Potassium deficiency and cardiac function: experimental and clinical aspects.
Intra- and extracellular potassium and magnesium gradients in cellular membranes are essential factors of physiologic functions. Intestinal and renal loss of these ions cause predominantly a decrease in cellular potassium and magnesium by lowering the extra-cellular concentrations. In close connection with these changes, the permeability of cellular membranes for ions and, consequently, the excitability of skeletal and heart muscle cells are altered. Changes in the excitation, i.e. increased rising rate of the action potential and alterations of the refractory period, provoke cardiac arrhythmias. It is assumed that in contrast to chronic potassium deficiency the net changes which are caused by a reduction of extracellular potassium in acute deficiency states predispose to glycoside toxicity. These changes may therefore explain the clinical observation that acute hypokalemia is associated with a greater glycoside sensitivity than chronic potassium deficiency. Recent findings indicate that antikaliuretic substances can prevent the incidence of cardiac arrhythmias and may reduce glycoside sensitivity of the heart not only by antikaliuretic effects, but also by a possible direct action on the myocardium. Positive inotropic actions have also been reported. The meachanism of these effects is not yet sufficiently clarified. With regard to the broad clinical application of antikaliuretic diuretics (aldosterone antagonists, amiloride and triamterene), we studied their effects on myocardial membrane properties. Aldosterone antagonists led to a significant concentration-dependent prolongation of action potential duration and, correspondingly, to a lengthening of the refractory period. Action potential duration showed a significant increase under the influence of amiloride. A shortening of the refractory period induced by glycoside was antagonized by triamterene. Thus, the administration of antikaliuretic diuretics seems to be useful in the therapy of congestive heart failure also with respect to their extrarenal cardiac effects. Potassium and magnesium deficiency significantly alter cellular membrane functions, especially under pathologic conditions as far as ionic permeability and active ion transport are concerned. We assume that these findings may further explain the persistence of cardiac arrhythmias and increased glycoside sensitivity due to potassium deficiency even after restoring normal extracellular potassium concentrations. Therefore prolonged potassium and magnesium) substitution should be provided in these conditions in spite of normal extracellular potassium concentration.
D000818:Animals; D002301:Cardiac Glycosides / Q000494:pharmacology; D004232:Diuretics / Q000494:pharmacology*; D004573:Electrolytes / Q000378:metabolism; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D006801:Humans; D008274:Magnesium / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D011191:Potassium Deficiency / Q000503:physiopathology*; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013329:Structure-Activity Relationship
D002301:Cardiac Glycosides; D004232:Diuretics; D004573:Electrolytes; D012964:Sodium; D008274:Magnesium; D011188:Potassium