Chen P S, Wolf P D, Melnick S D, Danieley N D, Smith W M, Ideker R E
Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Circ Res. 1990 Jun;66(6):1544-60. doi: 10.1161/01.res.66.6.1544.
The purpose of this study was to map in detail the spread of activation away from sites of early postshock excitation following unsuccessful defibrillation to determine whether these activation fronts are the unaltered continuation of activation fronts present just before the shock. We recorded simultaneously from 120 bipolar electrodes on 40 plunge needles in a 20 x 35 x 5-mm volume of tissue of the right ventricular outflow tract immediately before and after shocks of 190-350 V were given via electrodes on the right atrium and left ventricular apex to six open-chest dogs with electrically induced ventricular fibrillation. For 20 shocks approximately 100 V below the defibrillation threshold, the site of earliest recorded activation following the shock was near the center of the mapped region. At the earliest recorded activation sites, there was an isoelectric window in the immediate postshock period lasting 42 +/- 15 msec after which activation fronts either spread away from a site in all directions in a focal pattern (12 episodes) or else spread away in only one direction (eight episodes). Comparison of activation patterns immediately before and after the shock revealed that in 18 of the 20 episodes, the location and pathway of activation fronts after the shock were markedly different from those before the shock. The preshock intervals at the sites of earliest activation following the shock, that is, the interval between the last activation at the site and the time of the shock, were not randomly distributed but were similar, averaging 64 +/- 11 msec, and were negatively correlated with the isoelectric postshock window (r = -0.70, p = 0.0001). These findings indicate that the presence and the site of origin of activation fronts after the shock are influenced by at least two factors: the shock itself and the electrophysiological state of the myocardium at the time of the shock. Thus, epicardial shocks approximately 100 V below the defibrillation threshold markedly alter the activation sequences of fibrillation but are unsuccessful because the activation fronts following the shock reinitiate fibrillation.
本研究的目的是详细描绘除颤失败后早期电击兴奋部位之外的激动传播情况，以确定这些激动波前是否是电击前存在的激动波前的未改变延续。我们在6只开胸犬身上诱发心室颤动后，通过右心房和左心室心尖处的电极给予190 - 350 V的电击，在电击前后，立即从位于右心室流出道20×35×5 mm组织体积内的40根穿刺针上的120个双极电极同时进行记录。对于低于除颤阈值约100 V的20次电击，电击后最早记录到激动的部位靠近标测区域的中心。在最早记录到激动的部位，电击后即刻存在一个持续42±15毫秒的等电位窗，之后激动波前要么以局灶性模式从一个部位向各个方向扩散（12次），要么仅向一个方向扩散（8次）。电击前后激动模式的比较显示，在20次中的18次中，电击后激动波前的位置和路径与电击前明显不同。电击后最早激动部位的电击前间期，即该部位最后一次激动与电击时间之间的间期，并非随机分布，而是相似的，平均为64±11毫秒，并且与电击后等电位窗呈负相关（r = -0.70，p = 0.0001）。这些发现表明，电击后激动波前的存在和起源部位受到至少两个因素的影响：电击本身以及电击时心肌的电生理状态。因此，低于除颤阈值约100 V的体表电击会显著改变颤动的激动顺序，但由于电击后的激动波前重新引发颤动，所以除颤失败。
