appropriate people present. Sit down, face the family, and minimize interruptions by putting your pager on silent  and putting your cell phone on vibrate. If language is a barrier, arrange for a translator to be present  and part of the discussion. 2.   Perception. Before conveying information, use open-ended questions to find out what the family  already knows. Asking, “ What have you been told so far?”  or  “ What is your understanding of what  has happened?” allows an opportunity to gauge how the family perceives the current situation — what  it is and its seriousness (Baile, et al., 2000). It also provides an opportunity to correct misinformation. 3.   Invitation. Ask the family how they prefer to receive the information that you have to share and how  much they want to know. For example,  “ Would you like me to tell you more about what happened? ” Keep in mind that ethnic and cultural values play a significant role in the need for information.  Although families are often clear about how much information they are ready to hear, it is possible that they may be too emotionally upset or overwhelmed to hear and comprehend the information that   you are about to convey.

BOX 4.3

SPIKES Protocol

S—Setting P—Perception of what the patient/family understand about the situation I—Invitation from the patient/family to give information

K—Knowledge (ie, relaying medical facts) E—Emotions (ie, address with empathetic responses) S—Summary

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4.   Knowledge. Beginning with a warning statement that unfavorable news is coming may lessen the shock that can follow the disclosure of bad news (Baile, et al., 2000). Say something like, “I am sorry  to tell you that …” or “I have some bad newsto tell you” and then pause. This allows the family time to grasp what has been said. While speaking slowly, proceed to convey the news in small chunks and in a  straightforward manner. To reduce the potential for misunderstanding, use words that the family will easily comprehend. Avoid the use of medical jargon and avoid excessive bluntness. Assume nothing as to how the news is going to be received. If the resuscitation effort was unsuccessful, allow time for the shock to be absorbed and as much time as necessary for questions and discussion. Recognize that the initial shock experienced by the family may prevent them from knowing what questions to ask. It may  be necessary to repeat answers or explanations to make sure they are understood. 5.   Emotions.  Give the family time to respond. Be sensitive and respectful of cultural differences.  The family ’s reaction may be anger, shock, withdrawal, disbelief, extreme agitation, guilt, or sorrow.  An expected death may elicit a response of acceptance and relief. The resuscitation efforts may have given the family time to accept the terminal outcome. In some cases, there may be no observable response, or the response may seem inappropriate. A statement such as, “ You have my (our) sincere sympathy ” may be used to express your feelings. However, there are times that silence is appropriate. Silence respects the family ’s feelings and allows them to regain composure at their own pace. 6.   Summarize. Offer to contact the patient ’s physician and to be available if there are further questions.  Arrange for follow-up and continued support during the grieving period. Allow the family the opportunity to see their relative. In cases involving severe traumatic cardiac arrest, this may not be advisable. If equipment is still connected to the patient, prepare the family for what they will see. The patient  should be gowned before the family views the body. Accompany them if necessary. Some caregivers may prefer not to view the body. If this is their preference, do not attempt to force them to do so.

Helping the Caregivers  An unsuccessful resuscitation effort is difficult for the family as well as the health care professionals involved in the resuscitation. Although each health care professional may deal with stress differently, reactions suggesting a need for assistance include persistent feelings of anger, self-doubt, sadness, depression, or a desire to withdraw from others. It is important to recognize the warning signs of stress in yourself and others and know how to deal with them. Strategies for dealing with stress may include engaging  in exercise, practicing relaxation techniques, talking with family or friends, or meeting with a qualified mental health professional.

CHAPTER 4  Cardiac Arrest Rhythms

PUTTING IT ALL TOGETHER  The chapter quiz and case studies presented on the following pages are provided to help you integrate the information presented in this chapter. As you work through the case studies, remember that there may be alternative actions that are perfectly acceptable, yet not presented in the case study. CHAPTER QUIZ

True/False  Indicate whether the statement is true or false.

____

1.

Transthoracic impedance is significantly increased when defibrillation is performed  without the use of conductive material.

____

2.

Vasopressin can be substituted for the first or second dose of epinephrine in cardiac arrest.

____

3.

Current resuscitation guidelines recommend the routine use of lidocaine after cardiac arrest.

____

4.

For intubated patients, failure to achieve an EtCO2  of greater than 10 mm Hg after  20 minutes of CPR is associated with extremely poor chances for ROSC and survival.

____

5.

When a monophasic defibrillator is used for shockable cardiac arrest rhythms, the initial recommended energy dose is 120 to 150 J; 360 J is recommended for all subsequent shocks.

____

6.

Patients in cardiac arrest associated with PEA or asystole should receive epinephrine early during the resuscitative effort.

 Multiple Choice  Identify the choice that best completes the statement or answers the question.

____

7.

What is meant by the term PEA?   A. PEA refers to a flat line on the cardiac monitor. B. PEA refers to a slow rhythm with a wide-QRS complex. C. PEA refers to a chaotic rhythm that is likely to degenerate into cardiac arrest. D. PEA refers to an organized rhythm on the cardiac monitor (other than VT), though a pulse is not present.

____

8.

Defibrillation is indicated in the management of:  A. VF and asystole. B. PEA and asystole. C. pVT and VF. D. pVT and PEA.

____

9.

A patient is in cardiac arrest. CPR is in progress. Two attempts to establish peripheral IV access have been unsuccessful. To administer medications to this patient, your  best  course of action in this situation will be to:  A. Proceed with insertion of a central line. B. Continue attempts to establish peripheral IV access. C. Intubate the patient and administer drugs via the tracheal tube. D. Establish vascular access by means of an IO infusion.

____

10.

In which of the following situations would an epinephrine IV bolus be indicated?  A. Junctional rhythm, pVT, and asystole B. Sinus bradycardia, junctional rhythm, and a ventricular escape rhythm C. PEA, pVT, and asystole D. PEA, VF, and a ventricular escape rhythm

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____

11.

Establishing vascular access is part of:  A. “ A”  in the primary survey. B. “B”  in the secondary survey. C. “C”  in the secondary survey. D. “D”  in the primary survey.

____

12.

The first medication used in the management of PEA is:  A. Lidocaine. B. Epinephrine. C. Amiodarone. D. Atropine or epinephrine.

____

13.

Which of the following statementsabout lidocaine dosingduring cardiacarrest is correct?  A. Lidocaine is given as a continuous IV infusion of 2 to 10 mcg/min. B. Lidocaine is given as a continuous IV infusion of 10 to 20 mcg/kg/min. C. The initial dose is 1 mg IV push, which may be repeated twice to a maximum dose of 3 mg. D. The initial dose is 1 to 1.5 mg/kg IV push; repeat doses of 0.5 to 0.75 mg/kg IV  push may be given at 5- to 10-minute intervals, to a maximum dose of 3 mg/kg.

____

14.

A 49-year-old man is found unresponsive, not breathing, and pulseless. The cardiac monitor reveals monomorphic VT. The most important actions in the management of  this patient are:  A. CPR and defibrillation. B. Defibrillation and resuscitation medications. C. CPR and prompt insertion of an advanced airway. D. Synchronized cardioversion and resuscitation medications.

____

15.

A 75-year-old man is on the telemetry floor recovering from an inferior wall myocardial infarction. The nursing staff arrives in the patient ’s room in response to an alarm from his cardiac monitor, which reveals a sinus bradycardia at 40 beats/min. The patient is unresponsive, pulseless, and apneic. An IV is in place. You should now:  A. Defibrillate immediately. B. Begin transcutaneous pacing. C. Begin CPR, ventilate with a bag-mask, and give epinephrine IV. D. Begin CPR, insert an advanced airway, and give atropine IV.

Completion Complete each statement.

16. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification _____________________________________

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17. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification: _____________________________________ 18. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification _____________________________________ 19. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification: _____________________________________

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 Matching  Match the cardiac rhythms with their descriptions by placing the letter of each correct answer in the space   provided.

 A. VF  B. Monomorphic VT C. PMVT D. Asystole ____

20.

A total absence of ventricular electrical activity 

____

21.

Chaotic rhythm with no discernible waveforms, complexes, pattern, or regularity 

____

22.

Rapid rhythm in which the QRS complex is wide and usually regular; QRS complexes are of same shape and amplitude

____

23.

Rapid rhythm in which the QRS complexes are wide and appear to twist from upright to negative or negative to upright and back 

Short Answer 

24. What is the purpose of defibrillation? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

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CASE STUDY 4-1  Your patient is a 52-year-old woman who was found unresponsive on her kitchen floor by a neighbor.  You have a sufficient number of advanced life support personnel available to assist you and carry out your  instructions. Emergency equipment, including a biphasic AED, is available. 1. As you approach the patient, you observe that she is supine on a stretcher. Her eyes are closed, her  lips are blue, and her skin is pale. You see no signs of breathing. What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 2. The patient is unresponsive. How would you like to proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 3. The patient is not breathing and a pulse cannot be felt. Her skin is cool, pale, and dry. How should  you proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 4. How will you ensure the performance of high-quality chest compressions throughout this resuscitation effort? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 5. What is the difference between manual defibrillation and automated external defibrillation? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 6. The AED pads are in place on the patient ’s chest and rhythm analysis is complete. The AED advises a shock. What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 7. The patient has been defibrillated and high-quality CPR is ongoing. How will youopen the patient ’s airway? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 8. The patient ’s airway is clear. What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 9. Chest compressions are ongoing. An oral airway has been inserted. The patient is being ventilated  with a BMD. You see gentle chest rise with bagging. Vascular access has been established. What  should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

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10. After 2 minutes of CPR, the defibrillation team member reanalyzed the patient ’s rhythm with the  AED, which indicated, “No shock advised.”  How would you like to proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 11. A carotid pulse is present. The patient is breathing about 8 times/min but remains unresponsive.  What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 12. The Five Hs and Five Ts are memory aids used to recall possible reversible causes of cardiac emergencies. Explain the meaning of each of the Five Hs and Five Ts. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 13. The patient ’s heart rate is strong and regular. Her blood pressure is 98/60 mm Hg and she has been placed on the cardiac monitor, which shows a sinus tachycardia at 118 beats/min. Ventilations are being assisted with a BMD. The following information has been obtained: Signs/Symptoms:  A llergies: Medications: Past history: Last oral intake: E vents prior:

Found unresponsive by neighbor  Unknown Azithromycin (Zithromax), alendronate (Fosamax), aspirin Osteoporosis, heart attack 3 months ago Unknown Found unresponsive on the kitchen floor by a neighbor who had last  spoken to the patient about 25 minutes prior 

 What would you like to do next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

CASE STUDY 4-2  Your patient is a 40-year-old man who was found unresponsive in the street. Paramedics have placed the patient on a backboard with cervical spine stabilization. An IV of normal saline is infusing when the patient arrives in the emergency department. You have a sufficient number of advanced life support  personnel available to assist you and carry out your instructions. Emergency equipment, including a  biphasic manual defibrillator, is available. 1. As you approach the patient, you see that he is supine on a backboard. His eyes are closed and his skin is pale. You observe blood dripping from the patient ’s right ear. What should be done next? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 2. The patient has occasional gasping breaths occurring at a rate of 4 breaths/min. There is no pulse. His skin is warm, pale, and moist. What should be done now? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________

CHAPTER 4  Cardiac Arrest Rhythms

3. As the patient ’s chest is exposed to apply the combination pads, you observe multiple abrasions, a  partial thickness laceration in the area of the right nipple, and what looks like footprints on the patient ’s chest and abdomen. What should be done next? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 4. The monitor reveals the following rhythm:

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification _____________________________________ 5. Information from the paramedics has been obtained and your physical examination findings are noted. Signs/Symptoms:  A llergies: Medications: Past history: Last oral intake: E vents prior:

Possible assault by unknown persons with unknown  weapons Unknown Unknown Unknown Unknown Found unresponsive in the street 

Focused Physical Examination Head/face: Neck:  Thorax:  Abdomen: Pelvis: Back: Extremities:

Blood dripping from right ear, bruising of left orbit, frontal bone contusion, left  temporal area contusion; both pupils deviated to left side Unremarkable Partial thickness laceration near right nipple; abrasions and footprints noted Markedly distended and firm; abrasions and footprints noted Unremarkable Unremarkable Multiple abrasions on upper extremities

 You estimate the patient ’s weight to be 70 kg. What would you like to do next? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 6. Chest compressions are ongoing. An oral airway has been inserted and the patient is being ventilated  with a BMD. What should be done next? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________

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7. Although the monitor remains unchanged, a team member informs you that a weak pulse is present. How would you like to proceed? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 8. The patient is unresponsive and there are no signs of spontaneous breathing. His heart rate is 125 beats/min and his blood pressure is 53/30 mm Hg. What should be done next? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ CHAPTER QUIZ ANSWERS

True/False

1. T. When using handheld paddles, the use of gels, pastes, or pre-gelled defibrillation pads aids the passage of current at the interface between the defibrillator paddles/electrodes and the body surface. Failure to use conductive material results in increased transthoracic impedance, a lack of penetration of current, and burns to the skin surface. Combination pads are pre-gelled and do not require the application of additional gel to the patient ’s chest. OBJ: Explain defibrillation, its indications, proper pad or paddle placement, relevant precautions, and the steps required to perform this procedure with a manual defibrillator and an AED. 2. F. Epinephrine and vasopressin, which are vasopressors, have been shown to improve ROSC after  administration during cardiac arrest. Because current evidence has revealed that the efficacy of these medications are similar and that there is no demonstrable benefit from administering both epinephrine and vasopressin compared with epinephrine alone, vasopressin has been removed from the adult  cardiac arrest algorithm (Link, et al., 2015). OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 3. F. Although there is inadequate evidence to support the routine use of lidocaine after cardiac arrest, the initiation or continuation of lidocaine may be considered immediately after a ROSC from cardiac arrest associated with pVT or VF (Link, et al., 2015). OBJ: Discuss immediate post  – cardiac arrest care upon ROSC. 4. T. For intubated patients, continuous EtCO 2  monitoring should be used to monitor the quality of  compressions during resuscitation efforts. Failure to achieve an EtCO 2  of greater than 10 mm Hg  immediately after intubation and after 20 minutes of CPR is associated with extremely poor chances for ROSC and survival (Link, et al., 2015). This finding, in combination with other factors, may be considered when deciding when to terminate resuscitation (Link, et al., 2015). OBJ: Discuss the use of continuous EtCO 2  monitoring during resuscitation efforts. 5. F. When a monophasic defibrillator is used for shockable cardiac arrest rhythms, the recommended energy dose is 360 J for all shocks (Link, et al., 2015). OBJ: Identify the energy levels that are currently recommended, and indicate if the shock delivered should be a synchronized or unsynchronized countershock, for pulseless monomorphic VT, PMVT, and VF. 6. T. Current guidelines state that it may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest associated with an initial nonshockable  rhythm (Link, et al., 2015). However, because optimal timing may vary based on patient factors and resuscitation conditions, there is insufficient evidence to make a recommendation as to the optimal timing of epinephrine,

CHAPTER 4  Cardiac Arrest Rhythms

particularly in relation to defibrillation, when cardiac arrest is associated with a  shockable   rhythm (Link, et al., 2015). OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and routeof administration of applicablemedications), and electrical therapy, whereapplicable.  Multiple Choice

7. D. PEA is a clinical situation, not a specific dysrhythmia. PEA exists when organized electrical activity (other than VT) is observed on the cardiac monitor, but the patient is unresponsive, not  breathing, and a pulse cannot be felt. OBJ: Identify four cardiac rhythms that are associated with cardiac arrest. 8. C. Defibrillation is indicated in the management of pVT and VF. It is not indicated in the management of PEA. Remember: defibrillation is performed to depolarize the myocardial cells at one time and provide an opportunity for one of the heart ’s natural pacemakers to take over. In PEA, an organized rhythm is present on the monitor. Thus pacemaker activity is already present but there is inadequate cardiac output and no pulse. PEA is not shocked because a shock could disrupt the organized rhythm and cause chaos (ie, VF). Defibrillation is not indicated in asystole. OBJ: Explain defibrillation, its indications, proper pad or paddle placement, relevant precautions, and the steps required to perform this procedure with a manual defibrillator and an AED. 9. D. When peripheral IV cannulation is unsuccessful or is taking too long, an IO infusion is an alternative method of gaining access to the vascular system and should be considered before considering placement of a central line. To improve flow rates during an IO infusion, the use of a pressure bag or infusion pump may be necessary. If IV or IO access cannot be achieved to give drugs during a cardiac arrest, the tracheal route can be used to give selected medications; however, intravascular drug administration provides more predictable drug delivery and pharmacologic effect (Link, et al., 2015). OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 10. C. An IV bolus of epinephrine is indicated in cardiac arrest. Cardiac arrest rhythms include PEA, asystole, pVT, and VF. Epinephrine is not given as an IV bolus to patients who have a pulse.  Although epinephrine may be given to patients for symptomatic bradycardia, it is given as an IV  infusion, not an IV bolus. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 11. C. The primary survey focuses on BLS assessment and intervention. The secondary survey focuses on advanced life support assessment and interventions. Thus establishing vascular access is part of  “C”  (ie, Circulation) in the secondary survey. OBJ: List the purpose and components of the primary and secondary surveys. 12. B. The first medication used in the management of PEA is epinephrine. Amiodarone, atropine, and lidocaine are not indicated in the management of PEA. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 13. D. The initial dose of lidocaine is 1 to 1.5 mg/kg IV push. Repeat doses of 0.5 to 0.75 mg/kg IV  push may be given at 5- to 10-minute intervals, to a maximum dose of 3 mg/kg. OBJ: Discuss immediate post  – cardiac arrest care upon ROSC.

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14. A. CPR and defibrillation are the most important treatments for the patient in cardiac arrest associated with pVT or VF. Insertion of advanced airways and administration of resuscitation medications are of secondary importance. Although synchronized cardioversion may be used in the treatment of an unstable patient in monomorphic VT with a pulse, it is not indicated for pVT. OBJ: Explain defibrillation, its indications, proper pad or paddle placement, relevant precautions, and the steps required to perform this procedure with a manual defibrillator and an AED. 15. C. Althoughan organizedrhythmis presenton themonitor, thepatienthas nopulse.Thisclinical situation is PEA. You should begin CPR immediately, ventilate the patient with a BMD, and give epinephrine 1 mg IV. Transcutaneous pacing, defibrillation, and atropine administration are not indicated for PEA. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. Completion

16. Sinus rhythm to monomorphic VT OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 17. PMVT OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 18. Sinus rhythm with a run of monomorphic VT OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 19. Coarse VF  OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable.  Matching

20. D 21. A 22. B 23. C Short Answer 

24. The purpose of defibrillation (ie, unsynchronized countershock) is to deliver a uniform electrical current of sufficient intensity to depolarize myocardial cells (including fibrillating cells) at the same time, briefly  “ stunning ” the heart. This provides an opportunity for the heart ’s natural pacemakers to resume normal activity. When the cells repolarize, the pacemaker with the highest degree of automaticity should assume responsibility for pacing the heart. OBJ: Explain defibrillation, its indications, proper pad or paddle placement, relevant precautions, and the steps required to perform this procedure with a manual defibrillator and an AED.

CHAPTER 4  Cardiac Arrest Rhythms

CASE STUDY 4-1 ANSWERS 1. Your general impression should focus on three main areas that can be remembered by the mnemonic  ABC: A ppearance, (work of) Breathing, and Circulation. As you finish forming your general impression, you will have a good idea if the patient is sick (ie, unstable) or not sick (ie, stable). Begin the primary survey by assessing responsiveness. Start by asking,  “ Are you all right?” or  “ Can you hear  me?”   If there is no response, then gently tap or squeeze the patient ’s shoulder while repeating   verbal cues. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient. 2. Call for help and ask someone to get an AED or defibrillator. Look at the chest for movement while simultaneously feeling for a pulse for 5 to 10 seconds. While your fingers are in contact with the patient ’s skin, note the patient ’s skin temperature, color, and moisture. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient. 3. Direct a team member to start chest compressions. Ask another team member to turn on the AED and apply the AED pads to the patient. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient. 4. High-quality chest compressions require compressing the chest at an adequate rate and depth, allowing full chest recoil after each compression (enabling the heart to refill with blood), minimizing  interruptions in chest compressions, and avoiding excessive ventilation. To avoid tiring, the chest  compressor and airway team member should rotate positions (ideally in less than 5 seconds) when chest compressions are interrupted (eg, while the AED is analyzing the patient ’s cardiac rhythm,  when the AED is delivering a shock). OBJ: Discuss the requirements for performing high-quality chest compressions. 5. Manual defibrillation refers to the placement of paddles or pads on a patient ’s chest, interpretation of  the patient ’s cardiac rhythm by a trained health care professional, and the health care professional ’s decision to deliver a shock, if indicated. Automated external defibrillation refers to the placement of  pads on a patient ’s chest and interpretation of the patient ’s cardiac rhythm by the defibrillator ’s computerized analysis system. OBJ: Explain defibrillation, its indications, proper pad or paddle placement, relevant precautions, and the steps required to perform this procedure with a manual defibrillator and an AED. 6. When the defibrillation team member indicates that he is ready to shock, ensure that all team members clear the patient. After the shock is delivered, instruct the team to resume CPR without pausing for a pulse or rhythm check. Ask a team member to establish vascular  access. OBJ: Explain defibrillation, its indications, proper pad or paddle placement, relevant precautions, and the steps required to perform this procedure with a manual defibrillator and an AED. 7. Although there are no visible signs of trauma, open the patient ’s airway with the use of a jaw thrust   without neck extension maneuver because the patient was found on the floor and you cannot rule out  trauma because of a possible fall injury. Look in the mouth for blood, broken teeth or loose dentures, gastric contents, and foreign objects. OBJ: Describe and demonstrate the steps needed to perform the head tilt  – chin lift and jaw  thrust without neck extension maneuvers and relate the mechanism of injury to the opening of  the airway. 8. While continuing chest compressions, ask the airway team member to size and insert an oral airway. With the help of an assistant, ask the airway team member to begin positive pressure  ventilation with a BMD connected to 100% oxygen. Ventilate the patient with just enough force to produce gentle chest rise. Assess the patient ’s baseline breath sounds while the patient is being   ventilated.

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OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 9. While CPR continues, instruct a team member to administer epinephrine 1 mg or   vasopressin 40 units IV/IO. Consider the need for placement of an advanced airway and waveform capnography. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 10. Check for a pulse and repeat the primary survey. If a pulse is present, obtain the patient ’s vital signs. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 11. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor.  Ask the airway team member to continue to assist the patient ’s breathing with a BMD connected to O2. Obtain a 12-lead ECG and order laboratory tests. Find out if there is someone available  who can provide additional information about the patient so that factors that may have caused the arrest can be identified and treated. Because the patient remains unresponsive, consider TTM. OBJ: Discuss immediate post  – cardiac arrest care upon ROSC. 12. H ypovolemia  H ypoxia  H ypothermia  H ypokalemia/Hyperkalemia  H ydrogen ion (acidosis)

Tamponade, cardiac Tension pneumothorax Thrombosis: lungs (ie, massive pulmonary embolism) Thrombosis: heart (ie, acute coronary syndromes) Tablets/toxins: drug overdose

OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 13. Arrange for a cardiology consult and continue to monitor the patient ’s vital signs and ECG every  5 minutes as you prepare to transfer the patient for continued care. Request a team debriefing after  the patient ’s transfer is complete. OBJ: Discuss immediate post  – cardiac arrest care upon ROSC.

CASE STUDY 4-2 ANSWERS 1. Look at the chest for movement while assessing for a carotid pulse for up to 10 seconds, and assess the patient ’s skin, noting the patient ’s skin temperature, color, and moisture. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient. 2. Direct a team member to start chest compressions. While CPR continues, instruct a team member  to attach combination pads to the patient ’s bare chest in the position recommended by the manufacturer. Turn the power to the monitor/defibrillator on and identify the patient ’s cardiac rhythm. OBJ: Discuss a systematic approach to the initial emergency care of an unresponsive patient.

CHAPTER 4  Cardiac Arrest Rhythms

3. While CPR continues, perform a focused physical examination, looking for possible clues as to the cause of the arrest. Obtain, or direct a team member to obtain, additional information from the paramedics with regard to the circumstances in which the patient was found. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 4. The monitor shows a sinus tachycardia; however, because the patient has no pulse with this rhythm the clinical situation is PEA. OBJ: Identify four cardiac rhythms that are associated with cardiac arrest. 5. Activate the trauma team, if not already done, and consider the possible causes of the patient ’s cardiac arrest. On the basis of the information provided, hypovolemia (ie, firm distended abdomen) is one possible cause. Ask the IV team member to establish a second IV line and give a fluid challenge of normal saline. The amount given often varies depending on agency policy/local protocol. For the purposes of this scenario, we will give a 20 mL/kg fluid challenge of normal saline to start with. Because this patient weighs about 70 kg, our initial fluid challenge will be 1400 mL. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 6. While CPR continues, ask the IV team member to give 1 mg of 1:10,000 epinephrine IV push now  and repeat the same dose every 3 to 5 minutes as long as the patient has no pulse. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 7. Check the patient ’s other vital signs and repeat the primary survey. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 8. Ask the airway team member to continue to assist the patient ’s breathing with a BMD connected to 100% oxygen. Continue to monitor the patient ’s vital signs and ECG every 5 minutes as you prepare to transport the patient to the operating room (OR). Weigh the decision to place an advanced airway  and giving additional IV fluids now (delaying definitive care) versus transporting the patient to the OR and having these interventions performed by the anesthesiologist. Request a team debriefing  after the patient ’s transfer is complete. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable.

REFERENCES  Atkins, D. L., Berger, S., Duff, J. P., Gonzales, J. C., Hunt, E. A., Joyner, B. L., et al. (2015, Oct). 2015 American Heart Association guidelines for CPR & ECC.  Retrieved Jan 11, 2016, from American Heart Association. In  Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care—part  11: Pediatric basic life support and cardiopulmonary resuscitation quality:  Eccguidelines.heart.org .  Attaran, R. R., & Ewy, G. A. (2010). Epinephrine in resuscitation: Curse or cure? Future Cardiol ,  6(4), 473 – 482.

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Baile, W. F., Buckman, R., Lenzi, R., Glober, G., Beale, E. A., & Kudelka, A. P. (2000). SPIKES — A six-step protocol for delivering bad news: Application to the patient with cancer. Oncologist ,  5 (4), 302 – 311. Bissing, J. W., & Kerber, R. E. (2000). Effect of shaving the chest of hirsute subjects on transthoracic impedance to selfadhesive defibrillation electrode pads. Am J Cardiol ,  86(5), 587 – 589, A10. Boutsikaris, D., & Winters, M. E. (2012). Postresuscitation care. Emerg Med Clin North Am, 30 (1), 123 – 140. Callaway, C. W., Donnino, M. W., Fink, E. L., Geocadin, R. G., Golan, E., Kern, K. B., et al. (2015, Oct). 2015   American Heart Association guidelines for CPR & ECC. Retrieved Nov 7, 2015, from American Heart Association. In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care —part  8: Post  – cardiac arrest care:  Eccguidelines.heart.org . Dahl, C. F., Ewy, G. A., Warner, E. D., & Thomas, E. D. (1974). Myocardial necrosis from direct current countershock. Effect of paddle electrode size and time interval between discharges. Circulation, 50 (5), 956 – 961. Davidson, J. E., Powers, K., Hedayat, K. M., Tieszen, M., Kon, A. A., Shepard, E., et al. (2007). Clinical practice guidelines for support of the family in the patient-centered intensive care unit: American College of Critical Care Medicine Task Force 2004 – 2005. Crit Care Med ,  35 (2), 605 – 622. de Caen, A. R., Berg, M. D., Chameides, L., Gooden, C. K., Hickey, R. W., Scott, H. F., et al. (2015, Oct). 2015   American Heart Association guidelines for CPR & ECC.  Retrieved Oct 23, 2015, from American Heart Association. In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular  care—part 12: Pediatric advanced life support:  Eccguidelines.heart.org . Herlitz, B., Bång, A., Alsen, B., & Aune, S. (2002). Characteristics and outcome among patients suffering from in hospital cardiac arrest in relation to whether the arrest took place during office hours.  Resuscitation, 53(2), 127 – 133. Herlitz, J., Ekstr om, L., Wennerblom, B., Axelsson, A., Bång, A., & Holmberg, S. (1995). Adrenaline in out-ofhospital ventricular fibrillation. Does it make any difference? Resuscitation, 29(3), 195 – 201. Hummel, R. S., III, Ornato, J. P., Weinberg, S. M., & Clarke, A. M. (1988). Spark-generating properties of electrode gels used during defibrillation. A potential fire hazard. JAMA ,  260 (20), 3021 – 3024. Hunziker, S., Johansson, A. C., Rschan, F., Semmer, N. K., Rock, L., Howell, M. D., et al. (2011). Teamwork and leadership in cardiopulmonary resuscitation. J Am Coll Cardiol ,  57 (24), 2381 – 2388.  Jacobs, I. G., Finn, J. C., Jelinek, G. A., Oxer, H. F., & Thompson, P. L. (2011). Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial.   Resuscitation, 82(9), 1138 – 1143. Kaplan, M. (2010). SPIKES: A framework for breaking bad news to patients with cancer.  Clin J Oncol Nurs , 14 (4), 514 – 516. Kleinman, M. E.,Brennan, E. E., Goldberger, Z. D., Swor, R. A.,Terry, M., Bobrow, B. J.,et al.(2015, Oct). 2015   American Heart Association guidelines for CPR & ECC. Retrieved Jan 11, 2016, from American Heart Association. In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care— part 5: Adult basic life support and cardiopulmonary resuscitation quality:  Eccguidelines.heart.org . Kronick,S. L., Kurz, M.C., Lin, S., Edelson,D. P., Berg, R. A., Billi,J. E., etal. (2015). Part4: Systems ofcare and continuous quality improvement: 2015 American Heart Association guidelines update for cardiopulmonary  resuscitation and emergency cardiovascular care. Circulation, 132(suppl 2), S397 – S413. Lavonas, E. J., Drennan, I. R., Gabrielli, A., Heffner, A. C., Hoyte, C. O., Orkin, A. M., et al. (2015, Oct). 2015   American Heart Association guidelines for CPR & ECC. Retrieved Jan 11, 2016, from American Heart Association. In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care —part  10: Special circumstances of resuscitation:  Eccguidelines.heart.org . Li, Y., & Tang, W. (2012). Optimizing the timing of defibrillation: The role of ventricular fibrillation waveform analysis during cardiopulmonary resuscitation. Crit Care Clin, 28 (2), 199 – 210. Link, M. S., Atkins, D. L., Passman, R. S., Halperin, H. R., Samson, R. A., White, R. D., et al. (2010). Part 6: Electrical therapies: Automated external defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 122 (suppl 3), S706 – S719. Link, M. S., Berkow, L. C., Kudenchuk, P. J., Halperin, H. R., Hess, E. P., Moitra, V. K., et al. (2015, Oct). 2015   American Heart Association guidelines for CPR & ECC.  Retrieved Oct 30, 2015, from American Heart Association. In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular  care—part 7: Adult advanced cardiovascular life support:  Eccguidelines.heart.org . Littmann, L.,Bustin,D. J.,& Haley, M. W. (2014). A simplifiedand structured teaching tool for the evaluation and management of pulseless electrical activity. Med Princ Pract ,  23(1), 1 – 6. Martinez, J. P. (2012). Prognosis in cardiac arrest. Emerg Med Clin North Am, 30 (1), 91 – 103. Morrison, L. J., Neumar, R. W., Zimmerman, J. L., Link, M. S., Newby, L. K., McMullan, P. W., Jr., et al. (2013). Strategies for improving survival after in-hospital cardiac arrest in the United States: 2013 consensus recommendations. Circulation, 127 , 1538 – 1563. Opie, L. H., & Hasenfuss, G. (2012). Mechanisms of cardiac contraction and relaxation. In R. O. Bonow, D. L. Mann, D. P. Zipes, & P. Libby (Eds.), Braunwald s heart disease: A textbook of cardiovascular medicine  (9th ed., pp. 459 – 486). Philadelphia: Saunders. 

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Pagan-Carlo, L. A., Spencer, K. T., Robertson, C. E., Dengler, A., Birkett, C., & Kerber, R. E. (1996).  Transthoracic defibrillation: Importance of avoiding electrode placement directly on the female breast. J Am Coll Cardiol ,  27 (2), 449 – 452. Panacek, E. A., Munger, M. A., Rutherford, W. F., & Gardner, S. F. (1992). Report of nitropatch explosions complicating defibrillation. Am J Emerg Med ,  10 (2), 128 – 129. Peberdy, M. A.,Callaway, C. W., Neumar, R. W., Geocadin, R. G.,Zimmerman,J. L.,Donnino, M., et al.(2010). Part 9: Post  – cardiac arrest care: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 122 (suppl 3), S768 – S786. Phrampus, P. E., & O’Donnell, J. M. (2013). Debriefing using a structured and supported approach. In  A. I. Levine, S. DeMaria, Jr., A. D. Schwartz, & A. J. Sim (Eds.), The comprehensive textbook of healthcare simulation (pp. 73 – 84). New York: Springer Science. Sado, D. M., Deakin, C. D., Petley, G. W., & Clewlow, F. (2004). Comparison of the effects of removal of chest  hair with not doing so before external defibrillation on transthoracic impedance. Am J Cardiol ,  93(1), 98 – 100. Schmid, M. M., Kindlimann, A., & Langewitz, W. (2005). Recipients ’ perspective on breaking bad news: How you put it really makes a difference. Patient Educ Couns , 58 (3), 244 – 251. Sunde, K., & Steen, P. A. (2012). The use of vasopressor agents during cardiopulmonary resuscitation. Emerg Med  Clin North Am, 30 (1), 189 – 198.  Wecker, L., Crespo, L. M., Dunaway, G., Faingold, C., & Watts, S. (2010). Brody s human pharmacology   (5th ed., pp. 122 – 137) Philadelphia: Mosby.  Wrenn, K. (1990). The hazards of defibrillation through nitroglycerin patches. Ann Emerg Med , 19(11), 1327 – 1328. ’  

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Tachycardias INTRODUCTION  The tachycardia algorithm is a treatment guideline that is used when providing care to patients who have a tachycardia with a pulse. You must be able to recognize if a patient is asymptomatic, symptomatic but  stable, symptomatic but unstable, or pulseless. Care of the pulseless  patient with a tachycardia is provided using the cardiac arrest algorithm, which was discussed in Chapter 4. Familiarity with the tachycardia  algorithm requires patient assessment, rhythm recognition, and knowledge of medications, vagal maneu vers, and electrical therapy.  The signs and symptoms that are experienced by a patient with a tachycardia depend on the ventricular rate, how long the tachycardia lasts, the patient ’s general health, and the presence of underlying heart  disease. The faster the heart rate, the more likely the patient is to have signs and symptoms resulting from the rapid rate.  When a patient presents with signs and symptoms related to a tachycardia, ask yourself these questions: 1. Is the patient asymptomatic, symptomatic but stable, symptomatic and unstable, or pulseless? 2. Is the QRS wide or narrow? If it is wide, is it monomorphic or polymorphic? 3. Is the ventricular rhythm regular or irregular?  The answers to these questions will help to guide your treatment decisions. Most tachycardias do not  cause serious signs and symptoms until the ventricular rate exceeds 150 beats per minute (beats/min) unless the patient has impaired ventricular function (Link, et al., 2015). Serious signs and symptoms are those that affect vital organ function. Examples of serious signs and symptoms are shown in Box 5.1. If the patient is symptomatic but does not have serious signs and symptoms because of the rapid rate, the patient is considered to be stable. For example, a patient who has symptoms such as lightheadedness or palpitations with stable vital signs is symptomatic, but he or  she is not in imminent danger of cardiac arrest. After their airway, breathing, and circulation (ie, ABCs) have been assessed, stable but symptomatic patients are given oxygen (if indicated), intravenous (IV) access is established, and medication therapy is begun. Frequent patient reassessment is essential. If  the tachycardia produces serious signs and symptoms, typically with heart rates of 150 beats/min or more, the patient is considered unstable. Unstable patients who have a pulse and serious signs and symptoms caused by the tachycardia should receive immediate synchronized cardioversion.  The management of patients who present with a tachycardia is often complex. As an advanced cardiac life support provider, it is important for you to recognize when to consult expert advice with regard to rhythm interpretation, medications, or patient-management decisions.

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BOX 5.1

Signs and Symptoms of Hemodynamic Compromise

 Acute changes in mental status Chest pain Cold, clammy skin Fall in urine output Heart failure

Hypotension Pulmonary congestion Shortness of breath Signs of shock 

DESIRED RESULTS

G O A L  Given a patient situation, and working in a team setting, competently direct the initial emer gency care (including mechanical, pharmacologic, and electrical therapy where applicable) for a  patient experiencing a tachycardia.

LEARNING OBJECTIVES

 After completing this chapter, you should be able to: 1.  Differentiate among narrow-QRS tachycardias, wide-QRS tachycardias, and irregular  tachycardias. 2.  Given a patient situation, describe the electrocardiogram (ECG) characteristics and initial emergency care for narrow-QRS tachycardias, wide-QRS tachycardias, and irregular  tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 3.  Identify a patient who is experiencing a tachycardia as asymptomatic, symptomatic but stable, symptomatic but unstable, or pulseless. 4.  Explain synchronized cardioversion, describe its indications, and list the steps required to perform this procedure safely. 5.  For each of the following rhythms, identify the energy levels that are currently recommended: monomorphic ventricular tachycardia (VT), narrow-QRS tachycardia, atrial fibrillation (AFib), and atrial flutter.

LEARNING PLAN • •

•

•

•

Read this chapter before class. Remember to highlight important concepts as you read. Develop and use flashcards, flowcharts, and mnemonics to help enhance your retention of  the information presented. Flashcards can be particularly helpful with the recall of  medication dosages and rhythm recognition. Master identification of the following rhythms: sinus tachycardia, atrial tachycardia (AT), atrioventricular (AV) nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT), monomorphic VT, and polymorphic VT (PMVT). Master the following medications: O2, adenosine, amiodarone, beta-blockers, diltiazem, magnesium sulfate, procainamide, sotalol, and verapamil. Master the following skills: Ensure scene safety and the use of personal protective equipment. Assign team member roles or performing as a team member in a simulated patient situation. Direct or perform an initial patient assessment. Obtain vital signs, establish vascular access, attach a pulse oximeter and blood pressure and cardiac monitor, give supplemental O2  if indicated, and order a 12-lead ECG. Quickly identify an ECG rhythm, determining whether the QRS is narrow or wide (and if  it is wide, if the QRS is monomorphic or polymorphic), regular or irregular. Quickly recognize if a patient is asymptomatic, symptomatic but stable, symptomatic but unstable, or pulseless. • •

• •

•

•

CHAPTER 5   Tachycardias

Demonstrate familiarity with the tachycardia algorithm. Demonstrate an understanding of what vagal maneuvers are and when they are indicated. Demonstrate an understanding of the actions, indications, dosages, adverse effects, and contraindications for the medications used in the treatment of a narrow-QRS or  wide-QRS tachycardia. Deliver the correct type of energy (synchronized cardioversion versus defibrillation) and the correct energy level for the tachycardia if electrical therapy is indicated. Demonstrate safe operation of the defibrillator if electrical therapy is indicated. Recognize the need to change from synchronized cardioversion to defibrillation if the rhythm changes to pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF). Consider the possible reversible causes of a cardiac emergency. Verbalize when it is best to seek expert consultation. Review your performance as a team leader or team member during a postevent debriefing. Complete the chapter quiz and review the quiz answers provided. Read the case studies at the end of this chapter and compare your answers with the answers provided. • •

•

•

• •

• • •

• •

KEY TERMS

Delta wave  Slurring of the beginning portion of the QRS complex, caused by preexcitation. Supraventricular arrhythmias Rhythms that begin in the sinoatrial (SA) node, atrial tissue, or  the AV junction. Synchronized cardioversion  The timed delivery of a shock during the QRS complex.

NARROW-QRS TACHYCARDIAS Supraventricular arrhythmias begin above the bifurcation of the bundle of His. This means that supraventricular arrhythmias include rhythms that begin in the SA node, the atrial tissue, or the AV   junction.

Sinus Tachycardia [Objectives 1, 2, 3] If the SA node fires at a rate faster than normal for the patient ’s age, the rhythm is called sinus tachycardia. In adults, the rate associated with sinus tachycardia is usually between 101 and 180 beats/min; however, some experts calculate the upper rate as about 220 beats/min, minus the patient ’sageinyears(Link, et al., 2015) ( Table 5.1, Fig. 5.1). Sinus tachycardia is a normal response to the body ’s demand for increased cardiac output, which results from many conditions (Box 5.2). The patient is often aware of an increase in heart rate. Some patients complain of palpitations, a racing heart, or a feeling of pounding in their chests. In a patient with coronary artery disease, any tachycardia can cause problems. The heart ’s demand for  oxygen increases as the heart rate increases. As the heart rate increases, there is less time for the ventricles to fill and less blood for the ventricles to pump out with each contraction, which can lead to decreased TABLE 5.1

Regularity Rate P waves PR interval QRS duration

Characteristics of Sinus Tachycardia R to R and P to P intervals are regular Usually between 101 and 180 beats/min; some experts calculate the upper rate as about  220 beats/min, minus the patient ’s age in years Positive (ie, upright) in lead II; one precedes each QRS complex; P waves look alike 0.12 to 0.20 sec and constant from beat to beat  0.11 sec or less unless abnormally conducted

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Fig. 5.1   Sinus tachycardia. (From Aehlert B: ECG study cards,  St. Louis, 2004, Mosby.)

BOX 5.2 • • • •

• • • • •

Causes of Sinus Tachycardia

Acute MI Caffeine-containing beverages Dehydration, hypovolemia Drugs (eg, cocaine, amphetamines, “ecstasy,”  cannabis)   Exercise Fear and anxiety   Fever  Heart failure   Hyperthyroidism

• • •

• • • • •

  Hypoxia   Infection Medications (eg, epinephrine, atropine, dopamine)   Nicotine   Pain Pulmonary embolism   Shock  Sympathetic stimulation

cardiac output. Because the coronary arteries fill when the ventricles are at rest, rapid heart rates decrease the time available for coronary artery filling. This decreases the heart ’s blood supply. Chest discomfort  can result if the supplies of blood and oxygen to the heart are inadequate. Sinus tachycardia in a patient   who is having an acute myocardial infarction (MI) may be an early warning signal for heart failure, cardiogenic shock, and more serious dysrhythmias.  Treatment for sinus tachycardia is directed at correcting the underlying cause. Sinus tachycardia in a  patient experiencing an acute MI may be treated with medications to slow the heart rate and decrease myocardial oxygen demand (eg, beta-blockers), provided there are no signs of heart failure or other  contraindications.

ACLS Pearl Some dysrhythmias with very rapid ventricular rates (ie, above 150 beats/min) require the delivery of  medications or a shock to stop the rhythm. However, it is important to remember that shocking a sinus tachycardia is inappropriate; rather, treat the cause of the tachycardia.

Supraventricular Tachycardia [Objectives 1, 2] Supraventricular tachycardias (SVTs) involve tissue within the bundle of His or above and are associated  with ventricular rates faster than 100 beats/min at rest (Page, et al., 2015). Three examples of SVTs are shown in Fig. 5.2.

ACLS Pearl Some SVTs need the AV node to sustain the rhythm and some do not. For example, AVNRT and AVRT require the AV node as part of the reentry circuit to continue the tachycardia. Other  SVTs use the AV node only to conduct the rhythm to the ventricles. For example, AT, atrial flutter, and AFib arise from a site (or sites) within the atria; they do not need the AV node to sustain the rhythm.

CHAPTER 5   Tachycardias

 Atrial Tachycardia [Objectives 1, 2, 3]  AT consists of a series of regular rapid beats from an irritable site in the atria at a rate faster than 100 beats/min (Ellenbogen & Stambler, 2014). Although the P waves preceding each QRS complex appear  upright, they tend to look different from those seen when the impulse is initiated from the SA node ( Table 5.2, Fig. 5.3).  The term paroxysmal  is used to describe a rhythm that starts or ends suddenly. AT that starts or ends suddenly is called  paroxysmal supraventricular tachycardia (PSVT),  once called paroxysmal AT (PAT) (Fig. 5.4). PSVT may last for minutes, hours, or days. If the onset or end of PSVT is not observed on the ECG, the dysrhythmia is simply called SVT. Normal sinus rhythm

Atrial tachycardia (AT)

Atrioventricular nodal reentrant tachycardia (AVNRT)

Atrioventricular reentrant tachycardia (AVRT) BT

X SA

SA

SA

A

AV

AV

AV

B II

SA AV

C II

D II

II

Fig. 5.2   Types of SVTs. A, Normal sinus rhythm is shown here as a reference. B, With AT,a focus (X) outside theSA node fires off  automatically at a rapid rate. C, With AVNRT, the cardiac stimulus originates as a wave of excitation that spins around the AV   junctional area. As a result, P waves may be buried in the QRS or appear immediately before or just after the QRS complex (arrows) because of nearly simultaneousactivation of theatria andventricles.D, A similar type of reentrant(circus movement) mechanism in Wolff-Parkinson-White(WPW)syndrome. This mechanism is referred to as AVRT. Note theP wave in lead II somewhat after theQRS complex. BT, bypass tract. (From Goldberger AL: Clinical electrocardiography: a simplified approach, ed 7, St. Louis, 2006, Mosby.)

TABLE 5.2

Regularity Rate P waves

PR interval QRS duration

Characteristics of Atrial Tachycardia Regular 101 to 250 beats/min One P wave precedes each QRS complex in lead II; these P waves differ in shape from sinus P waves; an isoelectric baseline is usually present between P waves; if the atrial rhythm originates in the low portion of the atrium, P waves will be negative in lead II; with rapid rates, it may be difficult to distinguish P waves from T waves. May be shorter or longer than normal; may be difficult to measure because P waves may be hidden in the T waves of preceding beats 0.11 sec or less unless abnormally conducted

Atrial tachycardia

Sinus rhythm P'

P

Fig. 5.3 An AT (a type of SVT) that ends spontaneously with the abrupt resumption of sinus rhythm. The P waves of the tachycardia (rate: about 150 beats/min) are superimposed on the preceding T waves. (From Goldberger AL:  Clinical electro-  cardiography: a simplified approach, ed 7, St. Louis, 2006, Mosby.)

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Fig. 5.4   PSVT. (From Clochesy J:  Critical care nursing, ed 2, Philadelphia, 1996, Saunders.)

Focal AT   is a type of AT that begins in a small area (ie, focus) within the atria. Its atrial rate is often between 100 and 250 beats/min (Page, et al., 2015). A patient with focal AT often presents with PSVT.  Automatic AT, which is also called ectopic AT, is another type of focal AT in which a small cluster of cells  with altered automaticity fire. Vagal maneuvers do not usually stop the tachycardia, but they may slow the  ventricular rate. Multifocal AT is discussed later in this chapter with irregular tachycardias.  A rhythm that lasts from three beats up to 30 seconds is a  nonsustained rhythm. A sustained rhythm is one that lasts more than 30 seconds. Focal AT can be sustained or nonsustained. If episodes of AT are short, the patient may be asymptomatic. Nonsustained focal AT typically does not require treatment  (Page, et al., 2015). If AT is sustained and the patient is symptomatic because of the rapid rate, treatment  should include applying a pulse oximeter and administering oxygen (if indicated), obtaining the patient ’s  vital signs, and establishing IV access. A 12-lead ECG should be obtained. If the patient is not hypotensive, vagal maneuvers may be tried. Although AT will rarely stop with vagal maneuvers, they are used to try to better identify the mechanism of the SVT (ie, automatic, triggered activity, reentry) (Page, et al., 2015). Vagal maneuvers are discussed in the next section of this chapter. If vagal maneuvers fail, antiarrhythmic medications should be tried. Adenosine is the drug of choice for regular narrow-QRS complex tachycardias (Link, et al., 2015) ( Table 5.3, Fig. 5.5). If needed, calcium channel blockers ( Table 5.4) or beta-blockers ( Table 5.5) may be used to slow the ventricular rate. TABLE 5.3

Adenosine (Adenocard)

Class Mechanism of Action

Indications (Link, et al., 2015)

Dosage (Link, et al., 2015) Considerations

Endogenous chemical, antiarrhythmic • Naturally present throughout the body • Rapidly metabolized in the blood vessels • Slows sinus rate • Slows conduction time through AV node • Can interrupt reentry pathways through AV node • Half-life is less than 10 sec; doses of 12 mg or less terminate 92% of SVTs, usually within 30 sec (Miller & Zipes, 2012) • Stable narrow-QRS regular tachycardias • Unstable narrow-QRS regular tachycardia while preparations are made for synchronized cardioversion • Stable, regular, monomorphic wide-QRS tachycardia Initial dose is 6 mg rapid IV push over 1 to 3 sec. If no response within 1 to 2 min, give 12 mg rapid IV push. May repeat 12 mg dose once in 1 to 2 min. Follow each adenosine dose immediately with a 20 mL normal saline flush. • Constant ECG monitoring is essential. • Use with caution in patients with reactive airway disease. • Contraindicated in WPW pattern (Page, et al., 2015). • Adverse effects (eg, flushing, dyspnea, chest pressure) common but transient  and usually resolve within 1 to 2 min. Discontinue in any patient who develops severe respiratory difficulty. • If the dysrhythmia is not caused by reentry involving the AV node or sinus node (ie, AFib, AT, or VT), adenosine will not terminate the dysrhythmia but may produce transient AV block that may clarify the diagnosis. • After administration, many patients report a feeling of impending doom or feel that they are about to die ( Appelboam, et al., 2015). • Reduce the dose by one-half in patients on dipyridamole (Persantine), carbamazepine (Tegretol), those with transplanted hearts, or if given via a central IV line (Page, et al., 2015).

 AT, atrial tachycardia; AV, atrioventricular; ECG, electrocardiogram; IV, intravenous; SVT, supraventricular tachycardia; VT, ventricular tachycardia; WPW, Wolff-Parkinson-White

Flush

Adenosine

Fig. 5.5  Because of adenosine’s extremely short half-life, start the IV line as proximal to the heart as possible, such as the antecubital fossa. Follow each adenosine dose immediately with a 20 mL normal saline flush. (From  Roberts and Hedges  clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

’  

Calcium Channel Blockers

TABLE 5.4

Mechanism of Action

• • •

Indications (Link, et al., 2015)

• •

Dosage (Link, et al., 2015)

•

•

Considerations

•

• • •

Inhibit movement of calcium ions across cell membranes in the heart and vascular smooth muscle Slow conduction through the AV node and prolong the refractory period of the  AV node Decrease myocardial contractility Stable narrow-QRS tachycardia if the rhythm persists despite vagal maneuvers or adenosine or if the tachycardia is recurrent  To control the ventricular rate in patients with AFib or atrial flutter Diltiazem: Initial dose is 15 to 20 mg (0.25 mg/kg) IV over 2 min. If needed, follow in 15 min with 20 to 25 mg (0.35 mg/kg) IV over 2 min. Subsequent IV bolus doses should be individualized for each patient. Verapamil: 2.5 to 5 mg slow IV push over 2 min (give over 3 to 4 min in older adults or when BP is within the lower range of normal). May repeat with 5 to 10 mg in 15 to 30 min (if no response and BP remains normal or elevated). Maximum total dose 20 to 30 mg. Can worsen hypotension and should not be given to patients with a systolic BP of  less than 90 mm Hg. Use with caution in patients with mild to moderate hypotension. Monitor BP, heart rate, and ECG closely. Avoid in patients with impaired ventricular function or heart failure (Link, et al., 2015). Avoid in patients with wide-QRS tachycardia and preexcited AFib/atrial flutter (Mottram & Svenson, 2011). IV calcium channel blockers and IV beta-blockers should not be given together or in close proximity (within a few hours); may cause severe hypotension.

 AFib, atrial fibrillation; AV, atrioventricular; BP, blood pressure; ECG, electrocardiogram; IV, intravenous TABLE 5.5

  Beta-Blockers

Mechanism of   Action

• • • •

Indications (Link, et al., 2015)

• • •

Considerations

• • • •

Slow sinus rate Depress AV conduction Reduce blood pressure Decrease myocardial oxygen consumption Stable narrow-QRS tachycardias if the rhythm persists despite vagal maneuvers or adenosine or if the tachycardia is recurrent  For ventricular rate control in AFib and atrial flutter if no signs of heart failure Specific forms of PMVT (eg, ischemic PMVT, congenital long-QT syndrome PMVT, catecholaminergic PMVT) In general, patients with reactive airway disease should not receive beta-blockers. Some beta-blockers should be used with caution in patients with impaired renal or liver function. Adverse effects include hypotension, bradycardia, and the precipitation of heart failure. Avoid in patients with wide-QRS tachycardia, preexcited AFib, and atrial flutter (Mottram & Svenson, 2011).

 AFib, atrial fibrillation; AV, atrioventricular; PMVT, polymorphic ventricular tachycardia

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If AT is sustained at a rate faster than 150 beats/min and it is causing persistent signs of hemodynamic compromise, sedation should be administered and synchronized cardioversion should be performed. Synchronized cardioversion is most likely to be successful for ATs caused by reentry; it may or may  not be successful for ATs that result from triggered activity, and it is unlikely to be effective for automatic  ATs (Page, et al., 2015). Synchronized cardioversion is discussed later in this chapter.

ACLS Pearl Calcium channel blockers inhibit the entry of calcium into vascular smooth muscle cells and myocardial cells, which inhibits both myocardial and vascular smooth muscle contraction. By inhibiting the contractility of vascular smooth muscle and coronary vessels, vascular resistance is reduced, thereby reducing blood pressure. There are two major categories of calcium channel blockers: the dihydropyridines (including amlodipine and nifedipine) and the nondihydropyridines (including diltiazem and verapamil). The dihydropyridines primarily affect the peripheral vasculature, resulting in peripheral vasodilation, with little or no effect on the SA or AV nodes. The nondihydropyridines decrease heart rate and myocardial contractility, slow conduction through the AV node, and have some peripheral arterial dilatory effects as well. The major adverse effects of calcium channel blockers include hypotension, worsening heart failure, bradycardia, and AV block.

Vagal Maneuvers  Vagal maneuvers are methods that are used to stimulate baroreceptors located in the internal carotid arteries and the aortic arch. The stimulation of these receptors results in reflex stimulation of the vagus nerve and the release of acetylcholine. Acetylcholine slows conduction through the AV node, thereby  resulting in the slowing of the heart rate. Vagal maneuvers have been shown to be successful in converting   AVRT or AVNRT to sinus rhythm 17.9% to 54% of the time (Pandya & Lang, 2015). Common vagal maneuvers include the following: Application of a cold stimulus to the face for up to 10 seconds (eg, a washcloth soaked in iced water, a  • cold pack, or crushed ice mixed with water in a plastic bag or glove). This method is often effective in children, but seldom effective in adults. When using this method, do not obstruct the patient ’s mouth or nose or apply pressure to the eyes. The Valsalva maneuver is the forced expiration of air against a closed glottis (ie, deep cough, bearing  • down). A 2010 study showed improved success rates with the patient supine while forcefully exhaling  for at least 15 seconds ( Walker & Cutting, 2010). A more recent study showed improved success with a modified Valsalva maneuver during which the patient was placed in a semirecumbent position and asked to blow into a 10 mL syringe until the plunger moved ( Appelboam, et al., 2015). The patient   was then immediately moved to a supine position with passive leg elevation by a staff member at 45 degrees for 15 seconds, and then returned to a semirecumbent position for 45 seconds before reassessment of the patient ’s cardiac rhythm. Study results showed that conversion to sinus rhythm was significantly more common in the modified-maneuver group (43%) versus the control group (17%) ( Appelboam, et al., 2015). Carotid sinus massage (CSM), which is also called carotid sinus pressure. This procedure is performed •  with the patient ’s neck extended. The carotid pulse is palpated and then steady pressure is applied to the right or left carotid sinus for 5 to 10 seconds ( Page, et al., 2015) (Fig. 5.6). Carotid sinus pressure should be avoided in older adults and in patients who have a history of stroke, known carotid artery  stenosis, or a carotid artery bruit on auscultation ( Olgin, 2008). Simultaneous, bilateral carotid pressure is not recommended.

ACLS Pearl Before performing a vagal maneuver, place the patient on a cardiac monitor, apply a pulse oximeter  and blood pressure monitor, and establish IV access. Ensure that a defibrillator with pacing capability and antiarrhythmic medications are at the bedside.

Reentrant Tachycardias Reentry  is the spread of an impulse through tissue already stimulated by that same impulse; an electrical impulse is delayed, blocked, or both, in one or more areas of the conduction system while the impulse is

CHAPTER 5   Tachycardias

External carotid artery Angle of mandible

Internal cartoid artery Carotid sinus

Thyroid cartilage

Sternocleidomastoid muscle

Fig. 5.6   Location of the carotid sinus. (From  Roberts and Hedges   clinical procedures in emergency medicine , ed 6, ’  

Philadelphia, 2014, Saunders.)

conducted normally through the rest of the conduction system. This results in the delayed electrical impulse entering cardiac cells that have just been depolarized by the normally conducted impulse. Reentry is a common mechanism for AVNRT, which is also called  AV nodal reciprocating tachycardia,  and  AVRT, which is also called AV reciprocating tachycardia. With AVNRT, the electrical circuit or loop (ie, the reentrant circuit) exists within the AV node. With AVRT, an accessory AV conduction pathway  and either the AV node or another accessory pathway form the two parts of the electrical circuit or loop (Goel, et al., 2013). Atrioventricular Nodal Reentrant Tachycardia  [Objectives 1, 2, 3]  AVNRT is the most common SVT (Page, et al., 2015). Typical AVNRT is usually caused by a premature atrial complex (PAC) that is spread by the electrical circuit. This allows the impulseto spin around in a circle indefinitely and to reenter the normal electrical pathway with each pass around the circuit. The result is a very rapid and regular ventricular rhythm that ranges from 150 to 250 beats/min ( Table 5.6, Fig. 5.7). Because AVNRT may be short-lived or sustained, treatment depends on the duration of the tachycardia and severity of the patient ’s signs and symptoms. Assessment findings and symptoms that may be associated with rapid ventricular rates may include the following: • • • • • •

Chest pain or pressure   Dizziness   Dyspnea   Heart failure   Lightheadedness   Nausea

TABLE 5.6

Regularity Rate P waves

PR interval QRS duration

• • • • •

  Nervousness, anxiety   Palpitations (common) Signs of shock    Syncope   Weakness

Characteristics of Atrioventricular Nodal Reentrant Tachycardia Ventricular rhythm is usually very regular 150 to 250 beats/min; typically 180 to 200 beats/min in adults P waves are often hidden in the QRS complex; if the ventricles are stimulated first and then the atria, a negative (ie, inverted) P wave will appear after the QRS in leads II, III, and aVF; when the atria are depolarized after the ventricles, the P wave typically distorts the end of the QRS complex  P waves are not seen before the QRS complex, therefore the PR interval is not measurable 0.11 sec or less unless abnormally conducted

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Fig. 5.7   AVNRT.

If the patient is stable but symptomatic and the symptoms are the result of the rapid heart rate, apply a  pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and consider possible reversible causes of the tachycardia. A 12-lead ECG should be obtained to assist with rhythm identification; if the patient is unstable, do not delay cardioversion to obtain a 12-lead ECG (Link, et al., 2015). While continuously monitoring the patient ’s ECG, attempt  a vagal maneuver if there are no contraindications. AVNRT is usually responsive to vagal maneuvers. If   vagal maneuvers do not slow the rate or cause conversion of the tachycardia to a sinus rhythm, the first  antiarrhythmic given is adenosine (Link, et al., 2015). Treatment with calcium channel blockers or betablockers is indicated when AVNRT fails to convert to sinus rhythm, recurs, or when treatment with vagal maneuvers or adenosine reveals AFib or atrial flutter (Mottram & Svenson, 2011).  An unstable patient is one who has signs and symptoms of hemodynamic compromise. Examples of  these signs and symptoms include acute changes in mental status, chest pain or discomfort, hypotension, shortness of breath, pulmonary congestion, heart failure, acute MI, or signs of shock. If the patient is unstable, treatment should include application of a pulse oximeter and administration of supplemental oxygen (if indicated), IV access, and sedation (if the patient is awake and time permits), followed by  synchronized cardioversion. In clinical practice, health care practitioners sometimes consider a trial of  adenosine before cardioversion for patients who are mildly unstable with a narrow-QRS SVT that is not a sinus tachycardia. This practice is based on retrospective evidence that has shown that adenosine may promptly convert an unstable narrow-QRS SVT and resolve hemodynamic instability ( Mottram &  Svenson, 2011). Atrioventricular Reentrant Tachycardia  [Objectives 1, 2, 3]  AVRT is caused by the presence of an abnormal accessory pathway that serves as a conduit for impulses that originate from the SA node and allows rapid conduction, bypassing the AV node either on its way to the ventricles or on its return to the atria, resulting in a reentrant circuit (Mottram & Svenson, 2011). Ventricular preexcitation occurs when a supraventricular impulse travels by means of an accessory path way and excites the ventricles earlier than would be expected if the impulse traveled only by way of the normal AV conduction system (Hamdan, 2010). The number of atrial impulses reaching the ventricles may approach 300 to 350 beats/min, which significantly increases the risk of development of VF.  The most common form of preexcitation is the Wolff-Parkinson-White (WPW) pattern, which includes a triad of findings that consist of the following: (1) a short PR interval, (2) a delta wave, and (3) a wide-QRS complex (Fig. 5.8). A delta wave is the initial slurred deflection at the beginning  of the QRS complex. It represents the relatively slow ventricular depolarization over the accessory path way (Fig. 5.9) (Mark, et al., 2009). The QRS is wide because it reflects a fusion complex created by ventricular activation through both the AV node and the accessory pathway ( Hamdan, 2010). A patient is said to have WPW  syndrome   when a WPW preexcitation pattern is present on the ECG and a tachydysrhythmia occurs that is related to the accessory pathway ( Olgin & Zipes, 2012). An example of the  WPW pattern is shown in Fig. 5.10, and its ECG characteristics are summarized in  Table 5.7.  Although some people with AVRT never have symptoms, common signs and symptoms associated  with AVRT and a rapid ventricular rate include anxiety, chest discomfort, dizziness, lightheadedness, palpitations (common), shortness of breath during exercise, signs of shock, and weakness. Consultation  with a cardiologist is recommended when caring for a patient with AVRT. If a delta wave is noted on the ECG but the patient is asymptomatic, no specific treatment is required (Hamdan, 2010). If the patient is symptomatic because of the rapid ventricular rate, treatment will depend on how unstable the patient is,

CHAPTER 5   Tachycardias

Normal Sinus Rhythm

SA AV

LEAD II WPW: Sinus Rhythm

WPW: Atrioventricular   Reentrant   Tachycardia   (AVRT)

SA

SA BT

AV

AV

LEAD II

BT

LEAD II Delta Wave

P Wave

Fig. 5.8  Conduction during sinus rhythm in the normal heart (top) spreads from the SA node to the AV node and then down the bundle branches. The jagged line indicates physiologic slowing of conduction in the AV node. With WPW syndrome (bottom left), an abnormal accessory conduction pathway called a bypass tract (BT) connects the atria and ventricles. With WPW, during sinus rhythm the electrical impulse is conducted quickly down the BT, preexciting the ventricles before the impulse arrives via the AV node. Consequently, the PR interval is short and the QRS complex is wide, with slurring at  its onset (ie, delta wave). WPW predisposes patients to develop an AVRT (bottom right) in which a premature atrial beat  may spread down the normal pathway to the ventricles, travel back up the BT, and recirculate down the AV node again. This reentrant loop can repeat itself, resulting in a tachycardia. Notice the normal QRS complex and often negative P wave in lead II during this type of BT tachycardia. (From Goldberger AL: Clinical electrocardiography: a simplified approach, ed 7, St. Louis, 2006, Mosby.)

Normal conduction

WPW

or

A Delta

B

Delta

or

Fig. 5.9 Characteristic WPW pattern (ie, short PR interval, QRS widening, and delta wave) compared with normal conduction.  A, The usual appearance of WPW in leads where the QRS complex is mainly upright. B, The usual appearance of WPW when the QRS is predominantly negative. Negative delta waves may simulate pathologic Q waves —mimicking MI. (From Grauer K:  A practical guide to ECG interpretation , ed 2, St Louis, 1998, Mosby.)

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Fig. 5.10 This rhythm strip shows an example of intermittent preexcitation. The first three beats show preexcitation. This is followed by abrupt normalization of the QRS complex in the next two beats. The preexcitation pattern returns for the final three beats. (From Zipes DP, Jalife J:  Cardiac electrophysiology: from cell to bedside,  ed 3, Philadelphia, 2000, Saunders.)

TABLE 5.7

Regularity Rate P waves PR interval QRS duration

Characteristics of the Wolff-Parkinson-White Preexcitation Pattern Regular, unless associated with AFib Usually 60 to 100 beats/min, if the underlying rhythm is sinus in origin Normal and positive in lead II unless WPW is associated with AFib 0.12 sec or less if P waves are observed because the impulse travels very quickly across the accessory pathway, bypassing the normal delay in the AV node Usually more than 0.12 sec; slurred upstroke of the QRS complex (ie, delta wave) may be seen in one or more leads

 AFib, atrial fibrillation; AV, atrioventricular; WPW, Wolff-Parkinson-White

the width of the QRS complex (ie, wide or narrow), and the regularity of the ventricular rhythm. Obtain the patient ’s vital signs, apply a pulse oximeter, and administer supplemental oxygen, if indicated. Establish IV access and obtain a 12-lead ECG. If the tachycardia persists, the patient is stable, and the QRS is regular and narrow, current resuscitation guidelines recommend the use of adenosine (Link, et al., 2015). Because adenosine can precipitate AFib with a rapid ventricular rate in a patient with WPW, it is prudent  to have a defibrillator readily available for cardioversion before giving adenosine (Page, et al., 2015).

ACLS Pearl Medications such as adenosine, digoxin, diltiazem, and verapamil should be avoided for preexcited  AFib or atrial flutter ( Link, et al., 2015 ). These medications are contraindicated because they slow or  block conduction across the AV node but they may speed up conduction through the accessory pathway, thereby resulting in a further  increase in the ventricular rate. If the patient is unstable, preparations should be made for synchronized cardioversion.

 WIDE-QRS TACHYCARDIAS [Objectives 1, 2]  The QRS duration of a wide-QRS tachycardia is 0.12 second or more. Most wide-complex tachycardias are VT. Some wide-complex tachycardias are actually SVT with a bundle branch block (BBB) or aberrant  conduction. Still others are ventricular-paced rhythms or a tachycardia with AV conduction associated  with or mediated by an accessory pathway (ie, preexcited tachycardia). It is best to seek expert consultation when treating a patient who has a wide-complex tachycardia. If the patient is stable, the QRS is wide, the rhythm is regular, and the QRS complexes are of similar  shape (ie, monomorphic), adenosine is administered to try to identify the origin of the tachycardia while continuously monitoring the patient ’s ECG (Link, et al., 2015). With few exceptions, adenosine will generally have no effect if the rhythm is VT. If the wide-QRS rhythm is actually SVT with aberrancy, adenosine administration will usually result in a transient slowing or conversion to a sinus rhythm. For  the pharmacologic termination of a stable wide-QRS tachycardia that is most likely VT, procainamide ( Table 5.8), amiodarone, or sotalol ( Table 5.9) can be used (Link, et al., 2015). These medications are

CHAPTER 5   Tachycardias

considered first-line antiarrhythmics for monomorphic VT, and they have complex mechanisms of  action. They are used for both atrial and ventricular dysrhythmias. Although lidocaine is a ventricular  antiarrhythmic, it is considered a second-line antiarrhythmic for the management of monomorphic VT because it is reportedly less effective for the termination of VT than the first-line agents. If the decision is made to administer procainamide, amiodarone, or sotalol, it is recommended that expert consultation be sought before another drug is administered (Link, et al., 2015). If the diagnosis of SVT cannot  be proved or cannot be made easily, then the patient should be treated as if VT were present.

TABLE 5.8

Class Mechanism of Action

Indications Dosage

Considerations

Procainamide (Pronestyl) Class IA antiarrhythmic Blocks sodium and potassium channels, prolonging the effective refractory period and action potential duration in the atria, the ventricles, and the His-Purkinje system • Suppresses ectopy in atrial and ventricular tissue • Prolongs the PR and QT intervals • Exerts a peripheral vasodilatory effect  • To control the ventricular rate in the patient with preexcited AFib • Stable monomorphic VT with a normal QT interval • 20 mg/min IV infusion or 100 mg every 5 min until one of the following occurs: dysrhythmia resolves, hypotension ensues, QRS prolongs by more than 50% of original width, or total cumulative dose of 17 mg/kg is administered (Link, et al., 2015) • Up to 50 mg/min may be used in urgent situations (Gahart, et al., 2016b) • Maintenance infusion of 1 to 4 mg/min • During administration, carefully monitor the patient ’s ECG and BP. If the BP falls 15 mm Hg or more, temporarily discontinue administration. Watch the ECG closely for increasing PR and QT intervals, widening of the QRS complex, heart block, and/or onset of TdP. • Reduce the maintenance infusion rate in patients with impaired or reduced renal function. • Avoid use in patients with QT prolongation or heart failure. •

 AFib, atrial fibrillation; BP, blood pressure; ECG, electrocardiogram; IV, intravenous; TdP, torsades de pointes; VT, ventricular tachycardia

TABLE 5.9

Class Mechanism of Action

Indications Dosage Considerations

Sotalol (Betapace) Class III antiarrhythmic Slows heart rate • Decreases AV nodal conduction • Increases AV nodal refractoriness • Prolongs the effective refractory period of atrial muscle, ventricular muscle, and AV  accessory pathways (where present) in both anterograde and retrograde directions •   Negative inotrope Stable monomorphic VT (Link, et al., 2015) 1.5 mg/kg IV over 5 min; however, U.S. package labeling recommends any dosage should be infused slowly over a period of 5 hours (Link, et al., 2015) • Sotalol is not a first-line antiarrhythmic. • Use with caution in patients with bronchospastic disease. • Monitor carefully for bronchospasm, bradycardia, hypotension, and new dysrhythmias, including TdP. • Closely monitor the QT interval every 2 to 4 hours after each dose; if the QT interval lengthens to 0.5 sec or greater, reduce the dose or discontinue the drug (Page, et al., 2015). • Avoid in patients with a prolonged QT interval, those taking other QT-prolonging drugs, those with uncontrolled heart failure, and those with hypokalemia. •

 AV, atrioventricular; BP, blood pressure; IV, intravenous; TdP, torsades de pointes; VT, ventricular tachycardia

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 Ventricular Tachycardia [Objectives 1, 2, 3] VT exists when three or more sequential premature ventricular complexes (PVCs) occur at a rate of more than 100 beats/min. VT may occur as a short run that lasts less than 30 seconds and spontaneously ends (ie, nonsustained VT ) (Fig. 5.11). Sustained VT   persists for more than 30 seconds and may require therapeutic interventions to terminate the rhythm. VT may occur with or without pulses, and the patient may  be stable or unstable with this rhythm. VT, like PVCs, may originate from an ectopic focus in either ventricle. When the QRS complexes of  VT are of the same shape and amplitude, the rhythm is called  monomorphic VT. When the QRS complexes of VT vary in shape and amplitude from beat to beat, the rhythm is called  polymorphic VT. In PMVT, the QRS complexes appear to twist from upright to negative or negative to upright and back. PMVT is discussed later in this chapter with irregular tachycardias. Signs and symptoms associated with VT vary. The patient who has sustained monomorphic VT may  be stable for long periods. However, when the ventricular rate is very fast, or when myocardial ischemia is present, monomorphic VT can deteriorate to PMVT or VF. Syncope or near-syncope may occur because of an abrupt onset of VT. The patient ’s only warning symptom may be a brief period of lightheadedness.

ACLS Pearl  An SVT with an intraventricular conduction delay may be difficult to distinguish from VT. Keep in mind that VT is considered a potentially life-threatening dysrhythmia. If you are unsure whether a regular, wide-QRS tachycardia is VT or SVT with an intraventricular conduction delay, treat the rhythm as VT until proven otherwise. Obtaininga 12-lead ECGmay help differentiate VT from SVT, butdo notdelay treatment if the patient is symptomatic.

During VT, the severity of the patient ’s symptoms is related to a number of factors, including how  rapid the ventricular rate is, how long the tachycardia has been present, the presence and extent of underlying heart disease, and the presence and severity of peripheral vascular disease ( Martin & Wharton, 2001). Hemodynamic stability should not be used to differentiate between VT and SVT with an intra ventricular conduction delay (Mottram & Svenson, 2011). Signs and symptoms of hemodynamic instability related to VT may include the following: • Acute altered mental status Chest pain or discomfort  • •   Hypotension •   Pulmonary congestion •   Shock  Shortness of breath •

ACLS Pearl  VT may occur in a patient who has an implantable cardioverter-defibrillator (ICD) in place. If the rate of  the VT is below the programmed tachycardia detection rate, the ICD will not treat it. It is important to identify this situation and request expert consultation immediately. It is possible that the VT can be terminated painlessly with the use of the programmer that corresponds with the implanted device.

Fig. 5.11 Nonsustained VT. (From Crawford MV, Spence MI: Commonsense approach to coronary care, rev ed 6, St Louis, 1994, Mosby.)

CHAPTER 5   Tachycardias

 Treatment is based on the patient ’s signs, symptoms, and the type of VT. If the rhythm is monomorphic VT (and the patient ’s symptoms are caused by the tachycardia): Cardiopulmonary resuscitation (CPR) and defibrillation are used to treat the pulseless patient  •  with VT. Stable but symptomatic patients are treated with oxygen (if indicated), IV access, and ventricular anti• arrhythmics (eg, procainamide, amiodarone, sotalol) to suppress the rhythm. Procainamide should be avoided if the patient has a prolonged QT interval or signs of heart failure. Sotalol should also be avoided if the patient has a prolonged QT interval. Unstable patients (usually a sustained heart rate of 150 beats/min or more) are treated with oxygen, IV  • access, and sedation (if the patient is awake and time permits), followed by synchronized cardioversion. In all cases, an aggressive search must be made for the cause of the VT. For example, VT that occurs in the presence of hypokalemia may be terminated by treatment with replacement potassium.

ACLS Pearl  A rapid, wide-QRS rhythm associated with pulselessness, shock, or heart failure should be presumed to be VT until proven otherwise.

IRREGULAR TACHYCARDIAS  The severity of signs and symptoms associated with an irregular tachycardia varies depending on the  ventricular rate, how long the rhythm has been present, and the patient ’s cardiovascular status. The patient may be asymptomatic and not require treatment or may experience serious signs and symptoms. It is best to seek expert consultation when treating a patient who has an irregular tachycardia.

Multifocal Atrial Tachycardia [Objectives 1, 2, 3] Multifocal AT (MAT) is an automatic tachycardia that is the result of the random and chaotic firing of  multiple ectopic sites in the atria. At least three different P wave configurations (seen in same lead) are required for a diagnosis of MAT ( Table 5.10, Fig. 5.12). MAT is an irregular rhythm with a ventricular  rate faster than 100 beats/min; it is most often found in patients with advanced pulmonary disease. Because MAT can be difficult to treat, it is best to consult a cardiologist before starting treatment.  Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and obtain a 12-lead ECG.  The treatment of MAT is directed at the underlying cause (eg, hypoxia, acidosis, electrolyte disturbances). If the rhythm persists, evaluate the clinical signif icance of the tachycardia before considering the use of antiarrhythmics (Mottram & Svenson, 2011). Because MAT does not involve reentry through the  AV node, it is unlikely that vagal maneuvers or giving adenosine will terminate the rhythm. Metoprolol has been shown to be effective for rate control, but it should be avoided in patients with impaired left   ventricular function or bronchospastic pulmonary disease; in such cases, amiodarone may be preferred (Mottram & Svenson, 2011; Olgin & Zipes, 2012). MAT is unresponsive to cardioversion (Link, et al., 2015). TABLE 5.10

Regularity Rate P waves PR interval QRS duration

Characteristics of Multifocal Atrial Tachycardia

Irregular; the pacemaker site shifts from the SA node to ectopic atrial locations or the AV   junction Ventricular rate faster than 100 beats/min Size, shape, and direction may change from beat to beat; at least three different P wave configurations (seen in same lead) are required for a diagnosis of MAT Varies; the pacemaker site shifts from the SA node to ectopic atrial locations or the AV junction 0.11 sec or less unless abnormally conducted

 AT, atrial tachycardia; AV, atrioventricular; MAT, multifocal atrial tachycardia; SA, sinoatrial.

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CHAPTER 5   Tachycardias

Fig. 5.12 MAT. (From Braunwald E, Libby P, Zipes DP, et al.: Heart disease: a textbook of cardiovascular medicine, ed 6, St. Louis, 2001, Mosby.)

 Atrial Flutter [Objectives 1, 2, 3]  Atrial flutter is a macroreentrant AT in which an irritable site within the atria fires regularly at a very rapid rate ( Table 5.11). Because of this extremely rapid stimulation, atrial waveforms are produced that resemble the teeth of a saw, or a picket fence; these are called  flutter waves  or   F waves  (Fig. 5.13).  Typical atrial flutter is caused by reentry in which an impulse circles around a large area of tissue, such as the entire right atrium in a counterclockwise direction. F waves are predominantly negative in leads II, III, and aVF, and positive in V 1  ( January, et al., 2014). The atrial rate is typically 240 to 300 beats/min ( January, et al., 2014). It is best to consult a cardiologist when considering treatment options. Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and obtain a 12-lead ECG. Vagal maneuvers may help to identify the rhythm by temporarily slowing AV  conduction and revealing the underlying flutter waves (see Fig. 5.13). When vagal maneuvers are used in the management of atrial flutter, the response is usuallysudden slowing and then a return to the former  rate. Vagal maneuvers will not usually convert atrial flutter because the reentry circuit is located in the atria, not the AV node.

ACLS Pearl The two primary treatment strategies used to control symptoms associated with atrial flutter or AFib are rate control and rhythm control. With rate control, the patient remains in atrial flutter or AFib but the ventricular rate is controlled to decrease acute symptoms, reduce signs of ischemia, and reduce or prevent signs of heart failure from developing. With rhythm control, sinus rhythm is reestablished.

 When a rate control strategy is considered for the patient with atrial flutter and a rapid ventricular  response, medications such as beta-blockers or nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) are the drugs of choice (Link, et al., 2015). When a rhythm control strategy is considered, it is best to consult a cardiologist (Link, et al., 2015). The short-acting antiarrhythmic ibutilide ( Table 5.12) may be ordered for pharmacologic rhythm control, provided there are no contraindications to its use (Bontempo & Goralnick, 2011). Successful pharmacologic cardioversion with ibutilide has reportedly occurred in 60% to 90% of episodes of atrial flutter (Olgin & Zipes, 2012). Excessive QT

TABLE 5.11

Regularity Rate

P waves PR interval QRS duration

 AV, atrioventricular

Characteristics of Atrial Flutter

Atrial: regular; ventricular: regular or irregular, depending on AV conduction and blockade The atrial rate generally ranges from 240 to 300 beats/min; the ventricular rate varies and is determined by AV blockade; the ventricular rate will usually not exceed 180 beats/min as a result of the intrinsic conduction rate of the AV junction No identifiable P waves; saw-toothed “flutter”  waves are present  Not measurable 0.11 sec or less but may be widened if flutter waves are buried in the QRS complex or if  abnormally conducted

CHAPTER 5   Tachycardias

II

A II

B

CSM II

C

Fig. 5.13   Atrial flutter. A, This rhythm strip shows a narrow-QRS tachycardia with a ventricular rate just under 150 beats/min. B, The same rhythm shown in A with arrows added indicating possible atrial activity. C, When CSM is performed, the rate of conduction through the AV node slows, revealing atrial flutter. (From Grauer K: A practical guide to ECG interpre-  tation, ed 2, St Louis, 1998, Mosby.)

interval prolongation, which can cause torsades de pointes (TdP), is a potential complication that can occur during and shortly after ibutilide administration. Because most episodes of ibutilide-induced  TdP occur within 1 hour after treatment and almost all occur within 6 hours, continuous ECG monitoring is essential throughout ibutilide administration and for 6 to 8 hours thereafter  (Bontempo & Goralnick, 2011; Olgin & Zipes, 2012). Other medications that are useful for the pharmacologic cardioversion of atrial flutter or AFib include flecainide, dofetilide, and propafenone ( January, et al., 2014). Prompt synchronized cardioversion should be considered for any patient who is hemodynamically  unstable (Link, et al., 2015). If synchronized cardioversion is performed, atrial flutter can be successfully  converted to a sinus rhythm with the use of low energy levels. Sedation should be considered when circumstances permit.

 Atrial Fibrillation [Objectives 1, 2, 3]  AFib is a SVT characterized by uncoordinated atrial activation and consequently ineffective atrial contraction ( January, et al., 2014). It occurs because of altered automaticity in one or several rapidly firing  sites in the atria or reentry involving one or more circuits in the atria ( Table 5.13, Fig. 5.14). Cardiac output is decreased because of various mechanisms including the loss of effective atrial contraction, irregular cardiac cycle length, rapid heart rates, and decreased coronary blood flow (Goel, et al., 2013). Patients who experience AFib are at increased risk of atrial thrombus formation, leading to stroke, peripheral thromboembolism, or both ( January, et al., 2014).

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TABLE 5.12

Class Mechanism of   Action

Indications Dosage

Considerations

Ibutilide (Corvert) Class III antiarrhythmic Potassium channel blocker; prolongs action potential duration and QT interval • Mild slowing of the sinus rate and AV conduction • Rhythm conversion usually occurs within 30 min but may take up to 90 min after the start of the infusion (Gahart, et al., 2016a) Rapid conversion of recent onset AFib or atrial flutter to sinus rhythm 1 mg IV over 10 min; if the dysrhythmia does not terminate within 10 min after the end of the initial dose, a repeat dose of 1 mg may be administered 10 min after completion of the first infusion (Olgin & Zipes, 2012) • Avoid if the QTc is longer than 0.44 sec or when uncorrected hypokalemia or bradycardia exists (Olgin & Zipes, 2012) • Should not be given concurrently with Class IA antiarrhythmics or other Class III antiarrhythmics (eg, amiodarone, sotalol). • Lengthens the QT interval, increasing the risk of ventricular dysrhythmias, including TdP and monomorphic VT • During administration, resuscitation equipment must be immediately available and continuous ECG monitoring is essential; ECG monitoring should be continued for at  least 4 hours after administration (January, et al., 2014). • Pretreatment with IV magnesium may reduce the risk of ventricular dysrhythmias (January, et al., 2014). •

 AFib, atrial fibrillation; AV, atrioventricular; ECG, electrocardiogram; IV, intravenous; QTc, corrected QT interval; TdP, torsades de pointes; VT, ventricular tachycardia

TABLE 5.13

Characteristics of Atrial Fibrillation

Regularity Rate P waves PR interval QRS duration

Ventricular rhythm usually irregularly irregular Atrial rate usually 400 to 600 beats/min; ventricular rate variable No identifiable P waves; fibrillatory waves present; erratic, wavy baseline Not measurable 0.11 sec or less unless abnormally conducted

II

MCLI

Fig. 5.14   AFib. (From Aehlert B: ECG study cards,  St. Louis, 2004, Mosby.)

 Atrial flutter or AFib that has a rapid ventricular rate is described as uncontrolled  (Figs. 5.15, 5.16).  Atrial flutter or AFib with a rapid ventricular response is commonly called Aflutter with RVR  or   AFib  with RVR. Obtaining a thorough medical history and patient assessment are important. When obtaining the patient ’s history, asking about the number of episodes of AFib, their frequency, the nature of the patient ’s symptoms, and possible triggers may help to determine the pattern of the dysrhythmia. It is best to consult a cardiologist when considering specific therapies. Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and obtain a 12-lead ECG.

CHAPTER 5   Tachycardias

II

Fig. 5.15  AFib with a rapid ventricular response. (From Aehlert B:  ECGs made easy study cards, St. Louis, 2004, Mosby.)

Lead I

Fig. 5.16 AFib with a rapid ventricular response and left BBB. (From Goldberger AL: Clinical electrocardiography: a simplified  approach, ed 7, St. Louis, 2006, Mosby.)

 With a rate control strategy, the ventricular rate associated with the AFib is slowed without termination of the AFib and it is achieved using medications that prolong the refractory period of the AV node or catheter ablation (Fuster, et al., 2011; Bontempo & Goralnick, 2011). Treatment of precipitating or  reversible causes of AFib is recommended before starting antiarrhythmic therapy ( Wann, et al., 2011). IV administration of beta-blockers (eg, esmolol, metoprolol, propranolol) or nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) is recommended to slow the ventricular response to  AFib ( Anderson, et al., 2013; January, et al., 2014). These medications must be used with caution in patients with hypotension or heart failure. IV amiodarone can be useful for rate control in critically  ill patients without preexcitation, but it is less effective than nondihydropyridine calcium channel blockers ( January, et al., 2014). Rhythm control, that is, termination of AFib and restoring sinus rhythm, is achieved using a combination of approaches including pharmacologic or electric cardioversion and radiofrequency catheter  ablation. Because pharmacologic or electric cardioversion carries a risk of thromboembolism, anticoagulation is recommended before attempting conversion of AFib to a sinus rhythm when the duration of the  AFib exceeds 48 hours ( January, et al., 2014). Shorter durations of AFib do not exclude the possibility of  thromboembolism (Link, et al., 2015). For patients who are symptomatic and stable, but the duration of  atrial flutter or AFib is unknown, issues with regard to anticoagulation are important. Rate control can be attempted while expert consultation is sought. Patients who are hemodynamically unstable (eg, angina, heart failure, symptomatic hypotension, ongoing myocardial ischemia, shock, pulmonary edema) should receive prompt synchronized cardioversion ( January, et al., 2014). Sedation should be considered when circumstances allow. Anticoagulation should be started as soon as possible and continued for at least 4 weeks after cardioversion unless contraindicated ( January, et al., 2014).  Although atrial flutter often converts to a sinus rhythm with the use of low energy levels during synchronized cardioversion, higher energy levels are required for AFib (Fuster, et al., 2011). Although resuscitation guidelines have traditionally recommended that the energy used during the cardioversion of   AFib be increased in successive increments, experts state that the initial use of a higher-energy shock  is more effective and may minimize the number of shocks required, as well as the duration of sedation ( January, et al., 2014). Pretreatment with selected antiarrhythmic medications such as ibutilide can be useful to enhance the success of synchronized cardioversion, prevent recurrent AFib, and increase the likelihood of maintenance of sinus rhythm ( January, et al., 2014). For cardioversion of AFib, a biphasic  waveform is more effective than a monophasic waveform ( January, et al., 2014). Some, but not all, studies

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have shown anterior  – posterior electrode placement superior to anterolateral placement. If cardioversion is attempted using one electrode placement and fails, experts recommend using the alternative placement  before attempting another shock ( January, et al., 2014).

Polymorphic Ventricular Tachycardia [Objectives 1, 2, 3]  With PMVT, the QRS complexes vary in shape and amplitude from beat to beat and appear to twist  from upright to negative or negative to upright and back, resembling a spindle (Fig. 5.17). The ECG characteristics of PMVT are shown in Table 5.14. Several types of PMVT and their possible causes have been identified. PMVT that occurs in the presence of a long QT interval (generally, 0.50 second or more) is called torsades de pointes (TdP). A long QT interval may be congenital, acquired (typically precipitated by antiarrhythmic drug use or hypokalemia,  which are typically associated with bradycardia), or idiopathic (neither familial nor with an identifiable acquired cause). PMVT that occurs in the presence of a normal QT interval is simply referred to as  polymorphic VT  or   normal-QT PMVT.  The signs and symptoms associated with PMVT are usually related to the decreased cardiac output  that occurs because of the fast ventricular rate. Signs of shock are often present. The patient may experience a syncopal episode or seizures. The rhythm may occasionally terminate spontaneously and recur  after several seconds or minutes, or it may deteriorate to VF. The patient with sustained PMVT is rarely  hemodynamically stable.  Apply a pulse oximeter and administer supplemental oxygen, if indicated. Obtain the patient ’s vital signs, establish IV access, and obtain a 12-lead ECG. It is best to seek expert consultation when treating  the patient with PMVT because of the diverse mechanisms of PMVT, for which there may or may not be clues as to its specific cause at the time of the patient ’s presentation. Treatment options vary and can be contradictory. For example, a medication that may be appropriate for the treatment of TdP may be contraindicated when treating another form of PMVT. In general, if the patient is symptomatic because of  the tachycardia, treat ischemia (if it is present) and correct electrolyte abnormalities. If the QT interval is prolonged, the cause of the long QT should be determined and corrected, if possible (Olgin & Zipes, 2012). Discontinue any medications that the patient may be taking that prolong the QT interval. Generally, IV magnesium ( Table 5.15) is the initial treatment for the stable patient with PMVT associated  with a long QT interval (ie, TdP). Beta-blockers may be effective for certain forms of PMVT

Fig. 5.17 When the QRS complexes of VT vary in shape and amplitude, the rhythm is called PMVT. (From Aehlert B: ECGs  made easy study cards, St. Louis, 2004, Mosby.)

TABLE 5.14

Regularity Rate P waves PR interval QRS duration

Characteristics of Polymorphic Ventricular Tachycardia

Ventricular rhythm may be regular or irregular Ventricular rate is 150 to 300 beats/min; typically 200 to 250 beats/min None None 0.12 sec or more; there is a gradual alteration in the amplitude and direction of the QRS complexes; a typical cycle consists of 5 to 20 QRS complexes

CHAPTER 5   Tachycardias

TABLE 5.15

Magnesium Sulfate

Class Mechanism of Action

Antiarrhythmic, electrolyte Essential for activity of many enzyme systems • Plays an important role with regard to neurochemical transmission and muscular excitability PMVT with prolonged QT interval • If pulseless, give 1 to 2 g IV diluted in 10 mL D5W. • If pulse present, give 1 to 2 g IV diluted in 50 to 100 mL D5W over 15 min. • Use with caution in patients receiving digitalis, patients with impaired renal function, and patients with preexisting heart blocks. • Calcium is the antidote for magnesium toxicity.

Indications Dosage Considerations

•

D5W, dextrose 5% in water; IV, intravenous; PMVT, polymorphic ventricular tachycardia

(eg, ischemic PMVT, congenital long-QT syndrome PMVT, catecholaminergic PMVT). Amiodarone may be effective for PMVT with a normal QT interval. PMVT that is associated with Brugada syndrome may be responsive to isoproterenol (Link, et al., 2015). Adenosine should not be given for PMVT because it may cause degeneration of the dysrhythmia to VF (Link, et al., 2015). Because the QRS complexes of PMVT are disorganized (ie, they differ in amplitude and direction), synchronized cardioversion is generally not possible when managing an unstable patient with this rhythm. Therefore if the patient with PMVT is unstable or has no pulse, proceed with defibrillation as for VF. The tachycardia algorithm is shown in  Fig. 5.18.

Fig. 5.18   Tachycardia algorithm. (American Heart Association tachycardia algorithm. Reprinted with permission. 2015  American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care—Part 7: Adult   Advanced Cardiovascular Life Support. ECC guidelines.heart.org. © Copyright 2015 American Heart Association, Inc.)

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SYNCHRONIZED CARDIOVERSION [Objectives 4, 5] Synchronized cardioversion is a type of electrical therapy during which a shock is timed or programmed for delivery during ventricular depolarization (ie, the QRS complex). When the “Sync” control is pressed, a synchronizing circuit in the machine searches for the QRS complex and delivers the shock a few milliseconds after the QRS. The delivery of a shock during this portion of the cardiac cycle reduces the potential for the delivery of current during ventricular repolarization, which includes the vulnerable period of the T wave (ie, the relative refractory period). Because the machine must be able to detect a QRS complex so that it can “sync,”  synchronized cardioversion is used to treat rhythms that have a clearly identifiable QRS complex and a rapid ventricular  rate (eg, some narrow-QRS tachycardias, monomorphic VT). Synchronized cardioversion is not used to treat disorganized rhythms (eg, PMVT) or those that do not have a clearly identifiable QRS complex (eg, VF).

Procedure [Objectives 4, 5] Before performing synchronized cardioversion, take appropriate standard precautions and obtain a 12lead ECG. Identify the rhythm on the cardiac monitor and verify that the procedure is indicated. Printan ECG strip to document the patient ’s rhythm, and assess the patient for serious signs and symptoms from the tachycardia. Make sure that suction and emergency medications are available. Give supplemental oxygen, if indicated, and start an IV. If the patient is awake, explain the procedure and obtain an informed consent. If time and the patient ’s clinical condition permit, sedation should be administered before performing the procedure. Place the patient in a supine position and remove clothing from the patient ’s upper body. With gloves, remove transdermal medication patches, bandages, jewelry, and any other materials from the sites that   will be used for paddle or pad placement; do not attempt to administer shocks through them. Keep monitoring electrodes and wires well away from the area where paddles or combination pads will be placed. Contact may cause electrical arcing and patient skin burns during defibrillation or cardioversion.  Turn the power to the defibrillator on. If using combination pads, place them in proper position on the patient ’s bare chest. If using handheld paddles, remember to use appropriate conductive gel or disposable gel pads between the paddle electrode surface and the patient ’s skin. Press the  “ Sync” control on the defibrillator to select the synchronized mode (Fig. 5.19). Select a lead  with an optimum QRS complex amplitude and no artifact. Make sure the machine is marking or flagging  each QRS complex and that no artifact is present. The sense marker should appear near the middle of  each QRS complex. If sense markers do not appear or are seen in the wrong place (eg, on a T wave), adjust  the ECG size, or select another lead. Select the energy level appropriate for the patient ’s rhythm on the defibrillator (Fig. 5.20). Turnon the ECG recorder for a continuous printout. Next, press the “Charge” button on the defibrillator and recheck  the ECG rhythm (Fig. 5.21). If using handheld paddles, place the paddles on pre-gelled defibrillator  pads on the patient ’s chest and apply firm pressure. If the rhythm is unchanged, call “Clear!” and look  around you. Make sure that everyone is clear of the patient, the bed, and any equipment that is connected to the patient. Make sure oxygen is not flowing over the patient ’s chest to decrease the risk of combustion in the presence of electrical current. After confirming that the area is clear, depress the “Shock ” control until the energy is delivered (Fig. 5.22). If using handheld paddles, simultaneously depress both buttons on the paddles and hold until the shock is delivered. A slight delay may occur while the machine detects the next QRS complex. Release the “Shock ”  control after the shock has been delivered. Reassess the rhythm and the patient (Fig. 5.23). If the tachycardia persists, make sure that the machine is in “Sync” mode before delivering another shock. This is important because many defibrillators default to the unsynchronized mode after cardioversion. If the rhythm changes to VF, confirm that the patient has no pulse while another team member quickly verifies that all electrodes and cable connections are secure. If no pulse is present, ensure that the machine is not in “Sync”  mode and defibrillate (see Chapter 4). See Table 5.16 for a summary of cardioversion.

CHAPTER 5   Tachycardias

Fig. 5.19 Place combination pads in proper position on

Fig. 5.20 Select the appropriate energy level on the defi-

the patient ’s bare chest according to the defibrillator manufacturer’s instructions. Press the “Sync”  control on the defibrillator. Make sure the machine is marking each QRS complex and that no artifact is present. (From Roberts  and Hedges    clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

brillator. (From Roberts and Hedges    clinical procedures in  emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

Fig. 5.21   Press the “Charge”  button on the defibrillator

Fig. 5.22   Depress the “Shock ”  button until the energy is

and recheck the ECG rhythm. (From  Roberts and Hedges  clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

delivered. (From Roberts and Hedges    clinical procedures in  emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

’  

’  

’  

’  

Fig. 5.23 Reassess the rhythm and the patient. (From Roberts and Hedges   clinical procedures in emergency medicine, ed 6, ’  

Philadelphia, 2014, Saunders.)

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TABLE 5.16

Synchronized Cardioversion—Summary*

Rhythm

Recommended Energy Doses

Unstable narrow regular tachycardia (ie, atrial flutter, other SVTs) Unstable narrow irregular tachycardia (ie, AFib)

The biphasic dose is typically 50 to 100 J initially; increase in a stepwise fashion if the initial shock fails The biphasic dose is typically 120 to 200 J initially; increase in a stepwise fashion if the initial shock fails; begin with 200 J if using monophasic energy, and increase if unsuccessful The monophasic or biphasic dose is typically 100 J initially; it is reasonable to increase in a stepwise fashion if the initial shock fails

Unstable wide regular tachycardia (ie, monomorphic VT)

*Use energy doses recommended by the device manufacturer.  AFib, atrial fibrillation; J, Joule; SVT, supraventricular tachycardia; VT, ventricular tachycardia

CHAPTER 5   Tachycardias

PUTTING IT ALL TOGETHER  The chapter quiz and case studies presented on the following pages are provided to help you integrate the information presented in this chapter. As you work through the case studies, remember that there may be alternative actions that are perfectly acceptable, yet not presented in the case study. CHAPTER QUIZ

 Identify the choice that best completes the statement or answers the question.  Multiple Choice

____

1.

A 72-year-old man is anxious and complaining of palpitations. His blood pressure is 110/64 millimeters of mercury (mm Hg), his pulse is 190 beats/min, and his  ventilatory rate is 16 breaths/min. The patient denies chest pain. Breath sounds are clear. The cardiac monitor reveals monomorphic VT. Recommended treatment  in this situation includes:  A. Beginning CPR and defibrillating immediately. B. ABCs, O2, IV, and epinephrine 1 mg rapidly IV. C. ABCs, O2, IV, and procainamide 20 to 50 mg/min IV. D. ABCs, O2, IV, sublingual nitroglycerin, and adenosine 6 mg rapidly IV.

____

2.

With which type of tachycardia does the impulse begin above the ventricles but travel  via a pathway other than the AV node and bundle of His?  A. Sinus tachycardia  B. AT C. AVRT D. AVNRT

____

3.

Which of the following reflects the correct initial dosage of adenosine?  A. 6 mg IV bolus over 1 to 2 minutes B. 3 mg rapid IV bolus over 1 to 3 seconds followed by a 20 mL saline flush C. 6 mg rapid IV bolus over 1 to 3 seconds followed by a 20 mL saline flush D. 12 mg rapid IV bolus over 1 to 3 seconds followed by a 20 mL saline flush

____

4.

Synchronized cardioversion:  A. Is used only for atrial dysrhythmias. B. Delivers a shock during the QRS complex. C. Delivers a shock between the peak and end of the T wave. D. Is used only to treat rhythms with a ventricular rate of less than 60/min.

____

5.

The most common type of SVT is:  A. AT. B. Ventricular escape rhythm. C. AVRT. D. AVNRT.

____

6.

A 29-year-old man presents with acute altered mental status. His blood pressure is 50/P, ventilations 14 breaths/min. The cardiac monitor reveals PMVT. Your best  course of action in this situation will be to:  A. Give adenosine rapid IV push. B. Give diltiazem IV push over 2 minutes. C. Consider sedation and defibrillate immediately. D. Perform immediate synchronized cardioversion.

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____

7.

Examples of irregular tachycardias include:  A. Sinus tachycardia, accelerated junctional rhythm, and atrial flutter. B. PMVT, asystole, and sinus tachycardia. C. AFib, atrial flutter, and PMVT. D. Accelerated idioventricular rhythm, AFib, and accelerated junctional rhythm.

____

8.

Select the incorrect   statement regarding vagal maneuvers.  A. Carotid sinus pressure should be avoided in older patients. B. Carotid sinus pressure should be avoided if carotid bruits are present. C. An ECG monitor should be used when a vagal maneuver is performed. D. Simultaneous bilateral carotid pressure is recommended to ensure slowing of the heart rate.

____

9.

Which of the following correctly describes MAT?  A. In MAT, at least three different P wave configurations are observed. B. MAT is an irregularly irregular rhythm with no normal looking waveforms. C. Waveforms resembling teeth of a saw or picket fence are observed before each QRS complex. D. P waves are uniform in appearance, positive (ie, upright) in lead II, and one precedes each QRS complex.

____

10.

A 68-year-old man is complaining of chest pain. His level of responsiveness is rapidly  decreasing. His blood pressure is 50/32 mm Hg, his pulse is 230 beats/min, and his  ventilatory rate is 6 breaths/min. The cardiac monitor reveals a regular, narrow-QRS tachycardia. Your best course of action will be to:  A. Defibrillate with 360 J. B. Begin immediate transcutaneous pacing. C. Sedate and perform synchronized cardioversion with 50 J. D. Sedate and perform synchronized cardioversion with 120 J.

____

11.

When administering procainamide, the maximum dose is ____ and the maintenance infusion dose is ____.  A. 0.25 mg/kg, 5 to 15 mg/hour  B. 0.5 mg/kg, 50 mcg/kg/min C. 17 mg/kg, 1 to 4 mg/min D. 150 mg, 0.5 mg/min

____

12.

A 73-year-old woman is complaining of palpitations and chest pain. Her blood pressure is 72/50 mm Hg, her heart rate is 188 beats/min, and her ventilatory rate is 16 breaths/min. The cardiac monitor reveals a wide-QRS tachycardia. Your best course of action will be to:  A. Defibrillate immediately. B. Begin immediate transcutaneous pacing. C. Perform synchronized cardioversion with 100 J. D. Begin CPR and ventilate using a bag-mask device.

____

13.

A 56-year-old woman is complaining of palpitations. When questioned, she denies chest pain or shortness of breath. Her blood pressure is 134/82 mm Hg, pulse 180,  ventilations 18 breaths/min. The cardiac monitor shows a regular narrow-QRS tachycardia without visible P waves. Which of the following reflects your best course of  action to take at this time?  A. O2, IV, vagal maneuvers, and adenosine 6 mg rapid IV bolus B. O2, IV, vagal maneuvers, and verapamil 2.5 mg slow IV bolus C. O2, IV, sedate and perform synchronized cardioversion with 50 J D. O2, IV, and atropine 0.5 mg IV every 3 to 5 minutes to a maximum of 3 mg 

CHAPTER 5   Tachycardias

____

14.

A 62-year-old man is complaining of palpitations that came on suddenly after   walking up a short flight of stairs. His symptoms have been present for about  20 minutes. He denies chest pain and is not short of breath. His skin is warm and dry; breath sounds are clear. His blood pressure is 144/88 mm Hg, pulse 186, ventilations 18 breaths/min. The cardiac monitor reveals sustained monomorphic VT. An IV has been established. Which of the following medications is most appropriate in this situation?  A. Dopamine or sotalol B. Furosemide or atropine C. Nitroglycerin or morphine D. Procainamide or amiodarone

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CASE STUDY 5-1  A 72-year-old man presents with complaints of palpitations and chest heaviness. You have a sufficient  number of advanced life support personnel available to assist you and carry out your instructions. Emergency equipment, including a biphasic manual defibrillator, is available. 1. As you approach the patient, you observe that he is sitting upright on a stretcher. He appears anxious, his breathing is not labored, and his skin is pink. The patient speaks hurriedly, telling   you that his heart is “racing and feels like it is going to pound out of my chest.”  What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 2. The patient ’s ventilatory rate is 18 breaths/min and unlabored. His radial and carotid pulses are strong but too fast to count accurately. You estimate the rate to be about 200 beats/min. His skin is warm, pink, and dry. How would you like to proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 3. The patient ’s vital signs are as follows: Blood pressure: 142/90 mm Hg; heart rate 214 beats/  min; and ventilatory rate 18 breaths/min. Breath sounds are clear and equal. The patient ’s SpO 2   on room air is 96%, and he has been placed on the cardiac monitor, which reveals the following rhythm:

II

(From Aehlert B: ECG study cards , St. Louis, 2004, Mosby.)

 The following information has been obtained from the patient: Signs/Symptoms: Palpitations and chest “heaviness” began 1 hour ago when the patient began feeling as if  everything was spinning around him and felt heaviness in his chest at the same time; says this has happened once before but only lasted a minute or two; rates his chest  discomfort at 1/10  A llergies: None Medications: Lisinopril, hydrochlorothiazide Past history: Hypertension Last oral intake: Lunch 1 hour ago E vents prior: Patient was walking from his kitchen to his living room when his symptoms began

 The physical examination reveals no abnormalities. What is the rhythm shown on the monitor?  What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

CHAPTER 5   Tachycardias

4. An IV has been started in the right antecubital vein. A 12-lead ECG has been ordered. On the basis of the information provided, would you categorize this patient as asymptomatic, symptomatic but  stable, symptomatic but unstable, or pulseless? How would you like to proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 5. A cardiology consult has been requested. The patient has complied with your instructions, but no change is observed on the cardiac monitor. What would you like to do next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 6. After administering the initial dose of the ordered medication, a team member tells you that the patient ’s blood pressure is now 74/52 mm Hg and he is difficult to arouse. The rhythm on the monitor remains unchanged. What action(s) should be taken at this time? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 7. Intubation equipment, suction, and resuscitation medications are within arm’s reach. Sedation has been administered. Will you perform synchronized cardioversion or will you defibrillate the patient? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 8. A biphasic manual defibrillator is available to you. What initial energy setting will you use? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 9. What precautions should be observed to ensure that this procedure is performed safely? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 10. A shock was delivered as instructed. The cardiologist has arrived. The cardiac monitor reveals this rhythm. What is the rhythm?

II

V

(From Aehlert B: ECG study cards , St. Louis, 2004, Mosby.)

Identification: _____________________________________

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11. The patient is awake and alert. Strong carotid and radial pulses are present. His ventilatory rate is 14 breaths/min. Breath sounds are clear and equal. The patient ’s blood pressure is 108/88 mm Hg, and his SpO2  is 98% on room air. What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

CASE STUDY 5-2  A 61-year-old man presents with dizziness and difficulty breathing. You have a sufficient number of  advanced life support personnel available to assist you and carry out your instructions. Emergency equipment, including a biphasic manual defibrillator, is available. 1. The patient is sittinguprighton a stretcher and he is aware of your approach. His breathing is slightly  labored, and his skin is pale. Are these general impression findings normal or abnormal? If abnormal,  what are the abnormal findings? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 2. On the basis of the information provided, would you categorize this patient as sick (ie, unstable) or  not sick (ie, stable)? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 3. The patient is alert and oriented to person, place, time, and event. He reports several episodes of  dizziness since 5:30 am today and says that during these episodes he can feel his heart beating  faster than normal. The patient is allergic to codeine. He has a history of high cholesterol and hypertension for which he takes Lipitor and lisinopril. How would you like to proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 4. The patient ’s vital signs are as follows: Blood pressure: 63/40 mm Hg; heart rate 150 beats/min; and ventilatory rate 20 breaths/min. Breath sounds are clear and equal and his skin is cool, pale, and dry. The patient ’s SpO2  on room air is 88%, and he has been placed on the cardiac monitor,  which reveals the following rhythm:

(From Aehlert B: ECG study cards , St. Louis, 2004, Mosby.)

Identification: _____________________________________

CHAPTER 5   Tachycardias

5. How would you like to proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 6. Supplemental oxygen is being administered and an IV has been started. A cardiology consult has been requested. What would you like to do next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 7. Will you perform synchronized cardioversion or will you defibrillate the patient? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 8. A biphasic manual defibrillator is available to you. What initial energy setting will you use? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 9. A shock was delivered as instructed. You observe this rhythm on the cardiac monitor. What is the rhythm?

(From Aehlert B: ECG study cards , St. Louis, 2004, Mosby.)

Identification: _____________________________________ 10. What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 11. Chest compressions are being performed. What additional actions should be performed at this time? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 12. What actions can be taken during cardiac arrest to help ensure the delivery of medications from an extremity to the central circulation? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

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13. Chest compressions are continuing, bag-mask ventilation is being performed, and a vasopressor has been administered. The patient ’s cardiac rhythm remains unchanged. How would you like to proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 14. The patient has been defibrillated a second time. The IV team member is preparing to administer  amiodarone while chest compressions are being performed. What are the initial and repeat doses of  this medication during cardiac arrest? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 15. Despite the efforts of your team, the resuscitation effort is unsuccessful. Discuss the use of the SPIKES protocol when conveying bad news to the patient ’s family. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

CHAPTER QUIZ ANSWERS

 Multiple Choice

1. C. Because the patient has a pulse, CPR, defibrillation, and epinephrine are not indicated. The patient denies chest pain so nitroglycerin is not indicated. Procainamide, amiodarone, or sotalol can be considered for a stable patient in monomorphic VT. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 2. C. The AV node is normally the only electrical connection between the atria and ventricles.  Preexcitation is a term used to describe rhythms that originate from above the ventricles but in which the impulse travels via a pathway other than the AV node and bundle of His. Thus the supraventricular impulse excites the ventricles earlier than would be expected if the impulse traveled by way of  the normal conduction system. Patients with preexcitation syndromes are prone to AVRT. When the AV junction is bypassed by an abnormal pathway, the abnormal route is called an accessory pathway. An accessory pathway is an extra bundle of working myocardial tissue that forms a connection between the atria and ventricles outside the normal conduction system. OBJ: Differentiate among narrow-QRS tachycardias, wide-QRS tachycardias, and irregular  tachycardias. 3. C. The initial dose of adenosine is 6 mg rapid IV push over 1 to 3 seconds. If there is no response  within 1 to 2 minutes, give 12 mg rapid IV push. The 12 mg dose may be repeated once in 1 to 2 minutes. Follow each adenosine dose immediately with a 20 mL normal saline flush. Reduce the dose of adenosine by one-half in patients on dipyridamole (Persantine), carbamazepine (Tegretol), those with transplanted hearts, or if given via a central IV line. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 4. B. Synchronizedcardioversion is thetimeddeliveryof a shock duringthe QRScomplex. It is indicated in the management of a patient with a pulse who is exhibiting serious signs and symptoms related to a  tachycardia. It is used to treat rhythms that have a clearly identifiable QRS complex and a rapid ventricular rate (such as some narrow-QRS tachycardias and monomorphic VT).

CHAPTER 5   Tachycardias

OBJ: Explain synchronized cardioversion, describe its indications, and list the steps required to perform this procedure safely. 5. D. AT, AVNRT, and AVRT are types of SVT. The most common type of SVT is AVNRT. The next most common is AVRT. A ventricular escape rhythm is a bradycardia (ie, 20 to 40 beats/min), not a tachycardia, and it is a ventricular, not a supraventricular, rhythm. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 6. C. The patient is unstable (acute altered mental status, hypotension). Consider sedation and defibrillate immediately. Although synchronized cardioversion is an appropriate treatment for unstable patients with a tachycardia and a pulse, it is used for tachycardias that have a relatively uniform amplitude. Because the amplitude of the waveforms in PMVT varies, defibrillation should be used instead. Adenosine and diltiazem are not indicated. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 7. C. Examples of irregular tachycardias include AFib, atrial flutter, MAT, and PMVT. Asystole, accelerated idioventricular rhythm, and accelerated junctional rhythm are not tachycardias. OBJ: Differentiate among narrow-QRS tachycardias, wide-QRS tachycardias, and irregular  tachycardias. 8. D.   When using vagal maneuvers, make sure oxygen, suction, a defibrillator, and emergency  medications are available before attempting the procedure. Continuous monitoring of the patient ’s ECG is essential and a 12-lead ECG recording is desirable. Carotid sinus pressure should be avoided in older adults and in patients who have a history of stroke, known carotid artery stenosis, or a carotid artery bruit on auscultation. Simultaneous, bilateral carotid pressure is not  recommended. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 9. A. Wandering atrial pacemaker is a rhythm in which the size, shape, and direction of the P waves  vary, sometimes from beat to beat. The difference in the look of the P waves is a result of the gradual shifting of the dominant pacemaker between the SA node, the atria, and/or the AV junction. When a wandering atrial pacemaker is associated with a ventricular rate greater than 100 beats/min, the rhythm is called multifocal atrial tachycardia (MAT). MAT is also called chaotic AT. At least three different P wave configurations (seen in the same lead) are required for a diagnosis of wandering  atrial pacemaker or MAT. The rhythm may be irregular as the pacemaker site shifts from the SA node to ectopic atrial locations and the AV junction. OBJ: Differentiate among narrow-QRS tachycardias, wide-QRS tachycardias, and irregular  tachycardias. 10. C. The patient ’s chest pain, decreasing level of responsiveness, and hypotension indicate that he is clearly unstable. Your best course of action will be to administer sedation and perform synchronized cardioversion. The initial biphasic energy level is typically 50 to 100 J (use energy levels recommended by the defibrillator manufacturer). Transcutaneous pacing is not indicated. Defibrillation  with an initial shock of 360 J is warranted for pulseless VT, VF, and unstable, sustained PMVT (when using a monophasic defibrillator). OBJ: For each of the following rhythms, identify the energy levels that are currently recommended: monomorphic VT, narrow-QRS tachycardia, AFib, and atrial flutter. 11. C. The initial dose of procainamide is 20 to 50 mg/min IV. The maximum dose is 17 mg/kg, and the maintenance infusion dose is 1 to 4 mg/min.

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OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 12. C.  The patient ’s chest discomfort and hypotension indicate that her condition is unstable. You should administer sedation and perform synchronized cardioversion. The initial biphasic energy  level is typically 100 J (use energy levels recommended by the defibrillator manufacturer). Transcutaneous pacing and CPR are not indicated. Defibrillation is warranted for pulseless VT, VF, and unstable (ie, sustained) PMVT. OBJ: Explain synchronized cardioversion, describe its indications, and list the steps required to perform this procedure safely. 13. A. The patient appears stable but symptomatic because of the rapid rate. Treatment usually includes oxygen (if indicated), IV access, and vagal maneuvers. Vagal maneuvers are used to try to stop the rhythm or slow conduction through the AV node. If vagal maneuvers fail, antiarrhythmic medications should be tried. Adenosine is the drug of choice, except for patients with severe asthma. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 14. D. From the information provided, the patient appears to be clinically stable at this time. Procainamide would be appropriate to consider in this situation. Acceptable alternatives include amiodarone and sotalol. Dopamine increases the force of myocardial contraction, heart rate, and blood pressure. Because this patient is not hypotensive and he has a rapid heart rate, dopamine is not indicated. Nitroglycerin is a vasodilator. The patient has no complaint of chest pain and shows no signs of  heart failure so nitroglycerin is not indicated. Furosemide (Lasix) is also not indicated because there are no signs of pulmonary congestion. Atropine is not indicated because the patient has a tachycardia, not a bradycardia. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable.

CASE STUDY 5-1 ANSWERS 1. Assess the patient ’s breathing with regard to rate, quality, and regularity. Quickly estimate the patient ’s heart rate and determine the quality of the pulse (ie, fast or slow, regular or irregular, weak  or strong). Evaluate the patient ’s skin temperature, color, and moisture to assess perfusion. Perform a  brief neurologic evaluation (ie, obtain a Glasgow Coma Scale score), and assess the need for a  defibrillator. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 2. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor. Ask the airway team member to administer supplemental O 2 if indicated. Ask a team member to obtain the patient ’s baseline vital signs while you obtain, or direct a team member to obtain, a SAMPLE history  and perform a focused physical examination. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 3. The monitor shows a narrow-QRS tachycardiawith ST segment depression.Ask the IV team member to start an IV of normal saline and order a 12-lead ECG. OBJ: Differentiate among narrow-QRS tachycardias, wide-QRS tachycardias, and irregular  tachycardias. 4. On the basis of the patient ’s history and physical findings, the patient is symptomatic but stable at  this time. Order a cardiology consult. Ask the patient to perform a vagal maneuver.

CHAPTER 5   Tachycardias

OBJ: Identify a patient who is experiencing a tachycardia as asymptomatic, symptomatic but stable, symptomatic but unstable, or pulseless. 5. Because the patient is stable and the rhythm is a narrow-QRS tachycardia, ask the IV team member  to give adenosine 6 mg rapid IV bolus over 1 to 3 seconds and to follow with a 20 mL IV normal saline flush. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 6. The patient ’s change in mental status and blood pressure indicates that he is now symptomatic and unstable. Electrical therapy is warranted. Ensure that the code cart, including intubation equipment, suction, and resuscitation medications, is within arm ’s reach. Ask the defibrillation team member to apply combination pads to the patient ’s bare chest. While preparing to shock the patient, ask the IV  team member to sedate the patient. OBJ: Identify a patient who is experiencing a tachycardia as asymptomatic, symptomatic but  stable, symptomatic but unstable, or pulseless. 7. Because the patient has a pulse and the rhythm is a narrow-QRS tachycardia, ask the defibrillation team member to perform synchronized cardioversion. OBJ: Explain synchronized cardioversion, describe its indications, and list the steps required to perform this procedure safely. 8. The biphasic energy setting is typically 50 to 100 J initially for an unstable patient with a narrowQRS tachycardia; increase in a stepwise fashion if the initial shock fails. OBJ: For each of the following rhythms, identify the energy levels that are currently recommended: monomorphic VT, narrow-QRS tachycardia, AFib, and atrial flutter. 9. Ensure that the energy level appropriate for the patient ’s rhythm has been selected on the defibrillator. If the rhythm is unchanged, call “Clear!”   and make sure that everyone is clear of  the patient, the bed, and any equipment that is connected to the patient. Make sure oxygen is not flowing over the patient ’s chest to decrease the risk of combustion in the presence of electrical current. After confirming that the area is clear, depress the “Shock ”   control until the shock is delivered. OBJ: Explain synchronized cardioversion, describe its indications, and list the steps required to perform this procedure safely. 10. The monitor shows a sinus rhythm. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 11. Repeat the primary survey and monitor the patient ’s vital signs every 5 minutes for the next  30 minutes. Transfer patient care to the cardiologist. Request a team debriefing after the transfer  of patient care is complete. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable.

CASE STUDY 5-2 ANSWERS 1. The general impression findings are abnormal (Appearance: normal; Breathing: abnormal; Circulation: abnormal skin color). OBJ: State three areas to assess when forming a general impression of a patient.

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2. An abnormal finding that is observed when assessing any of the general impression areas (ie, appearance, work of breathing, circulation) suggests that the patient is sick (ie, unstable); move quickly and proceed immediately   to the primary survey. OBJ: State three areas to assess when forming a general impression of a patient. 3. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor and obtain the patient ’s baseline vital signs while you perform a focused physical examination. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 4. The monitor shows monomorphic VT. OBJ: Differentiate among narrow-QRS tachycardias, wide-QRS tachycardias, and irregular  tachycardias. 5. Ask the airway team member to administer supplemental O2 by nonrebreather mask for now and to monitor the patient ’s oxygen saturation. Direct the IV team member to start an IV of normal saline. Order a 12-lead ECG and cardiology consult as soon as possible. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 6. Because the patient is symptomatic and unstable, ask the defibrillation team member to apply combination pads to the patient ’s bare chest and prepare to shock the patient. Ensure that the code cart, including intubation equipment, suction, and resuscitation medications, is within arm’s reach.  While preparing to shock the patient, ask the IV team member to sedate the patient. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 7. Because the patient has a pulse and the rhythm is a monomorphic VT, ask the defibrillation team member to perform synchronized cardioversion. OBJ: Explain synchronized cardioversion, describe its indications, and list the steps required to perform this procedure safely. 8. The initial monophasic or biphasic energy dose is typically 100 J for an unstable patient with monomorphic VT. Use the energy setting recommended by the manufacturer. OBJ: For each of the following rhythms, identify the energy levels that are currently recommended: monomorphic VT, narrow-QRS tachycardia, AFib, and atrial flutter. 9. The monitor shows VF. OBJ: Identify four cardiac rhythms that are associated with cardiac arrest. 10. It is important to recognize that VF is a shockable cardiac arrest rhythm. Instruct the defibrillation team member to ensure that the  “ Sync” control is off and to prepare to defibrillate the patient, using  the energy levels recommended by the manufacturer. Ensure that all team members are clear of the patient and that oxygen is not flowing over the patient ’s chest before the shock is delivered. Instruct  the team to resume chest compressions immediately without pausing for a rhythm or pulse check  after the shock is delivered. OBJ: Differentiate between shockable and nonshockable cardiac arrest rhythms. 11. Instruct the airway team member to remove the nonrebreather mask, insert an oral airway, and begin  ventilating the patient with a bag-mask device connected to 100% oxygen. Consider placement of an advanced airway. Direct the IV team member to prepare and administer epinephrine 1 mg (1:10,000 solution) every 3 to 5 minutes as long as the patient is in cardiac arrest. Remember to rotate the compressor every 2 minutes to avoid tiring. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable.

CHAPTER 5   Tachycardias

12. During cardiac arrest, ensure that the IV team member follows each drug administered with a 20 mL bolus of IV fluid and brief (ie, about 10 to 20 seconds) elevation of the extremity during and after  drug administration to aid delivery of the drug into the central circulation. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 13. Direct the defibrillation team member to clear the patient, ensure oxygen is not flowing over the patient ’s chest, and then defibrillate the patient. After the shock has been delivered, instruct the team to immediately resume CPR. Direct the IV team member to prepare and administer amiodarone or  lidocaine IV while chest compressions are being performed. Consider reversible causes of the arrest  using the Five Hs and Five Ts. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 14. Amiodarone is an antiarrhythmic that may be considered for VF or pulseless VT unresponsive to CPR, defibrillation, and vasopressor therapy. The initial dose is 300 mg IV/IO, which can be followed by one dose of 150 mg IV/IO. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 15. SPIKES is an acronym for a six-step protocol that is used for conveying distressing information to patients and families. Following the SPIKES protocol can help ease the distress felt by the patient or  family who is receiving the news and the health care professional who is breaking the news. S—Setting (Select a location that provides for privacy with all appropriate people present) • P—Perception of what the family understands about the situation (Find out what the family  • already knows by asking, “ What have you been told so far?” or  “ What is your understanding  of what has happened?”) • I—Invitation from the family to give information (Ask the family how they prefer to receive the information that you have to share and how much they want to know; keep in mind that ethnic and cultural values play a significant role in the need for information) K —Knowledge (Begin with a warning statement that unfavorable news is coming and then • pause; “I am sorry to tell you that  …”) E—Emotions (Give the family time to respond; be sensitive and respectful of cultural differences) • S—Summarize (Offer to contact the patient ’s physician and to be available if there are further  • questions, arrange for follow-up support, allow the family the opportunity to see their relative if they wish to do so) OBJ: Discuss the use of the SPIKES protocol when conveying bad news.

REFERENCES  Anderson, J. L., Halperin, J. L., Albert, N. M., Bozkurt, B., Brindis, R. G., Curtis, L. H.,et al. (2013). Management of patients with atrial fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS guideline recommendations): A report of the American College of Cardiology Foundation/American Heart   Association Task Force on Practice Guidelines. J Am Coll Cardiol ,  61(18), 1935 – 1944.  Appelboam, A., Reuben, A., Mann, C., Gagg, J., Ewings, P., Barton, A.,et al. (2015). Postural modifica tion to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): A randomised controlled trial. Lancet ,  386(10005), 1747 – 1753. Bontempo, L. J., & Goralnick, E. (2011). Atrial fibrillation.  Emerg Med Clin North Am, 29(4), 747 – 758. Ellenbogen, K. A., & Stambler, B. S. (2014). Atrial tachycardia. In D. P. Zipes, & J. Jalife (Eds.),  Cardiac  electrophysiology: From cell to bedside  (6th ed., pp. 699 – 722). Philadelphia: Saunders.

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Fuster, V., Ryd en, L. E., Cannom, D. S., Crijns, H. J., Curtis, A. B., Ellenbogen, K. A.,et al. (2011). 2011 ACCF/   AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 guidelines for the management of  patients with atrial fibrillation. J Am Coll Cardiol ,  57 (11), 1330 – 1337. Gahart, B. L.,Nazareno, A. R., & Ortega,M. Q. (2016a). Ibutilide fumarate. In 2016 intravenous medications  (32nd ed., pp. 679-680). St. Louis: Mosby. Gahart, B. L., Nazareno, A. R., & Ortega, M. Q. (2016b). Procainamide hydrochloride. In  2016 intravenous medications  (32nd ed., pp. 1043 – 1046). St. Louis: Mosby. Goel, R., Srivathsan, K., & Mookadam, M. (2013). Supraventricular and ventricular arrhythmias.  Prim Care , 40 (1), 43 – 71. Hamdan, M. H. (2010). Cardiac arrhythmias. In T. E. Andreoli, I. J. Benjamin, R. C. Griggs, & E. J. Wing (Eds.),  Andreoli and Carpenter ’ s Cecil essentials of medicine  (8th ed., pp. 118 – 144). Philadelphia: Saunders.  January, C. T., Wann, L. S., Alpert, J. S., Calkins, H., Cigarroa, J. E., Cleveland, J. C.,et al. (2014). 2014 AHA/   ACC/HRS guideline for the management of patients with atrial fibrillation: A report of the American College of  Cardiology/American Heart Association TaskForce on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol ,  64 (21), e1 – e76. Link, M. S., Berkow, L. C., Kudenchuk, P. J., Halperin, H. R., Hess, E. P., Moitra, V. K.,et al. (2015, Oct).  2015   American Heart Association guidelines for CPR & ECC . Retrieved Jan 11, 2016, from American Heart Association. In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care—part  7: Adult advanced cardiovascular life support:  Eccguidelines.heart.org . Mark, D. G.,Brady, W. J., & Pines, J. M. (2009). Preexcitation syndromes: Diagnostic consideration in the ED. Am  J Emerg Med ,  27 (7), 878 – 888. Martin, D., & Wharton, J. M. (2001). Sustained monomorphic ventricular tachycardia. In P. J. Podrid, & P. R. Kowey (Eds.),  Cardiac arrhythmia: Mechanisms, diagnosis, and management   (2nd ed., pp. 573 – 601). Philadelphia: Lippincott Williams & Wilkins. Miller,J. M., & Zipes, D.P. (2012). Therapy forcardiacarrhythmias. In R. W. Bonow, D. L. Mann,D. P. Zipes, &  P. Libby (Eds.),   Braunwald ’ s heart disease —a  textbook of cardiovascular medicine   (9th ed., pp. 710 – 744). Philadelphia: Saunders. Mottram, A. R., & Svenson, J. E. (2011). Rhythm disturbances. Emerg Med Clin North Am, 29(4), 729 – 746. Olgin, J. E. (2008). Approach to the patient with suspected arrhythmia. In L. Goldman, & D. Ausiello (Eds.),  Cecil  medicine  (23rd ed., pp. 394 – 400). Philadelphia: Saunders. Olgin, J., & Zipes, D. P. (2012). Specific arrhythmias: Diagnosis and treatment. In R. O. Bonow, D. L. Mann, D. P. Zipes, & P. Libby (Eds.), Braunwald ’s  heart disease —a  textbook of cardiovascular medicine  (9th ed., pp. 771 –  824). Philadelphia: Saunders. Page, R. L., Joglar, J. A., Caldwell, M. A., Calkins, H., Conti, J. B., Deal, B. J.,et al. (2016).2015ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia.   Circulation, 133(14), e506 – e574. Pandya, A., & Lang, E. (2015). Valsalva maneuver for termination of supraventricular tachycardia.  Ann Emerg Med , 65 (1), 27 – 29.  Walker, S., & Cutting, P. (2010). Impact of a modified Valsalva manoeuvre in the termination of paroxysmal supraventricular tachycardia. Emerg Med J ,  27 (4), 287 – 291.  Wann, L. S., Curtis, A. B., January, C. T., Ellenbogen, K. A., Lowe, J. E., Estes, N.,et al. (2011). 2011 ACCF/   AHA/HRS focused update on the management of patients with atrial fibrillation (updating the 2006 guideline):  A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation, 123(10), 104 – 123. 

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6

Bradycardias INTRODUCTION [Objectives 1, 2]  The bradycardia algorithm is a treatment guideline that is used when providing care to patients who are symptomatic with a bradycardia. You must be able to recognize if a patient is asymptomatic, symptomatic but stable, symptomatic but unstable, or pulseless. Familiarity with the bradycardia algorithm requires patient assessment, rhythm recognition, knowledge of medications, and transcutaneous pacing (TCP). Cardiac output ¼ Stroke volume  Heart rate. Therefore a decrease in either stroke volume or heart  rate may result in a decrease in cardiac output. An absolute bradycardia  is a heart rate of less than 60 beats per minute (beats/min). When a patient has a  relative bradycardia, his or her heart rate may be more than 60 beats/min. This may occur when a hypotensive patient needs a tachycardia (as in hypovolemia) but is unable to increase his or her heart rate because of sinoatrial (SA) node disease, beta-blockers, or other medications. A patient with an unusually slow heart rate may complain of weakness, or dizziness and fainting (ie, syncope) can occur. Decreasing cardiac output will eventually produce hemodynamic compromise. If a patient presents with a bradycardia, assess how the patient is tolerating the rhythm. If the patient  has no symptoms, no treatment is necessary but he or she should be observed closely. Many patients tolerate a heart rate of 50 to 60 beats/min but become symptomatic when the rate drops below  50 beats/min. The term symptomatic bradycardia   is used to describe a patient who experiences signs and symptoms of hemodynamic compromise related to a slow heart rate. Examples of common signs and symptoms associated with symptomatic bradycardia are shown in Box 6.1.  Treatment of a symptomatic bradycardia should include assessment of the patient ’s oxygen saturation level and determining whether signs of increased work of breathing are present (eg, retractions, tachypnea, paradoxical abdominal breathing). Give supplemental oxygen if oxygenation is inadequate, and assist breathing if ventilation is inadequate. Establish intravenous (IV) access and obtain a 12-lead electrocardiogram (ECG). Atropine, administered IV, is the drug of choice for symptomatic bradycardia  (Link, et al., 2015). Reassess the patient ’s response and continue monitoring the patient. Other inter ventions that may be used in the treatment of symptomatic bradycardia include epinephrine, dopamine, or isoproterenol IV infusions, or TCP (discussed later in this chapter).

DESIRED RESULTS

G O A L  Given a patient situation, and working in a team setting, competently direct the initial emer gency care (including mechanical, pharmacologic, and electrical therapy where applicable) for a  patient experiencing a bradycardia.

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BOX 6.1 • • • • • • •

Symptomatic Bradycardia—Common Signs and Symptoms

Acute altered mental status   Diaphoresis   Dizziness   Fatigue Heart failure   Hypotension   Lightheadedness

• • • • • • •

Ongoing ischemic chest discomfort Pulmonary congestion Shortness of breath Signs of shock    Syncope Weak pulses   Weakness

LEARNING OBJECTIVES

 After completing this chapter, you should be able to: 1.  Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 2.  Identify a patient who is experiencing a bradycardia as asymptomatic, symptomatic but stable, symptomatic but unstable, or pulseless. 3.  Discuss the procedure for TCP, as well as its indications and possible complications.

LEARNING PLAN • •

• •

•

Read this chapter before class. Master identification of the following rhythms: sinus bradycardia, junctional rhythm, ventricular escape rhythm, and atrioventricular (AV) blocks: first-degree, second-degree type I, second-degree type II, 2:1 AV block, and third-degree AV block. Master the following medications: O2, atropine, dopamine, epinephrine, and isoproterenol. Master the following skills: primary and secondary surveys, supplemental O2  delivery devices, attachment and use of ECG monitoring leads, IV access, IV medication administration, and operation of a transcutaneous pacemaker. Master the following skills: Assign team member roles or perform as a team member in a simulated patient situation. Direct or perform an initial patient assessment. Obtain vital signs, establish vascular access, attach a pulse oximeter and blood pressure and cardiac monitor, give supplemental O2  if indicated, and order a 12-lead ECG. Quickly recognize if a patient is asymptomatic, symptomatic but stable, symptomatic but unstable, or pulseless. Demonstrate familiarity with the bradycardia algorithm. Demonstrate an understanding of the actions, indications, dosages, adverse effects, and contraindications for the medications used in the treatment of a symptomatic bradycardia. Administer medications and perform TCP when indicated. Consider reperfusion therapy if the patient’s signs and symptoms are consistent with an acute coronary syndrome (ACS) and there are no contraindications. Consider the possible reversible causes of a cardiac emergency. Verbalize when it is best to seek expert consultation. Review your performance as a team leader or team member during a postevent debriefing. Complete the chapter quiz and review the quiz answers provided. Read the case studies at the end of this chapter and compare your answers with the answers provided. •

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CHAPTER 6   Bradycardias

KEY TERMS

 Absolute bradycardia  A heart rate of less than 60 beats/min. Relative bradycardia A term that refers to a situation in which a patient’s heart rate may be more than 60 beats/min but, physiologically, the patient needs a tachycardia (as in hypovolemia) and is unable to increase his or her heart rate because of SA node disease, beta-blockers, or other medications. Symptomatic bradycardia  A term used to describe a patient who experiences signs and symptoms of hemodynamic compromise related to a slow heart rate.

SINUS BRADYCARDIA  [Objectives 1, 2] If the SA node fires at a rate that is slower than normal for the patient ’s age, the rhythm is called sinus  bradycardia. In adults and adolescents, a sinus bradycardia has a heart rate of less than 60 beats/min ( Table 6.1, Fig. 6.1). The term severe sinus bradycardia  is sometimes used to describe a sinus bradycardia   with a rate of less than 40 beats/min.  Assess how the patient tolerates the rhythm at rest and with activity. If the patient has no symptoms, no treatment is necessary. If the patient is symptomatic because of the slow rate, initial treatment generally includes supplemental oxygen (if indicated), starting an IV, obtaining a 12-lead ECG, and giving  IV atropine if the bradycardia persists despite adequate oxygenation and ventilation ( Table 6.2).

ACLS Pearl In the setting of a myocardial infarction (MI), sinus bradycardia is often temporary. A slow heart rate can be beneficial in the patient who has had an MIif nosymptoms are caused by the slowrate. This is because the heart’s demand for oxygen is less when the heart rate is slow.

TABLE 6.1

Regularity Rate P waves PR interval QRS duration

Characteristics of Sinus Bradycardia R to R and P to P intervals are regular Less than 60 beats/min Positive (ie, upright) in lead II; one precedes each QRS complex; P waves look alike 0.12 to 0.20 sec and constant from beat to beat  0.11 sec or less unless abnormally conducted

Fig. 6.1  Sinus bradycardia with ST segment depression.

JUNCTIONAL ESCAPE RHYTHM [Objectives 1, 2] Because a junctional rhythm starts from above the ventricles, the QRS complex is usually narrow and its rhythm is very regular at a rate of 40 to 60 beats/min ( Table 6.3, Fig. 6.2). If the AV junction paces the heart at a rate slower than 40 beats/min, the resulting rhythm is called a  junctional bradycardia. This may 

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TABLE 6.2

Class Mechanism of   Action

Indications Dosage Precautions

Atropine Sulfate Vagolytic, parasympatholytic, antimuscarinic, muscarinic antagonist, anticholinergic, parasympathetic antagonist, parasympathetic blocker • Competes with acetylcholine at muscarinic receptor sites • Increases heart rate and AV conduction velocity by blocking the effects of the vagus nerve on the SA and AV nodes • Relaxes bronchial smooth muscle •   Dilates pupils • Decreases secretion from salivary glands, sweat glands, bronchial glands, and acidsecreting cells of the stomach • Decreases motility of the gastrointestinal tract  First-line drug for symptomatic bradycardia (eg, sinus bradycardia, sinus arrest, AV block  at the level of the AV node) (Link, et al., 2015) 0.5 mg IV every 3 to 5 min to a total dose of 3 mg (Link, et al., 2015) • Second-degree AV block type II and third-degree AV blocks are unlikely to respond to atropine. In these situations, an IV infusion of a beta-adrenergic drug (ie, dopamine, epinephrine, or isoproterenol) or TCP is preferred while preparing for transvenous pacing (Link, et al., 2015). • Do not push slowly or in smaller than recommended doses; may cause paradoxical slowing of the heart rate. • May result in tachycardia, palpitations, and ventricular ectopy. • Use with caution in acute coronary syndromes; excessive increases in heart rate may further worsen ischemia or increase size of infarction. • Transplanted hearts do not usually respond to atropine because they lack vagal nerve innervation.

 AV, atrioventricular; IV, intravenous; SA, sinoatrial; TCP, transcutaneous pacing

TABLE 6.3

Regularity Rate P waves PR interval QRS duration

Characteristics of Junctional Escape Rhythm Very regular 40 to 60 beats/min May occur before, during, or after the QRS; if visible, the P wave is inverted in leads II, III, and aVF If a P wave occurs before the QRS, the PR interval will usually be 0.12 sec or less; if no P wave occurs before the QRS, there will be no PR interval 0.11 sec or less unless abnormally conducted

Fig. 6.2 Junctional escape rhythm with ST segment elevation. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

seem confusing because the AV junction’s normal pacing rate is bradycardic; however, the term junctional  bradycardia  refers to a rate slower than normal for the AV junction.  The patient may be asymptomatic with a junctional escape rhythm, or he or she may experience signs and symptoms that may be associated with the slow heart rate and decreased cardiac output. Treatment  depends on the cause of the dysrhythmia and the patient ’s presenting signs and symptoms. If the patient ’s signs and symptoms are related to the slow heart rate, treatment should include application of a pulse oximeter and administration of supplemental oxygen if indicated. Establish IV access, obtain a 12-lead ECG, and administer IV atropine. Reassess the patient ’s response and continue monitoring the patient.

CHAPTER 6   Bradycardias

TABLE 6.4

Class Mechanism of Action

Indications

Dosage Precautions

Dopamine (Intropin, Dopastat) Direct- and indirect-acting sympathomimetic; cardiac stimulant and vasopressor; natural catecholamine • Naturally occurring immediate precursor of norepinephrine in the body • Effects of dopamine are dose-related (there is some overlap of effects). At low doses, causes renal vasodilation. Moderate doses increase cardiac contractility and stroke volume. Higher doses increase peripheral resistance, BP, and renal vasoconstriction. • Temporizing measure in the management of symptomatic bradycardia that has not  responded to atropine, or for which atropine is inappropriate, while waiting for a pacemaker • Hypotension that occurs after return of spontaneous circulation • Hemodynamically significant hypotension in the absence of hypovolemia Give as a continuous IV infusion of 2 to 20 mcg/kg/min (Link, et al., 2015); titrate infusion rate according to BP and other clinical responses. • Monitor the BP, ECG, and drip rate closely. • Correct hypovolemia before beginning dopamine therapy for the treatment of  hypotension and shock. • Administer using an infusion pump. • Extravasation into surrounding tissue may cause necrosis and sloughing. • Gradually taper this drug before discontinuing the infusion.

BP, blood pressure; ECG, electrocardiogram; IV, intravenous

TABLE 6.5

Class Mechanism of Action Indications

Dosage Precautions

Isoproterenol (Isuprel) Sympathomimetic, cardiac stimulant, antiarrhythmic Increases heart rate and causes bronchodilation • Onset of action is immediate and lasts 1 to 2 hours Temporizing measure in the management of symptomatic bradycardia that has not  responded to atropine, or for which atropine is inappropriate, while waiting for a pacemaker Give as a continuous IV infusion of 2 to 10 mcg/min (Link, et al., 2015); titrate infusion rate according to heart rate and rhythm response. • Administer using an infusion pump. • Monitor the BP, ECG, and drip rate closely. •

BP, blood pressure; ECG, electrocardiogram; IV, intravenous

Other interventions that may be considered for the treatment of symptomatic bradycardia include epinephrine, dopamine ( Table 6.4), or isoproterenol ( Table 6.5) IV infusions, or TCP (discussed later in this chapter).

ACLS Pearl Recognizing the similarities and differences among dopamine, epinephrine, and isoproterenol administration is important when treating a symptomatic bradycardia. Although these drugs are given by continuous IV infusion, their dosing differs. Because the correct infusion rate for dopamine depends on the patient ’s weight, its dose range is 2 to 10 mcg/kg/min. An isoproterenol infusion is  not  based on the patient ’s weight and it is infused at 2 to 10 mcg/min. With symptomatic bradycardia, an epinephrine infusion is administered at a dose range of 2 to 10 mcg/min; however, during post–cardiac arrest care, epinephrine is infused at a rate of 0.1 to 0.5 mcg/kg/min. In all cases, the infusion is titrated to the desired clinical response.

 VENTRICULAR ESCAPE RHYTHM [Objectives 1, 2]  A ventricular escape rhythm, which is also called an idioventricular rhythm, occurs at a rate of 20 to 40 beats/min. The QRS complexes seen with this rhythm are wide because the impulses begin in the

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TABLE 6.6

Regularity Rate P waves PR interval QRS duration

Characteristics of Ventricular Escape Rhythm Ventricular rhythm is essentially regular Ventricular rate is 20 to 40 beats/min Usually absent or with retrograde conduction to the atria; may appear after the QRS (usually upright in the ST segment or T wave) None 0.12 sec or greater; the T wave is frequently in the opposite direction of the QRS complex 

Fig. 6.3   Ventricular escape rhythm. (From Aehlert B: ECGs made easy, ed 3, St. Louis, 2006, Mosby.)

 ventricles, bypassing the normal conduction pathway. When the ventricular rate slows to a rate of less than 20 beats/min, some clinicians refer to the rhythm as an  agonal rhythm or  dying heart. The characteristics of a ventricular escape rhythm are described in  Table 6.6, and an example is shown in Fig. 6.3. If the patient has a pulse and is symptomatic because of the slow rate, treatment should include application of a pulse oximeter and administration of supplemental oxygen if indicated. Establish IV access, obtain a 12-lead ECG, and administer IV atropine. Reassess the patient ’s response and continue monitoring the patient. TCP or a dopamine, epinephrine, or isoproterenol IV infusion may be tried if atropine is ineffective. Ventricular antiarrhythmics (eg, lidocaine) should be avoided during the management of this rhythm because they may abolish ventricular activity, possibly causing asystole in a  patient with a ventricular escape rhythm. If the patient is not breathing and has no pulse despite the appearance of organized electrical activity  on the cardiac monitor, pulseless electrical activity (PEA) exists. PEA was discussed in Chapter 4. The management of PEA should include high-quality cardiopulmonary resuscitation, giving oxygen, establishing vascular access, possible placement of an advanced airway, and an aggressive search for  the underlying cause of the situation.

 ATRIOVENTRICULAR BLOCKS  An AV block  is a delay or block in the transmission of an impulse from the atria to the ventricles.  AV blocks occur in 12% to 25% of patients with acute MI (Issa, et al., 2012). They are classified into (1) first-degree AV block, (2) second-degree AV block, and (3) third-degree AV block. With firstdegree AV block, impulses from the SA node to the ventricles are  delayed; they are not blocked. With second-degree AV blocks, there is an intermittent  disturbance in the conduction of impulses between the atria and the ventricles. With third-degree AV block, there is a  complete   block in the conduction of  impulses between the atria and the ventricles.

First-Degree Atrioventricular Block  [Objectives 1, 2]  A first-degree AV block is associated with a delay in impulse conduction that results in a constant PR  interval of more than 0.20 second in duration ( Table 6.7, Fig. 6.4). First-degree AV block may be permanent or transient (Latcu & Nadir, 2010). When the QRS complex associated with a first-degree AV  block is narrow, the conduction abnormality is most commonly in the AV node (Hamdan, 2010). When the QRS complex associated with a first-degree AV block is wide, the conduction abnormality may be located in the AV node, the bundle of His, or the bundle branches.

CHAPTER 6   Bradycardias

TABLE 6.7

Regularity Rate P waves PR interval QRS duration

Characteristics of First-Degree Atrioventricular Block  Regular Usually within normal range, but depends on underlying rhythm Every positive (ie, upright) P wave is followed by a QRS complex   Fixed duration of more than 0.20 sec Usually 0.11 sec or less unless abnormally conducted

Fig. 6.4  Sinus rhythm with a first-degree AV block, ST-segment depression. (From Aehlert B:  ECG study cards, St. Louis, 2004, Mosby.)

 The patient with a first-degree AV block is often asymptomatic; however, marked first-degree AV  block can lead to symptoms even in the absence of higher degrees of AV block ( Barold, 1996). Firstdegree AV block that occurs with acute MI should be monitored closely to detect progression to higher-degree AV block (Blank, et al., 2014). If first-degree AV block accompanies a symptomatic bradycardia, treat the bradycardia.

Second-Degree Atrioventricular Blocks  The term second-degree AV block is used when one or more, but not all, sinus impulses are blocked from reaching the ventricles. Intermittent AV conduction is reflected on the ECG as more P waves than QRS complexes. Second-degree AV block is classified as type I or type II, depending on the behavior of the PR inter vals associated with the dysrhythmia. The type I or type II designation is used to describe the ECG pattern of the PR intervals and should not be used to describe the anatomic site (ie, location) of the AV block  (Issa, et al., 2012). At least two consecutively conducted PR intervals must be observed to determine their  pattern. Second-Degree Atrioventricular Block Type I [Objectives 1, 2] Blockage of the right coronary artery resulting in an inferior MI or right ventricular infarction can result  in conduction delays such as first-degree AV block and second-degree AV block type I. Second-degree  AV block type I is also known as type I block, Mobitz I, or Wenckebach. The term Wenckebach phenomenon is used to describe a progressive lengthening of conduction time in any cardiac conducting tissue that eventually results in the dropping of a beat or a reversion to the initial conduction time. It is generally recognized that all of the classic Wenckebach features are found in less than 50% of cases (Latcu &  Nadir, 2010). Second-degree AV block type I is associated with a cyclic pattern that consists of conducted P waves (ie, each P wave is followed by a QRS) and then a P wave that is not conducted (ie, the P wave is not  followed by a QRS) ( Table 6.8, Fig. 6.5). The P wave that is not conducted ends a  group   of beats. The cycle then begins again. The repetition of this cyclic pattern is called grouped beating.  The patient with this type of AV block is usually asymptomatic because the ventricular rate often remains nearly normal, and cardiac output is not significantly affected. If the patient is symptomatic and the dysrhythmia is a result of medications (eg, digoxin, beta-blockers), these substances should be withheld. When it is associated with an acute inferior MI, this dysrhythmia is usually transient  and resolves within 48 to 72 hours as the effects of parasympathetic stimulation disappear.

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TABLE 6.8

Regularity Rate P waves PR interval

QRS duration

Characteristics of Second-Degree Atrioventricular Block Type I Ventricular irregular; atrial regular; grouped beating may be present  Atrial rate is greater than the ventricular rate Normal in size and shape; some P waves are not followed by a QRS complex  Progressive prolongation of the PR interval (although lengthening may be very slight) until a P wave appears without a QRS complex; the PR interval after a nonconducted P wave is shorter than the interval preceding the nonconducted beat  Usually 0.11 sec or less; complexes are periodically dropped

Fig. 6.5   Second-degree AV block type I. (From Aehlert B: ECG study cards,  St. Louis, 2004, Mosby.)

If the heart rate is slow and serious signs and symptoms occur because of the slow rate, treatment  should include applying a pulse oximeter and administering oxygen (if indicated), obtaining the patient ’s  vital signs, and establishing IV access. A 12-lead ECG should be obtained. Atropine, administered IV, is the drug of choice. Reassess the patient ’s response and continue monitoring the patient. When this rhythm occurs in conjunction with acute MI, the patient should be observed closely for increasing   AV block and expert consultation should be sought with regard to patient management decisions. Second-Degree Atrioventricular Block Type II [Objectives 1, 2] Second-degree AV block type II is also called  type II block or   Mobitz II   AV block ( Table 6.9, Fig. 6.6).  The site of block in type II block is most often in the bundle branches (Issa, et al., 2012). Although second-degree AV block type II is less common than type I, type II is more serious and it is associated

TABLE 6.9

Regularity Rate P waves PR interval QRS duration

Characteristics of Second-Degree Atrioventricular Block Type II Ventricular irregular; atrial regular Atrial rate is greater than the ventricular rate; ventricular rate is often slow Normal in size and shape; some P waves are not followed by a QRS complex  Within normal limits or prolonged, but constant for the conducted beats; the PR intervals before and after a blocked P wave are constant  Within normal limits if the block occurs above or within the bundle of His; greater than 0.11 sec if the block occurs below the bundle of His; complexes are periodically absent  after P waves

Lead II

Fig. 6.6   Second-degree AV block type II. (From Aehlert B: ECG study cards,  St. Louis, 2004, Mosby.)

CHAPTER 6   Bradycardias

 with an increased risk of mortality because it has a relatively high risk of progression to advanced or thirddegree AV block (Blank, et al., 2014). Because second-degree AV block type II may abruptly progress to third -degree AV block, the patient  should be closely monitored for increasing AV block. If the heart rate is slow and serious signs and symptoms occur because of the slow rate, treatment should include obtaining the patient ’s vital signs, applying  a pulse oximeter and administering oxygen (if indicated), and establishing IV access. Although atropine is the first-line drug for acute symptomatic bradycardia, it is unlikely to be effective when the site of an  AV block is below the AV node. In situations such as this, pacing or the administration of betaadrenergic medications is preferable (Link, et al., 2015). The choice of transcutaneous versus temporary  transvenous pacing varies by institution and equipment availability. If TCP is available, it should be readied for immediate use should the patient ’s condition deteriorate and become unstable. A 12-lead ECG should be obtained and a cardiology consult should be sought. 2:1 Atrioventricular Block   With second-degree AV block in the form of 2:1 AV block, there is one conducted P wave followed by a  blocked P wave; thus two P waves occur for every one QRS complex (ie, 2:1 conduction) ( Table 6.10). Because there are no two PQRST cycles in a row from which to compare PR intervals, 2:1 AV block  cannot be conclusively classified as type I or type II. To determine the type of block with certainty, it is necessary to continue close ECG monitoring of the patient until the conduction ratio of P waves to QRS complexes changes to 3:2, 4:3, and so on, which would enable PR interval comparison. If the QRS complex measures 0.11 second or less, the block is likely to be a form of second-degree AV block type I. A 2:1  AV block associated with a wide QRS complex (ie, more than 0.11 second) is usually a type II block. The causes and emergency management for 2:1 AV block are those of type I or type II block previously  described. A comparison of the types of second-degree AV blocks is shown in  Fig. 6.7. TABLE 6.10

Characteristics of Second-Degree 2:1 Atrioventricular Block 

Regularity Rate P waves PR interval QRS duration

Ventricular regular; atrial regular Atrial rate is twice the ventricular rate Normal in size and shape; every other P wave is not followed by a QRS complex  Constant   May be narrow or wide; complexes are absent after every other P wave

Lead II

A Lead II

B Lead II

C

Fig. 6.7 Types of second-degree AV block. A, Second-degree AV block type I. B, Second-degree AV block type II. C, 2:1  AV block. (From Grauer K: A practical guide to ECG interpretation,  ed 2, St Louis, 1998, Mosby.)

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 Third-Degree Atrioventricular Block  [Objectives 1, 2]  With third-degree AV block, there is a  complete   block in conduction of impulses between the atria and the ventricles ( Table 6.11, Fig. 6.8). The site ofblock may occur atthe level ofthe AVnode,the bundle of  His, or distal to the bundle of His. A secondary pacemaker (either junctional or ventricular) stimulates the ventricles; therefore the QRS may be narrow or wide, depending on the location of the escape pacemaker and the condition of the intraventricular conduction system. If the patient is symptomatic because of the slow rate, treatment should include obtaining the patient ’s  vital signs, applying a pulse oximeter, administering oxygen (if indicated), establishing IV access, and obtaining a 12-lead ECG. Because atropine is unlikely to be effective in the management of a thirddegree AV block, TCP may be used as a temporizing measure to provide immediate stabilization while preparations are made for transvenous pacing. Other interventions that may be used in the treatment of  third-degree AV block include epinephrine, dopamine, or isoproterenol IV infusions (Link, et al., 2015). Frequent patient reassessment is essential. Most patients with third-degree AV block have an indication for permanent pacemaker placement. The bradycardia algorithm is shown in Fig. 6.9.

ACLS Pearl  Although calcium administration is not part of the symptomatic bradycardia algorithm, IV calcium is useful in the treatment of many types of bradydysrhythmias, especially those that occur because of  an overdose of a calcium channel blocker (eg, verapamil, diltiazem) or because of hyperkalemia.

TABLE 6.11

Regularity Rate P waves PR interval QRS duration

Characteristics of Third-Degree Atrioventricular Block 

Ventricular regular; atrial regular; no relationship between the atrial and ventricular rhythms (ie, AV dissociation is present) The ventricular rate is determined by the origin of the escape pacemaker; the atrial rate is greater than (and independent of) the ventricular rate Normal in size and shape; some P waves are not followed by a QRS complex  None: the atria and the ventricles beat independently of each other, thus there is no true PR interval Narrow or wide, depending on the location of the escape pacemaker and the condition of  the intraventricular conduction system

 AV, atrioventricular

Fig. 6.8  Third-degree AV block with ST segment depression and inverted T waves. (From Aehlert B:  ECG study cards, St. Louis, 2004, Mosby.)

 TRANSCUTANEOUS PACING  TCP is the use of electrical stimulation through pacing pads that are positioned on a patient ’s torso to stimulate the contraction of the heart. TCP is also called temporary external pacing  or  noninvasive pacing.  TCP requires attaching two pacing electrodes to the skin surface of the patient ’s outer chest wall.  Although TCP is a type of electrical therapy, the current delivered is considerably less than that  used for cardioversion or defibrillation. The stimulating current selected for TCP is measured in

CHAPTER 6   Bradycardias

Fig. 6.9 Bradycardia algorithm. (American Heart Association bradycardia algorithm. Reprinted with permission. 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care—Part 7: Adult   Advanced Cardiovascular Life Support. ECC guidelines.heart.org. ©2015 American Heart Association, Inc.)

milliamperes (mA). The power delivered during each pacing impulse is less than 1 ⁄ 1000 of that delivered during defibrillation (Bessman, 2013). The range of output current of a transcutaneous pacemaker varies depending on the manufacturer. Because TCP is painful in conscious patients, sedation, analgesia, or  both may be needed to minimize the patient ’s discomfort associated with this procedure.

Indications [Objective 3]  TCP is indicated for symptomatic bradycardias unresponsive to atropine therapy or when atropine is not immediately available or indicated. It may also be used as a bridge until transvenous pacing can be accomplished or until the cause of the bradycardia is reversed (as in cases of drug overdose or hyperkalemia). Some clinicians prophylactically apply pacing electrodes to all critically ill patients with bradycardia to facilitate immediate TCP should decompensation occur (Bessman, 2013). Whether  or not TCP is effective, the patient should be prepared for transvenous pacing and expert consultation sought.

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Procedure [Objective 3]  Take appropriate standard precautions, and verify that the procedure is indicated. Place the patient on oxygen, if indicated. Assess the patient ’s vital signs and establish IV access. Because continuous monitoring of the patient ’s ECG is essential throughout the procedure, apply ECG electrodes. Position the ECG electrodes as far away as possible from where the pacing pads will be applied to minimize distortion of the ECG signal by the pacing current (Boehm, 2007; Del Monte, 2006). Identify the rhythm on the cardiac monitor. Record a rhythm strip and verify the presence of a paceable rhythm.  To improve electrode adherence and maximize the delivery of energy through the chest wall, prepare the skin on the patient ’s chest (and back if the anterior  – posterior pad position will be used) by washing   with a nonemollient soap and water (Spotts, 2011). When preparing the skin, avoid the use of flammable liquids (eg, alcohol, benzoin) because of the increased potential for burns (Spotts, 2011). Remove any  transdermal medication patches that may be present and wipe away any residue.  Apply adhesive pacing pads to the patient according to the manufacturer ’s recommendations (Fig. 6.10). Do not place the pads over open cuts, sores, drains, dressings, or over an implanted pacemaker or defibrillator. Avoid placing the pacing pads over bone (eg, sternum, spine, scapula) because this increases the level of energy needed to achieve capture, increases patient discomfort, and increases the possibility of noncapture (Spotts, 2011). When using the anterior  – posterior position for pad placement, the anterior electrode is placed between the xiphoid process and the left nipple, which corresponds  with the V 2  to V 3  ECG electrode position (Boehm, 2007; Del Monte, 2006). Ensure that the upper  edge of the electrode is below the nipple. If the patient is female, place the electrode beneath the breast  and against the chest wall (Bessman, 2013). The posterior electrode is placed beneath the left scapula and lateral to the spine at the level of the heart. Some clinicians recommend placing the posterior pad first to prevent buckling of the anterior electrode when rolling the patient to the side (Boehm, 2007). When using the anterolateral position for pad placement, which is also called the sternum – apex position, the lateral (ie, apex) pad is placed lateral to the left nipple in the left midaxillary line, which corresponds with the V 6 ECG electrodeposition. The anterior electrode is placed to the rightof the sternum and belowthe clavicle. Do not reverse placement of the pacing pads; doing so can result in the need for more current to achieve capture, which can result in increased patient discomfort (Del Monte, 2006). Next, connect the pacing cable to the pacemaker and to the adhesive pads on the patient. Turn the power to the pacemaker on. Set the pacing rate to the desired number of paced pulses per minute (ppm) (Fig. 6.11). Generally, a rate that is between 60 and 90 pulses/min will maintain an adequate blood pressure and cerebral perfusion in an adult (Del Monte, 2006).  After the rate has been regulated, start the pacemaker (Fig. 6.12). Slowly increase the stimulating  current (ie, output or mA) until pacer spikes are visible before each QRS complex (ie, capture). This control is usually labeled “Current,” “Pacer output, ”  or  “mA.”  Electrical capture   occurs when a pacing  stimulus leads to ventricular depolarization and is achieved in many patients between 50 and 100 mA (Del Monte, 2006). Although the amount of current necessary to achieve capture varies among individuals, it does not appear to correlate with body surface area or patient weight ( Boehm, 2007; Del Monte, 2006). Electrical capture usually is seen in the form of a wide QRS and a broad T wave on the ECG (Fig. 6.13). The captured QRS complex may be deflected in a positive or negative direction ( Del

Fig. 6.10   Apply adhesive pacing pads to the patient 

Fig. 6.11 Turn the pacemaker on and set the pacing rate

according to the manufacturer ’s recommendations. (From Roberts and Hedges    clinical procedures in emergency  medicine, ed 6, Philadelphia, 2014, Saunders.)

to the desired number of ppm. (From  Roberts and Hedges  clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

’  

’  

CHAPTER 6   Bradycardias

Fig. 6.12 After the rate has been regulated, start the pace-

Fig. 6.13   After electrical capture is achieved, assess for

maker and slowly increase the current output until electrical capture is achieved. (From Roberts and Hedges   clinical pro-  cedures in emergency medicine,   ed 6, Philadelphia, 2014, Saunders.)

mechanical capture by palpating for a pulse. (From  Roberts  and Hedges   clinical procedures in emergency medicine, ed 6, Philadelphia, 2014, Saunders.)

’  

’  

Monte, 2006). For some patients, electrical capture is less obvious; it may only be indicated as a change in the shape of the QRS.

ACLS Pearl During TCP, the muscle twitching that occurs with skeletal muscle contraction is not an indicator of  electrical or mechanical capture ( Boehm, 2007 ).

 Assess mechanical capture. Mechanical capture   refers to contraction of the myocardium and occurs  when pacing produces a response that can be measured, such as a palpable pulse. Other signs of increased cardiac output resulting from mechanical capture include an improved level of responsiveness, a rise in blood pressure, and improved oxygen saturation and skin color (Boehm, 2007; Del Monte, 2006).  To minimize confusion between the presence of an actual pulse and skeletal muscle contractions caused by the pacemaker, assess mechanical capture by assessing the patient ’s femoral pulse, right brachial pulse, or right radial pulse. If available, bedside ultrasound may be useful in determining mechanical capture (Bessman, 2013). After capture is achieved, continue pacing at an output level slightly higher than the threshold of initial electrical capture.  Assess the patient ’s level of responsiveness, oxygen saturation, blood pressure, and other vital signs. Closely monitor the patient, and assess the skin under the pacing electrodes for irritation after the first  30 minutes of pacing and periodically thereafter (Boehm, 2007). Documentation should include the following (Boehm, 2007; Del Monte, 2006): The date and time pacing was initiated (including baseline and pacing rhythm strips) • • The current required to obtain capture The pacing rate selected • •   The patient ’s response with capture (ie, mental status, blood pressure, oxygen saturation) • Medications administered during the procedure The date, time, and reason pacing was terminated, if applicable •

Limitations  The main limitation of TCP is patient discomfort. The discomfort is proportional to the intensity of  skeletal muscle contraction and the direct electrical stimulation of cutaneous nerves (Box 6.2). Patients have described the sensations associated with skeletal muscle contractions as tapping, twitching, or thudding (Boehm, 2007; Del Monte, 2006). Sensations associated with cutaneous nerve stimulation have been described as tingling, stinging, pinching, or burning (Boehm, 2007; Del Monte, 2006). When using the anterior  – posterior position for pacing pad placement, discomfort may be reduced in some patients by moving the anterior electrode from its V 2 to V 3 position more laterally to a V 6 position, recognizing that pacing will be temporarily discontinued during the period in which the pacing pad is moved (Boehm, 2007; Del Monte, 2006).  Another possible limitation of TCP is the use of incompatible pacing electrodes. For example, TCP electrodes used in the out-of-hospital setting may be incompatible with those used in the emergency 

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BOX 6.2

Patient Responses to Current with Transcutaneous Pacing*

OUTPUT (mA)

RESPONSE

20 30 40 50 60 70 80 90 100

Prickly sensation on skin Slight thump on chest   Definite thump on chest   Coughing   Diaphragm pacing and coughing   Coughing and knock on chest   More uncomfortable than 70 mA Strong, painful knock on chest   Leaves bed because of pain

*Responses with Zoll transcutaneous pacemaker. From Flynn, JB: Introduction to critical care skills. St. Louis, 1993, Mosby-Year Book.

department. Similarly, TCP electrodes/connectors used in the emergency department may be incompatible with those used in other areas of the hospital (Bessman, 2013). Capture may be difficult to achieve or it may be inconsistent for some patients. Increased stimulating  current may be required for patients with increased chest wall muscle mass, chronic obstructive pulmonary disease, pleural effusions, dilated cardiomyopathy, hypoxia, or metabolic acidosis because of the extremely high current thresholds required.

Possible Complications [Objective 3] Possible complications of TCP include the following: •   Coughing  •   Skin burns Interference with sensing from patient agitation or muscle contractions • • Discomfort as a result of the electrical stimulation of the skin and muscles Failure to recognize that the pacemaker is not capturing  • Tissue damage, including third-degree burns, with improper or prolonged TCP • When pacing is prolonged, pacing threshold changes, thereby leading to capture failure •

CHAPTER 6   Bradycardias

PUTTING IT ALL TOGETHER  The chapter quiz and case studies presented on the following pages are provided to help you integrate the information presented in this chapter. As you work through the case studies, remember that there may be alternative actions that are perfectly acceptable, yet not presented in the case study. CHAPTER QUIZ

 Multiple Choice  Identify the choice that best completes the statement or answers the question.

____

1.

An ECG rhythm strip shows a regular ventricular rhythm at a rate of 30 beats/min, more P waves than QRS complexes (the P waves occur regularly), a variable PR interval, and a QRS duration of 0.14 second. This rhythm is:  A. 2:1 AV block. B. Third-degree AV block. C. Second-degree AV block type I. D. Second-degree AV block type II.

____

2.

Depending on the severity of the patient ’s signs and symptoms, management of slow  rhythms may require intervention including:  A. Defibrillation. B. IV atropine. C. Synchronized cardioversion. D. Vagal maneuvers and/or adenosine.

____

3.

With 2:1 AV block, the PR interval:  A. Is absent. B. Shortens. C. Lengthens. D. Remains constant.

____

4.

Which of the following dysrhythmias has the greatest potential for sudden, third-degree AV block?  A. Junctional rhythm B. Sinus bradycardia  C. First-degree AV block  D. Second-degree AV block type II

____

5.

Which of the following best describes a ventricular escape rhythm?  A. Rapid, chaotic rhythm with no pattern or regularity  B. Gradual alteration in the amplitude and direction of the QRS; atrial rate indiscernible; ventricular rate 150 to 250 beats/min C. Essentially regular ventricular rhythm with QRS complexes measuring 0.12 second or greater; atrial rate not discernible; ventricular rate 20 to 40 beats/min D. Regular ventricular rhythm with QRS complexes measuring less than 0.10 second; P waves may occur before, during, or after the QRS; ventricular  rate 40 to 60 beats/min

____

6.

With second-degree and third-degree AV blocks:  A. P waves occur regularly. B. Every other P wave is dropped. C. P waves are periodically dropped. D. There are more QRS complexes than P waves.

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____

7.

TCP may be useful in which of the following situations?  A. Asystole B. Ventricular fibrillation C. Sinus tachycardia; blood pressure 108/70 millimeters of mercury  (mm Hg), unresponsive D. Second-degree AV block type II; blood pressure 64/42 mm Hg, altered mental status

____

8.

Which of the following medications increases heart rate by accelerating the rate at   which the SA node discharges and by blocking the vagus nerve?  A. Digitalis B. Atropine C. Amiodarone D. Beta-blocker 

____

9.

Which of the following best describes third-degree AV block?  A. Absent P waves, wide QRS, ventricular rate 40 beats/min or less B. Rapid rhythm in which the QRS complexes are wide and appear to twist  from upright to negative or negative to upright and back  C. More P waves than QRSs, P waves occur regularly, regular ventricular  rhythm, no pattern to PR intervals, QRS narrow or wide D. Rapid rhythm in which the QRS complex is wide and usually regular; QRS complexes are of same shape and amplitude

____

10.

A 47-year-old man is complaining of dizziness, nausea, and chest discomfort that he rates 4 out of 10. His blood pressure is 74/40 mm Hg; ventilations 16 breaths/min.  The patient ’s breath sounds are clear. The cardiac monitor displays the rhythm shown.

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Recommended treatment for this patient includes:  A. ABCs, O2, IV, and atropine IV push. B. ABCs, O2, IV, and adenosine rapid IV push. C. ABCs, O2, IV, and morphine titrated to pain relief. D. ABCs, O2, IV, sublingual nitroglycerin, and TCP. ____

11.

How would you differentiate a junctional escape rhythm at 40 beats/min from a   ventricular escape rhythm at the same rate?  A. It is impossible to differentiate a junctional escape rhythm from a ventricular  escape rhythm. B. The junctional escape rhythm will have a narrow QRS complex; the  ventricular escape rhythm will have a wide QRS complex. C. The rate (40 beats/min) would indicate a junctional escape rhythm, not a ventricular escape rhythm. D. The junctional escape rhythm will have a wide QRS complex; the ventricular  escape rhythm will have a narrow QRS complex.

CHAPTER 6   Bradycardias

Completion Complete each statement.

12. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification: _____________________________________ 13. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification: _____________________________________ 14. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification: _____________________________________

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15. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification: _____________________________________ 16. Identify the following rhythm (lead II):

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification: _____________________________________

CHAPTER 6   Bradycardias

CASE STUDY 6-1  A 75-year-old man presents with dizziness and generalized weakness. You have a sufficient number of  advanced life support personnel available to assist you and carry out your instructions. Emergency  equipment, including a biphasic manual defibrillator with TCP capability, is available. 1. The patient is lying supine on a stretcher and is aware of your approach. His breathing is not labored, and his skin is pale. Are these general impression findings normal or abnormal? If abnormal, what are the abnormal findings? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 2. How would you like to proceed? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 3. The patient ’s blood pressure is 72/44 mm Hg and his ventilatory rate is 18 breaths/min. Breath sounds are clear and equal and his skin is cool, pale, and dry. The patient ’s blood oxygen saturation level (SpO2) on room air is 94% and he has been placed on the cardiac monitor, which reveals the following rhythm: ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________

II

(From Aehlert B: ECGs made easy, ed 3, St. Louis, 2006, Mosby.)

Identification: _____________________________________ 4. The patient is alert and oriented to person, place, time, and event. He reports that while preparing  breakfast he felt as if he was going to “pass out ”  and promptly sat down until his symptoms passed.  The patient has no known allergies. He has a history of chronic obstructive pulmonary disease, for   which he occasionally uses a Combivent Respimat inhaler, and hypertension, for which he takes captopril daily. The patient denies chest pain and shortness of breath. How would you like to proceed? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 5. IV access has been established, a cardiology consult has been requested, and a 12-lead ECG has been obtained. On the basis of the information provided, would you classify this patient as asymptomatic, symptomatic but stable, symptomatic but unstable, or pulseless? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________

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6. What should be done now? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 7. The patient ’s blood pressure is now 114/63 mm Hg and his ventilatory rate is 16 breaths/min. His skin is warm, pink, and dry. The cardiac monitor reveals a sinus rhythm at 75 beats/min. The patient  states that he is feeling much better. What would you like to do next? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________

CASE STUDY 6-2  A 70-year-old man presents with nausea and dizziness. His symptoms began about 15 minutes ago while at rest. You have a sufficient number of advanced life support personnel available to assist you and carry  out your instructions. Emergency equipment, including a biphasic manual defibrillator with TCP capability, is available. 1. The patientis semireclined on a stretcher and is aware of your approach. You can see equal rise and fall of his chest and his skin is pale. How would you like to proceed? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 2. The patient is alert and oriented to person, place, time, and event, but he is slow to respond to your  questions. You are unable to palpate a radial pulse. A slow carotid pulse is present. The patient denies chest pain and has no known allergies. He has a history of diabetes, an abdominal aneurysm, and has had an angioplasty three times (he is uncertain of dates). His medications include furosemide, nitroglycerin (NTG), trazodone, warfarin, and hydrocodone.  The patient ’s blood pressure is 57/32 mm Hg and his ventilatory rate is 16 breaths/min. Breath sounds are clear and equal and his skin is cool, pale, and moist. The patient ’sSpO2 on room air is 96%.  The cardiac monitor reveals the following rhythm:

(From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)

Identification: _____________________________________ 3. On the basis of the information provided, would you classify this patient as asymptomatic, symptomatic but stable, symptomatic but unstable, or pulseless? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________

CHAPTER 6   Bradycardias

4. What should be done now? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 5. IV access has been established, a cardiology consult has been requested, a 12-lead ECG has been obtained, and laboratory results are pending. What factors must be considered when determining  the next steps in the management of this patient? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 6. On the basis of the patient ’s ECG rhythm, you elect to begin TCP. Pacing pads have been applied to the patient ’s chest and the procedure has been explained to the patient. At what rate should the pacemaker be set? What current (ie, output) settings should be used? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________ 7. The cardiac monitor reveals a 100% ventricular paced rhythm at 70 pulses/min. The patient ’s blood pressure is now 104/60 mm Hg and his ventilatory rate is 16 breaths/min. His skin is warm, pink, and dry. What would you like to do next? ______________________________________________________________________________ ______________________________________________________________________________ ______________________________________________________________________________

CHAPTER QUIZ ANSWERS

 Multiple Choice

1. B. With a third-degree block, the ventricular and atrial rhythms are regular; however, AV dissociation is present. The ventricular rate is determined by the origin of the escape rhythm. Based on the description provided (ie, a QRS duration of 0.14 second and a ventricular rate of 30 beats/min), the escape pacemaker is probably ventricular in origin. P waves are normal in size and shape, but some P  waves are not followed by a QRS complex. There is no true PR interval because the atria and the  ventricles beat independently of each other. The QRS may be narrow or wide, depending on the location of the escape pacemaker and the condition of the intraventricular conduction system. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and routeof administration of applicablemedications), and electrical therapy, whereapplicable. 2. B. Atropine, administered IV, is the drug of choice for symptomatic bradycardia. Defibrillation, synchronized cardioversion, vagal maneuvers, and adenosine are not indicated in the treatment  of bradycardias. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 3. D. Second-degree 2:1 AV block is characterized by P waves that are normal in size and shape, but  every other P wave is not followed by a QRS. The atrial rate is twice the ventricular rate. The PR  interval for the conducted beats is constant. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable.

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4. D. Second-degree AV block type II is often associated with anteroseptal MI. It is associated with an increased risk of mortality because it has a relatively high risk of progression to advanced or thirddegree AV block. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses,and routeof administration of applicablemedications), and electricaltherapy, where applicable. 5. C. A ventricular escape rhythm, which is also called an idioventricular rhythm, exists when three or  more ventricular beats occur in a row at a rate of 20 to 40 beats/min (ie, the intrinsic firing rate of the Purkinje fibers). The QRS complexes seen with this rhythm are wide because the impulses begin in the ventricles, bypassing the normal conduction pathway. When the ventricular rate slows to a rate of  less than 20 beats/min, some clinicians refer to the rhythm as an  agonal rhythm or   dying heart. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses,and routeof administration of applicablemedications), and electricaltherapy, where applicable. 6. A. With second-degree and third-degree AV blocks there are more P waves than QRS complexes and the P waves occur regularly. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses,and routeof administration of applicablemedications), and electricaltherapy, where applicable. 7. D. TCP may be useful for symptomatic bradycardias when the patient ’s signs and symptoms are caused by the slow heart rate. TCP is not indicated for any of the other rhythms listed. OBJ: Discuss the procedure for TCP, as well as its indications and possible complications. 8. B. Atropine is a vagolytic drug that is used to increase the heart rate.  Vago refers to the vagus nerves (right and left), which are the main nerves of the parasympathetic division of the autonomic nervous system. Lytic  refers to  “ lyse,” which means  “ to interfere with.” Atropine works by blocking acetylcholine at the endings of the vagus nerves. The vagus nerves innervate the heart at the SA and AV nodes.  Thus atropine is most effective for narrow-QRS bradycardias. By blocking the effects of acetylcholine, atropine allows more activity from the sympathetic division of the autonomic nervous system. As a  result, the rate at which the SA node can fire is increased. Areas of the heart that are not innervated or that are minimally innervated by the vagus nerves (eg, the ventricles) will not respond to atropine.  Thus atropine is usually ineffective for the treatment of wide-QRS bradycardias. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 9. C. A third-degree AV block has more P waves than QRSs, P waves occur regularly, there is a regular   ventricular rhythm, there is no pattern to PR intervals, and the QRS may be narrow or wide. Absent  P waves, wide QRS, and a ventricular rate 40 beats/min or less describes a ventricular escape (idio ventricular) rhythm. A rapid rhythm in which the QRS complexes are wide and appear to twist from upright to negative or negative to upright and back describes polymorphic ventricular tachycardia.  A rapid rhythm in which the QRS complex is wide and usually regular and QRS complexes are of the same shape and amplitude describes monomorphic ventricular tachycardia. 10. A. The cardiac monitor displays a junctional bradycardia. Atropine is often effective in increasing the heart rate in symptomatic narrow-QRS bradycardias. Because atropine will likely result in an increase in heart rate, the resulting increased rate will also increase myocardial oxygen demand. This must be considered when giving atropine to a patient who may be experiencing an acute MI. Adenosine is used to slow the heart rate in symptomatic narrow-QRS tachycardias. Because this patient  has a bradycardia, adenosine is not indicated. Sublingual nitroglycerin should not be given at this time because the patient ’s heart rate is less than 50 beats/min and his blood pressure is low. Nitrates are contraindicated in patients with hypotension (ie, systolic blood pressure less than 90 mm Hg, or 30 mm Hg or more below baseline). Although morphine is used to relieve pain, the patient ’s blood pressure is very low. Because the patient ’s breath sounds are clear, consider 

CHAPTER 6   Bradycardias

a 250 mL IV fluid challenge of normal saline to try to increase the patient ’s blood pressure. Give nitroglycerin and morphine as needed for pain relief if the patient ’s systolic blood pressure rises above 90 to 100 mm Hg (check your local protocols) and the heart rate increases to more than 50 beats/min. OBJ:  Given a patient situation, describe the ECG characteristics and initial emergency care for symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 11. B. Although junctional and ventricular rhythms are ectopic pacemaker sites, their rhythms can generally be differentiated by the width of their QRS complexes. The junctional escape rhythm will have a narrow QRS complex; the ventricular escape rhythm will have a wide QRS complex. OBJ:   Given a patient situation, describe the ECG characteristics and initial emergency  careforsymptomaticbradycardia,includingmechanical,pharmacologic(ie,indications,contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. Completion

12. 100% ventricular paced rhythm OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and routeof administration of applicablemedications), and electrical therapy, whereapplicable. 13. 2:1 AV block with ST segment depression OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and routeof administration of applicablemedications), and electrical therapy, whereapplicable. 14. Ventricular escape rhythm OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and routeof administration of applicablemedications), and electrical therapy, whereapplicable. 15. Sinus rhythm with first-degree AV block  OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 16. Third-degree (ie, complete) AV block with ST segment elevation OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and routeof administration of applicablemedications), and electrical therapy, whereapplicable.

CASE STUDY 6-1 ANSWERS 1. The general impression findings are abnormal (Appearance: normal; Breathing: normal; Circulation: abnormal skin color). OBJ: State three areas to assess when forming a general impression of a patient. 2. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor and obtain the patient ’s baseline vital signs while you perform a focused physical examination. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 3. The monitor shows sinus bradycardia at 33 beats/min changing to junctional bradycardia at  32 beats/min.

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OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses,and routeof administration of applicablemedications), and electricaltherapy, where applicable. 4. Ask the airway team member to monitor the patient ’s oxygen saturation. Direct the IV team member  to start an IV of normal saline. Order a 12-lead ECG, a cardiology consult, laboratory studies, and a  portable chest radiograph. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 5. This patient is symptomatic but unstable because he is hypotensive and his symptoms appear to be directly related to his bradycardia. Although the patient ’s mental status is normal, a blood pressure of  72/44 mm Hg is a concern for a patient who is being treated for hypertension. OBJ: Identify a patient who is experiencing a bradycardia as asymptomatic, symptomatic but  stable, symptomatic but unstable, or pulseless. 6. Instruct the IV team member to administer atropine 0.5 mg IV. This dose may be repeated every 3 to 5 minutes to a total dose of 3 mg. Closely monitor the patient ’s cardiac rhythm and vital signs after  each atropine dose. Although sinus bradycardia and junctional escape rhythms typically respond well to atropine, it is prudent to ask the defibrillation team member to prepare for TCP in the event that  atropine is ineffective. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses,and routeof administration of applicablemedications), and electricaltherapy, where applicable. 7. Continue to closely monitor the patient ’s ECG and vital signs. Review the results of the patient ’s 12-lead ECG and laboratory studies to try to determine the cause of the patient ’s bradycardia.  Arrange for the patient ’s transfer for continued care and request a team debriefing after the transfer  of patient care is complete. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses,and routeof administration of applicablemedications), and electricaltherapy, where applicable.

CASE STUDY 6-2 ANSWERS 1. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor and obtain the patient ’s baseline vital signs while you perform a primary survey and obtain a focused history. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 2. The rhythm shown is a third-degree AV block at 46 beats/min. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses,and routeof administration of applicablemedications), and electricaltherapy, where applicable. 3. This patient is symptomatic but unstable because he is hypotensive. OBJ: Identify a patient who is experiencing a bradycardia as asymptomatic, symptomatic but  stable, symptomatic but unstable, or pulseless. 4. Ask the airway team member to monitor the patient ’s oxygen saturation. Direct the IV team member  to start an IV of normal saline. Order a 12-lead ECG, a cardiology consult, laboratory studies, and a  portable chest radiograph. Instruct the defibrillation team member to prepare for TCP. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses,and routeof administration of applicablemedications), and electricaltherapy, where applicable.

CHAPTER 6   Bradycardias

5. Whenapatientexperiencesabradycardiaandthebradycardiaisthecauseofserioussignsandsymptoms, thepatientneeds immediate emergency care. Several factorsmustbe considered, such as theuseof pharmacologictherapy,electrical therapy, or both. Becauseatropine is unlikelyto be effective whenthe siteof  an AV block is belowthe AVnode, pacing or theuse of beta-adrenergicagents is preferable (Link,etal., 2015). The choice of transcutaneous versus temporary transvenous pacing varies by institution and equipment availability. Some clinicians prefer to administer IV atropine while external pacing pads are simultaneously placed on the patient. In the setting of bradycardia and coronary ischemia or MI, consideration must be given to atropine’s effects. For example, if the bradycardia is responsive to atropine administration, the resulting increased heart rate may increase myocardial oxygen demand, resulting in worsened ischemia or  extension of the infarction. Additional considerations in the setting of MI include the administration of aspirin, completion of a reperfusion checklist, and reperfusion therapy (ie, percutaneous coronary  intervention or fibrinolytics). Consultation with a cardiologist is advised. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and routeof administration of applicablemedications), and electrical therapy, whereapplicable. 6. Set the pacing rate to the desired number of ppm. Generally, a rate that is between 60 and 90 pulses/  min will maintain an adequate blood pressure and cerebral perfusion in an adult. After the rate has been regulated, start the pacemaker. Titrate the stimulating current (ie, output or mA) slowly but  steadily until pacer spikes are visible before each QRS complex. After capture is achieved, continue pacing at an output level slightly higher than the threshold of initial electrical capture. OBJ: Discuss the procedure for TCP, as well as its indications and possible complications. 7. Continue to closely monitor the patient ’s ECG and vital signs. Assess the skin under the pacing  electrodes for irritation after the first 30 minutes of pacing and periodically thereafter. Review the results of the patient ’s 12-lead ECG and laboratory studies to try to determine the cause of the patient ’s bradycardia. Arrange for patient transfer for continued care and request a team debriefing  after the transfer of patient care is complete. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and routeof administration of applicablemedications), and electrical therapy, whereapplicable.

REFERENCES Barold, S. S. (1996). Indications for permanent cardiac pacing in first-degree AV block: Class I, II, or III?  PACE , 19(5), 745 – 751. Bessman, E. S. (2013). Emergency cardiac pacing. In J. R. Roberts (Ed.), Roberts and Hedges    clinical procedures in emergency medicine  (6th ed., pp. 277 – 297). Philadelphia: Saunders. Blank, A. C., Loh, P., & Vos, M. A. (2014). Atrioventricular block. In D. P. Zipes, & J. Jalife (Eds.),  Cardiac electrophysiology: From cell to bedside  (6th ed., pp. 1043 – 1049). Philadelphia: Saunders. Boehm, J. (2007, Jul). Tried and true: Noninvasive transthoracic pacing . Retrieved Jan 28, 2015,fromZollCode Communications: www.zoll.com/CodeCommunicationsNewsletter/CCNLPacing/CCNLPacing.htm. Del Monte, L. (2006). Noninvasive pacing: What you should know. Redmond, WA: Medtronic Emergency Response Systems. Hamdan, M. H. (2010). Cardiac arrhythmias. In T. E. Andreoli, I. J. Benjamin, R. C. Griggs, & E. J. Wing (Eds.),  Andreoli and Carpenter  s Cecil essentials of medicine  (8th ed., pp. 118 – 144). Philadelphia: Saunders. Issa, Z. F.,Miller, J. M.,& Zipes, D. P. (2012). Atrioventricular conduction abnormalities. In Clinical arrhythmology  and electrophysiology: A companion to Braunwald  s heart disease  (2nd ed., pp. 175 – 193). Philadelphia: Saunders. Latcu, D.-G., & Nadir, S. (2010). Atrioventricular and intraventricular conduction disorders. In M. H. Crawford, J. P. DiMarco, & W. J. Paulus (Eds.), Cardiology  (3rd ed., pp. 725 – 739). Philadelphia: Elsevier. Link, M. S., Berkow, L. C., Kudenchuk, P. J., Halperin, H. R., Hess, E. P., Moitra, V. K., et al. (2015, Oct).  2015   American Heart Association guidelines for CPR & ECC. Retrieved Jan 11, 2016, from American Heart Association. In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care — part 7: Adult advanced cardiovascular life support: Eccguidelines.heart.org . Spotts, V. (2011). Temporary transcutaneous (external) pacing. In D. J. Lynn-McHale Wiegand (Ed.),  AACN   procedure manual for critical care  (6th ed., pp. 413 – 420). St. Louis: Saunders. ’  

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CHAPTER

7

Acute Coronary Syndromes INTRODUCTION  Acute coronary syndromes (ACSs), also called acute ischemic coronary syndromes (AICSs), are a group of  conditions that are caused by an abrupt reduction in coronary artery blood flow ( Amsterdam, et al., 2014). The sequence of events that occurs during an ACS results in conditions that range from myocardial ischemia (ie, unstable angina pectoris) to infarction (with or without associated ST segment ele vation [STE] on the electrocardiogram [ECG]). This chapter discusses the pathophysiology, history and clinical presentation, patient evaluation, and initial management of the patient experiencing an ACS.

DESIRED RESULTS

G O A L Given a patient situation, and working in a team setting, competently direct the initial emer gency care for a patient experiencing an ACS.

LEARNING OBJECTIVES

 After completing this chapter, you should be able to: 1.  Explain the pathophysiology of ACSs. 2.  Describe the forms of ACSs. 3. Discuss the typical clinical presentation of the patient with a suspected ACS. 4.  Identify key components that should be included in the history and physical examination of the patient with a suspected ACS. 5.  Explain and give examples of anginal equivalents. 6.  Explain atypical presentation and its significance in ACSs. 7.  Identify the ECG changes that are associated with myocardial ischemia, injury, and infarction. 8. Identify the ECG leads that view the anterior wall, the inferior wall, the lateral wall, the septum, the inferobasal wall, and the right ventricle. 9.  Explain the clinical and ECG features of a right ventricular infarction (RVI). 10. Describe the initial management of a patient who is experiencing an ACS. 11. Explain the importance of the 12-lead ECG for the patient with an ACS. 12. Discuss the three groups that are used when categorizing the 12-lead ECG findings of the patient experiencing an ACS.

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LEARNING PLAN • •

• •

Read this chapter before class. Master identification of the following rhythms: sinus rhythm, sinus bradycardia, sinus tachycardia, atrial fibrillation (AFib), atrial flutter; atrioventricular (AV) blocks: first-degree, second-degree type I, second-degree type II, third-degree; premature atrial complexes, premature ventricular complexes (PVCs). Master the following medications: O2, nitroglycerin (NTG), morphine sulfate, aspirin. Master the following skills: Ensure scene safety and the use of personal protective equipment. Assign team member roles or perform as a team member in a simulated patient situation. Direct or perform an initial patient assessment. Recognize signs and symptoms of ACSs. Recognize signs of myocardial ischemia, injury, and infarction on an ECG. Develop and implement a treatment plan on the basis of the patient’s presentation, history, physical examination, and diagnostic test results. Obtain vital signs, establish vascular access, attach a pulse oximeter and blood pressure and cardiac monitor, and give supplemental O2  if indicated. Know the actions, indications, dosages, adverse effects, and contraindications for the medications used in the treatment of ACSs. If applicable, use a reperfusion checklist to evaluate the patient’s candidacy for  fibrinolytic therapy. Review your performance as a team leader or team member during a postevent debriefing. Develop and use flashcards, flowcharts, and mnemonics to help enhance your retention of  the information presented. Complete the chapter quiz and review the quiz answers provided.   Read the case studies at the end of this chapter and answer the questions within each case study. Compare your answers with the answers provided. • •

• • • •

•

•

•

•

•

• •

KEY TERMS

 Anginal equivalent  Symptom other than chest pain or discomfort resulting from myocardial ischemia that may occur either alone or in combination in a patient with ischemic heart disease (IHD).  Arteriosclerosis  A chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls.  Atherosclerosis  A form of arteriosclerosis in which the thickening and hardening of the vessel walls are caused by a buildup of fat-like deposits in the inner lining, specifically of  large- and middle-sized muscular arteries.  Atypical presentation  Uncharacteristic signs and symptoms experienced by some patients.

PATHOPHYSIOLOGY OF ACUTE CORONARY  SYNDROMES [Objective 1]  Arteriosclerosis is a chronic disease of the arterial system characterized by abnormal thickening and loss of elasticity of the vessel walls. Atherosclerosis is a form of arteriosclerosis in which the thickening and hardening of the vessel walls are caused by a buildup of fat-like deposits in the inner lining of large- and middle-sized muscular arteries. The speed of progression of atherosclerosis is unpredictable and varies among individuals (Bentzon & Falk, 2011). The usual cause of an ACS is the rupture of an atherosclerotic plaque (Fig. 7.1).

CHAPTER 7   Acute Coronary Syndromes

FIBROUS CAP (smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization) NECROTIC CENTER (cell debris, cholesterol crystals, foam cells, calcium) MEDIA

Fig. 7.1 The basic structure of an atheromatous plaque. (From Kumar V, Abbas AK, Aster JC: Robbins basic pathology, ed 9, Philadelphia, 2013, Saunders.)

 Types of atherosclerotic lesions include the fatty streak, the fibrous plaque, and the advanced (ie, complicated) lesion (Fig. 7.2). Although not all fatty streaks evolve into plaques (Kumar, et al., 2013a), progression from a fatty streak to an advanced lesion is associated with injured endothelium that activates the inflammatory response. As the inflammatory response continues, the fatty streak becomes a fatty plaque, then a fibrous plaque, and finally an advanced lesion. Initially the walls of the blood vessel outwardly  expand (ie, remodel) as plaque builds up inside of it. This occurs so that the size of the vessel stays relatively constant, despite the increased size of the plaque. When the plaque fills about 40% of the inside of  the vessel, remodeling stops because the vessel can no longer expand to make room for the increase in plaque size. As an atherosclerotic plaque increases in size, the vessel becomes severely narrowed (ie, stenosed). Generally, arterial stenosis of 70% of the vessel ’s diameter is required to produce anginal symptoms (Kumar, et al., 2013a). The extent of arterial narrowing and the amount of reduction in blood flow  are critical determinants of coronary artery disease (CAD).  Atherosclerotic plaques differ with regard to their makeup, their vulnerability to rupture, and their tendency to form a blood clot. A “stable” or “nonvulnerable” atherosclerotic plaque has a relatively thick fibrous cap that separates it from contact with the blood and that covers a core that contains a large amount of  collagen and smooth muscle cells but a relatively small lipid pool (Fig. 7.3). A stable plaque may produce significant luminal obstruction, but it has a lower tendency to rupture or erode ( Sapin & Muller, 2003).  A plaque that is prone to rupture is called a  “ vulnerable”  plaque because it has a thin cap of fibrous tissue over a large, soft, fatty center that separates it from the opening of the blood vessel. If the fibrous cap erodes or ruptures, the contents of the plaque (ie, collagen, smooth muscle cells, tissue factor, inflammatory cells, and lipid material) are exposed to flowing blood, activating the clotting cascade, promoting  thrombus formation, and disrupting blood flow (Shah, 2003).  Although a thrombus is the most common cause of the blockage of a coronary artery, less commonly, an ACS may occur as a result of coronary artery spasm (eg, with cocaine abuse), severe luminal narrowing 

Fig. 7.2 The natural history, morphologic features, main pathogenic events, and clinical complications of atherosclerosis. ECM, extracellular matrix; SMC, smooth muscle cell. (From Kumar V, Abbas AK, Aster JC: Robbins basic pathology,  ed 9, Philadelphia, 2013, Saunders.)

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Vulnerable plaque

Stable plaque

Media

Media

Lumen

Lumen

Lipid core

Fibrous cap

Lipid core

Fibrous cap

Fig. 7.3 Vulnerable and stable atherosclerotic plaques. (From Kumar V, Abbas AK, Aster JC: Robbins basic pathology, ed 9, Philadelphia, 2013, Saunders.)

from atherosclerosis or restenosis after percutaneous coronary intervention (PCI), coronary dissection, hypercoagulation, trauma to the coronary arteries, or coronary artery emboli (rare) ( Basra, et al., 2014; Karve, et al., 2007).

MYOCARDIAL ISCHEMIA, INJURY, AND INFARCTION [Objective 2]  When a temporary or permanent blockageoccursin a coronary artery, the blood supply to the heartmuscle is impaired and myocardial cells distal to the site of the blockage are starved for oxygen and other nutrients. IHD is a consequence of reduced coronary blood flow as a result of obstructive atherosclerotic vascular disease in more than 90% of cases (Kumar, et al., 2013b). Clinical presentations of IHD may include angina  pectoris, silent myocardial ischemia, acute myocardial infarction (AMI), or sudden cardiac death. Partial or intermittent blockage of a coronary artery by a thrombus may result in no clinical signs and symptoms (ie, silent ischemia), unstable angina (UA), non – ST elevation MI (NSTEMI), or, possibly, sudden death. Complete blockage of a coronary artery may result in ST elevation MI (STEMI) or  sudden death.  The area supplied by a blocked coronary artery goes through a sequence of events that have been identified as zones of ischemia, injury, and infarction. Each zone is associated with characteristic ECG changes (Fig. 7.4).

Myocardial Ischemia [Objective 3] Myocardial ischemia can occur because of increased oxygen demand (ie, demand ischemia), reduced myocardial oxygen supply (ie, supply ischemia), or both. If the cause of the ischemia is not reversed and blood flow restored to the affected area of the heart muscle, ischemia may lead to cellular injury  and, ultimately, cellular death (ie, infarction). Early assessment and emergency care are essential to pre vent worsening ischemia. Because ischemia affects repolarization, its effects can be viewed on the ECG as ST segment depression (STD) and T wave changes in the leads that face the affected area of the ventricle (see Fig. 7.4). Methods to reduce the heart ’s oxygen demand include resting or slowing the patient ’s heart  rate with medications such as beta-blockers. Methods to increase blood flow to the ischemic myocardium include giving medications such as NTG.

ACLS Pearl The complete blockage of a coronary artery may cause an MI. However, because a plaque usually increases in size over months and years, other vascular pathways may enlarge as portions of a coronary artery become blocked. These vascular pathways (ie, collateral circulation) serve as an alternative route for blood flow around the blocked artery to the heart muscle. Thus the presence of  collateral arteries may prevent infarction despite complete blockage of the artery.

CHAPTER 7   Acute Coronary Syndromes

Zone of ischemia Zone of injury Zone of infarction R P

Q

T

Left ventricle

Fig. 7.4 Zonesof ischemia, injury,and infarction showing indicative ECGchanges andreciprocal changes correspondingto eachzone. (From Urden LD, Stacy KM, Lough ME: Critical care nursing: diagnosis and management, ed 6, St. Louis, 2010, Mosby.)

 Angina pectoris  is chest discomfort that occurs when the heart muscle does not receive enough oxygen (ie, myocardial ischemia). The discomfort that is associated with angina occurs because of the stimulation of nerve endings by lactic acid and carbon dioxide that build up in ischemic tissue. Angina most often occurs in patients with CAD that involves at least one coronary artery. However, it can be present in patients with normal coronary arteries. Angina also occurs in persons with uncontrolled high blood pressure or valvular heart disease. Chest discomfort associated with my ocardial ischemia usually begins in the central or left chest and then radiates to the arm (especially the little finger [ulnar] side of the left arm), the  wrist, the jaw, the epigastrium, the left shoulder, or between the shoulder blades (Fig. 7.5). Common  words used by patients experiencing angina to describe the sensation they are feeling are shown in Box 7.1.

ACLS Pearl Monitoring of ST segment changes can provide useful diagnostic and predictive information in the patient experiencing an ACS.

Stable Angina [Objective 3] Stable (ie, classic) angina remains relatively constant and predictable in terms of severity, signs and symptoms, precipitating events, and response to treatment. It is characterized by brief episodes of chest discomfort related to activities that increase the heart ’s need for oxygen such as emotional upset, exercise or  exertion, and exposure to cold weather. Possible related signs and symptoms are shown in  Box 7.2. Symptoms usually last less than 5 minutes and are typically relieved within 5 minutes with rest, short-acting NTG, or both ( Amsterdam, et al., 2014).

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A

B

C

D

E

F

G

H

Fig. 7.5  Common sites for anginal discomfort. A, Upper part of chest. B, Beneath the sternum radiating to neck and jaw. C, Beneath the sternum radiating down left arm. D, Epigastric. E, Epigastric radiating to the neck, jaw, and arms. F, Neck and  jaw. G, Left shoulder and arm. H, Interscapular. (From Urden LD, Stacy KM, Lough ME: Critical care nursing: diagnosis and  management, ed 6, St. Louis, 2010, Mosby.)

BOX 7.1

Common Terms Patients Use to Describe Angina

 A band across my chest”  A vise tightening around my chest” “ A weight in the center of my chest” “Burning” “Bursting” “Constricting”

Grip-like” Heaviness” “Pressing” “Squeezing” “Strangling” “Suffocating”

•

“

•

“

•

“

•

“

• • • •

BOX 7.2

• •

• • •

Stable Angina

Common Precipitating Events •

•

Emotional upset Exercise or exertion Exposure to cold weather 

Related Signs and Symptoms • • • •

Nausea or vomiting   Palpitations Shortness of breath   Sweating

Unstable Angina [Objective 3] UA, which is also known as preinfarction angina, accelerating  or   crescendo angina, intermediate coronary  syndrome, and  preocclusive syndrome, is a condition of intermediate severity between stable angina and  AMI. It is characterized by symptoms that occur at rest or with minimal exertion and last for 10 minutes

CHAPTER 7   Acute Coronary Syndromes

ormore ( Amsterdam, et al., 2014). The chest discomfort associated with UA may be described as painful and be accompanied by dyspnea, diaphoresis, nausea, syncope, or dysrhythmias. UA and NSTEMI may occur when blood flow through a coronary artery is partially or intermittently  blocked. The clinical presentations of patients with these conditions are similar, and it is often difficult to distinguish between them. UA and NSTEMI are often grouped together as  non – ST elevation acute coronary syndromes (NSTE-ACSs) because ECG changes associated with these conditions usually include STD and T wave inversion in the leads that face the affected area. UA and NSTEMI differ primarily by   whether myocardial ischemia is severe enough to cause cellular damage leading to detectable quantities of  cardiac biomarkers ( Amsterdam, et al., 2014). Cardiac biomarkers, discussed later in this chapter, are elevated when an infarction is present. Biomarkers are not elevated in patients with UA because there is no tissue death. Prinzmetal s Angina Prinzmetal’s angina, which is also called Prinzmetal s variant angina  or   variant angina, is the result of  intense spasm of a segment of a coronary artery. This variant angina may occur in otherwise healthy  individuals (usually in their 40s or 50s) with no demonstrable coronary heart disease or in patients with a nonobstructive atheromatous plaque. Although the episode of coronary artery spasm can be precipitated by exercise, emotional stress, hyperventilation, or exposure to cold, it usually occurs at rest, often occurs between midnight and 8 am, and may awaken the patient from sleep ( Kawano, et al., 2002). Episodes may occur in clusters of two or three within 30 to 60 minutes. Although episodes usually  last only a few minutes, this may be long enough to produce serious dysrhythmias including AV block  and ventricular tachycardia (VT), as well as sudden death. If the spasm is prolonged, infarction may  result. It can be difficult to suspect Prinzmetal ’s angina from the patient ’s clinical presentation. Patients  with Prinzmetal’s angina are generally younger and have fewer coronary risk factors (except for smoking) compared with patients with chronic stable angina. The patient with Prinzmetal ’s angina complains of chest pain that is often described as severe and may be accompanied by syncope. Chest  discomfort is usually relieved by NTG. Although typical angina produces ST segment  depression, Prinzmetal’s angina produces ST segment   elevation during periods of chest pain. After the episode of chest  discomfort is resolved, ST segments usually return to the baseline. Because NTG is effective at relieving  the coronary spasm, the ECG evidence of Prinzmetal ’s angina may be lost if no pretreatment ECG is obtained. ’

’  

ACLS Pearl Obtain a baseline 12-lead ECG before initiating treatment in any patient presenting with a possible ACS.

Myocardial Injury  Ischemia that is prolonged by more than just a few minutes can result in myocardial  injury. Myocardial  injury refers to myocardial tissue that has been cut off from, or experienced a severe reduction in, its blood and oxygen supply. Myocardial injury can be extensive enough to produce a decrease in pump function or  electrical conductivity in the affected cells. On the ECG, epicardial injury may cause elevation of the ST segment (in the leads that face the affected area) and depression of the baseline, whereas endocardial injury may cause depression of the ST segment and elevation of the baseline (Surawicz & Knilans, 2008).  “ It must be emphasized that acute injury is not synonymous with acute MI. Acute injury pattern can appear in the absence of MI, as a precursor of MI, concomitant with the pattern of acute MI, or in the presence of a preexisting MI pattern.  The hallmark of acute injury is STE, which is usually accompanied by reciprocal STD. An acute injury  pattern can also produce a primary STD (eg, a subendocardial or posterior wall injury) ”  (Surawicz &  Knilans, 2008, p. 126).  Although injured myocardial cells are still alive, they will die (ie, infarct ) if the blood flow isnot quickly  restored to the injured area. Methods to restore blood flow include giving fibrinolytics or performing a  PCI, among others.

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Myocardial Infarction  An MI occurswhen blood flow to the heartmusclestops or is suddenlydecreased long enoughto causemyocardial celldeath andnecrosis of themyocardium(Kurz,etal.,2014). Chest discomfort associated withacute MI usually lasts more than 20 minutes ( Thygesen, et al., 2012). The discomfort is often diffuse and may be accompanied by diaphoresis, dyspnea, nausea, abdominal pain, or syncope ( Amsterdam, et al., 2014).  The walls of the ventricles consist of an outer layer (ie, the epicardium), middle layer (ie, the myocardium), and an inner layer (ie, the endocardium). The myocardium is subdivided into two areas. The innermost half of the myocardium is called the subendocardial area  and the outermost half is called the subepicardial area. The main coronary arteries lie on the epicardial surface of the heart. The endocardial and subendocardial areas of the myocardial wall are the least perfused areas of the heart and the most   vulnerable to ischemia because these areas have a high demand for oxygen and are fed by the most distal branches of the coronary arteries. Transmural  is a term that is used to describe ischemia, injury, or infarction that extends from the endocardium through the myocardium to the epicardium. For example, an infarction that involves the entire thickness of the left ventricular wall is called a  transmural MI. Possible locations of infarctions in the ventricular wall are shown in Fig. 7.6.  When a coronary artery is blocked, the region of the heart supplied by the affected artery is called the area at risk (Fig. 7.7). Ischemia occurs immediately in the area supplied by the affected artery. Anaerobic metabolism ensues and lactic acid accumulates in the cardiac cells, which quickly results in a loss of myocardial contractility (Schoen & Mitchell, 2010). Diastolic and systolic dysfunction appear within 30 to 45 seconds of blood flow deprivation (Blanc-Brude, 2011). Ischemia also contributes to dysrhythmias, probably by causing electrical instability of ischemic areas of the heart (Schoen & Mitchell, 2010). If blood flow is not restored to the affected artery, myocardial cells within the subendocardial area  begin to reveal signs of injury within 20 to 40 minutes. If blood flow is quickly restored, the area at risk  can potentially be salvaged; aerobic metabolism resumes, cellular repair begins, and myocardial contractility is restored. Death of myocardial cells occurs when the area at risk has been deprived of blood flow for an extended interval, usually 2 to 4 hours or longer, depending on factors such as the presence of collateral circulation to the ischemic area, persistent or intermittent coronary vessel blockage, the metabolic/oxygen needs of  the myocardium at risk, and the sensitivity of the myocardial cells to ischemia (Schoen & Mitchell, 2010;  Thygesen, et al., 2012). Without clinical intervention (ie, reperfusion therapy), the infarction can expand to involve the entire thickness of the myocardial wall. Because time is muscle when caring for patients  with an ACS, the benefits of reperfusion therapy are greatest when it is performed early.

Subendocardial infarction Endocardium

Transmural infarction

Epicardium Intramural infarction Subepicardial infarction

Fig. 7.6 Possible locations of infarctions in the ventricular wall. (From Urden LD, Stacy KM, Lough ME: Critical care nursing:  diagnosis and management, ed 6, St. Louis, 2010, Mosby.)

CHAPTER 7   Acute Coronary Syndromes

Aorta Pulmonary artery

Left circumflex coronary artery Right coronary artery

Left anterior descending coronary artery Acute coronary arterial occlusion Zone of perfusion (area at risk) Completed infarct involving nearly the entire area at risk

Cross-section of myocardium Obstructed coronary artery

Endocardium Zone of necrosis

Zone of perfusion (area at risk)

0 hr

Zone of necrosis

2 hr

24 hr

Fig. 7.7 Progression of myocardial necrosis after coronary artery occlusion. A transmural segment of myocardium that is dependent on the occluded vessel for perfusion constitutes the area at risk (outlined). Necrosis begins in the subendocardial region in the center of the ischemic zone and with time expands to involve the entire wall thickness. Note that a very narrow zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion from the ventricle. (From Kumar V, Abbas AK, Aster JC:  Robbins basic pathology, ed pathology,  ed 9, Philadelphia, 2013, Saunders.)

PATIENT EVALUATION [Objective 4] Because not all chest discomfort is cardiac-related, patients with suspected ACS must be evaluated rapidly to identify those with an emergent condition versus those with a less urgent condition. The answers to two questions must be sought during the initial patient evaluation: (1) What is the likelihood that the patient ’s signs and symptoms represent an ACS, and (2) What is the likelihood of an adverse clinical outcome? outcome? ( Amsterdam, et al., 2014 2014)) Several risk assessment scores and clinical algorithms have been developed that encompass the patient ’s history, physical examination, ECG, and cardiac biomarkers to help identify patients with ACS who are at increased risk of adverse outcomes and to help guide clinical decision making ( Amsterdam, ( Amsterdam, et al., 2014 2014). ).

Patient History  Obtaining an accurate history is important to help determine whether a patient ’s signs and symptoms are most likely related to ischemia as a result of CAD. It is important to ask targeted questions to determine the patient ’s probability of an ACS and to not delay reperfusion therapy, if indicated.

ACLS Pearl When obtaining the patient ’s history, use the patient ’s words words for the discomfort discomfort.. For example, example, the patien patientt may not consid consider er his or her sympto symptom m “discomfort” or “pain” but instea instead d have have anothe anotherr approappropriate priately ly descri descripti ptive ve term term to descri describe be his or hersymptom. hersymptom. Whatev Whatever er term term the patien patientt uses, uses, contin continue ue to use that term when interacting with the patient.

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SAMPLE History  S igns • igns and Symptoms . Ask the patient what prompted him or her to seek medical assistance. A llergies  • llergies . Ask the patient about allergies to medications, food, environmental elements (eg, pollen), and products (eg, latex). M edications  • edications . Ask the patient about the prescription and over-the-counter medications he or she is currently taking. Find out if the patient has taken any medication for erectile dysfunction in the past 24 to 48 hours. Ask about the use of any herbal supplements or recreational drugs, such as cocaine. • ast medical history . Ask if the patient has a history of a heart attack, angina, heart failure, high blood P ast pressure, or abnormal heart rhythm. If the patient answers yes to this question, ask how the current  symptoms compare with the previous episode. Ask if the patient has ever had a heart-related medical procedure such as a bypass (ie, open-heart surgery), cardiac catheterization, angioplasty, transplant,  valve replacement, or pacemaker implantation. Determine whether the patient has a history of stroke; diabetes; lung, liver, or kidney disease; or other medical condition. Find out the patient ’s risk factors for heart disease. Ask the patient if he or she smokes. If the answer is yes, ask how many packs per day.  Ask the patient if a history of heart disease is in the family. If the answer is yes, ask whether anyone died of heart disease and at what age. Ask about a family history of high blood pressure, diabetes, and high cholesterol. Also, ask about any recent hospitalizations and any recent surgeries. Last oral intake . Ask the patient when he or she last had anything to eat or drink and if any recent  • changes changes in eating patterns patterns or fluid intake (or output) output) have occurred. occurred. E vents precipitated the patient  patient ’s current symptoms. For  • vents leading to the incident . Try to find out what precipitated example, example, did an event event or activity activity cause cause the patient  patient ’s symptoms, such as strenuous strenuous exercise, sexual activactivity, or unusual unusual stress? OPQRST History   The OPQRST mnemonic m nemonic is used to explore the characteristics of the patient ’s symptoms. Onset . When did did your symptoms symptoms begin? begin? Did they begin begin suddenly suddenly or gradually? gradually? Have you ever had had this • discomfo discomfort rt before before?? When? When? How long did it last? last? Were Were you you seen, seen, evalua evaluated ted,, or or treate treated d for it? If so, what  what   was the diagnosis? How does the discomfort you are feeling right now compare with that? P rovocation/   P osition. • rovocation/  P alliation/  alliation/  P  osition. What were you doing when your symptoms started? What makes the discomfort better or worse? What have you tried to relieve the problem? Does a change in position lessen the discomfort? Quality . What does your discomfort feel like? • Region/  Radiation/  Referral . Wher Wheree is your your disc discom omfo fort rt?? Does Does it stay stay in one one area area?? Do youhave symp sympto toms ms • in a different area of your body? S everity  • everity . On a scale of 0 to 10, with 0 being the least and 10 being the worst, what number would you assign your discomfort? iming . Is your discomfort still present? Is it getting better, worse, or staying about the same? Does it  T iming  • come and go or is it constant?

 Atypical Presentation [Objectives 5, 6] Not all all patien patients ts experi experienc encing ing an ACS ACS presen presentt similar similarly. ly. Althou Although gh chest chest pain pain is a common common sympt symptom om of an  ACS, in a study of nearly 435,000 patients who were ultimately diagnosed with acute MI, 33% did not   Anginal equivalent sym equivalent sympto have chest chest pain on presentatio presentation n (Ca (Cant nto, o, et al al., ., 20 2000 00). ). Anginal ptoms ms are sympto symptoms ms other  other  than chest pain or discomfort resulting from myocardial ischemia that may occur either alone or in combina binati tion on in a pati patien entt with with IHD IHD (Bo Boxx 7. 7.33). Being Being mindfu mindfull of angina anginall equival equivalent entss is essent essential ial to recogn recognizi izing  ng  presentation refers to the uncharacteristic signs and symptoms atypical presentations of ACS. Atypical ACS.  Atypical presentation refers that are experienced by some patients.  The American College of Cardiology (ACC) and American American Heart Association (AHA) guidelines list  the following as pain descriptions uncharacteristic  descriptions  uncharacteristic  of  of myocardial ischemia ( Amsterdam, ( Amsterdam, et al., 2014 2014): ): Pleuritic pain (ie, sharp or knife-like pain provoked by breathing or coughing) • Primary Primary or sole location of the discomfort discomfort in the middle or lower abdominal abdominal region • localized by the tip of one finger, particular particularly ly over the left ventricular ventricular apex or  • Pain that may be localized costochondral junction Pain reproduce reproduced d with movement or palpation palpation of the chest wall or arms •

CHAPTER 7   Acute Coronary Syndromes

BOX 7.3 • • • • • • •

Examples Exampl es of Anginal Equivalent Equivalent Symptoms Symptoms

Difficulty breathing   Dizziness   Dysrhythmias Epigastric pain or burning burning Excessive sweating   Fatigue Generalized weakness

• • • • • •

  Indigestion Isolated arm, back, jaw, or or neck discomfort New dyspnea on exertion   Palpitations Syncope or near-syncope Unexplained nausea nausea or vomiting

Brief episodes episodes of pain that last last a few seconds or less maximal intensity intensity at onset  • Pain that is of maximal • Pain that radiates into the lower extremities  Although typical characteristics increase the probability of CAD, features that are not characteristic of  ischemic chest pain do pain  do not exclude  the  the possibility of ACS ( Amsterdam, ( Amsterdam, et al., 2014 2014). ). Patients who are experiencing an ACS and who are most likely to present atypically include older  adults, diabetic individuals, women, patients with impaired renal function, patients with dementia, patients with prior cardiac surgery, and patients during the immediate postoperative period after noncardiac surgery ( Amsterdam, ( Amsterdam, et al., 2014; Karve, et al., 2007 2007). ). Older adults may have atypical symptoms such as dyspnea, shoulder or back pain, weakness, fatigue, a  change in mental status, syncope, unexplained nausea, and abdominal or epigastric discomfort. They are also more more likely than a younger patient patient to present present with more more severe severe preexisting preexisting conditions, conditions, such as hyperhypertension, heart failure, or a previous acute MI.  Three-quarters of all deaths among patients with diabetes mellitus are related to CAD (O (O’Gara Gara,, et al., 2013). 2013 ). Diabetic individuals may present atypically because of autonomic dysfunction. Signs and symptoms may include a change in mental status, fatigue, nausea or vomiting, dyspnea, generalized weakness, or lightheadedness. It is estimated that 30% of patients with STEMI are women ( O’Gara, et al., 2013). 2013 ). Although chest  pain or discomfort is the most common symptom of an ACS, it is less common in women than in men ( Woo & Schneider, 2009). 2009 ). When chest discomfort is present, it may be located in the front neck, jaw, right arm or shoulder, or upper back. Studies reveal that women refer to their chest discomfort differently  differently  from men using descriptors such as “sharp,” “stabbing,” “aching,”  or  “tightness”  (McSweeney,  ( McSweeney, et al., 2003; 200 3; Woo & Sch Schnei neider der,, 200 20099). When When experi experienc encing ing an ACS, ACS, women women may report report sympto symptoms ms that that includ includee shortness of breath, weakness, unusual fatigue, cold sweats, sleep disturbance, loss of appetite, nausea or   vomiting, abdominal discomfort, and dizziness or fainting (McSweeney, et al., 2003). 2003). •

Physical Examination [Objective 4]  Although the physical examination for patients who are being evaluated for possible ACS is often normal, performing a physical examination is important to identify potential precipitating causes of  myocardial ischemia (eg, uncontrolled hypertension, gastrointestinal [GI] bleeding), to assess the hemodynamic effect of the ischemic event, to identify coexisting conditions (eg, pulmonary disease, malignancies) that could influence treatment decisions ( Anderson, ( Anderson, et al., 2007 2007), ), and to evaluate the patient for  complications related to ACS (O ( O’Connor, et al., 2015). 2015). Because the goals of reperfusion therapy for  STEMI are to give fibrinolytics within 30 minutes of patient arrival or to provide PCI PCI within 90 minutes of arrival (O (O’Connor, et al., 2015), 2015), the targeted history and focused physical examination must be performed quickly and efficiently. efficiently. The physical physical examination examination should include the following: Measurement Measurement of vital signs (obtain blood pressure pressure readings in both arms if dissection dissection is suspected) suspected) • Auscultation of breath sounds for crackles (ie, rales) • Auscultation of cardiac sounds for murmurs, gallops, and friction rubs • Assessment for jugular venous distention (JVD), peripheral peripheral pulse deficits, and the presence of bruits bruits • •   Neurologic evaluation Identification of contraindications to antiplatelet or fibrinolytic therapy  •

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Electrocardiog Electro cardiogram ram Findi Findings ngs [Objective 7] Obtaining and reviewing a 12-lead ECG is important when evaluating a patient presenting with symptoms suggestive of ACS. The first 12-lead ECG should be obtained and interpreted within 10 minutes of patient contact ( Amsterdam, ( Amsterdam, et al., 2014 2014). ). Because it may be normal or initially nondiagnostic, the ECG should be repeated at 15- to 30-minute intervals during the first hour, especially if symptoms recur  ( Amsterdam, et al., 2014 2014). ). Indicative changes, which are ECG findings that are seen in leads that look directly at the area fed by  the blocked blocked vessel, vessel, are signific significant ant when when they are seen seen in two anatomically anatomically contigu contiguous ous leads. leads. Two leads are contiguous if they look at the same or adjacent areas of the heart or if they are numerically consecutive ches chestt lead leadss (Fi Fig. g. 7. 7.88). Reci Recipr proc ocal al ECG ECG chan changesmay gesmay be seen seen in lead leadss oppo opposit sitee (ie, (ie, abou aboutt 180 180 degr degree eess away  away  from) the leads that show the indicative change. Hyperacute T Waves [Objective 7]  Within minutes of an interruption of coronary blood flow, hyperacute T waves may be observed on the ECG in the leads facing the affected area. The presence of hyperacute T waves has been reported as early  as 30 minutes after the onset of chest pain, and hyperacute T waves usually appear before elevation in cardiac biomarkers or ST changes on the ECG (Sovari, ( Sovari, et al., 2007). 2007). Hyperacute T waves are tall, positive, peaked, and broad-based (Sovari, (Sovari, et al., 2007). 2007). Clinically, hyperacute T waves are often not  observed because these ECG changes have typically resolved by the time the patient seeks medical assistance. In addition to acute myocardial ischemia and infarction, possible causes of tall T waves include hyperkalemia, left ventricular hypertrophy, left BBB, acute pericarditis, acute central nervous system events (eg, intracranial hemorrhage), and benign early repolarization, among others. ST Segment Changes [Objective 7]  As the ACS progresses, changes in the ST segment (eg, elevation, depression) may be evident on the ECG. Recognizing Recognizing these ECG changes and communicati communicating ng these findings is important important when caring  for the patient with a suspected ACS. In a patient who is experiencing an ACS, new horizontal or downsloping STD of 0.5 mm or more is highly suggestive of myocardial ischemia when it is viewed in two or more anatomically contiguous leads ( Thygesen, et al., 2012 2012). ). Negative (ie, inverted) T waves may also be present.

Lateral I, aVL, V 5, V6

Inferior II, III, aVF

Anteroseptal V1, V2, V3, V4

Fig. 7.8  The surfaces of the heart. The posterior surface is not shown. (From Wesley K:  Huszar ’ ’s  ECG and 12-lead inter-  pretation, ed pretation,  ed 5, St. Louis, 2016, Mosby JEMS.)

CHAPTER 7   Acute Coronary Syndromes

Evidence of myocardial injury can be seen on the ECG as STE. New or presumed new STE of 1 mm or more at the J point in all leads other than V 2 and V 3 in a patient who is experiencing an ACS is suggestive of myocardial injury when observed in two or more anatomically contiguous leads (O ( O’Gara, et al., 2013). 2013 ). For leads V 2 and V 3, STE is considered significant if it is elevated 2 mm or more in men older  than 40 years or elevated 1.5 mm or more in women ( O’Gara, et al., 2013). 2013). Continuous ST segment  monitoring can be helpful for detecting ST segment changes that confirm the diagnosis of an ACS as well as for detecting detecting silent or unrecognized unrecognized myocardial ischemia. ischemia.

ACLS Pearl  A 2007 study evaluated the ability of clinicians in the emergency department, coronary care unit, and telemetry unit to differentiate ischemic from nonischemic ECG patterns and to detect the affected ECG leads and the location of ischemia ( Stephens, Stephens, et al., 2007 ). 2007 ). Only 19% of the clinicians correctly identi identifie fied d the presen presence ce or absenc absence e of ischem ischemia ia on all 12-lea 12-lead d ECG test test strips strips.. Of the three three ECGs ECGs with with an acute MI pattern, none was able to determine the correct leads, location, or amplitude of STE. These findings emphasize the importance of continuing education and ECG interpretation practice.

QRS Change Changes s [Objective 7] In the past, an MI was classified according to its location (eg, anterior, inferior) and whether or not it  produced Q waves on the ECG over several days. A Q A  Q wave infarction was infarction  was generally considered to be infarction  and a  non  non – Q wave infarction was infarction was referred to as a  subendocardial  synonymous with transmural with transmural infarction and a  subendocardial  infarction ( infarction (Scirica Scirica & Morrow, 2015). 2015). This terminology has been replaced because a pathologic Q wave may take hours to develop (and, in some cases, never develop) and because cardiac magnetic resonance studies indicate that the development of a Q wave on the ECG is determined more by the size of the infarction than by the depth of mural involvement (Scirica ( Scirica & Morrow, 2015). 2015).  Today, the 12-lead ECG is used to differentiate between those patients with STE and those without  STE and guide guide treatm treatment ent decisio decisions ns with with regard regard to reperf reperfusi usion on therap therapy. y. If the ST segmen segments ts are elevat elevated ed in two contig contiguou uouss leads leads and elevat elevated ed cardia cardiacc biomar biomarker kerss are presen present, t, the diagno diagnosis sis is STEMI. STEMI. Most Most patien patients ts  with STEMI will develop ECG evidence of pathologic Q waves (O’Gara, et al., 2013). 2013). If STE is not  present but biomarker levels are elevated, the diagnosis is NSTEMI. If the ST segments are not elevated and cardiac biomarkers are not elevated, the diagnosis is UA ( Thygesen, ( Thygesen, et al., 2012 2012). ). An MI may be further classified into five types, depending on the circumstances in which the MI occurs ( Table ( Table 7.1 7.1). ). T Wave Inversion [Objective 7] In a patient experiencing an ACS, inverted T waves suggest possible myocardial ischemia. T wave inversion may precede ST segment changes, or they may occur at the same time. Inverted T waves associated  with ischemia and infarction are usually narrow and symmetrically inverted (Kurz, et al., 2014). 2014). They  may remain inverted for varying periods ranging from days, weeks, or months, or they may remain permanently ( Wagner, ( Wagner, et al., 2009 2009). ). TABLE 7.1

Classification of Myocardial Infarction

Classification

Description

Type Type Type Type Type Type Type

Spontaneous MI related to ischemia MI secondary to an ischemic imbalance MI resul ting in death when biomar ker values are unavailable MI associated with PCI MI associated with stent thrombosis MI associated with restenosis MI associated with coronary artery bypass grafting

1 2 3 4a 4b 4c 5

Source: Thygesen, Source: Thygesen, et al., 2012. 2012 . MI, myocardial infarction; PCI, percutaneous coronary intervention

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CHAPTER 7   Acute Coronary Syndromes

 Anatomic Location of a Myocardial Infarction [Objective 8]  Anatomic regions of the left ventricle include the septal, anterior, lateral, inferior, and inferobasal (ie, posterior) surfaces (see  Fig. 7.8). 7.8). The areas of the heart supplied by the three major coronary arteries are shown in Fig. in  Fig. 7.9. 7.9. Leads that view the same surfaces of the heart can be grouped together and analyzed for ECG evidence of myocardial ischemia, injury, or infarction. Because ECG evidence must be found in at least two contiguous leads, assessing assessing lead groupings for indicative changes is helpful in determining the location of  the the area area at risk risk and and pred predict ictin ingg whic which h coro corona nary ry arte artery ry is affe affect cted ed ( Table 7.2 7.2). ). In gene genera ral, l, the the more more prox proxim imal al the the block blockag agee in the the vess vessel el,, the the larg larger er the the infa infarc rcti tion on and and the the grea greate terr thenumber thenumber of lead leadss show showin ingg indi indica cativ tivee changes (Morris (Morris & Brady, 2002). 2002). It is important to mention that localization of an infarction works reasonably well for STEMI. However, STD and T wave changes that suggest the presence of myocardial ischemia, as in NSTE-ACS, are less reliable in localizing the culprit vessel because these ECG changes reflect subendocardial rather than transmural ischemia ( Halim, et al., 2010). 2010). Factors including the anatomic position and size of the heart, the patient ’s unique pattern of coronary artery distribution, the location of the occlusion along the length of the coronary artery, the presence of collateral circulation,

RCA

LAD

1. Four chamber

Cx

RCA or Cx

2. Two chamber

4.   Base 4.

5. Mid

LAD or Cx

LAD or RCA

3. Long axis

6.  Apex 6. 

Fig. 7.9 Typical myocardial segments supplied supplied by the right coronary artery (RCA), left anterior descending artery (LAD), and circumflex circumflex (CX) coronary coronary arteries. arteries. The coronary coronary anatomy is shown on the left with the correspond corresponding ing wall segments segments in standard echocardiographic views on the right. The arterial distribution varies between patients. Some segments have variable coronary perfusion as indicated by the hatched regions. (From Lang RM, Bierig M, Devereux RB, et al.: Recommendations for chamber quantification: A report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Cardiology.  J Am Soc Echocardiogr 18 (12):1440-1463, (12):1440-1463, 2005.)

TABLE 7.2

Relationships Relationshi ps among Ventricular Ventricular Surfaces, Facing Leads, Leads, and Coronary Arteries

Ven Ve ntr tric icul ular ar Su Surrfa fac ce  Anterior Inferior Lateral Septal Inferobasal (posterior) Right ventricle

Indi In dica cati tive ve Ch Chan ang ges (F (Fac acin ing g Le Lead ads) s)

Affe Af fect cted ed Co Coro rona narry Art rter eryy

V 3, V 4 II, III, aVF I, aVL, V5,  V 6 V1,  V 2 V7  , V 8, 8,  V 9 V1 R to V 6R

LAD RCA (most common) or CX CX LAD RCA or CX RCA  

CX , circumflex circumflex;; LAD, left anterior descending descending;; RCA, right coronary coronary artery

CHAPTER 7   Acute Coronary Syndromes

TABLE 7.3

Contiguous Electrocardiographic Leads

I

Lateral

aVR

---------

V1  

Septum

V4 

 

Anterior

II

Inferior

aVL

Lateral

V2  

Septum

V5 

 

Lateral

III

Inferior

aVF

Inferior

V3  

Anterior

V6 

 

Lateral

Y

Interventricular septum

Left ventricle V6

Right atrium

X V5

Right ventricle

Lateral chest leads

V4 V1

V2

Septal leads

V3

Anterior leads

Fig. 7.10 The areas of the heart as seen by the chest leads. Leads V 1, V 2, and V 3  are contiguous. Leads V 3, V 4, and V 5  are contiguous, as well as V 4, V 5, and V 6. Note that neither the right ventricular wall (X)  nor the inferobasal (posterior) surface of the left ventricle (Y)  is well visualized by any of the usual six chest leads. (From Grauer K: A practical guide to ECG interpretation, ed 2, St. Louis, 1998, Mosby.)

previous infarctions, and concomitant drug- and electrolyte-related ECG changes may also affect the perceived location of an infarction versus its actual location.  When viewing the 12-lead ECG of a patient who is experiencing an ACS, look at each lead for  the presence of ST segment displacement (ie, elevation or depression). If ST segment displacement  is present, note its displacement in mm. Inspect the T waves for any changes in orientation, shape, and size. Examine each lead for the presence of a Q wave. If a Q wave is present, measure its duration.  The area of the left ventricle viewed by each lead of a standard 12-lead ECG is shown in Table 7.3. Leads II, III, and aVF are contiguous leads because they view the inferior wall of the left ventricle; thus they appear the same color in Table 7.3. Leads I, aVL, V 5, and V 6 are contiguous because they all look at  adjoining tissue in the lateral wall of the left ventricle. Numerically consecutive chest leads are also contiguous leads (Fig. 7.10). Anterior Infarction  [Objective 8]  The left anterior descending artery (LAD) supplies the anterior wall of the heart by means of its diagonal branches and the anterior two-thirds of the interventricular septum by means of its septal perforating  branches (Fig. 7.11). Evidence of an anterior infarction can be seen in leads V 3  and V 4, which face the anterior wall of the left ventricle. Septal involvement is evidenced by changes in leads V 1  and V 2 (Fig. 7.12). If an infarction involves the anterior wall and septum, ECG changes will be visible in V 1, V 2, V 3, and V 4, and the descriptive name anteroseptal   MI is used (Fig. 7.13). Because the LAD supplies a large portion of the left ventricle, a blockage in this area can lead to complications such as left ventricular dysfunction, including left-sided heart failure and cardiogenic shock.

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CHAPTER 7   Acute Coronary Syndromes

Aorta

Left main occlusion

Proximal LAD occlusion

Septal artery Circumflex artery Obtuse marginal artery

Diagonal artery Mid-LAD occlusion

Left anterior descending artery (LAD)

I Lateral

aVR

V1 Septum

V4 Anterior

II Inferior

aVL Lateral

V2 Septum

V5 Lateral

III Inferior

aVF Inferior

V3 Anterior

V6 Lateral

Fig. 7.11 Anterior wall infarction. Occlusion of the midportion of the LAD results in an anterior infarction. Proximal occlusion of the LAD may become an anteroseptal infarction if the septal branch is involved or an anterolateral infarction if the marginal branch is involved. If the occlusion occurs proximal to both the septal and diagonal branches, an extensive anterior infarction will result. (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syndromes,  ed 3, St. Louis, 2012, Mosby.)

Aorta Left main coronary artery

Right coronary artery (RCA)

Circumflex artery

Left anterior descending artery (LAD)

I Lateral

aVR

V1 V4 Septum Anterior

II Inferior

aVL Lateral

V2 Septum

V5 Lateral

III Inferior

aVF V3 Inferior Anterior

V6 Lateral

Fig. 7.12 Septal infarction. (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)

CHAPTER 7   Acute Coronary Syndromes

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 7.13 Anteroseptal infarction. (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)

Aorta Left main coronary artery Circumflex artery

Right coronary artery (RCA) a

Obtuse marginal c

b

Diagonal artery

Right ventricular marginal branch

Left anterior descending artery (LAD)

Posterior descending artery I Lateral

aVR

V1 Septum

V4 Anterior

II Inferior

aVL Lateral

V2 Septum

V5 Lateral

III Inferior

aVF Inferior

V3 Anterior

V6 Lateral

Fig. 7.14 Lateral wall infarction. Coronary artery anatomy shows (a)   blockage of the circumflex artery, (b)   blockage of the proximal LAD, and (c)   blockage of the diagonal artery. (From Phalen T, Aehlert BJ:  The 12-lead ECG in acute coronary syn-  dromes, ed 3, St. Louis, 2012, Mosby.)

 An anterior MI may cause dysrhythmias including PVCs, atrial flutter, or AFib. A blockage in the area of  the septum, which contains the bundle branches, may result in right or left bundle branch block (BBB), second-degree AV block type II, and third-degree AV block. Lateral Infarction  [Objective 8] Lateral wall infarctions often occur as extensions of anterior or inferior infarctions because the lateral wall of the left ventricle may be supplied by the circumflex (CX) artery, the LAD, or a branch of the right  coronary artery (RCA) (Fig. 7.14). Because the lateral wall of the left ventricle is viewed by a combination of chest (V 5 and V 6) and limb (I and aVL) leads, evidence of a lateral wall infarction may be seen in some or all of the following leads: I, aVL, V 5, and V 6. An example of an infarction involving the lateral wall is shown in Fig. 7.15. Inferior Infarction  [Objective 8]  The inferior wall of the left ventricle is perfused by the RCA in most individuals (Fig. 7.16); however, in some patients the CX artery supplies the inferior wall through the posterior descending artery (Fig. 7.17).

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CHAPTER 7   Acute Coronary Syndromes

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 7.15 Lateral wall infarction. Lead I shows a small Q wave with STE. A larger Q wave with STE can be seen in lead aVL. This patient had an anterior NSTEMI 4 days earlier with STE and T wave inversion in leads V 2  through V 6. A coronary arteriogram at that time showed a blocked LAD distal to its first large septal perforator. The STE evolved and the T waves in all of  the chest leads had become upright the day before this tracing was recorded. The patient then had another episode of chest  pain associated with the appearance of signs of acute lateral infarction as shown in this tracing. A repeat coronary arteriogram showed new blockage of the obtuse marginal branch of the circumflex artery. (From Surawicz B, Knilans TK: Chou's electrocardiography in clinical practice: adult and pediatric, ed 5, Philadelphia, 2001, Saunders.)

Examine limb leads II, III, and aVF for ECG evidence of an ACS involving the inferior wall. STE in lead V 1 in the presence of an inferior STEMI (with elevation greater in lead III than in lead II) suggests SA RVI (Kurz, et al., 2014). Parasympathetic nervous system hyperactivity is common with inferior wall MIs, resulting in bradydysrhythmias, hypotension, or both (Scirica & Morrow, 2015). Conduction delays such as first-degree  AV block and second-degree AV block type I are common and usually transient. An example of an infarction involving the inferior wall is shown in Fig. 7.18.

Aorta Left main coronary artery Dominant right coronary artery (RCA)

Septal artery Circumflex artery

a

Obtuse marginal artery

b Right ventricular marginal branch

Diagonal artery

Posterior descending artery

Left anterior descending artery (LAD)

Posterolateral branch of the circumflex artery

Fig. 7.16 Inferior wall infarction. Coronary anatomy shows a dominant RCA. A blockage at point  a  results in an inferior infarction and RVI. A blockage at point  b  involves only the inferior wall, sparing the right ventricle. (From Phalen T, Aehlert  BJ: The 12-lead ECG in acute coronary syndromes,  ed 3, St. Louis, 2012, Mosby.)

CHAPTER 7   Acute Coronary Syndromes

Aorta Left main coronary artery

Nondominant right coronary artery (RCA)

Dominant circumflex artery

b

Obtuse marginal artery

a

Diagonal artery

Right ventricular marginal branch

Left anterior descending artery (LAD)

Posterior descending artery

I Lateral

aVR

V1 Septum

V4 Anterior

II Inferior

aVL Lateral

V2 Septum

V5 Lateral

III Inferior

aVF Inferior

V3 Anterior

V6 Lateral

Fig. 7.17 Inferior wall infarction. Coronary anatomy shows a dominant CX artery. A blockage at point  a  results in an inferior infarction. A blockage at  b   may result in a lateral and inferobasal infarction. (From Phalen T, Aehlert BJ:  The 12-lead ECG in  acute coronary syndromes, ed 3, St. Louis, 2012, Mosby.)

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 7.18 STE in leads II, III, and aVF suggests an inferior wall injury pattern. Reciprocal STD is seen in leads I and aVL. (From Johnson R, Schwartz M:  A simplified approach to electrocardiography , Philadelphia, 1986, Saunders.)

Inferobasal Infarction  [Objective 8] Posterior wall MIs reportedly occur in 15% to 20% of acute MIs ( Lawner, et al., 2012). Current expert  opinion recommends that the term inferobasal wall   be used instead of   posterior wall  ( Thygesen, et al., 2012). The inferobasal wall of the left ventricle is supplied by the CX coronary artery in most patients; however, in some patients it is supplied by the RCA (Fig. 7.19). Although isolated inferobasal infarctions do occur, an inferobasal infarction more commonly occurs with lateral wall or inferior wall infarctions. If  the inferobasal wall is supplied by the RCA, complications may include dysrhythmias that involve the SA node, the AV node, and the bundle of His. Because no leads of a standard 12-lead ECG directly view the inferobasal wall of the left ventricle, posterior chest leads V 7, V 8, and V 9 should be used to detect evidence of an inferobasal infarction. Indicative changes of an inferobasal infarction include ST elevation in these leads. In a small study published in 2012, a 15-lead ECG (adding leads V 4R, V 8, and V 9 to the standard 12 leads) was obtained for patients presenting with STEMI. Forty percent of patients with inferior or lateral MI had an associated right or  posterior infarction that was not directly detected by a standard 12-lead ECG (Pickham & Sickler, 2012). Placement of additional posterior chest leads in the right midscapular line (V 10), right paraspinal line (V 11), and left scapular line (V 12) has been suggested and may increase the likelihood of identifying  an inferobasal infarction (Vasaiwala & Schreiber, 2008). An example of an inferobasal infarction is shown in Fig. 7.20.

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CHAPTER 7   Acute Coronary Syndromes

Aorta Left coronary artery Circumflex artery Obtuse marginal artery

Posterior descending artery

Left anterior descending branch

A

Right coronary artery

Aorta Left coronary artery Circumflex artery

Posterior descending artery

Obtuse marginal artery Left anterior descending branch

Right coronary artery

B

I Lateral

aVR

V1 Septum

V4 V7 Anterior Posterior

II Inferior

aVL Lateral

V2 Septum

V5 Lateral

V8 Posterior

III Inferior

aVF Inferior

V3 Anterior

V6 Lateral

V9 Posterior

Fig. 7.19 Inferobasal (posterior) infarction. A, Coronary anatomy shows a dominant RCA. Blockage of the RCA commonly results in an inferior and inferobasal infarction. B, Coronary anatomy shows a dominant CX artery. Blockage of a marginal branch is the cause of most isolated inferobasal infarctions. (From Phalen T, Aehlert BJ:  The 12-lead ECG in acute coronary  syndromes, ed 3, St. Louis, 2012, Mosby.)

I

aVR

V1

V4 RV4

II

III

aVL

V1

aVF

V1

V5 V8

V6 V9

Fig. 7.20 Fifteen-lead ECG with inferior, lateral, posterior, and right ventricular acute myocardial infarction (AMI). The standard 12-lead ECG reveals the typical STE in the inferior and lateral leads as well as STD with prominent R wave in the right  precordial leads. Posterior AMI is indicated by both the right precordial STD with a prominent R wave and the STE in posterior leads V 8  and V 9. Note that the degree of STE is less pronounced than that seen in the inferior leads because of a relatively longer distance from the posterior epicardium to surface leads. The RVI is noted in this case, using the simplified approach with only RV4, which demonstrates STE of relatively small magnitude. (From Marx JA, Hockberger RS, Walls RM: Rosen ’ s emer-  gency medicine —c  oncepts and clinical practice, ed 8, Philadelphia, 2014, Saunders.)

CHAPTER 7   Acute Coronary Syndromes

ACLS Pearl If a patient presents with a possible ACS and the only ST segment change seen on a standard 12-lead ECG is depression (particularly in leads V 1 through V 4 ), strongly consider obtaining posterior  chest leads V 7  through V 9  to assess for a possible inferobasal (ie, posterior) infarction.

Right Ventricular Infarction  [Objective 9]  When a RVI occurs, it is most often the result of an occlusion of the RCA (Fig. 7.21). However, the CX  artery supplies a significant proportion of the right ventricle in about 10% of patients (Hutchinson &  Rudakewich, 2009). Because about one-third of patients with inferior STEMI have RVI, all patients with inferior STEMI should be evaluated for evidence of RVI (O’Gara, et al., 2013). The most sensitive ECG signs of right   ventricular injury include 1 mm ST elevation in lead V 1 and in lead V 4R  (O’Gara, et al., 2013). Leads V 2 and V 3 may also show ST elevation in some patients. Some researchers have found that the sensitivity of  V 4R in detecting RVI is greater when measured 0.06 second after the J pointthan when measured at the J point (Seo, et al., 2011). The finding of ST elevation in V 4R is often temporary, lasting only 24 to 48 hours and normalizing in half of cases within 10 hours (Hutchinson & Rudakewich, 2009). An example of an infarction involving the right ventricle is shown in Fig. 7.22. It has been estimated that only 25% of patients with RVI develop clinically evident hemodynamic manifestations (Goldstein, 2012). Patients may present with, or subsequently develop, hypotension caused by bradydysrhythmias or caused by a reduction in preload after the administration of vasodilators such as NTG (Goldstein, 2012). Complications associated with RVI include bradydysrhythmias, AV  blocks, ventricular dysrhythmias, hypotension, right ventricular rupture, right ventricular papillary muscle rupture, and right ventricular thrombi (Hutchinson & Rudakewich, 2009). Right BBB, observed in up to 48% of cases of RVI, is associated with a poor prognosis ( Hutchinson & Rudakewich, 2009).

Lead aVR Lead aVR has been called “the forgotten lead ”  because many clinicians believe that lead aVR reflects reciprocal changes from leads aVL, II, V 5, and V 6 (Gorgels, et al., 2001). However, research has shown Aorta Left main coronary artery Right coronary artery (RCA) Circumflex artery

a b Right ventricular marginal branch

Left anterior descending artery (LAD)

Posterior descending artery Posterolateral branch of the circumflex artery I Lateral

aVR

V1 Septum

V4R V4 Anterior Rt ventricle

II Inferior

aVL Lateral

V2 Septum

V5 Lateral

V5R Rt ventricle

III Inferior

aVF Inferior

V3 Anterior

V6 Lateral

V6R Rt ventricle

Fig. 7.21  RVI. At  a, blockage of the RCA proximal to the right ventricular marginal branch results in an inferior infarction and RVI. At  b, blockage of the right ventricular marginal branch results in an isolated RVI. (From Phalen T, Aehlert BJ:  The 12-lead  ECG in acute coronary syndromes , ed 3, St. Louis, 2012, Mosby.)

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CHAPTER 7   Acute Coronary Syndromes

Right-sided leads

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

V1

II

V5

Fig. 7.22 The right-sided chest leads in a patient with acute inferior STEMI show STE in leads V 4R and V 5R, consistent with concomitant RVI. (From Adams JG,  Emergency medicine, ed 2, Philadelphia, 2013, Saunders.)

 value in the use of lead aVR in evaluating CAD and clinical situations including pericarditis, pulmonary  embolism, tricyclic antidepressant toxicity, tension pneumothorax, stress-induced cardiomyopathy, and as a means of differentiating atrial tachydysrhythmias (Vorobiof & Ellestad, 2011). Lead aVR has also been used to differentiate between left main coronary artery (LMCA) disease and disease of the proximal LAD. STE in lead aVR that is greater than or equal to that in V 1 suggests LMCA disease; conversely, STE that is greater in V 1  than in aVR suggests disease of the proximal LAD ( Yamaji, et al., 2001).

Cardiac Biomarkers Injured myocardial cells release enzymes and proteins that pass through broken cell membranes and leak  into the bloodstream. Examples include myoglobin, cardiac troponins T (TnT) and I (TnI), creatine kinase (CK) and its myocardial band (MB) isoform, and lactate dehydrogenase, among others (Halim, et al., 2010). The presence of these substances in the blood, which are called cardiac biomarkers, serum cardiac markers, or serum biomarkers, can subsequently be measured by means of blood tests to verify  the presence of an infarction. Cardiac biomarkers are useful for confirming the diagnosis of MI for  patients with STEMI. They are also useful for confirming the diagnosis of MI when patients present   without STE on their ECG, when the diagnosis may be unclear, and to distinguish patients with UA from those with NSTEMI. Cardiac troponins (ie, TnI and TnT) are components of the contractile apparatus of myocardial cells and are the biomarkers of choice for diagnosing MI because of their increased specificity and sensitivity  compared with CK-MB ( Amsterdam, et al., 2014; O’Connor, et al., 2015; Thygesen, et al., 2012). Because the ranges of normal biomarker levels vary among laboratories, current clinical practice guidelines define an increased cardiac troponin concentration as a value that exceeds the 99th percentile compared with a normal reference population ( Amsterdam, et al., 2014). Current resuscitation guidelines recommend against using high-sensitivity TnT and TnI alone measured at 0 and 2 hours (without performing clinical risk stratification) to identify patients at low risk for   ACS (O’Connor, et al., 2015). High-sensitivity TnI measurements that are less than the 99th percentile, measured at 0 and 2 hours, may be used together with low-risk stratification (Thrombolysis in MI [TIMI] score of 0 or 1, or low risk per Vancouver rule) to predict a less than 1% chance of 30-day major  adverse cardiac event (MACE) (O’Connor, et al., 2015). Negative TnI or TnT measurements obtained at the patient ’s initial presentation and again between 3 and 6 hours after symptom onset may be used together with very low-risk stratification (TIMI score of 0, low-risk score per Vancouver rule, North

CHAPTER 7   Acute Coronary Syndromes

 American Chest Pain score of 0 and age less than 50 years, or low-risk HEART score) to predict a less than 1% chance of 30-day MACE (O’Connor, et al., 2015).  Troponin levels remain elevated for several days after myocardial necrosis and may remain elevated for  up to 2 weeks with a large infarction ( Amsterdam, et al., 2014). Elevated troponins may also occur after  recent catheter ablation of a dysrhythmia because of direct cardiac trauma. CK-MB may be used to estimate the size of an MI ( Amsterdam, et al., 2014) and is the preferred alternative when cardiac troponin markers are unavailable ( Thygesen, et al., 2012). It is important to recognize that elevated cardiac troponin levels may be present with a number of  conditions other than MI. For example, abnormal elevations have been observed with heart failure, chronic kidney disease, pulmonary embolism, myocarditis, pericarditis, sepsis, transplant rejection, chemotherapy, and direct or indirect cardiac trauma (Giugliano, et al., 2015; Ibrahim, et al., 2014).

Imaging Studies  A portable chest radiograph should be obtained for patients with a suspected ACS within 30 minutes of  patient presentation. Two-dimensional transthoracic echocardiography is useful for the evaluation of left  and right ventricular function, including the assessment of myocardial thickness, thickening, and motion at rest. Echocardiography is also helpful for detecting mechanical complications of acute MI including  acute mitral regurgitation, pericardial effusion, myocardial free wall rupture, acute ventricular septal defect, and intracardiac thrombus formation. Limitations of the two-dimensional echocardiogram include the inability to distinguish between an acute MI and previous MI (Bolooki & Askari, 2010) and the inability to distinguish regional wall motion abnormalities caused by myocardial ischemia from that caused by infarction ( Thygesen, et al., 2007). Other imaging studies such as transesophageal echocardiography, a contrast-enhanced computed tomography scan of the chest, or magnetic resonance imaging are useful for excluding some of the nonischemic causes of acute chest pain, such as valvular heart disease, aortic dissection, and pulmonary  embolism.

INITIAL MANAGEMENT OF ACUTE CORONARY  SYNDROMES [Objectives 10, 11, 12]  Treatment of the patient with a suspected ACS is time sensitive and it must be done efficiently. Therapeutic interventions are aimed at improving myocardial tissue oxygen supply, reducing myocardial oxygen demand, protecting ischemic myocardium, restoring coronary blood flow, and preventing  reocclusion of the artery (Brown, 2013).

Prehospital Management  When arriving on the scene of a patient who is complaining of chest discomfort or an anginal equivalent, quickly perform a primary survey and stabilize the patient ’s airway, breathing, and circulation (ABCs) as necessary. Allow the patient to assume a position of comfort. Assess vital signs and oxygen saturation. Supplemental oxygen is warranted if the patient is having difficulty breathing, has obvious signs of heart  failure, or if he or she is hypoxemic (ie, oxygen saturation less than 90%) ( Amsterdam, et al., 2014; O’Connor, et al., 2015; O’Gara, et al., 2013). Titrate oxygen therapy to maintain an oxygen saturation of 94% or greater (O’Connor, et al., 2015). Because the usefulness of supplemental oxygen therapy has not been established in patients with normal oxygen saturation, the withholding of supplemental oxygen may be considered for normoxic patients with known or suspected ACS in the prehospital, emergency  department, and hospital settings (O’Connor, et al., 2015).

ACLS Pearl Results of the AirVersus Oxygen in ST-ElevationMyocardial Infarction (AVOID) trial, which were published after the systematic review by the International Liaison Committee on Resuscitation (ILCOR), found that supplemental oxygen therapy in patients with STEMI but without hypoxia may increase early myocardial injury and was associated with larger myocardial infarct size assessed at 6 months ( Stub, et al., 2015 ).

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Obtain a focused history, including the time of symptom onset. Assess and document the degree of  the patient ’s pain or discomfort using a 0-to-10 scale. Give aspirin if no contraindications are present. Establish cardiac monitoring and obtain a diagnostic-quality 12-lead ECG as soon as possible (O’Connor, et al., 2015). Perform a secondary survey during transport as dictated by the patient ’s condition. STEMI alert programs have been implemented in many emergency medical services (EMS) systems and hospitals across the country in an attempt to minimize total ischemic time, which is defined as the time from onset of symptoms of STEMI to successful reperfusion (O’Gara, et al., 2013). If the prehospital 12-lead ECG clearly shows evidence of STEMI, alert the receiving hospital and begin completing a reperfusion checklist. Establish intravenous (IV) li nes in transit and give medications for pain control per local or system protocol. Experts encourage the development of local protocols that  allow preregistration and direct transport to the catheterization laboratory of a PCI-capable hospital (bypassing the emergency department) for patients who do not require emergent stabilization upon arrival (O’Gara, et al., 2013). Although prehospital fibrinolytic therapy is not used in most U.S. communities, multiple studies have demonstrated its safety (O’Gara, et al., 2013). In communities where prehospital fibrinolysis is part of a STEMI system of care, current guidelines state that prehospital fibrinolysis is reasonable when transport time is more than 30 minutes and in-hospital fibrinolysis is the alternative treatment strategy (O’Connor, et al., 2015). In communities where prehospital fibrinolysis is available and transport directly to a PCI-capable hospital is available, transport directly to the PCI facility  may be preferred because the incidence of intracranial hemorrhage, although relatively rare, is greater   with fibrinolysis (O’Connor, et al., 2015).

Emergency Department Management  Although patients experiencing ischemic chest pain symptoms may arrive in the emergency department  by ambulance, many arrive by means of private vehicle. Patients who arrive by private vehicle should be triaged immediately. Quickly assess the patient ’s ABCs, and ensure that the patient has a secure airway and adequate breathing. Frequent assessment of the patient ’s mental status, vital signs, and oxygen saturation level is important and continuous ECG monitoring is essential during the prehospital, emergency department, and early hospital phases of care. Administer supplemental oxygen if indicated. If not already done, give aspirin if no contraindications are present and establish IV access. While completing a reperfusion checklist, obtain a chest radiograph within 30 minutes and draw initial laboratory tests including cardiac biomarkers, electrolytes, and coagulation studies. Obtain a targeted history and physical examination. This can be done at the same time as other procedures. Assess and document the character of the patient ’s chest discomfort, the presence of risk factors for CAD, and the presence of associated signs and symptoms. Consider the possibility of other conditions that mimic acute MI such as aortic dissection, acute pericarditis, acute myocarditis, and pulmonary  embolism. Continually reassess the degree of the patient ’s pain or discomfort using a 0-to-10 scale, and reassess the patient ’s response to medications given. Risk assessment tools should be used to determine the patient ’s risk of death and ischemia in STEMI and NSTE-ACS (Kurz, et al., 2014).  An initial 12-lead ECG should be obtained and interpreted within 10 minutes of patient contact  ( Amsterdam, et al., 2014). Obtain a repeat 12-lead ECG with each set of vital signs, when the patient ’s symptoms change, and as often as necessary. After the 12-lead has been obtained, it should be reviewed carefully for ECG evidence of an ACS. Patients experiencing a STEMI are considered the most emergent, followed by those with NSTE-ACS, and then persons experiencing chest pain of probable cardiac origin. On the basis of the 12-lead ECG findings, categorize the patient into one of the three following  groups: 1.   STE. Patients with ST elevation in two or more contiguous leads are classified as having a STEMI and should be evaluated for immediate reperfusion therapy by means of pharmacologic reperfusion (ie, fibrinolytics) or mechanical perfusion (ie, PCI) (discussed later in this chapter). The goals of  reperfusion are to administer fibrinolytics within 30 minutes of arrival or to provide PCI within 90 minutes of arrival (O’Connor, et al., 2015). Patients with obvious STE in leads II, III, and/or  aVF should also be evaluated for a possible RVI. 2.   STD. ST depression or transient ST segment/T wave changes that occur with chest pain or discomfort suggest myocardial ischemia. Patients with obvious STD in leads V 1 and V 2 should be evaluated for possible inferobasal MI. Patients presenting with NSTE-ACS, including those with recurrent 

CHAPTER 7   Acute Coronary Syndromes

symptoms, ischemic ECG changes, or positive cardiac troponins should be admitted to a monitored bed for further evaluation ( Amsterdam, et al., 2014). Stabilized patients with NSTE-ACS should be admitted to an intermediate (or step-down) care unit ( Amsterdam, et al., 2014). Patients with continuing angina, hemodynamic instability, uncontrolled dysrhythmias, or a large MI should be admitted to a coronary care unit ( Amsterdam, et al., 2014). Treatment options for NSTE-ACS are based on risk stratification and include antianginal, antiplatelet, and anticoagulant therapy (O’Connor, et al., 2015). Because the presence of depressed left ventricular function can influence pharmacologic therapies and can influence revascularization choices (ie, PCI versus coronary artery bypass graft surgery), assessment of left ventricular function is recommended ( Amsterdam, et al., 2014). 3.  Normal or nondiagnostic ECG. A normal ECG or nonspecific ST- and T wave changes are nondiagnostic and should prompt consideration for further evaluation. Consider admission of the patient with signs and symptoms suggesting an ACS and a nondiagnostic ECG to the emergency department  chest pain unit or to an appropriate bed (O’Connor, et al., 2015). Obtaining serial ECGs at 5- to 10-minute intervals or continuous monitoring of the ST segment should be performed to detect  the potential development of ST elevation if the initial ECG is not diagnostic of STEMI but the patient remains symptomatic and there is a high clinical suspicion of STEMI. Noninvasive tests (eg, computed tomography angiography, cardiac magnetic resonance, myocardial scintigraphy, stress echocardiography) can be useful in identifying patients suitable for discharge from the emergency  department (O’Connor, et al., 2015). The ACSs algorithm appears in Fig. 7.23.

Pharmacologic Therapies [Objective 10] Relief of cardiac-related discomfort is a priority for the management of a patient who is experiencing an  ACS and often requires a combination of oxygen, NTG, and opioid analgesics. The relief of pain decreases anxiety, myocardial oxygen demand, and the risk of dysrhythmias. Nitroglycerin NTG dilates the capacitance vessels (ie, veins), which causes a reduction in ventricular filling and cardiac preload. NTG also dilates normal and atherosclerotic epicardial coronary arteries and increases coronary  collateral flow ( Amsterdam, et al., 2014). Before giving NTG, assess the degree of the patient ’s pain or discomfort with the use of a 0-to-10 scale. Also record the pain ’s duration, time of onset, the activity that was being performed, and the pain quality. Reassess and document the patient ’s vital signs and level of discomfort after each dose. Common adverse effects of NTG administration include headache, flushing, tachycardia, dizziness, and orthostatic hypotension. Hypotension usually responds to supine positioning and the administration of IV fluids. Make sure that the patient has not used a phosphodiesterase inhibitor such as sildenafil (eg, Viagra)  within 24 hours or tadalafil (eg, Cialis) within 48 hours before NTG administration ( Table 7.4). The combination of a phosphodiesterase inhibitor and nitrates may result in severe hypotension. NTG should be avoided in inferior wall MI with a possible associated RVI. Consider the presence of RVI if the patient   with an inferior wall MI becomes hypotensive after nitrate administration.  Analgesic Therapy  Morphine sulfate is a potent narcotic analgesic and anxiolytic ( Table 7.5). It causes venodilation, and it  can lower heart rate (through increased vagal tone) and systolic blood pressure, thereby reducing myocardial oxygen demand. The adverse effects of morphine administration include nausea and vomiting, bradycardia, and respiratory depression. Hypotension may occur, particularly among patients who are  volume depleted or who have received vasodilators. Some studies have demonstrated increased adverse events associated with the use of morphine sulfate in patients with ACS and acute decompensated heart  failure ( Amsterdam, et al., 2014). Supine positioning or IV boluses of normal saline are used to restore blood pressure. Respiratory depression or excessive morphine-related bradycardia may require administration of a narcotic antagonist (eg, naloxone). Other narcotics may be considered for patients who are allergic to morphine. Before giving morphine, assess the degree of the patient ’s pain or discomfort with the use of a 0-to-10 scale. Also determine the duration, the time of onset, the activity being performed, and the pain quality. Reassess and document the patient ’s vital signs and level of discomfort after each morphine dose.

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Fig. 7.23   American Heart Association acute coronary syndromes algorithm. (Reprinted with permission. 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care —Part 9: Acute Coronary Syndromes. ECCguidelines.heart.org. © 2015 American Heart Association, Inc.)

Because of the increased risk of MACEs (eg, reinfarction, hypertension, heart failure, myocardial rupture) associated with the use of nonsteroidal antiinflammatory drugs (NSAIDs), these drugs (except for  aspirin) should not be initiated in the acute phase of care and should be discontinued in patients using  them before hospitalization ( Amsterdam, et al., 2014; O’Connor, et al., 2015; O’Gara, et al., 2013). Many health care professionals are using fentanyl (ie, Sublimaze) for pain relief as well as vasodilation in place of morphine in patients experiencing an ACS. Fentanyl is a lipid-soluble synthetic opioid that  has minimal cardiovascular effects, as well as a more rapid onset and shorter duration of action than morphine. The adverse effects of fentanyl are similar to those of morphine.

CHAPTER 7   Acute Coronary Syndromes

TABLE 7.4

  Nitroglycerin NSTE-ACS

Sublingual Indications and Dosage

STEMI

Class I recommendation: Patients with ongoing ischemic discomfort  ( Amsterdam, et al., 2014) should receive sublingual NTG (0.4 mg) Sublingual NTG may be given at 5-min every 5 min up to three doses as BP intervals to a maximum of three doses. allows (O’Gara, et al., 2013). Class I recommendation: May be useful to treat patients with STEMI ( Amsterdam, et al., 2014) and hypertension or HF (O’Gara, et al., IV NTG is indicated for patients with NSTE-ACS 2013) for treatment of persistent ischemia, HF, or hypertension. Nitrates should not be administered to patients with a systolic BP less than 90 mm Hg or 30 mm Hg or more below baseline, marked bradycardia or tachycardia, phosphodiesterase inhibitor use within the previous 24 to 48 hours, or suspected RVI (O’Gara, et al., 2013).

IV Indications

Notes

BP, blood pressure; HF, heart failure; IV, intravenous; mm Hg, millimeters of mercury; NSTE-ACS, non–ST elevation acute coronary syndrome; NTG, nitroglycerin; RVI, right ventricular infarction; STEMI, ST elevation myocardial infarction

TABLE 7.5

Morphine Sulfate

NSTE-ACS Indications and Dosage

Notes

STEMI

Class IIb recommendation: Morphine sulfate (4 to 8 mg IV initially [use Morphine sulfate (1 to 5 mg IV) may be lower doses in the elderly] with increments reasonable for patients with NSTE-ACS if  of 2 to 8 mg IV repeated at 5- to 15-min there is continued ischemic chest pain intervals if needed) is the analgesic of  despite maximally tolerated antiischemic choice for patients with STEMI, especially therapy ( Amsterdam, et al., 2014). Repeat  those whose course is complicated by every 5 to 30 min as needed to relieve acute pulmonary edema (O’Gara, et al., symptoms and maintain patient comfort. 2013). • Ensure that a narcotic antagonist and airway equipment is readily available before administration. • Factors such as patient age, body size, BP, and heart rate influence the dose of morphine needed to achieve adequate pain control (O’Gara, et al., 2013). • When indicated, administer naloxone 0.1 to 0.2 mg IV every 15 min to reverse the narcotic effects of morphine (O’Gara, et al., 2013). • Excessive morphine-related bradycardia may require the administration of atropine 0.5 to 1.5 mg IV (O’Gara, et al., 2013).

BP, blood pressure; IV, intravenous; NSTE-ACS, non –ST elevation acute coronary syndrome; STEMI, ST elevation myocardial infarction

Beta-Blockers  The inhibition of beta 1-adrenergic receptor sites decreases heart rate and the force of myocardial contraction, thereby reducing myocardial oxygen demand ( Table 7.6). It is essential to closely monitor  the patient ’s heart rate, blood pressure, pulmonary status, and ECG rhythm during treatment with a  beta-blocker. Simultaneous IV administration with IV calcium channel blockers (CCBs) (eg, verapamil, diltiazem) can cause severe hypotension. Calcium Channel Blockers Nondihydropyridine CCBs (eg, verapamil, diltiazem) decrease heart rate and myocardial contractility, slow conduction through the AV node, and have some peripheral arterial dilatory effects ( Table 7.7).  Although CCBs may be useful in relieving ischemia or lowering BP in patients who are intolerant of  beta-blockers, randomized controlled trials have demonstrated no beneficial effect on infarct size or  the rate of reinfarction when CCB therapy was initiated during either the acute or convalescent phase of STEMI (O’Gara, et al., 2013).

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TABLE 7.6

  Beta-Blockers

NSTE-ACS Indications

Class I recommendation:  (Amsterdam, et al., 2014) • Initiate oral beta-blockers within the first 24 hours in the absence of  HF, low output state, risk for cardiogenic shock, or other. contraindications to beta blockade • Use of sustained-release metoprolol succinate, carvedilol, or bisoprolol is recommended for beta-blocker therapy with concomitant NSTE-ACS,   stabilized  HF, and reduced systolic function. • Reevaluate to determine subsequent eligibility in patients with initial contraindications to beta-blockers. Class IIa recommendation: ( Amsterdam, et al., 2014) • It is reasonable to continue betablocker therapy in patients with normal LV function with NSTE-ACS.

Notes

•

•

STEMI

Class I recommendation: (O’Gara, et al., 2013) • Oral beta-blockers should be initiated in the first  24 hours in patients with STEMI who do not have any of the following: signs of HF, evidence of a low output state, increased risk for cardiogenic shock, or other contraindications to use of oral beta-blockers (PR interval more than 0.24 sec, second- or thirddegree heart block, active asthma, or reactive airway disease). • Beta-blockers should be continued during and after hospitalization for all patients with STEMI and with no contraindications to their use. • Patients with initial contraindications to the use of  beta-blockers in the first 24 hours after STEMI should be reevaluated to determine their subsequent eligibility. Class IIa recommendation: (O’Gara, et al., 2013) • It is reasonable to administer IV beta-blockers at the time of presentation to patients with STEMI and no contraindications to their use who are hypertensive or have ongoing ischemia. Risk factors for cardiogenic shock are age greater than 70 years, systolic BP less than 120 mm Hg, heart rate greater than 110 beats/min, or increased time since onset of STEMI symptoms (O’Gara, et al., 2013). Carefully monitor the patient ’s blood pressure, heart rate, and cardiac rhythm after beta-blocker administration.

BP, blood pressure; HF, heart failure; IV, intravenous; LV, left ventricular; mm Hg, millimeters of mercury; NSTE-ACS, non –ST elevation acute coronary syndrome; STEMI, ST elevation myocardial infarction

TABLE 7.7

Indications

Calcium Channel Blockers

NSTE-ACS

STEMI

Class I recommendations  (Amsterdam, et al., 2014): In patients with NSTE-ACS, continuing or frequently recurring ischemia, and a contraindication to beta-blockers, a nondihydropyridine CCB should be given as initial therapy in the absence of clinically significant LV dysfunction, increased risk  for cardiogenic shock, PR interval greater than 0.24 sec, or second- or third-degree AV block without a cardiac pacemaker. • Oral nondihydropyridine calcium antagonists are recommended in patients with NSTE-ACS who have recurrent ischemia in the absence of contraindications, after appropriate use of  beta-blockers and nitrates. • CCBs are recommended for ischemic symptoms when beta-blockers are not successful, are contraindicated, or cause unacceptable side effects. • Long-acting CCBs and nitrates are recommended in patients with coronary artery spasm.

May be useful to relieve ischemia, lower BP, or control the ventricular response rate to AFib in patients who are intolerant of betablockers (O’Gara, et al., 2013).

•

 AFib, atrial fibrillation; AV, atrioventricular; BP, blood pressure; CCB, calcium channel blocker; HF, heart failure; IV, intravenous; LV, left ventricular; NSTE-ACS, non–ST elevation acute coronary syndrome; STEMI, ST elevation myocardial infarction

CHAPTER 7   Acute Coronary Syndromes

TABLE 7.8

Statin Therapy Indications

Lipid Management

NSTE-ACS

STEMI

Class I recommendation  (Amsterdam, et al., 2014): High-intensity statin therapy should be initiated or continued in all patients with NSTE-ACS and no contraindications to its use Class IIa recommendation ( Amsterdam, et al., 2014): It is reasonable to obtain a fasting lipid profile in patients with NSTE-ACS, preferably within 24 hours of presentation

Class I and Class IIa recommendations same as for NSTE-ACS (O’Gara, et al., 2013)

NSTE-ACS, non–ST elevation acute coronary syndrome; STEMI, ST elevation myocardial infarction

Lipid Management Several studies have demonstrated that in patients stabilized after an ACS, treatment with statin drugs lowers the risk of coronary heart disease death, stroke, recurrent MI, and the need for coronary revascularization ( Amsterdam, et al., 2014; O’Gara, et al., 2013) ( Table 7.8). High-dose atorvastatin (ie, 80 mg daily) has been shown to reduce death and ischemic events among patients with ACS (O’Gara, et al., 2013). Renin-Angiotensin-Aldosterone System Inhibitors  Angiotensin-converting enzyme (ACE) inhibitors produce vasodilation by blocking the conversion of  angiotensin I into angiotensin II ( Table 7.9). Because angiotensin is a potent vasoconstrictor, limiting  its production decreases peripheral vascular resistance, thereby reducing the pressure that the heart must  pump against and decreasing the myocardial workload. ACE inhibitors also increase renal blood flow,  which helps rid the body of excess sodium and fluid accumulation. ACE inhibitors have been shown to reduce fatal and nonfatal major cardiovascular events in patients with STEMI (O’Gara, et al., 2013). An angiotensin receptor blocker (eg, valsartan) may be substituted for patients who are intolerant of ACE inhibitors (O’Gara, et al., 2013).  Antiplatelet Therapy   Antiplatelet and anticoagulant therapies are important components of ACS patient management because exposure of a ruptured plaque ’s contents triggers activation of the coagulation cascade. Antiplatelet  medications target specific platelet functions at different levels in the pathway of platelet aggregation (Fig. 7.24, Table 7.10).  Aspirin is an antiplatelet agent that inhibits cyclooxygenase, an enzyme required by platelets to synthesize thromboxane A 2. Non – enteric-coated aspirin (162 mg to 325 mg) should be administered to patients experiencing an ACS as soon as possible after symptom onset, unless contraindicated ( Amsterdam, et al., 2014; O’Gara, et al., 2013). Recommendations with regard to the use of aspirin in NSTE-ACS and STEMI are shown in Table 7.11.  The thienopyridines (eg, clopidogrel, prasugrel, ticlopidine) are drugs that target P2Y 12  receptors,  which are key adenosine diphosphate (ADP) receptors on the platelet surface ( Weitz, 2013). By blocking  P2Y 12  receptor sites, ADP is inhibited from activating additional platelets. Clopidogrel, prasugrel, and ticlopidine are irreversible platelet inhibitors that impede platelet function for the lif e of the platelet. Prasugrel, a newer thienopyridine, has more rapid and consistent platelet inhibition than clopidogrel ( Amsterdam, et al., 2014). Unlike the thienopyridines, ticagrelor binds reversibly to P2Y 12  receptors and has a more rapid and consistent onset of action compared with clopidogrel ( Amsterdam, et al., 2014). ADP inhibitors have a synergistic effect when used with aspirin because they inhibit different  platelet-activating pathways. For patients with suspected STEMI intending to undergo primary PCI (PPCI), current resuscitation guidelines note that it may be reasonable to begin ADP inhibition in either  the prehospital or in-hospital setting (O’Connor, et al., 2015). Glycoprotein (GP) IIb/IIIa receptors are the most abundant receptors on the platelet surface ( Weitz, 2013). GP IIb/IIIa inhibitors are potent antiplatelet medications that inhibit the final common pathway  of platelet aggregation (Mistry & Vesely, 2012). These agents are used in patients undergoing PCIs,

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TABLE 7.9

ReninAngiotensinAldosterone System Inhibitors  ACE inhibitors (eg, lisinopril, captopril, ramipril)

 ARBs (eg, valsartan)

 Aldosterone antagonists (eg, eplerenone)

Notes

Renin-Angiotensin-Aldosterone System Inhibitors

NSTE-ACS

STEMI

Class I recommendation: ( Amsterdam, et al., 2014)  An ACE inhibitor should be started and continued indefinitely in all patients with a LVEF less than 0.40 and in those with hypertension, diabetes mellitus, or stable chronic kidney disease unless contraindicated.

Class I recommendation: (O’Gara, et al., 2013)  An ACE inhibitor should be administered within the first 24 hours to all patients with STEMI with anterior location, HF, or LVEF less than or equal to 0.40, unless contraindicated. Class IIa recommendation: (O’Gara, et al., 2013)  ACE inhibitors are reasonable for all patients with STEMI and no contraindications to their use. Class I recommendation: Class I recommendation: ( Amsterdam, et al., 2014) (O’Gara, et al., 2013)  ARBs are recommended in patients  An ARB should be given to patients with with HF or MI with LVEF less than STEMI who have indications for but are 0.40 who are ACE inhibitor intolerant. intolerant of ACE inhibitors. Class I recommendation: Class I recommendation: ( Amsterdam, et al., 2014) (O’Gara, et al., 2013)  Aldosterone blockade is recommended  An aldosterone antagonist should be given to in patients post –MI without  patients with STEMI and no significant renal dysfunction or contraindications who are already hyperkalemia who are receiving receiving an ACE inhibitor and beta-blocker therapeutic doses of an ACE inhibitor and who have a LVEF less than or equal to and beta-blocker and have a LVEF of  0.40 and either symptomatic HF or 0.40 or less, diabetes mellitus, or HF. diabetes mellitus. ACE inhibitors may cause a profound drop in BP after the first dose or if used with diuretics. ACE inhibitors and ARBs should be avoided in patients with hypotension, renal failure, or hyperkalemia.

 ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blockers; BP, blood pressure; HF, heart failure; LVEF, left  ventricular ejection fraction; MI, myocardial infarction; NSTE-ACS, non –ST elevation acute coronary syndrome; STEMI, ST elevation myocardial infarction

particularly those with STEMI ( Weitz, 2013). GP IIb/IIIa inhibitors are administered IV. When the use of any of these medications is planned, minimize arterial and venous punctures; intramuscular injections; and the use of urinary catheters, nasotracheal intubation, and nasogastric tubes. When establishing IV  access, avoid noncompressible sites (eg, the subclavian or jugular veins).  Anticoagulant Therapy   Anticoagulants have been a mainstay in the management of patients with ACS, in the prevention of  stroke in patients with AFib, and in the prevention and treatment of venous thromboembolism, among  other conditions (Garg & Halperin, 2013). Older anticoagulants typically require frequent coagulation monitoring to ensure that a therapeutic response is achieved. For example, warfarin requires coagulation monitoring because its anticoagulant effects are influenced by dietary vitamin K intake, other medications, and various disease states ( Weitz, 2013). Dabigatran (Pradaxa), rivaroxaban (Xarelto), and apixaban (Eliquis) are newer oral anticoagulants that have a wide therapeutic window, fewer drug  – drug  interactions, an absence of major dietary effects, and less risk of intracranial bleeding than warfarin. Routine coagulation monitoring is not required in the majority of patients with these new agents; however, strict compliance is critical because missing even one dose could result in a period without protection from thromboembolism ( January, et al., 2014). Examples of anticoagulants appear in  Table 7.12. For patients with NSTE-ACS, anticoagulation, in addition to antiplatelet therapy, is recommended for all patients regardless of whether an invasive or conservative treatment strategy is planned

CHAPTER 7   Acute Coronary Syndromes

Plaque disruption Platelet adhesion and aggregation

A

Activation of coagulation cascade

B Thrombin formation Stable thrombus Fibrinogen

Fibrin Clot dissolution

Plasminogen

Plasmin

C Degradation products

Fig. 7.24 Site of action of medications used in the treatment of ACSs. A, Site of action of antiplatelet agents such as aspirin, thienopyridines, and GP IIb/IIIa inhibitors. B, Heparin bonds with antithrombin III and thrombin to create an inactive complex. C, Fibrinolytic agents convert plasminogen to plasmin, an enzyme responsible for degradation of fibrin clots. (From Urden LD, Stacy KM, Lough ME: Critical care nursing: diagnosis and management, ed 6, St. Louis, 2010, Mosby.)

TABLE 7.10

Antiplatelet Medications

Category

Action

Example(s)

Route

Cyclooxygenase inhibitors

Inhibit cyclooxygenase, an enzyme required by platelets to synthesize thromboxane A 2 Bind to ADP P2Y 12 receptors on the platelet  surface, thereby inhibiting ADP from activating additional platelets

 Aspirin

Oral

Clopidogrel (Plavix) Prasugrel (Effient) Ticagrelor (Brilinta) Ticlopidine (Ticlid)  Abciximab (ReoPro) Eptifibatide (Integrilin) Tirofiban (Aggrastat)

Oral

 ADP P2Y 12   receptor inhibitors

GP IIb/IIIa receptor inhibitors

Act on the GP IIb/IIIa receptors on the platelet membrane to inhibit platelet  aggregation and to prevent platelets from binding with fibrinogen

IV 

 ADP, adenosine diphosphate; GP, glycoprotein; IV, intravenous

( Amsterdam, et al., 2014). For patients with STEMI who are undergoing PPCI, Class I anticoagulant  therapy recommendations include the use of unfractionated heparin (UFH) with or without a GP IIb/  IIIa inhibitor, or bivalirudin (O’Gara, et al., 2013). Current resuscitation guidelines recommend that  EMS systems that do not currently administer heparin to suspected STEMI patients do not add this treatment, whereas those that do administer it may continue their current practice ( O’Connor, et al.,

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TABLE 7.11

Indications and Dosage

  Aspirin

NSTE-ACS

STEMI

Class I recommendations: ( Amsterdam, et al., 2014)

Class I recommendations: (O’Gara, et al., 2013) • Aspirin 162 to 325 mg should be given before primary PCI. • After PCI, aspirin should be continued indefinitely. • A loading dose of a P2Y 12  receptor inhibitor should be given as early as possible or at the time of  primary PCI to patients with STEMI. • P2Y 12   inhibitor therapy (maintenance doses) should be given for 1 year to patients with STEMI who receive a stent during primary PCI.

•

•

•

Non–enteric-coated, chewable aspirin (162 mg to 325 mg) should be given to all patients with NSTE ACS without contraindications as soon as possible after presentation, and a maintenance dose of  aspirin (81 mg/d to 162 mg/d) should be continued indefinitely. In patients with NSTE-ACS who are unable to take aspirin because of hypersensitivity or major GI intolerance, a loading dose of clopidogrel followed by a daily maintenance dose should be administered. A P2Y 12  inhibitor (either clopidogrel or ticagrelor) in addition to aspirin should be administered for up to 12 months to all patients with NSTE-ACS without  contraindications who are treated with either an early invasive or ischemia-guided strategy.

GI, gastrointestinal; NSTE-ACS, non–ST elevation acute coronary syndrome; PCI, percutaneous coronary intervention; STEMI, ST elevation myocardial infarction

TABLE 7.12

  Anticoagulants

Anticoagulant

Action

Route

 Apixaban (Eliquis)  Argatroban (Acova) Bivalirudin (Angiomax) Dabigatran (Pradaxa) Dalteparin (Fragmin)*

Factor Xa inhibitor Direct thrombin inhibitor Direct thrombin inhibitor Direct thrombin inhibitor Indirect thrombin inhibitor

Desirudin (Iprivask) Enoxaparin (Lovenox)*

Direct thrombin inhibitor Indirect thrombin inhibitor

Fondaparinux (Arixtra) Rivaroxaban (Xarelto) Unfractionated heparin Warfarin (Coumadin)

Factor Xa inhibitor Factor Xa inhibitor Indirect thrombin inhibitor Vitamin K antagonist

Oral IV  IV   Oral SC; IV if rapid anticoagulant  response needed SC SC; IV if rapid anticoagulant  response needed SC Oral IV or SC Oral

*

Low-molecular-weight heparin IV, intravenous; SC, subcutaneous

2015). Administration of UFH can occur either in the prehospital or in-hospital setting for STEMI patients for whom there is a planned PPCI reperfusion strategy (O’Connor, et al., 2015).

Reperfusion Therapies Of the patients who are experiencing ACSs, those who are experiencing a STEMI are most likely to benefit from reperfusion therapy. The primary choices for reperfusion therapy are fibrinolysis and PCI. Fibrinolytics (“clot-busters”) are medications that work by activating the conversion of plasminogen to plasmin, which then breaks down fibrinogen and fibrin clots. A PCI is a procedure in which a catheter  is used to open a coronary artery that has been blocked or narrowed by CAD. The term  primary PCI  is used when PCI is done alone as the primary treatment after diagnostic angiography. PPCI is the recommended reperfusion strategy when it can be performed in a timely manner by experienced personnel (O’Gara, et al., 2013). Current clinical practice guidelines with regard to PPCI in STEMI are shown in Box 7.4.

CHAPTER 7   Acute Coronary Syndromes

BOX 7.4

Primary PCI in STEMI Recommendations

Class I Recommendations •

•

Primary PCI should be performed in patients with STEMI and ischemic symptoms of less than 12 hours ’  duration.   Primary PCI should be performed in patients with STEMI and ischemic symptoms of less than 12 hours’   duration who have contraindications to fibrinolytic therapy, irrespective of the time delay from first medical contact.

•

Primary PCI should be performed in patients with STEMI and cardiogenic shock or acute severe HF, irrespective of time delay from MI onset.

Class IIa Recommendation •

Primary PCI is reasonable in patients with STEMI if there is clinical and/orECG evidence of ongoing ischemia between 12and 24hours after symptom onset.

Source: O ’Gara, et al., 2013, p. e90. ECG, electrocardiogram; HF, heart failure; MI, myocardial infarction; PCI, percutaneous coronary intervention; STEMI, ST elevation myocardial infarction

 The first physician who encounters a patient with STEMI should determine the need for reperfusion therapy and determine the means by which it is performed (pharmacologic versus mechanical) (O’Connor, et al., 2015). Because consultation delays therapy, routine consultation with a cardiologist  or other physician is not recommended except in equivocal or uncertain cases ( O’Connor, et al., 2015). Several factors must be considered when deciding to use fibrinolytic therapy versus PPCI including  the time from onset of symptoms, the patient ’s clinical presentation and hemodynamic status, the patient ’s age, the location of the infarction, the duration of STEMI at the time of initial emergency  department presentation, patient comorbidities, the risk of bleeding, the presence of contraindications, the time delay to PCI, and the abilities of the PCI cardiologist and hospital (O’Connor, et al., 2015; O’Gara, et al., 2013). For adult patients who present with STEMI at a non – PCI capable hospital, current guidelines recommend the immediate transfer of the patient without fibrinolysis to a PCI center  (O’Connor, et al., 2015). Fibrinolytic therapy with routine transfer for angiography may be an acceptable alternative to immediate transfer to PPCI when a STEMI patient cannot be transferred to a PCI-capable hospital in a timely manner (O’Connor, et al., 2015). Strategies that have been suggested for decreasing door-to-balloon time include the following  (Bradley, et al., 2006; O’Gara, et al., 2013): Use of the prehospital 12-lead ECG to diagnose STEMI; activation of the reperfusion team while the • patient is in transit to the hospital Activation of the reperfusion team by the emergency physician without waiting to consult a  • cardiologist  Activation of the reperfusion team by means of a single call from the emergency department to a cen• tral page operator, who then pages the interventional cardiologist and the catheterization laboratory staff  Goal established for the reperfusion team to arrive in the catheterization laboratory within 20 minutes • of being paged • Prompt feedback and analysis provided from a multidisciplinary quality improvement team to members of the STEMI care team  Although mechanical catheter-based intervention has been proven to produce better outcomes when performed in a timely manner, fibrinolytic therapy continues to play a major role in the treatment of  STEMI because only a minority of U.S. hospitals have PCI capabilities (O’Gara, et al., 2013). In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI and an onset of ischemic symptoms within the previous 12 hours when it is anticipated that primary  PCI cannot be performed within 120 minutes of first medical contact (O’Gara, et al., 2013). Fibrinolytic therapy is generally not recommended for patients presenting between 12 and 24 hours after onset of  symptoms unless ischemic pain persists with continuing STE; fibrinolytic therapy should not be administered to patients who present more than 24 hours after symptom onset (O’Connor, et al., 2015). STEMI patients with contraindications to fibrinolytic therapy and who are in cardiogenic shock are not candidates for fibrinolytic therapy (O’Connor, et al., 2015). PCI or a coronary artery bypass graft  is the preferred reperfusion strategy for STEMI patients who present in shock ( O’Connor, et al., 2015). There is no role for fibrinolytic therapy in patients with NSTE-ACS ( Amsterdam, et al., 2014; O’Connor, et al., 2015).

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Before starting fibrinolytic therapy, choose an ECG monitoring lead that shows clear evidence of ST elevation. During fibrinolytic therapy, monitor the ECG and the patient ’s vital signs closely. Watch for  ST changes, dysrhythmias, and hypotension, and question the patient about chest discomfort. When reperfusion occurs, the patient ’s chest discomfort typically stops abruptly as blood flow to the ischemic myocardium is restored. Watch for reperfusion dysrhythmias (eg, PVCs, bradycardias, heart block, VT,  ventricular fibrillation [VF]) as blood flow is reestablished through the infarct-related artery. Previously  elevated ST segments should quickly return to baseline as blood flow is restored to the affected myocardium. Reocclusion may occur. Pay careful attention to all potential bleeding sites (including catheter  insertion sites, arterial and venous puncture sites, cutdown sites, and needle puncture sites).

CHAPTER 7   Acute Coronary Syndromes

PUTTING IT ALL TOGETHER  The chapter quiz and case studies presented on the following pages are provided to help you integrate the information presented in this chapter. As you work through the case study, remember that there may be alternative actions that are perfectly acceptable, yet not presented in the case study. CHAPTER QUIZ

 Multiple Choice  Identify the choice that best completes the statement or answers the question.

____

1.

Whichof thefollowing isthe most commoncause ofthe blockageof a coronaryartery?  A. A thrombus B. Coronary artery spasm C. Coronary artery trauma  D. Coronary artery dissection

____

2.

Beta-blockers:  A. Increase heart rate. B. Decrease the force of myocardial contraction. C. Block the conversion of angiotensin I into angiotensin II. D. Are contraindicated in patients experiencing an ACS.

____

3.

Indicative changes, which are ECG findings that are seen in leads that look directly at  the area fed by a blocked coronary artery, are significant when they are seen in two anatomically contiguous leads. Which of the following reflects a pair of contiguous leads?  A. I and aVF  B. V 1  and V 6 C. V 2  and V 3 D. II and aVL

____

4.

Which of the following patients is most likely to present atypically with an ACS?  A. A 34-year-old man with no history of heart disease B. A 56-year-old woman with a history of type 1 diabetes C. A 65-year-old man with a history of two previous MIs D. A 58-year-old man with angina and a strong family history of CAD

____

5.

ECG changes characteristic of myocardial ischemia include temporary changes in the:  A. P wave and ST segment. B. ST segment and T wave. C. P wave and QRS complex. D. QRS complex and T wave.

____

6.

A 66-year-old woman presents in acute distress. She describes a suddenonset ofsevere chest discomfort and nausea that have been present for 2 hours. An initial 12-lead ECG should be obtained within __ minutes of contact with this patient.  A. 10 B. 30 C. 60 D. 90

____

7.

Which of the following is preferred for the relief of persistent chest discomfort  associated with a STEMI?  A. Aspirin B. Morphine C. Midazolam D. NSAIDs

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____

8.

Which of the following is (are) the preferred cardiac biomarker(s) for diagnosing MI?  A. Myoglobin B. TnI and TnT C. Ischemia-modified albumin D. CK-MB

____

9.

The recommended initial dose of aspirin is:  A. 35 to 81 mg. B. 81 to 162 mg. C. 162 to 325 mg. D. 325 to 500 mg.

____

10.

A 52-year-old woman is complaining of chest pain. The cardiac monitor reveals a  sinus rhythm at 68 beats/min. Her blood pressure is 88/60 millimeters of mercury  (mm Hg) and her ventilatory rate is 14 breaths/min. Breath sounds are clear. There are no signs of pedal edema. A standard 12-lead ECG is obtained that reveals 3-mm STE in leads II, III, and aVF. The patient is being given oxygen at 2 L/min by nasal cannula. An IV has been established. You should now:  A. Give sublingual NTG and aspirin. B. Give morphine sulfate and a calcium channel blocker. C. Attach right-sided chest leads to rule out RVI. D. Give a beta-blocker and determine the patient ’s eligibility for reperfusion therapy.

 Matching  Match each description with its corresponding answer 

 A. The zone of ischemia produces ST segment _____ in the leads facing the affected area  B. View the anterior wall of the left ventricle C. Indication for supplemental oxygen administration D. Blood tests used to help verify the presence of a MI E. View the inferior wall of the left ventricle F. The period from STEMI symptom onset to successful reperfusion G. Phosphodiesterase inhibitor use within the previous 24 to 48 hours H. This type of angina is the result of intense spasm of a segment of a coronary artery  I. View the interventricular septum  J. Examples of ACE inhibitors K. A procedure in which a catheter is used to open a coronary artery blocked or narrowed by CAD L. View the lateral wall of the left ventricle M. UA and NSTEMI N. The zone of injury produces ST segment _____ in the leads facing the affected area  O. Components of the treatment plan for NSTE-ACS P. Example of an antiplatelet agent  Q. View the inferobasal wall of the left ventricle R. Example of a condition that can mimic an acute MI S. PR interval more than 0.24 seconds, second- or third-degree heart block, reactive airway disease  T. Examples of beta-blockers ____

11.

Elevation

____

12.

PCI

____

13.

II, III, and aVF 

____

14.

Atenolol, metoprolol

____

15.

NSTE-ACSs

CHAPTER 7   Acute Coronary Syndromes

____

16.

Cardiac biomarkers

____

17.

Leads V7 , V 8, and V 9

____

18.

Contraindications for beta-blocker administration

____

19.

Depression

____

20.

Leads I, aVL, V5  , and V 6

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21.

Prinzmetal’s

____

22.

Total ischemic time

____

23.

Oxygen saturation level of less than 90%

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24.

Clopidogrel (Plavix)

____

25.

Leads V1   and V 2

____

26.

Pericarditis

____

27.

Lisinopril, captopril, ramipril

____

28.

Leads V3   and V 4

____

29.

Contraindication for nitrate administration

____

30.

Antianginal, antiplatelet, and anticoagulant therapy 

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CASE STUDY 7-1  Your patient is a 68-year-old man who is complaining of chest discomfort. The patient is hospitalized at a  PCI-capable facility. You have a sufficient number of advanced life support personnel available to assist   you and carry out your instructions. Emergency equipment, including a biphasic manual defibrillator, is available. 1. You see the patient sitting upright on a stretcher with beads of sweat visible on his forehead. He is awake and watches as you approach. The patient appears anxious and his skin is pale. His breathing  does not appear to be labored. Are these general impression findings normal or abnormal? If  abnormal, what are the abnormal findings? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 2. How would you like to proceed? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 3. The patient ’s blood pressure is 168/94 mm Hg and his ventilatory rate is 22 breaths/min. Breath sounds are clear and equal and his skin is cool, pale, and moist. The patient ’s SpO2  on room air is 95%. He has been placed on the cardiac monitor, which reveals a sinus tachycardia at 110 beats/min. The following information has been obtained from the patient: Signs/Symptoms: Discomfort located in the center of his chest and radiates to his left arm;  A llergies: Medications: Past history: Last oral intake: E vents prior:

rates his chest discomfort at 9 out of 10 None Aspirin 81 mg daily  Heart attack at age 45, RCA stent inserted Lunch 2 hours ago Patient was reading the newspaper when his discomfort began about 1½ hours ago.

 The physical examination reveals no abnormalities. What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 4. Should aspirin be administered to this patient? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 5. IV access has been established and a 12-lead ECG has been obtained. Which components of the ECG should be carefully examined to determine the most appropriate treatment course for this patient? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 6. When viewing the ECG of a patient experiencing an ACS, what does the presence of STE in the leads facing the affected area suggest? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

CHAPTER 7   Acute Coronary Syndromes

7. The patient ’s 12-lead ECG is shown here (Fig. 7.25). Are there any significant findings on this 12lead ECG?

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 7.25 (From Phalen T, Aehlert BJ: The 12-lead ECG in acute coronary syndromes,  ed 3, St. Louis, 2012, Mosby.)

_____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 8. What complications should be reasonably anticipated with this type of infarction? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 9. Sublingual NTG is ordered for this patient. What is the rationale for giving NTG in this situation? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 10. What precautions should be taken before giving NTG? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 11. After three doses of sublingual NTG, the patient rates his discomfort as 7/10. His vital signs are essentially unchanged. What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 12. Cardiac biomarkers and the 12-lead ECG confirm a STEMI. What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

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CHAPTER QUIZ ANSWERS

 Multiple Choice

1. A. A thrombus is the most common cause of the blockage of a coronary artery. Less common causes of an ACS include coronary artery spasm (eg, with cocaine abuse), severe luminal narrowing from atherosclerosis or restenosis after PCI, coronary dissection, hypercoagulation, trauma to the coronary  arteries, or coronary artery emboli (rare). OBJ: Explain the pathophysiology of ACSs. 2. B. The inhibition of beta 1-adrenergic receptor sites decreases heart rate and the force of myocardial contraction, thereby reducing myocardial oxygen demand. ACE inhibitors block the conversion of  angiotensin I into angiotensin II. In the absence of contraindications to their use, oral beta-blockers should be initiated in the first 24 hours in patients experiencing an ACS. OBJ: Describe the initial management of a patient experiencing an ACS. 3. C. Two leads are contiguous if they look at the same or adjacent areas of the heart or if they are numerically consecutive chest leads. Examples of contiguous leads include V 1  and V 2, V 2 and V 3, V 3  and V 4, V 4  and V 5, V 5  and V 6, I and aVL, II and aVF, and II and III, among others. OBJ:   Identify the ECG changes that are associated with myocardial ischemia, injury, and infarction. 4. B. Patients who are experiencing an ACS who are most likely to present atypically include older  adults, diabetic individuals, women, patients with impaired renal function, patients with dementia, patients with prior cardiac surgery, and patients during the immediate postoperative period after  noncardiac surgery. OBJ: Explain atypical presentation and its significance in ACSs. 5. B. The effects of myocardial ischemia can be viewed on the ECG as STD and T wave changes in the leads that face the affected area of the ventricle. OBJ: Identify the ECG changes associated with myocardial ischemia, injury, and infarction. 6. A. Obtaining and reviewing a 12-lead ECG is part of the initial assessment of the patient presenting   with ischemic chest discomfort and important in determining an appropriate treatment plan. Obtain thefirst 12-lead ECG within 10 minutes of patient contact. Obtain a repeat 12-lead ECG with each set of vital signs, when the patient ’s symptoms change, and as often as necessary. OBJ: Explain the importance of the 12-lead ECG for the patient with an ACS. 7. B. Morphine is the preferred analgesic for patients with STEMI who experience persistent chest  discomfort unresponsive to nitrates. Other narcotics may be considered in patients allergic to morphine. NSAIDs are contraindicated in patients with STEMI. OBJ: Describe the initial management of a patient experiencing an ACS. 8. B. Cardiac biomarkers include CK-MB, myoglobin, TnI, and TnT. Cardiac troponins are the biomarkers of choice for diagnosing MI because of their increased specificity and sensitivity compared  with CK-MB. Ischemia-modified albumin has been recognized as a marker of inflammation and myocardial ischemia but has been less well studied than those previously mentioned. OBJ: Describe the initial management of a patient who is experiencing an ACS. 9. C. Non – enteric-coated chewable aspirin should be given as early as possible after presentation to patients with an ACS, assuming there are no contraindications to its use. The initial dose is 162 to 325 mg. OBJ: Describe the initial management of a patient experiencing an ACS.

CHAPTER 7   Acute Coronary Syndromes

10. C. RVI should be suspected when ECG changes suggesting an inferior infarction (ST elevation in leads II, III, and/or aVF) are observed. The most sensitive ECG signs of right ventricular injury  include 1 mm ST elevation in lead V 1  and in lead V 4R. Patients with RVI may present with, or  subsequently develop, hypotension caused by bradydysrhyth mias or caused by a reduction in preload after the administration of vasodilators such as NTG. OBJ: Explain the clinical and ECG features of a RVI.  Matching

11. N

21. H

12. K 

22. F 

13. E

23. C

14. T

24. P

15. M

25. I

16. D

26. R 

17. Q  

27. J

18. S

28. B

19. A 

29. G

20. L

30. O

CASE STUDY 7-1 ANSWERS 1. The general impression findings are abnormal (Appearance: normal; Breathing: normal; Circulation: abnormal skin color). OBJ: State three areas to assess when forming a general impression of a patient. 2. Assess the patient ’s breathing with regard to rate, quality, and regularity. Quickly estimate the patient ’s heart rate and determine the quality of the pulse (ie, fast or slow, regular or irregular,  weak or strong). Evaluate the patient ’s skin temperature, color, and moisture to assess perfusion. Perform a brief neurologic evaluation (ie, obtain a Glasgow Coma Scale score) and assess the need for a defibrillator. Ask a team member to attach a pulse oximeter, ECG monitor, and blood pressure monitor. Ask the airway team member to administer supplemental O 2  if indicated. Ask a team member to obtain the patient ’s baseline vital signs while you obtain, or direct a team member to obtain, a SAMPLE history and perform a focused physical examination. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 3. When a patient presents with symptoms suggestive of ischemia or infarction, initial care should include primary and secondary surveys and administration of supplemental oxygen (if indicated). Direct the IV team member to start an IV of normal saline. Because it should be obtained within 10 minutes of patient contact, order a 12-lead ECG. In addition, order laboratory studies including  cardiac biomarkers, electrolytes, and coagulation studies, and a portable chest radiograph. OBJ: Describe the initial management of a patient who is experiencing an ACS.

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4. Yes. Non – enteric-coated chewable aspirin should be given as early as possible after presentation to patients with an ACS, assuming there are no contraindications to its use. Although the patient currently takes 81 mg of aspirin daily, the recommended initial dose is 162 to 325 mg. OBJ: Describe the initial management of a patient who is experiencing an ACS. 5. Once the 12-lead ECG has been obtained, it should be reviewed carefully. Look at each lead for the presence of ST segment displacement (ie, elevation or depression). If ST segment displacement is present, note its displacement in mm. Inspect the T waves for any changes in orientation, shape, and size. Examine each lead for the presence of a Q wave. If a Q wave is present, measure its duration.  Assess for areas of ischemia or injury by assessing lead groupings. Remember: ECG evidence must  be found in at least two contiguous leads. OBJ: Explain the importance of the 12-lead ECG for the patient with an ACS. 6. When viewing the ECG of a patient experiencing an ACS, the presence of STE in the leads facing  the affected area suggests myocardial injury. OBJ:   Identify the ECG changes that are associated with myocardial ischemia, injury, and infarction. 7. STE is seen in leads V 1, V 2, V 3, and V 4. STE in these leads suggests an anteroseptal MI. STD is seen in leads II, III, aVF, V 5, and V 6. OBJ: Identify the ECG leads that view the anterior wall, the inferior wall, the lateral wall, the septum, the inferobasal wall, and the right ventricle. 8. Because the LAD supplies a large portion of the left ventricle, a blockage in this area can lead to complications such as left ventricular dysfunction, including left-sided heart failure and cardiogenic shock. An anterior infarction may cause dysrhythmias including PVCs, atrial flutter, or AFib. A blockage in the area of the septum, which contains the bundle branches, may result in right  BBB, left BBB (this is more common), second-degree AV block type II, and third-degree AV block. OBJ: Describe the initial management of a patient who is experiencing an ACS. 9. NTG dilates the capacitance vessels (ie, veins), which causes a reduction in ventricular filling and cardiac preload. NTG also dilates normal and atherosclerotic epicardial coronary arteries and increases coronary collateral flow. OBJ: Describe the initial management of a patient who is experiencing an ACS. 10. Before giving NTG, assess the degree of the patient ’s pain/discomfort using a 0-to-10 scale, duration, time started, activity being performed, and pain quality. Reassess (and document) the patient ’s  vital signs and level of discomfort after each dose. Make sure that the patient has not used a phosphodiesterase inhibitor such as sildenafil (Viagra) within 24 hours or tadalafil (Cialis) within 48 hours before NTG administration. The combination of a phosphodiesterase inhibitor and nitrates may result in severe hypotension. Nitrates should not be administered to patients with a  systolic blood pressure less than 90 mm Hg or 30 mm Hg or more below baseline, severe bradycardia  or tachycardia, or suspected RVI. OBJ: Describe the initial management of a patient who is experiencing an ACS. 11. Morphine, which is generally given in 2 mg increments, should be administered for pain relief. Give additional doses at 5- to 15-minute intervals. Reassess and document the patient ’s vital signs and level of discomfort after each morphine dose. OBJ: Describe the initial management of a patient who is experiencing an ACS. 12. Reperfusion therapy is recommended for all eligible patients with STEMI who present within 12 hours of symptom onset. Primary PCI is the recommended method of reperfusion when it  can be performed in a timely fashion by experienced professionals. When the patient has a STEMI, is a candidate for reperfusion, and is initially seen at a PCI-capable hospital, he or she should be sent  to the cardiac catheterization laboratory for primary PCI, which should be accomplished within 90 minutes (O’Gara, et al., 2013). OBJ: Describe the initial management of a patient who is experiencing an ACS.

CHAPTER 7   Acute Coronary Syndromes

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 American Heart Association. In Web-based integrated guidelines for cardiopulmonary resuscitation and emergency cardiovascular care—part 9: Acute coronary syndromes:  Eccguidelines.heart.org . O’Gara, P. T., Kushner, F. G., Ascheim, D. D.,Casey, Jr., D. E.,Chung, M. K., de Lemos,J. A., et al.(2013).2013  ACCF/AHA guideline for the management of ST-elevation myocardial infarction. J Am Coll Cardiol ,  61(4), e78 – e140. Pickham, D., & Sickler, K. (2012). Concomitant infarct locations identified with 15 lead electrocardiogram.  Heart  Lung Circ ,  21(Suppl 1), S34. Sapin, P. M., & Muller, J. H. (2003). Triggers of acute coronary syndromes. In C. Cannon (Ed.), Management of   acute coronary syndromes  (2nd ed., pp. 61 – 94). Totowa, NJ: Humana Press. Schoen, F. J., & Mitchell, R. N. (2010). The heart. In V. Kumar, A. K. Abbas, N. Fausto, & J. C. Aster (Eds.), Robbins and Cotran pathologic basis of disease  (8th ed., pp. 529 – 587). Philadelphia: Saunders. Scirica, B. M., & Morrow, D. A. (2015). ST-elevation myocardial infarction: Pathology, pathophysiology, and clinical features. In D. L. Mann, D. P. Zipes, P. Libby, R. O. Bonow, & E. Braunwald (Eds.),  Braunwald s heart  disease: A textbook of cardiovascular medicine  (10th ed., pp. 1068 – 1094). Philadelphia: Saunders. Seo, D. W., Sohn, C. H., Ryu, J. M., Yoon, J. C., Ahn, S., & Kim, W. (2011). ST elevation measurements differ in patients with inferior myocardial infarction and right ventricular infarction. Am J Emerg Med , 29(9), 1067 – 1073. Shah, P. K. (2003). Mechanisms of plaque vulnerability and rupture. J Am Coll Cardiol ,  41(4 Suppl S), 15S – 22S. Sovari, A. A., Assadi, R., Lakshminarayanan, B., & Kocheril, A. G. (2007). Hyperacute T wave, the early sign of  myocardial infarction. Am J Emerg Med ,  25 (7), 859.e1 – 859.e7. Stephens, K. E., Anderson, H., Carey, M. G., & Pelter, M. M. (2007). Interpreting 12-lead electrocardiograms for  acute ST-elevation myocardial infarction: What nurses know. J Cardiovasc Nurs ,  22(3), 186 – 195. Stub, D., Smith, K., Bernard, S., Nehme, Z., Stephenson, M., Bray, J. E., et al. (2015). Air versus oxygen in ST-segment elevation myocardial infarction. Circulation, 131(24), 2143 – 2150. Surawicz, B., & Knilans, T. K. (2008). Acute ischemia. In Chou s electrocardiography in clinical practice  (6th ed, pp. 124 – 161). Philadelphia: Saunders.  Thygesen, K., Alpert, J. S., & White, H. D. (2007). Universal definition of myocardia l infarction. J Am Coll Cardiol , 50 (22), 2173 – 2195.  Thygesen, K., Alpert, J. S., Jaffe, A. S., Simoons, M. L., Chaitman, B. R., & White, H. D. (2012). Third universal definition of myocardial infarction. Circulation, 126(16), 2020 – 2035. Vasaiwala, S. C., & Schreiber, R. (2008). Posterior myocardial infarction: Unique diagnosis to an elusive problem.  Am J Emerg Med ,  26(4), 520.e5 – 520.e6. Vorobiof, G., & Ellestad, M. H. (2011). Lead aVR: Dead or simply forgotten?  JACC Cardiovasc Imaging ,  4 (2), 187 – 190.  Wagner, G. S., Macfarlane, P., Wellens, H., Josephson, M., Gorgels, A., Mirvis, D. M., et al. (2009). AHA/   ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI:  Acute ischemia/infarction; a scientific statement from the American Heart Association Electrocardiography  and Arrhythmias Committee. J Am Coll Cardiol ,  53(11), 1003 – 1011.  Weitz, J. I. (2013). Antithrombotic drugs. In R. Hoffman, E. J. Benz, Jr., L. E. Silberstein, H. E. Heslop, J. I. Weitz, &   J. Anastasi (Eds.), Hematology: Basic principles and practice  (6th ed., pp. 2102 – 2119). Philadelphia: Elsevier.  Woo, K. C., & Schneider, J. I. (2009). High risk chief complaints I: Chest pain—the big three. Emerg Med Clin  North Am, 27 (4), 685 – 712.  Yamaji, H., Iwasaki, K., Kusachi, S., Murakami, T., Hirami, R., Hamamoto, H., et al. (2001). Prediction of acute left main coronary artery obstruction by 12 lead electrocardiography: ST segment elevation in lead aVR with less ST segment elevation in V1. J Am Coll Cardiol ,  38 (5), 1348 – 1354. ’  

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8

Acute Ischemic Stroke INTRODUCTION [Objective 1] Stroke is the fourth leading cause of death in the United States, after heart disease, cancer, and chronic lower respirato respiratory ry disease disease ( Jauch, et al., 2013 2013). ). The Americ American an Heart Heart Associ Associati ation on (AHA) (AHA) estima estimates tes that that on average, someone in the United States experiences a stroke every 40 seconds ( Mozaffarian, et al., 2015). 2015). Of the 795,000 strokes that occur in the United States each year, about 610,000 of these are first attacks, and 185,000 185,000 are recurr recurrent ent attacks attacks ( Mozaf Mozaffarian farian,, et al., 2015 2015). ). Nearly half half of stroke survivors survivors have residual residual deficits, including weakness or cognitive dysfunction, 6 months after stroke (Bushnell, (Bushnell, et al., 2014). 2014). In the United States women are more often institutionalized after stroke and have poorer recovery from stroke than men (Bushnell, (Bushnell, et al., 2014). 2014). Beforethe Beforethe introd introduct uctionof ionof fibrin fibrinoly olytic tic therap therapyy in thetreatmen thetreatmentt of stroke stroke,, a strokewas strokewas notalwaysviewed notalwaysviewed as a medical emergency as there was little to offer patients to stop the process (Saunorus ( Saunorus Baird & Bethel, 2011). 2011 ). It is now recognized that early identification of a stroke is essential so that emergency care can be initiated as rapidly as possible. Like the Chain of Survival that is used to describe the sequence of events needed needed to to survive survive sudden sudden cardiac cardiac arrest arrest,, the Stroke Stroke Chain Chain of Surviva Survivall is a metaph metaphor or for for the series series of events events that must occur during during the emergency emergency care of the possible possible stroke patient patient to optimize optimize his or her chances chances of  full recovery ( Table ( Table 8.1). 8.1). The chain consists of eight links, which are also referred to as the  “ Ds of stroke care”: detection, dispatch, delivery, door, data, decision, drug, and disposition ( Jauch, ( Jauch, et al., 2013). 2013 ).  Types of strokes, stroke systems of care, and the initial emergency care for acute ischemic stroke are discussed in this chapter.

ACLS Pearl  A stroke is also called a  brain attack.  The public is familiar with the phrase  heart attack.  Because a stroke happens in the brain rather than in the heart, the phrase  brain attack  may   may convey the events involved in a stroke more clearly to the public than the word  stroke.  The term  brain attack  and   and its application to stroke are credited to Vladimir C. Hachinski, MD, and John Norris, MD, who are neurologists from Canada. The NSA began using the term in 1990. The term   cerebrovascular accident, whic which h was was usedfor usedfor manyyear manyyears s as a syno synony nym m for for the the wordstro wordstroke ke,, has has lost lost favo favor,beca r,becaus use e stro stroke kes s are are not really accidents ( Zivin, Zivin, 2012 ).

DESIRED RESULTS

G O A L   Given a patient situation, and working in a team setting, competently direct the initial  emergency care for a patient experiencing an acute ischemic stroke.

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TABLE 8.1

Stroke Chain of Surviv Survival al

Chain Cha in Lin Link k

Descri Des cripti ption on

Detect Detection ion Dispat Dispatch ch Deliver Deliveryy

Recogn Recognitio ition n of stroke stroke sign signss and symp symptoms toms by by the pati patient, ent, famil family, y, or byst bystand anders ers Activa Activation tion of the the EMSS, EMSS, priorit priorityy EMSS EMSS disp dispatc atch, h, and and prom prompt pt EMSS EMSS respon response se Prompt Prompt trans transpor portt to an an appro appropria priate te stroke stroke hospit hospital al while while prov providin iding g appro appropria priate te preh prehosp ospital ital assessment and care as well as prearrival notification Immediate ED triage ED evalu evaluati ation on,, stro stroke ke team team activ activat ation ion,, labo labora rator toryy stud studie ies, s, and and brai brain n imagi imaging ng Decisio Decision n about about poten potential tial ther therapie apiess made made on the the basis basis of the the data data gather gathered ed and and stroke stroke type type,, location location (eg, carotid, vertebrobasilar), vertebrobasilar), and stroke severity Adminis Administra tration tion of approp appropriat riatee medicat medication ionss and postad postadmin ministr istratio ation n monitor monitoring ing Promp Promptt admiss admissionto ionto a strokeunit strokeunit,, intens intensivecareunit,or ivecareunit,or transf transfer er forongoingcareand forongoingcareand closeobser closeobservat vation ion

Door Data Data Decisio Decision n Drug Drug Disposition Disposition

ED, emergency department; EMSS, emergency medical services system

LEARNING OBJECTIVES

 After completing this chapter, you should be able to: 1. Discuss Discuss the links in the Stroke Stroke Chain of Survival. Survival. 2.   Discuss the brain’s arterial blood supply. 3.  Describe the major types of stroke. 4. Explain Explain what a transient transient ischemic ischemic attack (TIA) is and how it differs differs from stroke. 5.  Explain why rapid identification of stroke is critical. 6.  Differentiate between the hyperacute and acute phases of stroke care. 7.  Describe the initial emergency care for acute ischemic stroke. 8. Compare Compare elements of acute stroke care facilities in the United United States. State the recomm recommend ended ed target target times times for key interv intervent ention ions s during during the hypera hyperacut cute e phase phase of  9. State acute stroke care. 10.  Give examples of medical conditions that mimic stroke.

LEARNING PLAN • • • •

Read this this chapter before before class. class. Master identification of the following following rhythms: sinus sinus rhythm and atrial fibrillation Master the following following medications: medications: O2, dextrose, fibrinolytics Master the following skills: Ensure scene safety and the use of personal protective equipment. equipment. Assignteam Assignteam membe memberr roles roles or perfo perform rm as a team team member member in a simula simulated ted patien patientt situat situation ion.. Direct or perform an initial patient assessment. assessment. Recognize signs signs and symptoms symptoms of acute ischemic stroke. Develop Develop and implement implement a treatment plan on the basis of the patient patient’s presentation, history, physical examination, and diagnostic test results. Obtain Obtain vital signs, establish establish vascular access, access, attach a pulse oximeter oximeter and blood pressure and cardiac monitor, and give supplemental O2  if indicated. Know the actions, indications, indications, dosages, adverse effects, and and contraindications for the medications used in the treatment of acute ischemic stroke. If applicable, applicable, use a reperfusion reperfusion checklist checklist to evaluate evaluate the patient’s candidacy for  fibrinolytic therapy. Review Review your performance performance as a team leader or team member during during a postevent postevent debriefing. Develo Develop p and use flashc flashcard ards, s, flowch flowchart arts, s, and mnemo mnemonic nics s to help help enhanc enhance e your your retent retention ion of  the information presented. Complete Complete the chapter quiz and review the quiz answers answers provided. provided. Read the case study at the end of this chapter and answer answer the questions questions within the case study. Compare your answers with the answers provided. • • • • •

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CHAPTER 8  Acute Ischemic Stroke

KEY TERMS

comprehen hensive sive,, divers diverse e system system that that addres addresses ses all aspect aspects s of strok stroke e Strok Str oke e system system of care care   A compre care in a coordinated fashion. Transient ischemic attack (TIA)  A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.

DEFI DE FINI NITI TION ON OF ST STRO ROKE KE In 2013, the Stroke Council of the American Heart Association/American Stroke Association (AHA/   ASA) developed an updated definition of stroke for the 21st century (Sacco, et al., 2013). 2013). The expert  consensus document generated by this group notes that the term stroke  term stroke  should  should be broadly used to include all of the following (Sacco, (Sacco, et al., 2013): 2013): • Definition of central central nervous system (CNS) (CNS) infarction: CNS infarction infarction is brain, spinal cord, or retina retinall cell cell death attributable to ischemia, based on 1. Pathological, imaging, or other objective evidence of cerebral, cerebral, spinal cord, or retinal focal focal ischemic injury injury in a defined defined vascular vascular distributio distribution; n; or  2. Clinical evidence of cerebral, spinal cord, or retinal focal focal ischemic injury based on symptoms persisting 24 hours or more or until death, and other etiologies excluded. (Note: CNS infarction includes hemorrhagic infarctions, types I and II.) • Definition of ischemic stroke: An stroke: An episode of neurological dysfunction caused by focal cerebral, spinal, or  retinal infarction. (Note: Evidence of CNS infarction is defined above.) • Definition of silent CNS infarction: Imaging infarction: Imaging or neuropathological evidence of CNS infarction, without  a history of acute neurological dysfunction attributable to the lesion. Definition of intracerebral hemorrhage: A hemorrhage: A focal collection of blood within the brain parenchyma or ven• tricular system that is not caused by trauma. (Note: Intracerebral hemorrhage includes parenchymal hemorrhages hemorrhages after CNS infarction, infarction, types I and II.) • Definition of stroke caused by intracerebral hemorrhage: Rapidly hemorrhage: Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular  system that is not caused by trauma.  A focal collection of chronic blood products within the brain • Definition of silent cerebral hemorrhage: hemorrhage: A parenchyma, parenchyma, subarachnoid subarachnoid space, space, or ventricular ventricular system on neuroimagin neuroimagingg or neuropatho neuropathological logical examination that is not caused by trauma and without a history of acute neurological dysfunction attributable to the lesion. hemorrhage: Bleeding into the subarachnoid space (ie, the space between the • Definition of subarachnoid hemorrhage: Bleeding arachnoid membrane and the pia mater of the brain or spinal cord). • Definition Definition of stroke stroke caused caused by subarachnoid subarachnoid hemorrhage: hemorrhage:   Rapidly developing signs of neurological dysfunction and/or headache because of bleeding into the subarachnoid space (ie, the space between the arachnoid arachnoid membran membranee and the pia mater mater of the brain or spinal spinal cord), which is not caused caused by trauma. trauma. • Definition of stroke caused caused by cerebral venous thrombosis: thrombosis: Infarction or hemorrhage in the brain, spinal cord, or retina because of thrombosis of a cerebral venous structure. Symptoms or signs caused by  reversible edema without infarction or hemorrhage do not qualify as stroke. stroke, not otherwise specified: specified: An  An episode of acute neurological dysfunction presumed to • Definition of stroke, be caused by ischemia or hemorrhage, persisting 24 hours or more or until death, but without sufficient evidence to be classified as one of the above.

 ANATOMY REVIEW  [Objective 2]  The brain makes up about 2% of an adult ’s total body weight, it receives 15% to 17% of the total cardiac output, and it consumes about 20% of the oxygen used by the body (Haines (Haines & Lancon, 2013). 2013). The brain is supp suppli lied ed with with blood blood by the the inte interna rnall caro carotid tid and and vert verteb ebra rall arte arteri ries es (Fi Fig. g. 8. 8.11). The intern internal al carotid carotid arteri arteries es branch branch into into the anteri anterior or and middle middle cerebr cerebral al arteri arteries. es. Stroke Strokess involvin involvingg the caroti carotid d arteri arteries es are called called anterior circulation strokes  or  strokes  or    carotid territory strokes.  They usually involve the cerebral hemispheres. After 

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Right anterior cerebral Anterior communicating Right middle cerebral Left internal carotid

Right posterior cerebral

Left posterior communicating Left superior cerebellar

Basilar Anterior spinal

Left vertebral

Fig. 8.1 Arterial blood supply to the brain. (From Solomon Solomon EP. Introduction to human anatomy and physiology,  ed 3, St. Louis, 2009, Mosby.)

passing through the foramen magnum, the vertebral arteries join to form the basilar artery, which div ides into into right right andleft poster posteriorcere iorcerebra brall arteri arteries es ( Haines&Lancon,2013 Haines&Lancon,2013).Strokesaffectingthevertebralarter).Strokesaffectingthevertebralarteries are called called posterior  They usually affect the brainstem  posterior circulation strokes or  strokes or vertebr vertebrobasi obasilar lar territory territory strokes. strokes. They or cerebe cerebellum llum.. The anteri anterior or and poster posterior ior circul circulatio ations ns form form a circul circular ar connec connectio tion n of arteri arteries es called called the circle  of Willis, which Willis, which is located at the base of the brain. Because anatomic variations are frequent, particularly in the vertebral artery system, the area supplied with blood by a given artery is not entirely predictable; as a  result, result, stroke stroke syndro syndromes mes do not always always correl correlate ate well well with with the locati location on of the vascul vascular ar injury injury (Zivi Zivin, n, 201 20122).

ACLS Pearl Most individuals will lose consciousness if the brain is deprived of blood and oxygen for 10 to 12 seconds; in the absence of hypothermia, irreparable brain damage or death may result after  3 to 5 minutes ( Haines Haines & Lancon, 2013 ). 2013 ).

STRO ST ROKE KE TY TYPE PES S ACLS Pearl For many years, the primary types of stroke were categorized as either ischemic or hemorrhagic. Experts now recommend that the term  hemorrhagic stroke  be discontinued because the term is confusing; confusing; it can refer to primary primary subarachno subarachnoid id hemorrhag hemorrhage e (SAH), (SAH), primary primary intracereb intracerebral ral hemorrhage hemorrhage (ICH), (ICH), or hemorr hemorrhag hage e after after infarc infarctio tion n that that occursspont occursspontane aneous ously ly or becaus because e of antith antithrom rombot botic ic or fibri fibri-nolytic therapy ( Sacco, Sacco, et al., 2013 ).

Subarachnoid Hemorrhage [Objective 3] SAH SAH is blee bleedin dingg into into thesubara thesubarachn chnoidspac oidspace. e. Blood Blood in the the suba subara rach chnoi noid d spac spacee may may be theresult theresult of traumaor  traumaor  nontrau nontraumat matic iccaus causes essuchas suchas a ruptur ruptured edcere cerebra brall aneurysmor aneurysmor an arteri arterioven ovenousmalfor ousmalformati mation on(( Fig.8.2 Fig.8.2).About  ).About  3% of all strokes are the result of SAH (Mozaffar ( Mozaffarian, ian, et al., 2015). 2015). Pati Patien ents ts ofte often n repo report rt a sudde sudden n onse onsett of a seve severe re head headac ache he or desc descri ribe be the the feel feeling ing as “the worst worst headac headache he of my life life..” Associated signs and symptoms vary and may include vomiting, focal neurologic deficits, neck  stiffness, dizziness, visual disturbances (eg, blurry or double vision), loss of consciousness, and seizures.

CHAPTER 8  Acute Ischemic Stroke

A

Subarachnoid hemorrhage

Intracerebral hemorrhage

Ruptured cerebral aneurysm

Ruptured blood vessel

B

Cerebral thrombosis

Cerebral embolism

Fig. 8.2  A, SAH, ICH. B, Ischemic stroke. (From Brooks ML, Brooks DL.   Exploring medical language, a student-directed  approach,  ed 9, St. Louis, 2014, Mosby.)

 Warning or sentinel signs and symptoms can occur minutes to weeks before a rupture because of blood leakage or because of nerve compression as the aneurysm expands. The sudden onset of a severe headache, vision problems, and nausea and vomiting are examples of possible warning signs and symptoms. Misdiagnosis or delayed diagnosis in patients with SAH is common because of the variability in types of  headaches and associated symptoms (Nentwich ( Nentwich & Veloz, 2012). 2012). Frequent vital sign checks including oxygen saturation readings, electrocardiogram (ECG) monitoring, and neurologic assessments are essential. ECG changes that may be observed in the acute phase of  SAH include peaked or deeply inverted T waves and increased U wave amplitude. The patient should be admitted to a neurologic intensive care unit for continuous monitoring for bleeding, hydrocephalus,  vasospasm, and other potential complications.

Intracerebral Intracer ebral Hemorr Hemorrhage hage [Objective 3]  About 10% of all strokes are the result of an ICH (Mozaffarian, (Mozaffarian, et al., 2015). 2015). Patients who experience an ICH have a 30-day mortality rate of 30% to 50%, with 75% of patients severely disabled or deceased at  1 year (Brouwers (Brouwers & Goldstein, 2012). 2012 ). Chronic hypertension and aging are among the risk factors associated with ICH. ICH is most often caused by the spontaneous rupture of small arteries within the substance of the brain. Less common causes of ICH include aneurysm, arteriovenous malformation, hemorrhagic transformation of ischemic stroke, and neoplasms (Brouwers ( Brouwers & Goldstein, 2012). 2012). Signs and symptoms may  include a severe headache, vomiting, neck stiffness, seizures, and coma or decreased level of consciousness. ness. Sympto Symptoms ms may progre progress ss over over minutes minutes or hours. hours. Becaus Becausee none none of these these finding findingss are specif specific ic for ICH, ICH, neuroimaging is essential to establish a definitive diagnosis (Brouwers ( Brouwers & Goldstein, 2012). 2012). Rapid diagnosis nosis and approp appropria riate te manage managemen mentt are import important ant becaus becausee neurol neurologi ogicc deteri deteriora oratio tion n is common common in the first  first  few hours of ICH onset (Morgenstern, (Morgenstern, et al., 2010). 2010 ).

ACLS Pearl It is estimated that more than 20% of patients who experience an ICH will experience a decrease in the GCS score of two points or more between the prehospital assessment and the patient’s initial evaluation in the emergency department ( Morgenstern, Morgenstern, et al., 2010 ). 2010 ).

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 About 73% of patients with ICH experience ongoing bleeding after hospital arrival (Brouw Brouwers ers &  Goldstein, 2012). 2012). Admission to a neurologic intensive care unit is recommended with monitoring of  intracranial pressure and cerebral perfusion pressure, in addition to vital sign and oxygen saturation monitoring (Morgenstern, (Morgenstern, et al., 2010). 2010 ). During the acute phase of care, strategies to minimize ongoing  bleeding may include reversal of anticoagulation and modest blood pressure reduction (Brouwers ( Brouwers &  Goldstein, Goldst ein, 2012 2012). ). Select Selected ed patien patients ts may benefi benefitt from from hemato hematoma ma evacua evacuatio tion n or extern external al ventri ventricul cular ar draindrainage (Brouwers (Brouwers & Goldstein, 2012). 2012).

Ischemic Isch emic Str Stroke oke [Objective 3] Statistics indicate that 87% of strokes are ischemic (Mozaffarian, ( Mozaffarian, et al., 2015). 2015). An ischemic stroke, also stroke, is an infarction of CNS tissue that occurs when a blood vessel supplying  described as an occlusive an  occlusive stroke, is the brain is blocked. The middle middl e cerebral artery is the blood vessel most often inv olved in ischemic stroke (Zivin, 2012). 2012). It is estimated that about 20% of ischemic strokes are caused by atherosclerosis of the extracranial or intracranial segments of the carotid or vertebrobasilar arteries, about 25% are caused by penetrating artery disease, another 20% are caused by cardiogenic emboli, and the stroke cause is unknown in about 30% of cases (Summers, (Summers, et al., 2009). 2009). Ischemic strokes may be symptomatic or silent  (ie, asymptomatic) (Ea (East ston, on, et al al., ., 20 2009 09). ). Signs and symptoms symptoms of ischemic ischemic stroke are are shown in Table in Table 8.2. 8.2.  A thrombotic stroke is the most common cause of ischemic stroke. With a thrombotic stroke, a  thrombus (ie, blood clot) develops in arteries that perfuse the brain (see  Fig. 8.2). 8.2). When the blood clots are of sufficient size to block blood flow through the artery, the area that was previously supplied by that  artery becomes ischemic. Ischemia is poorly tolerated by the brain because the brain is unable to store the glucose it needs to function. The patient ’s signs and symptoms depend on the location of the artery  affected affected and the areas of brain ischemia. ischemia.  With an embolic stroke, material from an area outside of the brain (eg, heart, aorta, other major artery) becomes dislodged and travels through the bloodstream to the brain (ie, cerebral embolism). Embolic TABLE 8.2

Signs and Symptom Symptoms s of Ischemic Ischemic Stroke

Affe Af fect cted ed Ar Arte tery ry

Clin Cl inic ical al Sig Signs ns an and d Sym Sympt ptom omss

 Anterior cerebral

Behavioral changes, emotional lability, impaired decision-making ability (especially if bilateral bilateral infarction) infarction) Contralateral hemiparesis Contralateral Contralateral sensory sensory loss Loss of coordination coordination Urinary incontinence Amnesi Amnesiaa Disturbances Disturbances in gait, speech, swallowing, vision Quadriplegia or hemiplegia  Vertigo Alte Altered red level level of resp respons onsiv iven enes esss Headaches Ipsilateral blindness Profound aphasia Weakness, paralysis, numbness, sensory changes, and visual deficits (eg, blurring) on the affected side Cont Contral ralat atera erall hemi hemipa pares resis is Contralateral Contralateral sensory sensory loss Contralateral Contralateral visual field deficits Deviation of the eyes to the side of the lesion Language deficit (dominant hemisphere) Spatial-perceptual deficit (nondominant hemisphere) Contral Contralate ateral ral sensor sensoryy impairm impairment ent or loss loss Inability to recognize familiar faces Ipsilateral Ipsilateral visual field deficits deficits Memory impairment 

Basilar Basilar and vertebr vertebral al

Inte Interna rnall caro carotid tid

Midd Middle le cereb cerebral ral

Poster Posterior ior cerebra cerebrall

CHAPTER 8  Acute Ischemic Stroke

Area of permanent damage Penumbra, area of salvageable damage Normal brain external to penumbra

Fig. 8.3 After an occlusive stroke, the penumbra is an interface between a region of permanent tissue damage and an area that will most likely survive. Rapid and appropriate treatment, with reperfusion of the penumbra, may salvage this region and reduce the neurologic deficits suffered by the patient. (From Haines DE.  Fundamental neuroscience for basic and clinical  applications,  ed 4, Philadelphia, 2013, Saunders.)

material may consist of fragments of tumors or plaques; air; fat; amniotic fluid; a foreign body; or a blood clot. An embolus tends to become lodged where arteries branch, because blood flow is most turbulent in these areas. Fragments of the embolus may become lodged in smaller vessels. Atrial fibrillation is the cardiac source of emboli in 50% of cardioembolic strokes ( Babarro, et al., 2009). As with thrombotic strokes, the patient ’s signs and symptoms depend on the location of the artery affected and the areas of  brain ischemia. Lacunar strokes, also called lacunar infarcts, are small infarctions caused by the blockage of a penetrating branch of a large cerebral artery. Lacunar strokes are usually associated with chronic hypertension, diabetes, and hyperlipidemia, and they most often occur in the basal ganglia, thalamus, cerebellum, white matter of the internal capsule, and pons. Blockageof a cerebral artery usually results in a core area that is irreversibly damaged within minutes or  hours (Nolte, 2009). The area of dead tissue is often surrounded by an area of hypoperfused tissue called the ischemic penumbra   or the transitional zone  (Fig. 8.3). The penumbra is supplied with blood by collateral arteries that connect with branches of the blocked vessel. Brain cells in the penumbra may be sal vaged depending on how quickly blood flow is restored. The earlier the treatment for stroke is given, the more favorable the results are likely to be.

 Transient Ischemic Attack  [Objective 4]  A transient ischemic attack (TIA),  also called a  ministroke, a  warning stroke, or a  transient stroke, is “a  transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without  acute infarction” (Easton, et al., 2009). A TIA is one of the most important warning signs of acute stroke. It is estimated that about 15% of all strokes are preceded by a TIA (Mozaffarian, et al., 2015). Most TIAs last less than 2 hours, but prolonged episodes do occur (Easton, et al., 2009).

STROKE SYSTEMS OF CARE [Objectives 5, 6] Forseveral years,organizationssuchas theBrain AttackCoalition(BAC),the AHA/ASA, andthe National Stroke Association(NSA)havebeen activein thedevelopmentof initiativesdesigned to optimizestrokecare

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in theUnited States. In 2000 the BAC recommended the establishment of primarystroke centers (PSCs) as an approach to improve the medical care of patients with stroke ( Alberts, et al., 2000). In 2005 the BAC published recommendations for comprehensive stroke centers (CSCs) ( Alberts, et al., 2005). During the same year, the AHA/ASA published recommendations with regard to the establishment of a stroke system of care, recognizing that U.S. citizens should have access to the full range of activities and services associated with stroke prevention and the timely identification, transport, treatment, and rehabilitation of  stroke patients regardless of geographic location, geopolitical boundaries, or socioeconomic disparities (Schwamm,etal.,2005). A strokesystemofcare isacomprehensive,diversesystemthataddressesallaspects ofstrokecareinacoordinatedfashion( Silva&Schwamm,2013).Itincludesthespectrumofstrokecarefrom primary prevention to activation of emergency medical services (EMS), acute care, secondary prevention, rehabilitation and return to the community (Silva & Schwamm, 2013). In acute stroke management, the phrase  “ time is brain ” or  “ time lost is brain lost ” reflects the need for  rapid assessment and intervention, because delays in diagnosis and treatment may leave the patient neurologically impaired and disabled (Gorelick, et al., 2008). The hyperacute phase of stroke care  refers to the key interventions involved in the assessment, stabilization, and treatment in the first hours after stroke onset (Casaubon & Suddes, 2013). During this time-sensitive phase, which encompasses all prehospital and initial emergency care for TIA and stroke, attention is focused on identifying stroke symptoms and stroke type, identifying treatment options, and executing the treatment plan as quickly as possible. The acute phase of stroke care  refers to key interventions involved in the assessment, treatment or management, and early recovery in the first days after stroke onset (Casaubon & Suddes, 2013). This phase focuses on confirming the cause of stroke and preventing medical complications, preparing the patient and family  for discharge, and establishing long-term secondary prevention measures (Summers, et al., 2009).

Public Education  The recognition of stroke signs and symptoms by the patient, family, or bystanders is critical. According to the AHA, a study was conducted of patients admitted to an emergency department with possible stroke to determine their knowledge of the signs, symptoms, and risk factors of stroke. Of the patients who were able to respond, 39% did not know a single sign or symptom and 43% did not know a single risk factor  (Mozaffarian, et al., 2015). Despite public education programs with regard to stroke warning signs (Box8.1),datashowthatfewer than half of 9-1-1calls forstrokeeventsweremadewithin 1 hour of symptom onset, andfewer than half ofthosecallers thoughtstrokewas thecauseof theirsymptoms ( Jauch,et al., 2013).  The intravenous (IV) administration of tissue plasminogen activator (tPA) has proved to be an effective cerebral reperfusion therapy. Currently, the window of opportunity for the use of IV tPA for the treatment of ischemic stroke is within 3 hours of symptom onset in a broad range of patients and between 3 and 4.5 hours of symptom onset in a more selective spectrum of patients. Unfortunately, delay in seeking treatment is a common reason for ineligibility for tPA. The main causes for delayed patient presentation to an emergency department include a lack of patient and public awareness of stroke signs and symptoms, the urgency of immediate care, and the need to call 9-1-1 for EMS activation (Higashida, et al., 2013). Despite efforts to educate the public about the importance of calling 9-1-1 upon recognition of stroke signs and symptoms, a significant percentage of patients (up to 50% in some studies) with an acute or subacute stroke present at a hospital by means of a private car, taxi, or another  mode of transportation (other than an ambulance) (Higashida, et al., 2013).

Emergency Medical Services Emergency medical services systems (EMSSs) play a critical role in optimizing stroke care ( Jauch, et al., 2013). Activation of the EMSS, priority EMS dispatch, prompt EMS response, triage and stabilization in the field, and ground or air ambulance transport are important components with regard to EMS and

BOX 8.1 •

• •

Stroke Warning Signs –  The Five “Suddens”

Sudden difficulty speaking (eg, an inability to say what is meant, slurred speech) Sudden dizziness Suddensevere headache with no knowncause

• •

Sudden visual changes in one or both eyes Sudden weakness or numbness of the face, arm, or leg (particularly on one side of the body)

CHAPTER 8  Acute Ischemic Stroke

the care of the stroke patient. Advance notification of stroke patient arrival by EMS personnel shortens the time to be seen for initial evaluation by an emergency physician, shortens the time to brain imaging, and increases the use of IV tPA ( Jauch, et al., 2013).  A 2007 AHA/ASA policy statement addressed specific parameters with regard to EMS and stroke systems of care, including the following ( Acker, et al., 2007): • All 9-1-1 call centers should use dispatch guidelines that prioritize patients experiencing stroke as requiring a high-priority EMS response at the highest care level available. The period between the receipt of the call and the dispatch of the response team should be less than • 90 seconds for 90% of calls involving stroke. To rapidly and accurately identify acute stroke patients, EMS personnel should use validated stroke • screening algorithms for the prehospital setting (eg, Cincinnati Prehospital Stroke Scale [CPSS], Los  Angeles Prehospital Stroke Screen [LAPSS]). After identifying a stroke patient using a validated screening form, EMS personnel should use validated stroke severity scales developed specifically  for prehospital use (eg, Los Angeles Motor Scale, Shortened National Institutes of Health Stroke Scale [NIHSS]). The EMSS response time should be less than 9 minutes at least 90% of the time for suspected acute • stroke patients. Response time  reflects the amount of time elapsed from the receipt of the call by the dispatch entity to the arrival on the scene of a properly equipped and staffed ambulance. The dispatch time, which is the interval between the time a call is received at the EMS answering point  • and the time the EMS unit is selected and notified of the need to respond, should be less than 1 minute. The  turnout time, which is the interval between the time the EMS unit is notified of the need to • respond and the time the EMS unit starts moving (ie, wheels turning), should be less than 1 minute. The on-scene time, which is the amount of time spent with the patient before the start of transport, • should be less than 15 minutes (unless there are extenuating circumstances or extrication difficulties). Stroke system transport protocols should be developed collaboratively with prehospital and hospital • providers, as well as with other stakeholders. Transport destination protocols should reflect optimal patient care with transport to a stroke center. Protocols for the transfer of stroke patients from non  –  stroke center hospitals to stroke centers should be established. Stroke patients should be transported to stroke-ready hospitals regardless of the patients ’  geopolitical location. Prearrival notification of hospitals should be provided for all suspected stroke patients. • Prehospital Assessment and Management [Objective 7] Prehospital professionals should quickly perform a primary survey andstabilize thepatient ’s airway, breathing, and circulation (ABCs) as necessary. A focused history should be obtained and the patient ’s normal baseline mentalstatusdetermined.Because families often confuse thetype of symptom onset with thetime thepatient   wasfound,the patient, patient ’s family,coworkers,or othersat thesceneshouldbeasked when thepatient was last known to be symptom-free (ie, last known normal or last known-well time) (Demaerschalk, et al., 2016). Determining and documenting the timeof symptom onset is critical and the single most important determinant of treatment options during thehyperacute phase of strokecare (Summers, et al., 2009). Allmedications that the patient is currently taking should be collected and documented. Medications that are particularly  important include anticoagulants, antiplatelet agents, antihypertensives, insulin, oral hypoglycemics, and sympathomimetics. Ascertain if the patient has a history of conditions that increase the likelihood that his orher symptomsarecausedbystrokesuchaspreviousTIAs andtheirfrequency,priorstroke,seizures,diabetes mellitus, hypertension, and atrial fibrillation ( Jauch, et al., 2013).  A neurologic assessment should be performed using a validated prehospital stroke screening tool.  Three commonly used screening tools include the CPSS, the LAPSS, and the Face Arm Speech Test  (FAST). The CPSS is taught as the three Ds of  “d rift (arm), d roop (facial weakness), and  d  ysarthria  (slurred speech). ”   The FAST assesses facial droop, arm drift, and speech (dysarthria and aphasia), and the time of symptom onset. If stroke is suspected, use a validated stroke severity scale to rate the severity of the stroke. The Los Angeles Motor Scale, which assigns point values to the LAPSS items of facial weakness, arm strength, and grip, is often used for this purpose. More recently, the Rapid Arterial oCclusion Evaluation (RACE) scale has been used to help identify large vessel occlusions (Perezdela  Ossa, et al., 2014). The RACE scale, which is based on the NIHSS, assesses the following areas in patients with suspected acute ischemic stroke: facial palsy (scored 0 to 2), arm motor function (0 to 2), leg motor function (0 to 2), gaze (0 to 1), and aphasia (if right hemiparesis is present) or agnosia  (if left hemiparesis is present) (0 to 2). 

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Regardless of the stroke scale used, if the patient ’s assessment findings and symptoms suggest an acute stroke, immediately begin transport as soon as the patient s condition is assessed as stable  (ie, load and go) to a  stroke-ready hospitaland notify thereceiving facility thatthe patientis in transit. Considerair medicaltransport when ground transport to the nearest stroke-ready hospital is longer than 1 hour ( Jauch, et al., 2013). Perform a secondary survey during transport as dictated by the patient ’s condition. Monitor the patient ’s breathing effort and be prepared to assist ventilations. Apply a pulse oximeter and a cardiac monitor. Use the least invasive method possible to maintain oxygen saturation above 94% ( Jauch, et al., 2013). Obtain a 12-lead ECG and establish IV access with normal saline. Avoid dextrosecontaining fluids in nonhypoglycemic patients because these solutions can worsen cerebral injury  ( Jauch, et al., 2013). Check the patient ’s serum glucose level; this helps to differentiate stroke from other  common causes of stroke symptoms (eg, hypoglycemia). Give dextrose if the patient is hypoglycemic. If  consistent with local protocols, obtain blood samples for laboratory testing and transfer the samples to receiving facility staff on arrival. Do not delay transport to perform these procedures.  A supine position is recommended if the patient is not hypoxic and can tolerate it ( Jauch, et al., 2013). Elevate the head of the stretcher 15 to 30 degrees if the patient is at risk for airway obstruction or aspiration or if increased intracranial pressure is suspected ( Jauch, et al., 2013). Monitor vital signs at least  every 15 minutes and more frequently if any vital sign is abnormal. In general, hypertension should not be treated in the prehospital setting. Hypotension should be treated in accordance with the underlying cause of the hypotension. Encourage family members or bystanders to accompany the patient to the hospital so they can provide historical information to the stroke team and provide support to the patient. If the patient ’s family cannot  go to the hospital, obtain a telephone number where they can be contacted, preferably a cell phone number, andbe certain to documentthis information forsubsequent retrievalby othermembers ofthehealth care team. Because strokes are dynamic processes, reassess the patient often during transport. Document any  changes in the patient ’s presentation from your initial assessment findings and relay this information to the appropriate staff on arrival at the receiving facility. ’  

Stroke Centers [Objectives 8, 9]  At present, acute stroke care in the United States consists of a tiered system of hospitals: nonstroke hospitals, acute stroke – ready hospitals (ASRHs), PSCs, and CSCs ( Table 8.3). Acute stroke teams (ASTs) are a key element for the delivery of stroke care within a stroke center. The AST is responsible for  TABLE 8.3

Comparison of Elements of Acute Stroke Care Facilities

Element

NonStroke Center

 Access to neurosurgical services  AST available

No

IV tPA capability 24/7

No

Rapid brain imaging 24/7

No

Stroke unit

No

Typical bed count 

20 to 50

No

ASRH

PSC

CSC

Yes, avail able within 3 hours or by transfer At bedside within 15 min 60-min or less doorto-needle time

 Yes, available within 2 hours, in-house or by transfer  At bedside within 15 min

 Yes, 24/7 coverage

Completed and read within 45 min of  order Not required unless patient admitted 30 to 100

Completed and read within 45 min of order

60-min or less door-toneedle time

Required for admitted patients 100 to 400

At bedside within 15 min 60-min or less door-to-needle time Completed and read within 45 min of  order Required for admitted patients 400 to 1500

 ASRH, acute stroke–ready hospital; AST, acute stroke team; CSC, comprehensive stroke center; IV, intravenous; PSC, primary stroke center; tPA, tissue plasminogen activator Sources: ( Alberts, et al., 2013; Higashida, et al., 2013)

CHAPTER 8  Acute Ischemic Stroke

responding to patients with an acute stroke and initiating diagnostic testing and immediate care (not  ongoing in-hospital care) ( Alberts, et al., 2011).  The role of an ASRH is to stabilize the patient, provide specific acute stroke care therapies, and arrange transportation of patients to the nearest PSC or CSC as determined by the patient ’s clinical status (Higashida, et al., 2013). Minimum staffing of the AST at an ASRH should include a nurse (or nurse practitioner or physician assistant) and a physician who have received training in acute stroke care ( Alberts, et al., 2013). Stroke team members should be available 24 hours a day, 7 days a week, responding   within 15 minutes of patient arrival ( Alberts, et al., 2013). An ASRH should establish a telemedicine link  to a PSC or CSC within 20 minutes of when it is deemed medically necessary ( Alberts, et al., 2013). This link can be used to obtain clinical stroke expertise, interpret brain imaging, initiate fibrinolytic therapy if  indicated, and address issuessuch as active bleeding or high intracranialpressures(Higashida, et al.,2013). PSCs are able to care for the majority of stroke patients with typical ischemic strokes who do not require endovascular therapy, neurosurgical interventions, or intensive care unit  – level care or who have multisystem disease(Higashida,etal.,2013).Intensivecareunit  – levelcareisofferedbysomePSCs(Higashida,etal.,2013). CSCs are capable of providing care for the most complex stroke patients, including those with large ischemic strokes, all types of hemorrhagic strokes, or multisystem involvement, as well as those who require surgical or endovascular interventions and intensive care unit  – level care (Higashida, et al., 2013). Established recommended target times for hospitals that receive acute stroke patients include the following: (1) emergency department physician evaluation within 10 minutes of arrival; (2) stroke team notification within 15 minutes of arrival; (3) brain computed tomography (CT) scan within 25 minutes of arrival; (4) interpretation of the CT scan within 45 minutes of arrival; (5) if indicated, door-to-drug  time of 60 minutes or less from arrival in the emergency department for at least 80% of patients; (6) and door-to-stroke-unit admission within 3 hours of arrival ( Jauch, et al., 2013). Triage and Initial Evaluation [Objective 7] Proper triage of stroke patients requires that emergency nurses be familiar with both typical and unusual stroke presentations (Summers, et al., 2009). Within minutes of the patient ’s arrival, reassess the patient ’s  ABCs and ensure that the patient has a secure airway and adequate breathing. Assess the patient ’s temperature,heartrate, blood pressure,ventilatoryrate,and oxygen saturation. Give oxygenif neededto maintain an oxygen saturation above 94%; supplemental oxygen is not recommended in nonhypoxic patients  with acute ischemic stroke ( Jauch, et al., 2013).Performa fingerstick glucose test toassessfor hypoglycemia  and administer dextrose if the blood glucose is less than 60 mg/dL ( Jauch, et al., 2013).  A minimum of two IV lines should be established if it is anticipated that the patient will receive fibrinolytic therapy. One site is used for infusing IV fluids (ie, normal saline) and medications and the other is used for the administration of tPA. Generally, normal saline is infused at a rate of 75 to 100 mL/hr to maintain normovolemia (Summers, et al., 2009) unless contraindications exist (eg, renal failure, heart  failure, pulmonary edema).  All patients with suspected acute stroke should receive continuous ECG monitoring to detect myocardial ischemia and cardiac dysrhythmias (eg, atrial fibrillation) and monitoring should be continued for  at least the first 24 hours after stroke ( Jauch, et al., 2013). A 12-lead ECG should be obtained to evaluate for preexisting cardiac disease and concurrent myocardial injury (Gorelick, et al., 2008). Patient History  [Objective 7] Verify the patient ’s last known-well time. Was anyone with the patient with his or her symptoms started?  What was the patient doing when the symptoms began? Did the patient complain of a headache? Did he or she have a seizure? Has there been a change in his or her level of responsiveness? Is there a history of  any recent trauma? Review the patient ’s past medical history and determine the presence of stroke risk  factors. Ask if there is any history of drug abuse, migraine, seizure, infection, trauma, or pregnancy  ( Jauch, et al., 2013). Find out the medications the patient is currently taking and his or her allergies to medications. Physical Examination [Objectives 7, 10]  When performing a physical examination, consider the presence of conditions that mimic stroke (Box 8.2). Examine the head and face for signs of trauma or recent seizure activity (eg, contusions, tongue

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BOX 8.2

Conditions That Mimic Stroke

  Bell’s palsy • CNS abscess or tumor •   Complicated migraine

•

•

Concussion with head injury   Conversion disorder • Drug toxicity (eg, carbamazepine, lithium, phenytoin) •   Eclampsia

•

•

•

•

•

  Encephalitis, meningitis   Hypertensive encephalopathy Metabolic disorders (eg, hyperglycemia, hypoglycemia, hyponatremia)   Positional vertigo   Seizures   Subdural hematoma

•

  Wernicke’s encephalopathy

• •

laceration). Auscultate the neck for carotid bruits, which suggests the presence of carotid atherosclerotic disease. Assess for jugular venous distention, which may be a sign of heart failure. Auscultate heart  sounds, which may reveal murmurs or gallops, and lung sounds. Examine the extremities for asymmetric strength and movement and asymmetric or diminished pulses. Inspect the skin for petechiae, purpura, or  ecchymoses, which may be the result of trauma, a platelet disorder, or a coagulation disorder. Neurologic Examination [Objective 7] Perform a brief neurologic screening assessment using a validated stroke scale. If the initial history, physical examination, and neurologic examination are suggestive of stroke, the stroke team should be mobilized.  The NIHSS is widely used and takes less than 10 minutesto perform. Trainingis required to use the scale accuratelyand to ensure interraterreliability. Useof theNIHSS is helpful in objectively ratingstroke severity, promoting comparisons with NIHSS examinations performed by other members of the stroke team (Nye,etal.,2012), recognizing (anddocumenting) improvement or deterioration in the patient ’s neurologic status, improving communication among members of the health care team, providing prognostic information, and influencing acute treatment decisions. The NIHSS assigns points for neurologic deficits with possible scores ranging from 0 to 42; the lower the score, the less the impairment. A score of 0 indicates no impairment, a score between 1 and 20 indicates mild to moderate impairment, and a score of more than 20 indicates severe impairment. An increase of 2 or more points on serially administered NIH stroke scales suggests stroke progression, although smaller changes may be equally significant. Diagnostic Tests [Objective 7] Diagnostic laboratory tests should be drawn immediately and before IV fluids are started. Of the laboratory tests recommended during the initial emergency evaluation (see  Box 8.3), only the assessment of  blood glucose must precede the initiation of IV tPA ( Jauch, et al., 2013).  Additional diagnostic studies should be obtained in selected cases such as pregnancy testing, blood alcohol level, blood and urine toxicology screen (for patients with possible substance abuse), blood cultures (if endocarditis is suspected), liver function tests and ammonia level (for patients with an unexplained altered level of consciousness), lumbar puncture (for suspected meningitis or if SAH is suspected and CT is negative for blood), electroencephalogram (for suspected seizures), and arterial blood gas tests (for suspected hypoxia).  The usefulness of chest radiography in the absence of clinical evidence of underlying pulmonary, cardiac, or vascular disease is unclear; if chest radiographs are obtained, they should not delay administration of IV tPA unless there are specific concerns about intrathoracic issues, such as aortic dissection ( Jauch, et al., 2013). BOX 8.3 • • •

•

Laboratory Studies for Suspected Stroke

Activated partial thromboplastin time Cardiac biomarkers; troponin is preferred Complete blood count, including platelet count Prothrombin time or international normalized ratio

• • •

Renal function tests Serum electrolytes Serum glucose

CHAPTER 8  Acute Ischemic Stroke

Brain Imaging [Objective 7]  A noncontrast brain CT or brain magnetic resonance imaging (MRI) scan should be obtained for all patients with suspected acute ischemic stroke to confirm or exclude the presence of cerebral hemorrhage ( Jauch, et al., 2013). Although MRI has been shown to be equivalent to CT in the detection of acute hemorrhage, CT remains the traditional initial imaging modality for the evaluation of suspected stroke because of its widespread availability, short acquisition time of 1 to 2 minutes, noninvasiveness, and general safety for both stable and unstable patients (Nentwich & Veloz, 2012). In patients presenting with a  history and clinical examination consistent with acute stroke, brain imaging is useful in determining  stroke location and vascular distribution, the presence of bleeding, the severity of ischemic stroke, and the presence of large-vessel occlusion ( Jauch, et al., 2013). Brain imaging is also useful for identifying  the size of the core of irreversibly infarcted tissue and determining the amount of hypoperfused tissue at  risk for subsequent infarction unless adequate perfusion is restored, which can affect treatment decisions (Nentwich & Veloz, 2012). Brain imaging should be completed within 25 minutes and interpreted  within 45 minutes of emergency department arrival ( Jauch, et al., 2013). Intravenous Fibrinolysis [Objective 7] Fibrinolytic therapy with IV tPA is recommended for selected patients who may be treated within 3 hours of onset of ischemic stroke ( American Stroke Association, 2014). IV tPA is recommended for administration to a select group of eligible patients who present within a 3- to 4.5-hour window after the onset  of acute stroke symptoms ( American Stroke Association, 2014). The eligibility criteria for treatment in this time frame are similar to those for patients treated within 3 hours of symptom onset, but with additional exclusion criteria. The AHA recommends that physicians review current inclusion and exclusion criteria to determine patient eligibility ( Jauch, et al., 2013). A recently published statement by the AHA/   ASA reflects the scientific rationale behind the eligibility criteria for the use of IV tPA in acute ischemic stroke (Demaerschalk, et al., 2016). Hospital and registry estimates of tPA treatment rates for stroke range from 20% to 30%, but national estimates of tPA use have ranged only from 3% to 5% since 2004 (Demaerschalk, et al., 2016). Reasons suggested for this low use include a lack of public education about stroke signs and symptoms and the need for rapid response, the slow adoption of tPA by the medical community, the complex systems  within the hospital necessary for safe and timely tPA administration, and the low eli gibility rate of ischemic stroke patients for tPA (Demaerschalk, et al., 2016). It is estimated that the eligibility for tPA within a population of ischemic stroke patients range from 6% to 8% of all strokes, with the most common reason for exclusion being delays in presentation for medical attention (Demaerschalk, et al., 2016). To reduce symptom onset  – to-treatment time, experts recommend that patients who are eligible for IV  tPA and who did not have intracranial vascular imaging as part of their initial evaluation should begin receiving IV tPA before being transported for additional imaging and before being transferred for endo vascular treatment (Powers, et al., 2015). IV tPA is a weight-based therapy. Although a small retrospective study found that documented estimated weights for patients receiving tPA were not significantly different from actual weights, it is preferable to obtain the patient ’s actual weight before tPA administration (Graves, et al., 2013).The tPA dose is 0.9 mg/kg, not to exceed 90 mg. Ten percent of the dose is given as an initial IV bolus over 1 minute followed by the remaining 90% of the dose infused using an infusion pump during the next hour. Calculate the desired dose, withdraw any excess amount from the vial, and then discard the excess amount to prevent accidental overdose (Summers, et al., 2009). Bleeding is the major complication of treatment with IV tPA. Although bleeding may occur from any  site, intracranial bleeding is of particular concern. Close monitoring of the patient is critical. In addition to using the NIHSS scale to assess neurologic deficits, assess pupil size, and use the Glasgow Coma Scale (GCS) to monitor the patient ’s level of responsiveness. These assessments should be performed every  hour for the first 24 hours after tPA administration and more often if indicated ( Summers, et al., 2009). The physician should be notified, the tPA infusion stopped (if tPA is still infusing), and an emergent CT scan obtained if the patient develops acute hypertension, nausea or vomiting, or severe headache, or if the patient has a worsening neurologic examination ( Jauch, et al., 2013). Closely observe for swelling of the tongue, lips, or oropharynx (ie, orolingual angioedema). Although this complication of tPA administration occurs in a small number of patients, it can lead to airway 

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obstruction. Patients taking angiotensin-converting enzyme inhibitors and those with infarctions that  involve the insular and frontal cortex appear to be at highest risk ( Jauch, et al., 2013). Treatment includes the administration of IV ranitidine, diphenhydramine, and methylprednisolone ( Jauch, et al., 2013). Measure the patient ’s blood pressure (BP) every 15 minutes during and after the tPA infusion for  2 hours, then every 30 minutes for 6 hours, and then every hour until 24 hours after the infusion ( Jauch, et al., 2013). Assess the patient ’s BP more frequently if his or her systolic BP is more than 180 millimeters of mercury (mm Hg) or if the diastolic BP is more than 105 mm Hg ( Jauch, et al., 2013). Administer antihypertensive medications per physician’s orders to maintain the patient ’s BP at or below these levels ( Jauch, et al., 2013). Obtain a brain CT or MRI scan 24 hours postinfusion before starting anticoagulants or antiplatelet agents ( Jauch, et al., 2013). Other Therapies [Objective 7] In addition to IV tPA, other therapies for acute ischemic stroke include invasive catheter-based reperfusion therapies that include intraarterial (IA) fibrinolysis, mechanical thrombectomy, or balloon angioplasty with or without stent placement (Ramee & White, 2014). Use of these therapies requires stroke centers with the resources and physician expertise to safely perform these procedures ( Jauch, et al., 2013). Patients eligible for IV tPA should receive IV tPA even if endovascular treatments are being considered (Powers, et al., 2015). Best Practices  Although current stroke guidelines recommend a door-to-needle time of 60 minutes or less for tPA administration to eligible ischemic stroke patients, research has shown that less than 30% of patients are treated within this period in the United States (Fonarow, et al., 2014). Target: Stroke is a national quality improvement program launched in 2010 by the AHA/ASA in partnership with other organizations. The program aims to assist hospitals in improving acute ischemic stroke care by reducing door-toneedle time for eligible patients being treated with tPA.  The primary goal during phase I of the program was for participating hospitals to administer tPA to at  least 50% of their patients with acute ischemic stroke within 60 minutes of hospital arrival ( American Stroke Association, 2014). After the start of the Target: Stroke initiative, research has shown a marked improvement in the timeliness of tPA administration, with the proportion of patients with a door-toneedle time of 60 minutes or less increasing from 29.6% to 53.3% (Fonarow, et al., 2014). Study results also showed that the improvement in timeliness in tPA administration was associated with improved clinical outcomes including lower in-hospital mortality, more frequent discharge to a more independently functioning environment, and lower rates of tPA complications, including symptomatic intracranial hemorrhage (Fonarow, et al., 2014). OnthebasisofthesuccessofphaseI,theAHA/ASAlaunchedphaseIItocontinueeliminatingtreatment  delays forpeople who suffer ischemicstrokes by challenginghospitals to provide tPAto eligiblepatients even more promptly ( American Stroke Association, 2014). The primary goal of phase II of Target: Stroke is to achieve a door-to-needle time within 60 minutes in 75% or more of acute ischemic stroke patients treated  with IV tPA; a secondary goal is to achievea door-to-needle time within 45 minutes in 50% or more of acute ischemic stroke patients treated with IV tPA ( American Stroke Association, 2014).  Target: Stroke encourages participating hospitals to adopt 11 evidence-based best practice strategies that can improve the speed with which tPA is administered in acute ischemic stroke. These strategies include the following ( American Stroke Association, 2014): • Encouraging prenotification of receiving hospitals by EMS personnel Using stroke-specific order sets, guidelines, and stroke tools • Using a rapid triage protocol to aid in the prompt recognition of stroke • Activating the entire stroke team with a single call or page, including notification to ensure prompt  • availability of the CT/MRI scanner  When appropriate, transferring eligible stroke patients from the emergency department triage area  • directly to the CT/MRI scanner for initial neurologic examination and brain imaging  Rapid acquisition and interpretation of brain imaging  • Rapid laboratory testing, including point of care testing if indicated • • Premixing tPA for high likelihood candidates, even before brain imaging  Prompt administration of IV tPA to eligible patients • Using a stroke team – based approach • Providing prompt and rapid feedback to the stroke team with regard to performance •

CHAPTER 8  Acute Ischemic Stroke

PUTTING IT ALL TOGETHER  The chapter quiz and case studies presented on the following pages are provided to help you integrate the information presented in this chapter. As you work through the case study, remember that there may be alternative actions that are perfectly acceptable, yet not presented in the case study. CHAPTER QUIZ

 Multiple Choice  Identify the choice that best completes the statement or answers the question.

____

1.

What is the most common cause of stroke?  A. A thrombus B. An embolus C. A ruptured cerebral aneurysm D. An arteriovenous malformation

____

2.

Paramedics are at the home of a 62-year-old man presenting with signs and symptoms suggestive of stroke. Which of the following is the most important question that  should be asked of this patient, family members, or others at the scene?  A. “ When did you last see a physician?” B. “ When did your symptoms begin?” C. “Do you have a history of hypertension? ” D. “ Are you currently taking any blood thinners?”

____

3.

Which of the following dysrhythmias is most likely to precipitate a stroke?  A. Junctional rhythm B. Atrial fibrillation C. Sinus bradycardia  D. Ventricular escape rhythm

____

4.

A 52-year-old woman presents with a sudden onset of numbness and weakness in her right arm and leg. Family members state her signs and symptoms began while the patient was preparing breakfast 1 hour ago. Examination reveals unequal grips with marked weakness on the patient ’s right side. Her blood pressure is 174/86 mm Hg, pulse 88 beats/min, and ventilatory rate 16 breaths/min. Her oxygen saturation on room air is 96%. As you establish vascular access, you note improvement in the patient ’s symptoms. After 25 minutes, her grips become equal and there is no  weakness on the patient ’s right side. You suspect:  A. Hypoglycemia  B. Acute ischemic stroke C. TIA D. SAH

____

5.

The acute phase of stroke care:  A. Includes prehospital care for stroke B. Seeks to identify stroke symptoms and stroke type C. Is a time-sensitive phase in the first hours after stroke onset  D. Focuses on confirming the cause of stroke and preventing complications

____

6.

During which of the following links of the Stroke Chain of Survival is immediate emergency department triage performed?  A. Data  B. Drug  C. Door  D. Delivery 

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____ 7.

For hospitals that receive acute stroke patients, a patient presenting with a possible stroke should be seen by a physician within __ of his or her arrival.  A. 5 minutes B. 10 minutes C. 25 minutes D. 45 minutes

____ 8.

Which of the following   must   be performed before IV tPA is administered?  A. Serum glucose B. Serum electrolytes C. Cardiac biomarkers D. Activated partial thromboplastin time

____ 9.

Fibrinolytic therapy with IV tPA is recommended for selected patients who may be treated within 3 hours of onset of ischemic stroke. Which of the following is a  contraindication to fibrinolytic therapy for this patient?  A. The patient ’s age is 55. B. The patient ’s symptoms began 45 minutes ago. C. The patient has an international normalized ratio of 2.2. D. The patient has a history of a myocardial infarction in 1996.

____

10.

Which of the following is true of acute stroke care facilities in the United States?  A. Neurosurgical coverage is available 24/7 at ASRHs. B. Acute stroke care facilities should have a stroke team at the patient ’s bedside within 15 minutes of arrival. C. Acute stroke care facilities should have IV tPA capability 24/7 with a 90-minute or  less door-to-needle time. D. The results of brain imaging should be obtained within 60 minutes of the order at a  stroke-ready facility.

CHAPTER 8  Acute Ischemic Stroke

CASE STUDY 8-1 Paramedics are called to a private residence for a 78-year-old man with a  “ possible stroke.” The patient ’s  wife is present. 1. The general impression reveals an elderly man sitting in a recliner. He is awake and aware of the paramedics’  approach. His breathing appears unlabored and equal chest risk and fall is observed.  The patient ’s skin color is pink. What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 2. The patient attempts to answer questions, but his speech is garbled. His breathing is quiet  and unlabored at a rate of 16 breaths/min. The patient ’s radial and carotid pulses are strong but  irregular. His skin is warm, pink, and dry. What should be done next? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 3. Differentiate between the CPSS and the Los Angeles Motor Scale. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 4. The examination reveals the patient has left facial droop, left arm drift, slurred speech, and a weak  left grip. His symptoms began about 35 minutes ago while watching television with his wife. The patient ’s blood pressure is 180/94 mm Hg, his heart rate is irregular at 80 to 110 beats/min, and the cardiac monitor reveals atrial fibrillation. The patient has a history of hypertension, for which he takes lisinopril and hydrochlorothiazide daily, and has no known allergies. What should be done now? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 5. The patient ’s glucose level is within normal limits. Why should the serum glucose level be determined during the initial management of a patient with suspected stroke? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 6. Describe the initial interventions that should be performed upon the patient ’s arrival in the emergency department. _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 7. The patient ’s oxygen saturation level is 96% on room air. Should supplemental oxygen be administered to this patient? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 8. Why is ECG monitoring recommended for patients with suspected acute stroke? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________

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9. The patient has a NIHSS score of 8. Shortly after physician evaluation and arrival of the stroke team, a brain CT scan is obtained and the results revealed no evidence of bleeding. After reviewing the inclusion and exclusion criteria for treatment with IV tPA, the decision is made to begin fibrinolytic therapy. How is this medication administered? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ 10. What assessments should be performed during and after treatment with tPA? _____________________________________________________________________________ _____________________________________________________________________________ _____________________________________________________________________________ CHAPTER QUIZ ANSWERS

1. A. Most strokes are the result of blockages caused by blood clots that develop within the brain artery  itself (ie, cerebral thrombosis) or clots that arise elsewhere in the body and then migrate to the brain (ie, cerebral embolism). OBJ: Describe the major types of stroke. 2. B. Determining and documenting the time of symptom onset is critical and the single most  important determinant of treatment options during the hyperacute phase of stroke care (Summers, et al., 2009). The patient, patient ’s family, coworkers, or others at the scene should be asked when the patient was last known to be symptom-free (ie, last known normal or last  known-well time). OBJ: Describe the initial emergency care for acute ischemic stroke. 3. B.  Atrial fibrillation is the cardiac source of emboli in 50% of cardioembolic strokes (Babarro, et al., 2009). OBJ: Describe the major types of stroke. 4. C. A TIA is a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. A TIA should be treated with the same urgency as a completed stroke. OBJ: Explain what a transient ischemic attack (TIA) is and how it differs from stroke. 5. D. The hyperacute phase of stroke care   refers to the key interventions involved in the assessment, stabilization, and treatment in the first hours after stroke onset (Casaubon & Suddes, 2013). During this time-sensitive phase, which encompasses all prehospital and initial emergency care for TIA and stroke, attention is focused on identifying stroke symptoms and stroke type, identifying treatment options, and executing the treatment plan as quickly as possible. The acute phase of   stroke care   refers to key interventions involved in the assessment, treatment or management, and early recovery in the first days after stroke onset (Casaubon & Suddes, 2013). This phase focuses on confirming the cause of stroke and preventing medical complications, preparing the patient and family for discharge, and establishing long-term secondary prevention measures (Summers, et al., 2009). OBJ: Differentiate between the hyperacute and acute phases of stroke care. 6. C. The door   link in the Stroke Chain of Survival refers to immediate emergency department triage upon the patient ’s arrival. OBJ: Discuss the links in the Stroke Chain of Survival. 7. B. For hospitals that receive acute stroke patients, a patient presenting with a possible stroke should be seen by a physician within 10 minutes of his or her arrival ( Jauch, et al., 2013). OBJ: State the recommended target times for key interventions during the hyperacute phase of  acute stroke care.

CHAPTER 8  Acute Ischemic Stroke

8. A. Of the laboratory tests recommended during the initial emergency evaluation of a patient with a  possible stroke, only the assessment of blood glucose must precede the administration of IV tPA ( Jauch, et al., 2013). OBJ: Describe the initial emergency care for acute ischemic stroke. 9. C. Some of the contraindications to fibrinolytic therapy include a history of previous intracranial hemorrhage, symptoms that suggest SAH, a patient who is anticoagulated and has an international normalized ratio greater than 1.7, significant head trauma or prior stroke within the last 3 months, and a systolic BP greater than 185 mm Hg or a diastolic BP greater than 110 mm Hg ( Jauch, et al., 2013). OBJ: Describe the initial emergency care for acute ischemic stroke. 10. B. Acute stroke care facilities should have a stroke team at the patient ’s bedside within 15 minutes of  arrival. Neurosurgical coverage is available 24/7 at a CSC; it is available within 2 hours, in-house, or  by transfer at a PSC; and it is available within 3 hours or by transfer at an ASRH. Acute stroke care facilities should have IV tPA capability 24/7 with a 60-minute or less door-to-needle time. Rapid brain imaging should be completed within 25 minutes of patient arrival and the results obtained  within 45 minutes of the order. OBJ: Compare elements of acute stroke care facilities in the United States.

CASE STUDY 8-1 ANSWERS 1. The next step is to perform a primary survey. Ask the patient questions to determine his level of  responsiveness and the adequacy of his airway and breathing. Quickly estimate the patient ’s heart  rate and determine the quality of his pulse (ie, fast or slow, regular or irregular, weak or strong). Evaluate his skin temperature, color, and moisture to assess perfusion. Perform a brief neurologic evaluation, assess the need for a defibrillator, and expose the patient for further evaluation. OBJ: Differentiate between the purposes and components of the primary and secondary surveys. 2. A focused history should be obtained and the patient ’s normal baseline mental status determined.  The patient, patient ’s family, or others at the scene should be asked when the patient was last known to be symptom-free (ie, last known normal or last known-well time). Determining and documenting  the time of symptom onset is critical and the single most important determinant of treatment  options during the hyperacute phase of stroke care (Summers, et al., 2009). OBJ: Explain why rapid identification of stroke is critical. 3. The CPSS is a commonly used stroke screening tool. The CPSS is taught as the three Ds of  “d rift  (arm), d roop (facial weakness), and d  ysarthria (slurred speech).” The Los Angeles Motor Scale is a  tool used to rate stroke severity in the field. It assigns point values to the LAPSS items of facial  weakness, arm strength, and grip. OBJ: Explain why rapid identification of stroke is critical. 4. Because the patient ’s assessmentfindings suggestan acute stroke, transport should begin immediatelyto a stroke-ready hospital. EMS personnel should notify the receiving facility that the patient is en route. OBJ: Explain why rapid identification of stroke is critical. 5. Assessment of the patient ’s serum glucose level is important because it helps to differentiate stroke from other common causes of stroke symptoms, such as hypoglycemia. OBJ: Give examples of medical conditions that mimic stroke. 6. Within minutes of the patient ’s arrival, reassess the patient ’s ABCs and ensure that the patient has a  secure airway and adequate breathing. Assess the patient ’s temperature, heart rate, blood pressure,  ventilatory rate, and oxygen saturation. If not already done, perform a fingerstick glucose test to assess for hypoglycemia. Establish a minimum of two IV lines if it is anticipated that the patient   will receive fibrinolytic therapy. OBJ: Describe the initial emergency care for acute ischemic stroke.

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7. No, not at this time. Give oxygen if needed to maintain an oxygen saturation above 94%; supplemental oxygen is not recommended in nonhypoxic patients with acute ischemic stroke ( Jauch, et al., 2013). OBJ: Describe the initial emergency care for acute ischemic stroke. 8. All patients with suspected acute stroke should receive continuous ECG monitoring to detect myocardial ischemia and cardiac dysrhythmias (eg, atrial fibrillation) and monitoring should be continued for at least the first 24 hours after stroke ( Jauch, et al., 2013). A 12-lead ECG should be obtained to evaluate for preexisting cardiac disease and concurrent myocardial injury ( Gorelick, et al., 2008). OBJ: Describe the initial emergency care for acute ischemic stroke. 9. IV tPA is a weight-based therapy. The tPA dose is 0.9 mg/kg, not to exceed 90 mg. Ten percent of  the dose is given as an initial IV bolus over 1 minute followed by the remaining 90% of the dose infused using an infusion pump during the next hour. Calculate the desired dose, withdraw any  excess amount from the vial, and then discard the excess amount to prevent accidental overdose (Summers, et al., 2009). OBJ: Describe the initial emergency care for acute ischemic stroke. 10. Use the NIHSS scale to assess neurologic deficits, assess the patient ’s pupil size, and use the GCS to monitor the patient ’s level of responsiveness. These assessments should be performed every hour for  thefirst 24 hours after tPA administration and more often if indicated (Summers, et al., 2009). Measure the patient ’s BP every 15 minutes during and after the tPA infusion for 2 hours, then every  30 minutes for 6 hours, and then every hour until 24 hours after the infusion ( Jauch, et al., 2013). Assess the patient ’s BP more frequently if his or her systolic BP is more than 180 mm Hg or if the diastolic BP is more than 105 mm Hg ( Jauch, et al., 2013). Administer antihypertensive medications per physician’s orders to maintain the patient ’s BP at or below these levels ( Jauch, et al., 2013). OBJ: Describe the initial emergency care for acute ischemic stroke.

REFERENCES  Acker, J. E., Pancioli, A. M., Crocco, T. J., Eckstein, M. K., Jauch, E. C., Larrabee, H., et al. (2007). Implementation strategies for emergency medical services within stroke systems of care. Stroke ,  38 (11), 3097 – 3115.  Alberts, M. J., Hademenos, G., Latchaw, R. E., Jagoda, A., Marler, J. R., Mayberg, M. R., et al. (2000). Recommendations for the establishment of primary stroke centers. JAMA ,  283(23), 3102 – 3109.  Alberts, M. J., Latchaw, R. E., Jagoda, A., Wechsler, L. R., Crocco, T., George, M. G., et al. (2011). Revised and updated recommendations for the establishment of primary stroke centers: A summary statement from the brain attack coalition. Stroke ,  42(9), 2651 – 2665.  Alberts, M. J., Latchaw, R. E., Selman, W. R., Shephard, T., Hadley, M. N., Brass, L. M., et al. (2005). Recommendations for comprehensive stroke centers: A consensus statement from the Brain Attack Coalition. Stroke , 36 (7), 1597 – 1616.  Alberts, M. J., Wechsler, L. R., Jensen, M. E., Latchaw, R. E., Crocco, T. J., George, M. G., et al. (2013). Formation and function of acute stroke-ready hospitals within a stroke system of care recommendations from the brain attack coalition. Stroke ,  44 (12), 3382 – 3393.  American Stroke Association (2014). Target: Stroke Campaign manual.  Dallas: American Stroke Association. Babarro, E. G., Rego, A. R., & González-Juanatey, J. R. (2009). Cardioembolic stroke: Call for a multidisciplinary  approach. Cerebrovasc Dis ,  27 (Suppl 1), 82 – 87. Brouwers, H. B., & Goldstein, J. N. (2012). Therapeutic strategies in acute intracerebral hemorrhage. Neurotherapeutics ,  9(1), 87 – 98. Bushnell, C., McCullough, L. D., Awad, I. A., Chireau, M. V., Fedder, W. N., Furie, K. L., et al. (2014). Guidelines for the prevention of stroke in women: A statement for healthcare professionals from the American Heart   Association/American Stroke Association. Stroke ,  45 (5), 1545 – 1588. Casaubon, L. K., & Suddes, M. (2013). Hyperacute stroke care. In M. P. Lindsay, G. Gubitz, M. Bayley, &  S. Phillips (Eds.),  Canadian best practice recommendations for stroke care: 2013   (4th ed., pp. 3 – 7). Ottawa, Ontario, Canada: Canadian Stroke Network and Heart and Stroke Foundation of Canada. Demaerschalk, B. M., Kleindorfer, D. O., Adeoye, O. M., Demchuk, A. M., Fugate, J. E., Grotta, J. C. , et al. (2016). Scientific rationale for the inclusion and exclusion criteria for intravenous alteplase in acute ischemic stroke: A

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statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke , 47 (2), 581 – 641. Easton, J. D., Saver, J. L., Albers, G. W., Chaturvedi, S., Feldmann, E., Hatsukami, T. S., et al. (2009). Definition and evaluation of transient ischemic attack. Stroke ,  40 (6), 2276 – 2293. Fonarow, G. C.,Zhao, X.,Smith, E. E., Saver, J. L.,Reeves, M. J.,Bhatt, D. L.,et al. (2014). Door-to-needle times for tissue plasminogen activator administration and clinical outcomes in acute ischemic stroke before and after a  quality improvement initiative. JAMA ,  311(16), 1632 – 1640. Gorelick, A. R., Gorelick, P. B., & Sloan, E. P. (2008). Emergency department evaluation and management of  stroke: Acute assessment, stroke teams and care pathways. Neurol Clin, 26(4), 923 – 942, viii. Graves, A., VerHage, A., Richlik, B., & Makic, M. B. (2013). Estimated versus actual weight when dosing rt-PA in acute ischemic stroke: Is there a difference? J Neurosci Nurs ,  45 (4), 180 – 185. Haines, D. E., & Lancon, J. A. (2013). A survey of the cerebrovascular system. In D. E. Haines (Ed.), Fundamental  neuroscience for basic and clinical applications  (4th ed., pp. 109 – 123). Philadelphia: Saunders. Higashida, R., Alberts, M. J., Alexander, D. N., Crocco, T. J., Demaerschalk, B. M., Derdeyn, C. P., et al. (2013). Interactions within stroke systems of care: A policy statement from the American Heart Association/American Stroke Association. Stroke ,  44 (10), 2961 – 2984.  Jauch, E. C., Saver, J. L., Adams, H. P., Jr., Bruno, A., Connors, J. J., Demaerschalk, B. M., et al. (2013). Guidelines for the early management of patients with acute ischemic stroke: A guideline for healthcare professionals fromthe  American Heart Association/American Stroke Association. Stroke ,  44 (3), 870 – 947. Morgenstern, L. B., Hemphill, J. C., Anderson, C., Becker, K., Broderick, J. P., Connolly, E. S., et al. (2010). Guidelines for the management of spontaneous intracerebral hemorrhage: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke ,  41(9), 2108 – 2129. Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman M., et al. (2015). Heart disease and stroke statistics—2015 update: A report from the American Heart Association.  Circulation, 131, e29 – e322. Nentwich, L. M., & Veloz, W. (2012). Neuroimaging in acute stroke. Emerg Med Clin North Am, 30 (3), 659 – 680. Nolte, J. (2009). Blood supply of the brain. In The human brain: An introduction to its functional anatomy  (6th ed., pp. 122 – 148). Philadelphia: Mosby. Nye, B. R., Hyde, C. E., Tsivgoulis, G., Albright, K. C., Alexandrov, A. V., & Alexandrov, A. W. (2012). Slim stroke scales for assessing patients with acute stroke: Ease of use or loss of valuable assessment data? Am J Crit  Care ,  21(6), 442 – 447. Perez de la Ossa, N., Carrera, D., Gorchs, M., Querol, M., Millán, M., Gomis M., et al. (2014). Design and  validation of a prehospital stroke scale to predict large arterial occlusion: The rapid arterial occlusion evaluation scale. Stroke ,  45 (1), 87 – 91. Powers, W. J., Derdeyn, C. P., Biller, J., Coffey, C. S., Hoh, B. L., Jauch, E. C., et al. (2015). 2015 American Heart   Association/American Stroke Association focused update of the 2013 guidelines for the early management of  patients with acute ischemic stroke regarding endovascular treatment: A guideline for healthcare professionals. Stroke ,  46(10), 3020 – 3035. Ramee, S. R., & White, C. J. (2014). Acute stroke intervention.  Curr Probl Cardiol ,  39(3), 59 – 76. Sacco, R. L., Kasner, S. E., Broderick, J. P., Caplan, L. R., Connors, J. J., Culebras A., et al. (2013). An updated definition of stroke for the 21st century: A statement for healthcare professionals from the American Heart   Association/American Stroke Association. Stroke ,  44 (7), 2064 – 2089. Saunorus Baird, M., & Bethel, S. (2011). Neurologic disorders. In   Manual of critical care nursing   (6th ed., pp. 619 – 694). St. Louis: Mosby. Schwamm, L. H., Pancioli, A., Acker, J. E., Goldstein, L. B., Zorowitz, R. D., Shephard, T. J., et al. (2005). Recommendations for the establishment of stroke systems of care. Stroke ,  36(3), 690 – 703. Silva, G. S., & Schwamm, L. H. (2013). Review of stroke center effectiveness and other get with the guidelines data. Curr Atheroscler Rep ,  15 (9), 350. Summers, D., Leonard, A., Wentworth, D., Saver, J. L., Simpson, J., Spilker, J. A., et al. (2009). Comprehensive overview of nursing and interdisciplinary care of the acute ischemic stroke patient. Stroke ,  40 (8), 2911 – 2944. Zivin, J. A. (2012). Approach to cerebrovascular diseases. In L. Goldman, & A. L. Schafer (Eds.), Goldman s Cecil  medicine  (24th ed., pp. 2304 – 2310). Philadelphia: Saunders. 

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9

Post Test  Multiple Choice  Identify the choice that best completes the statement or answers the question.

____

1.

A 48-year-old man became unresponsive shortly after presenting to you with nausea  and generalized chest discomfort. You observe gasping breathing and are unsure if   you feel a pulse. You should now:  A. Call for help and begin chest compressions. B. Wait until breathing stops and then check again for a pulse. C. Begin chest compressions only if you are certain a pulse is absent. D. Observe the patient for 2 minutes, then reassess his breathing and pulse.

____ 2.

Which of the following is the most likely complication of inferior wall myocardial infarction (MI)?  A. Cardiogenic shock  B. Ventricular rupture C. Bradydysrhythmias D. Tachydysrhythmias

____ 3.

A 52-year-old man is complaining of palpitations that came on suddenly after   walking up a short flight of stairs. His symptoms have been present for about  20 minutes. He denies chest pain and is not short of breath. His skin is warm and dry; breath sounds are clear. His blood pressure (BP) is 144/88 millimeters of  mercury (mm Hg), his heart rate is 186 beats per minute (beats/min), and his  ventilatory rate is 18 breaths/min. The cardiac monitor reveals the rhythm here. Vascular access has been established. Which of the following medications is most  appropriate in this situation?

(From Aehlert B:  ECG study cards,  St. Louis, 2004, Mosby.)

 A. B. C. D.

Dopamine or sotalol Furosemide or atropine Nitroglycerin (NTG) or morphine Procainamide or amiodarone

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____ 4.

Your general impression of a 78-year-old woman reveals that her eyes are closed, she is not moving, you can see no rise and fall of her chest or abdomen, and her skin color is pale. When you arrive at the patient ’s side, you confirm that she is unresponsive. Your best action in this situation will be to:  A. Open her airway and give two breaths. B. Apply an automated external defibrillator (AED). C. Assess breathing and determine whether she has a pulse. D. Prepare the necessary equipment to insert an advanced airway.

____ 5.

A 60-year-old woman has suffered a cardiac arrest. A health care professional trained in endotracheal intubation has intubated the patient. Which of the following  findings would indicate inadvertent esophageal intubation?  A. Jugular vein distention B. Subcutaneous emphysema  C. Gurgling sounds heard over the epigastrium D. Breath sounds heard on only one side of the chest 

____ 6.

Hypotension (ie, a systolic BP of less than 90 mm Hg) after the return of spontaneous circulation (ROSC) may necessitate the use of:  A. Fluid boluses and isoproterenol. B. Procainamide, epinephrine, or dopamine. C. Epinephrine, dopamine, or norepinephrine. D. Fluid boluses, procainamide, and isoproterenol.

____ 7.

Which of the following is incorrect  with regard to a postevent debriefing?  A. The facilitator should use open-ended questions to encourage discussion. B. Team members are encouraged to identify lessons learned in a nonpunitive environment. C. The gather phase of the debriefing includes a comparison of the team’s actions  with current resuscitation algorithms. D. Team members are given an opportunity to reflect on their performance and how  their performance can be improved.

____ 8.

Assuming there are no contraindications, which of the following can be performed as an initial intervention for a stable but symptomatic patient with the rhythm shown?

II

III

(From Aehlert B:  ECG study cards,  St. Louis, 2004, Mosby.)

 A. B. C. D.

Defibrillation Vagal maneuvers Administration of intravenous (IV) diltiazem Administration of IV epinephrine

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____ 9.

A 62-year-old man received IV tissue plasminogen activator (tPA) 2 hours ago after a diagnosis of acute ischemic stroke. While assessing the patient ’s vital signs,  you observe swelling of the patient ’s lips and tongue. Your best course of action will be to:  A. Administer aspirin and IV heparin. B. Administer IV antihistamines and steroids. C. Observe and reassess the patient every 15 minutes. D. Request an emergent brain computed tomography scan.

____ 10.

During a cardiac arrest, multiple attempts to establish a peripheral IV have proved unsuccessful. Your best course of action at this time will be to:  A. Insert a central line. B. Attempt intraosseous access. C. Discontinue resuscitation efforts. D. Continue peripheral IV attempts until successful.

____ 11.

Synchronized cardioversion:  A. Is used only for atrial dysrhythmias. B. Delivers a shock during ventricular depolarization. C. Delivers a shock between the peak and end of the T wave. D. Is used only for rhythms with a ventricular rate of less than 60 beats/min.

____ 12.

An 84-year-old man presents with an acute onset of altered mental status. The cardiac monitor shows the rhythm here. The patient ’s BP is 58/30 mm Hg and his ventilatory rate is 14 breaths/min. His skin is cool, moist, and pale. His blood oxygen saturation level (SpO2) on room air is 95%. An IV has been established.

II

(From Aehlert B:  ECG study cards,  St. Louis, 2004, Mosby.)

On the basis of the information provided, your best course of action will be to:  A. Prepare for transcutaneous pacing. B. Give amiodarone 300 mg IV push. C. Give epinephrine 1 mg IV bolus and reassess. D. Observe the patient and monitor for signs of deterioration. Questions 13 through 23 pertain to the following scenario Paramedics are on the scene with a 55-year-old man who is complaining of severe chest discomfort. He describes his discomfort as a  “heavy pressure”  in the middle of his chest that has been present for  about 1 hour.

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____ 13.

Which of the following actions performed at the scene is most likely to reduce subsequent treatment delays at the hospital?  A. Giving aspirin B. Obtaining a 12-lead electrocardiogram (ECG) C. Assessing vital signs and oxygen saturation D. Assessing the patient ’s degree of discomfort 

____ 14.

The patient rates his discomfort 9/10. His BP is 126/72 mm Hg and ventilations 14 breaths/min. His SpO2 on room air is 95%. The cardiac monitor shows a sinus rhythm at 60 beats/min. Immediate management of this patient should include:  A. Giving aspirin and NTG. B. Establishing IV access and giving aspirin. C. Administering oxygen and establishing IV access. D. Administering oxygen and obtaining a targeted history.

____ 15.

Current guidelines recommend obtaining an initial 12-lead ECG within ____ of  patient contact when an acute coronary syndrome (ACS) is suspected.  A. 10 minutes B. 30 minutes C. 45 minutes D. 60 minutes

____ 16.

When the patient ’s 12-lead ECG is reviewed, the results should be used to classify the patient into one of three groups.Which of the followingcorrectly reflects these categories?  A. ST elevation (STE), normal ECG, Q waves B. Q waves, ST depression (STD), inconclusive ECG C. STD, normal ECG, inconclusive ECG D. STE, STD, normal or nondiagnostic ECG

____ 17.

A 12-lead ECG has been obtained.

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

V1

II

V5

(From Phalen T, Aehlert B:  The 12-lead ECG in acute coronary syndromes,  ed 3, St. Louis, 2012, Mosby.)

 The patient ’s 12-lead ECG shows:  A. STE in leads II, III, and aVF. B. STD in leads I, II, III, and aVL. C. STE in leads I, aVL, and V 2  to V 6. D. STD in leads V 1, V 4, V 5, and V 6.

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____ 18.

To be considered significant, ECG findings, such as STE or STD, need to be  viewed in two or more contiguous leads. Which of the following are contiguous leads?  A. V 1, V 4, and V 5 B. V 2, V 3, and V 4 C. III, aVF, and V 1 D. I, II, III, and aVL

____ 19.

The patient ’s 12-lead ECG findings suggest a(n) _____ MI.  A. Posterior  B. Inferolateral C. Anterolateral D. Non – ST elevation

____ 20.

On the basis of the patient ’s 12-lead ECG findings:  A. The patient should be classified as having a nondiagnostic ECG and discharged  with follow-up instructions. B. The patient should be classified as having an ST elevation MI (STEMI) and should be evaluated for immediate reperfusion therapy. C. The patient should be classified as having a normal ECG; serial ECGs should be obtained at 30-minute intervals to detect the development of ST elevation. D. The patient should be classified as having a non – ST elevation ACS (NSTE-ACS) and should be admitted to a monitored bed for further evaluation.

____ 21.

Vascularaccess has beenestablished. The patient ’s BPis 130/70 mm Hg, his pulse is 60 beats/min, and his ventilatory rate is 14 breaths/min. Assuming there are no contraindications for any of the following medications, which of the following would be appropriate for this patient at this time?  A. Aspirin and NTG B. Aspirin and a nonsteroidal antiinflammatory drug (NSAID) C. An oral beta-blocker and an NSAID D. Aspirin and a calcium channel blocker (CCB)

____ 22.

NTG has been ordered for administration to this patient. NTG:  A. Is contraindicated in hypotensive patients. B. Should be administered via the IV route for maximum benefit. C. Should be used with caution in patients with anterior infarction. D. Should be given every 15 to 20 minutes until chest discomfort is relieved.

____

23.

The patient’ s chest discomfort was unrelieved after the maximum recommended dosage of NTG tablets. Morphine sulfate was ordered and a 4 mg dose was given IV. The patient ’s BP is now 80/60 mm Hg and his skin is cool, moist, and pale. His breath sounds are clear. You should:  A. Prepare a lidocaine infusion at 1 to 4 mg/min. B. Prepare an epinephrine infusion at 2 mcg/min. C. Give a 250 mL IV fluid bolus of normal saline. D. Prepare a dopamine infusion at 2 to 10 mcg/kg/min.

____ 24.

Which of the following is not recommended when performing defibrillation?  A. Check for a pulse immediately after defibrillation to determine next steps. B. Visually check and ensure that everyone is clear of the patient before shock  delivery. C. Remove transdermal medication patches or ointment from the patient ’s chest  before the procedure. D. All team members with the exception of the chest compressor should clear the patient as the machine charges.

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____ 25.

Atypical symptoms of ACSs are more common in:  A. Older adults, women, and diabetic individuals. B. Men, older adults, and individuals who have liver disease. C. Women, diabetic individuals, and individuals who have liver disease. D. Men, patients who have a history of coronary artery disease, and patients whohave a  history of hypertension.

____ 26.

A 53-year-old woman is unresponsive. The cardiac monitor initially showed a  narrow-QRS tachycardia at 220 beats/min. Her BP was 50 mm Hg by palpation and her ventilatory rate was 10 breaths/min. Supplemental oxygen therapy was initiated and an IV established before the patient ’s collapse. You promptly delivered a synchronized shock. Reassessment reveals the patient is not breathing and has no pulse. The cardiac monitor now reveals the rhythm shown. What course of action should you take at this time?

(From Aehlert B,  ECGs made easy,  ed 5, St. Louis, 2013, Mosby.)

 A. Defibrillate immediately. B. Perform cardiopulmonary resuscitation (CPR) for 2 minutes and then prepare to defibrillate. C. Place an advanced airway and then begin transcutaneous pacing. D. Press the “Sync”  control and deliver another synchronized shock. ____ 27.

An unstable patient with a narrow-QRS tachycardia requires electrical therapy.  You have a biphasic defibrillator available to you. Which of the following  correctly reflects the recommended energy dose that should be delivered in this situation?  A. Defibrillate with 120 joules (J). B. Defibrillate with 360 J. C. Perform synchronized cardioversion with 50 to 100 J for the initial shock. D. Perform synchronized cardioversion with 100 to 200 J for the initial shock.

____ 28.

The preferred method used to verify the proper placement of an endotracheal tube is:  A. Obtaining a chest radiograph. B. Using continuous waveform capnography. C. Auscultating the presence of bilateral breath sounds. D. Observing adequate chest rise with positive pressure ventilation.

____ 29.

Which of the following is incorrect  with regard to the events of a typical resuscitation effort?  A. The team leader should state his or her instructions one at a time. B. The team leader should encourage a respectful exchange of ideas. C. Team members must be knowledgeable about current resuscitation algorithms. D. Team members should be encouraged to confer among themselves throughout the resuscitation effort.

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____ 30.

Which of the following statements is correct about the use of medications during  cardiac arrest?  A. Amiodarone is the drug of choice for cardiac arrest resulting from asystole. B. Lidocaine is contraindicated in cardiac arrest associated with a shockable rhythm. C. Epinephrine should be given as soon as feasible after the onset of cardiac arrest  associated with a nonshockable rhythm. D. Vasopressin can be substituted for either the first or second dose of epinephrine in the treatment of cardiac arrest.

____ 31.

This 12-lead ECG is from a 50-year-old man complaining of chest discomfort.

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

(From Phalen T, Aehlert B:  The 12-lead ECG in acute coronary syndromes,  ed 3, St. Louis, 2012, Mosby.)

 Which of the following is true regarding this 12-lead ECG?  A. This 12-lead reveals no significant findings. B. STE is present in leads V 1  to V 4. An anterior STEMI is suspected. C. STE is present in leads I, aVR, and V 6. A lateral STEMI is suspected. D. STD is present in leads III and aVF. An inferior STEMI is suspected. Questions 32 and 33 pertain to the following scenario  A 65-year-old man is complaining of a sudden onset of dizziness. He is awake, alert, and diaphoretic.  The patient states that his symptoms began 45 minutes ago while cleaning his garage. He denies chest  pain, shortness of breath, and nausea. The patient ’s breath sounds are clear bilaterally. His BP is 78/50 mm Hg, ventilations 18 breaths/min. His SpO2  on room air is 96%.

____ 32.

The cardiac monitor reveals the following rhythm.

(From Aehlert B:  ECG study cards,  St. Louis, 2004, Mosby.)

 This rhythm is:  A. Junctional rhythm. B. Sinus bradycardia. C. Third-degree atrioventricular (AV) block. D. Second-degree AV block (2:1 AV block).

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____ 33.

An IV is in place. Your best course of action will be to:  A. Defibrillate immediately. B. Administer atropine 0.5 mg IV. C. Administer amiodarone 300 mg IV. D. Administer vasopressin 40 units IV.

Questions 34 through 36 pertain to the following scenario  An 89-year-old man is complaining of a  “racing heart.” He states his symptoms began while playing a  card game with friends. He had an MI 15 years ago and a coronary artery bypass graft 5 years ago. His BP is 140/90 mm Hg and his ventilatory rate is 16 breaths/min. Breath sounds are clear and his tidal volume is adequate. His SpO2  on room air is 88%.

____ 34.

On the basis of the information provided, supplemental oxygen:  A. Is unnecessary at this time. B. Is indicated and should be delivered using a nasal cannula. C. Is indicated for all patients who are experiencing a tachycardia. D. Should ideally be administered only after placement of an advanced airway.

____ 35.

You have started an IV and placed the patient on the cardiac monitor, which reveals the following rhythm:

(From Aehlert B:  ECG study cards,  St. Louis, 2004, Mosby.)

 This rhythm can best be described as a:  A. Regular, polymorphic, wide-QRS tachycardia. B. Regular, monomorphic, wide-QRS tachycardia. C. Irregular, polymorphic, wide-QRS tachycardia. D. Irregular, monomorphic, wide-QRS tachycardia. ____ 36.

Which of the following statements is true with regard to the management of this patient?  A. The patient is unstable. Sedate the patient and defibrillate as quickly as possible. B. The patient is stable. Administration of IV verapamil is recommended for  termination of the rhythm. C. The patient is stable. Administration of IV adenosine can be used as a therapeutic and diagnostic maneuver. D. The patient is unstable. Because there are recognizable QRS complexes on the monitor, synchronized cardioversion should be performed.

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Questions 37 and 38 pertain to the following scenario  A 72-year-old woman presented with a sudden onset of shortness of breath and collapsed. After  confirming the patient was unresponsive, apneic, and pulseless, CPR was begun.

____ 37.

The cardiac monitor shows the following rhythm. II

(From Aehlert B:  ECG study cards,  St. Louis, 2004, Mosby.)

 Which of the following ACLS treatment guidelines should be used in the initial treatment of this patient?  A. Symptomatic bradycardia  B. Narrow-QRS tachycardia  C. Pulseless electrical activity (PEA) D. ACSs ____ 38.

An IV has been established and the patient is being ventilated with a bag-mask device (BMD). You observe gentle bilateral chest rise with ventilations. Your next action should be to:  A. Defibrillate immediately. B. Give 0.5 mg of atropine IV. C. Give 1 mg of epinephrine IV. D. Begin transcutaneous pacing.

____ 39.

A 73-year-old woman presents with symptoms of acute stroke 3.5 hours after symptom onset. She has a history of an acute MI 6 years ago, chronic atrial fibrillation, and diabetes mellitus.Thepatient ’s BPis 168/100 mmHg, herheartrateis 88to 100 beats/min,andher   ventilations are 12 breaths/min. Her National Institutes of Health Stroke Scale (NIHSS) score is 22. Daily medications include lisinopril, metformin, and warfarin. Which of the following statements with regard to fibrinolytic therapy for this patient is true?  A. This patient is not a candidate for fibrinolytic therapy because of her age. B. This patient is not a candidate for fibrinolytic therapy because she is hypertensive. C. This patient is not a candidate for fibrinolytic therapy because she is taking an oral anticoagulant. D. This patient is not a candidate for fibrinolytic therapy because too much time has lapsed between symptom onset and hospital arrival.

____ 40.

Which of the following is true with regard to procainamide?  A. Procainamide is a potent vasoconstrictor. B. Procainamide may cause widening of the QRS complex. C. Procainamide is indicated in the treatment of asystole and slow PEA. D. Procainamide is a first-line drug in the management of torsades de pointes (TdP).

____ 41.

A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min delivers about _____oxygen to the patient when a reservoir is not used.  A. 21% B. 40% to 60% C. 60% to 90% D. 90% to 100%

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____ 42.

A 35-year-old woman presents with a narrow-QRS tachycardia. She is stable but  symptomatic. Vagal maneuvers and an initial dose of adenosine were ineffective. You should now:  A. Perform synchronized cardioversion. B. Administer 6 mg of adenosine rapid IV push. C. Administer 12 mg of adenosine rapid IV push. D. Administer diltiazem 0.25 mg/kg IV over 2 minutes.

____ 43.

A patient is unresponsive with spontaneous ventilations at a rate of 4 per minute. Chest movement is barely visible with each breath. A pulse is present. Which of the following oxygen delivery devices would be most appropriate to use in this situation?  A. A nasal cannula at 4 L/min B. A simple face mask at 6 L/min C. A nonrebreather mask at 12 L/min D. A BMD with a reservoir at 15 L/min

____ 44.

If a patient wakes from sleep or is found with symptoms of a stroke, the time of onset of  symptoms is defined as the time:  A. Of awakening. B. The patient retired for sleep. C. The patient was last known to be symptom-free. D. The patient was last seen by a health care professional.

____ 45.

The most common adverse effects of giving amiodarone are:  A. Nausea and asystole. B. Bradycardia and hypotension. C. Tachycardia and hypertension. D. Blurred vision and abdominal pain.

____ 46.

A 49-year-old man is found unresponsive, not breathing, and pulseless. The cardiac monitor reveals monomorphic ventricular tachycardia. The most important actions in the management of this patient are:  A. CPR and defibrillation. B. Defibrillation and resuscitation medications. C. CPR and prompt insertion of an advanced airway. D. Synchronized cardioversion and resuscitation medications.

____ 47.

Diltiazem may be used:  A. Concurrently with IV beta-blockers. B. In the management of symptomatic bradycardia. C. In the management of a stable patient with a wide-QRS tachycardia. D. To control the ventricular rate with atrial flutter or atrial fibrillation.

____ 48.

CPR is ongoing for a 66-year-old man in cardiac arrest. The cardiac monitor  reveals asystole. Vascular access has been achieved and an advanced airway has been inserted. Which of the following statements is correct with regard to this situation?  A. The depth of chest compressions should be 1.5 to 2 inches. B. Chest compressions should be delivered at a rate of 100 per minute. C. The ratio of chest compressions to ventilations delivered should be 30:2. D. Ventilations should be delivered at a rate of one breath every 6 seconds.

____ 49.

What precautions should be taken before giving NTG?  A. Make sure the patient ’s heart rate is at least 70 beats/min. B. Make sure there is no evidence of a right ventricular infarction. C. Make sure the patient ’s systolic BP is more than 140 mm Hg. D. Make sure the patient has not used a diuretic or an antihypertensive medication in the past 24 hours.

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____ 50.

A simple face mask:  A. Requires a minimum oxygen flow rate of 2 L/min. B. Can only be used in a spontaneously breathing patient. C. Does not permit the mixing of the patient ’s exhaled air with 100% oxygen. D. Delivers an oxygen concentration of 70% to 85% at recommended flow rates.

POST TEST ANSWERS

 Multiple Choice

1. A. Gasping breathing is not effective breathing. After recognizing that the patient is unresponsive and is not breathing normally, activate the emergency response system and check for a pulse for no more than 10 seconds. If you do not feel a pulse or are unsure if you feel a pulse during that period, begin chest compressions. OBJ:  Discuss a systematic approach to the initial emergency care of an unresponsive patient. 2. C.  Parasympathetic nervous system hyperactivity is common with inferior wall MIs, resulting in bradydysrhythmias. Ischemia of the AV node can result in first-degree or second-degree type I  AV block. These dysrhythmias are relatively common with an inferior infarction, usually transient  (resolving within 2 to 3 days), generally do not warrant treatment, and have a low mortality rate unless associated with hypotension, heart failure, or both. OBJ:  Describe the initial management of a patient who is experiencing an ACS. 3. D. The rhythm shown is monomorphic ventricular tachycardia. From the information provided, the patient appears to be clinically stable at this time. Procainamide would be appropriate to consider in this situation. Acceptable alternatives include amiodarone and sotalol. Dopamine increases the force of myocardial contraction, heart rate, and BP. Because this patient is not hypotensive and he has a  rapid heart rate, dopamine is not indicated. NTG is a vasodilator. The patient has no complaint of  chest pain so NTG is not indicated. Furosemide (Lasix) is also not indicated because there are no signs of pulmonary congestion. Atropine is not indi cated because the patient has a tachycardia, not a  symptomatic bradycardia. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 4. C.  After forming a general impression, you should approach the patient and assess her level of  responsiveness. If the patient is unresponsive, quickly determine whether the patient is not breathing  (or only gasping) and simultaneously check for a pulse for up to 10 seconds. If there is no pulse, begin chest compressions. OBJ:  Discuss a systematic approach to the initial emergency care of an unresponsive patient. 5. C. Absence of chest wall expansion and gurgling heard over the epigastrium indicate misplacement  of the endotracheal tube into the esophagus. If breath sounds were present bilaterally with bag-mask   ventilation before placement of a tracheal tube, the presence of breath sounds on only one side of the chest after placement of the tube suggests right primary bronchus intubation. OBJ:  Describe methods that are used to confirm correct endotracheal tube placement. 6. C. IV fluid boluses can be considered if the patient is hypotensive after the ROSC. Vasopressor IV  infusions such as epinephrine, dopamine, or norepinephrine may be started if necessary and titrated to achieve a minimum systolic BP of less than 90 mm Hg. Isoproterenol is an alternative agent that is primarily used to increase heart rate in a patient with a symptomatic bradycardia. Because it is not a vasopressor, it is not used to treat hypotension. Procainamide is an antiarrhythmic used to treat many atrial and ventricular dysrhythmias. Procainamide is not a vasopressor and because an adverse effect of procainamide administration is hypotension, it would not be used to treat hypotension. OBJ:  Discuss immediate postcardiac arrest care upon ROSC.

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7. C.  During a debriefing, each member of the code team has an opportunity to engage in honest  dialogue to gain understanding and to identify lessons learned in a nonpunitive environment.  An opportunity is provided for each team member to reflect on  what   they did,  when  they did it, how  they did it, why  they did it, and how   they can improve (Phrampus & O’Donnell, 2013).  The facilitator uses open-ended questions to encourage discussion and listens to the team members describe their perceptions of their behaviors. The actions of the team can be compared with current  resuscitation algorithms, professional standards, institution policies, best evidence, and local protocols to enhance understanding and support discussion during the analysis phase of the debriefing. OBJ:  Recognize the opportunities provided when a postevent debriefing is held. 8. B. The rhythm shown is AV nodal reentrant tachycardia (AVNRT) at 167 beats/min. Vagal maneu vers are methods used to stimulate baroreceptors located in the internal carotid arteries and the aortic arch. Stimulation of these receptors results in reflex stimulation of the vagus nerve and release of  acetylcholine. Acetylcholine slows conduction through the AV node, resulting in slowing of the heart rate. Vagal maneuvers can be attempted as an initial intervention in a stable patient with a  regular narrow-QRS tachycardia. Defibrillation is not indicated. Diltiazem is a CCB that is used in the treatment of stable, narrow-QRS tachycardias if the rhythm remains uncontrolled or uncon verted by adenosine or vagal maneuvers or if the tachycardia is recurrent. Epinephrine is not  indicated in the management of a stable patient with a tachycardia. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 9. B. Orolingual angioedema is an uncommon complication of tPA administration, but it can lead to airway obstruction. Patients taking angiotensin-converting enzyme inhibitors and those with infarctions that involve the insular and frontal cortex appear to be at highest risk ( Jauch, et al., 2013).  Treatment includes the administration of IV ranitidine, diphenhydramine, and methylprednisolone ( Jauch, et al., 2013). OBJ:  Describe the initial emergency care for acute ischemic stroke. 10. B.  If peripheral IV access is unsuccessful during cardiac arrest, consider an intraosseous infusion before considering placement of a central line. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 11. B.   Synchronized cardioversion is a type of electrical therapy in which a shock is “timed” or  “programmed”  for delivery during ventricular depolarization (ie, the QRS complex). It is indicated in the management of a patient who is exhibiting serious signs and symptoms related to a tachycardia. Because the machine must be able to detect a QRS complex in order to “sync,”  synchronized cardioversion is used to treat rhythms that have a clearly identifiable QRS complex and a rapid  ventricular rate (such as some narrow-QRS tachycardias and ventricular tachycardia). OBJ: Explain synchronized cardioversion, describe its indications, and list the steps required to perform this procedure safely. 12. A.  The rhythm shown is a third-degree AV block at a rate of about 30 beats/min. This patient is clearly symptomatic and needs immediate emergency care. A reasonable course of action will be to prepare for immediate transcutaneous pacing. Amiodarone is not indicated in the management of a  symptomatic bradycardia. Although epinephrine may be used in the management of a symptomatic bradycardia, it is given as a continuous IV infusion,  not  as an IV bolus. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable.

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13. B.  Although it is not yet known if this patient is experiencing a STEMI or if he is a candidate for  reperfusion therapy, obtaining a prehospital 12-lead ECG is associated with shorter reperfusion time and a lower mortality rate from STEMI (O’Gara, et al., 2013). OBJ:  Describe the initial management of a patient who is experiencing an ACS. 14. B.  Frequent assessment of the patient ’s mental status, vital signs, and oxygen saturation level is important, and continuous ECG monitoring is essential. Supplemental oxygen is warranted if  the patient is having difficulty breathing, has obvious signs of heart failure or shock, or if his oxygen saturation level declines below 90% ( Amsterdam, et al., 2014; O’Gara, et al., 2013). Establish IV access, obtain a targeted history and physical examination, and consider the possibility of  other conditions that mimic acute MI. Give aspirin if no contraindications are present. NTG should not be administered until a 12-lead ECG has been obtained and a right ventricular infarction has been ruled out. OBJ:  Describe the initial management of a patient who is experiencing an ACS. 15. A.  An initial 12-lead ECG should be obtained and interpreted with 10 minutes of patient contact  ( Amsterdam, et al., 2014). Obtain a repeat 12-lead ECG with each set of vital signs, when the patient ’s symptoms change, and as often as necessary. OBJ:  Describe the initial management of a patient who is experiencing an ACS. 16. D. The patient ’s initial 12-lead ECG should be reviewed and the patient classified into one of three categories: STE, STD, or normal or nondiagnostic ECG. OBJ: Discuss the three groups used when categorizing the 12-lead ECG findings of the patient  experiencing an ACS. 17. C.  The patient ’s 12-lead ECG shows STE in leads I, aVL, and V 2  to V 6. OBJ:  Identify the ECG leads that view the anterior wall, the inferior wall, the lateral wall, the septum, the inferobasal wall, and the right ventricle. 18. B.  Two leads are contiguous if they look at the same or adjacent area of the heart or if they are numerically consecutive chest leads. V 2, V 3, and V 4  are numerically consecutive chest leads. OBJ:  Relate the cardiac surfaces or areas represented by the ECG leads. 19. C.  The patient ’s 12-lead ECG shows STE in lead I, aVL, and V 2 through V 6. Because these leads  view the lateral and anterior surfaces of the left ventricle, an extensive anterolateral infarction is suspected. OBJ:  Recognize the changes on the ECG that may reflect evidence of myocardial ischemia, injury, and infarction. 20. B. Patients with STE in two or more contiguous leads are classified as having a STEMI and should be evaluated for immediate reperfusion therapy. OBJ: Discuss the three groups used when categorizing the 12-lead ECG findings of the patient  experiencing an ACS. 21. A.  Aspirin should be administered as soon as possible after symptom onset to patients with suspected ACSs (if there are no contraindications). NTG relaxes vascular smooth muscle and decreases myocardial oxygen consumption. An oral beta-blocker should be started within the first  24 hours after hospitalization in the absence of contraindications to beta blockade. Because of the increased risk of major adverse cardiac events associated with the use of NSAIDs, these drugs should not be initiated in the acute phase of care and should be discontinued in patients using them before hospitalization ( Amsterdam, et al., 2014; O’Gara, et al., 2013). Although CCBs may be useful in relieving ischemia or lowering BP in patients who are intolerant of beta-blockers, randomized controlled trials have demonstrated no beneficial effect on infarct size or the rate of reinfarction when CCB therapy was initiated during either the acute or convalescent phase of STEMI ( O’Gara, et al., 2013). OBJ:  Describe the initial management of a patient who is experiencing an ACS.

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22. A.   Patients with ischemic discomfort should receive up to three doses of sublingual NTG tablets or spray at 3- to 5-minute intervals until chest discomfort is relieved or hypotension limits its use. Nitrates are contraindicated in patients with hypotension (systolic BP below  90 mm Hg or 30 mm Hg or more below baseline), marked bradycardia or tachycardia, phosphodiesterase inhibitor use within the previous 24 to 48 hours, or suspected right ventricular  infarction. OBJ:  Describe the initial management of a patient who is experiencing an ACS. 23. C. Your best course of action will be to place the patient supine and give a 250 mL IV fluid bolus of  normal saline. Reassess his BP (and other vital signs) and breath sounds after administration. OBJ:  Describe the initial management of a patient who is experiencing an ACS. 24. A. Be sure that high-quality CPR is continued as the defibrillator is readied for use. While CPR continues, instruct a team member to expose the patient ’s chest and to remove any  transdermal medication patches or ointment from the patient ’s chest, if present. All team members with the exception of the chest compressor should clear the patient as the machine charges. When the defibrillator is charged, the chest compressor should  immediately   clear the patient. Call “Clear! ”   Look around you (360 degrees) to be sure that  everyone —including you—is clear of the patient, the bed, and any equipment that is connected to the patient. Be sure oxygen is not flowing over the patient ’s chest. Press the “Shock ”   control to defibrillate the patient. Release the “Shock ”   control after the energy  dose has been delivered. Instruct the team to resume chest compressions immediately   without pausing for a rhythm or pulse check. OBJ: Explain defibrillation; describe proper pad/paddle placement, indications, precautions, and the steps in performing this procedure with a manual defibrillator and automated external defibrillator. 25. A.  Patients who are experiencing an ACS who are most likely to present atypically include older  adults, diabetic individuals, women, patients with impaired renal function, patients with dementia, patients with prior cardiac surgery, and patients during the immediate postoperative period after  noncardiac surgery. OBJ:  Explain atypical presentation and its significance in ACSs. 26. A.  The cardiac monitor shows ventricular fibrillation (VF). Appropriate care at this time includes immediate defibrillation. Transcutaneous pacing can be used in the management of symptomatic bradycardia; it is not used for cardiac arrest rhythms such as VF. Synchronized cardioversion is not used to treat disorganized rhythms (eg, polymorphic VT) or those that do not have a clearly  identifiable QRS complex (eg, VF). OBJ: Explain defibrillation; describe proper pad/paddle placement, indications, precautions, and the steps in performing this procedure with a manual defibrillator and automated external defibrillator. 27. C.  If an unstable patient with a narrow-QRS tachycardia requires electrical therapy and a  biphasic defibrillator is available, perform synchronized cardioversion using 50 to 100 J initially (or the energy levels recommended by the defibrillator manufacturer), increasing in stepwise fashion if the initial shock fails. For example, if the initial synchronized shock was delivered using 50 J and failed, reasonable energy levels to use for the second and subsequent  shocks would be 100 J, then 200 J, 300 J, and 360 J (assuming the rhythm failed to convert   with each shock). OBJ:  For each of the following rhythms, identify the energy levels that are currently recommended: monomorphic VT, narrow-QRS tachycardia, atrial fibrillation, and atrial flutter. 28. B.  In addition to clinical assessment, continuous quantitative waveform capnography is recommended as the most reliable method for confirmation and monitoring of endotracheal tube placement. OBJ:  Describe methods that are used to confirm correct endotracheal tube placement.

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29. D. Each member of the resuscitation team must have clear roles and responsibilities, must know his or her limitations, must be knowledgeable about current resuscitation algorithms, must be practiced in resuscitation skills, and must be prepared to question other team members if an action is about to occur that may be inappropriate. To avoid information overload and to help ensure that what is  said  by the team leader is what is  heard   by the team members, the team leader should state his or her  instructions one at a time using terms that are known and shared by all team members. The team member ’s name should be used, if known. A good team leader values his or her team members, fosters an environment in which team members feel comfortable speaking up, and encourages a respectful exchange of ideas. Team members must clearly acknowledge when procedures and medications are complete. Because there are often a large number of persons present during a code, sidebar con versations among team members that can be distracting to other team members must be avoided. OBJ:  Discuss the events of a typical resuscitation effort. 30. C.  Because research has shown an association among the early administration of epinephrine and increased ROSC, survival to hospital discharge, and neurologically intact survival, current guidelines consider it reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest  associated with a nonshockable rhythm (Link, et al., 2015). Amiodarone is an antiarrhythmic that  can be used for shockable cardiac arrest rhythms (ie, VF, pulseless ventricular tachycardia [pVT]). It is not indicated for nonshockable cardiac arrest rhythms (ie, asystole and PEA). The initiation or  continuation of lidocaine may be considered immediately after ROSC from VF/pVT cardiac arrest  (Link, et al., 2015). Epinephrine and vasopressin are vasopressors that, when administered during  cardiac arrest, have been shown to improve ROSC ( Link, et al., 2015). Because the efficacy of both drugs is similar and research has shown no benefit from administering both drugs compared with epinephrine administered alone, vasopressin was removed from the adult cardiac arrest algorithm (Link, et al., 2015). OBJ:  Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 31. B. The rhythm shown is a sinus rhythm at 92 beats/min. STE is noted in V 1 to V 4; it is borderline in V 5. QS complexes (ie, pathologic Q waves) are noted in V 1 to V 5. An anterior STEMI is suspected. STD is present in lead aVF. OBJ:  Recognize the changes on the ECG that may reflect evidence of myocardial ischemia, injury, and infarction. 32. D.  The rhythm shown is second-degree AV block (2:1 AV block). OBJ:  Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 33. B. The drug of choice for symptomatic bradycardia is atropine. The initial dose is 0.5 mg, which may  be repeated every 3 to 5 minutes to a maximum dose of 3 mg. Defibrillation, amiodarone, and vasopressin are not indicated in the management of symptomatic bradycardia. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  symptomatic bradycardia, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 34. B. Administer supplemental oxygen as needed to maintain the patient ’s oxygen saturation at 94% or  higher. Because it is generally better tolerated than a mask, it is reasonable to use a nasal cannula. If the patient ’s oxygensaturation does not adequately improve with theuse of thecannula, it may be necessary  toswitchtooxygendeliverybymask.Becausethepatient ’sbreathingisadequate,advancedairwayplacement and positive pressure ventilation are not necessary at this time; however, if the patient becomes unresponsive or his breathing becomes inadequate, administer oxygen by positive pressure ventilation. OBJ: Describe the advantages, disadvantages, oxygen liter flow per minute, and estimated oxygen percentage delivered for each of the following devices: nasal cannula, simple face mask, partial nonrebreather mask, and nonrebreather mask.

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35. B. Monomorphic is a term used to describe QRS complexes that are of the same shape and amplitude.  When the QRS complexes vary in shape and amplitude from beat to beat, the term  polymorphic  is used. The rhythm shown is a regular, monomorphic, wide-QRS tachycardia. A 12-lead ECG should be obtained. It is wise to seek expert consultation when treating a patient with a wideQRS tachycardia. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 36. C. On the basis of the information provided, the patient is stable at this time. Administration of IV  adenosine can be used as a therapeutic and diagnostic maneuver. Verapamil is a CCB and should only be given to patients with a narrow-QRS tachycardia. It should not be given to patients with a   wide-complex tachycardia. Because electrical therapy is used for  unstable   patients, neither synchronized cardioversion nor defibrillation is indicated for this patient.  If   he were unstable, synchronized cardioversion would be used because the patient has a pulse and there are recognizable QRS complexes on the monitor. Defibrillation would be performed if the rhythm observed was polymorphic VT, pulseless monomorphic VT, or VF. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 37. C.  Despite the presence of an organized rhythm on the monitor, the patient has no pulse. This situation is PEA. OBJ:  Given a patient situation, describe the ECG characteristics and initial emergency care for cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 38. C.   Give 1 mg of 1:10,000 epinephrine IV. Defibrillation attempts to deliver a uniform electrical current of sufficient intensity to depolarize myocardial cells (including fibrillating cells) at the same time. This provides an opportunity for the heart ’s natural pacemakers to resume normal activity. In this situation, organized electrical activity is already present on the cardiac monitor; therefore defibrillation is contraindicated. Atropine, although once used for asystole and slow PEA, is no longer recommended. Transcutaneous pacing is not indicated in cardiac arrest. OBJ:  Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 39. C.  IV tPA is recommended for administration to a select group of eligible patients who present   within a 3- to 4.5-hour window after the onset of acute stroke symptoms ( American Stroke  Association, 2014). The eligibility criteria for treatment in this time frame are similar to those for patients treated within 3 hours of symptom onset, with the following additional exclusion criteria  ( American Stroke Association, 2014; Jauch, et al., 2013): patients older than age 80, those taking  oral anticoagulants regardless of their international normalized ratio, those with a baseline NIHSS score of more than 25, those with imaging evidence of ischemic injury involving more than one-third of the middle cerebral artery territory, or those with a history of both prior ischemic stroke and diabetes mellitus. OBJ:  Describe the initial emergency care for acute ischemic stroke. 40. B. Procainamide exerts a peripheral vasodilatory effect; therefore hypotension is a potential adverse effect. Procainamide may cause widening of the QRS complex. The drug should be discontinued if  the QRS widens more than 50% of its pretreatment width. Procainamide is used to control the  ventricular rate in the patient with preexcited atrial fibrillation and in the management of stable monomorphic VT with a normal QT interval. It is not used in the treatment of asystole or  PEA. Because it can cause prolongation of the PR and QT intervals, procainamide is not used in the management of TdP.

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OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable.

41. B. A BMD that is used with supplemental oxygen set at a flow rate of 10 to 15 L/min delivers about  40% to 60% oxygen to the patient when a reservoir is not used. OBJ: Describe the oxygen liter flow per minute and the estimated inspired oxygen concentration delivered with a pocket face mask and a BMD. 42. C. Vagal maneuvers are used to try to stop the rhythm or slow conduction through the AV node. If   vagal maneuvers fail, antiarrhythmic medications should be tried. Adenosine is the drug of choice, except for patients with severe asthma. The initial dose is 6 mg rapid IV push over 1 to 3 seconds. If  there is no response within 1 to 2 minutes, give 12 mg rapid IV push. The 12 mg dose may be repeated once in 1 to 2 minutes. If needed, CCBs or beta-blockers may be used to slow the ventricular rate. If the tachycardia is sustained and causing persistent signs of hemodynamic compromise, synchronized cardioversion should be performed. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 43. D. Remember that an open airway does not ensure adequate ventilation. This patient ’s breathing is inadequate as evidenced by his rate and depth of ventilations. The patient with inadequate breathing  requires positive pressure ventilation with supplemental oxygen. Of the choices listed, the only  device that can provide positive pressure ventilation is the BMD. If readily available, an oral airway  should be inserted before beginningbag-mask ventilation (if the patient does not have a gag or cough reflex). OBJ:  Describe and demonstrate how to ventilate a patient with a BMD and two rescuers. 44. C. For a patient with symptoms of stroke on awakening, the time of onset is assumed to be the time the patient was last known to be symptom-free before retiring (last known-well time). If a patient  had mild impairments but then had worsening over the subsequent hours, the time the first symptom began is assumed to be the time of onset. OBJ:  Describe the initial emergency care for acute ischemic stroke. 45. B.  Hypotension and bradycardia are most common adverse effects of amiodarone administration. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable. 46. A. CPR and defibrillation are the most important treatments for the patient in cardiac arrest associated with pVT or VF. Insertion of advanced airways and administration of resuscitation medications are of secondary importance. Although synchronized cardioversion may be used in the treatment of an unstable patient in monomorphic VT with a pulse, it is not indicated for pVT. OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  cardiac arrest rhythms, including mechanical, pharmacologic (ie, indications, contraindications, doses, and route of administration of applicable medications), and electrical therapy, where applicable. 47. D. Diltiazem is a CCB that may be used in stable narrow-QRS tachycardias if the rhythm persists despite vagal maneuvers or adenosine, if the tachycardia is recurrent, or to control the ventricular rate in patients with atrial fibrillation or atrial flutter. IV CCBs and IV beta-blockers should not be given together or in close proximity (within a few hours) because severe hypotension may result. CCBs should be avoided in patients with wide-QRS tachycardia and preexcited atrial fibrillation/atrial flutter (Mottram & Svenson, 2011). OBJ: Given a patient situation, describe the ECG characteristics and initial emergency care for  narrow-QRS tachycardias, wide-QRS tachycardias, and irregular tachycardias, including mechanical, pharmacologic, and electrical therapy, where applicable.

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48. D.  After insertion of an advanced airway, chest compressions should be delivered continuously at a  rate of 100 to 120 per minute without pauses for ventilation, unless ventilation is inadequate when compressions are not paused (Link, et al., 2015). Ventilations should be delivered at a rate of one breath every 6 seconds (10 breaths/min). For an average adult, chest compressions should be performed to a depth of at least 2 inches (5 cm) but not more than 2.4 inches (6 cm). OBJ:  Describe the role of each member of the resuscitation team. 49. B. Before giving NTG, assess the degree of the patient ’s pain/discomfort using a 0-to-10 scale, duration, time started, activity being performed, and pain quality. Reassess (and document) the patient ’s  vital signs and level of discomfort after each dose. Make sure that the patient has not used a phosphodiesterase inhibitor such as sildenafil (Viagra) within 24 hours or tadalafil (Cialis) within 48 hours before NTG administration. The combination of a phosphodiesterase inhibitor and nitrates may result in severe hypotension. Nitrates should not be administered to patients with a  systolic BP less than 90 mm Hg or 30 mm Hg or more below baseline, severe bradycardia or tachycardia, or suspected right ventricular infarction. OBJ:  Describe the initial management of a patient who is experiencing an ACS. 50. B.  A simple face mask, which is also called a   standard mask,  is a plastic reservoir that has been designed to fit over the nose and mouth of a spontaneously breathing patient. When using a simple face mask, the oxygen flow rate must be higher than 5 L/min to flush the buildup of the patient ’s exhaled carbon dioxide from the mask. At 5 to 10 L/min, the simple face mask can deliver an inspired oxygen concentration of about 35% to 60%. The patient ’s actual inspired oxygen concentration will vary, because the amount of air that mixes with supplemental oxygen is dependent on the patient ’s inspiratory flow rate. A nonrebreather mask, also called a   nonrebreathing mask,  does not  permit the mixing of the patient ’s exhaled air with 100% oxygen. A one-way valve between the mask  and the reservoir bag and a flap over one of the exhalation ports on the side of the mask prevent the inhalation of room air. OBJ: Describe the advantages, disadvantages, oxygen liter flow per minute, and estimated oxygen percentage delivered for each of the following devices: nasal cannula, simple face mask, partial nonrebreather mask, and nonrebreather mask.

REFERENCES  American Stroke Association. (2014).  Target: Stroke Campaign manual.  Dallas: American Stroke Association.  Amsterdam, E. A., Wenger, N. K., Brindis, R. G., Casey, Jr., D. E., Ganiats, T. G., Holmes, Jr., D. R., et al. (2014). 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes.  J Am Coll Cardiol ,  64 (24), 1 – 150.  Jauch, E. C., Saver, J. L., Adams, Jr., H. P., Bruno, A., Connors, J. J., Demaerschalk, B. M., et al. (2013). Guidelines for the early management of patients with acute ischemic stroke: A guideline for healthcare professionals from the American Heart Association/American Stroke Association.  Stroke ,  44 (3), 870 – 947. Link, M. S., Berkow, L. C., Kudenchuk, P. J., Halperin, H. R., Hess, E. P., Moitra, V. K., et al. (2015, Oct). 2015   American Heart Association Guidelines for CPR & ECC.   Retrieved Oct. 30, 2015, from American Heart   Association. In Web-based integrated guide lines for cardiopulmonary resuscitation and emergency cardiovascular care—part 7: Adult advanced cardiovascular life support:  Eccguidelines.heart.org . Mottram, A. R., & Svenson, J. E. (2011). Rhythm disturbances.  Emerg Med Clin North Am,  29 (4), 729 – 746. O’Gara, P. T., Kushner, F. G., Ascheim, D. D.,Casey, Jr., D. E.,Chung, M. K., de Lemos,J. A., et al.(2013).2013  ACCF/AHA guideline for the management of ST-elevation myocardial infarction.  J Am Coll Cardiol ,  61 (4), e78 – e140. Phrampus, P. E., & O’Donnell, J. M. (2013). Debriefing using a structured and supported approach. In A. I. Levine, S. DeMaria, Jr., A. D. Schwartz, & A. J. Sim (Eds.),  The comprehensive textbook of healthcare simulation (pp. 73 – 84). New York: Springer Science.

GLOSSARY   Absolute bradycardia  A heart rate of less than 60 beats/min.  Absolute refractory period  Corresponds with the onset of the QRS complex to about the peak of the  T wave on the electrocardiogram; cardiac cells cannot be stimulated to conduct an electrical impulse, no matter how strong the stimulus.  Accessory pathway  An extra bundle of working myocardial tissue that forms a connection between the atria and ventricles outside the normal conduction system.  Action potential A five-phase cycle that reflects the difference in the concentration of charged particles across the cell membrane at any given time.  Acute coronary syndrome (ACS) A group of conditions that are caused by an abrupt reduction in coronary artery blood flow; ACSs consist of three major syndromes: unstable angina, non – ST segment  elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).  Anginal equivalent  Symptom other than chest pain or discomfort resulting from myocardial ischemia  that may occur either alone or in combination in a patient with ischemic heart disease.  Arteriosclerosis  A chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls.  Atherosclerosis A form of arteriosclerosis in which the thickening and hardening of the vessel walls are caused by a buildup of fat-like deposits in the inner lining, specifically of large- and middle-sized muscular arteries.  Atypical presentation  Uncharacteristic signs and symptoms experienced by some patients.  Atrioventricular (AV) junction  AV node and the bundle of His.  Atrioventricular (AV) node Specialized cells located in the lower portion of the right atrium; delays the electrical impulse to allow the atria to contract and complete filling of the ventricles.  Automated external defibrillation  The placement of paddles or pads on a patient s chest and interpretation of the patient s cardiac rhythm by the defibrillator  s computerized analysis system. Depending  on the type of automated external defibrillator (AED) used, the machine will deliver a shock (if a  shockable rhythm is detected) or instruct the operator to deliver a shock.  Automated external defibrillator (AED)  A machine with a sophisticated computer system that analyzes a patient s heart rhythm using an algorithm to distinguish shockable rhythms from nonshockable rhythms and provides visual and auditory instructions to the rescuer to deliver an electrical shock, if a  shock is indicated. Bundle of His  Fibers located in the upper portion of the interventricular septum that conduct an electrical impulse through the heart; also called the  common bundle   or the  AV bundle. Capnography   The continuous analysis and recording of carbon dioxide concentrations in respiratory  gases. Cardiopulmonary (cardiac) arrest  The absence of cardiac mechanical activity, which is confirmed by  the absence of a detectable pulse, unresponsiveness, and apnea or agonal, gasping breathing. Cardiovascular collapse  A sudden loss of effective blood flow that is caused by cardiac and/or peripheral vascular factors that may reverse spontaneously (eg, syncope) or only with interventions (eg, cardiac arrest). Cardiovascular disease (CVD) A collection of conditions that involve the circulatory system, which contains the heart   (cardio)  and blood vessels (vascular), including congenital cardiovascular diseases. Carina  The point where the trachea divides into the right and left primary bronchi. Chain of Survival  The essential elements of a system of care that are necessary to link the victim of  sudden cardiac arrest with survival. ’

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Conduction system A system of pathways in the heart composed of specialized electrical (ie, pacemaker) cells. Coronary artery disease (CAD)  Disease affecting the arteries that supply the heart muscle with blood. Coronary heart disease (CHD) Disease of the coronary arteries and their resulting complications, such as angina pectoris and acute myocardial infarction. Cricothyroid membrane  A fibrous membrane located between the cricoid and thyroid cartilages. Defibrillation  Delivery of an electrical current across the heart muscle over a very brief period to terminate an abnormal heart rhythm; also called unsynchronized countershock or asynchronous countershock because the delivery of current has no relationship to the cardiac cycle. Defibrillator  A device used to administer an electrical shock at a preset energy level to terminate a cardiac dysrhythmia. Delta wave Slurring of the beginning portion of the QRS complex; caused by preexcitation. Depolarization Movement of ions across a cell membrane, causing the inside of the cell to become more positive; an electrical event expected to result in contraction. Effective refractory period  Period of the cardiac action potential that includes the absolute refractory  period and the first half of the relative refractory period. Electrocardiogram (ECG)   A recording of the heart s electrical activity from the body surface that  appears on ECG paper as specific waveforms and complexes. Electrode   Adhesive pad that contains a conductive gel and is applied at a specific location on the patient s chest wall and extremities and is connected by cables to an ECG machine. Epiglottis  A small piece of cartilage located at the top of the larynx that prevents foreign material from entering the trachea during swallowing. Glottis The true vocal cords and the space between them. Hard palate  Bony portion of the roof of the mouth that forms the floor of the nasal cavity. Heart disease A broad term that refers to conditions affecting the heart. His-Purkinje system   Portion of the conduction system consisting of the bundle of His, bundle branches, and Purkinje fibers. Interval  On the ECG, a waveform and a segment. Lead  A record (ie, tracing) of electrical activity between two electrodes. Manual defibrillation  The placement of paddles or pads on a patient  s chest, interpretation of the patient s cardiac rhythm by a trained health care professional, and the health care professional s decision to deliver a shock (if indicated). Myocardial cells Working cells of the myocardium that contain contractile filaments and form the muscular layer of the atrial walls and the thicker muscular layer of the ventricular walls. Nasal cannula  A piece of plastic tubing with two soft prongs that project from the tubing; used to deliver supplemental oxygen to a spontaneously breathing patient. Oxygenation The process of getting oxygen into the body and to its tissues for metabolism. Pacemaker cells  Specialized cells of the heart  s electrical conduction system, capable of spontaneously  generating and conducting electrical impulses. Pulse oximeter  A small instrument with a light sensor that quickly calculates the percentage of hemoglobin that is saturated with oxygen in a pulsating capillary bed. Refractoriness  A term used to describe the period of recovery that cells need after being discharged before they are able to respond to a stimulus. Relative bradycardia  A term that refers to a situation in which a patient  s heart rate may be more than 60 beats/min but, physiologically, the patient needs a tachycardia (as in hypovolemia) and is unable to increase his or her heart rate because of sinoatrial node disease, beta-blockers, or other medications. Relative refractory period  Corresponds with the downslope of the T wave on the ECG; cardiac cells can be stimulated to depolarize if the stimulus is strong enough. Repolarization Movement of ions across a cell membrane in which the inside of the cell is restored to its negative charge. Respiration  The exchange of oxygen and carbon dioxide during cellular metabolism. Risk factors  Traits and lifestyle habits that may increase a person s chance of developing a disease. Segment  On the ECG, a line between waveforms that is named by the waveform that precedes or follows it. Simple face mask  An oxygen delivery device that consists of a plastic reservoir that fits over a patient  s nose and mouth and a small diameter tube connected to the base of the mask through which oxygen is delivered; also called a  standard mask. ’

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Soft palate  The back part of the roof of the mouth that is made up of mucous membrane, muscular  fibers, and mucous glands. Stroke system of care  A comprehensive, diverse system that addresses all aspects of stroke care in a  coordinated fashion. Sudden cardiac death (SCD)  A natural death of cardiac cause that is preceded by an abrupt loss of  consciousness within 1 hour of the onset of an acute change in cardiovascular status; sudden cardiac  arrest  is a term commonly applied to such an event when the patient survives. Supernormal period  Period during the cardiac cycle when a weaker-than-normal stimulus can cause cardiac cells to depolarize. Supraventricular arrhythmias  Rhythms that begin in the sinoatrial node, atrial tissue, or the atrioventricular junction (ie, above the bifurcation of the His bundle). Symptomatic bradycardia  A term used to describe a patient who experiences signs and symptoms of  hemodynamic compromise related to a slow heart rate. Synchronized cardioversion The timed delivery of a shock during the QRS complex.  Transient ischemic attack (TIA)  A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.  Transthoracic impedance (resistance) The resistance of the chest wall to current. Uvula  Fleshy tissue that hangs down from the soft palate and into the posteriorportion of the oral cavity.  Vallecula  The space or  pocket   between the base of the tongue and the epiglottis.  Ventilation  The mechanical movement of gas or air into and out of the lungs. “

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INDEX  Note: Page numbers followed by  f   indicate figures, t   indicate tables, b   indicate boxes and ge   indicate glossary.

 A   ABC mnemonic, for general impression, 14 – 15  Absolute bradycardia, 167  Absolute refractory period (ARP), 68  ACC. See   American College of Cardiology (ACC)  Accelerating angina, 198 – 199  Accessory pathway, 70  ACE inhibitors. See   Angiotensin-converting enzyme (ACE) inhibitors  ACSs. See   Acute coronary syndromes (ACSs)  Action potential, 67 cardiac, 66 – 69, 66b , 66  f    Acute coronary syndromes (ACSs), 78 – 79, 78b , 193 – 236 algorithm, 218  f   analgesic therapy in, 217 – 218, 219t  anticoagulant therapy in, 222 – 224, 224t  atypical presentation of, 202 – 203 cause of, 194 electrocardiogram findings of, 204 – 214 hyperacute T waves, 204 – 214 QRS changes, 205, 205t  ST segment changes, 204 – 205, 205b   T wave inversion, 205 evaluation of, 201 – 215 patient history, 201 – 202, 201b  imaging studies for, 215 initial management of, 215 – 226 emergency department, 216 – 217 pharmacologic therapies, 217 – 224 prehospital, 215 – 216, 215b  pathophysiology of, 194 – 196, 195  f   patient evaluation for, 201 – 215 physical examination of, 203  Acute ischemic coronary syndromes (AICSs), 193 – 194  Acute ischemic stroke, 237 – 258, 237b , 238t   Acute stroke, 243 – 244. See also Stroke  Acute stroke-ready hospitals (ASRHs), 246 – 247  Acute stroke teams (ASTs), 246 – 247  Adam's apple, 26  Adenoids, 25  Adenosine, 134 – 136, 134t , 140b   Advanced airways, 49 – 59, 50 – 51b  endotracheal tube placement, confirming, 51 – 59, 51b   Advanced cardiac life support (ACLS), 1, 63  Advanced life support, effective, 8  AECDs. See  Automated external cardioverter-defibrillators (AECDs)  AED. See  Automated external defibrillator (AED)  AFib. See   Atrial fibrillation (AFib)  Agonist, 88b   AHA. See   American Heart Association (AHA)

 AHA/ASA. See  American Heart Association/American Stroke Association (AHA/ASA)  AICSs. See   Acute ischemic coronary syndromes (AICSs)  Airway(s) advanced, 49 – 59, 50 – 51b  lower, 27 – 28 management of, 23 – 62 manual, maneuvers for, 37 – 38, 38t  primary survey assessment of, 15 suctioning of, 39 – 40 upper, 25 – 27, 26 – 27b   Airway adjuncts, 40 – 44 nasal airway, 42 – 44, 43  f  , 44t  oral airway, 40 – 41, 41 – 42  f  , 44t   Alveolar ducts, 28  American College of Cardiology (ACC), 202 – 203  American Heart Association (AHA), 6, 202 – 203, 237  American Heart Association/American Stroke Association (AHA/ASA), 243 – 244  Amiodarone (Cordarone), 88, 89t   Analgesic therapy, 217 – 218, 219t   Anesthesiologist, 103b   Angina  Prinzmetal's, 199, 199b  stable, 197, 198b  terminology for, 198b  unstable, 198 – 199  variant, 199  Angina pectoris, 3, 197, 197 – 198b , 198  f    Anginal equivalent, 202 examples of, 203b   Angiotensin-converting enzyme (ACE) inhibitors, 221  Anterior circulation strokes, 239 – 240  Anterior interventricular artery, 65  Anterior myocardial in farction, 207 – 209, 208 – 209  f    Anterior oropharynx, 25 – 26  Anterolateral, 95  Anteroseptal myocardial infarction, 207  Anticoagulant therapy, 222 – 224, 224t   Antiplatelet therapy, 221 – 222, 223  f  , 223 – 224t   Apex-anterior position, 95  Area at risk, myocardial infarction, 200, 201  f    Arrhythmia, 63 – 65  Arteriosclerosis, 194, 195 – 196  f    Arytenoid cartilages, 26  Aspirin, 221, 224t   ASRHs. See   Acute stroke-ready hospitals (ASRHs)  ASTs. See   Acute stroke teams (ASTs)  Asynchronous countershock. See  Defibrillation

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 Asystole, 4, 88 – 89, 90  f   cardiac arrest rhythms, 88 – 89, 90  f   characteristics of, 90t  P-wave, 88, 90  f    ventricular, 88  AT. See   Atrial tachycardia (AT)  Atheromatous plaque, basic structure of, 195  f    Atherosclerosis, 194  Atherosclerotic lesions, types of, 195  Atherosclerotic plaques, 195  Atrial fibrillation (AFib), 145 – 148, 146 – 147  f  , 146t   Atrial flutter, 144 – 145, 144b , 144t , 145  f    Atrial tachycardia (AT), 133 – 136, 133  f  , 133t , 135  f    Atrioventricular blocks, 172 – 176 first-degree, 172 – 173, 173t , 173  f   second-degree, 173 – 175, 175  f   2:1, 175, 175t  type I, 173 – 174, 174  f  , 174t  type II, 174 – 175, 174  f  , 174t  third-degree, 176, 176  f  , 176b , 176t   Atrioventricular bundle. See   Bundle of His  Atrioventricular junction, 70 atrioventricular node and, 70 bundle of His and, 70  Atrioventricular nodal reciprocating tachycardia, 136 – 137  Atrioventricular nodal reentrant tachycardia (AVNRT), 137 – 138, 137t , 138  f    Atrioventricular node, 70  Atrioventricular reciprocating tachycardia, 136 – 137  Atrioventricular reentrant tachycardia (AVRT), 138 – 140, 139  f    Atropine sulfate, 170t   Atypical presentation, of acute coronary syndromes, 202 – 203  Augmented limb leads, 73, 73  f    Automated external cardioverter-defibrillators (AECDs), 100  Automated external defibrillation, 91, 99 operation of, 99  Automated external defibrillator (AED), 6  Automatic atrial tachycardia, 134  Automatic cells. See  Pacemaker cells  Automaticity, 66  AVNRT. See   Atrioventricular nodal reentrant tachycardia  (AVNRT)  AVRT. See   Atrioventricular reentrant tachycardia (AVRT)

B BAC. See   Brain Attack Coalition (BAC) Bad news, conveying, resuscitation efforts and, 111 – 112, 111b  Bag-mask device (BMD), 47, 47  f   supplemental oxygen, with/without, 48 Bag-mask resuscitator. See   Bag-mask device (BMD) Bag-mask ventilation, 47 – 49, 47  f  , 48b , 49  f   oxygen delivery, 47 – 48 troubleshooting, 49 Bag-valve-mask device. See   Bag-mask device (BMD) Basic life support (BLS), 1 cardiopulmonary resuscitation and, 6 BBB. See   Bundle branch block (BBB) Berman airway, 40 – 41, 41  f   Beta-blockers, 135t , 219, 220t  Biphasic defibrillation, 93 – 94 Biphasic defibrillators, 94 Biphasic truncated exponential (BTE) waveform, 93 – 94 Biphasic waveforms, 93 – 94, 94  f   Bipolar lead, 73 BLS. See   Basic life support (BLS)

BMD. See   Bag-mask device (BMD) Bradycardias, 167 – 192. See also specific types  absolute, 167 algorithm of, 177  f   relative, 167 sinus, 169, 169b , 169  f  , 169 – 170t  symptomatic, 167, 168b  Brain, arterial blood supply to, 240  f   Brain attack, 237b .  See also Stroke Brain Attack Coalition (BAC), 243 – 244 Brain imaging, 249 Breathing, 16 Bronchi primary, left and right, 27 – 28 secondary, 28 tertiary, 28 Bronchioles, 28 BTE waveform. See   Biphasic truncated exponential (BTE)  waveform Bulb-type esophageal detector devices, 51, 52  f   Bundle branch block (BBB), 140, 147  f  , 207 – 209 Bundle branches left, 70 right, 70 Bundle of His, 70. See also Bundle branches

C CAD. See   Coronary artery disease (CAD) Calcium channel blockers, 135t , 136b , 219 – 220, 220t  Capacitor, 92 Capnograms, interpreting, 31b  Capnography, 30 Capnometers, digital, 31 Carbon dioxide, monitoring of, 30 – 32 Cardiac action potential, 66 – 69, 66b , 66  f   phases of, 67 – 68, 68b , 68  f   Cardiac anatomy, 63 – 82 Cardiac arrest, 3 algorithm, 90 – 91, 92  f   heart rhythms in, 4, 83 – 128 in-hospital, 5 out-of-hospital, 4 – 5 phases of, 4t  pregnancy and, 107 primary, 4 sudden, 4 Cardiac Arrest Management station, 101b  Cardiac arrest rhythms, 83 – 128 asystole, 88 – 89, 90  f   pulseless electrical activity, 90 – 91, 90b , 91  f   resuscitation team, 100 – 124, 101b   ventricular fibrillation, 85 – 88  ventricular tachycardia, 85 Cardiac biomarkers, 214 – 215 Cardiac cells, 66 action potential of, 66 – 69, 66b , 66  f   Cardiac output, 10 Cardiac troponins, 214 Cardiopulmonary arrest, 3. See also Cardiac arrest  Cardiopulmonary resuscitation (CPR), 1 – 2, 10 – 13 barriers to effective, 10 – 11, 11b  cardiac output associated with, 10 in Chain of Survival, 6, 9 chest compressions mechanical devices, 12 – 13, 13 – 14  f   physiology of, 10, 10b  feedback during, 11 – 12, 12  f  

Index 

Cardiovascular care, after ROSC, 109 – 110 Cardiovascular collapse, 3 Cardiovascular disease (CVD), 2 – 3 risk factors for, 2 – 3, 3t  Cardioversion, synchronized, 150 Caregivers, assistance by resuscitation team, 112 – 124 Carina, 27 – 28 Carotid sinus, location of, 137  f   Carotid sinus massage (CSM), 136, 137  f   Carotid sinus pressure. See   Carotid sinus massage (CSM) Carotid territory strokes, 239 – 240 Centers for Disease Control and Prevention, 4 Central nervous system (CNS) infarction, definition of, 239 Cerebral hemorrhage, silent, 239 Cerebral venous thrombosis, stroke caused by, 239 Chain of Survival, 5 – 10 advanced life support, effective, 8 cardiopulmonary resuscitation and, 9 early, 6 defibrillation prompt, 9 rapid, 6 – 8, 7  f   definition, 5 in-hospital, 8 – 10 links in, 5 medical emergency team and, 8 notification and response, 9 out-of-hospital, 5 – 8 post-cardiac arrest care integration of, 8 intra-arrest and, 9 – 10 recognition and activation in, 6 surveillance and prevention, 8 – 9, 9b  CHD. See   Coronary heart disease (CHD) Chest compressions mechanical devices for, 12 – 13, 13 – 14  f   physiology of, 10, 10b  Chest hair, 94 – 95, 95b  Chest leads, 72 – 76 augmented limb, 73, 73  f   bipolar, 73 frontal plane, 73, 73t  horizontal plane, 73 – 76, 73 – 74b , 74  f  , 74 – 75t  standard limb, 73, 73  f   Chronotrope, 88b  Cilia, 28 Cincinnati Pre-hospital Stroke Scale (CPSS), 245 Circle of Willis, 239 – 240 Circulation, 16 Circumflex (CX) artery, 65 blockage of, 65 – 66 Closed-loop communication, resuscitation efforts, 105, 105b  Coarse  ventricular fibrillation, 85 – 86 Code, 5 Code blue, 5 Code director, 101 Code team, 100 Colorimetric capnometer, 31 – 32, 32  f   Common bundle, 70 Complexes of electrocardiogram, 76 – 77 Comprehensive stroke centers (CSCs), 247 Computed tomography (CT), 249 Conducting cells. See  Pacemaker cells Conduction system, 69 – 70, 71t  atrioventricular node, 70 bundle branches, right and left, 70 bundle of His, 70 “

”

Conduction system (Continued) Purkinje fibers, 70, 71t  sinoatrial node, 69 – 70, 69  f  , 70b  Conductive material, use of, 96 – 97, 96  f   Congenital cardiovascular disease, 2 – 3 Contributing risk factors, 2 – 3, 3t  Coronary arteries, 65 – 66 Coronary artery disease (CAD), 3 Coronary heart disease (CHD), 3 Coronary perfusion pressure, 10 CPR. See  Cardiopulmonary resuscitation (CPR) CPSS. See   Cincinnati Prehospital Stroke Scale (CPSS) Crash cart, 102 Crescendo angina, 198 – 199 Cricoid cartilage, 26 – 27 Cricothyroid membrane, 26 – 27 CRM. See   Powerheart Cardiac Rhythm Module (CRM) CSCs. See   Comprehensive stroke centers (CSCs) CSM. See   Carotid sinus massage (CSM) CT. See   Computed tomography (CT) CVD. See  Cardiovascular disease (CVD) CX artery. See   Circumflex (CX) artery  Cyclooxygenase inhibitors, 223t 

D Debriefing, resuscitation efforts, 110 – 111 Defibrillation, 91 – 100, 93b  automated external, 91, 99 biphasic, 93 – 94 manual, 91 monophasic, 93 – 94 primary survey assessment of, 16 procedure for, 97 – 99, 97 – 99b , 98  f   prompt, 9 rapid, 6 – 8 transthoracic impedance, 94 – 97, 94b  Defibrillation waveforms, 93 biphasic waveform, 93 – 94, 94  f   monophasic waveform, 93 – 94, 94  f   Defibrillators, 92 – 93, 93  f  . See also Defibrillation automated external, 6 biphasic, 94 monophasic, 94 Delta wave, 131 ge , 138 Depolarization, 67, 67b   wave of, 67 Digital capnometers, 31, 31  f   Disability, primary survey assessment of, 16 Dispatch time, 245 DNAR. See  Do-not-attempt-resuscitation (DNAR) Do-not-attempt-resuscitation (DNAR), 104 Dopamine, 171t , 171b  Dromotrope, 88b  Drug administration, 103, 103b  Ds of stroke care . See   Stroke Chain of Survival Dysrhythmia, 63 – 65 “

”

E E-C clamp technique, 46, 46  f   E-C grip, 46, 46  f   ECG. See  Electrocardiogram (ECG) Ectopic AT. See   Ectopic atrial tachycardia (ectopic AT) Ectopic atrial tachycardia (ectopic AT), 134 Ectopic pacemaker sites, 70, 70b  EDDs. See   Esophageal detector devices (EDDs) Effective refractory period (ERP), 68  f  , 69

283

284   Index 

Electrical capture, 178 – 179, 179  f   Electrical therapy, possible complications of, 100 Electrocardiogram (ECG), 71 – 78, 71  f  , 72b  absolute refractory period on, 68 chest leads for, 72 – 76 complexes of, 76 – 77 electrodes, 72, 72  f    waveforms of, 76 – 77, 76  f   Electrocardiography paper, 76, 76  f   Electrodes, 72, 72  f   Electromechanical dissociation, 90 Electrophysiology, 63 – 82 cardiac cells, 66 conduction system, 69 – 70 refractory periods, 68 – 69, 68  f   Embolic ischemic stroke, 242 – 243 Emergency cardiovascular care, 1 – 22 Chain of Survival, 5 – 10 coronary artery disease, 3 patient assessment, 14 – 19 sudden cardiac death, 4 Emergency medical services (EMS), 6 on stroke care, 244 – 246 Emergency medical technicians (EMTs), 100 EMS. See   Emergency medical services (EMS) EMTs. See   Emergency medical technicians (EMTs) Endotracheal intubation, 50, 50  f   Epiglottis, 25 – 26 Epinephrine, 86 – 88, 87t , 171b  ERP. See   Effective refractory period (ERP) Esophageal detector devices (EDDs), 51 – 59 Esophageal intubation detectors, 51 Exposure, assessment of patient's, 16 Extracorporeal CPR, 106b  Extraglottic airway devices, 49 – 50

F Face Arm Speech Test (FAST), 245 Family notification, resuscitation efforts, 111 – 112 FAST. See   Face Arm Speech Test (FAST) FBAO. See   Foreign body airway obstruction (FBAO) Fibrinolytics, 224 "Fine" ventricular fibrillation, 85 – 86 First-degree atrioventricular block, 172 – 173, 173t , 173  f   Five Hs, 86, 87b  Five Ts, 86, 87b  "Fixed" risk factors, 2 – 3, 3t  Flexible suction catheters, 39 Flow rates of nasal cannula, 33 of nonrebreather mask, 36b  of partial rebreather mask, 36 of simple face mask, 34 Flutter waves, 144, 145  f   Focal AT. See   Focal atrial tachycardia (focal AT) Focal atrial tachycardia (focal AT), 134 Foreign body airway obstruction (FBAO), 6 French suction catheters, 39 Frontal plane leads, 73, 73t 

G Gasping, 3 Gastric distention, 46b  GCS. See   Glasgow Coma Scale (GCS) Glasgow Coma Scale (GCS), 249 Glottic opening, 26

Glottis, 26 Glycoprotein (GP) IIb/IIIa receptor inhibitors,221 – 222,223t  Guedel airway, 40 – 41, 41  f  

H Hard palate, 25 – 26 Head tilt-chin lift, 37, 37  f  , 38t  Heart, surfaces of, 204  f   Heart attack, 237b  Heart disease, 1 Heart rhythms. See also specific types  in cardiac arrest, 83 – 128 asystole, 88 – 89, 90  f   pulseless electrical activity, 90 – 91, 90b , 91  f   resuscitation team, 100 – 124, 101b   ventricular fibrillation, 85 – 88  ventricular tachycardia, 85 nonshockable, 86 – 88, 106 – 107 shockable, 86 – 88, 97b , 105 – 106, 106b  Hemorrhagic stroke, 240b  HFNC systems. See   High-flow nasal cannula (HFNC) systems HI-D Big Stick suction tip, 39, 39  f   High-flow nasal cannula (HFNC) systems, 34 His-Purkinje system, 70 Horizontal plane leads, 73 – 76, 73 – 74b , 74  f  , 74 – 75t  Hyperacute T waves, 204 Hypercarbic respiratory failure, 28 Hyperventilation, 10b  Hypopharynx, 25 Hypoxemic respiratory failure, 28

I Ibutilide, 144 – 145, 146t  ICH. See  Intracerebral hemorrhage (ICH) Idioventricular rhythm, 171 – 172. See also Ventricular escape rhythm IHCA. See   In-hospital cardiac arrest (IHCA) In-hospital cardiac arrest (IHCA), 5 In-hospital Chain of Survival, 8 – 10 Inferior myocardial infarction, 209 – 210, 210 – 211  f   Inferobasal myocardial infarction, 211 – 213, 212  f  , 213b  Inferobasal wall myocardial infarction, 211 Inotrope, 88b  Intermediate coronary syndrome, 198 – 199 Intervals, 77 – 78, 77  f  , 78b  Intracerebral hemorrhage (ICH), 241 – 242, 241b  definition of, 239 stroke caused by, 239 Intravenous fibrinolysis, 249 – 250 Inverted T waves, 204 – 205 Irregular tachycardias, 143 – 149 atrial fibrillation, 145 – 148, 146 – 147  f  , 146t  atrial flutter, 144 – 145, 144b , 144t , 145  f   multifocal atrial tachycardia, 143, 143t , 144  f   polymorphic ventricular tachycardia (PMVT), 148 – 149, 148 – 149  f  , 148 – 149t  Ischemic penumbra, 243, 243  f   Ischemic stroke, 241  f  , 242 – 243 acute, 237 – 258, 237b , 238t  definition of, 239 embolic, 242 – 243 lacunar, 243 signs and symptoms of, 242t  thrombotic, 242 Isoproterenol, 171t , 171b 

Index 

J  J point , 77  Jaw thrust, 38, 38t , 38  f    Joint Commission National Patient Safety Goals , 8  Joint Commission on Accreditation of Healthcare Organizations, 8  Junctional bradycardia, 169 – 170  Junctional dysrhythmias, 70b   Junctional escape rhythm, 169 – 171, 170t , 170  f  , 171b 

L Lacunar infarcts, 243 Lacunar strokes, 243 LAD artery. See   Left anterior descending (LAD) artery  Laryngeal mask airway (LMA), 49 – 50, 50  f   Laryngopharynx, 26 Larynx, 26 Latent pacemaker, 70 Lateral myocardial infarction, 209, 209 – 210  f   LCA. See   Left coronary artery (LCA) Lead aVR, 213 – 214 Lead wire, 72 Leads. See   Chest leads Left anterior descending (LAD) artery, 65, 207 Left coronary artery (LCA), 65 Left main coronary artery (LMCA), 65 Lidocaine (Xylocaine), 88, 89t  Life support, advanced. See also Basic life support (BLS) effective, 8 Lipid management, 221, 221t  LMA. See   Laryngeal mask airway (LMA) LMCA. See   Left main coronary artery (LMCA) Los Angeles Motor Scale, 245 Lower airway, 27 – 28

M MACE. See   Major adverse cardiac event (MACE) Magnesium sulfate, 149t  Magnetic resonance imaging (MRI), 249 Major adverse cardiac event (MACE), 214 – 215 Manual airway maneuvers, 37 – 38, 38t  head tilt-chin lift, 37, 37  f  , 38t   jaw thrust, 38, 38t , 38  f   Manual defibrillation, 91 MAT. See   Multifocal atrial tachycardia (MAT) Mechanical cells, 66 Mechanical chest compression devices, 12 – 13, 13 – 14  f   Medical emergency team (MET), 8 Mega Code station, 101b  MET. See   Medical emergency team (MET) MEWS. See   Modified Early Warning Score (MEWS) MI. See   Myocardial infarction (MI) Ministroke. See   Transient ischemic attack (TIA) Modifiable risk factors, 2 – 3, 3t  Modified Early Warning Score (MEWS), 8 Modified jaw thrust, 38 Monomorphic ventricular tachycardia, 142 Monophasic defibrillation, 93 – 94 Monophasic defibrillators, 94 Monophasic waveform, 93 – 94, 94  f   Mouth-to-mask ventilation, 45 – 46, 47t , 47  f   MRI. See   Magnetic resonance imaging (MRI) Multifocal atrial tachycardia (MAT), 143, 143t , 144  f   Myocardial blood flow, 10 Myocardial cells, 66

Myocardial infarction (MI), 65, 196 – 200, 200 – 201  f   anatomic location of, 204  f  , 206 – 213, 206 – 207t , 206  f   anterior, 207 – 209, 208 – 209  f   inferior, 209 – 210, 210 – 211  f   inferobasal (posterior), 211 – 213, 212  f  , 213b  lateral, 209, 209 – 210  f   right ventricular, 213, 213 – 214  f   anteroseptal, 207 classification of, 205t  common cause of, 66b  coronary heart disease and, 3 transmural, 200 Myocardial injury, 196 – 200 Myocardial ischemia, 196 – 200, 196b , 197  f  , 198b  pain descriptions uncharacteristic of, 202 – 203

N Narrow-QRS tachycardias, 131 – 140, 134 – 135t , 135  f   atrial tachycardia, 133 – 136, 133  f  , 133t , 135  f   atrioventricular nodal reentrant tachycardia (AVNRT), 137 – 138, 137t , 138  f   atrioventricular reentrant tachycardia (AVRT), 138 – 140, 139  f   sinus tachycardia, 131 – 132, 131t , 132  f  , 132b  Nasal airway, 42 – 44, 43  f  , 44t  Nasal cannula, 33 – 34, 33b , 33  f  , 37t  Nasal prongs, 33 Nasal trumpet. See   Nasal airway  Nasopharyngeal airway (NPA). See   Nasal airway  Nasopharynx, 25 National Institutes of Health Stroke Scale (NIHSS), 248 National Stroke Association (NSA), 243 – 244 Negative T waves, 204 Neurologic care, after ROSC, 110 NIHSS. See   National Institutes of Health Stroke Scale (NIHSS) Nitroglycerin (NTG), 217, 219t  NIV. See   Noninvasive ventilation (NIV) Non-ST elevation acute coronary syndromes (NSTE-ACSs), 199 Noninvasive pacing. See   Transcutaneous pacing (TCP) Noninvasive positive pressure ventilation (NPPV), 44 – 45, 45b  Noninvasive ventilation (NIV), 44 – 45 "Nonmodifiable" risk factors, 2 – 3, 3t  Nonrebreather mask, 35  f  , 36, 36b , 37t  Nonshockable rhythms, 86 – 88, 106 – 107 Nonsustained rhythm, 134 NPPV. See  Noninvasive positive pressure ventilation (NPPV) NSA. See   National Stroke Association (NSA) NSTE-ACSs. See   Non-ST elevation acute coronary  syndromes (NSTE-ACSs) NTG. See   Nitroglycerin (NTG) Nurse anesthetist, 103b 

O Occlusive stroke, 242 OHCA. See   Out-of-hospital cardiac arrest (OHCA) On-scene time, 245 OPA. See   Oropharyngeal airway (OPA) Opioid overdose, 107 Oral airway, 40 – 41, 42  f  , 44t  Oropharyngeal airway (OPA), 40 Oropharynx, 25 – 26 Orotracheal intubation, 25 – 26 Out-of-hospital cardiac arrest (OHCA), 4 – 5 Out-of-hospital Chain of Survival, 5 – 8

285

286   Index 

Oxygen delivery devices, 32 – 36 bag-mask ventilation, 47 – 49 nasal cannula, 33 – 34, 33b , 33  f  , 37t  nonrebreather mask, 35  f  , 36, 36b , 37t  partial rebreather mask, 35 – 36, 35 – 36b , 35  f  , 37t  simple face mask, 34, 34  f  , 34b , 37t  Oxygenation, 29 pulse oximetry, 32b  ROSC and, 108

P P-wave, asystole, 88, 90  f   P2Y 12  receptor inhibitors, 221, 223t  PAC. See   Premature atrial complex (PAC) Pacemaker cells, 66 Paddle/pad position, 95 – 96, 95 – 96  f   size, 95 Paddle pressure, 97 Palatine tonsils, 25 – 26 Paroxysmal, definition of, 133 Paroxysmal AT. See   Paroxysmal atrial tachycardia (PAT) Paroxysmal atrial tachycardia (PAT), 133 Paroxysmal supraventricular tachycardia (PSVT), 133, 134  f   Partial rebreather mask, 35 – 36, 35 – 36b , 35  f  , 37t  PAT. See   Paroxysmal atrial tachycardia (PAT) PATCH-4-MD, 86, 86b  Patient assessment, 14 – 19 general impression of condition, 14 – 15 primary survey, 15 – 16, 15b  responsive patient, 15 – 16 unresponsive patient, 16, 16b   with respiratory compromise, 29 – 32 scene safety, 14 secondary survey, 17 – 19 components, 17b  Patient history, of acute coronary syndromes, 201 – 202, 201b  PCI. See   Percutaneous coronary intervention (PCI) PEA. See   Pulseless electrical activity (PEA) Percutaneous coronary intervention (PCI), 224 Pharyngeal tonsils, 25 Pharynx, 25 laryngopharynx, 26 nasopharynx, 25 oropharynx, 25 – 26 Physical examination, of acute coronary syndromes, 203 PMVT. See   Polymorphic ventricular tachycardia (PMVT) Pocket face mask, 45 – 46 Pocket mask, 45 – 46, 45  f   POCUS. See   Point of care ultrasound (POCUS) Point of care ultrasound (POCUS), 90 – 91 Polymorphic ventricular tachycardia (PMVT), 148 – 149, 148 – 149  f  , 148 – 149t  Poor R-wave progression, 77 Positive pressure ventilation, 44 – 49 bag-mask ventilation, 47 – 49, 48b , 49  f   mouth-to-mask ventilation, 45 – 46, 47t , 47  f   noninvasive positive pressure ventilation, 44 – 45, 45b  Post-cardiac arrest care, 102, 108 – 110, 108t , 109  f   integration of, 8 intra-arrest and, 9 – 10 Post-cardiac arrest syndrome, components of, 108t  Posterior chest lead, 75  f   Posterior circulation strokes, 239 – 240 Posterior wall myocardial infarction, 211 Postresuscitation support, 102. See also POst-cardiac arrest  care

Powerheart Cardiac Rhythm Module (CRM), 100 Pregnancy, cardiac arrest and, 107 Preinfarction angina, 198 – 199 Premature atrial complex (PAC), 137 Premature ventricular complexes (PVCs), 142 Preocclusive syndrome, 198 – 199 Primary bronchi, left and right, 27 – 28 Primary bronchi bifurcation, 27  f   Primary cardiac arrest, 4 Primary percutaneous coronary intervention, 224 in STEMI recommendations, 225b  Primary stroke centers (PSCs), 247 Primary survey, on patient, 15 – 16, 15 – 16b  Prinzmetal's angina, 199, 199b  Procainamide, 140 – 141, 141t  PSCs. See   Primary stroke centers (PSCs) PSVT. See  Paroxysmal supraventricular tachycardia (PSVT) Public access defibrillation, 6 Pulmonary compliance, 49 Pulse ox. See   Pulse oximeter  Pulse oximeter, 29, 30b  Pulse oximetry, 29 – 30, 30  f  , 32b  accuracy of, factors affecting, 30b  Pulseless electrical activity (PEA), 4, 90 – 91, 90b , 91  f   Pulseless ventricular tachycardia (pVT), 4 Purkinje fibers, 67 – 68, 70, 71t  PVCs. See  Premature ventricular complexes (PVCs) pVT. See   Pulseless ventricular tachycardia (pVT)

Q QRS complexes of polymorphic ventricular tachycardia, 148, 148  f   of ventricular tachycardia, 85  f   QT interval, 78

R R-wave progression, 77 RACE. See   Rapid Arterial Occlusion Evaluation (RACE) Rapid Arterial Occlusion Evaluation (RACE), 245 Rapid Response System (RRS), 8 calling criteria, 9b  Rapid response team (RRT), 8 RCA. See   Right coronary artery (RCA) Rectilinear biphasic (RLB) waveform, 93 – 94 Reentrant tachycardias, 136 – 140 Reentry, 136 – 137 Refractoriness, 68 Refractory periods, 68 – 69, 68  f   Relative bradycardia, 167 Relative refractory period (RRP), 69 Renin-angiotensin-aldosterone system inhibitors, 221, 222t  Reperfusion therapies, 224 – 226, 225b  Repolarization, 67 Respiration, 29 Respiratory compromise, patient with, 28 – 32 Respiratory failure hypercarbic, 28 hypoxemic, 28 Respiratory system, anatomy of, 25 – 28 Response time, 245 Resuscitation efforts, 104 – 112, 104b  caregivers, assisting, 112 – 124 closed-loop communication, 105, 105b  debriefing, 110 – 111 family notification, 111 – 112 conveying bad news, 111 – 112, 111b 

Index 

Resuscitation efforts (Continued) nonshockable rhythms, 106 – 107, 107b  patient transfer, 107 post-cardiac arrest care, 108 – 110, 109  f   cardiovascular care, 109 – 110 neurologic care, 110 oxygenation and ventilation, 108 shockable rhythms, 105 – 106, 106b  special resuscitation situations, 107 cardiac arrest and pregnancy, 107 known/suspected opioid overdose, 107 Resuscitation mask, 45 – 46 Resuscitation team, 100 – 124, 101b  team leader, responsibilities of, 101 – 102 team member, responsibilities of, 102 – 104, 103b  Return of spontaneous circulation (ROSC), 108 Right chest leads, 74, 75t , 75  f   Right coronary artery (RCA), 65, 65  f   blockage of, 65 Right ventricular infarction (RVI), 213, 213 – 214  f   Rigid suction catheters, 39, 39  f   Risk factors contributing, 2 – 3, 3t  defined, 2 – 3 fixed , 2 – 3, 3t  modifiable, 2 – 3, 3t  nonmodifiable , 2 – 3, 3t  RLB waveform. See   Rectilinear biphasic (RLB) waveform ROSC. See   Return of spontaneous circulation (ROSC) RRP. See   Relative refractory period (RRP) RRS. See   Rapid Response System (RRS) RRT. See   Rapid response team (RRT) RSVP system, 104b  RVI. See   Right ventricular infarction (RVI) “

“

”

”

S SAH. See  Subarachnoid hemorrhage (SAH) Saturation of peripheral oxygen (SpO 2), 29 SBAR acronym, 104b  SCD. See   Sudden cardiac death (SCD) Second-degree atrioventricular blocks, 173 – 175, 175  f   2:1, 175, 175t  type I, 173 – 174, 174  f  , 174t  type II, 174 – 175, 174  f  , 174t  Secondary bronchi, 28 Secondary survey, on patient, 17 – 19 Segments, 77 – 78, 77  f  , 78b  Selected energy, 97 Serum biomarkers, 214 Serum cardiac markers, 214 Severe sinus bradycardia, 169 Shockable rhythms, 86 – 88, 97b , 105 – 106, 106b  Silent central nervous system infarction, definition of, 239 Silent cerebral hemorrhage, definition of, 239 Simple face mask, 34, 34  f  , 34b , 37t  Sinoatrial node, 69 – 70, 69  f  , 70b  Sinus bradycardia, 169, 169b , 169  f  , 169 – 170t  Sinus tachycardia, 131 – 132, 131t , 132  f  , 132b  SNP. See   Supernormal period (SNP) Soft palate, 25 – 26 Soft suction catheters, 39, 40  f   Sotalol, 140 – 141, 141t  SPIKES protocol, 111 – 112, 111b  SpO2. See   Saturation of peripheral oxygen (SpO 2) ST junction, 77 ST segment, changes of, with acute coronary syndrome, 204 – 205, 205b 

Stable angina, 197, 198b  Standard limb leads, 73, 73  f   Standard mask, 34. See also Simple face mask  Stroke, 237b .  See also specific types  anatomy review, 239 – 240, 240b , 240  f   anterior circulation, 239 – 240 carotid territory, 239 – 240 cerebral venous thrombosis, caused by, 239 conditions mimicking, 248b  definition of, 239 hemorrhagic, 240b  intracerebral hemorrhage, caused by, 239 occlusive, 242 posterior circulation, 239 – 240 Stroke Chain of Survival for, 237, 238 t  subarachnoid hemorrhage, caused by, 239 types of, 240 – 243 intracerebral hemorrhage, 241 – 242, 241b  ischemic stroke, 241  f  , 242 – 243, 242t  subarachnoid hemorrhage, 240 – 241 transient ischemic attack, 243  vertebrobasilar territory, 239 – 240  warning signs of, 244b  Stroke centers, 246 – 250, 246t  best practices, 250 brain imaging, 249 diagnostic tests, 248, 248b  intravenous fibrinolysis, 249 – 250 neurologic examination, 248 other therapies, 250 patient history, 247 physical examination, 247 – 248, 248b  triage and initial evaluation, 247 Stroke Chain of Survival, 237, 238t  Stroke systems of care, 243 – 250 acute phase of, 244 emergency medical services on, 244 – 246 hyperacute phase of, 244 prehospital assessment and management, 245 – 246 public education, 244, 244b  Subarachnoid hemorrhage (SAH), 240 – 241, 241  f   definition of, 239 stroke caused by, 239 Subendocardial area, 200 Subepicardial area, 200 Suction catheters flexible, 39 French, 39 rigid, 39, 39  f   soft, 39, 40  f   tonsil tip, 39  whistle tip, 39  Yankauer, 39 Suctioning of airway, 39 – 40, 40b  possible complications of, 40b  Sudden cardiac arrest, 4 Sudden cardiac death (SCD), 2 – 5, 3  f   definition of, 4 Supernormal period (SNP), 69 Support roles, in resuscitation team, 103 – 104 Supraglottic airways, 49 – 50 Supraventricular arrhythmias, 131, 131 ge  Supraventricular dysrhythmias, 70b  Supraventricular tachycardia (SVT), 132 – 140, 132b , 133  f   Sustained rhythm, 134 SVT. See   Supraventricular tachycardia (SVT) Sympathetic receptors, 88b  Symptomatic bradycardia, 167, 168b 

287