Virtual electrode-induced reexcitation: A mechanism of defibrillation.
Virtual electrode-induced reexcitation: A mechanism of defibrillation.
复制标题
DOI：
10.1161/01.res.85.11.1056
复制
发表时间：
1999-11
影响因子：
20.1
通讯作者：
Yuanna Cheng;K. Mowrey;D. R. V. Wagoner;Patrick J. Tchou;Igor R. Efimov
中科院分区：
文献类型：
--
作者：
Yuanna Cheng;K. Mowrey;D. R. V. Wagoner;Patrick J. Tchou;Igor R. Efimov
除颤的机制仍然知之甚少。除颤的成功取决于消除颤动而不引起电击诱发心律失常。我们在不应期使用植入式除颤器电极施加电击期间，对兔子心脏（n = 20）的选定心外膜区域进行了光学映射。单相电击导致虚拟电极极化（VEP）。 VEP正值导致动作电位持续时间延长，而负极化则缩短动作电位持续时间，导致兴奋性部分或完全恢复。冲击后，新的传播波前出现在两个区域和重新激发的负极化区域之间的边界处。电击引起的激活的传导速度和最大动作电位上升速率 dV/dt (max) 取决于电击结束时的跨膜电位。线性回归分析显示，当电击后电压V(m)值为-56.7+/-0.6 mV时，电击后激活的dV/dt(max)达到正常动作电位的50%(n=9257)。负电位越少，传导速度越慢和阻滞，而负电位越多，传导速度越快。尽管在这两种情况下都会产生断波，但只有当传导缓慢时，它们才会退化为心律失常。电击引起的 VEP 对于消除颤动至关重要，但可以通过产生兴奋性间隙而重新诱发心律失常。通过逐渐增加冲击强度来重新激发这些间隙可以为脆弱性的下限和上限提供基础。前者可能对应于重激励的慢波前和相位奇点的起源。后者对应于快速传导，在此期间波断不再产生持续的心律失常。
Mechanisms of defibrillation remain poorly understood. Defibrillation success depends on the elimination of fibrillation without shock-induced arrhythmogenesis. We optically mapped selected epicardial regions of rabbit hearts (n=20) during shocks applied with the use of implantable defibrillator electrodes during the refractory period. Monophasic shocks resulted in virtual electrode polarization (VEP). Positive values of VEP resulted in a prolongation of the action potential duration, whereas negative polarization shortened the action potential duration, resulting in partial or complete recovery of the excitability. After a shock, new propagated wavefronts emerged at the boundary between the 2 regions and reexcited negatively polarized regions. Conduction velocity and maximum action potential upstroke rate of rise dV/dt (max) of shock-induced activation depended on the transmembrane potential at the end of the shock. Linear regression analysis showed that dV/dt(max) of postshock activation reached 50% of that of normal action potential at a V(m) value of -56.7+/-0.6 mV postshock voltage (n=9257). Less negative potentials resulted in slow conduction and blocks, whereas more negative potentials resulted in faster conduction. Although wavebreaks were produced in either condition, they degenerated into arrhythmias only when conduction was slow. Shock-induced VEP is essential in extinguishing fibrillation but can reinduce arrhythmias by producing excitable gaps. Reexcitation of these gaps through progressive increase in shock strength may provide the basis for the lower and upper limits of vulnerability. The former may correspond to the origination of slow wavefronts of reexcitation and phase singularities. The latter corresponds to fast conduction during which wavebreaks no longer produce sustained arrhythmias.