Abstract
Extracellular field shocks are applied between two extracellular electrodes placed on the body’s surface to convert ventricular fibrillation to sino-atrial rhythm. The basic question about the underlying mechanism relates to how electrical current flowing primarily through the extracellular space will flow across the cell membranes and affect the transmembrane potential of underlying cells. Experimental studies in whole hearts and cell cultures have shown that myocytes within the heart – at sites forming so-called virtual electrodes – can affect the shape of the action potential and/or excite the heart, and thereby interrupt reentrant circles and stop fibrillation. Small resistive obstacles formed by connective tissue or blood vessels in the order of few hundred micrometers in length may suffice to interrupt fibrillatory propagation. Overall, the connective tissue network, especially if it becomes more expressed in disease states or during evolving age, plays an important role in defibrillation.
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Kleber, A.G., Gillis, A.M. (2021). The Role of Microscopic Tissue Structure in Defibrillation. In: Efimov, I.R., Ng, F.S., Laughner, J.I. (eds) Cardiac Bioelectric Therapy. Springer, Cham. https://doi.org/10.1007/978-3-030-63355-4_11
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