There are several findings, however, that are not in total agreement with this hypothesis. One finding is that one or two rapid postshock cycles can appear following a defibrillation shock, yet the shock can still succeed (i.e., a type B successful defibrillation).24 This phenomenon may be similar to that of repetitive responses after shocks given during the
Figure 13: Example of the similarity of isochronal maps of the first postshock cycle after (a) the largest shock that induced ventricular fibrillation (VF) (2 J) and (b) the largest shock that failed to defibrillate (2 J) in the same animal. The display is similar to those in Fig. 11. Earliest postshock activation (arrows) was in the basal third of the ventricles for the shock given during the vulnerable period of paced rhythm (a) as well as for the failed defibrillation shock given during VF (b). The interval from the shock until earliest recorded activation for the first postshock cycle was 47 ms for the shock given during the vulnerable period and 50 ms for the shock given during VF. (Shibata et al. 1988)7
vulnerable period of regular rhythm. It may be in both of these cases that, even though a critical point is formed, activation propagates around it so quickly that the tissue that was directly excited by the shock field is still refractory when the postshock wavefront circles around to encounter it, causing the wavefront to block. This explanation is supported by the finding that waveforms that cause critical points to form in more recovered tissue, where the conduction velocity should be faster than in refractory tissue, have lower DFTs than waveforms with a similar critical potential gradient but a more refractory critical degree of recovery (Fig. 10).21
Another finding not in complete agreement with the refractory potential gradient critical point hypothesis for defibrillation is that earliest postshock activation, even when mapped with intramural electrodes, does not always appear immediately after the shock and appears to arise focally instead of immediately forming a reentrant circuit.25 However, this finding is consistent with the ULV hypothesis for the mechanism of defibrillation, because shocks given during the vulnerable period of regular rhythm can appear after an interval of tens of milliseconds and can appear focal (Figs. 11i and 13a).
Other findings not in agreement with the refractory potential gradient critical point hypothesis for defibrillation are that the critical potential gradient appears to increase as the distance from the S2 electrode to the critical point is increased by increasing shock strength,26 and that the ULV is not a single value but is a probability function. The DFT probability function can be explained by the fact that the state of the heart is different for each shock, so that a critical degree of refractoriness may or may not intersect the critical potential gradient at the time of the shock. The ULV shocks, however, are timed to occur at the same point in the vulnerable period, yet a probability function is still present, although with shocks given to scan the entire T wave, the ULV probability curve is steeper than that for the DFT.5 The existence of a ULV probability curve may indicate that the response to the shock is very sensitive to small variations in the electrophysiological state of the heart between one shock and the next.
A major limitation of the refractory potential gradient critical point hypothesis for defibrillation is that it does not explicitly consider the effects of the shock field and of the polarity of the shock electrodes on the transmembrane potential. One reason for this is that little was known about these effects at the time the hypothesis was put forward, and it was thought that the primary effect of the shock was to hyperpolarize the portion of each cell or each bundle of cells closer to the anode and depolarize the portion of each cell or each bundle of cells closer to the cathode, creating a "sawtooth"
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