DRUG INFLUENCES ON THERMOREGULATION
Causes for inadvertent hypothermia include not only patients’ exposure to a cold room environment and their inability to initiate behavior responses, but the proclivity of anesthetics to promote heat loss. Volatile anesthetics, propofol, and older opioids such as morphine and meperidine promote heat loss through vasodilation. This process is compounded further by the fact that these drugs, as well as fentanyl and its derivatives, directly impair hypothalamic thermoregulation in a dose-dependent manner. Opioids also depress overall sympathetic outflow, which further inhibits any attempts at thermoregulation. The depressant effect on the hypothalamus results in an elevated threshold for heat response, along with a diminished threshold for cold response such as vasoconstriction and shivering. Therefore, opioids widen the normal interthreshold range from ∼0.2°C to as much as 4°C, and patients are unable to adjust to cold environments and heat loss resulting from vasodilation (Figure 1). It is notable that nitrous oxide depresses thermoregulation to a lesser extent than equipotent concentrations of the volatiles, and midazolam has minimal or no influence.3 Presumably this would be true for other benzodiazepines as well.
Following induction of general anesthesia, the decline in body temperature occurs in three phases. The greatest decline occurs during the first half hour or phase 1. Normally body heat is maintained in an unevenly distributed manner; the temperature of core tissues is 2°C to 4°C greater than skin temperature. Following anesthesia induction, however, vasodilation combined with a lowered cold threshold in the hypothalamus allows a redistribution of body heat from core tissues to skin, where heat is lost primarily through radiation. Phase 2 commences after approximately 1 hour, as core temperature decreases at a slower rate and proceeds in a linear manner as heat lost from the body exceeds heat production. Finally, after 3 to 5 hours, phase 3 commences, as an equilibrium is reached where heat loss is matched by heat production and thermoregulated vasoconstriction commences to function.1,3
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Curiously, regional anesthesia also produces hypothermia. In dentistry, the region of blockade is so small that it presents no concern. Regional anesthesia in medicine however produces similar patterns of heat loss and hypothermia as are produced by general anesthesia. Hypothermia is very common following spinal and epidural anesthesia. Blockade of afferent fibers from large regions obviously prevents cold input to the hypothalamus. However, despite the fact that locally injected anesthetics have no direct action on the hypothalamus, the thermoregulatory center nevertheless becomes impaired. (This does not occur following the intravenous administration of lidocaine for cardiac arrhythmias.) For reasons yet to be explained, the thermoregulatory center incorrectly judges skin temperature in blocked regions to be abnormally elevated.1 The net result is that the interthreshold range increases 3 to 4 times (from 0.2°C to 0.6°C to 0.8°C), which of course is significantly less than the 20-fold increase that can be produced by general anesthesia (from 0.2°C to 4°C) (Figure 1). Despite this drop in core temperature, patients generally feel warm because the hypothalamus misinterprets skin temperature. In fact, patients may become hypothermic enough to commence shivering despite their subjective feeling of warmth. The concomitant use of sedation not only compounds the depression of thermoregulation but obtunds the patient’s subjective sensations.
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