Zhou X, Daubert J P, Wolf P D, Smith W M, Ideker R E
Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Circ Res. 1993 Jan;72(1):145-60. doi: 10.1161/01.res.72.1.145.
To study the mechanism of defibrillation and the reason for the increased defibrillation efficacy of biphasic waveforms, the potential gradient in a 32 x 30-mm region of the right ventricle in 15 dogs was progressively lowered in four steps while a strong potential gradient field was maintained throughout the rest of the ventricular myocardium. The volume of right ventricle beneath the plaque was 10 +/- 2% of the total ventricular mass. A 10-msec monophasic (eight dogs) or 5/5-msec biphasic (seven dogs) truncated exponential shock 30% above the defibrillation threshold voltage was given via electrodes on the left ventricular apex and right atrium to create the strong potential gradient field. Simultaneously, a weaker shock with the same waveform but opposite polarity was given via mesh electrodes on either side of the small right ventricular region to cancel part of the potential difference in the region and to create one of the four levels of potential gradient fields. Shock potentials and activations were recorded from 117 epicardial electrodes in the small region, and in one dog global epicardial activations and potentials were recorded from a sock containing 72 electrodes. Each gradient field was tested 10 times for successful defibrillation after 10 seconds of electrically induced fibrillation. For both monophasic and biphasic shocks, the percentage of successful defibrillation attempts decreased (p < 0.05) as the potential gradient decreased in the small region. Defibrillation was successful approximately 80% of the time for a mean +/- SD potential gradient of 5.4 +/- 0.8 V/cm for monophasic shocks and 2.7 +/- 0.3 V/cm for biphasic shocks (p < 0.05). No postshock activation fronts arose from the small region for eight waveform when the gradient was more than 5 V/cm. For both waveforms, the postshock activation fronts after the shocks were markedly different from those just before the shock and exhibited either a focal origin or unidirectional conduction.(ABSTRACT TRUNCATED AT 400 WORDS)
为研究除颤机制及双相波除颤效果增强的原因，在15只犬的右心室32×30mm区域内的电位梯度分四步逐渐降低，同时在心室其余心肌区域维持强电位梯度场。斑块下方右心室的体积为心室总质量的10±2%。通过左心室心尖和右心房的电极给予高于除颤阈值电压30%的10毫秒单相（8只犬）或5/5毫秒双相（7只犬）截断指数电击，以产生强电位梯度场。同时，通过小右心室区域两侧的网状电极给予相同波形但极性相反的较弱电击，以抵消该区域部分电位差并创建四个电位梯度场水平之一。从小区域内的117个心外膜电极记录电击电位和激活情况，在一只犬中，从包含72个电极的套囊中记录整体心外膜激活和电位。在电诱导颤动10秒后，对每个梯度场进行10次成功除颤测试。对于单相和双相电击，随着小区域内电位梯度降低，成功除颤尝试的百分比均下降（p<0.05）。单相电击时，平均±标准差电位梯度为5.4±0.8V/cm时，除颤成功率约为80%；双相电击时，平均±标准差电位梯度为2.7±0.3V/cm时，除颤成功率约为80%（p<0.05）。当梯度大于5V/cm时，8个波形在小区域均未出现电击后激活前沿。对于两种波形，电击后的激活前沿与电击前明显不同，表现为局灶性起源或单向传导。（摘要截断于400字）
