Thermoregulation
Adnan M. Bakar
Charles L. Schleien
KEY POINTS
Extreme variations in environmental temperature disrupt thermoregulatory function and lead to heat-related illness.
Prevention is essential in avoiding the complications of heat-related illness.
Modulation of the systemic inflammatory response is an important determinant of compensated versus decompensated response to heat-related injury.
Heat stroke is a medical emergency. Prompt and aggressive cooling to below 39°C within 30 minutes of onset of illness prevents a high mortality rate.
The superior method of cooling has not been proven.
Hypothermia can occur due to exposure to cold and other etiologies when thermoregulation is overwhelmed or dysfunctional.
Children are at increased risk for hypothermia due to their body morphology and faster cooling rates.
The choice of rewarming method for hypothermia depends on the degree of hypothermia and the presence or absence of cardiac arrest.
Resuscitation of the hypothermic patient with cardiac arrest should be continued until the core temperature is 34°C, spontaneous circulation has occurred, or lethal injuries are identified.
Prevention and early recognition can limit the incidence, morbidity, and mortality of accidental hypothermia.PHYSIOLOGY OF THERMOREGULATION
Normal body temperature is maintained constant by a balance of heat loss and heat gain with the assistance of an efficient thermoregulatory mechanism. Extreme environmental temperature variations, however, can overcome this effective 
thermoregulatory function and lead to heat- or cold-related illnesses.
thermoregulatory function and lead to heat- or cold-related illnesses.Body temperature consists of core and shell temperatures. Rectal, esophageal, bladder, and oral temperatures represent core temperature, whereas axillary and skin temperatures represent shell temperature. Core temperature determines the risk of injury to various organs in the body. Air temperature, air movement, thermal radiation, sweating, skin blood flow, and temperature of underlying tissue all influence shell temperature (1). Thermoreceptors for the shell reside in the skin. Core thermoreceptors exist in the cortex, hypothalamus, midbrain, medulla, spinal cord, and deep abdominal structures in addition to the skin (2,3). On sensing a temperature change, these receptors transmit afferent impulses via the lateral spinothalamic tract to the central thermostat located in the preoptic/anterior hypothalamus, which maintains the temperature set point (4). Thermoregulation is initiated when sensed temperature is different from the set point. The conditions associated with failed thermoregulatory mechanisms that lead to hyperthermia or hypothermia will be discussed in this chapter.
Heat Gain
Warm-blooded animals have the capacity to raise their body temperature above their environmental temperature, which occurs when endogenous or exogenous heat gain exceeds heat loss. Heat is generated in the human body from basal metabolism, physical activity, food consumption, metabolic activity, emotional change, hormonal effects, and certain medications that typically raise body metabolism. The body may also acquire heat passively when the environmental temperature exceeds body temperature.
Heat Loss
Heat is lost from the body via conduction, convection, radiation, and evaporation. In most situations, humans produce more heat than necessary and dissipate the excess heat into the environment.
Conduction is heat loss by the transfer of heat from a warmer to a cooler object when the two objects are in direct contact. The amount of heat loss depends on the contact area and the temperature difference between the body and the other surface. Typically, only 3% of body heat is lost by conduction; however, conduction may be a major source of heat loss in wet clothing or immersion incidents because of the excellent conductive properties of water.
Convection is heat loss by the movement of air or fluid that circulates around the skin. More heat is carried away from the body in windy conditions, as the movement of air rapidly removes the insulating layer of warmer air normally around the body surface. Approximately 12%-15% of body heat is lost by convection.
Radiation is heat loss due to infrared heat emission to surrounding air. Heat loss occurs primarily from the head and noninsulated areas of the body and usually occurs rapidly. Radiation can account for 55%-65% of heat loss.
Evaporation is heat loss by the change of water from a liquid (sweat) to a gas state via the skin or respiration. Evaporation normally accounts for 25% of heat loss, but depends on surface area, temperature difference, and humidity. Evaporative heat loss is highest in cold, dry, and windy conditions (5).
HYPERTHERMIA
Definitions
Hyperthermia refers to body temperature elevation beyond the hypothalamic set point because of inadequate heat loss and/or excessive heat gain. Cytokines do not mediate this temperature elevation in contrast to fever (see what follows), as the hypothalamic set point itself has not changed. Hence, antipyretics (aspirin, acetaminophen, nonsteroidal antiinflammatories), which lower the set point, have no effect. Extreme temperature elevations (>41°C) are common in the hyperthermic patient.
Fever represents a regulated temperature elevation (>38.5°C) to a new higher set point in the hypothalamus. It is caused by the release of pyrogens from macrophages/monocytes. These include the cytokines interleukin-1 (IL-1), tumor necrosis factor (TNF), interferon (IFN)-γ, and IL-6, which are released in response to inflammatory stimuli such as infection, malignancy, autoimmune disease, and other disease states. Cytokine-induced fever rarely exceeds 41°C, with the exception of some cases of encephalitis and meningitis.
Classification of Hyperthermia Syndromes
Hyperthermia syndromes may be classified as environmental (or exertional), drug (or toxin)-induced, or of genetic/unknown origin. Considerable overlap exists among these groups, as patients with a genetic predisposition may be more susceptible to environmental/exertional or drug-induced hyperthermia.
TABLE 36.1 RISK FACTORS FOR HEAT-RELATED ILLNESS | ||||||||||||||||
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These syndromes have similar patient presentation. However, certain aspects of the clinical presentation may be unique or exaggerated, depending on the specific entity. Hyperthermia may induce euphoria instead of discomfort, resulting in failure to seek prompt medical attention. Even in the most severe form of heat illness, early clinical signs are nonspecific. The severity of heat-related injury depends on the degree of core temperature elevation and its duration. Therefore, preventive measures, early diagnosis, and aggressive treatment are essential components of a good outcome (6).
Heat Stroke (Environmental/Exertional Heat-Related Illness)
Heat-related illnesses comprise a spectrum of diseases that ranges from heat stress—a benign condition—to heat stroke—a potentially fatal condition. The milder conditions (variously termed heat rash, heat cramps, heat edema, and heat exhaustion) generally do not require PICU management.
Between 1979 and 2002, there were 4780 heat-related deaths in the United States. Only 6% of these patients were <15 years of age, 50% were between 15 and 64 years old, and 44% were >65 years old. It is estimated that heat stroke caused more American deaths during this time period than the effects of hurricanes, lightning, earthquakes, tornadoes, and floods combined (7).
Heat stroke is characterized by an elevation of core temperature above 40°C, commonly with nervous system dysfunction manifesting in delirium, convulsions, or coma. Death associated with heat stroke has been estimated as high as 50%, and those who do survive may sustain permanent neurologic damage (8). Heat stroke is subdivided into classic (environmental) or exertional. The mechanism of classic heat stroke that follows exposure to high environmental temperature is more common in younger children who are unable to escape from the hot environment, or in those who may have an underlying condition that causes thermoregulatory dysfunction. While exertional heat stroke may occur in temperate environments, the risk is higher when the individual engages in heavy exercise in hot and humid conditions.
Exertional heat stroke often may be linked to a genetic predisposition. Individuals with a predominance of type II muscle fibers are more susceptible to exertional heat stroke. These individuals have lower exercise capacity and accumulate more lactate, which, in turn, directly activates the cell membrane sodium/potassium pump (Na/K-ATPase). Activation of Na/K-ATPase affects intracellular sodium and calcium resulting in depletion of cellular energy stores (9). The loss of mitochondrial function and disturbed calcium (Ca2+) homeostasis activate phospholipase A2, resulting in the production of free radicals, prostaglandins, leukotrienes, and calcium-dependent proteases and the eventual development of rhabdomyolysis (10). Rhabdomyolysis results from free radical-induced lipid peroxidation and overload of cellular and mitochondrial calcium, primarily resulting in muscle necrosis.
PreventionUnderstanding the risk factors for heat stroke better allows for more effective preventive measures. Previously it was thought that children were more prone to heat-related illness than adults because they were less effective at regulating body temperature, incurred greater cardiovascular strain for similar amounts of work, had diminished sweating capacity, and had a lower exercise tolerance in heat (11,12,13
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