Fotuhi P C, Epstein A E, Ideker R E
Department of Medicine, University of Alabama at Birmingham, USA.
Am J Cardiol. 1999 Mar 11;83(5B):24D-33D. doi: 10.1016/s0002-9149(98)00966-7.
Today, transthoracic and intracardiac defibrillation offer a well-accepted and widely used form of therapy for patients with life-threatening ventricular arrhythmias. Despite the wide clinical use of defibrillators, the mechanisms by which an electrical shock halts fibrillation are still not completely understood. During a shock, different amounts of current flow through the different parts of the heart and the current distribution is highly uneven. This current distribution is affected by changes in the shock potential gradient through the heart, changes in fiber orientation, and changes in myocardial conductivity caused by connective tissue barriers. It would be ideal if the potential gradient distribution throughout the ventricles could be measured directly for each individual patient during defibrillator implantation and follow-up and the shock strength could be programmed based on this measurement, but so far this is not possible. A more feasible approach is to determine, by trial and error, the magnitude of the shock strength delivered through the defibrillation electrodes for successful defibrillation. There is no distinct threshold value above which all shocks succeed and below which all shocks fail to defibrillate. Rather, increasing shock strength increases the likelihood the shock will succeed. Therefore, instead of a distinct defibrillation threshold, a probability of success curve exists. However, increasing the shock strength above an optimal range can actually decrease the success rate for defibrillation. One possible explanation is that the high voltage gradients caused by such large shocks damage cells and result in postshock arrhythmias that may reinitiate fibrillation. Another problem that can affect the probability of defibrillation success for a particular programmed energy setting is that the shock strength required for defibrillation may increase over time due to (1) the growth of fibrotic tissue around the defibrillation electrode; (2) migration of the lead; (3) acute ischemia; or (4) other changes in the underlying cardiac disease (e.g., worsening of heart failure). Such possible increases in the defibrillation shock strength requirement should be compensated for before they occur by adding a margin of safety to the shock strength needed for effective defibrillation. When programming an implantable defibrillator, it is important to keep in mind that the defibrillation shock should be (1) strong enough to defibrillate at least 98% of the time with the first shock; (2) weak enough not to cause severe post-shock arrhythmias or reinitiation of fibrillation; but (3) strong enough to compensate for changes of defibrillation energy requirements over time. This usually can be accomplished by setting the defibrillator 7-10 J higher than the defibrillation threshold determined by a standard step-down protocol.
如今，经胸和心内除颤为患有危及生命的室性心律失常的患者提供了一种广为接受且广泛应用的治疗方式。尽管除颤器在临床上被广泛使用，但电击终止颤动的机制仍未被完全理解。在电击过程中，不同量的电流流经心脏的不同部位，且电流分布极不均匀。这种电流分布会受到穿过心脏的电击电位梯度变化、纤维方向变化以及结缔组织屏障导致的心肌电导率变化的影响。要是在植入除颤器期间及随访过程中，能直接测量每位患者整个心室的电位梯度分布，并基于此测量结果来设定电击强度，那将是理想的情况，但目前这还无法实现。一种更可行的方法是通过反复试验来确定经除颤电极施加的、能成功除颤的电击强度大小。不存在一个明确的阈值，高于该阈值所有电击都能成功，低于该阈值所有电击都无法除颤。相反，增加电击强度会增加电击成功的可能性。因此，存在的是一条成功概率曲线，而非明确的除颤阈值。然而，将电击强度增加到超出最佳范围实际上可能会降低除颤成功率。一种可能的解释是，如此大的电击所产生的高电压梯度会损伤细胞，并导致电击后心律失常，进而可能重新引发颤动。对于特定的程控能量设置，另一个会影响除颤成功概率的问题是，由于以下原因，除颤所需的电击强度可能会随时间增加：(1)除颤电极周围纤维化组织的生长；(2)导线移位；(3)急性缺血；或(4)潜在心脏病的其他变化（如心力衰竭加重）。在这些可能导致除颤电击强度要求增加的情况发生之前，应通过在有效除颤所需的电击强度上增加安全余量来进行补偿。在程控植入式除颤器时，重要的是要记住，除颤电击应：(1)足够强，以便首次电击至少98%的时间能成功除颤；(2)足够弱，不会引起严重的电击后心律失常或重新引发颤动；但(3)足够强，以补偿除颤能量需求随时间的变化。这通常可以通过将除颤器设置得比通过标准逐步降低方案确定的除颤阈值高7 - 10焦耳来实现。
