Humans, as homeotherms, strive to maintain body temperature within acceptable limits—35° to 37°C (95° to 98.6°F) and do so in the face of wide variations in temperature, humidity, solar radiation, and other environmental parameters and with a variety of physiologic and behavioral adaptations.

There are two main avenues of heat production in the human body—basal metabolism and exercise. Basal metabolism produces an average of 65 to 85 kcal of heat per hour. This output increases 13% per degree Celsius rise in body temperature. 7 Muscular activity produces heat at a range of 300 to 1,000 kcal/h and can dramatically raise body temperature at a rate that well-conditioned athletes can sustain for hours. Even at rest, humans can produce enough heat that the excess must be dissipated. The addition of exercise, warm temperatures, humidity, solar radiation, and other environmental, physiologic (eg, underlying health, medications) and human-created (eg, excess clothing) parameters can greatly increase this challenge.

There are four main avenues of heat exchange with the environment: conduction, convection, radiation, and evaporation. These are discussed here in the context of heat illness.

Conductive heat transfer occurs when there is direct contact between two bodies of differing temperatures. Energy in the form of heat moves from the warmer to the cooler object. Human tissues are generally poor conductors of heat, especially areas with subcutaneous fat. In general, behavior limits the effect of conduction as a heat exchange mechanism; we insulate ourselves from both cold and warm surfaces.

Convective heat transfer occurs when two surfaces, in direct contact, are moving relative to each other; moving air and water are the obvious examples. Convection transfers heat within the body between blood and tissues and between blood vessels via counter current heat exchanges. This effect varies based on the temperature gradient, the thermal conductivity of the medium (air or water), surface exposure and protective clothing. In a cold environment wind chill occurs when a cool wind moves over warm skin. Moving cold water combines the increased conductivity of water with the convective mechanism to increase heat loss. In a warm environment a hot wind can theoretically add heat to the body, but its effect would be low due to the small thermal gradient. Hot wind is mostly an agent of overall heat stress.

Radiation heat transfer occurs from the emission of electromagnetic energy. The gradient of energy transfer is from a warmer to a colder object. In a cold environment humans are often the warmer objects in the environment (normal body temperature of 37°C [98.6°F]) and lose heat by emitting radiation from exposed skin. In a warm environment an increase in skin temperature facilitates heat loss from radiation as long as the surrounding environment is cooler than the skin. We receive radiation heat input from fires, from the sun or from warm objects in our surroundings such as concrete or rock walls. Bare skin is receptive to radiation heat input; clothing diminishes this response.

Evaporation is our most important means of heat dissipation. When perspiration evaporates from the skin’s surface the change in state from liquid to gas consumes energy from the surface of the skin—approximately 580 kcal/L of evaporated sweat. Evaporative heat loss accounts for 20% of the body’s total heat loss in normal conditions—much more when we are under heat stress or working hard. We use evaporation to our advantage to cool ourselves in hot environments.

For conceptual understanding the regulation of body temperature is often sketched as a negative feedback system consisting of central and peripheral sensors that signal to the anterior hypothalamus in the brain and a set of return signals that induce physiologic and behavioral responses for body temperature regulation. In homeostasis, body temperature fluctuates around a thermal set point, a homeostatic thermostat. Environmental heat exposure and exercise may raise the skin and core temperature above the set point, evoking autonomic responses (peripheral vasodilation, increased cardiac output, increased respirations, increased sweating) and behavioral responses (adjusting clothing, seeking shelter, fanning) to lower the temperature. Environmental cold exposure may lower the temperature below the set point, evoking autonomic (peripheral vasoconstriction, increased metabolic rate, cardiac output) and behavioral responses (adjusting clothing, seeking shelter, consuming food and warm fluids, exercise) to elevate the temperature back to the set point. Fever is a protective response, an increase in the set point to assist immune responses to infection, inflammation, or trauma. Protective hypothermia is used by some species to decrease metabolic demands.

For the WEMS provider, hydration impacts personal and team homeostasis and the ability of the responder to perform. It requires constant attention while in the field. Wilderness providers care for patients whose primary medical condition may be dehydration and for patients where dehydration underlies and complicates other injuries and illnesses.

Humans are bags of water: 50% to 70% of the body mass of an average young adult male is water. We hear through a medium of water. The brain is cushioned by fluid, and the joints are lubricated by fluid. Blood is 90% water, and every biochemical
reaction takes place in a medium of water. The inability to maintain fluid balance through a lack of fluid availability or exposure to extreme environments affects health, the ability to think clearly, and to perform physical work.

The term exercise-associated muscle cramps reflects the understanding that these cramps are not directly related to an elevated body temperature. They can happen in any exercise, in warm and cold temperature, during warm-up, during the exercise, or after exercise. The cause of exercise-associated muscle cramps remains a topic of debate. Discussions focus on exercise-associated muscle cramps as a result of local fluid and
electrolyte deficits, (eg, increased intracellular calcium stimulating muscle contraction), or as a result of central neuromuscular fatigue, or any combination of these factors.¹³ Exercise-associated muscle cramps are associated with other forms of heat illness, but they do not predispose a person to other forms of heat illness.

Lack of fitness, lack of acclimatization to exercise in the heat, and profuse sweating associated with sodium loss are characteristics of people who suffer from exercise-associated muscle cramps.¹⁴

Syncope is a sudden, transient loss of consciousness and postural tone. Heat syncope is commonly a limited period of altered mental status or loss of consciousness in the context of heat exposure. It is similar to vasovagal syncope and results from orthostatic blood pooling, peripheral vasodilation, and the absence of a robust vascular response to positional change. There is no evidence of severe, life-threatening causes in heat syncope and either no loss of consciousness or rapid return of normal mental status once the patient is in a supine position and removed from heat stress. Dehydration, a lack of heat acclimatization, prolonged standing, and underlying cardiovascular health are presumed contributing factors. It usually resolves promptly with rest, removal from heat stress, and hydration.¹⁵

Heat-associated postural hypotension, a term that can be used interchangeably with heat syncope, often refers to syncope from inadequate hydration and alterations in lower extremity vascular tone when exercise stops. For example, when a runner stops and the leg muscles are no longer contracting in the constant rhythmic manner of running, blood may pool in the legs. The stress of dehydration and the sudden cessation of movement may cause a sudden drop in blood pressure that triggers fainting.

Heat exhaustion, also known as heat prostration or heat collapse, is just what the term says, fatigue from the stress of coping with a hot environment. The work of heat dissipation along with the stress from coping with sunlight and heat exhaust the patient. Heat exhaustion is not low fluid volume from dehydration, although dehydration can occur alongside heat exhaustion.

Heat exhaustion is considered to be on the mild to moderate spectrum of heat illness, although for some patients it is debilitating. It may remain an entity by itself or progress to exertional heat stroke. It may occur with or without dehydration and elevated core temperature.¹⁶

It is usually seen in the context of exercise in the heat but can occur without exercise in people with underlying medical conditions and associated heat stress (cardiovascular insufficiency limiting robust response to the heat stress, medications that predispose to dehydration or drive metabolic rate, cumulative stress over multiple days).

In the spectrum of heat illness, heat stroke is the life-threatening emergency. Patients have exaggerated heat production and an inability to cool themselves due to extreme heat challenge and underlying health issues (classic heat stroke) or heat challenge and exertion (exertional heat stroke). Core temperature is usually above 40°C (104°F).

Current understanding of the pathophysiology of heat stroke, which is still incomplete, is that the need to dissipate heat from exertion or chronic heat stress results in an increase in blood flow to the skin and a decrease in blood flow to the gut. This triggers gut ischemia, increased epithelial membrane permeability, and leakage of endotoxin into the systemic circulation causing a systemic inflammatory response. Multi-organ system failure is the ultimate cause of heat stroke death.¹⁷

Classic heat stroke occurs in an at-risk population of the very young, the elderly, and the chronically ill, often accompanied by social and economic factors such as inability to access air-conditioning or cool surroundings during periods of heat stress.

High temperature and humidity that impair heat dissipation, often for several days, can precede classic heat stroke. Infants are vulnerable due to their high surface area to body mass ratio, which can increase heat gain and dehydration, poorly developed thermoregulation mechanisms, and inadequate behavioral responses. The elderly can have comorbidities such as mental illness, use of prescription medications that influence thermoregulation (diuretics, anticholinergics, antipsychotics, tranquilizers), diabetes, and cardiovascular disease.

Exertional heat stroke is typically seen in athletes unacclimatized to exercise in the heat. During exercise, excess heat must be dissipated from the body to avoid hyperthermia. The burden of the heat load can be slow to develop and accompanied by nausea, dizziness, feeling of heat oppression, and perceived high exertion. These may be overlooked as normal side effects of exertion or ignored from motivation to train, compete, work, or rescue. The presentation may also be acute with sudden collapse and altered mental status.

People vary in their tolerance for dehydration. A body mass water deficit of greater than 2% is often cited as a threshold for symptomatic dehydration, although trained athletes can tolerate greater deficits during competition. Dehydration causes increased body core temperature, increased cardiovascular strain, increased glycogen utilization, and altered central nervous system function. The impact of dehydration on prolonged work efforts is magnified by hot environments, and probably worsens as the level of dehydration increases.

The 2% dehydration threshold has been reported to affect cognitive performance. Outdoor people are aware of the irritability and dullness of intellect from dehydration. Studies
of performance when dehydrated have documented reduced visual motor tracking, impaired short-term memory, reduced attention span, reduced ability to do arithmetic calculations, and higher levels of perceived effort and concentration. This has clear implications for the quality of decisions and the effect on risk management in wilderness activities.¹⁸

Exercise-associated hyponatremia has been observed during marathon and ultramarathon competition, military training, and recreational activities. Hyponatremia describes a state of lower than normal blood sodium concentration, typically lower than 135 mEq/L. Exercise-associated hyponatremia tends to be more common in long-duration activities and most often occurs when individuals consume low-sodium drinks or sodium-free water in excess of sweat losses (typified by body mass gains), either during or shortly after completing exercise.

The primary cause of hyponatremia in the context of exercise in the heat is drinking fluids without electrolyte supplements in excess of fluid loss. In an effort to reduce heat stroke emergencies, Grand Canyon National Park emphasized “drink water, drink water, drink water” to its visitors. Pure water does not have electrolyte supplementation, and consequently, the incidence of hyponatremia increased. The same phenomenon was seen in marathon running where hyponatremia was virtually unknown before the modern advice to drink water to excess.

Contributing factors can include inappropriate increased antidiuretic hormone (vasopressin) secretion that causes fluid retention and a hypertonic urine. Sodium loss in sweat is not a cause of exercise-associated hyponatremia, although it may exacerbate the problem in some people. Most sports drinks are not protective as they tend to have insufficient sodium to compensate for excessive fluid intake.

At risk is anyone consuming excessive fluids, as well as smaller people, females, those exercising for longer than 4 hours, or those taking high doses of nonsteroidal antiinflammatories (NSAIDs), which slow kidney function.¹⁹