• D I Sessler.
• Department of Anesthesia, University of California-San Francisco 94143-0648, USA. sessler@anesthesia.ucsf.edu
• Anesthesiology. 2000 Feb 1;92(2):578-96.

AbstractHypothermia 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.

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