Abstract

Four patients with digitalis toxicity were found to be hypomagnesemic and normokalemic. A significantly lower mean serum magnesium was noted in a group of digitalized heart failure patients (1.40 mEq./L.) than in matched normal subjects (1.93 mEq./L.). These observations, coupled with the fact that both digitalis and magnesium deficiency lead to a decrease in intracellular potassium, suggested that hypomagnesemia might contribute to the development of digitalis toxicity. To determine whether hypomagnesemia facilitates the development of digitalis toxicity, serial acetyl strophanthidin infusions were performed in 19 adult mongrel dogs. Hypomagnesemia was achieved by Kiil kidney dialysis. While dialysate electrolyte concentration corresponded to normal canine plasma, acetyl strophanthidin was infused (100 μg per minute) three times at three hour intervals. Hypomagnesemia was then induced by three hours of magnesium-free dialysis and acetyl strophanthidin was again infused. Mean serum magnesium was reduced 44 per cent (1.67 to 0.93 mEq./L.). This was accompanied by a 26 per cent reduction in the amount of acetyl strophanthidin needed to produce a toxic arrhythmia (42.4 to 31.4 μg per kilogram). Restitution of sinus rhythm was observed in 13 dogs immediately after the intravenous infusion of 2 to 7 c.c. of 25 per cent magnesium sulfate. These studies have shown that hypomagnesemia facilitates digitalis toxicity which can be promptly terminated with magnesium sulfate. Since diuretic drugs may produce hypomagnesemia as well as hypokalemia and both may predispose to digitalis toxicity, it is suggested that serum magnesium as well as potassium levels be determined in patients with digitalis toxicity.

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