Skouibine, Trayanova, Moore, 1999

Model Structure

ABSTRACT: 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 spiral 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 electroporation. In both cases, the spiral wave is initiated via cross-field stimulation of the bidomain sheet. The extracellular defibrillation shock is delivered via two small electrodes located at opposite tissue boundaries. Modifications 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 simulations within reasonable time. The simulation results demonstrate that anode and/or cathode break excitations contribute significantly to the activity during and after the shock. For a successful defibrillation shock, the virtual electrodes and the break excitations restrict the spiral wave and render the tissue refractory so it cannot further maintain the reentry. The results also indicate that electroporation alters the anode/cathode break phenomena, the major impact being on the timing of the cathode-break excitations. Thus, electroporation results in different patterns of transmembrane potential distribution after the shock. This difference in patterns may or may not result in change of the outcome of the shock.

The original paper reference is cited below:

Anode/cathode make and break phenomena during defibrillation: Does electroporation make a difference?, Skouibine, K., Trayanova, N., Moore, P. 1999, IEEE Transactions on Biomedical Engineering, 46, 769-777. PubMed ID: 10396895

Schematic diagram of the cell model.