Effects of electroporation on the transmembrane potential distribution in a two-dimensional bidomain model of cardiac tissue

Electroporation in a Two-Dimensional Myocardium. Introduction: Defibrillation shocks, when delivered through internal electrodes, establish transmembrane potentials (V-m) large enough to electroporate the membrane of cardiac cells. The effects of such shocks on the transmembrane potential distribution are investigated in a two-dimensional rectangular sheet of cardiac muscle modeled as a bidomain with unequal anisotropy ratios. Methods and Results: The membrane is represented by a capacitance C-m, a leakage conductance g(l), and a variable electroporation conductance G, whose rate of growth depends exponentially on the square of V-m. The stimulating current I-o, 0.05-20 A/m, is delivered through a pair of electrodes placed 2 cm apart for stimulation along fibers and 1 cm apart for stimulation across fibers. Computer simulations reveal three categories of response to I-o: (1) Weak I-o, below 0.2 A/m, cause essentially no electroporation, and V-m increases proportionally to I-o. (2) Strong I-o, between 0.2 and 2.5 A/m, electroporate tissue under the physical electrode. V-m is no longer proportional to I-o; in the electroporated region, the growth of V-m is halted and in the region of reversed polarity (virtual electrode), the growth of V-m is accelerated. (3) Very strong I-o, above 2.5 A/m, electroporate tissue under the physical and the virtual electrodes. The growth of V-m in all electroporated regions is halted, and a further increase of I-o increases both the extent of the electroporated regions and the electroporation conductance G. Conclusion: These results indicate that electroporation of the cardiac membrane plays an important role in the distribution of V-m induced by defibrillation strength shocks. (J Cardiovasc Electrophysiol, Vol. 10, pp. 701-714, May 1999).