Sessler D I, McGuire J, Moayeri A, Hynson J
Department of Anesthesia, University of California, San Francisco 94143-0648.
Anesthesiology. 1991 Feb;74(2):226-32. doi: 10.1097/00000542-199102000-00006.
Central body temperature, which usually is well controlled, typically decreases more than 1 degree C during the 1st h of general anesthesia. This hypothermia has been attributed partially to an anesthetic-induced peripheral vasodilation, which increases cutaneous heat loss to the environment. Based on the specific heat of humans, heat loss would have to increase more than 70 W for 1 h (in a 70-kg person) to explain hypothermia after induction of general anesthesia. However, during epidural anesthesia, sympathetic blockade increases heat loss only slightly. Furthermore, thermoregulatory vasoconstriction in unanesthetized humans decreases heat loss to the environment only 15 W. Therefore, we tested the hypothesis that the hypothermia that follows induction of general anesthesia does not result from increased cutaneous heat loss. Heat loss and skin-surface and tympanic membrane temperatures, before and after induction of isoflurane anesthesia, were measured in five minimally clothed volunteers. Peripheral skin blood flow was evaluated with venous-occlusion volume plethysmography and skin-surface temperature gradients. Cutaneous heat losses in watts were summed from ten area-weighted thermal flux transducers. Tympanic membrane temperature, which was stable during the 30-min control period preceding induction, decreased 1.2 +/- 0.2 degrees C in the 50 min after induction. Isoflurane anesthesia decreased mean arterial blood pressure approximately 20%. Average skin-surface temperature increased over 15 min to 0.5 degree C above control. Heat loss from the trunk, head, arms, and legs decreased slightly, whereas loss from the hands and feet (10.5% of the body surface area) doubled (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
核心体温通常受到良好控制,但在全身麻醉的第1小时内,体温通常会下降超过1摄氏度。这种体温过低部分归因于麻醉诱导的外周血管扩张,这会增加皮肤向环境的热量散失。根据人体的比热,要解释全身麻醉诱导后的体温过低,1小时内(70千克体重的人)热量散失必须增加超过70瓦。然而,在硬膜外麻醉期间,交感神经阻滞只会轻微增加热量散失。此外,未麻醉的人体体温调节性血管收缩只会使向环境的热量散失减少15瓦。因此,我们检验了这样一个假设,即全身麻醉诱导后的体温过低并非由皮肤热量散失增加所致。在五名穿着极少衣物的志愿者身上,测量了异氟烷麻醉诱导前后的热量散失、皮肤表面温度和鼓膜温度。通过静脉阻塞容积描记法和皮肤表面温度梯度评估外周皮肤血流量。用十个面积加权热通量传感器计算以瓦为单位的皮肤热量散失。鼓膜温度在诱导前30分钟的对照期内保持稳定,诱导后50分钟下降了1.2±0.2摄氏度。异氟烷麻醉使平均动脉血压降低了约20%。平均皮肤表面温度在15分钟内升高至比对照高0.5摄氏度。躯干、头部、手臂和腿部的热量散失略有下降,而手部和脚部(占体表面积的10.5%)的热量散失增加了一倍(P<0.01)。(摘要截选至250字)