New insights into defibrillation of the heart from realistic simulation studies

Abstract

Cardiac defibrillation, as accomplished nowadays by automatic, implantable devices, constitutes the most important means of combating sudden cardiac death. Advancing our understanding towards a full appreciation of the mechanisms by which a shock interacts with the heart, particularly under diseased conditions, is a promising approach to achieve an optimal therapy. The aim of this article is to assess the current state-of-the-art in whole-heart defibrillation modelling, focusing on major insights that have been obtained using defibrillation models, primarily those of realistic heart geometry and disease remodelling. The article showcases the contributions that modelling and simulation have made to our understanding of the defibrillation process. The review thus provides an example of biophysically based computational modelling of the heart (i.e. cardiac defibrillation) that has advanced the understanding of cardiac electrophysiological interaction at the organ level, and has the potential to contribute to the betterment of the clinical practice of defibrillation.

Keywords: Computer simulation; Electric countershock; Ventricular fibrillation.

Figure 1

Transmembrane potential distribution at shock-end for various shock electrode configurations, waveforms, strengths, and polarities as indicated within each panel. The colour scale is saturated, i.e. V_m above 20 mV and below −90 mV appears as 20 and −90 mV, respectively. (A) External shocks are monophasic, 4 ms long, and of strengths shown in the figure; they are applied at a coupling interval of 105 ms. For each case, the anterior epicardium and endocardium, and a transmural view of the ventricles are shown. Images are based on figures published in Rodriguez and Trayanova. (B) External truncated-exponential monophasic shocks of reversed polarity and strength 5 V/cm. Anterior epicardium and transmural views of the ventricles are shown. Images are based on figures published in Rodriguez et al. (C) External truncated-exponential (62% tilt) monophasic and biphasic shocks are of 10 ms duration, coupling interval 220 ms, and of strengths shown in the figure. Anterior epicardium and transmural views of the ventricles are shown. Biphasic shock polarity reverses at 6 ms. In addition, the V_m distribution 10 ms after shock-end is shown in a transmural view. Images are based on figure published in Trayanova et al. (D) Implantable cardioverter-defibrillator-like electrode configuration delivers truncated-exponential (62% tilt) biphasic shocks of 10 ms duration at coupling interval 140 ms, and of strengths shown in the figure. Images are based on figure published in Trayanova et al.

Figure 2

Monophasic (top) and biphasic (bottom) shock episodes resulting in isoelectric window and arrhythmia initiation. Progression of activity from VEP through initiation of intramural activation (transparent view with activation marked by *) to epicardial breakthrough followed by focal activation pattern and ultimately a reentry. Shocks are external of duration 10 ms (6/4 ms for the biphasic shock) and of strengths 16 (monophasic) and 12 (biphasic) V/cm and are delivered at 220 ms coupling interval. Images based on figures published in Ashihara et al.

Figure 3

Tunnel propagation of activations following defibrillation shocks in the rabbit heart. Arrows indicate direction of propagation. Presented is the submerging of a pre-shock fibrillatory wavefront by a strong biphasic shock delivered from an ICD. The figure shows the model, the fibrillatory pre-shock state (with scroll-wave filaments, the organizing centres of reentry, shown in pink), and post-shock V_m maps for two shock strengths at different post-shock timings. In contrast to the 25 V shock, the near-DFT 175 V shock converted the LV excitable area into an intramural excitable tunnel (see triangular arrows in shock-end panel) with no apparent propagation on the epicardium; the wavefront propagated in it until epicardial breakthrough following the isoelectric window. Images based on figures published in Constantino et al.

Figure 4

Mechanisms for shock failure, for shocks far below (A) and near (B) the DFT. In (A), arrhythmia is induced right after the shock, initiated by a post-shock activation (typically a break excitation wave) that reenters in the heart. In (B), the presence of only intramural excitable areas results in propagation of post-shock activations initiated in these areas deep in the ventricular wall (‘tunnel propagation’). These intramural wavefronts cannot make a breakthrough on the ventricular surface because of the post-shock depolarization of the surfaces. Only when the surfaces recover from this depolarization, the intramural wavefronts propagating in the mid-wall tunnel are able to make a breakthrough on the wall surfaces, marking the end of the isoelectric window, and becoming the earliest propagated post-shock activations propagating globally (and thus on the ventricular surfaces). Image based on figure published in Trayanova et al.

Figure 5

MRI-based model of healed infarction in the rabbit. (A) Ex-vivo MRI scan of the rabbit heart with healed myocardial infarction and anterior view of the fibre orientations in the ventricles. (B) Left panel, anterior view of the ventricles submerged in a perfusing bath and placed between plate electrodes (blue, grounding electrode; red, shock electrode). The infarct scar is shown in blue, the peri-infarct (border) zone is shown in green. The pink square at the apex shows the location of the pacing electrode. The bottom inset shows the highly detailed structure of the scar and the PZ. The top inset shows the details of the computational mesh. (C) Distribution of shock-end V_m. Less tissue was excited in the infarction model (purple arrows). Right-most panel shows the V_m difference between infarction and control models, computed as control V_m minus infarction V_m. Images based on figures published in Rantner et al.

Figure 6

Implantable cardioverter-defibrillator configurations tested in the paediatric patient with tricuspid valve atresia. Figure modified with permission from Rantner et al.