Imaging of Ventricular Fibrillation and Defibrillation: The Virtual Electrode Hypothesis

Abstract

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.

Effects of high-frequency biphasic shocks on ventricular vulnerability and defibrillation outcomes through synchronized virtual electrode responses

“…Therefore, the electrical energy can propagate into tissue deeper than the superficial layers when the shock energy follows the cell bundles in accordance with the sawtooth mechanism. On the basis of the sawtooth model, if an electric field is sufficiently strong, the transmembrane potential in the depolarized areas of all cells reaches the activation threshold and initiates local excitation, which spreads to the hyperpolarized areas, and the entire cell chain is activated almost simultaneously [12]. In this study, the temporal sawtooth pattern was observed at the tissue level during high-frequency defibrillation.…”

“…In optical mapping experiments under real cathode stimulation, the cardiac tissue near the electrodes depolarizes, which generates two virtual anodes and causes lateral myocardium hyperpolarization. This phenomenon explains how remote tissue not directly under the shocking electrodes can have transmembrane potential responses from the shock [12,16,17]. The virtual electrode hypothesis is more applicable to biphasic shocks than to monophasic shocks possibly because of the immediate phase reversal of tissue responses during the shock [15,18].…”

Using Nanosecond Shocks for Cardiac Defibrillation

“…Isolated cardiomyocytes are still an important model to study defibrillation because stimulation can be used as a proxy for defibrillation. Stimulation is a viable proxy on theoretical grounds, because the success of defibrillation depends on whether a shock activates enough of the cardiac tissue 15,16,31 (but our data hereunder suggest that it has limitations). Stimulation of individual myocytes with nanosecond pulses is possible, 32,33 and the mechanism of stimulation likely involves electroporation of the plasma membrane.…”

Sudden cardiac death in children and young adults without structural heart disease: a comprehensive review

“…Reentry refers to a circus movement of advancing wave front of depolarization through a circuit within the heart muscle which usually involves a critical barrier around which the wave front advances (Mines, 1913;Wit , 1978). This barrier could be a fixed anatomic barrier such as a scar, area of ischemia, or an anatomic structure such as a valve, or it can be virtual and even be mobile (Boukens et al, 2015). In several types of arrhythmias, the circuit is large and macroscopic involving much of the heart.…”