Relation of Electrolyte Disturbances to Cardiac Arrhythmias

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.