Arrhythmias, electrolytes, and ACE inhibitor therapy in the elderly.

Elderly patients have a higher incidence of symptomatic cardiac arrhythmias and greater management problems than younger patients. This is due to the frequency of occult and overt cardiovascular disease, reduction in cardiac reserve as a consequence of the aging process, and coexistence of other disorders which provide a substrate for iatrogenic disease. The last problem is largely due to electrolyte disturbances induced by diuretic therapy for hypertension and heart failure. The major electrolyte disturbance implicated in arrhythmogenesis is diuretic-induced hypokalemia. There is no doubt that arrhythmias are caused by severe hypokalemia (less than 2.5 mEq/l), or by a milder degree of hypokalemia in digitalis-treated patients or those with left ventricular hypertrophy, but the literature contains conflicting data regarding the importance of milder hypokalemia. The most compelling study in support of its importance used a crossover study design in hypertensive patients with coronary disease and showed that mild degrees of hypokalemia induced by thiazide diuretics increased the tendency to arrhythmia when compared with normokalemia on a potassium-sparing diuretic. Diuretic-induced magnesium deficiency is also regarded by some to be as important as hypokalemia, but the evidence is less extensive. Thus, it appears reasonable to avoid hypokalemia and hypomagnesemia. The optimum therapeutic approach in using diuretics is to keep the dose as low as possible, restrict dietary sodium, and add potassium supplements. Since, in many cases of hypertension, hypokalemia is due to secondary hyperaldosteronism, the use of angiotensin-converting enzyme inhibitors is another therapeutic approach that is effective in hypertension and heart failure.