Das G, Talmers F N, Weissler A M
Am J Cardiol. 1975 Sep;36(3):281-5. doi: 10.1016/0002-9149(75)90476-2.
Previous observations of slowing of the heart rate after administration of atropine in doses smaller than 0.4 mg and recent reports of development of rhythm disorders in patients with acute myocardial infarction given atropine prompted us to evaluate systematically the effects of various doses of atropine (0.1 to 0.8 mg) on the response of the sinoatrial (S-A) and atrioventricular (A-V) nodes in healthy volunteers. The response of the S-A node to atropine was characteristically bimodal, slowing at smaller doses and accelerating at larger doses. In contrast, the A-V node showed acceleration of conduction in response to all doses of atropine used. A hypothesis based on current understanding of the electrophysiologic parameters governing impulse formation and impulse conduction is advanced to explain the apparent paradox in the S-A and A-V nodal responses to small doses of atropine. The results suggest the need for caution and continuous rhythm monitoring when giving atropine to patients with acute myocardial infarction.
先前观察到给予小于0.4毫克剂量的阿托品后心率减慢,以及近期有报道称急性心肌梗死患者使用阿托品后出现心律失常,这促使我们系统评估不同剂量(0.1至0.8毫克)的阿托品对健康志愿者窦房结和房室结反应的影响。窦房结对阿托品的反应具有典型的双峰性,小剂量时减慢,大剂量时加速。相比之下,房室结对所用的所有剂量阿托品均表现出传导加速。基于目前对控制冲动形成和冲动传导的电生理参数的理解,提出了一个假设来解释窦房结和房室结对小剂量阿托品反应中明显的矛盾现象。结果表明,给急性心肌梗死患者使用阿托品时需要谨慎并持续进行心律监测。