Unipolar stimulation-induced arrhythmias can be explained by the bidomain model with unequal anisotropy ratios, but none of the examined mechanisms adequately explain cross-field stimulation.
This review identifies a critical gap in theoretical models of cardiac electrophysiology, showing that current mechanisms cannot fully explain how cross-field stimulation induces reentry.
This review examines the initiation of reentry in cardiac muscle by strong electric shocks. Specifically, it concentrates on the mechanisms by which electric shocks change the transmembrane potential of the cardiac membrane and create the physiological substrate required by the critical point theory for the initiation of rotors. The mechanisms examined include (1) direct polarization of the tissue by the stimulating current, as described by the one-dimensional cable model and its two- and three-dimensional extensions, (2) the presence of virtual anodes and cathodes, as described by the bidomain model with unequal anisotropy ratios of the intra- and extracellular spaces, (3) polarization of the tissue due to changing orientation of cardiac fibers, and (4) polarization of individual cells or groups of cells by the electric field ("sawtooth potential"). The importance of these mechanisms in the initiation of reentry is examined in two case studies: the induction of rotors using successive stimulation with a unipolar electrode, and the induction of rotors using cross-field stimulation. These cases reveal that the mechanism by which a unipolar stimulation induces arrhythmias can be explained in the framework of the bidomain model with unequal anisotropy ratios. In contrast, none of the examined mechanisms provide an adequate explanation for the induction of rotors by cross-field stimulation. Hence, this study emphasizes the need for further experimental and theoretical work directed toward explaining the mechanism of field stimulation. (c) 1998 American Institute of Physics.
Roth et al. (Sun,) conducted a review in Cardiac arrhythmias. Electric shocks was evaluated. Unipolar stimulation-induced arrhythmias can be explained by the bidomain model with unequal anisotropy ratios, but none of the examined mechanisms adequately explain cross-field stimulation.