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  • Most patients with sudden cardiac death have underlying CHD.

  • In the absence of reversible cause, ICD is recommended.


Sudden cardiac death is defined as unexpected nontraumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms. The causative rhythm in most cases is ventricular fibrillation. Sudden cardiac arrest is a term reserved for the successful resuscitation of ventricular fibrillation, either spontaneously or via intervention (defibrillation).


Approximately 70% of cases of sudden cardiac death are attributable to underlying CHD; in up to 40% of patients, sudden cardiac death may be the initial manifestation of CHD. The initiating arrhythmia in most patients is unknown but is presumed to be sustained monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, or primary ventricular fibrillation (especially in the setting of acute ischemia). Complete heart block and sinus node arrest may also cause sudden death. A disproportionate number of sudden deaths occur in the early morning hours, which suggests that there is a strong interplay with the autonomic nervous system. In patients younger than 35, most sudden cardiac death (SCD) is caused by inherited heart disease (long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome, HCM, arrhythmogenic RV cardiomyopathy, dilated cardiomyopathy). Over the age of 35, CHD is the most common cause of SCD, although inherited causes are common up until the age of 50. Noninherited forms of heart disease can also lead to SCD, including valvular heart disease (aortic stenosis, pulmonic stenosis), congenital heart disease, and myocarditis. Prompt evaluation to exclude reversible causes of sudden cardiac arrest should begin immediately following resuscitation. Laboratory testing should be performed to exclude severe electrolyte abnormalities (particularly hypokalemia and hypomagnesemia) and acidosis and to evaluate cardiac biomarkers. Caution should be taken in attributing cardiac arrest solely to an electrolyte disturbance, however, because laboratory abnormalities may be secondary to resuscitation and not causative of the event. A 12-lead ECG should be performed to evaluate for ongoing ischemia or conduction system disease. Ventricular function should be evaluated with echocardiography. Evaluation for ischemic heart disease (CT or coronary angiography) should be performed to exclude coronary disease as the underlying cause, since revascularization may prevent recurrence. In the absence of coronary disease, contrast-enhanced cardiac MRI may be used to evaluate for the presence of myocardial scar, which is a strong predictor of recurrent ventricular tachycardia/ventricular fibrillation in patients with nonischemic cardiomyopathy.


Unless ventricular fibrillation occurs shortly after MI, is associated with ischemia, or is seen with a correctable process (such as an electrolyte abnormality or medication toxicity), surviving patients require intervention since recurrences are frequent. Survivors of cardiac arrest appear to have improved long-term outcomes if a targeted temperature management protocol is rapidly initiated and continued for 24–36 hours after cardiac arrest.

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