Abstract-It has been hypothesized that during ventricular fibrillation (VF), the fastest activating region, the dominant domain, contains a stable reentrant circuit called a mother rotor. This hypothesis postulates that the mother rotor spawns wavefronts that propagate to maintain VF elsewhere and implies that the ratio of wavefronts propagating off a region to those propagating onto it (propoff/propon) should be Ͼ1 for the dominant domain but Ͻ1 elsewhere. To test this prediction in the left ventricular (LV) epicardium of a large animal, most of the LV free wall was mapped with 1008 electrodes in 7 pigs. VF activation rate was faster in the posterior than in the anterior LV (10.0Ϯ1.3Hz versus 9.3Ϯ1.3Hz; PϽ0.001). The anterior LV had a higher fraction of wavefronts that blocked than did the posterior LV and had a propoff/propon ratio Ͻ1 (PϽ0.001). The mean conduction velocity vectors of the VF wavefronts pointed in the direction from the posterior to the anterior LV. Although these findings favor a dominant domain in the posterior LV, the facts that the anterior LV had a higher incidence of reentry than did the posterior LV and that the posterior LV did not have propoff/propon significantly different from 1 do not. Thus, quantitative regional differences are present over the porcine LV epicardium during VF. Although these differences are not totally consistent with the presence of a dominant domain within the LV free wall, the mean conduction velocity vector is consistent with one in the septum. Key Words: ventricular fibrillation Ⅲ electrical mapping Ⅲ mechanisms of arrhythmias V arious hypotheses have been presented to explain the complex activation sequences during ventricular fibrillation (VF). One hypothesis is drawn from a computer model of atrial fibrillation where "wandering wavelets" encounter tissue in which refractoriness is spatially dispersed heterogeneously, leading to reentry that changes pathways from cycle to cycle. 1 Another hypothesis states that instead of the spatial dispersion of refractoriness, the temporal restitution proportion of refractoriness causes block that sustains VF. 2,3 A third hypothesis is that a single stable dominant rotor, the "mother rotor," spawns wavefronts that spread away from it and block to form complex activation sequences that maintain fibrillation in the rest of the myocardium. 4 -9 Recent evidence for the mother rotor hypothesis comes from studies of optical mapping that imaged isolated rabbit hearts, 6,7 slabs of sheep right ventricular (RV) and left ventricular (LV), 8 and guinea pig hearts. 9 This last study reported that the mother rotor was localized to the anterior LV epicardium and was responsible for maintaining VF throughout both ventricles. However, others investigating the same location in the same species did not find evidence of a mother rotor. 10 In the intact swine heart, epicardial reentry also is uncommon in the anterior LV. 11 Optical mapping of slabs of sheep hearts suggests a mother rotor might be intramural. 8 Conversely, optical mapping o...
Background-Shocks that have defibrillated spontaneous ventricular fibrillation (VF) during acute ischemia or reperfusion may seem to have failed if VF recurs before the ECG amplifier recovers after shock. This could explain why the defibrillation threshold (DFT) for spontaneous VF appears markedly higher than for electrically induced VF. Methods and Results-The DFT for electrically induced VF (E-DFT) was determined in 15 pigs before ischemia, followed by left anterior ascending or left circumflex artery occlusion. VF was electrically induced 20 minutes after occlusion, followed 5 minutes later by reperfusion. Whether spontaneous or electrically induced, VF during occlusion or reperfusion was treated with up to 3 shocks at 1.5ϫE-DFT. If all 3 shocks failed, shock strength was increased. Thirty minutes after reperfusion, the other artery was occluded and the protocol was repeated. Defibrillation was considered successful if postshock sinus/idioventricular rhythm was present for Ն30 seconds. VF recurring within 30 seconds after the shock was considered immediate or delayed if the first postshock activation complex in a rapidly restored ECG recording was VF or sinus/idioventricular rhythm, respectively. Defibrillation efficacy at 1.5ϫE-DFT was significantly higher for electrically induced ischemic VF (76%) than for spontaneous VF (31%). The incidence of delayed recurrence after electrically induced nonischemic (3%) or ischemic (20%) VF was significantly lower than after spontaneous VF (75%). Mean VF recurrence time after spontaneous VF was 4.6Ϯ5.3 seconds. Conclusions-Spontaneous VF can be halted by a shock but then quickly restart before a standard ECG amplifier has recovered from postshock saturation, making it appear that the shock failed.
During internal defibrillation, potential gradients greater than 100 V/cm occur near defibrillation electrodes. Such strong fields may cause deleterious effects, including arrhythmias. This study determined 1) the effects of such strong fields on the propagation of activation and 2) whether these effects were different for monophasic and biphasic shocks. Voltages and potential gradients during the shock, as well as activation sequences before and after the shock, were mapped from 117 epicardial electrodes placed over a 3 x 3-cm area on the right ventricle in six dogs. Pacing at a cycle length of 350 msec was given from a long narrow electrode on the right side of the mapped area to generate parallel activation isochrones. A monophasic shock, 10 msec in duration, or a biphasic shock with both phases 5 msec in duration was delivered 300 msec after the last paced stimulus via a mesh electrode on the left side of the mapped area as the cathode, with the anode on the right atrium. Shocks of 70-850 V were given, and the potential gradient and current density at each recording electrode were calculated from the measured potentials and fiber orientation by using a finite element method. Pacing was resumed 200 msec after the shock, and activation sequences were mapped for up to 5 minutes. Potential gradients ranged from 1 to 189 V/cm with high fields on the left side and low fields on the right side of the mapped area. Where the potential gradient was weak, the first activation sequence after the shock was similar to that before the shock, but activation blocked without conducting into areas where the gradient was greater than 64 +/- 4 (mean +/- SD) V/cm for monophasic and greater than 71 +/- 6 V/cm for biphasic shocks. These values are significantly different (p less than 0.003). The higher the potential gradient, the longer was the duration of block before conduction returned. Block duration, however, was generally shorter for biphasic than for monophasic waveforms of the same field strength. In conclusion, conduction block can follow either waveform, but biphasic waveforms cause less block than monophasic waveforms. This effect may partially explain the increased defibrillation efficacy of biphasic shocks.
LPAs exist after successful and failed shocks near the DFT. Thus, the time from the shock to the GPA is not totally electrically silent.
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