1.1e Sudden Cardiac Arrest

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MEDICINE II 1.1E CARDIAC ARREST AND SUDDEN CARDIAC DEATH

Term Death

Cardiac Arrest

Cardiovascular Collapse

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DEFINITION OF TERMS Definition Qualifiers or Exceptions Irreversible cessation None of all biologic functions Abrupt cessation of Rare spontaneous cardiac pump reversions; likelihood function, which may of successful be reversible but will intervention relates to lead to death in the mechanism of arrest, absence of prompt clinical setting and intervention time of intervention A (sudden) loss of Nonspecific term that effective blood flow includes cardiac caused by cardiac arrest and its and/or peripheral consequences and vascular factors that also events that revert may revert spontaneously spontaneously (such as syncope) or only with intervention

CARDIAC ARREST Cardiac arrest is expected: - Life threatening illness - Severe injuries Cardiac arrest is not expected - Sudden cardiac death SUDDENT CARDIAC DEATH (SCD) Natural death from cardiac causes, heralded by an abrupt loss of consciousness within 1 hour after the onset of an acute change in CV status Pre-existing heart disease may or may not have been known to be present but the time and mode of death are unexpected

TIME REFERENCES IN SUDDEN CARDIAC DEATH Prodromes Onset of terminal Cardiac arrest Biological event death New or Abrupt change in Sudden Failure of worsening clinical status collapse resuscitation cardiovascular OR failure of  Arrhythmia  Loss of symptoms electrical, effective  Hypotension mechanical  Chest pain circulation  Chest pain or CNS  Palpitations  Loss of  Dyspnea function after consciousne  Dyspnea  Lightheadedness initial ss  Fatiguability resuscitation Days to months Up to 1 hour Minutes to weeks

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SUDDEN CARDIAC DEATH: EPIDEMIOLOGY >300,000 cases of SCD per year in US Account for 50% of all cardiac deaths Peak incidence: - Birth to 6 months: Sudden Infant Death Syndrome (SIDS) - > 45 years: 88% of deaths are cardiac in origin Male: Female = 4:1

RISK OF SCD BY DECILE OF MULTIVARIATE RISK SELECTED RISK FACTORS:  Age  Cigarettes  Diabetes  Heredity  Hyperlipidemia  Hypertension  Obesity  Sedentary STRUCTURAL CAUSES OF CARDIAC ARRESY AND SUDDENT CARDIAC DEATH  Coronary heart disease 80% - Coronary artery abnormalities - Myocardial ischemia and infarction  Myocardial hypertrophy 10-15% - Secondary - Hypertrophic cardiomyopathy  Dilated cardiomyopathy  Inflammatory and infiltritive diseases - Myocarditis - Infiltritive diseases  Valvular heart disease 5-10%  Electrographic abnomalities - Long QT syndrome - Short QT syndrome - Brugada syndrome (Sleep death in Southeast Asians; bangungot) - WPW syndrome - Conduction abnormalities AGE-RELATED & DISEASE SPECIFIC RISK FOR SCD Usual causes:  Myocarditis  Hypertrophic CM  Long QT syndromes  Right ventricular dysplasia  Anomalous coronary artery  Brugada syndrome  Idiopathic VF

Usual causes:  Coronary atherosclerosis  Dilated cardiomyopathy  Infiltrative heart disease  Valvular heart disease

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Medicine II

1.1D ACUTE CORONARY SYNDROME

PATHOPHYSIOLOGY OF SCD IN CORONARY DISEASE 

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HYPERTROPHIC CARDIOMYOPATHY The heart muscle (myocardium) becomes abnormally thick (hypertrophied). The thickened heart muscle can make it harder for the heart to pump blood.

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DILATED CARDIOMYOPATHY Usually starting in your heart's main pumping chamber (left ventricle). The ventricle stretches and thins (dilates) and can't pump blood as well as a healthy heart can.

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FUNCTIONAL CAUSES OF CARDIAC ARREST Alterations of coronary blood flow - Transient ischemia - Reperfusion after ischemia Low cardiac output states - Heart failure - Shock Systemic metabolic abnormalities - Electrolyte imbalance (ex. Hypokalemia) Neurophysiologic disturbances - Autonomic fluctuations Toxic responses - Proarrhythmic drug effects - Cardiac toxins (Ex. Cocaine, Digitalis intoxication) - Drug interactions

BIOLOGICAL MODEL OF SUDDEN CARDIAC DEATH STRUCTURE FUNCTION Myocardial infarction  Transient alterations of - Acute coronary blood flow - Healed Electrogenic - Vasomotor dynamics - Aneurysm Theory - Acute (transient) ischemia - Reperfusion after ischemia Hypertrophy PVCs - Secondary  Systemic factors - Primary - Hemodynamic factors - Hypoxemia, acidosis Myopathic ventricle - Electrolyte imbalance - Dilatation VT/VF  Neurophysiological interactions Structural electrical - Transmitters, receptors abnormality - Central influences  Toxic effects - Proarrhythmic drugs - Cardiac toxicity RISK OF SCD RELATED TO LEFT VENTRICULAR EJECTION FRACTION

ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA

PROGNOSTIC SIGNIFICANCE OF VENTRICULAR ARRHYTHMIAS AND LV EJECTION FRACTION AFTER MI

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A rare form of cardiomyopathy in which the heart muscle of the right ventricle (RV) is replaced by fat and/or fibrous tissue. The right ventricle is dilated and contracts poorly. As a result, the ability of the heart to pump blood is usually weakened.

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Medicine II 

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MECHANISMS OF CARDIAC ARREST Arrhythmic events - Ventricular fibrillation (VF) 62.4% - Bradyarrhythmias (including AV block & asystole 16.5% - Torsades des pointes 12.7% - Primary ventricular tachycardia (VT) 8.3% Pulseless electrical activity (PEA) - Previously referred to as electromechanical dissociation

1.1D ACUTE CORONARY SYNDROME VENTRICULAR TACHYCARDIA DUE TO MYOCARDIAL ISCHEMIA

VENTICULAR FIBRILLATION

SINUS ARREST / ASYSTOLE

VENTRICULAR TACHYCARDIA

TORSADES DE POINTES

CLINICAL PRESENTATION OF PATIENTS WITH VENTRICULAR ARRYTHMIAS AND SUDDEN CARDIAC DEATH  Asymptomatic individuals with or without ECG abnormalities  Patients with symptoms potentially attributable to ventricular arrythmias - Palpitations - Dyspnea - Chest pains - Syncope or presyncope  Hemodynamically stable VT  Hemodynamically unstable VT  Cardiac arrest - Asystole (sinus arrest, high grade AV block) - Ventricular tachycardia (VT) - Ventricular fibrillation (VF) - Pulseless electrical activity (PEA) EMERGENCY MANAGEMENT OF SCD: CARDIOPULMONARY RESUSCITATION  Basic life support - Airway > Head tilt > Chin tilt - Breathing > Mouth-to-mouth > Mas-to-mouth >30:2 (ratio of chest compressions to breaths) - Circulation > High quality chest compression - Hands maintain firm contact with lower sternum - Sternum must be depressed by 11/2 - 2 inches - Allow full chest recoil between compressions - Compression rate of 100/minute

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NEW BLS GUIDELINES Compressions - Effective, uninterrupted compressions alone result in equivalent survival Airway Breathing Page 3 of 4

Medicine II

1.1D ACUTE CORONARY SYNDROME

EXTERNAL CHEST COMPRESSIONS           

CAUSES OF PULSELESS ELECTRICAL ACTIVITY Hypoxia Hypovolemia Hydrogen ion (acidosis) Hypothermia Hypo / Hyperkalemia Hypoglycemia Tension pneumothorax Tamponade (cardiac) Thrombosis (coronary; pulmonary) Toxins (drug overdose; poisoning) Trauma SURVIVAL AFTER OUT OF HOSPITAL CARDIAC ARREST

ADVANCED CARDIAC LIFE SUPPORT (ACLS) FOR VF PULSELESS VT

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PREVENTION OF SCD Secondary prevention (postcardiac arrest survivors) Primary prevention - Advanced structural heart disease with LVEF < 35% - Less advanced structural heart disease with LVEF > 35% - Structurally normal heart with molecular disorders associated with increased risk of ventricular arrhythmias - General population Implantable cardioverter defibrillator (ICD); treatment of choice Pharmacologic therapy - Beta-blockers - Amiodarone - Sotalol SUCCESSFUL DEFIBRILLATION BY ICD

ADVANCED CARDIAC LIFE SUPPORT FOR PATIENTS WITH BRADYARRHYTHMIC ASYSTOLIC ARRESTS AND PULSELESS ELECTRICAL ACTIVITY

VT IN A PATIENT WITH BRUGADA SYNDROME

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