Membrane refractoriness and excitation induced in cardiac fibers by monophasic and biphasic shocks.

INTRODUCTION

This modeling study examines the effect of low-intensity monophasic and biphasic waveforms on the response of a refractory cardiac fiber to the defibrillation shock.

METHODS AND RESULTS

Two cardiac fiber representations are considered in this study: a continuous fiber and a discrete fiber that incorporates gap junctions. Each fiber is undergoing a propagating action potential. Shocks of various strengths and coupling intervals are delivered extracellularly at fiber ends during the relative refractory period. In a continuous fiber, monophasic shock strengths of three times the diastolic threshold either elicit no response or, for coupling intervals above 380 msec, reinitiate propagation. In contrast, biphasic shocks of same strength are capable of terminating the existing wavefronts by either invoking a nonpropagating response (coupling intervals 370 to 382 msec) that prolongs the refractory period or inducing wavefront collision (coupling intervals above 400 msec). The fiber response is similar for other shock strengths and when cellular discontinuity is accounted for. Thus, for a refractory fiber, biphasic shocks have only a small "vulnerable" window of coupling intervals over which propagation is reinitiated.

CONCLUSION

At short coupling intervals, a significant extension of refractoriness is generated at regions where the biphasic shock induced hyperpolarization followed by depolarization. At large coupling intervals, the enhanced efficacy of biphasic shocks is associated with their ability to induce wavefront collision, thus decreasing the probability of reinitiating fibrillation. Overall, the defibrillation shock affects the tissue through the induced large-scale hyperpolarization and depolarization, and not through the small-scale transmembrane potential oscillations at cell ends.