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Intraoperative thermoregulatory vasoconstriction, once triggered, is remarkably effective in preventing further
Mean body temperature will decrease when heat loss to the environment exceeds metabolic heat production. Heat production during anesthesia is approximately 0.8 kcal/kg/hr. Because the specific heat of the human body is about 0.83 kcal/kg, [151] body temperature decreases approximately 1°C/hr when heat lost to the environment exceeds metabolic production by a factor of 2. Normally, about 90% of metabolic heat is lost through the skin surface. During anesthesia, additional heat is lost directly from surgical incisions and by the administration of cold intravenous fluids.
Thermoregulatory vasodilation causes the initial core-to-peripheral redistribution of body heat[57] ; similarly, re-emergence of vasoconstriction in patients becoming sufficiently hypothermic produces a core temperature plateau.[46] It is thus evident that vasomotor tone alters intercompartmental heat transfer. In addition to thermoregulatory arteriovenous shunt status, arteriolar tone is directly modulated by anesthetics per se.[54] Both factors potentially influence the speed with which peripherally applied heat reaches the core thermal compartment.
Thermoregulatory vasoconstriction slightly impairs induction of therapeutic hypothermia during neurosurgery.[152] However, arteriovenous shunt tone has little effect on intraoperative cooling[153] or heating.[154] Intraoperative vasoconstriction thus only slightly impedes peripheral-to-core transfer of cutaneous heating and cooling. Little clinical effect presumably results because intraoperative thermoregulatory vasoconstriction is opposed by direct anesthetic-induced peripheral vasodilation.
During postanesthetic recovery, however, the situation differs markedly. Here, anesthetic-induced peripheral dilation[54] [155] dissipates, with thermoregulatory vasoconstriction left unopposed. As might be expected, this vasoconstriction then becomes an important factor and significantly impairs transfer of peripherally applied heat to the core thermal compartment. Patients with a residual spinal anesthetic block thus warm considerably faster than those recovering from general anesthesia alone ( Fig. 40-17 ).[156] Heat balance studies indicate that core warming is slowed because vasoconstriction constrains up to 30 kcal in peripheral tissues.[157]
Because postoperative thermoregulatory vasoconstriction decreases peripheral-to-core transfer of heat, applied warming is most effective during surgery when patients are vasodilated. From a practical point of view, this means that it is easier to maintain intraoperative normothermia (when most patients are vasodilated) than to rewarm them postoperatively (when virtually all hypothermic patients
Figure 40-17
Intraoperative and postoperative core temperatures in
patients assigned to general anesthesia (n = 20)
and spinal anesthesia (n = 20). All patients were
warmed with forced air during the postoperative period. Core temperature did not
differ significantly during surgery, but it increased significantly faster postoperatively
in patients given spinal anesthesia (1.2 ± 0.1°C/hr
versus 0.7 ± 0.2°C/hr, means ± SD). (Redrawn
from Szmuk P, Ezri T, Sessler DI, et al: Spinal anesthesia only minimally increases
the efficacy of postoperative forced-air rewarming. Anesthesiology 87:1050–1054,
1997.)
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