Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

Abstract

To test the hypothesis that a defibrillation shock is unsuccessful because it fails to annihilate activation fronts within a critical mass of myocardium, we recorded epicardial and transmural activation in 11 open-chest dogs during electrically induced ventricular fibrillation (VF). Shocks of 1-30 J were delivered through defibrillation electrodes on the left ventricular apex and right atrium. Simultaneous recordings were made from septal, intramural, and epicardial electrodes in various combinations. Immediately after all 104 unsuccessful and 116 successful defibrillation shocks, an isoelectric interval much longer than that observed during preshock VF occurred. During this time no epicardial, septal, or intramural activations were observed. This isoelectric window averaged 64±22 ms after unsuccessful defibrillation and 339±292 ms after successful defibrillation (P < 0.02). After the isoelectric window of unsuccessful shocks, earliest activation was recorded from the base of the ventricles, which was the area farthest from the apical defibrillation electrode. Activation was synchronized for one or two cycles following unsuccessful shocks, after which VF regenerated.Thus, (a) after both successful and unsuccessful defibrillation with epicardial shocks of 21 J, an isoelectric window occurs during which no activation fronts are present; (b) the postshock isoelectric window is shorter for unsuccessful than for successful defibrillation; (c) unsuccessful shocks transiently synchronize activation before fibrillation regenerates; (d) activation leading to the regeneration of VF after the isoelectric window for unsuccessful shocks originates in areas away from the defibrillation electrodes. The isoelectric window does not support the hypothesis that defibrillation fails solely because activation fronts are not halted within a critical mass of myocardium. Rather, unsuccessful epicardial shocks of 21 J halt all activation fronts after which VF regenerates.

Transmural and endocardial Purkinje activation in pigs before local myocardial activation after defibrillation shocks

“…Of the 24 successful shocks, 22 were Type B successes, which are defined as successful defibrillation shocks with the earliest first post-shock activation recorded in the working myocardium within 130 ms of the defibrillation shock. 15 Type A successes, which are defined as successful defibrillation shocks after which this interval is >130 ms, occurred twice and had an average earliest recorded post-shock activation time of 245 ms. The first five post-shock activation cycles in these two episodes were all sinus beats.…”

“…[11][12][13][14][15] Previous defibrillation studies have demonstrated that in pigs first postshock activation tends to arise closer to the epicardium than the endocardium.11 , 16 In pigs, Purkinje fibers traverse the ventricular wall and extend nearly to the epicardial surface. [17][18][19] Thus, the subepicardial location of the first recorded post-shock electrical activation in pigs raises the possibility that the earliest post-shock activation arises in the specialized conduction system.…”

Atria are more susceptible to electroporation than ventricles: Implications for atrial stunning, shock-induced arrhythmia and defibrillation failure

“…These results may also explain phenomenon of the "iso-electric window", which was observed after failed defibrillation shocks. (35) …”

Mechanisms of defibrillation

“…Monophasic shocks may be strong enough to terminate the wavefronts of VF, but fail to defibrillate because the shocks create virtual electrodes, which generate new wavefronts that reinitiate VF (60,61). Figure 11 shows the development of a virtual cathode and anode on the anterior epicardium of an optically mapped rabbit heart (62).…”