EFFECTS OF ELECTROPORATION ON TRANSMEMBRANE POTENTIAL INDUCED BY DEFIBRILLATION SHOCKS

This study uses a one-dimensional model of cardiac strand to investiga te the effects of electroporation on transmembrane potential (V-m) ind uced by defibrillation shocks. The strand is stimulated at the ends by extracellular electrodes. Its membrane, when exposed to large V-m, in creases its conductance in a manner consistent with reversible electri cal breakdown. Numerical simulations indicate that V-m increases propo rtionally to the shock strength only until the ends of the strand elec troporate. Beyond this point, further increases in shock strength resu lt 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 int o intracellular space. Consequently, only a fraction of the delivered current, I-cr, gives rise to V-m; the current in excess of I-cr divide s itself proportionally between intra- and extracellular space and doe s not contribute to macroscopic V-m. Thus, electroporation has a benef icial effect: the formation of pores prevents the development of an ex cessively high V-m and limits the damage to the tissue. In contrast, e lectroporation does not affect the ''sawtooth'' component of V-m that reflects polarization of individual cells by electric field. These res ults indicate that electroporation does not impair the ability of the shock to reach the distant myocardium and may actually aid defibrillat ion by reducing nonuniformity of electrical conditions between regions close to the electrodes and in the bulk of tissue.