The mechanisms of cardiac defibrillation, the most effective clinical procedure for termination of lethal cardiac arrhythmias, are not well understood. Shocks establish an electric field in the heart, which, in turn, induces changes in the transmembrane potential leading to defibrillation. The complexity of cardiac structure makes it difficult to explain, based on experiments alone, how exactly the electric field affects transmembrane potential. In an attempt to provide additional insight into the issue, in this computational study we explore the effects of strong electric shocks on myocardium in fibrillation.; Cardiac tissue is represented by the two-dimensional anisotropic bidomain model with active membrane kinetics and various fiber geometries. A single reentrant circuit of excitation serves as a simple model of the arrhythmic behavior. Bidomain model allows us to study currents introduced by the shock into the extracellular space of the myocardium.; We illustrate various mechanisms by which cardiac tissue structure, as well as the electrode shape, assists the changes in transmembrane potential throughout the myocardium that result in defibrillation. We observe the shock-induced regions of the reverse polarity of transmembrane potential, so-called virtual electrodes, that form at a distance from the physical electrodes. These regions affect the electrical state of the tissue globally by perturbing reentrant wavefronts and generating new excitations.; Our results support the hypothesis that virtual electrodes play an important role in defibrillation. The variety of simulation results described here offers a new level of understanding of the virtual electrode concept and provides a theoretical ground for future experimental studies.
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