Abstract
Core body temperature is highly regulated in humans by the autonomic nervous system and the hypothalamus. General anesthesia, neuraxial anesthesia and analgesia, and drugs such as opioids all reduce the ability of the hypothalamus to regulate core temperature. Intraoperative hypothermia is common and is caused by (1) redistribution of heat from the core to the periphery, (2) decreased metabolism, leading to decreased heat production, and (3) increased heat loss, primarily via radiation, convection, and in large, open surgeries, evaporation. Thus without intervention hypothermia (and, less commonly, hyperthermia) is a common consequence of anesthetic management. Although mild or moderate hypothermia may be protective in certain circumstances (e.g., after cardiac arrest), perioperative hypothermia is associated with multiple adverse outcomes, including increased postoperative discomfort and postanesthesia recovery time, blood loss and transfusion, cardiovascular morbidity, surgical site infection, deep vein thrombosis, and hospital length of stay. Intraoperative hypothermia can be prevented, mitigated, or corrected by preoperative and intraoperative active warming, which has also been shown to reduce complications.
Keywords
thermoregulation, core temperature, adverse effects of hypothermia, anesthetic-induced hypothermia, redistribution hypothermia, thermoregulatory vasoconstriction
Chapter Outline
Normal Physiologic Thermoregulation
Anesthetic Effects on Thermoregulation
Effects of Anesthetic Techniques and Agents
Consequences of Thermal Dysregulation Related to Anesthesia
Measuring Temperature Intraoperatively
Prevention and Correction of Intraoperative Hypothermia
Core body temperature is highly regulated in humans by the autonomic nervous system and the hypothalamus. General anesthesia, neuraxial anesthesia and analgesia, and drugs such as opioids all reduce the ability of the hypothalamus to regulate core temperature. Thus without intervention, hypothermia (and, less commonly, hyperthermia) is a common consequence of anesthetic management. In this chapter, we review normal thermoregulation, the mechanisms responsible for anesthesia-related hypothermia and hyperthermia, and the consequences of perioperative hypothermia. We use this framework to discuss methods to reduce, prevent, or correct perioperative hypothermia and hyperthermia.
Normal Physiologic Thermoregulation
Human body core temperatures are regulated by the hypothalamus in response to sensory inputs from the autonomic nervous system. Ambient and internal temperature is sensed by temperature-sensing elements in the skin and the dorsal root ganglia. The signals travel via ascending spinothalamic tracts and afferent somatosensory pathways, through the lateral parabrachial nucleus to the hypothalamus. Exercise, nutrition, infection, hypothyroidism or hyperthyroidism, and drugs such as opioids and general anesthetic agents affect temperature thresholds through inhibitory postsynaptic signals in the hypothalamus.
Core temperature in humans represents a balance between heat production via metabolism and heat loss mostly through the skin but also via gas exchange and urine output. Basal heat production is about 0.83 kcal/kg per degree centigrade. Well-perfused tissues are also generally the most metabolically active and produce the most heat. Heat production is increased during exercise, mostly as a result of increases in muscle metabolism. It is decreased during anesthesia owing to decreased metabolism, primarily in the brain, muscles, and heart. Mechanical ventilation and neuromuscular blocking agents further reduce metabolic rate.
There are four primary mechanisms for heat loss: radiation, convection, conduction, and evaporation ( Fig. 15.1 ). Radiation makes the largest contribution. Air movement displaces heat near the skin surface by displacing warm air with cooler air. Heat distribution from the core includes both blood-borne longitudinal convection and radial conduction into adjacent tissues. Heat transfer to peripheral tissues is slower than core heat transfer because of the lower rate of perfusion. Longitudinal convection via the blood is the primary mechanism for peripheral redistribution of heat, although radial diffusion also contributes. Administration of intravenous fluids that are below core temperature increases heat loss via conduction because the administered fluid is warmed to body temperature by surrounding blood and tissues. Evaporation via intact skin and exhalation of warmed, humidified air dissipates less than 15% of the basal metabolic rate during normal circumstances but increases substantially during sweating. The microenvironment around the skin surface influences heat loss through conduction, convection, and radiation. Likewise, heat loss may be augmented by relatively cool operating rooms, cool intravenous and irrigating fluids, and evaporation from large surgical incisions.
A useful model for understanding thermoregulation divides the human body into core and peripheral thermal compartments ( Fig. 15.2 ). The core consists of the well-perfused organs—that is, the brain and those within the trunk—and makes up about 60% of body mass. Because these organs are well perfused, heat distribution across the core is rapid and uniform. The hypothalamus normally regulates core temperature to the range of 36.5°C to 37.5°C. In a given individual, core temperature varies with diurnal rhythms, cytokines produced during inflammation, and other stimuli. The peripheral compartment consists of the skin and subcutaneous tissue, resting muscle, and the upper and lower extremities. The hypothalamus does not regulate peripheral temperature, but it does receive sensory temperature input from the periphery. Peripheral temperature under normal circumstances is usually about 2°C to 4°C less than core temperature, largely as a result of peripheral vasoconstriction to regulate heat loss to the environment.
Exposure to a cold environment causes peripheral vasoconstriction. Peripheral vasoconstriction directly reduces heat loss, which helps to maintain the balance of heat production and heat loss. Peripheral vasoconstriction also causes redistribution of heat content (tissue temperature) from the periphery to the core, thus immediately increasing core heat content while reducing peripheral heat content. This thermoregulatory response increases the core-to-peripheral temperature gradient, which may increase to more than 10°C in extreme circumstances. Conversely, exposure to a hot environment or an increase in heat production, as with increased metabolism, induces thermoregulatory vasodilation to increase heat loss, as well as to transfer heat from the core to the periphery. Under these circumstances, the core-to-peripheral temperature gradient may be less than 2°C.
Hormonal, cytokine, and endocrine inputs to the hypothalamus define the core temperature set point, which varies diurnally and in response to fever triggers such as interleukin (IL)-2. The hypothalamus integrates tissue and environmental temperature signals and maintains core temperature within a tight interthreshold range of about 0.2°C above or below the set point. Modification of heat production (shivering, behavioral modification) and modification of heat loss (behavioral modification, vasoconstriction or vasodilation, and sweating) facilitate this tight temperature control. Behavioral modification includes adding layers (e.g., clothing or covers) to reduce heat loss in response to cold exposure or a reduction in core temperature, and removing layers to increase heat loss in response to heat exposure or an increase in core temperature. It also includes reducing physical activity to reduce heat production or increasing physical activity, which may be voluntary or involuntary (shivering), to increase heat production.
In summary, normal thermoregulatory mechanisms tightly control human body core temperature within a narrow interthreshold range of about 0.2°C. Next, we consider the important ways that anesthetic agents alter these mechanisms.
Anesthetic Effects on Thermoregulation
Intravenous and inhaled anesthetic agents, neuraxial anesthesia and analgesia, and opioids all blunt the hypothalamic responses to changes in core and environmental temperature, thus increasing the interthreshold range (i.e., the range of tolerated temperatures) in a dose-dependent manner ( Fig. 15.3 ). A major mechanism for this is through inhibition of changes in vascular tone. Virtually all anesthetic techniques and agents induce vasodilation. Vasoconstriction in response to a reduction in core temperatures is inhibited until the core temperature is decreased by ~3°C to 4°C. Anesthetic agents not only increase the interthreshold range but also inhibit or eliminate responses to changes in core temperature. General anesthesia prevents behavioral modification in response to core and environmental temperature changes while the patient is unconscious, and neuraxial anesthesia and opioids reduce temperature perception, thus making behavioral modification less likely. General anesthesia abolishes the shivering response and limits sweating. Mechanisms that cause increased heat loss to the environment include cutaneous vasodilation, surgical exposure (including radiative and evaporative heat loss), inhalation of dry, cold gases that are warmed and humidified in the lungs and exhaled, and administration of ambient temperature intravenous fluids. Anesthetic agents also reliably reduce the metabolic rate and thus heat production. Neuromuscular blocking agents compound the effects of anesthetic agents by further reducing metabolic heat production.
As a result of the combination of reduction in heat production and reduced capacity to decrease heat loss leading to increased heat loss, in the absence of interventions to maintain normothermia, most patients exposed to general anesthesia become hypothermic, typically by 1°C to 3°C. A 3°C reduction in mean body temperature translates to a heat “debt” of approximately 175 kcal in an average 70-kg patient, equivalent to about 3 hours of basal metabolic heat production. Thus patients who become hypothermic intraoperatively may take hours to return to baseline thermal comfort.
Although core temperature is almost universally used as a measure of the state of thermoregulation of an individual, it does not accurately represent either total body heat content or mean body temperature because peripheral tissues are typically 2° to 4°C cooler than the trunk and the head. This normal core-to-peripheral tissue temperature gradient is maintained by tonic thermoregulatory vasoconstriction of arteriovenous shunts in the fingers and toes that maintain core temperature by reducing heat loss to the environment. Thus in addition to effects on normal thermoregulatory mechanisms, the direct vasodilation caused by all anesthetics causes dissipation of heat across the existing temperature gradients from the warmer core to the cooler periphery. Despite the early decrease in core temperature within the first 30 minutes of anesthetic induction, body heat content during early anesthesia remains constant; that is, net heat exchange to the environment remains close to zero. The redistribution of core heat to the periphery contributes about 65% of the total decrease in core temperature during the first 3 hours of anesthesia.
In the absence of interventions to minimize preinduction peripheral vasoconstriction or to add heat to the patient by active warming methods (these interventions are described in detail later), core temperatures under anesthesia typically decrease by 1°C to 1.5°C during the first hour. This is followed by a slower linear phase of temperature decrease over the next 2 to 3 hours. A plateau is then reached throughout the remainder of the procedure ( Fig. 15.4 ).
The initial large decrease is caused by redistribution of heat content as the result of vasodilation of previously constricted vessels. The linear phase results mainly from the decrease in metabolic rate induced by anesthesia, typically in the range of a 15% to 40% reduction. In this phase, heat loss exceeds metabolic heat production, which leads to a slow, linear decrease in temperature. During this phase, patient factors such as basal metabolic rate and obesity, the type of operation, and ambient temperature all may affect the rate of decrease. In a sufficiently long surgery (>4 hours) the linear phase is followed by a core temperature plateau, when heat loss and heat production reach equilibrium.
This state of equilibrium is also known as thermal steady state. Patients with sufficient initial body heat content remain relatively warm intraoperatively and tend to reach thermal steady state earlier. In patients in whom core temperature was maintained in the normal range preoperatively owing to thermoregulatory vasoconstriction, core temperature decreases by a greater amount and it takes longer to reach thermal steady state. Core hypothermia in general or regional anesthesia is a function of the initial thermoregulatory state of the patient and the site, duration, and magnitude of surgery.
Although the core temperature plateau usually occurs at about the same time as the temperature becomes low enough to trigger thermoregulatory vasoconstriction (~34°C-35°C), vasoconstriction, surprisingly, only slightly reduces cutaneous heat loss. The reason appears to be that constriction is largely restricted to arteriovenous shunts in the fingers and toes. The distribution of heat to the periphery is influenced by peripheral blood flow, heat exchange between adjacent arteries and veins, and the core-to-peripheral temperature gradient. Once heat reaches the periphery it cannot travel back to the core against the temperature gradient. Reemergence of vasoconstriction restricts further redistribution from the core but cannot recover heat already lost to peripheral tissues. After vasoconstriction, cutaneous heat loss decreases as less heat flows peripherally from the core and peripheral tissues gradually cool. However, core temperature plateau appears well before a thermal steady state, suggesting that it is a constraint of centrally generated metabolic heat to the core, rather than a reduction in cutaneous loss. Cutaneous heat alterations therefore represent a more accurate measure of heat loss than changes in central body temperature because as mentioned redistribution is the determinant of heat balance.
Thermoregulation under anesthesia is different in infants and children than in adults. Although respiratory losses are similar, infants have less mass with a high surface-area-to weight ratio. A greater fraction of their weight is distributed to their heads and torsos as opposed to their extremities. With less overall mass, infants have lower metabolic heat production and cannot absorb much heat from the core. They typically lose heat from their thin scalps and skin as opposed to redistribution, which is most apparent during the linear phase of hypothermia. Studies have also shown impaired thermoregulation in old age.
As patients emerge from anesthesia postoperatively, they slowly regain thermoregulatory control and, in the absence of intraoperative active warming, regain core normothermia in about 2 to 5 hours. Upon emergence, patients regain arteriovenous vasoconstriction and shivering and are able to decrease cutaneous heat loss, constrain metabolic heat to the thermal core, and increase metabolic heat production. Recovery, however, may be limited by residual volatile anesthetics or opioids administered at the end of surgery.
Effects of Anesthetic Techniques and Agents
General anesthesia decreases core temperature to a greater extent than neuraxial anesthesia. Patients under neuraxial anesthesia lose less heat from redistribution compared with those who have general anesthesia. Although neuraxial anesthesia inhibits thermoregulation centrally, more importantly, the inhibition of peripheral sympathetic motor nerves prevents thermoregulatory vasoconstriction and shivering. Neuraxial anesthesia also has a lesser impact on reducing metabolic heat production. As a result, patients under neuraxial anesthesia demonstrate a smaller initial reduction of core temperature related to redistribution and a slow, prolonged phase of linear hypothermia.
Hypothermia during neuraxial anesthesia for small surgeries is usually mild because a passive plateau develops in well-insulated patients. Patients undergoing long operations under neuraxial anesthesia, on the other hand, are at risk of developing more severe hypothermia comparable to that seen under general anesthesia. Neuraxial anesthesia inhibits both autonomic thermoregulatory control and thermoregulatory shivering in response to hypothermia.
Combined approaches, including anesthetic agents, analgesic/sedative agents, and/or neuraxial anesthesia/analgesia, produce a more pronounced inhibition of thermoregulation and a greater risk of perioperative hypothermia. Heat redistribution may be increased because of differential and additive mechanisms. Heat may be lost at a higher rate during the linear phase. When the effects of regional anesthesia on vasoconstriction are superimposed on those of general anesthesia, vasoconstriction occurs at a lower core temperature. Centrally initiated vasoconstriction will have a reduced effect on vascular tone in the lower extremities after neuraxial anesthesia.
Although hypothermia is more common and appears to have more severe consequences, the disruption in thermoregulation induced by anesthesia may also lead to hyperthermia. In patients having superficial surgery of long duration in which almost all of the skin is covered by drapes, active warming can lead to hyperthermia owing to transfer of heat to the patient in excess of heat loss. Adverse consequences of hyperthermia include increased heart rate and, if severe, neurologic consequences.
Consequences of Thermal Dysregulation Related to Anesthesia
Intraoperative core hypothermia was the norm in anesthesia management until at least the 1990s, and it was not thought to have adverse consequences. That view was incorrect, however. Even 0.5°C of hypothermia has adverse consequences, which include patient discomfort, prolonged duration (and cost) of immediate postoperative recovery in the postanesthesia care unit (PACU), prolonged drug metabolism, increased risk of blood loss and transfusion, increased risk of cardiovascular and wound morbidity, and increased risk of deep vein thrombosis ( Table 15.1 and Fig. 15.8 ).
| Consequence | Author | N | ΔT core (°C) | Normothermic | Hypothermic | P |
|---|---|---|---|---|---|---|
| Surgical wound infection | Kurz et al. | 200 | 1.9 | 6% | 19% | < 0.01 |
| Duration of hospitalization | Kurz et al. | 200 | 1.9 | 12.1 ± 4.4 days | 14.7 ± 6.5 days | <0.01 |
| Intraoperative blood loss | Schmied et al. | 60 | 1.6 | 1.7 ± 0.3 I | 2.2 ± 0.5 I | < 0.001 |
| Allogeneic transfusion requirement | Schmied et al . | 60 | 1.6 | 1 unit | 8 units | < 0.05 |
| Morbid cardiac events | Frank et al . | 300 | 1.3 | 1% | 6% | <0.05 |
| Postoperative ventricular tachycardia | Frank et al. | 300 | 1.3 | 2% | 8% | <0.05 |
| Urinary excretion of nitrogen | Carli et al . | 12 | 1.5 | 982 mmol/day | 1798 mmol/day | <0.05 |
| Duration of vecuronium | Heier et al . | 20 | 2.0 | 28 ± 4 min | 62 ± 8 min | < 0.001 |
| Duration of atracurium | Leslie et al. | 6 | 3.0 | 44 ± 4 min | 68 ± 7 min | < 0.05 |
| Postoperative shivering | Just et al. | 14 | 2.3 | 141 ± 9 mL/min/m 2 | 269 ± 60 mL/min/m 2 | < 0.001 |
| Duration of postanesthetic recovery | Lenhardt et al. | 150 | 1.9 | 53 ± 36 min | 94 ± 65 min | < 0.001 |
| Plasma [norepinephrine] | Frank et al. | 74 | 1.5 | 330 ± 30 pg/mL | 480 ± 70 pg/mL | < 0.05 |
| Thermal discomfort | Kurz et al. | 74 | 2.6 | 50 ± 10 mm VAS | 18 ± 9 mm VAS | < 0.001 |
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