The Virtual Electrode Hypothesis of Defibrillation

Ripplinger, Crystal M.; Efimov, Igor R.

doi:10.1007/978-0-387-79403-7_13

Cited by 7 publications

(7 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Experimentally, much of our current understanding of defibrillation mechanisms has been derived from whole-ventricle optical mapping investigations[2-4] which only probe polarization patterns from tissue layers close to the epicardial surface[5]. However, fine-scale discontinuities in tissue structure, known to be present throughout the myocardial wall, have been postulated to play a crucial role in defibrillation through the creation of virtual-electrodes, as current induced by the applied field is redistributed, assisting in the bulk activation of myocardium.…”

Section: Introductionmentioning

confidence: 99%

Investigating the Role of the Coronary Vasculature in the Mechanisms of Defibrillation

Bishop

Plank

Vigmond

2012

Circ: Arrhythmia and Electrophysiology

View full text Add to dashboard Cite

Background The direct role of coronary vessels in defibrillation, although hypothesized to be important, remains to be elucidated. We investigate how vessel-induced virtual-electrode polarizations assist reentry termination. Methods and Results A highly anatomically-detailed rabbit ventricular slice bidomain computer model was constructed from 25μm MR data, faithfully representing both structural and electrical properties of blood vessels. For comparison, an equivalent simplified model with intramural cavities filled-in was also built. Following fibrillation induction, 6 initial states were selected and biphasic shocks (5–70V) applied using a realistic Implanted Cardioverter Defibrillator electrode configuration. A fundamental mechanism of biphasic defibrillation was uncovered in both models, involving successive break excitations (after each shock phase) emanating from opposing myocardial surfaces (in septum/LV), which rapidly closed-down excitable gaps. The presence of vessels accelerated this process, achieving more rapid and successful defibrillation: defibrillation failed in 5 cases (all due to initiation of new activity), compared to 8 with the simplified model (5/8 failures due to surviving activity). At stronger shocks, virtual-electrodes formed around vessels, rapidly activating intramural tissue due to break excitations, assisting the main defibrillation mechanism and eliminating all activity <15ms of shock-end in 60% of successful shocks (36% in simplified model). Subsequent analysis identified only vessels approximately >200um diameter participated via this mechanism. Consequently, wavefronts could survive intramurally in the simplified model, leading to reentry and shock-failure. Conclusions We provide new insight into defibrillation mechanisms by showing how intramural blood vessels facilitate more effective elimination of existing wavefronts, rapid closing-down of excitable gaps and successful defibrillation, and give guidance towards the required resolution of cardiac imaging and model generation endeavors for mechanistic defibrillation analysis.

show abstract

Section: Introductionmentioning

confidence: 99%

Investigating the Role of the Coronary Vasculature in the Mechanisms of Defibrillation

Bishop

Plank

Vigmond

2012

Circ: Arrhythmia and Electrophysiology

View full text Add to dashboard Cite

show abstract

“…The success of the bidomain model suggests that it may also be useful for modeling the response of the heart to strong shocks during defibrillation. Indeed, another review at least as long as this one could be written describing the use of the bidomain model for studying defibrillation [100,101].…”

Section: Resultsmentioning

confidence: 99%

Numerical Simulations of Cardiac Tissue Excitation and Pacing Using the Bidomain Model

Roth¹

2011

TOPETJ

View full text Add to dashboard Cite

Abstract:The last two decades have produced significant advances in our theoretical understanding of cardiac pacing. The bidomain model, a mathematical representation of the anisotropic electrical properties of cardiac tissue, has provided insight into many long-standing mysteries of pacing, such as the mechanisms of make and break excitation, the shape of the strength-interval curve, and the induction of reentry by burst pacing. This paper reviews the application of the bidomain model to these and other topics, and summarizes our theoretical understanding of how electrical excitation of the heart works.

show abstract

“…It is based on solid experimental evidence and theoretical foundation. [59] Numerous optical mapping studies presented evidence that in addition to depolarization, shock also was capable to hyper-polarize or de-excite other regions of the heart resulting in action potential shortening instead of the consistent prolongation observed in Dillon’s first study. Figure14_9 shows the results of one such study from an anterior rabbit ventricle with recorded optical action potentials displaying both shock-induced shortening (observed at the virtual anode) and prolongation (observed at the virtual cathode).…”

Section: Mechanisms Of Defibrillationmentioning

confidence: 99%

“…Subsequent generalized activation function theory was formulated by Sobie et al, which laid the theoretical foundation for the virtual electrode hypothesis. [60] The generalized activating function shows mathematically how a combination of field gradients, underlying heterogeneities in refractoriness and anatomical discontinuities in conduction properties could create neighboring regions of virtual anodes and cathodes, which hyperpolarize and depolarize tissue serving as secondary sources to stimulate the tissue or to induce new fibrillatory wavefronts [9, 59, 61, 62]. …”

Section: Mechanisms Of Defibrillationmentioning

confidence: 99%

Imaging of Ventricular Fibrillation and Defibrillation: The Virtual Electrode Hypothesis

Boukens

Gutbrod

Efimov

2015

Advances in Experimental Medicine and Biology

Self Cite

View full text Add to dashboard Cite

Ventricular fibrillation is the major underlying cause of sudden cardiac death. Understanding the complex activation patterns that give rise to ventricular fibrillation requires high resolution mapping of localized activation. The use of multi-electrode mapping unraveled re-entrant activation patterns that underlie ventricular fibrillation. However, optical mapping contributed critically to understanding the mechanism of defibrillation, where multi-electrode recordings could not measure activation patterns during and immediately after a shock. In addition, optical mapping visualizes the virtual electrodes that are generated during stimulation and defibrillation pulses, which contributed to the formulation of the virtual electrode hypothesis. The generation of virtual electrode induced phase singularities during defibrillation is arrhythmogenic and may lead to the induction of fibrillation subsequent to defibrillation. Defibrillating with low energy may circumvent this problem. Therefore, the current challenge is to use the knowledge provided by optical mapping to develop a low energy approach of defibrillation, which may lead to more successful defibrillation.

show abstract

The Virtual Electrode Hypothesis of Defibrillation

Cited by 7 publications

References 67 publications

Investigating the Role of the Coronary Vasculature in the Mechanisms of Defibrillation

Investigating the Role of the Coronary Vasculature in the Mechanisms of Defibrillation

Numerical Simulations of Cardiac Tissue Excitation and Pacing Using the Bidomain Model

Imaging of Ventricular Fibrillation and Defibrillation: The Virtual Electrode Hypothesis

Contact Info

Product

Resources

About