Potassium is a major determinant of the electrophysiologic properties of the myocardial membrane, and it plays an important role in the occurrence of arrhythmia. Hypokalemia has been associated with an increased frequency of ventricular premature complexes (VPCs) in some studies of hypertensive patients treated with diuretics, but other studies have failed to confirm any association. Studies involving patients with an acute myocardial infarction have also provided conflicting data about the association between hypokalemia and VPCs. Whereas the role of potassium in the genesis of simple VPCs remains uncertain, animal and clinical studies have demonstrated a strong relation between hypokalemia and the occurrence of sustained ventricular tachycardia and ventricular fibrillation during acute ischemic states. Hypokalemia may also affect the action of antiarrhythmic drugs by altering the electrophysiologic properties of the myocardium, potentially negating some of the antiarrhythmic activity of these agents. Although diuretic use is the most frequent cause of hypokalemia, epinephrine can also lower serum potassium as a result of stimulation of the beta 2 adrenoreceptor. This mechanism may, in part, explain the ability of beta blockers to prevent sudden death in patients with a recent myocardial infarction.