David D, Lang R M, Neumann A, Borow K M, Akselrod S, Mor-Avi V
University of Chicago Medical Center, Department of Medicine, IL 60637.
Am Heart J. 1990 May;119(5):1061-8. doi: 10.1016/s0002-8703(05)80235-2.
Clinical experience has shown that the antiarrhythmic effect of lidocaine on atrial arrhythmias, and specifically for the conversion of atrial fibrillation to normal sinus rhythm, is minimal. This study summarizes our experience in 30 dogs in which atrial fibrillation was initiated and sustained (greater than or equal to 15 minutes) under increased vagal tone achieved by either alpha-chloralose anesthesia (26 dogs) or pentobarbital sodium anesthesia combined with direct external electrical vagal stimulation (four dogs). Under increased vagal tone (regardless of the procedure), an intravenous bolus of lidocaine (2 to 3 mg/kg) was 100% effective (101 of 101 episodes) in pharmacologically converting atrial fibrillation to normal sinus rhythm. This was associated with marked slowing of intra-atrial electrical activity, as shown by fast Fourier analysis of intra-atrial electrograms. Over a period of 3 to 5 minutes, lidocaine progressively shifted the peak frequency content from 84 +/- 18 mV2/Hz in the 10 to 20 Hz frequency band during the pre-lidocaine phase to 110 +/- 34 mV2/Hz in the 0 to 10 Hz frequency band immediately prior to conversion to normal sinus rhythm. When atropine was administered or electrical vagal stimulation was discontinued, the conversion of atrial fibrillation to normal sinus rhythm followed a similar electrophysiologic pattern. When isoproterenol was infused, it was difficult to induce atrial fibrillation; when the arrhythmia was initiated, it could not be sustained even with concomitant electrical vagal stimulation. Thus in this model of parasympathetically sustained atrial fibrillation, lidocaine was 100% effective in converting atrial fibrillation to normal sinus rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)
临床经验表明,利多卡因对房性心律失常的抗心律失常作用极小,尤其是对于将房颤转为正常窦性心律。本研究总结了我们在30只犬中的经验,这些犬通过α-氯醛糖麻醉(26只犬)或戊巴比妥钠麻醉联合直接体外电迷走神经刺激(4只犬)使迷走神经张力增加,从而引发并维持房颤(大于或等于15分钟)。在迷走神经张力增加的情况下(无论采用何种方法),静脉推注利多卡因(2至3mg/kg)在将房颤药理学转为正常窦性心律方面100%有效(101次发作中的101次)。这与心房内电活动明显减慢有关,心房内电图的快速傅里叶分析表明了这一点。在3至5分钟的时间内,利多卡因逐渐将峰值频率成分从前利多卡因阶段10至20Hz频段的84±18mV2/Hz,转变为即将转为正常窦性心律前0至10Hz频段的110±34mV2/Hz。当给予阿托品或停止电迷走神经刺激时,房颤转为正常窦性心律遵循类似的电生理模式。当输注异丙肾上腺素时,很难诱发房颤;当引发心律失常时,即使伴有电迷走神经刺激也无法维持。因此,在这种迷走神经维持的房颤模型中,利多卡因在将房颤转为正常窦性心律方面100%有效。(摘要截短于250字)