15 LECTURE's Final for Print

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LECTURES IN ANAESTHESIOLOGY FOR MEDICAL STUDENTS

BY PROF. BRIG. M. SALIM SI(M) MBBS: MCPS (Pak); D.A. (London); FFARCSI (Dublin) FRCA (London); FCPS (Pak); Ph.D ,FRCP; FICS, FACS. Diploma in Acupuncture (China); D.Sc. (Hony) Fellow Medicina Alternativa.

HIGHER EDUCATION COMMISSION ISLAMABAD

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Copyrights @ Higher Education Commission Islamabad Lahore Karachi

Peshawar

All rights are reserved. No part of this publication may be reproduced, or transmitted, in any form or by any means – including, but not limited to, electronic, mechanical, photocopying, recording, or, otherwise or used for any commercial purpose what so ever without the prior written permission of the publisher and, if publisher considers necessary, formal license agreement with publisher may be executed. Project: “Monograph and Textbook Writing Scheme” aims to develop a culture of writing and to develop authorship cadre among teaching and researcher community of higher education institutions in the country. For information please visit: www.hec.gov.pk HEC – Cataloging in Publication (CIP Data): Salim, M. Basics of pain medicine 1. Pain 2. Medicine Includes index 616.849-dc22 ISBN: 969-8963-00-6 First Edition 2007 (Published by HEC) Second Edition 2014 Copies Printed: 500 Published By: D. G. Administration, Higher Education Commission, Islamabad–Pakistan Disclaimer: The publisher has used its best efforts for this publication through a rigorous system of evaluation and quality standards, but does not assume, and hereby disclaims, any liability to any person for any loss or damage caused by the errors or omissions in this publication, whether such errors or emissions result from negligence, accident, or any other cause.

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LECTURES IN ANAESTHESIOLOGY FOR MEDICAL STUDENTS

BY PROF. BRIG. M. SALIM SI(M) MBBS: MCPS (Pak); D.A. (London); FFARCSI (Dublin) FRCA (London); FCPS (Pak); Ph.D ,FRCP; FICS, FACS. Diploma in Acupuncture (China); D.Sc. (Hony) Fellow Medicina Alternativa. 

Professor of Anaesthesiology & Pain Medicine Islamic International Medical College, Rawalpindi.



Honorary Consultant & Instructor Armed Forces Post Graduate Medical Institute, Rawalpindi.



President: Society for Treatment and Study of Pain (STSP)



Chief Editor, JIIMC



Chief Editor, Anaesthesia, Pain & Intensive Care



Patron,, Rawal Medical Journal

FORMERLY: 

Prof. of Anaesthesia, Rawalpindi Medical College Holy Family Hospital, Rawalpindi.



Professor of Anaesthesiology Army Medical College, Rawalpindi.



Advisor in Anaesthesia Armed Forces of Pakistan.



Dean faculty of Anaesthesiology College of Physicians and Surgeons of Pakistan. 3

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CONTENTS List of figure …………………………………………………………………………………………………………vii Dedication………………………………………………………………………………………………….………...ix Forewords………………………………………………………………………………………………….………...xi Preface……………………………………………………………………………………………………………….xiii Introduction…………………………………………………………………………………………………………..xv Lecuter-1 Preoperative Assessment and Premedication……………………………………………….……….……..1 Lecuter-2 Inhalational Anaesthetic Agents……………………….........................................................................15 Lecuter-3 Intravenous Anaesthetic Agents …………………………………………..…………………………………27 Lecuter-4 Muscle Relaxants ……………………………………………..……………..………………………………..31 Lecuter-5 Local Anaesthetic Agents …………………………………………………..………………………………..37 Lecuter-6 Regional Anaesthesia.........................................................................................................................41 Lecuter-7 Fluid Management ……………………………………………………………………………..…………......57 Lecuter-8 Acid-Base & Electrolyte Balance …………………………………………………………….……………...65 Lecuter-9 Blood Gases, Pulse Oximetry and Capnography…………………………………………..……………...73 Lecuter-10 Anaesthesia and Related Diseases ………………………………..……………………………………….79 Lecuter-11 Cardiopulmonary Resuscitation…………………………………………………………...…………….…..85 Lecuter-12 Pain………………………………………………………………………………………..……………….…...95 Lecuter-13 ICU…………………………………………………………………………………………………………..….99 Lecuter-14 Complications of Anaesthesia …………………………………………….………………………………..103 Lecuter-15 Post Operative Recovery and Care …………………………………………………….…………………111 Appendix……………………………………………………..……………………………………...................119 Suggested Reading………………………………………………………………………………..……………131 Index………………………………………………………..………………………………………………………133

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LECTURE 1

PREOPERATIVE ASSESSMENT AND PREMEDICATION Q:

WHAT IS THE AIM OF PREOPERATIVE ASSESSMENT?

The preoperative management affects outcome for better or worse, and central to achieving the best possible outcome is a thorough preoperative evaluation intended to:    

Identify the health problems that place the patient at increased risk. Resolve and control diseases as well as possible. Define a management plan that minimizes preoperative, intraoperative, and especially postoperative risks. The Aim of preoperative evaluation is to reduce morbidity and mortality.

Q: WHAT POINTS WOULD YOU KEEP IN MIND WHILE TAKING THE HISTORY? 1. General medical and surgical history. Ask especially about:          

2. 3. 4. 5. 6. 7. 8.

Cardiovascular system --- hypertension, angina, orthopnoea, ankle swelling, previous MI, rheumatic fever, valvular heart disease. Respiratory system --- shortness of breath, cough, sputum, wheezing, asthma, tobacco abuse. Hepatic --- viral hepatitis, jaundice, cirrhosis. Renal --- renal failure. Gastrointestinal --- peptic ulcer disease. CNS --- seizures, peripheral neurological deficit, stroke, muscle dystrophies. Musculoskeletal --- osteoarthritis, rheumatoid arthritis. Endocrine --- diabetes mellitus, thyroid disease. Haematology --- easy bruising or prolonged bleeding. Dental --- temporomandibular joint disorder, loose or missing teeth. Previous anaesthetics and ill effects. Drug therapy including oral contraceptives and aspirin. Excessive alcohol intake. Allergies. Pregnancy. Time of last intake of food and drink. A consent form.

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Q:

WHAT PHYSICAL EXAMINATION SHOULD BE DONE BY AN ANAESTHETIST?

1. Respiratory System:  Cyanosis.  Finger clubbing.  Pattern of breathing.  Mediastinal shift.  Localizing signs.  Presence of added sounds on auscultation. 2. Cardiovascular system:  Pulse (rate, rhythm and character).  Venous pressure and character.  Peripheral dependant oedema.  Blood pressure.  Apex beat.  Thrills.  Extra heart sounds and murmurs. 3. State of nutrition, malnutrition and obesity. 4. Skin colour, especially pigmentation.

pallor,

cyanosis,

jaundice

or

5. Psychological state of the patient, especially anxiety. 6. The airway(The Airway are assessed by Mallampati scoring system). 7. Ease of venous cannulation.

Q:

WHAT INVESTIGATIONS SHOULD BE AVAILABLE AT PREOPERATIVE ASSESSMENT?

Depending upon the age and condition of the patient following investigations may be required: 1. 2. 3. 4. 5.

Urine tests, especially for sugar, ketones and protein. Haemoglobin and blood count. Blood urea and Creatinine. Serum electrolytes. Blood glucose. 15

6. E.C.G. 7. Chest X-ray. 8. Echocardiogram. 9. Bedside pulse oximetry. 10. Other special investigations may be ordered when indicated. The above investigations help to assess the status of the patient condition. The anaesthetist should correct any abnormality in the investigation before giving anaesthesia. He may refer the patient to appropriate consultant.

Q: WHAT IS ASA (AMERICAN SOCIETY ANAESTHESIOLOGISTS) SCORING SYSTEM?

OF

The ASA scoring system describes the preoperative condition of a patient. It makes no allowances for the patient’s age, smoking history, any obesity or pregnancy. Addition of postscript E indicates emergency surgery. THE ASA SCORING SYSTEM I Healthy patient. II Mild systemic disease, no functional limitations. III Moderate systemic disease, definite functional limitation. IV Severe systemic disease that is a continuous threat to life. V Moribund patient, unlikely to survive 24 hours with or without operation.

Q: WHAT IS MALLAMPATI SCORING SYSTEM? Clinical assessment of airway is very essential. In Mallampati scoring system, the patient sits opposite the anesthetist with mouth open and tongue protruded. The structures visible at the back of the mouth are noted as described below.  

Class 1 – faucial pillars, soft palate and uvula visible. Class 2 – faucial pillars and soft palate visible, uvula masked by base of tongue.  Class 3 – only soft palate visible.  Class 4 – soft palate not visible. Mallampati scoring system helps the anaesthetist for easy intubation. Patients in class1 and 2 are intubated easily for other classes anaesthetist adopted other measures to intubate the patients such as stylet or fiber optic laryngoscope.

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Q: WHAT ARE THE EFFECTS OF PRE- EXISTING DURG THERAPY? 1. Antihypertensive drugs are normally continued up to the time of surgery, otherwise hypertensive crisis may occur. Adequate therapy restores a normal blood volume and minimizes the risk of a dangerous fall of arterial pressure at induction of anaesthesia. The avoidance of hypovolaemia during surgery is important. Bradycardia is common in those taking betablocking drugs. 2. Antianginal drugs such as calcium channel blockers or nitrates should not be stopped before surgery without a very specific reason, or angina may recur. 3. Lithium should be stopped 2 days before major surgery as it potentiates the non-depolarizing group of relaxants. In emergency cases Suxamethonium and regional blocks should be considered. 4. Monoamine oxidase inhibitors such as phenelzine should be discontinued 2 weeks before surgery, otherwise hypo or hypertensive crisis may occur and its prolongs analgesics effect particularly pethidine and opioids. 5. Levodopa should be continued upto the time of surgery to prevent the recurrence of severe Parkinsonism, dysphagia and aspiration pneumonia. 6. Steroid therapy suppresses ACTH production by the anterior pituitary. In time the adrenal cortex atrophies and is thus unable to increase its secretions in response to stress. This results in profound hypotension during and after anaesthesia with decreased sensitivity to catecholamine. Thus it is generally safer to assume some diminution of adrenal reserve and to give extra hydrocortisone over the period of surgery, e.g. hydrocortisone 100 mg i.m. just before surgery, and continued 6 to 8 hourly for 24 hours after minor surgery, or for 3 days in case of major surgery. 7. insulin should be continued. The patient should be NPO after midnight, no IV fluids, and half of the usual morning subcutaneous dose given. Hypoglycemia and hyperglycemia should be avoided. 8. Oral contraceptives should be discontinued 4 weeks prior to surgery as they increase the risk of DVT.

Q: WHAT ARE THE REASONS FOR THE ADMINISTRATION OF PREMEDICANTS? 

To reduce fear and anxiety.

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  

To reduce saliva secretion. To prevent vagal reflexes, due to surgical stimulation or associated with medication. For specific therapeutic affects, e.g. steroids, H2 blockers, etc.

Q: WHAT ARE THE PREMEDICATION?

DIFFERENT

DRUGS

USED

FOR

SEDATIVES BENZODIAZEPINES These are all good premedicants and can be given orally producing sedation, amnesia and freedom from anxiety. Midazolam: has been used for night sedation before surgery (7.5 – 15 mg) or as premedication. Dose is 70-100 mcg/kg i.v. 30-60 min before surgery. Diazepam: 10-20 mg, orally or i.v. duration 4-8 hrs. ANALGESICS Long acting NSAIDs gives useful background analgesia. Ketoprofen (100-200 mg oral or rectal, 30 mg i.m, i.v.), Piroxicam (20-40 mg oral), Diclofenac (50-100 mg oral or rectal) will all give useful analgesia in patients suffering from pain preoperatively. Pethidine or Morphine can also be used. ANTICHOLINERGIC AGENTS

ATROPINE

Effects on nervous system: 

Competitive blocking action on muscarinic receptors supplied by postganglionic cholinergic nerves.  Complete vagal blockade requires a dose of 3mg.  Inhibits sweating.  Stimulates the medulla and higher centres. Effects on eye:  Dilated pupils.  Loss of accommodation. Effects on respiratory system:  Sweat, bronchial and salivary glands are inhibited.  Bronchodilatation.  Slight increase in anatomical dead space. Effects on circulatory system.  Tachycardia.  Decreased filling time.

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 Increased myocardial oxygen consumption.  Cardiac output and blood pressure is increased. Effects on alimentary system.  Tone and peristalsis of gut are decreased.  Increases chances of regurgitation. Dose: usual adult dose, 0.6 mg i.m. (in children 0.015 mg/kg) 1 hr before operation. With neostigmine the dose is 1-2 mg.

HYOSCINE HYDROBROMIDE: Used as a gastrointestinal antispasmodic. It is a tertiary amine, so crosses the blood-brain barrier and causes sedation. Occasionally it produces central anticholinergic syndrome. It is a mild respiratory stimulant, while its actions on iris, salivary, sweat and bronchial glands are stronger than atropine. It is a moderately powerful antiemetic. Dose 10-30 mg.

GLYCOPYRONIUM BROMIDE:

It reduces the tone of lower oesophageal sphincter. It suppresses gastric secretions better than atropine or hyoscine. It causes tachycardia; so effective in preventing bradycardia due to suxamethonium. It efficiently dries up salivary secretion. Dose: premedication 0.2-0.4 mg (adult); 4-8 mcg/kg (child). Intravenous use to protect against bradycardia (adult) 0.2 mg, 4 mcg/kg (child). ANTACIDS These are commonly prescribed for patients thought to be at risk of regurgitation and aspiration. Ranitidine, 150 mg orally or 50 mg i.m. DRUGS FOR SPECIFIC EFFECTS These include all drugs used to ensure optimal treatment of specific conditions up to the time of surgery, e.g. salbutamol inhalation for asthmatics. NOTE: It is usually quoted that sympathetic words and reassurance to patients act as sedative effect. Remember:- reassurance + sympathetic words = 10 mg diazepam.

EQUIPMENT Q1: WRITE SHORT NOTES:-

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1. Anaesthesia Machine 2. Cylinders 3. Vaporizers 1. ANAESTHESIA MACHINE Def: Machine which delivers measured amount of gases & volatile anaesthetic agents from source of supply to patient through tubing. Basic functions of machine: To deliver compressed gases to patient at a safe pressure.  To allow the flow & composition of the gases to be easily adjusted.  To permit the addition of a precise concentration of volatile anaesthetic such as isoflurane.  To deliver this mixture to a common gas outlet & hence, to a breathing circuit on ventilation. Types of Anaesthesia Machine: - There are two types of Anaesthesia Machine. I) Continuous Flow: - Machine delivers a mixture of gases & vapours at a continuous flow set by anaesthetist into a reservoir bag from which the patient inhales. II) Demand Flow: - Machine delivers the preset mixture of gas at flow rates demanded by breathing pattern of the patient without interposition of reservoir bag.

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Fig:

The system is an anaesthetic machine of the Boyle’s type. Nitrous oxide and oxygen from cylinders on the left are measured by rotameters (flow meters). Control levers determine what proportion of the total flow goes through the bottle. A rod raises or lowers the hood. This is a simple anaesthetic apparatus design by Edmond Boyle. He was commonly known as “Cookie”. In place of ether vaporizer (as shown in the figure) these days other vaporizers such as halothane, isoflurane, sevoflurane etc are installed.

Components of Anaesthesia Machine:  Gas inlets receive medical gases from attached cylinders or hospital’s gas delivery system.  Pressure regulators reduce gas pressure.  Oxygen-Pressure failure devices signals low oxygen pressure.  Vaporizers blend gases with volatile anaesthetic agents.

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

A fresh gas out-let delivers the final gas composition to the breathing circuit.

2. CYLINDERS.

Cylinders are constructed from molybdenum steel. Cylinders are tested hydraulically every 5 years to ensure that they can withstand hydraulic pressures considerably in excess of those to which they are subjected in normal use & the tests recorded by a mark stamped on the neck of the shoulder. Gas cylinders are tested by I) Tensile test. II) Flattening, impact & band tests. III) Hydraulic or pressure test. Filling ratio of a cylinder is the ratio of weight of gas in the cylinders to weight of water the cylinder could hold. Great care is taken that the gases are free from water vapours, otherwise when the cylinder is opened, temperature fall & water vapours would freeze & block the exit valve. Cylinder are identified by:i. Size of cylinder e.g. oxygen cylinder are 6 different sizes C,D,E,F,G,J, & N2O cylinders are 5 different sizes C,D,E,F,G ii. Colour Codes a. N2O cylinder has Blue body & Shoulder. b. O2 cylinder carries black body & white shoulder. c. CO2 cylinder has grey body & shoulder. iii.Pin Index System is a device to prevent interchangeability of cylinders of different gases. The pegs on the inlet connection slot into corresponding holes (pits) on the cylinder valve. e.g. position of pit on cylinders: O2 --2, 5 N2O --3, 5 CO2 --1, 6 Different gas cylinders carry different pressures e.g. O 2 cylinder pressure is 137 bars N2O cylinder pressure is 44 bar at 15C. Cylinder valves should be opened slowly to prevent sudden surges of pressure & should be closed with no more force that is necessary otherwise valve seating may be damaged.

3. VAPORIZERS Definition: - A vaporizer is a device for adding clinically useful concentration of anaesthetic vapours to a stream of carrier gas. Types:-

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i.

Drawover vaporizers: In this type of vaporizers, gas is pulled through the vaporizer when the patient inspires, creating a subatmospheric pressure. Resistance to gas flow through a draw over vaporizer must be extremely small. ii. Plenum Vaporizers: - In this type of vaporizers gas is forced through the vaporizer by the pressure of fresh gas supply. Resistance of plenum vaporizers may be high enough to prevent its use as draw over vaporizers. Principles of both devices are similar. All the anaesthetic gas entering the vaporizer passes through the anaesthetic liquid and becomes saturated with vapour. 1 ml of liquid anaesthetic is equivalent of approximately 200ml of anaesthetic vapors. Concentration of anaesthetic in the gas mixture emerging from the outlet port is dependent upon:  

 

 

Saturated Vapour Pressure of the anaesthetic liquid in the vaporizer. Temperature of liquid anaesthetic agent, as this determines its saturated vapour pressure. Splitting ratio i.e. the flow rate of gas through the vaporizer chamber in comparison with that through bypass. Surface area of anaesthetic agent in the vaporizer. Duration of use as the liquid in the vaporizing chamber evaporate, its temperature falls & thus its saturated vapour pressure decreases. This leads to reduction in concentration of anaesthetic in mixture leaving the exit port. Nature of liquid Fresh gas flow

Q2: WRITE SHORT NOTE ON ENDOTRACHEAL TUBES? ENDOTRACHEAL TUBES There are many designs of endotracheal tubes. The general considerations determining their construction as follow. MATERIAL

Red rubber -

Not normally disposable

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- Relatively irritant, and not ideal for prolonged Intubation - Firm/curvature predetermined - May transmit infection Plastic (PVC) - Disposable - Non-irritant (implantation-tested) - Moulds to body contours at 37C CUFFS Red rubber cuffs are firm and rounded so that a seal between the endotracheal tube and the trachea exists over small areas. The mucosa is likely to be damaged, not only because of the chemical irritants but also because of compression, and hence hypoxia, of the mucosa. PVC tubes have cuffs of varying shapes. The shape of the cuff can be more cylindrical, thus, by increasing the area of seal, there is a reduction in the pressure necessary in the cuff. The seal between tracheal mucosa and endotracheal tube is required to prevent the escape of gas (during IIPV) and also to prevent the aspiration of saliva or gastric contents into the tracheobronchial tree. Age/4 + 4.5 is the accepted formula for determining the size (mm) of the endotracheal tube, for a child. The length of the tube for a child is determined by: Age/2 + 12 cm (oral) Age/2 + 15 cm (nasal)

Q3: WRITE A SHORT NOTE ON LARYNGOSCOPES LARYNGOSCOPES These are the instruments to see larynx.

There are many designs for use, depending on requirement:

1.

NEONATAL – STRAIGHT BLADE The epiglottis is relatively large and floppy; a straight blade is necessary to flatten and hold the epiglottis forward to allow the cords to be visualised. 2. INFANT–STRAIGHT OR CURVED BLADE The tongue of the infant is large in relation to the buccal cavity and blade design is aimed at keeping it out of the way. Blades which are almost tubular are used in infants with tissue flaps associated with palatal defects. The most commonly used paediatric laryngoscopes are the Anderson, Magill and the Robertshaw.

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Fig: INTRODUCING A LARYNGOSCOPE.

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Fig: HOW TO USE A LARYNGOSCOPE. (A) Insert the laryngoscope with your wrist straight, then extend your wrist. (B) Finally, lift the patient’s jaw forwards. (C)The secret of success is to have the patient’s head extended on his neck before you begin. (D) and to have his neck flexed forwards. (E). Arrange the pillow under his neck and shoulders so that you can achieve this. This has been likened to the position of “sniffing the morning air”.

3.

ADULT – STRAIGHT OR CURVED BLADE The primary aim is deflection of the tongue from the line of vision of the vocal cords; however, a variety of other problems have been overcome. a. A laryngoscope with an obtuse angle between the handle and the blade – to facilitate insertion into the mouth of patients with difficult access, e.g. in an iron lung, in severe fixed flexion or in a halo splint for stabilization of the cervical spine. b. A ‘left – handed blade’ – for use is patients where the right side of the mouth is invaded by tumour, or access is otherwise compromised. c. The addition of a prism to the blade allows the vocal cords to be visualized when they are not in direct line of sight. d. McCoy Laryngoscope. Resembles a conventional laryngoscope, but the distal part of the blade is hinged and can be tilted up or down by a lever on the handle. Allows 27

the larynx to be ‘lifted’ to improve vision in case of difficulty. 4. LARYNGEAL MASK AIRWAY (LMA) A revolution in airway control. The LMA is inserted into the mouth and advanced until it comes to lie against the posterior pharyngeal wall opposite the larynx. The large cuff is then inflated and this creates a seal around the laryngeal opening. The seal of airway to trachea is not so reliable as when using an endotracheal tube and a number of studies have shown some leakage past the LMA which could potentially enter the trachea. Some doubts have been expressed as to the suitability of the LMA for use during controlled ventilation and for surgery within the mouth and pharynx, e.g., tonsillectomy. Nevertheless, it has been used widely for these situations. Great care must be taken to ensure that airway inflation pressures remain low if using an LMA for controlled ventilation. 5. FIBREOPTIC LARYNGOSCOPE A thin flexible fibreoptic device that will pass through a tracheal tube. The fiberscope is passed through the nose or mouth (the nose is usually easier) and advanced under direct vision until it lies within the trachea. The tracheal tube, which has been previously slid onto the fiberscope is then advanced using the fiberscope as a guide. The fiberscope is then withdrawn. The use of the fibreoptic laryngoscope requires previous training. It is the safest technique for securing the airway is case of anticipated difficult Intubation and may be performed with the patient awake following local anaesthesia to the airway.

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Fig:

THE POSITIONS OF PTIENTS OF DIFFERENT AGES DURING INTUBATION. Put the pillow under an adult’s head and neck, but under a child’s back.

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LECTURE 2

INHALATIONAL ANAESTHETIC AGENTS Q: WHAT ARE THE CHARACTERISTICS OF AN IDEAL VOLATILE ANAESTHETIC AGENT? The characteristics of an ideal volatile anaesthetic agent are: 1. Non-inflammable, non explosive. 2. Stable physical characteristics. 3. Appropriate volatility, having low boiling point and high SVP. 4. Potent. 5. Cardiovascular and respiratory stability. 6. Low blood-gas solubility giving rapid induction/recovery. 7. Analgesic. 8. Low incidence of nausea and vomiting. 9. Should not sensitize the myocardium to adrenaline. 10. Non-irritant and pleasant smelling. 11. Non-metabolized. 12. Non-hepatotoxic and nephrotoxic. 13. Non-teratogenic. 14. Cheap. 15. No effect on CBF and intracranial pressure or effect easily antagonized by hyperventilation. 16. No effect on E.C.G.

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Fig: HOLDING THE MASK WITH ONE HAND.

Fig: HOW TO HOLD THE MASK WITH TWO HANDS.

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Q: WHAT IS THE CLASSIFICATION ANAESTHETIC AGENTS?

OF

INHALATIONAL

A: VOLATILE ANAESTHETIC AGENTS 1. ETHERS.  Methoxyflurane (not in use due to its nephrotoxic effects).  Enflurane.  Isoflurane. 2. HALOGENATED HYDROCARBONS.  Halothane.  Sevoflurane.  Desflurane.  Chloroform(not used these days due to its toxic effects).

B: GASEOUS ANAESTHETIC AGENTS

1. NITROUS OXIDE . 2. CYCLOPROPANE (not used these days due to its toxic effects and explosion hazards).

NITROUS OXIDE Q: HOW IS NITROUS OXIDE PREPARED? Nitrous oxide is also known as laughing gas. It is prepared commercially by heating Ammonium Nitrate crystals to a temperature of 245-270oC. Heat NH4NO3 ------N2O + H2O

Q: WHAT ARE THE IMPURITIES FORMED ALONG WITH N2O? The chief impurities are: Nitrogen which dilutes the anaesthetic.  Nitric oxide which combines with hemoglobin to produce anemic type of hypoxia.  Nitric acid causes pulmonary oedema.  Nitrogen dioxide which may damage the valves.  Ammonia.  Nitrous acid. Now-a-days 99.5% pure gas is supplied.

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Q: HOW IS NITROUS OXIDE STORED? Nitrous oxide is stored in compressed form as a liquid in blue cylinders at a pressure of 50 bar (5000kPa; 750 lb.in 2). Because the cylinder contains liquid and vapour, the total quantity of nitrous oxide contained in cylinder can be ascertained only by weighing. Nitrous oxide cylinders should be kept in a vertical position during use so that the liquid phase remains at the bottom of the cylinder.

Q: WHAT ARE THE PHYSICAL PROPERTIES OF NITROUS OXIDE?             

Sweet smelling. Non irritating. Colorless. Non inflammable but supports combustion. Formula N2 O Molecular wt: 44 Boiling point: -89oC Critical temperature: 36.5oC Critical pressure: 71.7 Atm. Blood/gas solubility coefficient: 0.468 Eliminated unchanged from the body mostly via lungs. Stable. Not affected by soda lime.

Q: WHAT ARE THE EFFECTS OF NITROUS OXIDE ON VARIOUS SYSTEMS OF THE BODY? 1. CNS  Causes CNS depression.  Paralysis of respiratory and vasoactive centre does not occur. 2. RESPIRATORY SYSTEM  Respiration is stimulated (both depth and rate).  Reduces the MAC of volatile anaesthetics by about 50%. 3. MUSCULAR SYSTEM 

Depression of skeletal system is minimal.

4. MISCELLANEOUS  No effect on kidney or liver function.  Nausea and vomiting are likely to occur. 33



Crosses placental barrier depression in fetus.

but

does

not

cause

respiratory

Q: WHAT ARE THE SIDE EFFECTS OF NITROUS OXIDE?          

May cause exhilaration and euphoria during induction. Unpleasant hallucinations and dysphoria can occur. Continual use for days or weeks may cause neutropenia or macrocytic anaemia. Interferes with nucleic acid synthesis. Diffuses into cavities and cause otological disturbances in middle ear. Prolonged use can lead to bone marrow depression and teratogenic effect. Respiratory depression and diffusion hypoxia. Pollution problem. Expensive. Difficulties of cylinder transport.

HALOTHANE Q: WRITE A SHORT NOTE ABOUT THE CHEMISTRY AND PHYSICAL PROPERTIES OF HALOTHANE? Halothane is 2-bromo-2-chloro-1, 1, 1-triflouroethane. Its formula is CI F   H------- C ----- C -------F   Br F The         

physical properties are:Halogenated hydrocarbon. Non inflammable and non explosive. Colourless and sweet smelling. Unstable in light. Stored in amber coloured bottles with thymol as preservative. Mol. wt: 197 o Boiling point: 50.2 C L.H.V: 35.2 Calories/gm Oil water solubility: 220 34

 

Blood gas solubility: 2.5 at 37oC MAC: 0.75 V %

Q: WRITE DOWN BRIEFLY THE EFFECTS OF HALOTHANE ON VARIOUS ORGAN SYSTEMS? CVS:          

Blocks sympathetic ganglion Increases vagal tone causing bradycardia Direct myocardial depressant effect. Direct depressant of vasomotor center. Increases impulse discharge from baroreceptors. Depresses S-A node. Direct depressant of vasculature of smooth muscles. Dose dependent hypotension due to decreased cardiac output and lowered peripheral resistance. Sensitizes heart to arrhythmic effects of adrenaline. Coronary artery vasodilator.

CNS  Increases the CSF pressure and cerebral blood flow.  Blunts autoregulation of cerebral blood pressure.  Not a very good analgesic. RESPIRATORY SYSTEM  Depresses respiration with shallow rapid breathing.  Rate increases with depth of anaesthesia.  Bronchodilator.  Increases apneic threshold.  Hypoxic drive depressed.  Attenuates airway reflex.  Depresses clearance of mucous secretions from respiratory tract. MUSCULAR SYSTEM  Potentiates the effect of non depolarizing muscle relaxant.  Moderate relaxation.  Triggering agent for malignant hyperpyrexia. UTERUS 

Uterine relaxation and bleeding only in parturient uterus.

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LIVER   

Halothane hepatitis. Decreases hepatic blood flow. Slows down the metabolism of drugs like fentanyl, phenytoin, verapamil.

HORMONAL EFFECTS  

Increase in growth hormone, serum thyroxine. Sensitivity to insulin is increased.

BODY TEMPERATURE 

Causes 1o C drop of esophageal temperature and 4o C rise of skin temperature.

MISCELLANEOUS HALOTHANE SHAKES: recovery from halothane is sometimes associated with restlessness or shivering. Cover with blankets and ensure adequate oxygenation.

Q: WHAT ARE THE CONTRAINDICATIONS TO THE USE OF HALOTHANE?    

Patient with hepatic dysfunction. Patient with increased intracranial pressure. Patient having history of malignant hyperpyrexia. Patients with hypovolaemia and severe cardiac disease such as aortic stenosis.

ENFLURANE Q: WRITE A SHORT NOTE ABOUT THE CHEMISTRY AND PHYSICAL PROPERTIES OF ENFLURANE. Enflurane is defluoro methyl ether of 1, 1, 2 trifluro-2-Chloroethane. F

F

F







H ----- C ---- O ----- C ----- C ------ H    F E CI The physical properties of enflurane are:-

36

       

Stable, colourless without added chemical stabilizers. Non inflammable, non explosive. Pleasant ethereal smell. Does not decompose when circulated with oxygen and water vapours through warm soda lime. Blood/gas solubility coefficient: 1.8 MAC: 1.7% Boiling point: 56oC SVP: 175 mmHg at 20oC

Q: WHAT ARE THE EFFECTS OF ENFLURANE ON VARIOUS ORGAN SYSTEMS? CVS       

Dose dependant depression of myocardial contractility. Reduction in cardiac output. Less likely to sensitise the heart to adrenaline. Dose dependant reduction in arterial pressure. No central vagal effect. Hypotension leads to reflex tachycardia. Preferable to halothane during surgery involving pheochromocytomas and other tumours associated with excessive secretion of catecholamines.

RESPIRATORY SYSTEM    

Non irritant. Does not increase salivary or bronchial secretions. Dose dependant depression of alveolar ventilation with reduction in tidal volume and an increase in ventilatory rate. Pharyngeal and laryngeal reflexes are diminished quickly.

UTERUS Dose related relaxation of uterine muscle. CNS    

Dose dependant depression of EEG activity. Produces epileptiform spike activity. Twitching of face and arm muscles. Avoided in epileptic patients.

MUSCLE RELAXATION

37

Enhances the effect of non-depolarizing muscle relaxants.

Q: WHAT ARE ENFLURANE?   

THE

INDICATIONS

FOR

THE

USE

OF

For induction and maintenance of general anaesthesia. For dental anaesthesia in view of rapidity of action and recovery with stability of cardiovascular system. May be used in children.

38

ISOFLURANE Q: WHAT IS THE FORMULA AND THE MAJOR PHYSICAL CHARACTERISTICS OF ISOFLURANE? Isoflurane, which is 1-chloro-2, 2, 2-triflouroethyl diflouromethyl ether, is an isomer of enflurane. Its formula is F

H

F    H ----- C ------ C ----- O ----- C ------ H    F CI F Its physical properties include  Colorless, volatile anaesthetic  Slightly pungent odour  Does not require preservatives  Non inflammable  Vapor pressure  MAC 1.2  Blood/gas partition coefficient 1.4

240 mmHg at 20oC

Q: WHAT ARE THE EFFECTS OF ISOFLURANE ON VARIOUS ORGAN SYSTEMS? RESPIRATORY SYSTEM  Dose dependant depression of ventilation.  Decrease in tidal volume with increase in ventilatory rate.  Blunts response to hypoxia and hypercapnia.  Bronchodilator. CVS   

Myocardial depressant but less depression of cardiac output than halothane potent peripheral vascular dilator. Systemic hypotension due to reduction in systemic vascular resistance coronary vasodilatation leading to Coronary Steal Syndrome. Does not sensitize the myocardium to catecholamines.

CNS

39

   

High inspired concentrations, Minimum Alveolar Concentration (MAC) > 1 lead to vasodilatation, an increased cerebral blood flow and intracranial pressure. No seizure activity on EEG. Does not blunt autoregulation. Decreases CMRO2 (Cerebral Metabolic Rate of Oxygen consumption).

MUSCULAR SYSTEM 

Dose dependant depression of neuromuscular transmission with potentiation of non depolarizing neuromuscular blocking drugs.

RENAL 

Decreases renal blood flow, GFR and urine output.

HEPATIC  

Total hepatic blood flow is decreased but to lesser extent than halothane LFT’s minimally affected.

Q: WRITE SHORT NOTE ON SEVOFLURANE. SEVOFLURANE This is non-flammable ether. It is devoid of significant cardio/respiratory side-effects. The major advantage is that its very low blood: gas solubility coefficient (0.6) allows its use for rapid face mask induction of anaesthesia, especially in children. It is in wide clinical use in Japan. It is 3% metabolised.    

MAC Blood: gas solubility at 37C Boiling point Saturated vapour pressure at 20C mmHg

2.0 0.65 58.5C 170

Q: WRITE SHORT NOTE ON DESFLURANE DESFLURANE Desflurane is also halogenated ether and is licensed for use in Europe and North America. It is not unpleasant to inhale and is non-irritant to the respiratory tract at low concentrations. It has a very low blood; gas

40

solubility (0.42) and is thus associated with short induction and wakeup times. It is 0.02% metabolised.  MAC 6.0  Blood: gas solubility at 37C 0.45  Boiling point 22.8C  Saturated vapour pressure at 20C 66 mmHg Both these agents are expensive to produce. They offer advantages over other anaesthetic vapours but sevoflurane produces a toxic product on contact with soda-lime whilst desflurane increases heart rate and is a respiratory irritant at concentrations > 1MAC.

41

LECTURE 3

INTRAVENOUS ANAESTHETIC AGENTS Q: DEFINE INTRAVENOUS ANAESTHETIC AGENTS? I/V anaesthetic agents may be defined as “drugs that will induce loss of consciousness in one arm brain circulation time when given in appropriate dosage”.

Q: NAME THE COMMON INTRAVENOUS AGENTS. Common I/V anaesthetic agents include: 1. 2. 3. 4. 5.

Thiopentone sodium Ketamine. Propofol. Etomidate. Methohexitone.

Q: WRITE A SHORT NOTE ON THIOPENTONE? Thiopentone sodium: It is the most commonly used I/V anaesthetic agent. It is usually used for induction of anaesthesia. It is a sodium salt of barbituric acid and is the sulphur analogue of pentobarbitone. The 2.5% solution, which is commonly prepared, has a pH of 10.5.        

It produces anaesthesia usually in less than 30 sec. after i/v injection. Duration of action is 5 – 10 min. Myocardial contractility is depressed and peripheral vasodilatation occurs, which leads to Hypotension. Ventilatory drive is decreased and a short period of apnoea is common, preceded by a few deep breaths. Skeletal muscle tone is reduced due to suppression of spinal cord reflexes. Intraocular Pressure (IOP) is reduced by 40% Antanalgesic If injected accidentally in the artery it will cause sever pain in the fingers. One should keep the needle in-situ and inject papaverine (Vasodilator) and local anaesthetic procaine to relief pain.

INDICATIONS:

42

Induction of anaesthesia, Maintenance of anaesthesia, Basal narcosis by rectal administration, Status epilepticus, Reduction of intracranial pressure. ABSOLUTE CONTRAINDICATIONS:  Airway obstruction.  Porphyria  Previous hypersensitivity reaction. DOSE: 

3 – 5 mg/kg body weight as 2.5% solution.

Q: WRITE A SHORT NOTE ON KETAMINE? KETAMINE: This is a phencyclidine derivative. It produces dissociative anaesthesia.  After i.v. injection it induces anaesthesia in 30 – 60 sec. duration of action is 10 – 15 min. After i.m. injection the effect starts within 3-4 min. and duration of action is 15 – 25 min.  There may be emergence delirium, restlessness, disorientation, nightmares and hallucinations.  Arterial pressure increases by up to 25%.  Heart rate increases by upto 20%. Myocardial oxygen demand also increases.  Transient apnoea may occur after i.v. injection, but ventilation is well maintained thereafter.  Pharyngeal and laryngeal reflexes and a patent airway are well maintained.  Muscle tone is increased & spontaneous movements may occur.  IOP increases. Dosage:   

2-mg/kg i.v. for induction. 1 – 1.5 mg/kg for maintenance. 8 – 10-mg/kg i.m.

PROPOFOL

Q: WHAT IS THE FORMULA OF PORPOFOL?

43

2, 6, di-isopropylphenol: 1% solution in egg white lecithin emulsion.

Q: WHAT ARE PRESENTATION?

THE

PHYSICAL

PROPERTIES

AND

Propofol is extremely lipid soluble, but almost insoluble in water. It is formulated in a white, aqueous emulsion containing soybean oil and purified egg phosphatide.

Q: WHAT ARE THE PHARMACOKINETICS OF PROPOFOL?     

Distributed rapidly Termination of action occurs by redistribution Metabolized at both hepatic and extra hepatic sites Very high clearance Excretion through kidneys

Q: WHAT IS THE DOSE OF PROPOFOL?   

2-3 mg/kg IV induction 100-200 μg/kg/min maintenance Sedation: 25-100 μg/kg/min

Q: WHAT ARE PROPOFOL?

THE

PHARMACOLOGIC

ACTIONS

OF

CNS EEG frequency decreases and amplitude increases Cerebral blood flow, intracranial pressure and cerebral metabolic oxygen demand decreases May have anticonvulsant effect Occasional excitatory activity CVS Venous dilatation, decreased depression lead to hypotension Heart rate may increase

peripheral

resistance

and

cardiac

RESPIRATORY Transient apnoea 44

Decreased rate and tidal volume Depression of laryngeal reflexes more than barbiturate HEPATIC None RENAL Decreased cardiac output may decrease renal blood flow MISCELLANEOUS Less postoperative nausea than barbiturates Possible antipruritic effect at low dose

Q: WHAT ARE THE ADVERSE EFFECTS? 1. 2. 3. 4. 5. 6. 7.

Very low incidence of anaphylaxis Caution if lipid disorder present Cardiovascular depression Respiratory depression Excitatory phenomena Pain on injection Occasional monoclinic movements.

45

LECTURE 4

MUSCLE RELAXANTS Q:

CLASSIFY MUSCLE RELAXANTS.

Muscle relaxants are classified as: 1. Depolarizing Muscle Relaxants  

Succinyl choline (commonly used) Decamethonium

2. Non-Depolarizing Muscle Relaxants. 

Long Acting    



Intermediate Acting   



Tubocurarine Doxacurium Pancuronium (commonly used) Gallamine (not used due to its ganglion blocking effects)

Atracurium (commonly used) Vecuronium Rocuronium

Short Acting  Mivacurium

Q: WHAT ARE DEPOLARIZING 1. 2. 3. 4. 5. 6. 7. 8.

THE SALIENT FEATURES MUSCLE BLOCK?

OF

NON-

Do not cause muscle fasciculation. Very hydrophilic. Relatively slow onset. Reversed by neostigmine and other anticholinesterases. Effects reduced by acetylcholine and adrenaline. Potentiated by volatile agents, Mg2, and hypokalemia. Mild cooling antagonizes their effects. Acidosis increases duration and degree of non-depolarizing block.

46

Q: WHAT ARE THE SALIENT FEATURES OF DEPOLARIZING MUSCLE BLOCKING DRUGS? 1. 2. 3. 4. 5. 6.

Cause muscle fasciculation’s but not in myasthenia gravis. Repolarization is interfered with; the resting membrane potential is held up until phase II block develops, when it returns to -70 mV. Not reversed with neostigmine and other anticholinesterases. potentiated with isoflurane, enflurane, Ach, respiratory alkalosis, hypothermia and Mg2+. Antagonized by ether, halothane, acidosis and non-depolarizing relaxants. Fast dissociation constants at receptor.

Q: WHAT CLINICAL SIGNS INDICATE THE NEED OF MORE RELAXANT DURING SURGERY? 1. 2. 3. 4. 5.

Hiccup, due to contraction of periphery of the diaphragm. Rigidity of abdominal wall. Increased resistance to inflation of lung. Bucking or coughing on tracheal tube. As indicated by neuromuscular monitoring.

Q: WHAT ARE THE CLINICAL SIGNS OF INCOMPLETE REVERSAL? 1. 2. 3.

6. 7.

Shallow respiration. Jerky respiration. “Tracheal tug” and “see-saw” respiration where, as the abdomen moves out, the chest moves in. Cyanosis. A restless, frightened, struggling patient, who says that he or she cannot breathe. Diplopia. Inability to raise head or extrude tongue.

Q:

WRITE A SHORT NOTE ON ATRACURIUM?

4. 5.

ATRACURIUM Physical structure: It is an isoquinolon compound belonging to quaternary group. Pharmacokinetics: Absorption: from I/M and I/V routes. 47

Distribution: Throughout ECF. Metabolism: Hoffmann degradation. Alkaline ester hydrolysis in plasma. Pharmacodynamics: Dose: 0.5-mg/kg i.v. as bolus dose. Top ups 0.3- 0.1mg/kg i.v. Neonates are slightly more resistant so dose is 0.3 mg/kg. Speed of onset: 1-2 min. Duration: 20-40 min . Reversed with: neostigmine. Side effects and clinical considerations 1. Release of histamine. 2. Hypotension and tachycardia, if given in excess of 0.5mg/kg bronchospasm so avoid in patients with bronchial asthma. 3. Laudanosine, a breakdown product of Hoffmann degradation, is epileptogenic. 4. Duration of action can be markedly prolonged in hypothermia and acidotic patients. 5. Atracurium precipitates as a free acid if given into an i.v. line containing an alkaline solution such as thiopentone.

Q:

WRITE A SHORT NOTE ON PANCURONIUM?

Physical structure: It is a long acting quaternary amino-steroid, devoid of hormonal activity. It resembles two acetylcholine molecules bound together. Pharmacokinetics:     

Strongly bound to gamma globulin and moderately bound to albumin. Metabolized by deacytylation in liver to limited degree. Excretion primarily through kidney (40%) but 10% is cleared through bile. Patients with renal failure show prolonged block. Patients with cirrhosis require increased loading dose due to large volume of distribution but decreased maintenance dose due to decreased plasma clearance.

Dose: 0.05mg/kg i.v. bolus. Duration: 40-60 min. Side effects and clinical considerations

48

1. 2. 3. 4. 5.

Can cause stimulation of the myocardium with rise in pulse rate and blood pressure. Vagal blockade and catecholamines release. Increased incidence of ventricular dysrythmias. Releases histamine from tissues. Should be avoided in renal failure and total biliary obstruction.

Q: WHAT IS SUXAMETHONIUM PHARMACOKINETICS?

AND

WHAT

IS

ITS

Suxamethonium is a dicholine ester of succinic acid. It belongs to quaternary ammonium group. Pharmacokinetics: Absorption: I/V, I/M or S/C. Distribution: throughout the ECF and slightly through placenta. Metabolism: hydrolysis by plasma cholinesterases. Dose: 1-1.5 mg/kg Duration: 10-15 min.

the

Q: WHAT ABNORMALITIES CAN OCCUR IN SUXAMETHONIUM METABOLISM, WHICH CAN PROLONG ITS DURATION OF ACTION? 1.

2.

Abnormal plasma cholinesterase (inherited)  Atypical cholinesterase.  Fluoride resistant cholinesterase.  Silent gene. Plasma cholinesterases deficiency:  Acquired  After X-ray therapy  After organophosphorous poisoning  In hyperpyrexia  In cardiac failure  Uraemia  Hypoproteinemia  Myasthenia gravis  Pregnancy  Myxoedema  Asthma  Obesity  Following treatment with: cyclophosphamide, ecothiopate, ketamine, pancuronium, MAO inhibitors, and oral contraceptives.

49

 3.

Congenital

Plasma cholinesterase Antagonism: by anticholinesterases such as neostigmine.

Q: WHAT ARE THE SIDE EFFECTS OF SUXAMETHONIUM. 1. PROLONGED APNOEA: The      

commonest causes are: Atypical serum cholinesterases. Dehydration and electrolyte imbalance. An overdose of muscle relaxant. A low serum cholinesterase level in blood. An excessive formation of succinyl monocholine. Dual block.

The management includes    2.

Artificial ventilation and sedation are maintained until monitoring shows that the block has worn off. A blood sample is taken for cholinesterase analysis. Fresh frozen plasma given. HYPERKALEMIA

A rise in serum potassium of 0.2-0.4 mmol/l occurs due to release from muscle, especially in burn patients. 3.

RAISED INTRA-OCCULAR PRESSURE Suxamethonium, 1 mg/kg, raises the pressure an average of 7 mm

Hg. 4.

MUSCLE PAIN More frequent in women and middle-aged patients.

5.

RAISED INTRAGASTRIC PRESSURE

6.

MALIGNANT HYPERPYREXIA Incidence is 1 in 100000 adults.

7.

EXACERBATES DYSTROPHIA MYOTONIA

8.

DIRECT MYOCARDIAL DEPRESSANT BRADYCARDIA AND CARDIAC ARREST MUSCARINIC EFFECTS

9.

LEADING

TO

10. ANAPHYLAXIS

50

Q: WHAT ARE THE SUXAMETHONIUM?

INDICATIONS

FOR

   

Endotracheal intubation. ECT. Short orthopaedic procedures. Short surgical procedures.

    

Hyperkalemia. Known case of atypical pseudocholinesterase. Hypersensitivity. In patients with increased intraocular pressure. Family history of malignant hyperpyrexia.

USE

OF

Q: WHAT ARE THE CONTRA-INDICATIONS TO THE USE OF SUXAMETHONIUM?

51

LECTURE 5

LOCAL ANAESTHETIC AGENTS Q: WHAT ARE LOCAL ANAESTHETIC AGENTS? Local anaesthetics cause reversible blockade of peripheral nerve conduction or inhibition of excitation at nerve endings with resultant loss of sensation in the particular area of the body.

Q: HOW DO YOU CLASSIFY LOCAL ANAESTHETIC AGENTS. A)

ACCORDING TO STRUCTURE 1. HAVING ESTER LINKAGE  Chloroprocaine  Cocaine  Procaine  Tetracaine 2. HAVING AMIDE LINKAGE  Lignocaine  Bupivacaine  Etidocaine  Cinchocaine

B)

ACCORDING TO POTENCY 1. LOW POTENCY AND SHORT DURATION  Procaine  Chloroprocaine 2. INTERMEDIATE POTENCY AND DURATION   

Mepivacaine Prilocaine Lignocaine

3. HIGH POTENCY AND LONG DURATION   

Tetracaine Bupivacaine Etidocaine

52

Q: WHAT IS THE SITE OF ACTION OF LOCAL ANAESTHETIC AGENTS? The site of action of local anesthetics drugs is at the surface membrane of cells of excitable tissues. In a myelinated nerve the site of action is the node of Ranvier.

Q: WHAT IS DIFFERENTIAL BLOCK? The minimum concentration of local anaesthetic drug necessary to cause block of a nerve fiber of given diameter is known as the Cm. The thicker the diameter of a nerve fibre the greatest the Cm required. In practice the sequence of blockade is autonomic, sensory, and finally motor block according to fibre diameter.

Q: WHAT DOES THE UPTAKE OF LOCAL ANAESTHETICS DEPEND UPON? Local anaesthetic drugs are lipid-soluble bases, which act by penetrating lipo-protein cell membranes in the non-ionized state. The blocking quality of a local anaesthetic drug depends on its:    

Potency. Latency (time between its injection and maximum effect) – this in turn depends on nerve diameter, local pH, diffusion rate and concentration of local drug. Duration of action. Regression time (time between commencement and completion of pain appreciation).

Q: WHAT TOXICITY?        

FACTORS

INFLUENCE

LOCAL

ANAESTHETIC

Quantity of solution. Concentration of drug. Presence or absence of adrenaline. Vascularity of site of injection. Rate of absorption of drug. Rate of metabolism of drug. Hypersensitivity of patient. Age, physical status and weight of patient.

53

Q: WHAT ARE THE SIGNS OF TOXICITY IN VARIOUS ORGAN SYSTEMS? CENTRAL NERVOUS SYSTEM       

Central stimulation followed by depression. Restlessness. Hysterical behaviour. Vertigo. Tremors. Convulsions. Respiratory failure.

Treatment: Artificial ventilation with O2 or air.  Intravenous injection of Suxamethonium or Thiopentone to control convulsions (10-150 mg).  Diazepam.

just

sufficient

CARDIOVASCULAR SYSTEM  

Hypotension. Acute collapse – primary cardiac failure, feeble pulse and cardiovascular collapse, bradycardia, pallor, sweating and hypotension. Treatment: Elevate legs.  Give oxygen by IPPV.  Rapid intravenous infusion.  Raise blood pressure.  Cardiac massage. RESPIRATORY SYSTEM   

Apnoea. Medullary depression. Respiratory muscle paralysis.

ALLERGIC PHENOMENA    

Bronchospasm. Urticaria. Angioneurotic oedema. Cross sensitivity.

54

Q: HOW CAN YOU IMPORVE DURATION AND QUALITY OF LOCAL ANAESTHETIC?    

Addition of adrenaline, 1:200 000 to 1:500 000 solution. Injection closer to nerve. The amount of free base. Adjusting the pH to about 7.

Q: WHAT ARE ANESTHESIA?       

THE

DIFFERENT

METHODS

OF

LOCAL

Simple topical application at operative site. Infiltration analgesia to abolish pain. Field block. Nerve block (conduction anaesthesia). Refrigeration analgesia (Cryoanalgesia). Intravenous local analgesia. Central neural blockade.

Q: WHAT IS THE MAXIMUM DOSE OF LOCAL ANAESTHETICS? Drug Lignocaine Bupivacaine

Maximum Dose mg/kg 3 to 7 (with adrenaline) 2.5

Remember: 1 ml of 1% lignocaine = 10 mg

55

Lecture 6 REGIONAL ANAESTHESIA Q:

What is the anatomy of spinal cord?

Spinal cord is a part of CNS, extending from foramen magnum to lower border of L1 or upper border of L2 in adults and L3 L4 in children. It is covered by fibro fatty tissue known as meninges. It consists of grey mater and white mater which represent ascending and descending tracts. There are 8 cervical. 12 thoracic, 5 lumbar and 5 sacral spinal nerves.

SPINAL ANAESTHESIA Q:

DEFINE SPINAL ANAESTHESIA?

Spinal anaesthesia is a type of regional block in which local anaesthetic is injected into the subarachnoid space. It causes major conduction block, which refers to blockade of spinal nerve roots. The resultant nerve block provides surgical anaesthesia as far cephalad as upper abdomen.

Q:

WHAT ARE THE INDICATIONS OF SPINAL ANAESTHESIA?

Indications are:i) ii) iii)

Q:

Lower abdominal surgery e.g. Cesarean Section, Herniotomy, Transvesical prostatectomy, TURP, Cystoscopies etc. Perineal surgery e.g. haemorrhoidectomy, fistulectomy, TURP, cystoscopies etc. Lower limb surgery e.g. Arthroscopy, amputation, open reduction internal fixation (ORIF) of fractures etc.

AT WHICH LEVELS THE BLOCK IS PERFORMED?

A typical subarachnoid block is performed in the lumbar region below the level of spinal cord i.e. L 3-4 in children and L2-3 in adults.

Q: WHICH STRUCTURES ARE PIERCED WHILE PERFORMING THE BLOCK? Following structures are pierced from behind forward:-

56

i) ii) iii) iv) v) vi)

Skin and subcutaneous tissues Supraspinous ligament Interspinous ligament Ligamentum Flavum Durmamater Arachnoid mater

Fig: EQUIPMENT FOR EPIDURAL AND SUBARACHNOID ANAESTHESIA.

Q: WHAT ARE ANAESTHESIA?

THE

COMPLICATIONS

OF

SPINAL

57

Complications are:i) Hypotension. ii) Post dural puncture headache (PDPH). iii) Nausea and vomiting. iv) Meningitis. v) Urinary retention.

Q:

WHICH AGENTS ARE COMMONLY USED?

Agents commonly used are:i) Inj. Lignocaine 2%. ii) Inj. Bupivacaine 0.5%. iii) Inj. Bupivacaine 0.75%.

Q: WHAT ARE ANAESTHESIA?

THE

CONTRAINDICATIONS

OF

SPINAL

Contraindications are:i) ii) iii) iv) v) vi) vii)

Patient’s disapproval. Infection at the injection site. Increased intracranial pressure. Coagulopathy. Meningitis. Hypovolaemia and Hypotension. Valvular heart disease.

EPIDURAL ANAESTHESIA Q:

WHAT IS EPIDURAL ANAESTHESIA?

In Epidural Anaesthesia local anaesthetics are injected in the epidural space. The epidural space lies just outside the dural sac, where there is a negative pressure. The structures pierced by epidural needle: Skin.  Subcutaneous fat.  Supraspinous ligament.  Interspinous ligament.  Ligamentum Flavum, and then is the epidural space.

Q:

DESCRIBE THE ANATOMY OF EPIDURAL SPACE?

Boundaries:

58

Superiorly: closed at foramen magnum. Inferiorly: closed at sacro-cocccygeal membrane. Anteriorly: posterior longitudinal ligaments, vertebral bodies. Posteriorly: vertebral lamina and Ligamentum Flavum. Laterally: open, pedicles and intervertebral foramina Shape: Triangular, with apex posteriorly. Contents: Veins, arteries, fat, lymphatic, nerve roots and dural cuffs.

Fig:

LUMBAR EPIDURAL ANAESTHESIA. Notice how the anaesthetist’s right hand rests against the patient’s back to support the needle.

Q: DIFFERENTIATE ANAESTHESIA?

BETWEEN

SPINAL

AND

EPIDURAL

In spinal anaesthetic: A small amount of local anaesthetic drug is placed directly in the CSF producing a total neural blockade caudal to the injection site.  It gives rapid, dense and predictable anaesthetic effect. In epidural anaesthesia:59

  

Ten-fold increase in dose of local anaesthetic (in comparison to spinal) is required to fill the potential epidural space. The onset is slower. The anaesthesia is segmental i.e. a band of anaesthesia is produced extending above and below the injection site.

Advantages of epidural anaesthesia:  Epidural anaesthesia causes less hypotension as compared to spinal anaesthesia. Catheter can be introduced inside the epidural space and drugs can be given repeatedly for post-operative pain relief.  Epidural analgesia is a popular technique for painless delivery.  Epidural anaesthesia can be applied at any level of vertebral column by expert hands.

60

Fig:

THE ANATOMY OF EPIDURAL AND SUBARACHNOID ANAESTHESIA. A, the anatomy for lumbar puncture with a patient in the sitting position. B, with the patient in the lying position. The line between his iliac crests passes between his 3rd and 4th lumbar spines. C and epidural needle goes first through his interspinous ligament and then through his ligamentum flavum before it reaches his extradural space. In this figure his interspinous ligament has been dissected away in the segment through which the needle is passing. For subarachnoid anaesthesia the needle goes further on through his dura and arachnoid mater into his subarachnoid space, which is filled with CSF.

Q:

HOW EPIDURAL SPACE IS IDENTIFIED?

61

Tuohy’s needle is passed in the intervertebral space, while passing through the skin, supraspinous ligament, interspinous ligament and ligamentum flavum. Two methods are applied for identification of epidural space.  Loss Of Resistance (LOR) method, using syringe.  Hanging drop method.

Q: WHAT ARE THE CONTRAINDICATIONS OF EPIDURAL ANAESTHESIA? Following are the contraindications of epidural anaesthesia: Patient’s refusal.  Sepsis with haemodynamic instability.  Uncorrected hypovolaemia.  Coagulopathy.

Q: WHAT ARE ANAESTHESIA?

THE

COMPLICATIONS

OF

EPIDURAL

These are: Hypotension, which can be prevented by fluid preload.  Intravascular injection of local anaesthetic.  Dural puncture and total spinal anaesthesia.  Epidural haematoma.

CAUDAL ANAESTHESIA Q:

DEFINE CAUDAL ANAESTHESIA?

The sacral epidural is called caudal anaesthesia. In this block local anaesthetic is injected through sacral hiatus into the epidural space. The caudal space is the sacral component of the epidural space, and access is through the sacral hiatus, a midline defect of caudal most aspect of the sacrum. The space is covered by sacrococccygeal ligament.

62

Fig:

CAUDAL EPIDURAL ANAESTHESIA. A, the position of the needle in relation to the sacrum. B, the patient ready for the anaesthetic with a pillow under his pubis. C, making a triangle with the anatomical landmarks. D, injecting.

63

Q:  

Q:

WHAT ARE ITS INDICATIONS? Surgical and obstetric procedures involving perineum and sacral distributions, such as anorectal region. Postoperative pain relief for operations on the lower extremities, perineum, male genitals and lower abdomen.

WHAT ARE ITS CONTRAINDICATIONS?

Absolute  Sepsis.  Bacteremia.  Skin infection at injection site.  Severe hypovolaemia.  Coagulopathy.  Therapeutic anticoagulation.  Increased intracranial pressure.  Lack of consent.  Sacral decubitus ulcers. Relative        

Q:       

Peripheral neuropathy. Mini-dose heparin. Aspirin or other antiplatelet drugs. Certain cardiac lesions. Psychologic or emotional instability. Morbid obesity. Prolonged surgery. Surgery of uncertain duration.

WHAT ARE THE COMPLICATIONS? Pain on injection. Backache. Headache. Urinary retention. Vascular injury, Nerve injury. Rarely in obstetric practice, injury to fetal head when placing the needle. Infections.

64

Q: HOW WOULD YOU GIVE LOCAL BLOCKS FOR THE MOUTH AND TEETH? (Following pages are for dental students. The students may practice these local blocks under the supervision of their teachers.) A tooth and its surrounding gum are innervated from three directions: (1) Its pulp is supplied by a nerve which passes up its root. The gum on (2) its labial and (3) its lingual sides is innervated separately. The tooth socket is partly supplied by the nerve that supplies the root and partly by those that supply the gum. If you are going to remove a patient’s tooth painlessly, you will have to anaesthetize all three sets of nerves. You can easily anaesthetize a patient’s labial and lingual gums by local infiltration, but instead of blocking his palatal gums close to this teeth, it is easier to block them in his palate. Infiltrating his gums or his palate will at the same time block the nerves that supply most of the roots of his teeth. The exceptions are his lower molars and second premolars. To anaesthetize them you will have to block his inferior alveolar nerve as it enters his mandibular canal. A patient’s inferior alveolar nerve supplies all the teeth of his lower jaw, so blocking this nerve should make all his lower teeth completely anaesthetic. Unfortunately, anaesthesia is sometimes incomplete, because small accessory branches enter the bone through other foramina and so escape the block. Also, his incisors may not be completely anaesthetized by a single block, because they are innervated from both sides. ANAESTHETIZING THE TEETH DRUGS AND EQUIPMENT For all methods, use 0.5% bupivacaine, or 2% lignocaine with or without adrenaline, preferably in 2 ml cartridges. If possible, a 10% lignocaine spray, or 5% lignocaine paste. A dental cartridge type syringe. If necessary, you can use an ordinary one, preferably one with a “Luer-lok”. Use thin needles – 0.323 and 42 mm. A spirit lamp to flame the end of the cartridge which has to be pierced. A pair of straight – nosed pliers, or artery forceps, to remove the broken end of a needle. A decontaminant, such as 0.5% chlorhexidine. Forceps and some pledgets of cotton wool. GENERAL METHOD Sedate the patient with diazepam 10 to 20mg. Explain to him what your are going to do. Clean his mucosa with the antiseptic. If possible, spray his mucosa with 10% lignocaine, or apply it as a 5% paste.

65

After a few seconds stretch his mucous membrane at the site of the injection and quickly pierce it with the bevel of the needle parallel to the bone. Inject quickly – there is nothing more painful than a local dental anaesthetic given slowly. Once you are through his mucosa, you can pause a little while you find the landmarks. When your needle is in the right position, inject. You cannot aspirate with a dental cartridge. Test for analgesia. If you are going to fill a patient’s tooth, drill its exposed dentine.. Before pulling it out, test the sensitivity of the gum around it.

66

Fig:

BLOCKING THE LINGUAL AND INFERIOR ALVEOLAR NERVES. A, is an injection which is too lateral and B is one which is too medial. X, is the initial position for the syringe, and Y, its final position. C, is the position of your fingers feeling the ascending ramus of the patient’s mandible. D, is the position to aim for , midway between your two fingers.

LOCAL INFILTRATION FOR ALL UPPER TEETH, THE LOWER INCISORS AND CANINES, AND ALL DECIDUOUS TEETH Infiltrate the solution outside the periosteum, near the apex of the tooth. This is where its nerves enter the bone, so this is your target. Labially is his upper jaw. Inject at the reflection of the mucous membrane where it forms the base of the sulcus, as in A, Fig. Inject 12ml of solution, or about half a cartridge. The tip of your needle should come to lie opposite the tip of the root of the tooth you are going to extract. For front teeth insert the needle in line with the tooth. This is impossible with molars, so, if you want to anaesthetize a patient’s third molar, insert the needle over his second molar, and aim it obliquely so that its point comes to lie over the root of his third. If you move the point of the needle fanwise, as in D, very carefully, you can anaesthetize 2 or 3 teeth without removing it. When you inject his upper molars (D), feel the gum on the outer surface of his upper back teeth. The crest of bone jutting down from above is his infrazygomatic crest. Insert your needle immediately behind this crest, distal to his second molar. Push your needle in 2 cm, as far as it will go, and inject 2 ml of solution. Move it as fanwise as you inject. This is also called a tuberosity block. Palatally in the upper jaw Inject at the points marked “X” about 1 cm from the tooth half way between the edge of the gum, and the mid line, as in B, Fig. This is a shallow injection because his palate lies close below a patient’s mucous membrane. Inject just enough solution to make his gum go white. You will not be able to inject much, and you will have to press quite hard. Labially in a patient’s lower jaw. Hold his lip out of the way so that you can see the sulcus clearly. Insert the needle next the chosen tooth, so that its point lies against the outside of his mandible, level with the tip of the root. Inject half a cartridge.

67

Lingually in the lower jaw. Insert the needle a short distance at the point where the mucosa is reflected off the lingual side of his alveolus, as in A, Fig. You may have to hold his tongue out of the way to see the floor of his mouth. Inject about a quarter of a cartridge. There will be a small swelling, which will quickly disappear. THE LOWER PREMOLARS Labially do a mental block like this: Pull down the patient’s lower lip. Use the tip of your index finger to feel the labial surface of his gum as it turns upwards to join his cheek just posterior to his first premolar tooth. You should be able to feel his mental nerve as it comes out of the mental foramen in his mandible. Inject from behind, as in F Fig. Pull the corner of the patient’s mouth out of the way. Tilt the needle medially between his first and second premolars. Aim to place the needle just outside his mental foramen. This is half way between his gingival margin and the lower border of his mandible. As a person gets older, his mandible is absorbed, so that his mental foramen comes to lie nearer the upper border of this mandible. Inject 2 ml of solution. If necessary, repeat the procedure on the other side. Try not to enter his mental foramen, because you may injure the vessels that come out of it, and so cause a large haematoma. Lingually inject his premolars in the same way as for his lower incisors and canines. LOWER MOLARS Do an inferior alveolar and lingual nerve block, as described below.

68

Fig:

INFILTRATING THE LOWER GUMS. A, infiltrating the lingual and B, the labial gum.

RIGHT INFERIOR ALVEOLAR AND LINGUAL NERVE BLOCK:Landmarks The secret of success is to visualize where the patient’s mandibular foramen is, and to aim the tip of a 42 mm needle at it. As usual, the details are all important. Adjust the headrest, so that when the patient’s mouth is wide open, the occlusal plane of his mandible is horizontal, as in D, Fig. When you are learning, use a dental stick dipped in gentian violet to draw a line QR on the mucous membrane of the inside of his cheek in the line of the occlusal surfaces of his lower teeth. If he has a denture, draw it with this in place. If marking it makes him retch, anaesthetize his mucosa first. 69

Feel the anterior and posterior borders of the ascending ramus of his mandible between the thumb and index finger of your left hand, as in C. Make sure that your index finger is as far up his mandible as it will go. The tips of your fingers should lie at either end of line QR. Aim at the mid point between them – usually 2 cm behind point R. Rest the syringe on the occlusal surfaces of the teeth.

Fig:

INFILTRATION ANAESTHESIA FOR THE TEETH. A, when you infiltrate a patient’s gum, put the needle into his buccal sulcus, make the bevel face his periosteum and inject just outside it. B, to anaesthetize his palatal gums inject at the point marked “X”. C, infiltrating the palatal gum of his first molar. D, infiltrating the buccal aspect of his third molar (tuberosity block). E, infiltrating the gum of his lateral incisor. F, blocking his mental nerve. His mental foramen lies on a vertical line between his 4th and 5th teeth, and in a young person is half way up his mandible.

70

The block Now you know the landmarks, put your left index finger into the patient’s mouth, above his lower third molar, as in the upper diagram in Fig. you will feel a depression in the bone immediately above and behind it (retromolar fossa). Behind this you will find a ridge (the oblique line), on the inner surface of his mandible. Ask him to open his mouth even wider. Insert the needle, as described above, immediately medial to the oblique line, 1 cm above the patient’s third molar. At first, place the syringe in the line of the body of his mandible. This is position ”X”. As you push the needle in 2 cm, move the barrel of the syringe across his teeth, so that it lies over his opposite premolar. This is position “Y”. As you move the needle, keep it in contact with his teeth all the time. If he has no teeth, keep it carefully horizontal in his mouth. As you do so, you will feel the needle pass through the buccinator muscle. As it goes through, inject 0.5 ml of solution. Push the needle 2.5 cm further in until it reaches the medial surface of the ramus of his mandible. Inject 2.5 ml here to block his inferior alveolar nerve. If you reach bone at a lesser depth, your needle is too far lateral (needle A in Fig). If you feel no bone, it is too far medial (needle B). After you have withdrawn the needle, inject the last 1 ml of solution into his buccal sulcus, just above the crown of his third molar tooth. This will block his buccal nerve, as it lies on the inner surface of his buccinator muscle. The latent period lasts 10 minutes. The whole of one side of the patient’s face will feel heavy, and his lower lip will feel dead on that side. If anaesthesia of his canine is not complete, infiltrate his gum, or block his mental nerve. CAUTION! (1) Don’t’ push the needle completely into the patient’s tissues, if it breaks you will have great difficulty removing it. (2) Before starting to extract a tooth, press the beak of the forceps hard on both sides of the tooth. If he feels pain, give him another injection.

71

Fig: INSERTING THE NEEDLE TO BLOCK THE INFERIOR ALVELAR NERVE. Notice the position of the point of the needle.

72

Lecture 7 FLUID MANAGEMENT Q: WHY IS NECESSARY?

EVALUATION

OF

INTRAVENOUS

VOLUME

Most of the patients undergoing surgical procedures require venous access and intravenous fluid therapy. The assessment of intravenous volume and replacement of any fluid or electrolyte deficits and ongoing losses is very important. Errors in fluid management or transfusion may result in considerable morbidity and mortality.

Q: WHAT ARE THE INTRAVENOUS VOLUME?

STEPS

OF

EVALUATION

OF

The following are the steps of evaluation of intravenous fluid volume:1. HISTORY:History of abnormal fluid loss. History of NPO hours. 2. PHYSICAL EXAMINATION:Physical examination is important to assess whether the patient is suffering from hypovolemia or hypervolemia. Signs of hypovolemia:Skin turgor is lost. Dry mucous membranes. Dull sensorium. Weak peripheral pulses. Increased pulse rate. Decreased blood pressure. Orthostatic changes in pulse and blood pressure. Urine output less than 0.5 ml/kg/hr. Late signs of hypervolemia are:Tachycardia. Pulmonary rales. Cyanosis. Wheezing. Pink frothy sputum. Presacral or pretibial pitting edema. Increased urinary flow. 3.

HAEMODYNAMIC MEASUREMENT:73

Body fluid status can be measured by measurement of CVP (Central Venous Pressure). PCWP (Pulmonary Capillary Wedge Pressure). 4. LABORATORY EVALUATION:Blood:Serum haematocrit ---- increases with dehydration. Arterial pH ---- metabolic acidosis in dehydration. Serum sodium ---- increases in dehydration. Serum urea ---- increases in dehydration. Urea to creatinine ratio ---- 10:1. Urine:Urine specific gravity ---- 1.010. Urine osmolarity > 650 m. osmol/kg. Urinary sodium concentration < 20meq/l. Urinary chloride concentration is decreased.

Q:

WHAT ARE THE TYPES OF INTRAVENOUS FLUIDS?

There are two types of intravenous fluid:Crystalloids. Colloids.

Q:

WHAT ARE CRYSTALLOIDS?

Crystalloids are aqueous solutions of low molecular weight with or without glucose. When given they rapidly equilibrate and distribute throughout the entire extracellular fluid space. Crystalloids are equally effective when given in sufficient amounts in restoring intravascular volume, usually 3-4 times the volume of blood lost.

Q:

WHAT ARE THE TYPES OF CRYSTALLOIDS?

A wide variety of solutions are available. e.g.  0.9% normal saline.  Hartman’s solution.  5% dextrose solution. The solutions should be chosen according to the type of fluid loss being replaced. 1. maintenance type solutions:Losses primarily due to water loss should be replaced with hypotonic solutions. 2. Replacement type solutions:-

74

Losses that involve both water and electrolyte deficit should be replaced with isotonic electrolyte solutions.

Q:

WHAT ARE COLLOID SOLUTIONS?

Colloid solutions contain high molecular weight proteins or large glucose polymers usually in normal saline. Colloid solutions maintain osmotic pressure and mostly remain intravascular for 3-6 hours. Severe intravascular fluid deficits can be more rapidly corrected using colloid solutions.

Q: WHAT COLLOIDS?   

Q:       

Q:     

ARE

THE

INDICATIONS

FOR

THE

USE

OF

Fluid resuscitation in patients with severe intravascular fluid deficit. Fluid resuscitation in patients with severe hypoalbunemia. Conditions associated with severe protein loss such as burn.

WHAT ARE THE TYPES OF COLLOIDS? Blood derived colloids. Albumin 5% and 25% solutions. Plasma protein fraction 5%. Dextrose starches. Dextran. Starch solution. Gelatins.

WHAT ARE THE SIDE EFFECTS OF DEXTRAN? Antiplatelets effect. May interfere with blood typing. May prolong bleeding time. May cause renal failure. Mild to severe anaphylactic reactions can occur.

Q: WHAT THERAPY?

ARE

THE

STEPS

OF

PERIOPERATIVE

FLUID

This includes normal maintenance requirements:This means replacement of normal losses such as: Urine formation. 75

     

GIT secretions. Sweating. Insensible loss from skin and respiratory tract. This is a hypotonic loss and is replaced with solutions such as. 5% Dextrose water with saline. 5% Dextrose water without saline.

Estimation of normal maintenance requirements:1st 10 kg ------------------ 4 ml/kg/hr Next 10 kg ---------------- 2 ml/kg/hr For each kg above 20 kg – 1ml/kg/hr Pre-existing deficits Fluid deficit due to period of fasting before surgery: Normal maintenance rate X duration of fast  Abnormal fluid loses  Pre operative bleeding  Vomiting  Diuresis  Diarrhoea  Occult loses  Third spacing  Ascites  Increased insensible losses due to hyperventilation, fever and sweating  To replace pre-existing deficits fluid should be similar in composition to the fluid lost. Surgical fluid losses:Blood loss is estimated;  Suction container.  Visual estimation of blood loss.  Sponges 4’’ x 4’’ --- 10 ml.  Laparotomy pads ---- 100 – 150 ml.  Blood loss can be measured by weighing sponges before and after use and by serial haematocrit and hemoglobin concentrations. Other fluid losses  Evaporation.

 Internal distribution.  Interstitial space (third spacing). 76

 Across serosal surface (Ascites).  Into bowel lumen.  Significant loss of lymphatic fluid may occur during extensive retroperitoneal dissection.

Q: What is Daily Fluid requirement Post-operatively? Daily Fluid Requirement Post-operative

Adult Patient According to Body wt. First 10kg  4  kg/hr (4  10) = 40 ml/hr Next 10kg  2  kg/hr (2 10) = 20 ml/hr Next 10kg  1  kg/hr (1  10) = 10 ml/hr For example 70 kg wt patient First 10kg 40 ml/hr Next 10 kg 20ml/hr Next 10 kg 50ml/hr Total 110ml/hr Adult open heart surgery 1st day 1ml/kg/hr 2nd day 1.5 ml/kg/hr Paediatric Cases First 10kg 4ml/kg/hr Next 10kg 2ml/kg/hr Then Next 1ml/kg/hr

BLOOD TRANSFUSION Q: WHAT ARE THE INDICATIONS OF BLOOD TRANSFUSION IN A SURGICAL PATIENT?

77

  

Hb % less than 7 gm/dl and / or Haematocrit less than 21% (in a patient undergoing elective surgery) 10-20% blood volume loss

Q: WHAT ARE TRANSFUSION? 1.

2. 3. 4. 5.

6. 7. 8. 9. 10. 11.

Q:

THE

COMPLICATIONS

OF

BLOOD

Infection a. Viruses  Hepatitis C  Hepatitis B  HIV  Cytomegalovirus b. Bacteria Syphilis c. Protozoa: Malaria, toxoplasmosis ABO incompatibility Anaphylaxis Adverse transfusion reaction Massive transfusion problems a. Hyperkalemia: high K+ levels in blood, may be if transfusion more than 1.5 ml/kg/min. b. Hypocalcaemia: citrate chelates ionized calcium c. Hypomagnesaemia d. Acid-base derangements: initial acidosis becomes alkalosis as citrate metabolized to bicarbonate e. Hypothermia Oxygen dissociation curve shifts to the left, so less oxygen is delivered to the tissue Micro embolism Hyperglycaemia Dilutional thrombocytopenia Dilutional coagulopathy Transfusion-related acute lung injury

HOW IS BLOOD STORED?

78

Red cells last well in refrigerated (4-6 C) stored blood. More than 70% survive 24 hrs after transfusion. Clotting factors deteriorate progressively after 24 hrs storage. Citrate-phosphate-dextrose (CPD) blood contains no functional platelets after 48h. citrate-phosphate – dextrose blood plus adenine preserves its adenosine triphosphate (ATP) and 2,3-DPG levels for up to 2 weeks with slow fall thereafter and is stored for up to 35 days.

Q:

WHAT ARE VARIOUS BLOOD PRODUCTS AVAILABLE? 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Q:

Saline adenine glucose mannitol blood Whole blood Frozen blood Plasma Human albumin Human fibrinogen Cryoprecipitate Platelets Factor VIII concentrate Factor IX Washed red cells

WHAT ARE THE SIGNS OF INCOMPATIBLE TRANSFUSION?

In the conscious 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Headache Precordial or lumbar pain Urticaria or pruritus Burning in limbs Bronchospasm Dyspnoea Tachycardia Restlessness Suffused face Nausea and vomiting Pyrexia and rigors Circulatory collapse Later, haemoglobinaemia, haemoglobinuria and oliguria.

Under anaesthesia Sometimes not easy to distinguish from the effects of hemorrhage itself, especially during rapid transfusion > 100 ml/min. 79

Immediate 1. Rapid severe and progressive hypotension 2. Tachycardia 3. General oozing from wound 4. Urticarial rash 5. Bronchospasm, raising airway pressures positive pressure ventilation.

on

intermittent

Late Jaundice and oliguria in 5-10% of these patients. It strongly resembles anaphylactic reaction and treatment is similar.

Q: WHAT IS THE MANAGEMENT OF SEVERE TRANSFUSION REACTION? The blood unit should be rechecked against blood slip and patient’s identity bracelet (Patient’s Chart). Blood should be drawn to identify haemoglobin and coagulation tests. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Stop the transfusion. Support blood pressure with intravenous colloids or crystalloids and ionotropes or vasoconstrictors if needed. 100% O2. Induce a diuresis with mannitol 50 g or frusemide 10-20 mg. Check acid-base balance and electrolyte. Exchange transfusion in the desperate case. High dose of steroids may be useful. Antihistamines may be indicated in the early stages but may increase hypotension. Where DIC is occurring, coagulation factors and platelets need to be replaced. Transfer to high-dependency unit or intensive therapy unit.

80

Lecture 8 ACID-BASE & ELECTROLYTE BALANCE ACID – BASE BALANCE

Q:

DEFINE THE FOLLOWING:

pH, ACID, BASE, ACIDOSIS, ACIDEMIA, ALKALOSIS, ALKALEMIA? pH: It is the negative logarithmic value of H+ concentration pH= 1/[H+] Acids: Substances that produce H+ when dissolved in water. Acid-Base disorders: Normal pH of body fluids is 7.36-7.44 Acidosis: Process that cause acids to accumulate Acidemia: Present when pH < 7.36 Alkalosis: Process that cause base to accumulate Alkalemia: Present when pH > 7.44

Q: WHAT ARE THE DIFFERENT ACID-BASE DISORDERS? EXPLAIN. Primary acid-base disorders are:Respiratory: if primary disturbance involves CO2 Metabolic: if primary disturbance is in HCO3 concentration. METABOLIC ACIDOSIS Characterized by decreased HCO3 and a variable degree of acidemia. Respiratory compensation is by hyperventilation thus washing out CO2.

81

Clinical features:Decreased cardiac output Pulmonary hypertension Arrhythmias Kussmaul breathing Hyperkalaemia Causes Overproduction of acids:Diabetic ketoacidosis Lactic acidosis Exogenous acid:Salicylates Reduced excretion:Renal failure Treatment Identification of cause and its treatment. If pH < 7.2, measures taken to restore pH. Sodium bicarbonate can be used for restoration of pH towards normal. Bicarbonate requirement: body wt. (in kg) x base deficit x 0.3 METABOLIC ALKALOSIS Characterized by primary increase in HCO3 and a variable degree of alkalemia. Compensatory respiratory hypoventilation is very limited and not effective. For diagnostic point of view, metabolic alkalosis is divided into: Chloride responsive Chloride resistant Chloride responsive: Loss of acid Vomiting N/G suction Gastrocolic fistula Chloride depletion Diarrhoea Diuretic abuse Excessive alkalies NaHCO3 administration Chloride resistance Primary or secondary hyperaldosteronism Cushing syndrome Severe hypokalemia 82

Treatment In chloride responsive alkalosis, administration of saline causes volume expansion and results in excretion of excess bicarbonate; if K + is required, it should be given as KCl. In patients to whom volume is administered, the use of acetazolamide results in renal loss of HCO 3 and an improvement in pH. In life threatening metabolic alkalosis, rapid correction is necessary and may be achieved by administration of H+ in the form of dilute HCl. Acid is given as 0.1 normal HCl in glucose 5 % at a rate no more than 0.2 mmol/kg/hr. RESPIRATORY ACIDOSIS Characterized by an increase in CO2, which results in acidemia proportional to degree of hypercapnia. Compensation is through kidneys, which excrete acid. Clinical features Usually hypoxemia and manifestations of underlying disease dominate the clinical picture but hypercapnia per se may result in coma, raised ICP and hyper dynamic CVS resulting, from release of catecholamine.

Causes:CNS Drug over dosage Trauma Tumor PNS Polyneuropathy Myasthenia gravis Poliomyelitis Tetanus Primary pulmonary disease Airway obstruction:Asthma Parenchymal disease:ARDS Loss of mechanical integrity:Flail chest Treatment Treatment of underlying cause and mechanical ventilation if required.

RESPIRATORY ALKALOSIS Primary decrease PaCO2, which increase pH above 7.44 Clinical features:83

Lightheadedness Confusion Seizures Circumoral paraesthesia Hyperreflexia Tetany Causes Hyperventilation voluntarily or hysteria Pain, anxiety Specific conditions CVS disease Meningitis Tumor Trauma Respiratory disease Pneumonia Pulmonary embolism Shock Cardiogenic Hypovolaemic Treatment Treatment of underlying cause

ELECTROLYTE BALANCE SODIUM BALANCE Q:

WHAT IS THE NORMAL SODIUM BALANCE OF THE BODY?

Daily ingestion amounts to 50-300 mmol. Losses in sweat and faces are minimal (approx. 10 mmol/day) and final adjustment are made by kidney. Urine Na may be as low as 2 mmol/day during salt restriction or may exceed 700 mmol/day after salt loading. Sodium balance is related intimately to ECFV and water balance.

Q:

DEFINE HYPERNATREMIA?

Hypernatremia is defined as a plasma sodium concentration of more than 150 mmol/litre. It may result from pure water loss, hypotonic fluid loss or salt gain. In the first two conditions, ECFV is reduced, whereas salt gain is associated with an expanded ECFV.

84

Q:

WHAT ARE THE VARIOUS CAUSES OF HYPERNATREMIA?

Pure water depletion External loss postoperative) Renal loss Hypotonic fluid loss External loss Renal loss Salt gain

Failure of water intake (coma, elderly, Mucocutaneous loss Fever, hyperventilation, thyrotoxicosis Diabetes inspidus (cranial, nephrogenic) Chronic renal failure Gastrointestinal (vomiting, diarrhea) Skin (excessive sweating) Osmotic diuresis (glucose, urea, mannitol) latrogenic (NaHCO3, hypertonic saline) Salt ingestion Steroid excess

Q:

WHAT ARE THE CONSEQUENCES OF HYPERNATREMIA?

 

Reduction in cell volume and water content of the brain. Increased permeability and even rupture of the capillaries in the brain and subarachnoid space. Pyrexia. Nausea, vomiting. Convulsions. Coma. Focal neurological syndrome.

    

Q:

WHAT IS THE TREATMENT OF HYPERNATREMIA?

For hypernatremic patients without volume depletion 5% glucose is sufficient to correct the water deficit. Water deficit is calculated as: Water deficit = (measured [Na +] /140xTBW)-TBW For hypernatremic patients with hypovolaemia, isotonic saline is the initial treatment of choice. Once volume depletion is corrected then further repair of any fluid deficit can be accomplished with hypotonic fluids.

Q:

DEFINE HYPONATREMIA?

This is defined as a plasma sodium concentration of less than 135 mmol/litre.

85

Q:

WHAT ARE THE CAUSES OF HYPONATRAEMIA? HYPONATREMIA

 EVALUATION OF EXTRACELLULAR FLUID VOLUME

 HYPOVOLAEMIA NORMOVOLEMIA

HYPERVOLAEMIA





(EDEMA)





osmolarity

plasma





 Renal Loss

EXTRA RENAL LOSS





-

-

Diuretic abuse Hypoadrenalis m - Salt losing nephropathy Renal tubular - Acidosis -

-

-

-

Diarrhoea Vomiting Third space losses

Congestive cardiac failure

       

      

 

Urine sodium < 15mmol/l

Urine sodium > 20mmol/l



NORMAL Psuedohypo natraemia

-

     

Urine sodium 60 years old, PaCO2 is equal to 80 mm Hg minus 1 mm Hg for every year over 60.

Q: HOW DO YOU INTERPRET ARTERIAL BLOOD GASES (ABG’s) VALUES? 1.

2.

3.

4. 5.

Check pH = Alkalosis = Acidosis Check pCO2 = CO2 retention (hypoventilation); respiratory acidosis or compensating for metabolic alkalosis. = CO2 blown off (hyperventilation); respiratory alkalosis or compensating for metabolic acidosis. Check HCO3 = Nonvolatile acid is lost; HCO3 gained (metabolic alkalosis or compensating for respiratory acidosis) = Nonvolatile acid is added; HCO3 is lost (metabolic acidosis or compensating for respiratory alkalosis) Determine imbalance Determine if compensation exists

90

Q: WHAT CHANGES IN PARAMETERS WILL HELP YOU TO DETERMINE IMBALANCE IN ABG’s? If pH



pH



If pH



pH



If pCO2  pCO 2  If pCO2  pCO 2 

Q:

and pCO2 or and pCO2



and HCO3 or and HCO3



and HCO3 or and HCO3



and HCO3 or and HCO3



Then respiratory disorder 

Then metabolic disorder 

Then compensation is occurring 

Then mixed imbalance 

HOW WOULD YOU DETERMINE COMPENSATION?

To determine the compensation for respiratory or metabolic disorders, pH and PaCO2 are the basic parameters. The normal range of PH = 7.30 – 7.50 PaCO2 = 30-50 mm Hg So remember range. 30-50 For compensation of respiratory alkalosis / acidosis: check the pH For compensation of metabolic alkalosis / acidosis: check pH and PaCO2 Now - If PaCO2 is normal and pH is outside the range – the disorder is uncompensated - If PaCO2 is increased or decreased and pH is outside the range – the disorder is partially compensated - If PaCO2 is increased or decreased and pH is within range – the disorder is fully compensated.

91

See for example. If ph = 7.26, PaCO2= 56, HCO3 = 24 then respiratory acidosis is uncompensated If ph = 7.38 PaCO2= 76, HCO3 = 24 then respiratory acidosis is compensated If ph=7.2, PaCO2=40, HCO3 =9 then metabolic acidosis is either acute or uncompensated If ph = 7.36 PaCO2= 25, HCO3 = 15 then metabolic acidosis is compensated

PULSE OXIMETRY Q:

WHAT IS PULSE OXIMETRY?

This is a non-invasive measurement of the arterial blood oxygen saturation at the level of the arterioles. A continuous display of the oxygenation is achieved by a simple, accurate and rapid method. Pulse oximetry has proved to be a powerful monitoring tool in the operation theatre, recovery wards, and intensive care units, general wards and during transport of critically ill patients.

Q:

WHAT ARE THE COMPONENTS OF A PULSE OXIMETER? 1. A probe positioned on the finger, toe, ear lobe or nose. The light emitting diodes (LEDs) producing beams at red and infrared frequencies on one side and a sensitive photodetector on the other side. The LEDs operate in sequence. 2. The case, which houses the microprocessor. There is a display of the oxygen saturation, pulse rate and a plethysmographic waveform of the pulse. Alarm systems can be set for a low saturation value and for both high and low pulse rates.

Q: WHAT IS THE MECHANISM OF ACTION OF PULSE OXIMETER? 1. The oxygen saturation is estimated by measuring the transmission of light, through a pulsatile vascular bed (e.g., finger). 2. The amount of light transmitted depends on many factors. The light absorbed by non-pulsatile tissues (e.g., skin soft tissues, bone and venous blood) is constant (DC). The non-constant absorption (AC) is the result of arterial blood pulsation. The sensitive photodetector generates a voltage proportional to the transmitted light. 92

3. The microprocessor is programmed to mathematically analyze both the DC and AC components. The result is the arterial saturation.

Q:

WHAT ARE THE FACTORS THAT AFFECT IT’S WORKING? 1. It is accurate in the range of 70-100%. Below the saturation of 70% readings are extrapolated. 2. Carbon monoxide poisoning (including smoking), coloured nail varnish, I/V injections of certain dyes and drugs responsible for the production of methaemoglobinemia are all sources of error. 3. Excessive movement or malposition of the probe is a source of error. 4. Inaccurate measurements can be caused by venous pulsations.

CAPNOGRAPHY, END TIDAL CO2 CONCENTRATION Q:

WHAT IS A CAPNOGRAPH?

An instrument, which gives a continuous recording of end-tidal carbon dioxide concentration, is known as a capnograph.

Q:

HOW IS INFRARED ANALYZER USED FOR THIS PURPOSE?

Gases with molecules that contain at least two dissimilar atoms absorb radiation in infrared region of spectrum. Using this property, carbon dioxide concentration can be measured directly and continuously throughout the respiratory cycle. End-tidal carbon dioxide reflects accurately the arterial carbon dioxide tension in the individuals with normal lungs.

Q:

WHAT ARE ITS COMPONENTS? 1. The sample chamber can either be positioned within the patient’s gas stream or connected to the distal end of the breathing system via a sampling tube. 2. A photodetector measures light reaching it from a light source at the correct infrared wavelength after passing through two chambers. One acts as a reference whereas the other one is the sample chamber.

Q:

WHAT IS THE MECHANISM OF ACTION? 93

1. CO2 absorbs the infrared radiation particularly at a wavelength of 4.3 um. 2. The amount of radiation absorbed is proportional to the number of CO2 molecules (partial pressure of CO 2) present in the chamber. 3. The electrical output from the detector is proportional to the partial pressure of CO2 in the chamber. 4. In the same way a beam of light passes through the reference chamber, which contains air. The absorption detected from the sample chamber is compared to that in the reference chamber. This allows the calculation of values.

Q:

WHAT ARE THE TYPES OF CO2 ANALYZERS? 1. Side stream analyzer 2. Main stream analyzer

Q:

WHAT ARE THE USES OF END TIDAL CO2?

Increased end-tidal CO2  Hypoventilation  Rebreathing  Sepsis  Malignant hyperpyrexia  Hyperthermia  Skeletal muscle activity Decreased end-tidal CO2  Hyperventilation  Pulmonary embolism  Hypoperfusion  Hypometabolism  Hypothermia

Q: WHAT ARE THE PROBLEMS IN THE USE OF INFRARED ANALYZER? 1. In patients with chronic obstructive airway disease, the waveform shows a sloping trace and does not reflect end-tidal CO2. 2. During pediatric anaesthesia, it can be difficult to produce and interpret end tidal CO2 due to high respiratory rates and small tidal volumes. 94

3. Dilution of end-tidal CO2 can occur, whenever there are loose connections or system leaks. 4. Nitrous oxide absorbs infrared light with an absorption spectrum overlapping that of CO2, thus causing inaccuracy. 5. The absorption of CO2 is increased due to the presence of nitrous oxide or nitrogen.

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Lecture 10

ANAESTHESIA AND RELATED DISEASES HYPERTENSION Q: HOW WILL YOU DEFINE HYPERTENSION? Hypertension is characterized by a persistent. Systolic blood pressure > 140 mm Hg. Diastolic blood pressure > 90 mm Hg.

Q: CLASSIFY HYPERTENSION. CLASSIFICATION OF BLOOD PRESSURE FOR ADULTS Category Normal High normal Hypertension Stage 1 (mild) Stage 2 (moderate) Stage 3 (severe) Stage 4 (very severe)

Systolic (mm Hg) 120

Q: HOW DOES HYPERTENSION AFFECT ADMINISTRATION OF ANAESTHESIA? Hypertension may lead to ischemia, myocardial infarction, acute LVF, CVA, haemorrhage, disruption of vascular suture lines. The three main features of hypertension which directly influence the administration of anaesthesia to these patients are:  

Altered vascular reactivity to drugs – due to altered flow resistance, smooth muscle shortening relationship in arteriole. Pre-existing coronary artery disease (CAD) with high blood pressure. Existence of LVF and renal failure.

Q: WHAT PROBLEMS CAN YOU FACE DURING ANAESTHESIA? 1. Excessive hypotension may occur during induction of anaesthetic agents:-

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Give slow I/V injection of anaesthetic agents. Stabilize the heart with I/V narcotic analgesic like ultra short acting Fentanyl. Inhalation of volatile anaesthetics over 5 mins with N2O: Oxygen. Give lignocaine 1mg/kg IV bolus dose to attenuate reflexes at intubation. 2. Excessive hypertension during intubation:Intubation leads to excessive sympathetic discharge, tachycardia, and dysrythmias. Give lignocaine 1mg/kg body wt. Short acting beta blockers such as esmolol I/V. Local spray of cords. 3. Acute hypertension during maintenance:Titrate volatile anaesthetic. Avoid hypocapnia and hypercapnia. 4. Rebound hypertension during recovery:If diastolic BP 120mm Hg, give anti-hypertensive agents such as nitroprusside, nitroglycerine.

ASTHMA Q: DEFINE ASTHMA? WHAT ARE THE FEATURES OF ASTHMA? Asthma is a disease characterized by an increased responsiveness of the trachea and bronchi to various stimuli manifested by a widespread narrowing of the airways that changes in severity either spontaneously or as a result of therapy. Salient features are:

Variable wheezing, dyspnoea and cough due to widespread airway narrowing.

Q: WHAT ARE THE TRIGGERING FACTORS FOR ASTHMA? 1. Anxiety, airway instrumentation, exercise, allergens (dust, pollens etc.) 2. Thiopentone, muscle relaxants and beta-blockers may cause bronchoconstriction. May be due to IgE mediated histamine release. 3. 10% of adult asthmatics are sensitive to aspirin and other NSAIDs.

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Q: WHAT ARE THE IMPORTANT HISTORICAL FEATURES OF AN ASTHMATIC PATIENT? A careful history allows a close estimate of severity of the disease and should include the following questions: 1. How and when the patient was first diagnosed? 2. How often the patient has attacks, what typically initiates them, and how long the illness has lasted? 3. Whether the patient has been treated as an outpatient or inpatient? If inpatient, ask for details of hospital stay, including length of admission, requirement of intensive care, and intubation. 4. What medication the patient takes, including as-needed usage and over-the counter medications. Has the patient ever taken steroids?

Q: WHAT PREOPERATIVE TESTS SHOULD BE ORDERED? Following investigations should be requested: 1.

2. 3. 4.

Routine investigations like blood C/P, urine R/E, serum electrolytes etc. Chest X-Ray. ECG. Lung function tests; FEV1, FEV1/FVC, ABG’s.

Q: WHAT IS THE ANAESTHETIC MANAGEMENT OF ASTHMA? Anaesthetic management:    

Except in emergency, patients with asthma should not be operated upon until their lungs condition is optimal. Premedication: Antihistamines are useful. Regional techniques are preferred. Volatile anaesthetics are bronchodilator and well tolerated. Nebulized Salbutamol can be given during the operation.

Asthma may get worse by: I./V Thiopentone  Clumsy inhalational induction  Tracheal intubation

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Incomplete relaxation Regurgitation Avoid beta blockers (Cardio selective, Metoprolol 2-10 mg may be used)   

Q: WHAT IS THE TREATMENT OF ACUTE BRONCHOSPASM? Treatment of acute Bronchospasm During operation 1. Deepen the Anaesthesia. 2. Adrenaline 1:1000,0.5 ml sc. 3. Salbutamol infusion 5 mg/ml. (5 ml of 1 mg/ml solution added to 500ml of 0.9% saline to give final conc. Of 10mg/ml). 4. Ketamine, sub anaesthetic dose 0.75mg/kg. 5. Aminophylline 5mg/kg (halothane can interact with Aminophylline to produce arrhythmias).

ANAESTHESIA AND LUNG DISEASES Q: WHAT ARE THE COMMON LUNG DISEASES FACED DURING ANAESTHESIA? 1. OBSTRUCTIVE LUNG DISEASE A. Increased resistance to airflow can be caused by pathology in the lumen, in the bronchial wall, or outside the airways.  Chronic obstructive lung disease  Chronic bronchitis  Emphysema Reactive airway diseases (asthma) 2. RESTRICTIVE LUNG DISEASE A. Pulmonary fibrosis B. Sarcoidosis C. Hypersensitivity Pneumonitis D. Systemic Sclerosis

Q: WHAT WILL BE THE ANAESTHETIC MANAGEMENT OF A PATIENT WITH LUNG DISEASE? 1. PREOPERATIVE EVALUTAION a) Pulmonary function tests b) ABG’s c) Chest X-ray

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2. PREOPERATIVE PREPARATION a) Minimizing bronchospasm b) Smoking cessation at least 2 weeks prior to surgery.

3. ANAESTHETIC MANAGEMENT a) Intubation 1) Direct oral: appropriate if intubation difficulty not suspected. 2) Fibroptic: appropriate for difficult airway 3) Nasal 4) Awake: indications include difficult airway, high risk of gastric aspiration, anatomic risk for inadequate cord visualization, jaw malformation, head and neck scar, congenital abnormalities of upper airway, morbid obesity 5) Endobronchial: appropriate when one lung ventilation desired b) Hypercarbia 1) May prolong time for resumption of spontaneous ventilation at the end of case 2) Increases cerebral blood flow c) Hypocarbia 1) May prolong time for resumption of spontaneous ventilation at the end of case 2) Decreases cerebral blood flow d) Hypoxemia: greatest risk 1) Low F1O2 due to anaesthetic circuit leakage or disconnection 2) Endobronchial intubation 3) Bronchospasm 4) Pulmonary odema 5) Pneumothorax 6) Unplanned extubation 7) Endotracheal tube obstruction 8) Airway obstruction in nonintubated patient 9) Alveolar hypoventilation 10) Atelactasis 11) Worsening of underlying pulmonary disease

Q: WHAT ARE THE MOST COMMON POSTOPERATIVE COMPLICATIONS? 1. Atelactasis 2. Pneumonia

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Lecture 11

CARDIOPULMONORY RESUSCITATION Q: DEFINE CPR. Cardiopulmonary resuscitation (CPR) is an emergency technique that anyone can learn to help someone whose heart and/or breathing has stopped.

Q: What are the basic rhythms of Cardiac Arrest? Rhythms of cardiac arrest are divided into two groups: 1. Shockable Rhythms 2. Nonshockable Rhythms Each of these two are further divided into two rhythms 1. Shockable Rhythms: a. Ventricular Fibrillation b. Pulseless Ventricular Tachycardia 2. Non Schockable Rhythms: a. Asystole b. Pulseless Electrical Activity

Q: WHAT ARE THE POTENTIALLY REVERSIBLE CAUSES OF CARDIAC ARREST. The potentially reversible causes of cardiac arrest can be remembered by keeping “5Hs” and “5Ts”. 1. 5Hs are as under:Hypovolemia. Hypoxia. Hydrogen Ion (Acidosis). Hyper / Hypokalemia. Hypothermia. 2. 5Ts are:Tablets (Drugs). Temponade. Tension pneumothorax. Thrombosis, coronary. Thrombosis, pulmonary.

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Q: WHAT ARE THE TWO COMMONLY USED TYPES OF CPR. 1. Basic Life Support (BLS) 2. Advanced Life Support (ALS)

Q: DESCRIBE THE STEPS OF BLS. Steps of BLS can be described in the form of “Primary ABCD Survey”. Primary ABCD Survey is composed of following. A – Airway, Open the airway. B – Breathing, Assess breathlessness Give two normal breaths that make chest rise (1 sec) C – Circulation ….. Assess circulation   

Lay Rescuers ….. No pulse check. Look for other signs of circulation (breathing, coughing or movement). Doctors and Paramedics ….. Check pulse (Carotid in Adults, Brachial in Infants and Children) If no signs of circulation ….. Start Chest Compressions

D – Defibrillate. Attach AED or give shocks from manual defibrillator. Single shock should be given. Monophasic 360 J and Biphasic 120200 J.

Q: WHAT ARE THE METHODS OF CLEARING THE AIRWAY? There are two methods of opening the airway. 1. Head tilt and Chin lift Maneuver. This is done in patients where it is confirmed that there is no risk of neck injury e.g. cardiac arrest in home, arrest in hospital wards. 2. Jaw Thrust Maneuver. This should be performed in patients in whom neck injury is suspected e.g. road side accidents, drowning in divers etc.

Q: HOW SHOULD ONE SUPPORT AND ASSESS BREATHING DURING BLS? 103

Assess breathing by using three senses i.e. look, listen and feel. Look for the movements of abdomen, listen the breath sounds, and feel the air coming out of patient’s nose or mouth by placing your ear near patient’s nose and mouth. If the person is breathing place him in recovery position, call for help and monitor his breathing efforts. If the person is not breathing then give two normal breaths that make chest rise, by blowing from your mouth after pinching his nose and getting a proper mouth to mouth seal. After two initial breaths give two breaths after every thirty chest compressions.

Q: DESCRIBE THE PROCEDURE OF CHEST COMPRESSIONS DURING BLS. Following are the essentials for chest compressions during CPR. 1. Hand placement. Place heal of your hands above the xiphoid process in the midline of the sternum. 2. Compress the chest by two inches in adults, and one inch in children (1 – 8 years). 3. Ratio of compression to ventilation (C:V) 30:2 in adults and children C:V should be 30:2 for single rescuer and 15:2 for two rescuers. 4. Compression rate should be 100/min.

Q: WHAT IS THE BEST TIME FOR DEFIBRILLATION? Best time for defibrillation is immediately after cardiac arrest or as early as possible. Chances of revival decrease by approximately 10% after every minute delay in defibrillation.

Q: WHAT ARE THE COMPONENTS OF SECONDARY ‘ABCD’ SURVEY? ALS can be described in the form of “Secondary ABCD Survey”. Secondary ABCD Survey consists of following steps. 

A – Airway Advanced airway control Tracheal Intubation

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

B – Breathing IPPV with Ambu Bag or Ventilator



C – Circulation IV access Rhythm appropriate drugs



D – Differential Diagnosis

Q: WHAT AIRWAY ADJUNCTS COULD BE USED DURING ACLS? 1. 2. 3. 4. 5. 6. 7. 8.

Laerdal Mask (Ambu rescue mask) Oropharyngeal airway Ambu bag and mask Laryngeal Mask Airway (LMA) Oesophagotracheal Combitube Endotracheal tube Cricothyroid puncture Tracheostomy (Percutaneous)

Q: ENUMERATE THE ESSENTIAL DRUGS REQUIRED FOR ACLS ALONG WITH THE DOSES. 1. 2. 3. 4. 5. 6. 7. 8.

Oxygen 10 – 15 l/min. Adrenaline 1mg every 3 – 5 minutes. Amiodarone 300mg IV push in adults and 5mg/kg in children Atropine 0.5 – 1mg (maximum dose is 0.03 to 0.04 mg/kg body weight). Lignocaine 1 – 1.5 mg/kg body weight. Magnesium sulphate 1 – 2 g IV in adults. Procainamide up to 17 mg/kg body weight. Sodium Bicarbonate 1 mmol/kg only in protracted CPR, known cases of bicarbonate responsive acidosis, hyperkalaemia.

Q: WHAT IS ALGORHITHM FOR BASIC LIFE SUPPORT? 105

ALGORHITHM FOR BASIC LIFE SUPPORT Check responsiveness Shake and shout

Unresponsive Shout for help

Open airway, Head tilt, Chin lift, jaw thrust

Check breathing Look, listen, feel

Breathing present, place in recovery position

No breathing two effective breaths

Assess circulation Movement/pulse

Circulation present continue rescue breathing @20/min, check circulation every minute

No circulation Compress chest 100/min.30:2ratio

Q: WHAT IS THE ALGORITHM FOR CPR? Cardiac arrest

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BLS algorithm if appropriate

Precordial thump if appropriate

Attach defib/monitor

Assess rhythm

VF/Pulseless VT

Defibrillate Shock 360J Monophasic 120-200J Biphesic

CPR 2 min

During CPR If not already:  Check electrode/paddle positions and contact  Attempt/verify: ETT i.v.access  Give adrenaline every 3min  Correct reversible causes  Consider: buffers antiarrhythmics atropine/pacing Potentially reversible causes: Hypoxia Hypovolaemia Hyper/hypokalaemia and metabolic disorders Hypothermia Tension pneumothorax Tamponade Toxic/therapeutic disturbances Thromboembolic/mechanical obsruction

Asystole or PEA

Up to 3 min CPR

Figure 1: Algorithm for advanced life support management. BLS=Basic life support.

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Fig: MOUTH – TO – MOUTH AND MOUTH –TO – NOSE VENTILATION. Start mouth – to – mouth, and if this fails try mouth – to – nose. A, and B, extend the patient’s head, pinch his nose and watch his chest expand. B, and C, when you ventilate mouth to nose, put one hand on his forehead and hold his chin up with the other one.

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30:2

After every 30 chest compressions 2 lung inflations are carried out

Fig: CARDIOPULMONARY RESUSCITATION. Note that the operator is using the heel of his hand.

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Q: HOW WOULD YOU KEEP THE AIRWAY CLEAR? Try these methods in the following order. If one method fails, quickly move on to the next. FLEX THE PATIENT’S NECK AND TILT HIS HEAD While he is lying flat, grasp his head with one hand and tilt it so that his nostrils point upwards. At the same time, flex his neck forward. Extending his head without flexing his neck is less effective. This combination of movements raises his mandible away from his cervical spine, and lifts his tongue off the posterior wall of his pharynx. A pillow under his head and neck helps to maintain this position. LIFT HIS CHIN Pull it upwards. This will usually clear the airway of a young adult with a good set of teeth.

Fig: TWO WAYS OF KEEPING A PATIENT’S AIRWAY CLEAR. Tilting a patient’s head backwards will usually clear his airway. If this does not, insert Guedel’s airway.

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LIFT THE ANGLES OF HIS JAW Sit at the head of the table, rest your elbows on it, and lift both the angles of his jaw with your middle fingers. Your thumb and first fingers will then be free, if necessary, to hold the mask, as in Fig. Lifting his chin, if it succeeds, is better than lifting the angles of his jaw, because lifting them can make his jaw stiff, and at worst dislocate it. Lifting the angles of the jaw is for more difficult patients only. GUEDEL’S AIRWAY If the above method fails to clear the patient’s airway, insert Guedel’s airway. Wet the airway. Open his mouth for a moment, and insert it with its tip pointing towards his hard palate. Then turn the airway through 180 so that its curve follows his soft palate and the back of his tongue and lifts his tongue forward. CAUTION! (1) Be careful not to push his tongue downwards as you insert the airway. (2) Don’t insert it during very light anaesthesia, or the patient will cough, retch, or vomit. (3) Even Guedel’s airway does not guarantee a clear airway, so you may also need to lift his chin or the angles of his jaw.

Fig: GUEDELS’S AIRWAY IN PLACE. If lifting a patient’s chin fails to clear his airway, you may need to lift the angles of his jaw.

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NASAL AIRWAY Put a soft wide rubber tube down one of his nostrils, and hold it with a large safety pin. This is useful in severe maxillofacial injuries, when opening the patient’s mouth may be impossible or painful. FERGUSSON’S GAG is useful if the patient clenches his teeth shut, and prevents you inserting an airway. Push the gag between his back teeth, and use it to open his jaw. Keep pieces of rubber tube on the ends of the gag to prevent them injuring his teeth. If his teeth are complete, so that you cannot insert a gag, force a wedge between his teeth. Rock it to and fro between them, until they are far enough apart for you to insert the ends of the gag. The danger of this is that you will break his teeth, but you may have to take this risk. If you don’t have a gag or a wedge, press your fingers between his gums behind his molar teeth. This will open his jaws enough for you to pass a laryngoscope. This is less traumatic than using a gag. Many anaesthetists prefer this method and seldom, if ever, use a gag.

Q: WHAT IS THE NEW GUIDE LINE OF CPR, GIVE SUMMARY? Summary of new ILCOR guidelines concerning BLS Following the new recommendations of the Resuscitation council 2005, here are the main improvements to BLS some of which we might try to get across during the WHO Earthquake training. Main Changes 1. Children are classified into only 2 age groups: infants < 1year and children (1year to puberty). 2. There are 5 initial rescue breaths (no mention that 2 must be effective). 3. When doing pulse check it is now a “circulation check: as follows: Start chest compressions if any of the following are present:  Absent central pulse for up to 10 seconds (carotid, brachial or femoral).  Inadequate pulse (< 60 bpm for all ages of Child) with signs of poor perfusion (include pallor, lack of responsiveness and poor muscle tone).  No signs of a circulation (include movement, coughing or normal breathing but not agonal gasps). 4. Chest compressions must compress the lower third of the sternum by one third of the anteroposterior diameter (use 2 fingers, 1 hand or 2 hands as needed to achieve this depending on age and size). 5. Position for all ages is 2 finger breadth above the xiphisternum.

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6. In infants hand encircling technique is best. 7. For all infants and children the ratio is 15 compressions 2 ventilations. 8. For all adults the ratio is 30 compressions to 2 ventilations. Lecture 12

PAIN Q: DEFINE PAIN. Pain is a complex but an important protective phenomenon it may be defines as: “An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.”

Q: WHAT ARE THE TYPES OF PAIN? Pain is divided into two types, acute pain and chronic pain. Acute pain: It is most often caused by an acute injury or pathological state, and lasts only as long as the tissue lesion exists. If it is not effectively treated, it may develop into chronic pain. Postoperative pain is an example of acute pain. Chronic pain: It is usually associated with a persistent tissue lesion, it may continue long after the normal healing of an acute injury, or disease has subsided. The term chronic is applied to pain which lasts for more than six months.

Q: WHAT ARE THE PAIN PRODUCING SUBSTANCES? PAIN PRODUCING SUBSTANCES: A number of pain producing substances have been discovered which are considered to be mediators of inflammatory reactions. These mediators include the hydrogen and potassium ions, kinins, histamine, 5-hydroxytryptamine, metabolites of arachidonic acid, namely prostaglandins and leukotrienes.

Q: WHAT ARE THE DIFFERENT METHODS FOR MEASUREMENT OF PAIN? Different methods used for measurement of pain include 1. Pakistan Coin Scale (PCS) 2. Verbal Rating Scales (VERS’s) 113

3. Numerical Rating Scales (NRS’s) 4. Visual Analogue Scales (VAS’s) Theses simple methods have been used effectively in hospitals, clinics and provide valuable information about pain and analgesia. General principals / options of pain relief. 1. Prevent initial excitation of nociceptive nerves e.g., NSAIDs are used, they inhibit prostaglandin activity. 2. Interrupt peripheral nociceptive transmission e.g., Local anaesthetic in acute pain. 3. Alter spinal modulation of nociceptive transmission e.g., spinal/epidural narcotics. Epidural local anaesthetics. Epidural local anaesthetic & narcotics. TENS and Acupuncture. There is inhibitory system in dorsal horn, TENS / acupuncture act there. Similarly spinal and epidural opiates act on receptors in dorsal horn. 4. Interrupt spinal cord nociceptive transmission e.g., destroy or cut the tract for intractable pain. 5. Alter central processing of nociceptive transmission e.g., opiates, N2 O etc. They act centrally also. 6. Alter emotional response to pain e.g., there is anxiety in acute pain and depression in chronic pain – appropriate drugs can be given. 7. Alter behavioral response to the pain e.g., in chronic pain patient’s pain may submerge in a complete picture of disability.

Q: WHAT ARE THE COMMON DRUGS GIVEN FOR PAIN RELIEF? 1. NSAIDs  Paracetamol  Aspirin  Diclofenac  Piroxicam  Mefenamic acid  Ketorolac 2. OPIODS  Morphine  Pethidine  Tramadol

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  

Nalbuphine Buprenorphine Pentazocine

Q: WHAT ARE THE DIFFERENT BLOCKS GIVEN FOR PAIN RELIEF? Plexuses blocks Brachial plexus block Paravertebral block Nerve blocks Sciatic nerve block Suprascapular nerve block Ulnar nerve block Radial nerve block Peroneal nerve block Bier’s block: IV Local anaesthetic is given after applying tourniquet to an extremity.

Q: WHAT IS PATIENT – CONTROLLED ANALGESIA(PCA) ? This refers to the on-demand, intermittent, self- administration of analgesic drugs by a patient. Predominately used to deliver opioid analgesic. The traditional route of drug delivery has been intravenous but subcutaneous and epidural routes can also be used. The quality of analgesia is normally good and shows wide inter-patient variation. PCA is also useful in children over 5 years, in obstetrics, in acute medical diseases, e.g. sickle-cell crisis and malignant pain.

Q: HOW IS PAIN PERCEIVED? Information signaling acute injury is transmitted along fast conduction velocity (20m/sec) unmyelinated C fibers (dull second pain). These first order neurons synapse with second order neurons in the dorsal horn of the spinal cord. There is an increased release of neuropeptides such as substance P, and excitatory amino acids such as glutamate, in the dorsal horn. Nociceptive information to thalamus is conducted up to the spinothalamic tracts. Synapse of second order with third order neurons in the ventral thalamus results in onward transmission of nociceptive impulse to sensory cortex, where it is ultimately perceived as pain.

Q: WHAT ARE PAIN CLINICS?

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Anaesthetists in conjunction with other specialties, including rheumatology, neurology, neurosurgery, psychiatry and other disciplines including nursing, usually head the pain clinics. The roles of pain clinic in patient care are:  Decrease subjective pain experience.  Increase general level of activity.  Decrease drug consumption.  Return to employment or full quality of life.  Decrease further use of health care resources.  Essential pain clinic equipment will include suitable imaging, suitable monitoring for sedation, radio-frequency lesion generator, cryoprobe machine and peripheral nerve stimulator. Pain clinics have been shown to be effective both for nerve block treatments and for psychologically based therapeutics.

Q: HOW IS CANCER PATIENT TREATED? Pain occurs in 70% of patient with advance cancer. Treatment of pain of advanced cancer include treatments such as radiotherapy which is effective for bony metastasis, chemotherapy, hormone manipulation, orthopaedic correction of pathological fractures, surgical correction of bowel obstruction and neurological decompression of cranium or spinal cord. Dexamethasone is commonly used to reduce painful tissue edema: WHO’s “step ladder” analgesia are used. When pain of advanced cancer is not adequately treated by active treatment or weak opioids, the following options can be used.  Morphine, orally or an elixir.  Fentanyl patches with 72-h duration.  Diamorphine give subcutaneously.  Co-analgesics added to augment opioids such as NSAIDs, tricyclic anti-depressants.  Epidural catheter analgesia using bupivacaine.  A number of neurolytic techniques are in common practice for pain of advanced cancer.  Coeliac plexus block using alcohol or phenol for carcinoma of pancreas, and pain arising from stomach, liver and small intestine.  Splanchnic nerve blocks.  Chemical sympathectomy, lumbar or presacral for refractory lower limb or pelvic pain.  Cordotomy done via radio-frequency of spinothalamic tract at C2 for mesothelioma.

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

Intrathecal neurolysis using phenol or alcohol for trunk pain.

Q: HOW PAIN IS RELIEVED DURING LABOUR. (PAINLESS DELIVERY)? Epidural catheter is passed during early stage of labour and local anaesthetic drug is injected intermittently through the catheter.

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Lecture 13

ICU Q: DEFINE ICU. An Intensive Care Unit usually provides 1 – 10% of total hospital beds, apart from specialized requirements e.g. cardiac surgery, neurosurgery, etc. Units larger than ten beds are sometimes subdivided into specialized units, a maximum of four beds is recommended. Anaesthesiologists in the UK run 85% of ICUs.

Q: HOW IS AN ICU DESIGNED? Design consideration include: Size of unit/bed (approx 20m2/ patient).  Proximity to OT, casualty department, X-Ray plus laboratory facilities.  Equipment: ventilators, monitoring, infusion pump, etc.  Staff and their facilities (one nurse/patient for 24hr/day).

Q: WHAT IS THE PATIENT SELECTION CRITERIA IN AN ICU? Patient selection criteria  Major organ failure requiring artificial support e.g., respiratory or cardiovascular, often in combination with other organ system failure (e.g. renal).  Intensive monitoring and treatment in severe disease states, e.g., septicemia, head injury, poisoning and overdose, burns, etc.  Postoperative monitoring of respiratory, cardiovascular, neurological problems, etc.  Other considerations – the disease state should be potentially reversible, pre morbid general health, age and mortality, premedication scores and availability of beds. Problems may be related to:  Original condition.  Multiple organ failure; may follow disease processes (e.g., renal failure and ARDS are common in critical illness of any cause. Prognosis worsens as more organ systems are involved.  Infection e.g., septicemia.  Adequate nutrition and fluid and electrolyte balance.  Gastric ulceration (stress ulcers).  Immobility: DVT and bed sores may occur.

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

Sedation.

MONITORING Q: WHAT TYPE OF MONITORING IS REQUIRED IN ICU? Monitoring required in an ICU include: Vital signs  ECG  CVP monitoring  ABG’s  Pulse oximetry  Capnography  Pupil size and Urine output

ARTIFICIAL VENTILATION Q: WHAT ARE THE MAIN TYPES OF ARTIFICIAL VENTILATION? TYPES:1. Negative pressure ventilation (not used nowadays). 2. Positive pressure ventilation.

Q: CLASSIFY VENTILATORS. Classification based on cycling from inspiration to expiration: Time cycled.  Volume cycled.  Pressure cycled.  Flow cycled.

Q: WHAT ARE THE INDICATION OF ARTIFICIAL VENTILATION? Indications:  PaO2 < 60mm Hg.  PaCO2>50mm Hg.  PH10-15 >5 12-20 -25 70 on FiO2 40% >16