Cardiac effect of diuretic drugs

Triamterene, amiloride, ethacrynic acid, and furosemide were studied to determine whether they modified the digitalis-induced egress of myocardial potassium which is thought to facilitate the development of digitalis arrhythmias. In a control group of 15 dogs, potassium was measured in samples obtained simultaneously from the femoral artery (FA) and the coronary sinus (CS) in a control period and at intervals after the administration of 1 mg. of acetylstrophanthidin. Acetylstrophanthidin caused a significant increase in cardiac A-V difference in the potassium concentration (CS-FA) averaging 0.47 mEq. per liter. In a group of 10 dogs, when 175 mg. of triamterene was infused prior to the acetylstrophanthidin, the rise in A-V differnece was abolished and the arrhythmias often aborted. In contrast, the infusion of potent diuretics (40 mg. of furosemide in five dogs and 100 mg. of ethacrynic acid in another five dogs) prior to acetylstrophanthidin, caused a doubling of the maximal A-V potassium difference. This study suggests that the clinical administration of antikaliuretic drugs may prevent the arrhythmias of digitalis toxicity not only by reducing kaliuresis and subsequent hypokalemia, but by a myocardial effect which antagonized the digitalis-induced loss of myocardial potassium. Contrariwise, potent diuretics may facilitate digitalis arrhythmias through a myocardial action causing a greater egress of myocardial potassium, thus explaining the development of arrhythmias despite normal serum potassium levels. These potent diuretics should be used cautiously, especially when given intravenously to patients receiving digitalis.