Sessler D I, Rubinstein E H, Moayeri A
Department of Anesthesia, University of California, San Francisco 94143-0648.
Anesthesiology. 1991 Oct;75(4):594-610. doi: 10.1097/00000542-199110000-00009.
To evaluate physiologic responses to mild perianesthetic hypothermia, we measured tympanic membrane and skin-surface temperatures, peripheral vasoconstriction, thermal comfort, and muscular activity in nine healthy male volunteers. Each volunteer participated on three separate days: 1) normothermic isoflurane anesthesia; 2) hypothermic isoflurane anesthesia (1.5 degrees C decrease in central temperature); and 3) hypothermia alone (1.5 degrees C decrease in central temperature) induced by iced saline infusion. Involuntary postanesthetic muscular activity was considered thermoregulatory when preceded by central hypothermia and peripheral cutaneous vasoconstriction. Tremor was considered normal shivering when electromyographic patterns matched those produced by cold exposure in unanesthetized individuals. During postanesthetic recovery, central temperatures in hypothermic volunteers increased rapidly when residual end-tidal isoflurane concentrations were less than or equal to 0.3% but remained 0.5 degree C less than control values throughout 2 h of recovery. All volunteers were vasodilated during isoflurane administration. Peripheral vasoconstriction occurred only during recovery from hypothermic anesthesia, at end-tidal isoflurane concentrations of less than approximately 0.4%. Spontaneous tremor was always preceded by central hypothermia and peripheral vasoconstriction, indicating that muscular activity was thermoregulatory. Maximum tremor intensity during recovery from hypothermic anesthesia occurred when residual end-tidal isoflurane concentrations were less than or equal to 0.4%. Three patterns of postanesthetic muscular activity were identified. The first was a tonic stiffening that occurred in some normothermic and hypothermic volunteers when end-tidal isoflurane concentrations were approximately 0.4-0.2%. This activity appeared to be largely a direct, non-temperature-dependent effect of isoflurane anesthesia. In conjunction with lower residual anesthetic concentrations, stiffening was followed by a synchronous, tonic waxing-and-waning pattern and spontaneous electromyographic clonus, both of which were thermoregulatory. Tonic waxing-and-waning was by far the most common pattern and resembled that produced by cold-induced shivering in unanesthetized volunteers; it appears to be thermoregulatory shivering triggered by hypothermia. Spontaneous clonus resembled flexion-induced clonus and pathologic clonus and did not occur during hypothermia alone; it may represent abnormal shivering or an anesthetic-induced modification of normal shivering. We conclude that among the three patterns of muscular activity, only the synchronous, tonic waxing-and-waning pattern can be attributed to normal thermoregulatory shivering.
为评估围麻醉期轻度低温的生理反应，我们测量了9名健康男性志愿者的鼓膜温度、皮肤表面温度、外周血管收缩、热舒适度和肌肉活动。每位志愿者在三个不同日期参与实验：1）正常体温下的异氟烷麻醉；2）低温异氟烷麻醉（中心温度降低1.5℃）；3）通过输注冰盐水诱导单独低温（中心温度降低1.5℃）。当麻醉后非自主肌肉活动之前出现中心体温过低和外周皮肤血管收缩时，被认为是体温调节性的。当肌电图模式与未麻醉个体冷暴露产生的模式相匹配时，震颤被认为是正常寒战。在麻醉后恢复期间，低温志愿者的中心体温在呼气末异氟烷残留浓度小于或等于0.3%时迅速升高，但在整个2小时的恢复过程中仍比对照值低0.5℃。所有志愿者在异氟烷给药期间血管扩张。外周血管收缩仅在低温麻醉恢复期间出现，呼气末异氟烷浓度小于约0.4%时发生。自发震颤总是先于中心体温过低和外周血管收缩，表明肌肉活动是体温调节性的。低温麻醉恢复期间最大震颤强度出现在呼气末异氟烷残留浓度小于或等于0.4%时。识别出三种麻醉后肌肉活动模式。第一种是强直性僵硬，在一些正常体温和低温志愿者中，当呼气末异氟烷浓度约为0.4 - 0.2%时出现。这种活动似乎主要是异氟烷麻醉的直接、非温度依赖性效应。随着残留麻醉浓度降低，僵硬之后是同步的、强直性的强弱交替模式和自发肌电图阵挛，两者均为体温调节性的。强直性强弱交替是迄今为止最常见的模式，类似于未麻醉志愿者冷诱导寒战产生的模式；它似乎是由低温触发的体温调节性寒战。自发阵挛类似于屈曲诱导阵挛和病理性阵挛，且仅在单独低温期间不出现；它可能代表异常寒战或麻醉诱导的正常寒战改变。我们得出结论，在这三种肌肉活动模式中，只有同步的、强直性的强弱交替模式可归因于正常的体温调节性寒战。
