Ventricular arrhythmias are probably the cause of sudden death due to myocardial ischemia or infarction. Such arrhythmias result from alterations in the transmembrane potentials of ventricular muscle and Purkinje fibers. Most of our knowledge concerning mechanisms for these arrhythmias has been derived from experimental studies on the canine heart. In this model, the early ventricular arrhythmias which occur within minutes after coronary artery occlusion probably have different electrophysiological mechanisms than the late arrhythmias which occur several or more hours after the onset of ischemia. The early arrhythmias probably result from reentry in ventricular muscle due to slow conduction in ischemic or infarcting muscle cells. The later arrhythmias most likely arise in subendocardial Purkinje fibers which develop spontaneous diastolic depolarization and abnormally prolonged action potential duration. It is important for future investigations to determine the relevance of electrophysiological studies on the canine heart to human ischemic and infarction arrhythmias.