Szatmáry L J
Eur Heart J. 1984 Aug;5(8):637-48. doi: 10.1093/oxfordjournals.eurheartj.a061720.
Autonomic blockade is commonly employed as a test of sinus node dysfunction. We compared primary and secondary atrial postpacing pauses and postextrasystolic sino-atrial responses before and after autonomic blockade in 56 patients with the clinical diagnosis of sick sinus syndrome. Pharmacological autonomic blockade was achieved by atropine 0.04 mg kg-1 and propranolol 0.2 mg kg-1, i.v. In a group of patients with a normal intrinsic heart rate the number of positive electrophysiologic variables associated with sinus node dysfunction declined after autonomic blockade. In 91% of these patients, sinus node function was characterized by a normal intrinsic recovery time, gradual exponential return to the constant sinus cycle length, and biphasic postextrasystolic return responses. Three patients in this group had intrinsic SA-block revealed by atrial pacing and verified by Holter monitoring. Besides normal intrinsic pacemaker properties in 53% of patients, rhythm monitoring revealed severe sinus node dysfunction as manifested by bradycardia and the tachycardia-bradycardia syndrome. SA-block and sinus arrest up to 29120 ms. In the abnormal intrinsic heart rate group, disturbed intrinsic rhythmicity was characterized in all by a prolonged corrected intrinsic recovery time (2320 +/- 2740 ms [+/- SD]), arrhythmia and/or bradycardia in the secondary postpacing cycles, chaotic postextrasystolic patterns, or prolonged sinoatrial conduction times. Significantly slow minimal heart rates during sleep significantly prolonged average sinus cycle lengths and positive ECGs for sinoatrial disorders in the waking period were present on the 24-h rhythm recording. It is concluded that intrinsic heart rate obtained by autonomic blockade is the best and most simple method for the diagnosis of intrinsic sinus node dysfunction. Combined autonomic blockade and electrophysiological tests can be of great value in unmasking the severity and degree of intrinsic dysfunction and analyzing the abnormality of secondary pacemaker function. These investigations, however, are rather insensitive and therefore ineffective in detecting autonomic sinus node dysfunction. To assess the role and significance of the autonomous neurovegetative tone in the genesis of sinoatrial disorders, rhythm monitoring is required.
自主神经阻滞常用于窦房结功能障碍的检测。我们比较了56例临床诊断为病态窦房结综合征患者在自主神经阻滞前后的原发性和继发性房性起搏后间歇以及早搏后窦房反应。通过静脉注射0.04mg/kg阿托品和0.2mg/kg普萘洛尔实现药理学自主神经阻滞。在一组固有心率正常的患者中,自主神经阻滞后与窦房结功能障碍相关的阳性电生理变量数量减少。在这些患者中,91%的窦房结功能表现为固有恢复时间正常、逐渐指数性恢复到恒定的窦性周期长度以及早搏后双相恢复反应。该组中有3例患者通过心房起搏揭示并经动态心电图监测证实存在固有窦房阻滞。除了53%的患者具有正常的固有起搏器特性外,节律监测显示严重的窦房结功能障碍,表现为心动过缓和心动过速 - 心动过缓综合征。窦房阻滞和窦性停搏长达29120毫秒。在固有心率异常组中,所有患者的固有节律紊乱表现为校正后的固有恢复时间延长(2320±2740毫秒[±标准差])、继发性起搏周期中的心律失常和/或心动过缓、早搏后混乱模式或窦房传导时间延长。睡眠期间显著缓慢的最低心率显著延长了平均窦性周期长度,24小时节律记录显示清醒期存在窦房紊乱的阳性心电图。结论是,通过自主神经阻滞获得的固有心率是诊断固有窦房结功能障碍的最佳且最简单的方法。联合自主神经阻滞和电生理检查对于揭示固有功能障碍的严重程度和分析次级起搏器功能异常具有重要价值。然而,这些检查对检测自主神经源性窦房结功能障碍相当不敏感,因此无效。为了评估自主神经张力在窦房紊乱发生中的作用和意义,需要进行节律监测。