Physiology of Heat

Heat Regulation

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

Acclimatization

Acclimatization is defined as “a constellation of physiologic adaptations that appear 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 in 7 to 14 days. This is characterized by an earlier onset of sweating (at a lower core temperature), increased sweat volume, and lowered sweat electrolyte concentration. Acclimatization is hastened by modest salt deprivation and delayed by high dietary salt intake. As acclimatization proceeds, the sweat sodium concentration decreases while the volume increases.¹¹

The cardiovascular system plays a major role in both acclimatization and endurance training, largely resulting from an expansion of plasma volume.¹² 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.¹²

Although many similarities exist between 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.¹²

Predisposing Factors for Heat Illness

Elderly patients, psychiatric patients, or those with chronic diseases who are taking medications predisposing to heat illness are prone to classic heatstroke during periods of high ambient heat and humidity. Adequate fluid intake is essential. Elderly patients sometimes dress inappropriately for hot weather; 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. 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, pleasantly 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 (500-600 mL) and cool temperatures (10-15.8° C). 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 or 3% body weight (1.5-2 L in a 70-kg man) should drink extra fluid and be permitted to compete only when 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, scanty urine, tachycardia, and increase in rectal temperature of approximately 2° C. Such 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 examined by a physician. Wrestlers frequently fast, restrict food and fluid intake, and exercise vigorously wearing vapor-impermeable clothing to lose weight quickly so that they can compete in a lower weight class.¹³

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 inhibition of aldosterone secretion. Excessive salt ingestion can also exacerbate potassium depletion.

Evaporative cooling can be lost when clothing inhibits air convection and evaporation. Loose-fitting clothing or ventilated fishnet jerseys allow efficient evaporation. Light-colored clothing reflects rather than absorbs light. Water evaporated from clothing is much less efficient for body cooling than is water evaporated from the skin.14,15

The body’s heat dissipation mechanisms are analogous to the cooling system of an automobile (Fig. 141-1). 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.

Effective circulation requires both an intact pump and adequate coolant levels. Individuals with cardiac disease or those taking beta-adrenergic blocking agents or calcium channel blockers may be unable to increase their cardiac output sufficiently 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 (“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 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 elderly 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 some drugs of abuse interfere with sweating and produce heat illness.¹¹ Various skin diseases, including miliaria (prickly heat rash), extensive burns, scleroderma, ectodermal dysplasia, and cystic fibrosis, are risk factors. Anhidrosis can be secondary to either central or peripheral nervous system disorders as well.

Increased heat production causing heat illness most often accompanies exercise in hot, humid environments. Athletes and military recruits are commonly affected. When heat and humidity are extreme, exertion is not necessary to produce heat-related problems. Several indices help objectify heat strain. The indices can be divided into two categories: heat scales that are based on meteorologic parameters only and heat scales that combine environmental and physiologic parameters.¹⁶

The wet bulb globe temperature heat index is an excellent meteorologic measure of environmental heat stress (Box 141-1). It includes the effects of temperature, humidity, and radiant thermal energy from the sun. When climatic conditions exceed 25° C wet bulb, even healthy people are at high risk if they choose to exercise. Above 28° C, exercise and strenuous work should be avoided or limited to extremely short periods.¹⁷

The heat strain index is widely accepted as an example of an index that includes environmental and physiologic factors. There are several variations and modified heat strain indices in existence, with varying ease of use and accuracy (Fig. 141-2).¹⁶

Before the advent of air conditioning, mortality increased threefold to fivefold in nursing homes and threefold in the general population during heat waves. Mortality in geriatric patients correlates with average weekly peak air temperature. Most deaths in the 2003 European heat wave occurred in elderly patients. Microclimates conducive to heat illness are produced in the interiors of automobiles, tanks, and tents in the sun as well as in engine rooms, hot tubs, and saunas.⁴ Children are more susceptible to heat stressors because the higher surface area–to–mass ratios allow increased absorption of heat. They also have lower sweat rates per gland.¹⁸

Endogenous factors, such as hyperthyroidism and pheochromocytoma, can also drastically increase heat production. An overdose of sympathomimetics or stimulants, such as amphetamines, cocaine, and phencyclidine, can cause fatal hyperpyrexia. High ambient temperature is associated with a significant increase in mortality from cocaine overdose. Many younger patients who die of hyperthermia test positive for cocaine.¹⁹ Heatstroke can occur with delirium resulting from ethanol withdrawal.²⁰ There are also reports of heatstroke occurring in well-trained military soldiers or athletes who ingest dietary supplements containing ephedrine or the ergogenic aid creatine.^21,22

Certain patients undergoing general anesthesia rapidly experience severe hyperthermia, muscle rigidity, and acidosis. This syndrome, termed malignant hyperthermia, is the result of a genetically determined instability of skeletal muscle sarcoplasmic reticulum that allows inappropriate intracellular calcium release. Dantrolene, which lowers myoplasmic calcium, is effective in the prevention and treatment of this syndrome.²³

Malignant hyperthermia is rarely seen in outpatient settings, but a clinically similar entity, neuroleptic malignant syndrome, is often encountered. This syndrome is induced by antipsychotic medications and is characterized by muscle rigidity, severe dyskinesia or akinesia, hyperthermia, tachycardia, dyspnea, dysphagia, and urinary incontinence. Although the lead-pipe rigidity and hyperthermia are reminiscent of malignant hyperthermia, the putative mechanism is different. Dopamine receptor blockade in the corpus striatum caused by butyrophenones and similar agents produces severe muscle spasticity and dystonia, leading to overproduction of heat. Some antipsychotics also cause suppression of thirst recognition. Other miscellaneous risk factors include obesity.²⁴ Individuals with a history of heatstroke, with or without an inherent aberration that predisposed them to the initial episode, are at increased risk for a recurrence.

Fever versus Hyperthermia

It is both diagnostically and therapeutically important to identify patients suffering from a febrile response rather than heat illness. For many years, fever was attributed to pyrogens released by bacteria or viruses (exogenous pyrogens) or to cells undergoing autolysis after phagocytic activity (endogenous pyrogens).²⁵ These circulating pyrogens would directly affect the thermoregulatory control center. It now appears that fever is the result of triggering by pyrogens of pathways involving cytokine receptors or other signals to reset the thermal set point in the preoptic area of the anterior hypothalamus to a new level above 37° C.²⁵

Once this temperature is established, the thermoregulatory center uses all available heat-regulatory servomechanisms to maintain the new temperature. Thus a patient with fever in an environment previously believed to be thermally comfortable begins to feel cold and chooses a warmer environment. This behavioral drive is coordinated with the autonomic mechanisms, such as shivering, to increase body temperature to the new set point. In most circumstances, temperature elevation is not a significant problem, and therapy is directed at the underlying disease state. 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, temperature must be artificially regulated.

Because fever is the product of a molecular interaction that establishes a new physiologic thermal set point, therapeutic attempts to lower temperature are opposed by body mechanisms that attempt to maintain the new set point. Thus attempts at whole-body cooling produce violent shivering and discomfort.²⁶ The use of agents to block the causative molecular interaction is the most clinically effective approach. Antipyretics block the action of the pyrogen at hypothalamic receptor sites through inhibition of prostaglandin synthesis.²⁷ These antipyretics are not effective against and should not be used to control environmental hyperthermia.

Heat Cramps