Takata Kotaro, Adachi Yushi U, Suzuki Katsumi, Obata Yukako, Sato Shigehito, Nishiwaki Kimitoshi
Department of Anesthesia, Japanese Red Cross Hamamatsu Hospital, Hamamatsu, Shizuoka, 4348533, Japan.
J Anesth. 2014 Feb;28(1):116-20. doi: 10.1007/s00540-013-1676-7. Epub 2013 Aug 16.
Sinus bradycardia is a well-known consequence of stimulation of presynaptic α2 adrenergic receptors due the adminstration of dexmedetomidine. One of the most serious adverse effects of dexmedetomidine is cardiac arrest. Some cases demonstrating such an arrest due to the indiscriminate use of this drug were recently reported. We continuously administered dexmedetomidine to a 56-year-old male patient at a rate of 0.3 μg/kg/h (lower than the recommended dose) without initial dosing for sedation in an intensive care unit. The patient had undergone open cardiac surgery and atrial pacing was maintained at a fixed rate, 90/min. The PQ interval in electrocardiography gradually prolonged during the infusion; finally, complete atrioventricular block and subsequent cardiac arrest occurred. Immediate cardiopulmonary resuscitation was carried out, including re-intubation, and recovery of spontaneous circulation was attained 15 min after the event. The patient was discharged from hospital on the 25th postoperative day without any neurological complications.
窦性心动过缓是由于使用右美托咪定刺激突触前α2肾上腺素能受体而产生的一种众所周知的后果。右美托咪定最严重的不良反应之一是心脏骤停。最近有报道称,一些因滥用该药物而导致心脏骤停的病例。在重症监护病房,我们以0.3μg/kg/h的速率(低于推荐剂量)持续给一名56岁男性患者输注右美托咪定,未进行初始镇静给药。该患者接受了心脏直视手术,心房起搏以固定频率90次/分钟维持。输注过程中,心电图的PQ间期逐渐延长;最终,发生了完全性房室传导阻滞及随后的心脏骤停。立即进行了心肺复苏,包括重新插管,事件发生15分钟后恢复了自主循环。患者术后第25天出院,无任何神经并发症。