• D I Sessler.
• Department of Anesthesia, University of California, San Francisco 94143-0648.
• FASEB J. 1993 May 1;7(8):638-44.

AbstractGeneral anesthesia markedly impairs normal control of body temperature, reducing the threshold (triggering core temperature) for thermoregulatory vasoconstriction from approximately 37 to approximately 34.5 degrees C. Sweating and active vasodilation thresholds similarly are increased, widening the range of temperatures not triggering regulatory compensations from approximately 0.2 to approximately 4 degrees C. However, once initiated, the gains (slopes of response intensity vs. core temperature curves) and maximum intensities of thermoregulatory responses are nearly normal. Intraoperative core temperature initially decreases rapidly because anesthetic-induced inhibition of tonic thermoregulatory vasoconstriction causes a core-to-peripheral redistribution of body heat. The subsequent slower, linear decrease in body temperature results from heat loss exceeding metabolic heat production. And finally, after 3-4 h of anesthesia, core temperature stabilizes at an abnormally low value. In patients experiencing minimal heat loss, and therefore not becoming sufficiently hypothermic to trigger vasoconstriction, this plateau can be passive steady state in which heat loss equals production. Conversely, patients becoming sufficiently hypothermic will trigger thermoregulatory vasoconstriction that both decreases cutaneous heat loss and sequesters some metabolic heat in the core. Epidural and spinal anesthesia also cause core hypothermia by inhibiting tonic thermoregulatory vasoconstriction, producing an internal redistribution of heat from the warm core to cooler peripheral tissues. Core hypothermia provokes thermoregulatory responses including vasoconstriction (above the block level) and shivering. Nonetheless, many patients feel warmer after induction of regional anesthesia, apparently because perceived skin temperature is elevated. The following review will focus on anesthetic-induced impairment of normal thermoregulatory control and the resulting alterations in heat balance.

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