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急性肺栓塞期间出现交替性右束支传导阻滞。

Right bundle branch block on alternate beats during acute pulmonary embolism.

作者信息

Shinde Rituparna S, Carbone Vincenzo, Shinde Suresh N, Oreto Giuseppe

机构信息

Ruby Hall Clinic, Shinde Clinic, Pune, India.

出版信息

Ann Noninvasive Electrocardiol. 2011 Jul;16(3):311-4. doi: 10.1111/j.1542-474X.2011.00434.x.

Abstract

The electrocardiogram of a patient with acute pulmonary embolism showed right bundle branch block (RBBB) on alternate beats; following thrombolysis, the pattern evolved to persistent RBBB and eventually to normal conduction. Analysis of serial tracings suggested that the mechanism of RBBB alternans was tachycardia-dependent bidirectional bundle branch block, caused by prolongation of both anterograde and retrograde refractory periods (RPs) of the right bundle branch (RBB). The sinus impulse found the RBB refractory, and was conducted over the left bundle branch only, depolarizing the left ventricle and then attempting to penetrate retrogradely the RBB; at that time, however, the RBB was still refractory. When a QRS complex had a RBBB configuration, therefore, the RBB was not depolarized; the ensuing sinus impulse found the RBB fully responsive as a consequence of the long period intervening between two successive depolarizations, and resulted in normal intraventricular conduction. With right ventricular afterload decrease, the recovery of RBB anterograde and retrograde excitability was asynchronous, since the retrograde RP became normal earlier than the anterograde one. In accordance with the relatively short retrograde RP, the RBB was retrogradely invaded by the transseptal impulse coming from the left ventricle; this "shifted to the right" the anterograde RP of the RBB. The RBB, thus, was still refractory to the next sinus impulse, and RBBB again occurred; the RBB, thus, was once more depolarized retrogradely, and this led to perpetuation of RBBB. Finally, intraventricular conduction became normal owing to full normalization of RBB anterograde and retrograde refractoriness.

摘要

一名急性肺栓塞患者的心电图显示交替出现右束支传导阻滞(RBBB);溶栓治疗后,这种模式演变为持续性RBBB,最终传导恢复正常。对系列心电图的分析表明,RBBB交替的机制是心动过速依赖性双向束支传导阻滞,由右束支(RBB)的前向和逆向不应期(RP)延长所致。窦性冲动发现RBB处于不应期,仅通过左束支传导,使左心室 depolarizing,然后试图逆向穿透RBB;然而,此时RBB仍处于不应期。因此,当QRS波群呈RBBB形态时,RBB未 depolarized;随后的窦性冲动发现RBB由于两次连续 depolarizations之间的长时间间隔而完全有反应,导致室内传导正常。随着右心室后负荷降低,RBB前向和逆向兴奋性的恢复不同步,因为逆向RP比前向RP更早恢复正常。根据相对较短的逆向RP,RBB被来自左心室的经间隔冲动逆向侵入;这使RBB的前向RP“右移”。因此,RBB对下一个窦性冲动仍处于不应期,再次出现RBBB;RBB再次被逆向 depolarized,这导致RBBB持续存在。最后,由于RBB前向和逆向不应期完全恢复正常,室内传导恢复正常。

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本文引用的文献

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Bundle branch block on alternate beats: by what mechanism?交替性束支阻滞:通过何种机制?
J Electrocardiol. 2002 Apr;35(2):147-52. doi: 10.1054/jelc.2002.32337.
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