THERMOREGULATORY VASOCONSTRICTION IMPAIRS ACTIVE CORE COOLING

被引:66
作者
KURZ, A
SESSLER, DI
BIRNBAUER, F
ILLIEVICH, UM
SPISS, CK
机构
[1] UNIV CALIF SAN FRANCISCO,SCH MED,DEPT ANESTHESIA,THERMOREGULAT RES LAB,SAN FRANCISCO,CA 94143
[2] UNIV VIENNA,DEPT ANESTHESIA & INTENS CARE,VIENNA,AUSTRIA
关键词
BRAIN PROTECTION; FORCED AIR; NEUROSURGERY; TEMPERATURE; HYPOTHERMIA; THERMOREGULATION; VASOCONSTRICTION;
D O I
10.1097/00000542-199504000-00008
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background: Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees C sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees C. However, the efficacy even of active cooling might be impaired by thermoregulatory vasoconstriction, which reduces cutaneous heat loss and constrains metabolic heat to the core thermal compartment. The authors therefore tested the hypothesis that the efficacy of active cooling is reduced by thermoregulatory vasoconstriction. Methods: Patients undergoing neurosurgical procedures with hypothermia were anesthetized with either isoflurane/nitrous oxide (n = 13) or propofol/fentanyl (n = 13) anesthesia. All were cooled using a prototype forced-air cooling device until core temperature reached 32 degrees C. Core temperature was measured in the distal esophagus. Vasoconstriction was evaluated using forearm minus fingertip skin-temperature gradients. The core temperature triggering a gradient of 0 degrees C identified the vasoconstriction threshold. Results: In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degrees C) occurred at a core temperature of 34.4 +/- 0.9 degrees C, 1.7 +/- 0.5 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 +/- 0.9 degrees C, 1.6 +/- 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees C. Core cooling rates were comparable in each anesthetic group. However, patients in whom vasodilation was maintained cooled fastest. Patients in whom vasoconstriction occurred required nearly an hour longer to reach core temperatures of 33 degrees C and 32 degrees C than did those in whom vasodilation was maintained (P < 0.01). Conclusions: Vasoconstriction did not produce a full core temperature ''plateau,'' because of the extreme microenvironment provided by forced-air cooling. However, it markedly decreased the rate at which hypothermia developed. The approximate to 1.h delay in reaching core temperatures of 33 degrees C and 32 degrees C could be clinically important, depending on the target temperature and the time required to reach critical portions of the operation.
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收藏
页码:870 / 876
页数:7
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