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本文报告三例窦房结病变患者注射较大剂量(≥1mg)阿托品后,分别出现窦房结恢复时间的相反延长,长达8.94秒的窦性停搏以及非阵发性交界性心动过速等窦房结功能障碍的表现。推测其发生机制可能为:1、阿托品改善窦房传导,增加窦房结内除极化而引起窦房结功能的抑制;2.阿托品在血浆药物浓度较低时,表现为拟副交感神经效应;3.阿托品在抑制病变的窦房结的同时,兴奋下级起搏点。本文提示较大剂量阿托品注射可以引起窦房结功能障碍。
This article reports three cases of sinus node lesions in patients with larger doses (≥ 1mg) atropine, respectively, the opposite extension of the sinus node recovery time, as long as 8.94 seconds sinus arrest and non-paroxysmal borderline tachycardia Such as sinus node dysfunction performance. Presumably, its mechanism may be: 1, atropine to improve sinoatrial conduction, increased sinus node depolarization caused sinus node function inhibition; 2. atropine in the plasma drug concentration is low, the performance of the parasympathetic effect; 3. Atropine in the suppression of lesions of the sinus node at the same time, excited subordinate pacemaker. This article suggests that larger doses of atropine injection can cause sinus node dysfunction.