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围手术期热平衡

Perioperative heat balance.

作者信息

Sessler D I

机构信息

Department of Anesthesia, University of California-San Francisco 94143-0648, USA.

出版信息

Anesthesiology. 2000 Feb;92(2):578-96. doi: 10.1097/00000542-200002000-00042.

Abstract

Hypothermia during general anesthesia develops with a characteristic three-phase pattern. The initial rapid reduction in core temperature after induction of anesthesia results from an internal redistribution of body heat. Redistribution results because anesthetics inhibit the tonic vasoconstriction that normally maintains a large core-to-peripheral temperature gradient. Core temperature then decreases linearly at a rate determined by the difference between heat loss and production. However, when surgical patients become sufficiently hypothermic, they again trigger thermoregulatory vasoconstriction, which restricts core-to-peripheral flow of heat. Constraint of metabolic heat, in turn, maintains a core temperature plateau (despite continued systemic heat loss) and eventually reestablishes the normal core-to-peripheral temperature gradient. Together, these mechanisms indicate that alterations in the distribution of body heat contribute more to changes in core temperature than to systemic heat imbalance in most patients. Just as with general anesthesia, redistribution of body heat is the major initial cause of hypothermia in patients administered spinal or epidural anesthesia. However, redistribution during neuraxial anesthesia is typically restricted to the legs. Consequently, redistribution decreases core temperature about half as much during major conduction anesthesia. As during general anesthesia, core temperature subsequently decreases linearly at a rate determined by the inequality between heat loss and production. The major difference, however, is that the linear hypothermia phase is not discontinued by reemergence of thermoregulatory vasoconstriction because constriction in the legs is blocked peripherally. As a result, in patients undergoing large operations with neuraxial anesthesia, there is the potential of development of serious hypothermia. Hypothermic cardiopulmonary bypass is associated with enormous changes in body heat content. Furthermore, rapid cooling and rewarming produces large core-to-peripheral, longitudinal, and radial tissue temperature gradients. Inadequate rewarming of peripheral tissues typically produces a considerable core-to-peripheral gradient at the end of bypass. Subsequently, redistribution of heat from the core to the cooler arms and legs produces an afterdrop. Afterdrop magnitude can be reduced by prolonging rewarming, pharmacologic vasodilation, or peripheral warming. Postoperative return to normothermia occurs when brain anesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2-5 h, depending on the degree of hypothermia and the age of the patient.

摘要

全身麻醉期间的体温过低呈现出典型的三个阶段模式。麻醉诱导后核心体温的最初快速下降是由于身体热量的内部重新分布。出现重新分布的原因是麻醉药抑制了通常维持较大核心体温与外周体温梯度的紧张性血管收缩。然后核心体温以由热量散失与产生之间的差异所决定的速率呈线性下降。然而,当外科手术患者体温过低到一定程度时,他们会再次触发体温调节性血管收缩,这会限制核心到外周的热量流动。代谢热的受限反过来会维持核心体温平台期(尽管全身仍在持续散热),并最终重新建立正常的核心到外周的体温梯度。这些机制共同表明,在大多数患者中,身体热量分布的改变对核心体温变化的影响大于全身热量失衡。与全身麻醉一样,身体热量的重新分布是接受脊髓或硬膜外麻醉患者体温过低的主要初始原因。然而,神经轴麻醉期间的重新分布通常仅限于腿部。因此,在主要传导麻醉期间,重新分布使核心体温降低的幅度约为全身麻醉时的一半。与全身麻醉期间一样,随后核心体温以由热量散失与产生之间的不平衡所决定的速率呈线性下降。然而,主要的区别在于,线性体温过低阶段不会因体温调节性血管收缩的再次出现而中断,因为腿部的血管收缩在外周被阻断。结果,在接受神经轴麻醉的大型手术患者中,存在发生严重体温过低的可能性。低温体外循环与身体热量含量的巨大变化有关。此外,快速降温和复温会产生较大的核心到外周、纵向和径向组织温度梯度。外周组织复温不足通常会在体外循环结束时产生相当大的核心到外周梯度。随后,热量从核心重新分布到较凉的手臂和腿部会产生体温后降。延长复温时间、药物性血管舒张或外周加温可以降低体温后降的幅度。当脑内麻醉药浓度充分降低以再次触发正常的体温调节防御时,术后体温恢复正常。然而,残留麻醉和用于治疗术后疼痛的阿片类药物会降低这些反应的有效性。因此,恢复正常体温通常需要2至5小时,这取决于体温过低的程度和患者的年龄。

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