This computational study provides a theoretical framework for understanding how the complex fibrous structure of the myocardium influences the distribution of electrical currents and transmembrane potentials during defibrillation.
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Does not yet inform defibrillation practice; extends computational models of fibrous polarization effects.
The purpose of this paper is to investigate the relationship between cardiac tissue structure, applied electric field, and the transmembrane potential induced in the process of defibrillation. It outlines a general understanding of the structural mechanisms that contribute to the outcome of a defibrillation shock. Electric shocks defibrillate by changing the transmembrane potential throughout the myocardium. In this process first and foremost the shock current must access the bulk of myocardial mass. The exogenous current traverses the myocardium along convoluted intracellular and extracellular pathways channeled by the tissue structure. Since individual fibers follow curved pathways in the heart, and the fiber direction rotates across the ventricular wall, the applied current perpetually engages in redistribution between the intra- and extracellular domains. This redistribution results in changes in transmembrane potential (membrane polarization): regions of membrane hyper- and depolarization of extent larger than a single cell are induced in the myocardium by the defibrillation shock. Tissue inhomogeneities also contribute to local membrane polarization in the myocardium which is superimposed over the large-scale polarization associated with the fibrous organization of the myocardium. The paper presents simulation results that illustrate various mechanisms by which cardiac tissue structure assists the changes in transmembrane potential throughout the myocardium.
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Trayanova et al. (1998) studied this question.
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