Thermoregulation and perioperative hypothermia

Published on 07/02/2015 by admin

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Thermoregulation and perioperative hypothermia

C. Thomas Wass, MD

Heat balance and thermoregulation

Body heat is unevenly distributed, with a typical core-to-peripheral temperature gradient of 2° C to 4° C. As with any other neurally mediated physiologic process, thermoregulation involves afferent thermal sensing, central processing, and efferent responses. Thermal receptors are distributed throughout the body (e.g., skin, abdominal and thoracic tissues, spinal cord, hypothalamus), with impulses in response to hypothermia and hyperthermia transmitted to the central nervous system via Aδ and C fibers, respectively. Central processing (primarily in the hypothalamus) results in voluntary (e.g., wearing appropriate attire, adjusting ambient temperature) and involuntary (autonomic) efferent responses. The slope of the efferent response intensity (e.g., magnitude of vasomotor changes) versus core temperature defines the gain.

In unanesthetized patients, cold-induced autonomic defenses follow a hierarchical pattern that progresses from vasoconstriction to nonshivering thermogenesis and, finally, shivering thermogenesis (Figure 161-1). Vasoconstriction decreases cutaneous blood flow and heat loss, primarily in the fingers and toes. Although its effects are minimal in adults, nonshivering thermogenesis can double metabolic heat production in the mitochondria-rich brown fat of neonates and infants. Shivering thermogenesis results from involuntary skeletal muscle activity that increases metabolic rate and heat production.

The threshold for warmth-induced autonomic responses, such as active vasodilation and sweating, is similar. Each gram of evaporated sweat dissipates approximately 540 calories of heat to the environment.

Core temperatures between the first cold-induced (i.e., vasoconstriction) and warmth-induced (i.e., vasodilation) responses define the interthreshold range (ITR). Temperatures within this 0.2° C range do not trigger thermoregulatory defense mechanisms.

Effects of anesthesia on thermoregulation

General anesthesia

Intravenously administered and inhaled anesthetic agents inhibit thermoregulation in a dose-dependent manner. That is, general anesthetic agents increase the thresholds for warmth-induced thermoregulatory responses and decrease the thresholds for cold-induced defenses. Accordingly, there is a 20-fold increase (i.e., from 0.2° C to 4.0° C) in the ITR. As a result, anesthetized patients are poikilothermic over this 4° C range, which renders them susceptible to developing heat loss and hypothermia.

Systemic side effects of perioperative hypothermia

Central nervous system

A large amount of experimental evidence indicates that hypothermia may protect the brain from ischemic and traumatic injury. In contrast, fever has been reported to worsen outcomes following cerebral ischemia or head trauma. Hypothermia decreases brain activity, as measured by electroencephalography, and increases latency in the somatosensory evoked potential. Changes in the amplitude of the somatosensory evoked potential are less clearly defined. Mild intraoperative hypothermia has also been reported to prolong postoperative recovery.

Cardiovascular

Decreased core temperature can slow intracardiac conduction, predispose patients to developing lethal cardiac arrhythmias, increase pulmonary and systemic vascular resistance, decrease myocardial contractility, decrease cardiac output, induce myocardial ischemia, and interfere with platelet function and the coagulation cascade (e.g., decreased thrombin production). Interestingly, myocardial ischemia is not entirely due to shivering-induced increases in whole-body metabolism. That is, other contributory mechanisms include increased myocardial work resulting from catecholamine-induced increases in systemic vascular resistance, blood pressure, and heart rate. In patients who have been successfully resuscitated after cardiac arrest due to ventricular fibrillation, two large prospective studies have shown that therapeutic mild hypothermia has been shown increases the rate of a favorable neurologic outcome and reduces chances of a fatal outcome. However, a more recent prospective study did not find any benefit to mild hypothermia (34° C vs. 37° C) in patients following a cardiac arrest.

Mechanisms and prevention of perioperative hypothermia

Perioperative hypothermia occurs via several heat-loss mechanisms: redistribution, convection, radiation, conduction, and evaporation. Although all of these mechanisms are important to some extent, the initial drop in core temperature—and the most important cause of perioperative hypothermia—is predominantly due to redistribution (i.e., transfer) of heat from the core to peripheral tissues (see Figure 161-1). Rapid core-to-peripheral heat transfer produces hypothermia in nearly all patients regardless of the type of anesthesia delivered (e.g., general or regional).

Prevention and treatment of hypothermia may be achieved using passive techniques (e.g., applying cotton blankets, sterile drapes, reflective “space” blankets) or active techniques (e.g., using forced-air convective warmers, resistive-heating blankets, conductive circulating water mattresses, intravenous fluid warmers, radiant infrared lamps, and airway heating and humidification). Of these techniques, heat conservation is most effectively achieved using forced-air convective surface warming or carbon-fiber resistive heating blankets.