Myocardial K + loss after countershock and the relation to ventricular arrhythmias after nontoxic doses of acetyl strophanthidin

Abstract

Since ventricular arrhythmias due to digitalis appear to be related to enhanced potassium egress from the heart, it was reasoned that the sensitivity of the digitalized heart during cardioversion may be related to an effect on myocardial K + transport. The application of transthoracic countershock in normal, intact, anesthetized dogs, at an energy level of 75 watt-seconds, produced increased concentrations of K + in the coronary sinus for as long as nine minutes. A similar cumulative loss of this ion from myocardium, estimated from the product of the A-V differences and coronary plasma flow, was seen after a second or third shock. Administration of acetyl strophanthidin, 0.03 mg. per kilogram, to a second group of animals was associated with no evidence of arrhythmias. The cumulative K + loss from the myocardium during the activity of drug averaged 119 μEq per 100 Gm. In a third group, countershock intervention four minutes after the administration of strophanthidin produced an enhanced potassium loss over that seen in Group II in the same time period (p < 0.02). There was an associated increase of ectopic activity in the postcountershock period, supporting the view that altered K + transport is the basis for this phenomenon.