EFFECTS OF ELECTROPORATION ON TRANSMEMBRANE POTENTIAL INDUCED BY DEFIBRILLATION SHOCKS

This study uses a one-dimensional model of cardiac strand to investigate the effects of electroporation on transmembrane potential (V-m) induced by defibrillation shocks. The strand is stimulated at the ends by extracellular electrodes. Its membrane, when exposed to large V-m, increases its conductance in a manner consistent with reversible electrical breakdown. Numerical simulations indicate that V-m increases proportionally to the shock strength only until the ends of the strand electroporate. Beyond this point, further increases in shock strength result in only a minor change in V-m. This arrest in the growth of V-m is caused by pores that develop in the cells immediately adjacent to the electrodes and that shunt part of the stimulating current directly into intracellular space. Consequently, only a fraction of the delivered current, I-cr, gives rise to V-m; the current in excess of I-cr divides itself proportionally between intra- and extracellular space and does not contribute to macroscopic V-m. Thus, electroporation has a beneficial effect: the formation of pores prevents the development of an excessively high V-m and limits the damage to the tissue. In contrast, electroporation does not affect the ''sawtooth'' component of V-m that reflects polarization of individual cells by electric field. These results indicate that electroporation does not impair the ability of the shock to reach the distant myocardium and may actually aid defibrillation by reducing nonuniformity of electrical conditions between regions close to the electrodes and in the bulk of tissue.