By increasing ambient temperature in the operating room to 26 degrees C (79 degrees F), the incidence of core hypothermia can be dramatically reduced in both younger and older patients.
1. Previous studies on the thermoregulatory effects of alpha-adrenoceptor antagonists have been performed primarily in animals and the findings have been inconsistent. There is evidence for thermoregulatory impairment by alpha-adrenergic antagonists in humans not exposed to cold, but the effects of alpha-adrenergic blockade during cold challenge have not been investigated. 2. Fourteen healthy human volunteers (seven elderly, aged 55-68 years and seven young, aged 19-27 years) were studied on three separate days and received three randomly assigned treatments; (i) control (no drug), (ii) low-dose phentolamine and (iii) high-dose phentolamine. On each day cold intravenous saline (4 degrees C) was given until both vasoconstriction and shivering were triggered or a maximum fluid volume (40 ml/kg) was delivered. Core temperature, peripheral vasoconstriction and metabolic heat production were measured. 3. The alpha-adrenoceptor antagonist caused a dose-dependent inhibition of vasoconstriction in the elderly but did not impair vasoconstriction in the young subjects at the doses that were given. Shivering and metabolic heat production were unaffected by alpha-adrenergic blockade in the elderly or in the young. 4. These findings illustrate the selective inhibition of vasoconstriction (but not shivering) by alpha-adrenoceptor antagonism in elderly individuals. Compared with the young, the elderly are more sensitive to the effects of alpha-antagonists, perhaps due to downregulation of the alpha-adrenoceptor. These findings lead us to conclude that thermoregulatory vasoconstriction is alpha-adrenergically mediated, and this response is attenuated by alpha-adrenoceptor blockade in elderly humans.
Postoperative hypothermia is common and associated with adverse hemodynamic consequences, including adrenergically mediated systemic vasoconstriction and hypertension. Hypothermia is also a known predictor of dysrhythmias and myocardial ischemia in high-risk patients. We describe a prospective, randomized trial designed to test the hypothesis that forced-air warming (FAW) provides improved hemodynamic variables after coronary artery bypass graft. After institutional review board approval and written informed consent, 149 patients undergoing coronary artery bypass graft were randomized to receive postoperative warming with either FAW (n = 81) or a circulating water mattress (n = 68). Core temperature was measured at the tympanic membrane. A weighted mean skin temperature was calculated. Heart rate, mean arterial blood pressure, central venous pressure, cardiac output, and systemic vascular resistance were monitored for 22 h postoperatively. Mean arterial blood pressure was maintained by protocol between 70 and 80 mm Hg by titration of nitroglycerin and sodium nitroprusside. The two groups had similar demographic characteristics. Tympanic and mean skin temperatures were similar between groups on intensive care unit admission. During postoperative rewarming, tympanic temperature was similar between groups, but mean skin temperature was significantly greater in the FAW group (P < 0.05). Heart rate, mean arterial pressure, central venous pressure, cardiac output, and systemic vascular resistance were similar for the two groups. The percent of patients requiring nitroprusside to achieve the hemodynamic goals was less (P < 0.05) in the FAW group. In conclusion, aggressive cutaneous warming with FAW results in a higher mean skin temperature and a decreased requirement for vasodilator therapy in hypothermic patients after cardiac surgery. This most likely reflects attenuation of the adrenergic response or opening of cutaneous vascular beds as a result of surface warming. IMPLICATIONS Forced-air warming after cardiac surgery decreases the requirement for vasodilator drugs and may be beneficial in maintaining hemodynamic variables within predefined limits.
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