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Title page for ETD etd-11232005-142052


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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