MEMBRANE REFRACTORINESS AND EXCITATION INDUCED IN CARDIAC FIBERS BY MONOPHASIC AND BIPHASIC SHOCKS

Cardiac Fiber Responses to Defibrillation Shocks. Introduction: This m odeling study examines the effect of low-intensity monophasic and biph asic waveforms on the response of a refractory cardiac fiber to the de fibrillation shock. Methods and Results: Two cardiac fiber representat ions are considered in this study: a continuous fiber and a discrete f iber that incorporates gap junctions. Each fiber is undergoing a propa gating action potential. Shocks of various strengths and coupling inte rvals are delivered extracellularly at fiber ends during the relative refractory period. In a continuous fiber, monophasic shock strengths o f three times the diastolic threshold either elicit no response or, fo r coupling intervals above 380 msec, reinitiate propagation. In contra st, biphasic shocks of same strength are capable of terminating the ex isting wavefronts by either invoking a nonpropagating response (coupli ng intervals 370 to 382 msec) that prolongs the refractory period or i nducing wavefront collision (coupling intervals above 400 msec). The f iber response is similar for other shock strengths and when cellular d iscontinuity is accounted for. Thus, for a refractory fiber, biphasic shocks have only a small ''vulnerable'' window of coupling intervals o ver which propagation is reinitiated. Conclusion: At short coupling in tervals, a significant extension of refractoriness is generated at reg ions where the biphasic shock induced hyperpolarization followed by de polarization. At large coupling intervals, the enhanced efficacy of bi phasic shocks is associated with their ability to induce wavefront col lision, thus decreasing the probability of reinitiating fibrillation. Overall, the defibrillation shock affects the tissue through the induc ed large-scale hyperpolarization and depolarization, and not through t he small-scale transmembrane potential oscillations at cell ends.