The effect of increasing extracellular potassium concentration (Ko) upon electrical ventricular defibrillation threshold was investigated in pentobarbital anesthetized dogs treated with intravenous potassium chloride. Defibrillation threshold fell during potassium intoxication. The percent decrease in defibrillation threshold was linearly related to the logarithm of Ko and to the potassium equilibrium potential, EK, calculated from measured extracellular and intracellular potassium concentrations of ventricular muscle. In dogs supported by left ventricular bypass in order to maintain the circulation during potassium intoxication, the values of Ko and EK required for spontaneous, K+ induced defibrillation (electrical defibrillation threshold = zero) were 16.6 mEq/L and -46 mV compared to the normal values of 3.9 mEq/L and -84 mV. Changes in defibrillation threshold related to changes in EK may be significant events in digitalis intoxication and in myocardial anoxia during prolonged fibrillation.

Defibrillation of the heart is often discussed as a large scale analog of cardiac pacing. Termination of atrial or ventricular fibrillation by a strong electric shock, applied with paddle electrodes across the chest or directly to the heart, is assumed to be the result of stimulation of a diffuse mass of potentially excitable cells (1, 2). The mechanism of defibrillation is usually stated to be the consequent production of a simultaneously refractory state in the entirety of a critical mass of the fibrillating myocardium (3, 4).


This is the author-accepted manuscript version of Babbs C.F., Whistler S.J., Yim G.K.W., Tacker W.A., Geddes L.A., Dependence of defibrillation threshold upon extracellular/intracellular K_8+_9 concentrations, J. Electrocardiol 13, 73-79, 1980. It is made available here with CC-BY-NC-ND. The version of record can be found at http://dx.doi.org/10.1016/S0022-0736(80)80013-6.


cardiac muscle, equilibrium potential, potassium, Nernst equation, transmembrane potential

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