Exposure to warm environments affects many physiologic functions and may cause dehydration. Most people experience mild but uncomfortable symptoms; however, effects may range from cramps and edema to syncope, heat exhaustion, and heatstroke. Core temperature is elevated in some types of heat illness. People with dehydration (see Fluid Metabolism: Volume Depletion and see Dehydration and Fluid Therapy in Children: Dehydration in Children) may have tachycardia, tachypnea, and orthostatic hypotension. CNS dysfunction suggests heatstroke, the most serious disorder; confusion and lethargy may further impair the ability to escape the heat and rehydrate.
Heat input comes from
Heat output occurs through the skin via the following:
The contribution of each of these mechanisms varies with environmental temperature and humidity. Radiation predominates at room temperature, but as environmental temperature approaches body temperature, evaporation becomes more important, providing essentially 100% of cooling at > 35° C. However, high humidity greatly limits evaporative cooling (see Heat Illness: Heatstroke).
Heat output is modulated by changes in cutaneous blood flow and sweat production. Cutaneous blood flow is 200 to 250 mL/min at normal temperatures but increases to 7 to 8 L/min with heat stress, requiring a marked increase in cardiac output. Also, heat stress increases sweat production from negligible to > 2 L/h; thus, significant dehydration can occur rapidly. Because sweat contains electrolytes, electrolyte loss may be substantial. However, prolonged exposure triggers physiologic changes to accommodate heat load (acclimatization); eg, sweat Na levels are 40 to 100 mEq/L in people who are not acclimatized but decrease to 10 to 70 mEq/L in acclimatized people.
The body can compensate for large variations in heat load, but significant or prolonged exposure to heat increases core temperature. Modest, transient core temperature elevations are tolerable, but severe elevations (typically > 41° C) lead to protein denaturation and, especially during hard work in the heat, release of inflammatory cytokines (eg, tumor necrosis factor-α, IL-1b). As a result, cellular dysfunction occurs and the inflammatory cascade is activated, leading to dysfunction of most organs and activation of the coagulation cascade. These pathophysiologic processes are similar to those of multiple organ dysfunction syndrome (see Shock and Fluid Resuscitation: Multiple organ dysfunction syndrome (MODS)), which follows prolonged shock.
Compensatory mechanisms include an acute-phase response by other cytokines that moderate the inflammatory response (eg, by stimulating production of proteins that decrease production of free radicals and inhibit release of proteolytic enzymes). Also, increased core temperature triggers expression of heat-shock proteins. These proteins transiently enhance heat tolerance by poorly understood mechanisms (eg, possibly by preventing protein denaturation) and by regulation of cardiovascular responses. With prolonged or extreme temperature elevation, compensatory mechanisms are overwhelmed or malfunction, allowing inflammation and multiple organ dysfunction syndrome to occur.
Heat disorders are caused by some combination of increased heat input and decreased output (see Table 1: Heat Illness: Common Factors Contributing to Heat Disorders).
Excess heat input typically results from strenuous exertion, high environmental temperatures, or both. Medical disorders and use of stimulant drugs can increase heat production.
Impaired cooling can result from obesity, high humidity, wearing heavy clothing, and anything that impairs sweating or evaporation of sweat.
Clinical effects of heat illnesses are exacerbated by the following:
The elderly and the very young and people with cardiovascular disorders or electrolyte depletion (eg, due to diuretic use) are at highest risk.
Common sense is the best prevention. Physicians should recommend the following measures:
Thirst is a poor indicator of dehydration during exertion; fluids should be drunk every few hours regardless of thirst. However, overhydration must be avoided; significant hyponatremia (see Electrolyte Disorders: Hyponatremia) has occurred in endurance athletes who drink very frequently during exercise. Plain water is adequate for hydration during most activity; cool water is absorbed more readily. Special hydrating solutions (eg, sports drinks) are not required, but their flavoring enhances consumption, and their modest salt content is helpful if fluid requirements are high.
Drinking fluids and consuming generously salted foods should be encouraged. Laborers or others who sweat heavily can lose ≥ 20 g of salt/day, making heat cramps more likely; such people need to replace the Na loss with drink and food. A palatable drink providing about 20 mmol of salt/L may be prepared by adding about 5 g (a rounded teaspoon) of table salt to 20 L (about 5 gallons) of any sweetened beverage prepared from a powdered mix. People on low-salt diets should increase salt intake.
Successively and incrementally increasing the level and amount of work done in the heat eventually results in acclimatization, which enables people to work safely at temperatures that were previously intolerable or life threatening. Progressing from 15 min/day of moderate activity (enough to stimulate sweating) during a hot time of day to 90 min of vigorous activity over 10 to 14 days is typically adequate. Acclimatization markedly increases the amount of sweat (and hence cooling) produced at a given level of exertion and markedly decreases the electrolyte content of sweat. Acclimatization significantly decreases risk of a heat illness.
Last full review/revision February 2010 by James P. Knochel, MD
Content last modified February 2012