Key result
Negative polarization (hyperpolarization) can deexcite cardiac cells, creating excitable tissue regions that influence both the induction of fibrillation and the success or failure of defibrillation.
Understanding the role of negative polarization and deexcitation provides new mechanistic insights into how defibrillation shocks can either succeed or induce fibrillation.
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Highlights hyperpolarization in defibrillation mechanisms; leaves open whether targeting deexcitation improves clinical outcomes.
Previous models of fibrillation induction and defibrillation stressed the contribution of depolarization during the response of the heart to a shock. This article reviews recent evidence suggesting that comprehending the role of negative polarization (hyperpolarization) also is crucial for understanding the response to a shock. Negative polarization can "deexcite" cardiac cells, creating regions of excitable tissue through which wavefronts can propagate. These wavefronts can result in new reentrant circuits, inducing fibrillation or causing defibrillation to fail. In addition, deexcitation can lead to rapid propagation through newly excitable regions, resulting in the elimination of excitable gaps soon after the shock and causing defibrillation to succeed.
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Efimov et al. (2000) conducted a review in Fibrillation induction and defibrillation. Negative polarization (hyperpolarization) was evaluated. Negative polarization (hyperpolarization) can deexcite cardiac cells, creating excitable tissue regions that influence both the induction of fibrillation and the success or failure of defibrillation.
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