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Ann Thorac Surg 1999;68:1454-1455
© 1999 The Society of Thoracic Surgeons
a Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
Address reprint requests to Dr Roy, Department of Anesthesiology, Wake Forest University, School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1009
Presented at Outcomes ’99, "The Key West Meeting," Key West, FL, May 26–30, 1999.
Unanesthetized man is homeothermic, capable of maintaining systemic normothermia independent of his surroundings. Anesthesia impairs thermoregulation [1]. Perioperative hypothermia is common. A key predictor of postoperative hypothermia is the lowest intraoperative temperature. Although it is widely accepted that hypothermia protects the central nervous system during times of potential cerebral ischemia, recent studies have demonstrated significant deleterious effects, including coagulopathy, morbid cardiac events, and infection [1].
"Warm heart surgery" and "normothermic cardiopulmonary bypass (CPB)" have been reported as equal if not superior to techniques of hypothermic CPB [2, 3], with significant improvement in postoperative outcomes.
Respiratory
The time to extubation is shorter after normothermic CPB [4, 5], although studies of lung function have failed to identify a reason for the difference. Diaphragmatic function is impaired by hypothermia [6]. Rewarming in the postoperative period has been identified as a time of potential hemodynamic and ventilatory instability [7].
Coagulation
Hypothermia reduces platelet aggregation and endothelial-associated coagulation with subsequent increases in postoperative bleeding and requirements for blood products [8, 9]. Decreased bleeding in the postoperative period is associated with a shorter intubation time and a lower requirement for inotropic support.
Hemodynamic
Normothermic heart surgery is accompanied by a significant reduction in systemic vascular resistance (SVR) [3]. The hypothesis that this is due to increased release of catecholamines during hypothermia has not been substantiated clinically. In fact, normothermia is associated with higher levels of circulating catecholamines [10]. There is evidence of temperature-dependent release of vasoactive cytokines, most notably tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 [11]. The reduction in SVR results in improved myocardial function and a reduction in the need for inotropic support. Hypothermia is associated with an increase in the incidence of postoperative atrial fibrillation [12].
Splanchnic
The splanchnic organs are susceptible to ischemia during periods of low cardiac output and reduced oxygen delivery during or immediately after CPB [13]. Hypothermia was thought to provide these organs with additional protection during periods of high risk. However, Croughwell and associates [14], using an indirect measure of gut perfusion, concluded splanchnic hypoperfusion was common after CPB and associated with postoperative complications, but the perfusion temperature had no significant effect on gut mucosal hypoperfusion.
Neurologic
Despite the systemic advantages, there is little evidence to support any neuroprotective benefits of normothermia and significant evidence to support increased risk of neurological deficit [15, 16]. Despite numerous published studies, there is no consensus of opinion regarding whether normothermic or hypothermic CPB is preferable. This uncertainty may reflect confusion concerning the definition of "normothermia" rather than a misunderstanding of cerebral physiology.
Normothermia has traditionally been defined as 37°C. The confusion in reported studies of "normothermia" appears to be twofold; firstly, a differentiation must be made between the systemic perfusion temperature and the myocardial perfusion temperature. Secondly, "normothermic perfusion" appears to encompass a variety of practices from actively heating the CPB circuit to maintain normothermia (37°C) to neither heating nor cooling the circuit and allowing the temperature to drift before active rewarming. These variations in technique are further complicated by a variation in the site used to monitor temperature.
In ongoing animal studies at Wake Forest University School of Medicine, we are characterizing the temperature profiles of different brain and body sites during CPB. The rate of cooling and rewarming between all body regions is highly variable, with no body region accurately reflecting brain temperature. Nasopharyngeal temperature is approximately 4°C lower than brain temperature during rewarming. In addition, there is variability between brain regions, with deeper structures cooling and rewarming fastest. These findings may explain the wide variation in outcomes described in studies of "normothermic" cardiac surgery. These results suggest that during rewarming it is possible to subject the brain to significant hyperthermia.
Cerebral blood flow is principally determined by cerebral metabolic demand. Cerebral metabolism is reduced 5% to 7% for each degree centigrade reduction in temperature [17]. Hypothermia results in an overall reduction in blood flow, which further aids neuroprotection by decreasing the number of emboli that may potentially be delivered to the brain [18, 19]. In addition, we have demonstrated a significant reduction in the size of the cerebral ischemic lesion caused by an embolus impacting during hypothermia as opposed to during normothermia.
Evidence supports the use of systemic normothermia to improve nonneurologic outcome. In contrast, evidence is contradictory and confusing regarding perfusion temperature and neurological outcome. According to basic physiological principles, neither cerebral normothermia nor hyperthermia during CPB can be neuroprotective. Ideally, a CPB technique that combines the advantages of cerebral hypothermia with systemic or corporeal normothermia would appear to optimize clinical outcome. Importantly, clinical researchers must be clear about their definition of normothermia, temperature management, and the method they used to monitor temperature when they compare data from different studies and institutions.
References
This article has been cited by other articles:
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  J. W. Hammon Jr. and L. H. Edmunds Jr. Extracorporeal Circulation: Organ Damage Card. Surg. Adult, January 1, 2003; 2(2003): 361 - 388. [Full Text]
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 S. E. Kasner, T. Wein, P. Piriyawat, C. E. Villar-Cordova, J. A. Chalela, D. W. Krieger, L. B. Morgenstern, S. E. Kimmel, J. C. Grotta, and H.-C. Koennecke Acetaminophen for Altering Body Temperature in Acute Stroke: A Randomized Clinical Trial * Editorial Comment: A Randomized Clinical Trial Stroke, January 1, 2002; 33(1): 130 - 135. [Abstract] [Full Text] [PDF]
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