Goldberg M E, Torjman M, Bartkowski R R, Mora C T, Boerner T, Seltzer J L
Department of Anesthesiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107.
Anesth Analg. 1992 Dec;75(6):965-71. doi: 10.1213/00000539-199212000-00015.
Postoperative respiratory depression after alfentanil administration has been described in several case reports. The effects of a prolonged alfentanil infusion on the CO2 response curve or cognitive function have not been studied. Twenty-one ASA physical status I or II patients were studied after a prolonged alfentanil infusion (> 90 min) to determine the incidence of postoperative respiratory depression, arterial O2 desaturation, and impairment of cognitive function. Each patient's recovery was observed at 30-min intervals for evidence of respiratory depression (utilizing the Read CO2 rebreathing method), desaturation by pulse oximetry (severe desaturation defined as arterial O2 saturation < 90%), and cognitive function (utilizing Trieger dot and digit substitution tests). Plasma samples were also examined for secondary elevations in alfentanil plasma concentrations. Significant depression of the CO2 response curve and cognitive function was found up to 1 h postoperatively. Arterial O2 desaturation was seen in 11 of 21 patients (52%). No correlation was found between arterial O2 desaturation and cognitive function scores or CO2 rebreathing results. Increased depression of the CO2 response curve was not necessarily associated with severe desaturation episodes. A secondary increase in plasma alfentanil concentration was detected in 5 of the 21 patients (24%), but these patients did not experience further depression of the CO2 response curve. We conclude that prolonged alfentanil administration may result in severe arterial O2 desaturation with significant depression of the hypercapnic respiratory drive during the first hour in the postanesthesia care unit, even though the majority of our patients were easily aroused in response to verbal stimuli.
多篇病例报告描述了使用阿芬太尼后出现的术后呼吸抑制情况。但尚未研究过长时间输注阿芬太尼对二氧化碳反应曲线或认知功能的影响。对21例美国麻醉医师协会（ASA）身体状况为I级或II级的患者在长时间输注阿芬太尼（>90分钟）后进行了研究，以确定术后呼吸抑制、动脉血氧饱和度降低和认知功能损害的发生率。每隔30分钟观察每位患者的恢复情况，以寻找呼吸抑制（采用Read二氧化碳重复呼吸法）、脉搏血氧饱和度测定的血氧饱和度降低（严重血氧饱和度降低定义为动脉血氧饱和度<90%）以及认知功能（采用特里格点和数字替代测试）的证据。还检测了血浆样本中阿芬太尼血浆浓度的二次升高情况。术后长达1小时发现二氧化碳反应曲线和认知功能有显著抑制。21例患者中有11例（52%）出现动脉血氧饱和度降低。未发现动脉血氧饱和度降低与认知功能评分或二氧化碳重复呼吸结果之间存在相关性。二氧化碳反应曲线抑制增加不一定与严重血氧饱和度降低发作相关。21例患者中有5例（24%）检测到血浆阿芬太尼浓度二次升高，但这些患者的二氧化碳反应曲线未进一步受到抑制。我们得出结论，即使我们的大多数患者在受到言语刺激后很容易被唤醒，但在麻醉后护理单元的第一个小时内，长时间输注阿芬太尼可能会导致严重的动脉血氧饱和度降低，并伴有高碳酸血症呼吸驱动的显著抑制。
