2134 American Family Physician www.aafp.org/afp Volume 71, Number 11 ��� June 1, 2005 is characterized by rapid onset���developing in hours���and frequently is associated with high core temperatures. Heat exhaustion is a more common and less extreme manifestation of heat-related illness in which the core temperature is between 37��C (98.6��F) and 40��C. Symptoms of heat exhaustion are milder than those of heatstroke, and include dizziness, thirst, weakness, headache, and malaise. Patients with heat exhaustion lack the profound cen- tral nervous system derangement found in those with heatstroke. Their symptoms typi- cally resolve promptly with proper hydration and cooling. Physiology Heat is exchanged with the environment in four ways: conduction, convection, radia- tion, and evaporation. Conduction refers to heat loss through direct contact with a cooler object. Convection is the dissipation of heat when relatively cool air passes over exposed skin. Radiation is the release of heat from the body directly into the environment. Evapo- ration through perspiration is the body���s most effective method of cooling under most circumstances, dissipating up to 600 kcal per hour in optimal conditions.5 Hypothalamic thermoregulation processes (peripheral vaso- dilation, thermal sweating, cardiac changes) are activated by core temperature increases of less than 1��C (1.8��F).6 Endurance athletes perspire at a rate of up to 1.5 L per hour, and the body is capable of twice that.7,8 Heat exchange is dependent on gradients of temperature and moisture as the ambient temperature and humidity increase, thermal transfer becomes less efficient. Thus hot, humid weather confers the highest risk of heat injury. Heart rate, cardiac output, and minute ventilation increase under hyper- thermic conditions, while visceral perfusion decreases. Medications such as vasocon- strictors and beta blockers can profoundly impact thermoregulation by decreasing the body���s ability to shunt large volumes of hyperthermic blood away from the core and to the skin (Table 1).9-11 After several weeks in a hot environ- ment the body can adapt and become more efficient. The primary response involves salt retention and increased fluid secretion through the sweat glands. Other changes include increased circulating plasma vol- Strength of Recommendations Key clinical recommendation Label References Cooling by evaporation is the most effective method in the field under normal conditions patients with heatstroke should initially be treated with evaporative cooling. B 25 Community collaboration and intervention programs decrease morbidity and mortality associated with heat. B 30, 32 Fans alone are inadequate in the prevention of heat-related illness, and physicians should encourage other preventive measures such as maintaining hydration, avoidance of heat, and acclimatization. C 9, 31 Early cooling is thought to reduce mortality associated with heatstroke treatment in the field should be initiated as soon as possible. C 22, 24 A = consistent, good-quality patient-oriented evidence B = inconsistent or limited-quality patient-oriented evidence C = consensus, disease-oriented evidence, usual practice, opinion, or case series. See page 2029 for more information. The Author JAMES L. GLAZER, M.D., is assistant director in the Department of Family Medicine and the Division of Sports Medicine at Maine Medical Center, Portland, Me. He completed a family practice residency at the Maine-Dartmouth Family Practice Residency, Augusta, Me., and a sports medicine fellowship at the University of Kentucky, Lexington. Address correspondence to James L. Glazer, M.D., Maine Medical Center, Department of Family Practice, 272 Congress St., Portland, ME 04101 (e-mail: glazej@mmc.org). Reprints are not available from the author.

June 1, 2005 ��� Volume 71, Number 11 www.aafp.org/afp American Family Physician 2135 Heatstroke ume, enhanced glomerular filtration rate, and an increase in the kidneys��� ability to withstand exertional rhabdomyolysis.12 A number of acute-phase reactants pro- tect against tissue injury in response to heat stress.13 In addition, cells transcribe heat shock proteins to protect themselves from the effects of sudden heating.14 These are thought to work as chaperones by attaching to cellular proteins and preventing them from unfolding in hot environments. Pathophysiology Heatstroke and heat exhaustion occur when the body���s thermoregulatory responses are inadequate to preserve homeostasis. This can result from extrinsic factors that make heat dissipation less efficient, such as extremes of temperature, physical effort, and environ- mental conditions. It also can result from physiologic limitations, putting children, elderly persons, and those who are chronically ill at increased risk. Chronic volume deple- tion, medication use, inability to increase cardiovascular output, normal deficiencies in heat shock protein responses associated with aging, and lack of acclimatization all can inhibit the body���s ability to respond to heat challenges. The term thermal maximum was devel- oped to measure the magnitude and dura- tion of heat that cells can encounter before becoming damaged. Human thermal maxi- mum has been established as a core body temperature of approximately 42��C (107.6��F) for between 45 minutes and eight hours.15 Cellular destruc- tion occurs more quickly and completely at higher temper- atures. Inflammatory factors are released and gastrointestinal permeability increases, which may allow endotoxins into the cir- culation.16 Hematologic and endothelial changes resembling disseminated intervas- cular coagulation also occur.17 Clinical Presentation HEAT EXHAUSTION Heat exhaustion is a milder entity than heat- stroke that exists on the same continuum of heat-related illness. Heat exhaustion typi- cally is associated with nonspecific signs and symptoms and mild pyrexia (Table 2).4,9,18,19 Patients may experience nausea and malaise, and show signs of circulatory collapse. Evi- dence of central nervous system dysfunction should trigger a diagnosis of heatstroke rather than heat exhaustion. Heat exhaustion can be associated with water or sodium depletion, which can compromise the patient���s ability to thermoregulate by sweating. Hyponatremic heat exhaustion represents a special case, requiring unique treatment. Clinically significant hyponatremia often results from voluntary overhydration and can be dangerous.20 Clinical manifestations of hyponatremia include nonspecific symp- toms involving the central nervous system, such as dizziness, nausea, and malaise, which may progress to seizures and even death.21 Heatstroke Heatstroke is a much more severe entity than heat exhaustion. The diagnosis of heatstroke rests on two critical factors: hyperthermia and central nervous system dysfunction. Heat- stroke is a medical emergency, and mortality TABLE 1 Medications and Substances that May Contribute to Heat-Related Illness Alcohol Alpha andrenergics Amphetamines Anticholinergics Antihistamines Benzodiazepines Beta blockers Calcium channel blockers Cocaine Diuretics Laxatives Neuroleptics Phenothiazines Thyroid agonists Tricyclic antidepressants Information from references 9 through 11. The diagnosis of heatstroke rests on two critical factors: hyperthermia and central nervous system dysfunction.