Anode cathode make and break phenomena in a model of defibrillation

The goal of this simulation study is to examine, in a sheet of myocardium, the contribution of anode and cathode break phenomena in terminating a spir al wave reentry by the defibrillation shock. The tissue is represented as a homogeneous bidomain with unequal anisotropy ratios. Two case studies are presented in this article: tissue that can electroporate at high levels of transmembrane potential, and model tissue that does not support electropora tion. In both cases, the spiral wave is initiated via cross-field stimulati on of the bidomain sheet, The extracellular defibrillation shock is deliver ed via two small electrodes located at opposite tissue boundaries. Modifica tions in the active membrane kinetics enable the delivery of high-strength defibrillation shocks, Numerical solutions are obtained using an efficient semi-implicit predictor corrector scheme that allows one to execute the sim ulations within reasonable time. The simulation results demonstrate that an ode and/or cathode break excitations contribute significantly to the activi ty during and after the shock. For a successful defibrillation shock, the v irtual electrodes and the break excitations restrict the spiral wave and re nder the tissue refractory so it cannot further maintain the reentry, The r esults also indicate that electroporation alters the anode/cathode break ph enomena, the major impact being on the timing of the cathode-break excitati ons. Thus, electroporation results in different patterns of transmembrane p otential distribution after the shock. This difference in patterns may or m ag not result in change of the outcome of the shock.