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Chapter: Clinical Anesthesiology: Perioperative & Critical Care Medicine: Thermoregulation, Hypothermia, & Malignant Hyperthermia

Thermoregulation & Hypothermia

Hypothermia reduces metabolic oxygen requirements and can be protective during cere-bral or cardiac ischemia.



Hypothermia, usually definedasabody tempera-ture less than 36°C, occurs frequently during anes-thesia and surgery. Unintentional perioperative hypothermia is more common in patients at the extremes of age, and in those undergoing abdominal surgery or procedures of long duration, especially with cold ambient operating room temperatures; it will occur in nearly every such patient unless steps are taken to prevent this complication.


Hypothermia reduces metabolic oxygen requirements and can be protective during cere-bral or cardiac ischemia. Nevertheless, hypother-mia has multiple deleterious physiological effects (Table 52–1). Infact, unintendedperioperativehypothermia has been associated with an increased mortality rate.


Core temperature is normally the same as the central venous blood temperature (except during periods of relatively rapid temperature change as can occur during extracorporeal perfusion). When there is no attempt to actively warm an anesthetized patient, core temperature usually decreases 1–2C during the first hour of general anesthesia (phase one), followed by a more gradual decline during the ensuing 3–4 h (phase two), eventually reaching a point of steady state (phase three). With general, epidural, or spinal anesthesia redistribution of heat from warm “central” compartments (eg, abdomen, thorax) to cooler peripheral tissues (eg, arms, legs) from anesthetic-induced vasodilation explains most of the initial decrease in temperature

during phase one, with actual heat loss from the patient to the environment being a minor contribu-tor. Continuous heat loss to the environment appears to be primarily responsible for the slower subse-quent decline during phase two. At steady state, heat loss equals metabolic heat production (Figure 52–1).In the normal unanesthetized patient the hypothalamus maintains core body temperature within very narrow tolerances, termed the interthreshold range, with the threshold for sweating and vasodilation at one extreme and the threshold for vasoconstriction and shivering at the other. Increasing core temperature a fraction of a degree induces sweating and vasodilation, whereas a mini-mally reduced core temperature triggers vasoconstriction and shivering. Anesthetic agents inhibit central thermoregulation by interfering with these hypothalamic reflex responses. For example, isoflurane produces a dose-dependent decrease in the threshold temperature that triggers vasoconstriction (3C decrease for each percent of inhaled isoflurane). Both general and regional anesthetics increase the interthreshold range, albeit by different mechanisms. Spinal and epidural anes-thetics, like general anesthetics, lead to hypothermia by causing vasodilation and internal redistribu-tion of heat. The accompanying thermoregulatory impairment from regional anesthetics that allows continued heat loss is likely due to altered percep-tion by the hypothalamus of temperature in the anesthetized dermatomes rather than a central drug effect, as with general anesthetics.

Intraoperative Considerations


A cold ambient temperature in the operating room, prolonged exposure of a large wound, and the use of large amounts of room-temperature intravenous fluids or high flows of unhumidified gases can con-tribute to hypothermia. Prewarming the patient forhalf an hour with convective forced-air warming blankets prevents phase one hypothermia by elim-inating the central–peripheral temperature gradi-ent. Methods tominimizephase twohypothermiafrom heat loss during anesthesia include use of forced-air warming blankets and warm-water blan-kets, heated humidification of inspired gases, warm-ing of intravenous fluids, and increasing ambient operating room temperature. Passive insulators such as heated cotton blankets or so-called space blankets have limited utility unless virtually the entire body is covered.

Postoperative Considerations


Shivering can occur in postanesthesia care units (PACUs) or critical care units as a result of actual hypothermia or neurological aftereffects of general anesthetic agents. Shivering is also common imme-diately postpartum. Shivering in such instances rep-resents the body’s effort to increase heat production and raise body temperature and may be associated with intense vasoconstriction. Emergence from even brief general anesthesia is sometimes also associated with shivering. Although the shivering can be part of nonspecific neurological signs (posturing, clonus, or the Babinski sign) that are sometimes observed during emergence, shivering is most often associ-ated with hypothermia and volatile anesthetics. Regardless of the mechanism, shivering appears to be more common after longer durations of surgery and the use of greater concentrations of a volatile agent. Occasionally it is intense enough to cause hyperthermia (38–39°C) and metabolic acidosis, both of which promptly resolve when the shivering stops. Both spinal and epidural anesthesia lower th shivering threshold and vasoconstrictive response to hypothermia; shivering may also be encountered in the PACU following regional anesthesia. Other causes of shivering should be excluded, such as sep-sis, drug allergy, or a transfusion reaction. Intense shivering may increase oxygen consumption, CO2 production, and cardiac output. These physiologi-cal effects are often poorly tolerated by patients with preexisting cardiac or pulmonary impairment.


Postoperative shivering may increase oxygen consumption as much as fivefold, may decrease arte-rial oxygen saturation, and may be associated with an increased risk of myocardial ischemia. Although postoperative shivering can be effectively treated with small intravenous doses of meperidine (12.5– 25 mg) in adults, the better option is to reduce the likelihood of shivering by maintaining normother-mia. Shivering in intubated and mechanically venti-lated patients can also be controlled with sedation and a muscle relaxant until normothermia is rees-tablished and the effects of anesthesia have dissipated.

Postoperative hypothermia should be treated with a forced-air warming device, if available;alternately (but less satisfactorily) warming lights or heating blankets can be used to restore body temper-ature to normal. Hypothermia has been associated with an increased incidence of myocardial ischemia, arrhythmias, increased transfusion requirements, and increased duration of muscle relaxant effects, the latter of which can be especially harmful in the recently extubated patient.

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