Most cases of sudden cardiac death (SCD) are due to malignant ventricular tachyarrhythmias, such as ventricular tachycardia (VT) and ventricular fibrillation (VF)(see Fig. 36.1). Both VF and pulseless VT require defibrillation as definitive therapy. If these or other arrhythmias persist despite basic life support and defibrillation, the current international advanced cardiac life support guidelines (ILCOR 2005) recommend administration of pharmacologic agents to help stabilize rhythm and restore cardiac output.

The pathophysiologic substrate of cardiac arrest: therapeutic implications

The pathophysiology of sudden cardiac death is relevant to both acute and long-term management. In most instances, the underlying cardiac pathology is ischemia and coronary artery disease. For instance, Liberthson and coworkers reported that 81% of a series of SCD victims had significant coronary artery disease. In another series, up to 50% of the victims of out-of-hospital cardiac arrest had suffered a recent acute myocardial infarction. Although the majority have a coronary disease etiology, numerous other pathologies can be involved in the genesis of sudden cardiac death, such as ventricular hypertrophy, cardiomyopathies, congenital disorders of ion channels (“channelopathies”), but also massive pulmonary embolism, as well as coronary dissection, and coronary inflammation or embolism to the coronary arteries. Froma clinical perspective, it is appropriate to assume that the cause of sudden death is coronary artery disease unless circumstances suggest otherwise. Although the creatine kinase (CK) and its MB fraction may not be diagnostic of acute myocardial ischemia, cardiac troponins can identify myocardial ischemic damage and thus prompt invasive coronary studies, which may make longterm antiarrhythmic treatment irrelevant.