The induction of reentry in cardiac tissue. The missing link: How electric fields alter transmembrane potential

Journal Article (Journal Article)

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. © 1998 American Institute of Physics.

Full Text

Duke Authors

Cited Authors

  • Roth, BJ; Krassowska, W

Published Date

  • January 1, 1998

Published In

Volume / Issue

  • 8 / 1

Start / End Page

  • 204 - 220

International Standard Serial Number (ISSN)

  • 1054-1500

Digital Object Identifier (DOI)

  • 10.1063/1.166298

Citation Source

  • Scopus