Patterns of and mechanisms for shock-induced polarization in the heart: a bidomain analysis

Abstract

This paper examines the combined action of cardiac fiber curvature and transmural fiber rotation in polarizing the myocardium under the conditions of a strong electrical shock. The study utilizes a three-dimensional finite element model and the continuous bidomain representation of cardiac tissue to model steady-state polarization resulting from a defibrillation-strength uniform applied field. Fiber architecture is incorporated in the model via the shape of the heart, an ellipsoid of variable ellipticity index, and via an analytical function, linear or nonlinear, describing the transmural fiber rotation. Analytical estimates and numerical results are provided for the location and shape of the "bulk" polarization (polarization away from the tissue boundaries) as a function of the fiber field, or more specifically, of the conductivity changes in axial and radial direction with respect to the applied electrical field lines. Polarization in the tissue "bulk" is shown to exist only under the condition of unequal anisotropy ratios in the extra- and intracellular spaces. Variations in heart geometry and, thus, fiber curvature, are found to lead to change in location of the zones of significant membrane polarization. The transmural fiber rotation function modulates the transmembrane potential profile in the radial direction. A higher gradient of the transmural transmembrane potential is observed in the presence of fiber rotation as compared to the no rotation case. The analysis presented here is a step forward in understanding the interaction between tissue structure and applied electric field in establishing the pattern of membrane polarization during the initial phase of the defibrillation shock.

The role of transmural ventricular heterogeneities in cardiac vulnerability to electric shocks

“…2), it leads to a significant change in VEP and thus plays a key role in vulnerability to shocks. Sub-epicardial gapjunctional uncoupling within the LV free wall represents a discontinuity in the bidomain intracellular conductivities, which leads to the formation of shock-induced VEP (Entcheva et al, 1999). Areas of positive and negative polarisation are induced alongside the boundary between epicardial and midmyocardial layers, as shown in Figs.…”

Mechanisms of Defibrillation Failure

“…The increase in isoelectric window after high strength shock can also be explained by the prolongation of the epicardial refractoriness (surface polarization), resulting in the longer tunnel propagation. This is because intramural virtual electrode polarization is lower magnitude than surface polarization (Entcheva et al, 1999) and thus the LV midmyocardium, less affected by the shock, still contributes to the excitable tunnel even for higher strength shocks. Considering the high probability of the existence of the postshock excitable tunnel even for above-DFT shocks, defibrillation success may be explained by the fact that initiating PAs, originating within the wall, cannot find an excitable exit onto the epicardium and die out in the mid-myocardium.…”

Cardiac Arrhythmias: Mechanistic Knowledge and Innovation from Computer Models

“…In the absence of a better strategy, strong electrical shocks have remained the only reliable treatment for cardiac fibrillation. Over the years, biophysically-detailed multi-scale models of defibrillation [3,6,105,107] have made major contributions to understanding how defibrillation shocks used in clinical practice interact with cardiac tissue [7,9,11,29,50,78,103,104,115,118]; these models have been validated by comparing to the results of optimal mapping experiments [20,24,25]. Computer modeling of whole-heart defibrillation has been instrumental in the development of the virtual electrode polarization (VEP) theory for defibrillation.…”