Hynson J M, Sessler D I, Moayeri A, McGuire J, Schroeder M
Department of Anesthesia, University of California, School of Medicine, San Francisco 94143-0648.
Anesthesiology. 1993 Aug;79(2):219-28, discussion 21A-22A. doi: 10.1097/00000542-199308000-00005.
Core temperature decreases rapidly after induction of anesthesia, largely because heat is redistributed to peripheral tissues. The hypothesis that warming peripheral tissues before induction of general anesthesia (prewarming) minimizes hypothermia was tested. Because circulating blood volume may be greater during exposure to heat compared to cold, the hypothesis that prewarming decreases the amount of hypotension associated with induction of anesthesia was tested also. Finally, the hypothesis that the difference between direct radial arterial blood pressure and blood pressure measured oscillometrically at the brachial artery depends on thermoregulatory and anesthetic conditions was tested.
Each of six volunteers underwent general anesthesia (propofol and nitrous oxide) twice on the same day. Each anesthetic lasted 1 h and was preceded by either 2 h of active warming with forced air or 2 h of passive cooling by exposure to a typical operating room environment. After induction of each anesthetic, volunteers were fully exposed to the ambient environment. Volunteers recovered for 2 h before starting the second preinduction treatment.
Initial tympanic membrane temperatures were similar before each preinduction treatment: 36.7 +/- 0.4 degrees C when volunteers were not warmed and 36.7 +/- 0.6 degrees C when volunteers were warmed. Tympanic membrane temperature did not change during the preinduction period without warming but increased slightly (delta T = 0.4 +/- 0.2 degree C) during warming. After induction of anesthesia, core temperatures decreased to 36.1 +/- 0.4 degree C over 1 h when volunteers were prewarmed but decreased to 34.9 +/- 0.4 degrees C when they were not. Radial arterial systolic, diastolic, and mean blood pressures were lower before induction of anesthesia when volunteers were warmed compared to when no warming was given. Oscillometric diastolic and mean pressures also were lower during prewarming; however, oscillometric systolic pressure did not differ significantly. Prewarming did not result in less hypotension after induction. Without warming, the difference (radial arterial minus oscillometric) in systolic blood pressure measurements was approximately 17 mmHg. Warming was associated with a reversal of the systolic pressure difference to approximately -6 mmHg. After induction of anesthesia, the differences in systolic and mean pressure measurements became more negative with respect to the preinduction values regardless of preinduction warming treatment.
These data confirm our hypothesis that redistribution hypothermia can be minimized by preinduction warming of peripheral tissues. Prewarming decreases blood pressure but does not prevent subsequent hypotension after induction. The difference between radical arterial blood pressure and oscillometric blood pressure depends on thermoregulatory vasomotor changes but also may be influenced by vasodilation associated with administration of propofol and nitrous oxide.
麻醉诱导后核心体温迅速下降，主要是因为热量重新分布到外周组织。我们对全身麻醉诱导前对外周组织进行升温（预升温）可将体温过低降至最低这一假设进行了检验。由于与寒冷环境相比，暴露于热环境时循环血容量可能更大，我们还对预升温可减少与麻醉诱导相关的低血压量这一假设进行了检验。最后，我们对桡动脉直接血压与肱动脉示波测量血压之间的差异取决于体温调节和麻醉条件这一假设进行了检验。
6名志愿者每人在同一天接受两次全身麻醉（丙泊酚和氧化亚氮）。每次麻醉持续1小时，在麻醉前分别进行2小时的主动强制空气升温或暴露于典型手术室环境中2小时的被动降温。每次麻醉诱导后，志愿者完全暴露于环境中。志愿者在开始第二次诱导前治疗前恢复2小时。
每次诱导前治疗前初始鼓膜温度相似：未升温时为36.7±0.4℃，升温时为36.7±0.6℃。在未升温的诱导前期鼓膜温度未变化，但在升温期间略有升高（ΔT = 0.4±0.2℃）。麻醉诱导后，预升温的志愿者核心体温在1小时内降至36.1±0.4℃，而未预升温的志愿者降至34.9±0.4℃。与未升温时相比，升温的志愿者在麻醉诱导前桡动脉收缩压、舒张压和平均血压较低。示波舒张压和平均血压在预升温期间也较低；然而，示波收缩压无显著差异。预升温并未导致诱导后低血压减轻。未升温时，收缩压测量值的差异（桡动脉减去示波）约为17 mmHg。升温与收缩压差逆转至约-6 mmHg相关。麻醉诱导后，无论诱导前升温治疗如何，收缩压和平均压测量值与诱导前值相比差异变得更负。
这些数据证实了我们的假设，即通过对外周组织进行诱导前升温可将再分布性体温过低降至最低。预升温可降低血压，但不能预防诱导后随后的低血压。桡动脉血压与示波血压之间的差异取决于体温调节性血管舒缩变化，但也可能受丙泊酚和氧化亚氮给药相关的血管舒张影响。
