The mechanisms of the vulnerable window: the role of virtual electrodes and shock polarity

Vulnerability and defibrillation are mechanistically dependent upon shock s trength, polarity, and timing. We have recently demonstrated that shock-ind uced virtual electrode polarization (VEP) may induce reentry. However, it r emains unclear how the VEP mechanism may explain the vulnerable window and polarity dependence of vulnerability. We used a potentiometric dye and opti cal mapping to assess the anterior epicardial electrical activity of Langen dorff-perfused rabbit hearts (n = 7) during monophasic shocks (+/- 100 V an d +/- 200 V, duration of 8 ms) applied from a transvenous defibrillation le ad at various coupling intervals. Arrhythmias were induced in a coupling in terval and shock polarity dependent manner: (i) anodal and cathodal shocks induced arrhythmias in 33.2 +/- 30.1% and 53.1 +/- 39.3% cases (P < 0.01), respectively, and (ii) the vulnerable window was located near the T-wave. O ptical maps revealed that VEP was also modulated by the coupling interval a nd shock polarity. Recovery of excitability produced by negative polarizati on, known as de-excitation, and the resulting reentry was more readily achi eved during the relative refractory period than the absolute refractory per iod. Furthermore, anodal shocks produced wavefronts propagating in an inwar d direction with respect to the electrode, whereas cathodal shocks propagat ed in an outward direction. Wavefronts produced by anodal shocks were more likely to collide and annihilate each other than those caused by cathodal s hocks. The probability of degeneration of the VEP-induced phase singularity into a sustained arrhythmia depends upon the gradient of VEP and the direc tion of the VEP-induced wavefront. The VEP gradient depends upon the coupli ng interval, while the direction depends upon shock polarity; these factors explain the vulnerable window and polarity-dependence of vulnerability, re spectively.