Wass C T, Cable D G, Schaff H V, Lanier W L
Department of Anesthesiology, Mayo Clinic and Mayo Medical School, Rochester, Minnesota 55905, USA.
Ann Thorac Surg. 1998 Feb;65(2):454-60. doi: 10.1016/s0003-4975(97)01235-6.
Because different anesthetics have different effects on cerebral blood flow and cerebral metabolism, we hypothesized that they also may have different effects on brain temperature during hypothermic cardiopulmonary bypass (CPB) and subsequent rewarming.
Sixteen dogs were anesthetized either with inhaled halothane, 1.0 minimum alveolar concentration (ie, an anesthetic that should increase cerebral blood flow and minimally affect cerebral metabolism; n = 8), or with intravenous high-dose pentobarbital (ie, an anesthetic that should reduce cerebral blood flow and cerebral metabolism by approximately one half; n = 8). Normocapnia (alpha-stat technique) and a blood pressure near 90 mm Hg were maintained. Thermistors were placed in the esophagus (ie, the body core), in the parietal epidural space, and in the parietal brain parenchyma at depths of 1 and 2 cm. Initially, all temperatures were controlled at 38.0 degrees +/- 0.2 degrees C (mean +/- standard deviation). Thereafter, atrial-femoral artery CPB was initiated, and after 15 minutes at 38 degrees C, the core temperature was decreased to 28 degrees C over approximately 21 minutes. After 30 minutes at 28 degrees C, the core temperature was returned to 38 degrees C over approximately 21 minutes and was maintained at 38 degrees C for the next 30 minutes.
In halothane-anesthetized dogs, the mean brain-to-core temperature gradient always was 1.0 degrees C or less for all brain sites during all phases of CPB. In contrast, in pentobarbital-anesthetized dogs, the mean brain temperature during active cooling typically exceeded the core temperature by 1.7 degrees to 2.2 degrees C. This brain-to-core temperature gradient persisted into the period of stable hypothermia. During the rewarming phase of CPB, the mean brain temperature was 2.9 degrees to 3.4 degrees C cooler than the core temperature. This trend of relative cerebral hypothermia persisted well into the period in which the core temperature was 38 degrees C.
Deep barbiturate anesthesia resulted in a brain-to-core temperature gradient during CPB that was of a magnitude greater than the 1 degrees C previously reported to modulate ischemic neurologic injury. We speculate that the timely administration of barbiturates (eg, during the latter stages of CPB) may be useful as part of a cerebroprotective regimen in humans undergoing CPB, in part because the barbiturates influence brain temperature.
