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Sudden cardiac death as a consequence of unexpected cardiac arrest claims the lives of >310,000 adult Americans each year and accounts for approximately 63% of all deaths from cardiovascular causes.1 Despite advances in resuscitation and EMS, only approximately 6% of all cardiac arrest victims survive to leave the hospital neurologically intact. However, there is substantial variability in the odds for survival among various geographic locations, with published survival to hospital discharge for patients with all initial rhythms ranging from 1% to 25%.2–4 This chapter reviews the epidemiology and pathophysiology of sudden cardiac death in adults and the strategies to prevent and treat the problem. Sudden infant death syndrome and cardiac arrest in children are discussed in Chapters 14, Resuscitation of Neonates; 112, Sudden Infant Death Syndrome and Apparent Life-Threatening Event; and 15, Resuscitation of Children, respectively.

Most episodes of unexpected sudden cardiac death in adults occur in the home.5 The most common victim is a male who is 50 to 75 years of age. The majority of sudden cardiac death victims have underlying structural heart disease, usually in the form of coronary atherosclerosis and/or cardiomegaly.6 Structural coronary artery abnormalities and their consequences (e.g., myocardial ischemia and infarction) are associated with 80% of fatal arrhythmias.7 Dilated and hypertrophic cardiomyopathies are the next most common cardiac abnormalities causing sudden cardiac death. Other cardiovascular disorders, including valvular or congenital heart disease, acquired infiltrative disorders, primary electrophysiologic abnormalities (e.g., hereditary prolonged Q-T interval syndromes), and genetically determined ion-channel abnormalities (e.g., Brugada syndrome), account for only a small proportion of sudden cardiac death cases. A small percentage of sudden cardiac death cases occur during exercise and/or athletic activities. Most commonly, hypertrophic cardiomyopathy or a blow to the anterior chest (“commotion cordis”) is the trigger for ventricular fibrillation.8

Epidemiologic studies have identified both a circadian and a seasonal pattern of sudden cardiac death and acute myocardial infarction (AMI), suggesting the presence of underlying biologic triggers of the onset of both disease processes.9 Both sudden cardiac death and AMI are most likely to occur within the first few hours after awakening from sleep, at a time when there is increased sympathetic stimulation. β-blockade appears to protect against sudden cardiac death, particularly in patients with known coronary artery disease who have had an AMI and have a low ejection fraction. In addition, both sudden cardiac death and AMI are much more likely to occur during climatic winter rather than summer.9,10 These and other epidemiologic and experimental findings suggest that neurophysiologic factors, such as autonomic tone, may alter the heart’s propensity to develop and sustain a serious ventricular dysrhythmia. An alternative possibility is that there are factors external to the atherosclerotic plaque, such as triggers of plaque rupture or thrombus formation, which may affect the onset of ischemic cardiac events.

Ventricular Tachyarrhythmias

Sudden cardiac death is usually caused by chance arrhythmic events ...

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