Relation of Electrolyte Disturbances to Cardiac Arrhythmias

Abstract

While a number of electrolytes play a role in the genesis of the transmembrane action potential (AP), the changes in the action potential most clearly related to arrhythmias are dependent to a large extent on K+. Potassium gradient is a major determinant of the magnitude of transmembrane resting potential (TRP), and secondarily the rate of rise (dV/dt) of phase 0, and consequently the speed of conduction. The cell membrane conductance for K+, or a decrease therein, is most likely the major determinant of spontaneous slow depolarization during phase 4. Thus K+has a pronounced effect on both conduction and automaticity. Furthermore, these electrophysiologic properties are altered within levels of K+encountered in clinical medicine, a situation which, with rare exceptions, is not seen with Ca++, Mg++, or Na–. These latter ions affect the action potential and induce experimental arrhythmias at concentrations which are unphysiologic and frequently incompatible with life. Consequently, of all the electrolytes, disturbed K+metabolism accounts for the vast majority of clinical arrhythmias. For the same reasons, with the exception of the ability of Na+and Ca++to reverse the K+-induced depression of conduction, K+is the only electrolyte with clinacally significant antiarrhythmic properties.