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由于室内传导缺陷导致按需起搏器感知功能缺失。

Lack of sensing by demand pacemakers due to intraventricular conduction defects.

作者信息

Vera Z, Mason D T, Awan N A, Hiliard G, Massumi R A

出版信息

Circulation. 1975 May;51(5):815-22. doi: 10.1161/01.cir.51.5.815.

Abstract

A previously unrecognized form of failure of normally functioning noncompetitive R-inhibited or R-triggered pacemakers to sense is described in 30 patients. The failure was produced by the delayed arrival of ventricular depolarization due to intraventricular conduction disturbances at the site of pacemaker sensing electrodes. These patinets with late activation of the right ventricle exhibited right bundle branch block (RBBB) during conducted sinus beats or had ectopic beats arising from the left ventricle. In both these situations, several late occurring QRS complexes were not sensed by the pacemaker electrodes in the right ventricular apex (RVA) and thereby the R-inhibited pacemaker spike discharged into the initial portion of the QRS complex. Activation of the RVA was delayed up to 65 msec in sinus beats with RBBB and even longer in premature beats arising from the left ventricle. The depolarization front of such beats reached the myocardium around the right ventricular pacemaker electrodes late in the QRS and thereby were not sensed up to 65 msec after the QRS onset as seen on the surface electrocardiogram (ECG). It was found in this study that if the inscription of such QRS complexes began up to 65 msec before the next due pacemaker impulse, these complexes were not sensed, allowing discharge of normally functioning R-inhibited pacemakers within the QRS which mimicked pacemaker malfunction. Failure to sense due to this phenomenon was observed in patients with noncompetitive pacemakers, both R-inhibited and R-triggered; temporary and permanent; with unipolar as well as bipolar electrodes. Similarly, patients with left ventricular epicardial electrodes and left bundle branch block in sinus beats also exhibited this phenomenon. Complete evaluation proved that pacemaker function was normal in the entire patient group. Recognition that failure to sense was the result of intraventricular conduction disorder prevented the untimely replacement of the pulse generator. This phenomenon of nonsensing by noncompetitive pacemakers should be considered in the presence of wide QRS complexes before the pacemaker is concluded to be malfunctioning.

摘要

在30例患者中描述了一种先前未被认识的正常功能的非竞争性R抑制或R触发起搏器感知失败的形式。这种失败是由于心室传导障碍导致心室去极化延迟到达起搏器感知电极部位所致。这些右心室晚期激活的患者在窦性传导搏动期间表现为右束支传导阻滞(RBBB),或有源于左心室的异位搏动。在这两种情况下,右心室心尖部(RVA)的起搏器电极未感知到几个晚发的QRS波群,从而使R抑制型起搏器的脉冲发放到QRS波群的起始部分。在伴有RBBB的窦性搏动中,RVA的激活延迟长达65毫秒,在源于左心室的早搏中延迟更长。此类搏动的去极化波在QRS波群晚期到达右心室起搏器电极周围的心肌,因此在体表心电图(ECG)上,在QRS波群起始后长达65毫秒都未被感知到。在本研究中发现,如果此类QRS波群的记录在下次预期的起搏器脉冲之前65毫秒内开始,则这些波群未被感知,从而使正常功能的R抑制型起搏器在QRS波群内发放脉冲,这模拟了起搏器故障。在非竞争性起搏器患者中,无论是R抑制型还是R触发型;临时和永久性的;单极和双极电极的患者,均观察到由于这种现象导致的感知失败。同样,窦性搏动时伴有左心室心外膜电极和左束支传导阻滞的患者也表现出这种现象。全面评估证明整个患者组的起搏器功能正常。认识到感知失败是室内传导障碍的结果,避免了过早更换脉冲发生器。在判定起搏器故障之前,当出现宽QRS波群时,应考虑非竞争性起搏器的这种无感知现象。

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