Humans are essentially biochemical furnaces that burn food to fuel with a complex array of metabolic functions. These chemical reactions consume substrate, generate usable energy, and produce byproducts that must be eliminated for continued operation of the system. Water and carbon dioxide are produced and eliminated in large quantities, as well as urea, sulfates, phosphates, and other chemical byproducts. These reactions are exothermic and combine to produce a basal metabolic rate that amounts to approximately 100 kCal/h for a 70-kg person. In the absence of cooling mechanisms, this baseline metabolic activity would result in a 1.1°C (2°F) hourly rise in body temperature.

Heat production can be increased 20-fold by strenuous exertion. Rectal temperatures as high as 42°C (107.6°F) have been recorded in trained marathon runners, without ill effects. Metabolic factors (hyperthyroidism and sympathomimetic drug ingestion) can dramatically increase heat production. Environmental heat not only adds to the heat load but also interferes with its dissipation. The physics of heat transfer as it relates to human physiology involves four mechanisms—conduction, convection, radiation, and evaporation.

The regulation of body temperature involves three distinct functions—thermosensors, a central integrative area, and thermoregulatory effectors.

Thermosensors

Temperature-sensitive structures are located peripherally in the skin and centrally in the body. However, skin temperature changes correlate poorly with changes in the rate of heat loss. Thermosensitive neurons, located in the preoptic anterior hypothalamus, are activated when the temperature of the blood circulating through that area exceeds a set point ( Fig. 129.1 ).

Preoptic Anterior Hypothalamus.

Adapted from Nuclei of the hypothalamus. bhavanajagat.files.wordpress.com/2012/07/nuclei-of-hypothalamus.jpg .

The skin temperature affects heat loss when a person resting in a warm environment initiates sweating, even though the core temperature remains constant. In contrast, changes in core temperature are more dominant than skin temperature changes in producing heat-dissipating responses.

Acclimatization is the constellation of physiologic adaptations that occur in a normal person as the result of repeated exposures to heat stress. Daily exposure to work and heat for 100 min/day results in near-maximal acclimatization within 7 to 14 days. This is characterized by an earlier onset of sweating (at a lower core temperature), increased sweat volume, and lowered sweat sodium concentration. Acclimatization is hastened by modest salt deprivation and delayed by high dietary salt intake.

The cardiovascular system plays a major role in acclimatization and endurance training, largely resulting from an expansion of plasma volume. Heart rate is lower and associated with a higher stroke volume. Other physiologic changes include earlier release of aldosterone, although acclimatized individuals generate lower plasma levels of aldosterone during exercise heat stress. Total body potassium depletion of up to 20% (500 mEq) by the second week of acclimatization can occur as a result of sweat and urine losses, coupled with inadequate repletion.

Although many similarities exist among thermoregulatory responses to heat and exercise, the well-conditioned athlete is not necessarily heat-acclimatized. For heat and exercise-induced adaptive responses to be maintained, heat exposure needs to continue intermittently, at least on 4-day intervals. Plasma volume decreases considerably within 1 week in the absence of heat stress.

Advanced age, psychiatric conditions, chronic disease, obesity, and certain medications increase the risk for classic heatstroke during periods of high heat and humidity. Adequate fluid intake is essential. Older adults often overdress during hot weather conditions. Heat loss is maximized by light, loose-fitting garments.

Exertional heatstroke is most likely to occur in young healthy people involved in strenuous physical activity, especially if they have not acclimatized to environmental factors that overwhelm heat-dissipating mechanisms. For example, wrestlers frequently fast, restrict food and fluid intake, and exercise vigorously wearing vapor-impermeable clothing in an effort to maintain or drop their current weight class. Pre-existing illness may not increase the risk of exertional heat stroke. Fluid intake is the most critical variable. Dehydration can be minimized by education on work-rest cycles and fluid consumption, and through provision of cool flavored fluids.

The goal is to maximize voluntary fluid intake and gastric emptying so that fluid can rapidly enter the small intestine, where it is absorbed. Gastric emptying is accelerated to 25 mL/min by large fluid volumes (500 to 600 mL) and cool temperatures (10°C to 15.8°C [50°F to 60.4°F]). High osmolality inhibits gastric emptying; osmolality of less than 200 mOsm/L is optimal. Most commercially available electrolyte solutions contain excessive sugar. Hydration can be monitored by measurement of body weight before and after training or athletic competition. An athlete with a loss of 2% to 3% body weight (1.5 to 2 L in a 70-kg man) should drink extra fluid and be permitted to compete only when his or her body weight is within 0.5 to 1 kg (1 or 2 pounds) of the starting weight on the previous day. A weight loss of 5% or 6% represents a moderately severe deficit and usually is associated with intense thirst, scant dark-colored urine, tachycardia, and increase in rectal temperature of approximately 2°C (3.6°F). These athletes should be restricted to light workouts after hydration until they return to normal weight. A loss of 7% or more of body weight represents severe water depletion; participation in sports should not be permitted until the athlete is evaluated by a physician or sports trainer. The administration of salt tablets during strenuous exercise can cause delayed gastric emptying, osmotic fluid shifts into the gut, gastric mucosal damage, and hypernatremic dehydration. A 6-g sodium diet is sufficient for successful adaptation for work in the heat, with sweat losses averaging 7 L/day. Excessively high salt intake in relation to salt losses in sweat during initial heat exposure can impair acclimatization because of the inhibition of aldosterone secretion. Excessive salt ingestion can also exacerbate potassium depletion.

Evaporative cooling can be lost when clothing inhibits air convection and evaporation. Water evaporated from clothing is much less efficient for body cooling than water evaporated from the skin. Loose-fitting clothing or ventilated fishnet jerseys allow efficient evaporation. Light-colored clothing reflects rather than absorbs light.

The heat dissipation mechanisms of the body are analogous to the cooling system of an automobile ( Fig. 129.2 ). Coolant (blood) is circulated by a pump (heart) from the hot inner core to a radiator (skin surface cooled by the evaporation of sweat). Temperature is sensed by a thermostat (CNS), which alters coolant flow by a system of pipes, valves, and reservoirs (vasculature). Failure of any of these components can result in overheating.

Predisposing factors for heat illness, an automotive analogy.

Effective circulation requires an intact pump and adequate coolant levels. β-adrenergic blocking agents or calcium channel blockers may prevent an increase in cardiac output sufficient to produce the necessary peripheral vasodilation to dissipate heat. Dehydration caused by gastroenteritis, diuretics, or inadequate fluid intake predisposes to heat illness. Individuals working in the heat seldom voluntarily drink as much fluid as they lose and replace only approximately two-thirds of net water loss (so-called voluntary dehydration). Dehydration alone increases body temperature at rest by increasing the work of the sodium-potassium adenosine triphosphatase pump, which accounts for 25% to 45% of the basal metabolic rate. This is particularly true in cases of hypernatremic dehydration. The pipes and valves of the coolant system may be abnormal in diabetic or older patients with extensive atherosclerosis.

Radiator function depends on the skin and sweat glands. Occlusive, vapor-impermeable clothing hinders evaporative and convective cooling. Anticholinergic medications and stimulant drugs of abuse interfere with sweating and contribute to heat illness. Various skin diseases, including miliaria (prickly heat rash), extensive burns, scleroderma, ectodermal dysplasia, and cystic fibrosis, are risk factors. Anhidrosis can also be secondary to central or peripheral nervous system disorders.

Increased heat production causing heat illness most often accompanies exercise in a hot humid environment. When heat and humidity are extreme, exertion is not necessary to produce heat-related problems. Several indices help objectify heat strain. These indices can be divided into two categories, heat scales based on meteorologic parameters and those that combine environmental and physiologic parameters.

The wet bulb globe temperature heat index is an excellent meteorologic measure of environmental heat stress ( Box 129.1 ). It measures the effects of temperature, humidity, and radiant thermal energy from the sun. When climatic conditions exceed 25°C (77°F) wet bulb, even healthy people are at high risk during exercise. Above 28°C (82.4°F), exercise and strenuous work should be avoided or limited to extremely short periods of time.

It is diagnostically and therapeutically important to identify patients suffering from a febrile response rather than heat illness. Fever does not cause primary pathologic or physiologic damage to humans and does not require primary emphasis in the therapeutic regimen, which is directed at the underlying disease state. If temperature-related physiologic changes such as febrile seizures and tachycardia compromise a patient with marginal cardiac reserve, the temperature should be artificially regulated with antipyretics. In contrast, antipyretics are not effective against heat illness and are not recommended to control environmental hyperthermia.

Miliaria produces intensely pruritic vesicles on an erythematous base. The rash is confined to clothed areas, and the affected area is often completely anhidrotic. During the next week, a keratin plug develops and fills these vesicles, causing a deeper obstruction of the sweat gland duct. The obstructed duct then ruptures a second time, producing a deeper vesicle within the dermis. This is known as the profunda stage, and it can persist for weeks. Profunda vesicles are not pruritic and closely resemble the white papules of piloerection. Chronic dermatitis is a common complication ( Fig. 129.3 ).

Prickly Heat.

From Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 3rd ed. St. Louis: Mosby; 1996.

Alternative diagnoses include contact dermatitis, cellulitis, and allergic reactions. A heat exposure history and distribution of the rash will solidify the diagnosis.

Laboratory data is not indicated with miliaria.

Miliaria rubra can be prevented by wearing light, loose-fitting, clean clothing and avoiding situations that produce continuous sweating. Avoid routine use of talcum or baby powder. Gentle exfoliation may help to remove debris that occlude the eccrine sweat ducts. However, soap may cause additional skin irritation. Topical corticosteroids, such as hydrocortisone 2.5% or triamcinolone 0.1% twice a day for one to two weeks, may decrease pruritus and inflammation but is not required for the resolution of miliaria. Patients can be discharged with dermatologic or primary care follow-up.

Athletes, roofers, steelworkers, coal miners, field workers, and boiler operators are among the most common victims of heat cramps. Heat cramps tend to occur after exercise, when the victim stops working and is relaxing ( Box 129.2 ). In this respect, they differ from the cramps experienced by athletes during exercise, which tend to last for several minutes, are relieved by massage, and resolve spontaneously.

Heat cramps are occasionally confused with hyperventilation tetany, which can occur during heat exhaustion. Hyperventilation tetany can be distinguished by the presence of carpopedal spasm and paresthesias in the distal extremities and perioral area.

Heat cramps accompanied by systemic symptoms may be part of salt depletion heat exhaustion. Check serum electrolyte levels as heat cramp victims often exhibit hyponatremia and hypochloremia. Rhabdomyolysis or resultant renal damage is not present with isolated heat cramps.

Heat cramps are rapidly relieved by salt solutions. Many commercially available flavored electrolyte solutions are available. Mild cases without concurrent dehydration are treated orally with a 0.1% or 0.2% salt solution (two to four 10-grain salt tablets [56 to 112 mEq] or ¼ to ½ teaspoon of table salt dissolved in 1 quart of water), which is the general limit of palatability. Severe cases respond rapidly to an infusion of normal saline. Salt tablets are gastric irritants, delay gastric emptying, and are not recommended as treatment. Although most patients do not seek medical treatment, most patients with heat cramps may be safely discharged after the administration of balanced salt solutions and clinical improvement.

Swollen feet and ankles are often reported by non-acclimatized individuals, especially older adults, who encounter climatic stresses of tropical and semitropical areas. They commonly have schedules that involve long periods of sitting or standing. The edema is usually minimal, is not accompanied by any significant impairment in function or ambulation, and often resolves after several days of acclimatization.

Differentiate heat edema from congestive heart failure, liver disease states, nephrosis, lower extremity infections, and deep venous thrombosis.

Awareness of this clinical presentation prevents overly vigorous diagnostic and therapeutic intervention. A brief diagnostic evaluation to rule out thrombophlebitis, lymphedema, or congestive heart failure may be appropriate, but invasive diagnostic techniques are not indicated.

Pharmacologic therapy is not indicated, and diuretic therapy is not effective. Simple leg elevation or thigh-high support hose should be used. In most individuals, the problem resolves through adequate acclimatization or with the individual’s return to a temperate climate. Given its benign nature, patients with heat edema can be safely discharged with outpatient follow-up.