The body produces heat as a direct result of its metabolic activities. The major organs, and in particular the brain, generate the greatest proportion of this heat. In addition, muscle can significantly contribute to this, but usually only during relatively brief periods of intense use.3,4 Thermal energy within the body is distributed between central (core) and peripheral compartments. The core compartment consists of the trunk (including the major organs) and the head. The skin (including superficial tissues of the trunk) as well as the arms and legs represent the peripheral compartment.5 Temperature in this peripheral compartment is usually 2°C to 4°C lower than the core—a gradient that becomes highly relevant when anesthesia is induced and vasodilation occurs.3,5
Just as defining terms for what comprises normothermia and hypothermia is important, choosing an appropriate site for monitoring is equally so. Wide discrepancies exist between different body sites and for different operative situations.6,7 The skin is a peripheral temperature monitoring site and correlates poorly to core temperature.8 Core temperature, a term widely used by anesthesiologists, is somewhat nebulously defined, but is generally accepted to reflect mean temperature of the well-perfused organs (ie, brain, heart, kidney, and lungs). Acceptable sites for measurement of core temperature include the tympanic membrane, nasopharynx, esophagus, and bladder.
Similar to many other physiologic systems, the thermoregulatory system has at least 3 major components: (1) sensory receptors (an afferent limb), (2) a central integrator or controller, and (3) an effector organ system (an efferent limb). The sensory receptors provide information from thermosensitive sites in the skin and other body structures (spinal cord and viscera) to a central controller that then integrates this information and compares it with a standard reference or set-point (Fig. 88-1).2,9 The skin, deep tissues (viscera), spinal cord, hypothalamus, and other brain structures each contribute approximately 20% of the input to the autonomic thermoregulatory control center. On the basis of the difference between the afferent input and the target set-point, the controller provides information to effector systems that then initiate changes to regulate heat production or loss.
There is general agreement that the anterior hypothalamus is the central controller for body temperature, comparing the afferent input with the central set-point, and instituting an appropriate autonomic neural response. Investigations by neuroanatomists and neurophysiologists have greatly increased understanding of how the 3 components of the thermoregulatory system function to maintain a thermal balance; details concerning these experimental studies are the subject of numerous books and review articles.2,5,10-15
An important concept to consider in the control of temperature is the inter-threshold range. This is defined as the range between which thermoregulatory responses to cold versus those for warmth are activated. That is, if body temperature is in this range, no autonomic thermoregulatory defenses are triggered. In the normal adult, this range is typically 0.2°C but may be wider in the elderly.9,16
Anesthesia significantly widens the inter-threshold range to as much as 4°C.17-20 With a range this wide, it becomes easy to understand that under anesthesia, body temperature is greatly influenced by the surrounding environment and trends toward equilibrating with ambient temperature, thus defining the anesthetized patient as poikilothermic. Thermoregulatory responses are diminished in the elderly and may also be attenuated in persons with poor general health. An impairment of the skin sympathetic nerve traffic responses to thermal challenge has been demonstrated in the elderly.21 This impairment of thermoregulation and vasoconstrictor response has been seen even in mild thermal (cold) challenges.22 In contrast to the elderly, premature infants appear to have an intact central thermoregulatory control.
Normal Thermoregulatory Efferent Responses
In normal, unanesthetized humans, behavioral regulation (dressing appropriately and/or modifying environmental temperature) is one of the most important mechanisms contributing to heat regulation. After this behavioral adjustment is made, humans further regulate heat exchange with their environment by balancing several thermoregulatory effects: (1) cutaneous vasomotor tone adjustments (vasodilation, vasoconstriction), (2) sweating, (3) shivering, and (4) nonshivering thermogenesis.
In hypothermic situations where the hypothalamus activates heat conservation and production mechanisms, thermoregulatory vasoconstriction occurs via the activation of arteriovenous shunts in the periphery.23 Arteriovenous shunts (approximately 100 μm in diameter, roughly 10 times the size of a capillary) are located primarily in the fingers, toes, and nose. Cutaneous vasoconstriction can reduce heat loss by modulating convection and radiation from the skin surface. Shunt vasoconstriction initially halves the heat loss from the fingers and toes via a reduction of peripheral blood flow. This ultimately leads to a gradual cooling of the arms and legs.24 These shunts are controlled by centrally mediated α-adrenergic receptors in response to the release of norepinephrine from presynaptic adrenergic nerve terminals.25 In addition to the centrally mediated vasoconstriction, there is also a component of nonadrenergic vasoconstriction that can occur in response to local cooling.26
Cutaneous vasoconstriction is usually the first and most consistent thermoregulatory response to hypothermia. This vasoconstriction raises thermal insulation provided by the skin and can decrease whole body heat loss by 25% to 50%.27,28 If heat loss continues and core temperature continues to fall, shivering, with its metabolically driven increases in heat production, is initiated.
The shivering response is the primary mechanism activated to increase heat production when hypothermic conditions persist in the presence of thermoregulatory constriction; it is dependent on central neuronal coordination and normal neuromuscular function. Shivering is initiated only after the failure of maximal vasoconstriction, nonshivering thermogenesis (in neonates), and behavioral adjustments have proven to be inadequate to maintain target body temperature (see Fig. 88-1). Shivering is an energy-inefficient means of heat production and can cause a 2- to 3-fold increase in whole-body oxygen consumption.29 Cardiac output is directly dependent on metabolic rate. As a result, patients who shiver have a higher cardiac index and heart rate during maximal muscular activity.30 This metabolic effect of shivering on oxygen consumption depends on its intensity and the affected muscle mass.31 The actual increase reported in the literature has been widely variable (from as low as 7% to >700%), depending on the clinical situation, selected sample, and measuring technique.32 More often, it is considered in the 200% to 400% range.4,8
Intermediate between the efferent vasoconstrictive and shivering thermoregulatory responses to cold is nonshivering thermogenesis. This response, occurring in both normal and premature infants, increases metabolic heat production without inducing any mechanical work.33 Brown adipose tissue is an important site of nonshivering heat production in the neonate. The brown fat is rich in mitochondria (which gives it its brownish macroscopic hue) and is distributed over the neck, back, viscera, and great vessels. The metabolism of brown fat is initiated by β3-adrenergic effects on terminal nerves within it.34 Although the exact mechanism of heat production is not clearly understood, it is thought that it is either related to an uncoupling of oxidative phosphorylation within the mitochondria in the presence of fatty acids or results from lipolysis-lipogenesis coupled with ATP utilization.2 It is generally agreed that nonshivering thermogenesis does not occur in adult humans.35
Under static conditions, heat produced by the body's metabolic process must eventually be dissipated to the environment. Close to 95% of this heat traverses the skin, with the remainder occurring via the respiratory tract. As a result, factors that modulate heat loss must involve the skin itself, either directly via sweating or indirectly via modifying cutaneous blood flow. Sweating is the most effective method of heat loss. Evaporation of sweat is an energy-absorbing process. In a dry environment, sweating alone can easily dissipate the heat generated at basal levels. Furthermore, an increase in temperature of 0.5°C can produce a 7-fold increase in sweat rate and body conductivity.10,36,37 Sweating is mediated by cholinergic sympathetic fibers and can be nearly abolished by even small doses of atropine—something to consider in the perioperative state. Vasodilation is important for the transfer of heat from the core to the periphery. Sweating and vasodilation responses work synchronously to counter any increases in core temperature, with vasodilation increasing cutaneous blood flow and heat delivery for the evaporative sweating heat loss mechanism.38