Although electric countershock is the treatment of choice for many atrial arrhythmias and is the only treatment available for the termination of ventricular fibrillation, many recent reports have shown that dose-dependent injurious side-effects result. In previous studies we showed that this post-shock dysfunction was related to a prolonged depolarization of the myocardial cell membrane and to a possible calcium overload. This work also indicated that the mechanisms producing post-shock dysfunction differed from those producing defibrillation, thus suggesting that the dysfunction could be minimized without sacrificing defibrillating efficacy. The present study utilizes photocell mechanogram and intracellular microelectrode techniques in cultured myocardial cells to examine in greater detail the mechanisms underlying post-shock dysfunction at the cellular level. In particular, the role of specific parameters of the defibrillating waveshape and timing in the cardiac cycle, as well as the effects of multiple shocks, will be examined. The results of these studies are expected to suggest specific modifications in countershock procedures which are based on a firm physiological understanding of the actions of the strong electric field on the myocardial cell and to increase our understanding of the fundamental mechanisms underlying the interaction of external electric fields with biological systems.
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