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交流泄漏电流导致完全血流动力学崩溃而不诱发颤动的机制。

Mechanisms by which AC leakage currents cause complete hemodynamic collapse without inducing fibrillation.

作者信息

Malkin R A, Hoffmeister B K

机构信息

Joint Program in Biomedical Engineering at The University of Memphis and The University of Tennessee-Memphis, 38152-3210, USA.

出版信息

J Cardiovasc Electrophysiol. 2001 Oct;12(10):1154-61. doi: 10.1046/j.1540-8167.2001.01154.x.

DOI:10.1046/j.1540-8167.2001.01154.x
PMID:11699524
Abstract

INTRODUCTION

The first study of weak alternating current (AC) stimulation in closed chest humans showed that complete hemodynamic collapse can occur below the threshold for inducing ventricular fibrillation (VF), a heretofore unknown danger to patients. This article, and the accompanying simulation article, explore the mechanisms responsible for the collapse.

METHODS AND RESULTS

A quadripolar pacing catheter was placed in the right ventricle (RV) of six dogs. The tip of the catheter (17 mm2) carried 5 seconds of AC stimulation ranging from 10 to 160 Hz and 10 to 1,000 microA. The lead II body surface ECG, femoral artery pressure, and a bipole from the proximal pair of electrodes on the RV catheter were recorded 2 seconds before, during, and 2 seconds after stimulation. Based on the blood pressure, every episode was categorized as VF, COLLAPSE without VF, extrasystolic without COLLAPSE (EFFECT), or having caused no effect (NSR). The electrical activation interval (interspike interval [ISI]) from the RV bipole was compared with the mechanical activation interval, determined from M-mode ultrasound. COLLAPSE is associated with a short ISI (NSR = 408+/-110 msec; EFFECT = 305+/-113 msec; COLLAPSE = 179+/-25 msec; P < 0.001) with a high degree of regularity (P < 0.001): coefficient of variation of ISI for COLLAPSE (0.038+/-0.069) versus VF (0.389+/-0.222), EFFECT (0.420+/-0.241), and NSR (0.016+/-0.048). Electrical activation and mechanical activation rates occurred at integer multiples of the AC stimulation period.

CONCLUSION

COLLAPSE (86+/-37 microA; minimum 50 microA in two animals) occurs below the VF threshold (108+/-28 microA) by causing rapid, regular excitation.

摘要

引言

首次针对闭胸人体进行的弱交流电(AC)刺激研究表明,在诱发心室颤动(VF)的阈值以下可能会发生完全血流动力学崩溃,这是此前未被认识到的对患者的危险。本文以及随附的模拟文章探讨了导致崩溃的机制。

方法与结果

将四极起搏导管置于6只犬的右心室(RV)中。导管尖端(17平方毫米)进行5秒的AC刺激,频率范围为10至160赫兹,电流为10至1000微安。在刺激前2秒、刺激期间和刺激后2秒记录标准肢体导联II体表心电图、股动脉压力以及RV导管近端一对电极的双极信号。根据血压,将每一次发作分类为VF、无VF的崩溃(COLLAPSE)、无崩溃的期外收缩(EFFECT)或无影响(NSR)。将来自RV双极的电激活间隔(峰间间隔[ISI])与通过M型超声确定的机械激活间隔进行比较。COLLAPSE与短ISI相关(NSR = 408±110毫秒;EFFECT = 305±113毫秒;COLLAPSE = 179±25毫秒;P < 0.001),且具有高度规律性(P < 0.001):COLLAPSE的ISI变异系数(0.038±0.069)与VF(0.389±0.222)、EFFECT(0.420±0.241)和NSR(0.016±0.048)相比。电激活和机械激活速率以AC刺激周期的整数倍发生。

结论

COLLAPSE(86±37微安;两只动物中最低为50微安)通过引起快速、规则的兴奋发生在VF阈值(108±28微安)以下。

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