ROSENS EMERGENCY MEDICINE Chapter 133

ROSENS EMERGENCY MEDICINE Chapter 133

Heat Illness

Melissa Platt and Timothy G. Price

PRINCIPLES

Background

Humans have been plagued by heat illness throughout recorded history, often as the result of military exercises, athletic events, or recreational activities. When environmental heat stress is maximal, strenuous exercise is not required to produce heat illness. Modern military organizations continue to encounter heat illness because of the requirement to train unacclimatized troops with heavy physical exercise. Heat stroke is the third leading cause of death among all U.S. athletes. Of the major sports, football has the greatest number of heat stroke fatalities and a 10 times higher rate for heat illnesses.1 The health hazards associated with extreme environmental working conditions in many industries are being increasingly recognized worldwide. 2,3,4

The elderly and poor, often lacking adequate air conditioning and nutrition, and those with preexisting disease are prone to heat illness during environmental extremes. It is estimated that at least 10 times as many heat-aggravated illnesses occur in patients with co-morbid conditions such as coronary artery disease, cerebrovascular disease, and diabetes. In heat wave years in the United States, approximately 10 times as many deaths are reported as during non–heat wave years. Climate models suggest an increase in both frequency and intensity of heat waves in temperate areas of the world.5,6 Before the advent of air conditioning, mortality increased three 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, military tanks, and tents in the sun as well as in engine rooms, mines, hot tubs, and saunas.7 Children are more susceptible to heat stressors because their higher surface area–to–mass ratios allow increased absorption of heat. They also have lower sweat rates per gland.20

Anatomy and Physiology

Heat Production

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 are urea, sulfates, phosphates, and other chemical products. These reactions are exothermic and combine to produce a basal metabolic rate that amounts to approximately 100 kcal/hr for a 70-kg person. In the absence of cooling mechanisms, this baseline metabolic activity would result in a 1.1° C hourly rise in body temperature.

Heat production can be increased 20-fold by strenuous exertion. Rectal temperatures as high as 42° C are recorded without ill effects in trained marathon runners. Metabolic factors, such as hyperthyroidism and sympathomimetic drug ingestion, can dramatically increase heat production. Environmental heat not only adds to the heat load but also interferes with heat dissipation. The physics of heat transfer as it relates to human physiology involves four mechanisms: conduction, convection, radiation, and evaporation.7

Conduction is the transfer of heat energy from warmer to cooler objects by direct physical contact. Air is a good insulator; therefore, only approximately 2% of the body heat loss is by conduction. In contrast, the thermal conductivity of water is at least 25 times that of air.

Convection is heat loss to air and water vapor molecules circulating around the body. As ambient temperature rises, the amount of heat dissipated by convection becomes minimal. Once air temperature exceeds the mean skin temperature, heat is gained by the body. Convective heat loss varies directly with wind velocity. Loose-fitting clothing maximizes convective (and also evaporative) heat loss.

Radiation is heat transfer by electromagnetic waves. Although radiation accounts for approximately 65% of heat loss in cool environments, it is a major source of heat gain in hot climates. Up to 300 kcal/hr can be gained from radiation when directly exposed to the hot summer sun.8

Evaporation is the conversion of a liquid to the gaseous phase. Evaporation of 1 mL of sweat from the skin cools the body by 0.58 kcal. As ambient temperature rises, evaporation becomes the dominant mechanism of heat loss. Panting mammals such as dogs have an oropharyngeal countercurrent flow mechanism (carotid rete mirabile) that results in selective cooling of the brain. In humans, respiratory and countercurrent mechanisms are minimal sources of heat loss.

Heat Regulation

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

Thermosensors. Temperature-sensitive structures are located both peripherally in the skin and centrally in the body. Skin temperature change however, correlate poorly with changes in the rate of heat loss.9 Thermosensitive neurons, located in the preoptic anterior hypothalamus. are activated when the temperature of the blood circulating through that area exceeds a “set point.” (Figure 133-1)

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.10

Central Integrative Area: The central nervous system (CNS) interprets information received from the thermosensors to properly instruct thermoregulatory effectors. The concept of a central thermostat by which an alteration shifts effector thresholds in the same direction fits a variety of clinical situations. For example, fever, the circadian rhythm of temperature variation, and the changes difference in rectal temperature after ovulation can be explained by variation of a thermal set point.

Thermoregulatory Effectors: Sweating and peripheral vasodilation are the major mechanisms by which heat loss can be accelerated. In a warm environment, evaporation of sweat from the skin is the most important mechanism of heat dissipation. Heat loss from the skin by convection and radiation is maximized by increased skin blood flow to facilitate sweating.

Humans possess apocrine and eccrine sweat glands. Apocrine glands are concentrated in the axillae and produce milky sweat rich in carbohydrate and protein. They are adrenergically innervated and respond to emotional stress as well as to heat. Most glands producing “thermal sweat” are eccrine glands. These are cholinergically innervated and distributed over the entire body, with the largest number on the palms and soles. Eccrine sweat is colorless, odorless, and devoid of protein. Individuals exercising in hot environments commonly lose 1 or 2 L/hr of sweat. Losses of up to 4 L/hr is possible with strenuous exercise.

Cooling is best achieved by evaporation from the body surface; sweat that drips from the skin does not cool the body. Each liter of completely evaporated sweat dissipates 580 kcal of heat. The ability of the environment to evaporate sweat is termed atmospheric cooling power and varies primarily with humidity but also with wind velocity. As humidity approaches 100%, evaporative heat loss ceases.

The vascular response to heat stress is cutaneous vasodilation and compensatory vasoconstriction of splanchnic and renal beds. These vascular changes are under neurogenic control and allow heat to be dissipated quickly and efficiently, but they place a tremendous burden on the heart.11 To maintain blood pressure, cardiac output increases dramatically. For this reason, saunas and hot tubs may be dangerous for patients with cardiac disease. Cardiovascular and baroreceptor reflexes also affect skin blood flow. Reduced forearm sweating and vasodilation are observed in severely dehydrated subjects exercising in a warm environment.14

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 within 7 to 14 days.13 This is characterized by an earlier onset of sweating (at a lower core temperature), increased sweat volume, and lowered sweat sodium concentration.9,14 Acclimatization is hastened by modest salt deprivation and delayed by high dietary salt intake.

The cardiovascular system plays a major role in both acclimatization and endurance training, largely resulting from an expansion of plasma volume.15 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.15

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.15

Pathophysiology

Predisposing Factors for Heat Illness

Advanced age, psychiatric conditions, chronic disease, obesity, and certain medications increase the risk for classic heatstroke during periods of high heat and humidity16,17. Adequate fluid intake is essential. Elderly patients often over dress 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. 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 (500-600 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 evaluated by a physician or sports trainer. 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.

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.18

The body’s heat dissipation mechanisms are analogous to the cooling system of an automobile (Fig. 133-2). 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.

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 stimulant drugs of abuse interfere with sweating and contribute to heat illness.14 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. 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 and heat scales that combine environmental and physiologic parameters.19

The wet bulb globe temperature heat index is an excellent meteorologic measure of environmental heat stress (Table 133-1). 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 during exercise. Above 28° C, exercise and strenuous work should be avoided or limited to extremely short periods.

The heat strain index is widely accepted as an example of an index that includes environmental

and physiologic factors. Several variations and modified heat strain indices exist,with varying

ease of use and accuracy.19

Fever versus Hyperthermia

It is both 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, temperature should be artificially regulated with antipyretics. These antipyretics are not effective against and are not recommended to control environmental hyperthermia.