Li Li, Nikolski Vladimir, Efimov Igor R
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106-7207, USA.
J Cardiovasc Electrophysiol. 2003 Oct;14(10 Suppl):S237-48. doi: 10.1046/j.1540.8167.90316.x.
Lidocaine is known to increase the defibrillation threshold (DFT) of monophasic shocks (MS) and have no effect on DFT of biphasic shocks (BS). The aim of this study was to enhance our understanding of the mechanisms of vulnerability and defibrillation through the investigation of this difference.
We studied the effect of 15 microM lidocaine on shock-induced vulnerability using fluorescent imaging of Langendorff-perfused rabbit hearts. Vulnerability was assessed as vulnerable window with shock strengths of 15 to 150 V and vulnerable period (VP) with shock delivery phase of 0% to 100% of action potential duration (% APD). With MS, lidocaine caused a significant increase in both the upper limit of vulnerability (ULV, 71 +/- 17 V vs 120 +/- 1.5 V, P < 0.01) and upper limit of VP (91 +/- 8.0% APD vs 110 +/- 4.2% APD, P < 0.01). With BS, lidocaine had no effect on ULV (40 +/- 3.4 V vs 45 +/- 4.5 V) and did not increase the upper limit of VP (78 +/- 8.9% APD vs 96 +/- 12% APD, P < 0.01). Lidocaine caused reduction of the conduction velocity during pacing (0.58 +/- 0.08 m/s vs 0.44 +/- 0.05 m/s, P < 0.01), shock-induced break excitation (0.82 +/- 0.17 m/s vs 0.30 +/- 0.07 m/s, P < 0.01), and postshock reentry (0.34 +/- 0.07 m/s vs 0.19 +/- 0.08 m/s, P < 0.01). Lidocaine had no effect on shock-induced virtual electrode polarization.
Lidocaine increased MS ULV due to slowing of shock-induced break-excitation wavefronts, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no effect on BS ULV because no break excitation was induced by BS. Reduction of conduction velocity by lidocaine resulted in increased dispersion of repolarization and led to upper limit of VP increase for both MS and BS.
已知利多卡因会增加单相电击（MS）的除颤阈值（DFT），而对双相电击（BS）的DFT没有影响。本研究的目的是通过对这一差异的研究，加深我们对易损性和除颤机制的理解。
我们使用Langendorff灌注兔心脏的荧光成像技术，研究了15微摩尔利多卡因对电击诱导易损性的影响。易损性通过15至150伏电击强度下的易损窗口以及动作电位持续时间（%APD）的0%至100%电击发放阶段的易损期（VP）来评估。对于MS，利多卡因使易损性上限（ULV，71±17伏对120±1.5伏，P<0.01）和VP上限（91±8.0%APD对110±4.2%APD，P<0.01）均显著增加。对于BS，利多卡因对ULV没有影响（40±3.4伏对45±4.5伏），且未增加VP上限（78±8.9%APD对96±12%APD，P<0.01）。利多卡因导致起搏期间传导速度降低（0.58±0.08米/秒对0.44±0.05米/秒，P<0.01）、电击诱导的破裂兴奋（0.82±0.17米/秒对0.30±0.07米/秒，P<0.01）以及电击后折返（0.34±0.07米/秒对0.19±0.08米/秒，P<0.01）。利多卡因对电击诱导的虚拟电极极化没有影响。
利多卡因增加MS的ULV是由于电击诱导的破裂兴奋波前减慢，这导致虚拟电极诱导的相位奇点存活概率增加。利多卡因对BS的ULV没有影响，因为BS不会诱导破裂兴奋。利多卡因导致的传导速度降低导致复极离散增加，并导致MS和BS的VP上限均增加。
