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利多卡因对人体希氏-浦肯野系统内折返的影响。

The effect of lidocaine on reentry within the His-Purkinje system in man.

作者信息

Ruskin J N, Akhtar M, Damato A N, Foster J R

出版信息

Circulation. 1980 Aug;62(2):388-400. doi: 10.1161/01.cir.62.2.388.

Abstract

The effects of intravenous lidocaine were assessed in 11 patients with normal intraventricular conduction in whom reentry within the His-Purkinje system (RE-HPS) occurred consistently over a narrow range of ventricular (S1S2) coupling intervals. RE-HPS was characterized by a spontaneous beat (V3) inducible by critically timed premature stimuli (S2) during constant ventricular drive (S1S1), and was dependent upon critical retrograde conduction delay within the HPS (S2H2 interval). Lidocaine abolished RE-HPS in six of 11 patients (group 1) and shortened the zone of RE-HPS in five of 11 patients (group 2). In group 1 after lidocaine, critical S2H2 intervals for RE-HPS were not attained at any S1S2 in four patients and critical S2H2 intervals were equaled but not exceeded in two patients without resulting in RE-HPS. In group 2 after lidocaine. RE-HPS was present in all patients at S2H2 intervals comparable to control values; however, significantly closer S1S2 intervals were necessary to achieve these requisite S2H2 delays (p < 0.005). The longest S2H2 intervals at comparable S1S2 intervals were significantly shortened by lidocaine in 11 of 11 patients (p < 0.001). Thus, lidocaine causes a significant decrease in retrograde refractoriness within the HPS in patients with normal intraventricular conduction.

摘要

对11名室内传导正常的患者进行了静脉注射利多卡因的效果评估,这些患者在希氏-浦肯野系统(RE-HPS)内的折返在较窄的心室(S1S2)耦合间期范围内持续发生。RE-HPS的特征是在恒定心室驱动(S1S1)期间,由临界定时的早搏刺激(S2)诱发的自发搏动(V3),并且依赖于希氏-浦肯野系统内的临界逆行传导延迟(S2H2间期)。利多卡因使11名患者中的6名(第1组)的RE-HPS消失,并使11名患者中的5名(第2组)的RE-HPS区域缩短。在第1组中,利多卡因注射后,4名患者在任何S1S2时均未达到RE-HPS的临界S2H2间期,2名患者的临界S2H2间期相等但未超过,未导致RE-HPS。在第2组中,利多卡因注射后,所有患者在与对照值相当的S2H2间期时均存在RE-HPS;然而,需要显著更短的S1S2间期才能达到这些必要的S2H2延迟(p<0.005)。在11名患者中的11名患者中,利多卡因使在相当的S1S2间期时最长的S2H2间期显著缩短(p<0.001)。因此,利多卡因可使室内传导正常的患者希氏-浦肯野系统内的逆行不应期显著降低。

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