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Theory of Heart pp 533–560Cite as

Basic Mechanisms of Ventricular Defibrillation

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Part of the book series: Institute for Nonlinear Science ((INLS))

Abstract

Recordings were made simultaneously from many electrodes placed on and in the hearts of animals to study the basic principles of ventricular defibrillation. The findings are listed below. Earliest activations following a shock slightly lower in strength than needed to defibrillate (a subthreshold defibrillation shock) occur in those cardiac regions in which the potential gradients generated by the shock are weakest. Activation fronts after subthreshold shocks do not appear to be continuations of activation fronts present just before the shock. An upper limit exists to the strength of shocks that induce fibrillation when given during the “vulnerable period” of regular rhythm. This upper limit of vulnerability correlates with and is similar in strength to the defibrillation threshold. To defibrillate, a shock must halt the activation fronts of fibrillation without giving rise to new activation fronts that reinduce fibrillation. The response to shocks during regular rhythm just below the upper limit of vulnerability is similar to the response to subthreshold defibrillation shocks. Shocks during regular rhythm initiate rotors of reentrant activation leading to fibrillation when a critical point is formed, at which a certain critical value of shock potential gradient field strength intersects a certain critical degree of myocardial refractoriness. This critical point may explain the existence of the upper limit of vulnerability. The critical point may also partially explain the finding that the relationship between shock strength and the success of the shock in halting fibrillation is better represented by a probability function rather than by a discrete threshold value. Very high potential gradients, approximately an order of magnitude greater than needed for defibrillation, have detrimental effects on the heart, including conduction block, induction of arrhythmias, decreased wall motion, and tissue necrosis.

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Authors and Affiliations

  1. Department of Medicine and Pathology, Duke University Medical Center, 27710, Durham, North Carolina, USA

    Raymond E. Ideker, Anthony S. L. Tang, David W. Frazier, Nitaro Shibata, Peng-Sheng Chen & J. Marcus Wharton

  2. The Engineering Research Center in Emerging Cardiovascular Technologies, Duke University, 27706, Durham, North Carolina, USA

    Raymond E. Ideker, Anthony S. L. Tang, David W. Frazier, Nitaro Shibata, Peng-Sheng Chen & J. Marcus Wharton

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  1. Raymond E. Ideker
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  2. Anthony S. L. Tang
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Editors and Affiliations

  1. Department of Physiology, McGill University, Montreal, Quebec, H3G 1Y6, Canada

    Leon Glass

  2. Department of Engineering Science, University of Auckland, Auckland, New Zealand

    Peter Hunter

  3. Department of Applied Mechanics and Engineering Science—Bioengineering, University of California, San Diego, La Jolla, CA, 92093, USA

    Andrew McCulloch

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Ideker, R.E., Tang, A.S.L., Frazier, D.W., Shibata, N., Chen, PS., Wharton, J.M. (1991). Basic Mechanisms of Ventricular Defibrillation. In: Glass, L., Hunter, P., McCulloch, A. (eds) Theory of Heart. Institute for Nonlinear Science. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3118-9_20

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