Type of Document	Dissertation
Author	Woods, Marcella Cherie
URN	etd-11232005-142052
Title	The Response of the Cardiac Bidomain to Electrical Stimulation
Degree	PhD
Department	Biomedical Engineering
Advisory Committee	Advisor Name Title John P. Wikswo Committee Chair Michael I. Miga Committee Member Richard A. Gray Committee Member Richard G. Shiavi Committee Member Robert L. Galloway Committee Member
Keywords	electric stimulation cardiac electrophysiology bidomain model optical mapping Heart -- Electric properties
Date of Defense	2005-11-08
Availability	unrestricted
Abstract Coronary heart disease is the single largest cause of mortality in the United States. Approximately 335,000 people die annually from sudden cardiac death, and the majority of these cases are believed to be from ventricular fibrillation. To effectively treat and prevent cardiac rhythm disturbances, the response of the heart to electrical stimulation must be understood. Although cardiac defibrillation therapy is an invaluable medical procedure, the mechanisms by which strong electrical shocks terminate potentially lethal fibrillation are still debated. Bidomain models of cardiac tissue successfully characterize many of the effects of electrical stimulation of the heart. In the bidomain, the intracellular and extracellular spaces are distinct and have differing electrical anisotropies. With unequal anisotropy ratios, bidomain theory predicts simultaneous positive and negative polarization in response to stimulation, in the form of virtual cathodes and anodes that lead to interesting cardiac activation dynamics. This research examined experimentally the response of cardiac tissue to electrical stimulation from a bidomain perspective. Changes in transmembrane potential during and following electrical stimulation were recorded optically using a voltage-sensitive fluorescent dye. Optical mapping allows noninvasive measurement with high spatiotemporal resolution and avoids electrical stimulus artifacts. We found that: 1. During unipolar anodal stimulation of diastolic tissue, the mechanism of excitation depends upon the extracellular potassium concentration. 2. With proper timing of unipolar stimulation close to refractoriness, damped waves with diminished amplitude and velocity either gradually die or sharply increase in amplitude after a delay to become a steadily propagating wave. 3. We confirmed bidomain model predictions that virtual electrodes from unipolar stimulation affect excitability through the cardiac cycle as shown by strength-interval curves. 4. Field stimulation of the diastolic heart revealed that increasing shock strength and duration do not necessarily result in faster activation because of virtual anode polarization. 5. Alternating regions of positive and negative virtual electrode polarization around an insulating heterogeneity occur during field stimulation and may affect plunge electrode measurements. An increased understanding of how cardiac tissue responds to electrical stimulation in various conditions will guide improvements in treatment and prevention of cardiac rhythm disorders.
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