Signs and symptoms of heat exhaustion

Treatment /management


Observations of humans living in tropical climates, working in industrial settings, and exercising in artificial laboratory environments distinguish two clusters of relevant physiological responses: (1) circulatory insufficiency and (2) electrolyte imbalance. These disorders have multiple common etiological factors

(1) Circulatory insufficiency occurs when the combined stresses of exercise and ambient heat exceed the cardiac capacity to maintain normal functions. Aggravated by fluid-electrolyte losses

(2) Electrolyte imbalance is defined as a low serum chloride (Cl) conc. of ≤100 mEq/L (sodium [Na+] conc. ≤139 mEq/L), primarily due to replacement of water loss in sweat without replacement of electrolytes

(1) Vertigo, fainting, collapse, nausea, headache, vomiting, respiratory disturbance, fatigue, and exhaustion are present in varying proportions.(2) Reduced serum Na+ and Cl conc. Loss of body weight. Tingling leading to muscle cramps. Vomiting and diarrhea. Normal rectal temperature

Heat exhaustion and heat cramps often are observed with overlapping symptoms. Hyperpyrexia (i.e., heat stroke) and life-threatening loss of body water (20–25% of body mass) are classified as distinct disorders

Both (1) and (2) respond rapidly to intravenous (i.v.) saline administration

Lee, report to the Royal Society of Tropical Medicine and Hygiene, UK [10]

Industrial labor, mining and military activities. Exercise-induced sweating that leads to dehydration and large salt losses in sweat. Elevated internal body temperature or skeletal muscle cramps may or may not be involved. Long duration of heat exposure each day

Classified four types of heat exhaustion:

anhydrotic: sweating deficiency usually preceded by severe prickly heat (miliaria rubra); salt deficiency: inadequate replacement of salt loss due to sweat and urine losses, leading to dehydration and reduced blood volume; water deficiency: lack of drinking water or low volume intake; and exercise-induced (e.g., marching or digging)

Anhydrotic: General physical and mental loss of energy and initiative, irritability, loss of appetite, difficulty sleeping and working. While under heat stress, intense warmth, dyspnea, tachycardia and distress. Eventual collapse with possible loss of consciousness. Skin is dry except on the face, palms, soles of the feet, and axillae. Salt deficiency (Type I): collapse with pallor, sweating, vomiting, and sometimes muscle cramps. Hemoconcentration. Urine is concentrated with small volume and low sodium concentration. Water deficiency (Type II): thirst, vague discomfort, anorexia, impatience, sleepiness, weariness, dizziness. Tingling, dyspnea, cyanosis in advanced cases. Walking pace cannot be maintained, inability to stand, incoordination, hysteria, or delirium. Exercise-induced: exertion is halted voluntarily due to exhaustion or collapse. Syncope may occur if upright posture is sustained after exercise

Heat exhaustion treatment options are not described

Weiner and Horne, UK Medical Research Council, Climatic Physiology Committee report [11]

As part of updated nomenclature and classification of heat illnesses, three types of heat exhaustion are recognized: (a) salt and/or water depletion, (b) anhidrotic, and (c) unqualified

The pathophysiologies of heat disorders are not described

In this one-page document, specific signs and symptoms of heat disorders are not described. General descriptions include (a) salt and/or water depletion is used as a compromise term in the field, where physicians rely on clinical observations and judgment without the aid of laboratory tools; (b) extensive obstruction of sweat-gland ducts leads to impaired evaporative cooling, with loss of heat tolerance; and (c) diagnosis by exclusion

Distinct from heat exhaustion, transient heat fatigue is presented as a new heat illness classification, to designate the deterioration of skilled performance occasionally observed in an otherwise normal adult during short exposures to extreme heat. Recovery is prompt upon return to a cool environment

Heat exhaustion treatment options are not described

Minard summary of UK and US government medical and research committee joint efforts [6]

Soldiers working or marching in hot or hot-wet environments. Heavy sweating with inadequate water and salt replacement. Excessive cardiovascular demand and water- electrolyte depletion exist in all cases. Two forms of heat exhaustion are distinguished: water depletion and salt depletion

Heat exhaustion is due to the combination of excessive cardiovascular demand (i.e., when cardiac output is insufficient to meet the competing circulatory demands of skin blood flow, skeletal muscle, and vital organs), reduced “effective” plasma volume, reduced venous return to the heart (due to vasodilation in skin and active muscle), and sweat-induced depletion of water and salt. A single episode of heat exhaustion does not imply predisposition to heat injury

The symptoms of heat exhaustion are non-specific. No combination of presenting symptoms and signs is characteristic of this illness. Each patient requires careful clinical evaluation addressed to the presenting complaints, including thirst, syncope, profound physical fatigue, nausea, vomiting, hyperventilation with carpopedal spasm, dyspnea, muscle cramps, confusion, anxiety and agitation, mood change, orthostatic dizziness, ataxia, hyperthermia, and frontal headache. Water depletion and salt depletion heat exhaustion exhibit subtly different signs and symptoms. This is a functional illness and is not associated with evidence of organ damage

Removal of gear or clothing and rest in a shaded-ventilated area encourages spontaneous cooling. Pouring cool water over the skin encourages skin vasoconstriction and venous return to the heart. Extracellular volume is replenished rapidly by i.v. fluid. Patients with tachycardia at rest or orthostatic signs should initially receive normal saline in i.v. boluses of 200–250 cc to restore circulatory function. More than 2 L of normal saline should not be administered without laboratory surveillance

USARIEM Heat Illness Guide for Medical Officers [12]

Endurance running in a hot environment, including training and competition. The most susceptible individuals are those who exercise at or near their maximal capacity, are dehydrated, are not physically fit, and are not heat acclimatized

Failure of the cardiovascular responses to strenuous workload, high ambient temperature, and dehydration. Such dehydration reduces exercise capacity due to decreased circulating blood volume, blood pressure, sweat rate, and skin blood flow

Heat exhaustion has no known harmful, chronic effects. Symptoms may include headache, extreme weakness, dizziness, vertigo, heat cramps in skeletal muscles, sensation of heat on the head or neck, vomiting, nausea, irritability, and goose flesh. Depending on the severity of signs and symptoms, agitation, hyperventilation, muscle incoordination, impaired judgment, and confusion may be seen. Fainting may or may not accompany heat exhaustion. During the early stage, the patient may appear ashen-gray, the blood pressure may be low, and the pulse rate may be elevated

Oral rehydration is preferred for patients who are conscious, coherent, and without vomiting. Intravenous fluids facilitate rapid recovery; 5% dextrose sugar in either 0.45% saline (NaCl) or 0.9% saline is most commonly administered

ACSM Exertional Heat Illness Position Stand [13]

During exercise, repetitive muscle pumping action assists venous return to the heart. On cessation of exercise, this muscle assistance to blood flow ceases, and venous blood return may diminish rapidly enough to produce nausea, collapse, or syncope. Although this form of syncope may occur in the absence of EHI, clinical evaluation is warranted because the symptoms may be due to hypovolemia

Exertional heat exhaustion is a reversible, non-life-threatening multisystem disorder reflecting the inability of the circulatory system to meet the demands of thermoregulatory, muscular, cutaneous, and visceral blood flow. It represents primarily a syndrome of dehydration without serious metabolic complications. This is a reversible system dysfunction without evidence of organ damage or severe metabolic consequences

This illness usually involves minor elevations of internal temperature (<40 °C), but it can be associated with a very high rectal temperature in cases of severe heat exhaustion. If hyperthermia greater than 104 °F (40 °C) is measured rectally, rapid cooling to a body temperature of less than 102 °F (38.99 °C), rest, and rehydration are essential to prevent progression to heat stroke.

Levels of progressive orthostatic signs and symptoms are proposed. Mild: faintness, dizziness, wobbly legs, stumbling gait, blurred or tunnel vision, blackout. Exertional heat syncope: collapse with brief (>3 min) loss of consciousness. Severe: evaluated via tilt tests. Shock or cardiovascular collapse are possible.

Mild: symptoms are rapidly improved by water and salt replacement, a cool environment, and rest. Moderate-to-Severe: patients with orthostatic hypotension are better treated with 1–2 liters of i.v. normal or half-normal saline, starting at a rate of 250–500 ml/h, and their responses are monitored. A history or evaluation that suggests hyponatremia (i.e., drinking large volume of water) or severe salt and water deficits indicates laboratory monitoring

Gardner and Kark, heat illness diagnosis, management, surveillancea [14]

In athletes, cumulative dehydration develops insidiously over several days and is typically observed during the first few days of a season or in tournament competition

Cumulative dehydration can be detected by measuring daily prepractice and postpractice weights. The cumulative effects of a 1% fluid loss per day occurring over several days create an increased risk for heat illness and decreased exercise performance

Exercise (heat) exhaustion is the inability to continue exercise and is associated with any combination of heavy sweating, dehydration, sodium loss, and energy depletion. It occurs most frequently in hot, humid environments

Athletes with exercise (heat) exhaustion may exhibit these signs and symptoms: dehydration, dizziness, lightheadedness, syncope, headache, nausea, anorexia, diarrhea, decreased urine output, persistent muscle cramps, pallor, profuse sweating, chills, cool/ clammy skin, weakness, intestinal cramps, hyperventilation, and a rectal temperature that ranges between 36 °C (97 °F) and 40 °C (104 °F). Severe heat exhaustion is difficult to distinguish from exertional heat stroke without measuring rectal temperature. Cognitive changes are usually minimal, but bizarre behavior, hallucinations, altered mental status, confusion, disorientation, and coma suggest more serious conditions

The goal of athlete safety is addressed through the recognition of heat illness and a well-developed plan to evaluate and treat affected athletes. This includes knowledge of the common early signs and symptoms, a rectal thermometer to measure deep body temperature, a cooling zone (shaded, fans, air conditioned), a plan for emergency evacuation if needed, and a mobile phone to communicate with emergency personnel

NATA Exertional Heat Illness Position Statement [15]

Selected intrinsic etiological factors: inadequate heat acclimatization, low physical fitness status, high percent body fat, dehydration, gastrointestinal illness, salt deficiency, medications (e.g., antihistamines, diuretics), dietary supplements (e.g., ephedra), motivation to push oneself to extreme limits. Selected extrinsic factors: Intense or prolonged exercise with few rest breaks; high ambient temperature, humidity, and sun exposure; minimal access to fluids before and during practice and rest periods; inappropriate work/rest ratios based on intensity and wet bulb globe temperature (WBGT); insulative clothing and equipment; lack of education and awareness of early warning signs among coaches, athletes, and medical staff; no emergency plan

Heat exhaustion is a moderate illness characterized by the inability to sustain adequate cardiac output, resulting from strenuous physical exercise and environmental heat stress. Inherent needs to maintain blood pressure and essential organ function, combined with a loss of fluid due to acute dehydration, create a challenge the body cannot meet, especially if intense exercise continues unabated

Most important criteria are (a) obvious difficulty continuing intense exercise in the heat, (b) lack of severe hyperthermia (usually <40 °C) although mild hyperthermia may be seen at the time of the incident (100°–103 °F, 37.7°–39.4 °C) and (c) lack of severe CNS dysfunction. Other salient findings may include physical fatigue, dehydration, electrolyte depletion, ataxia or coordination problems, syncope, dizziness, profuse sweating, pallor, headache, nausea, vomiting, diarrhea, stomach/intestinal cramps, persistent muscle cramps, and rapid recovery with treatment

The following procedures are recommended if heat exhaustion is suspected: move the athlete from activity to a shaded or air-conditioned area. Remove excess clothing and equipment. If hyperthermic, cool the athlete until rectal temperature is ~ 101 °F (38.3 °C). Lie the athlete supine with legs propped above heart level. If the athlete is not nauseated, vomiting, or experiencing CNS dysfunction, rehydrate orally with chilled water or sports drink. Alternatively, implement i.v. normal saline therapy. Monitor heart rate, blood pressure, respiratory rate, rectal temperature, and CNS status. Transport to an emergency facility if improvement is not rapid

Inter-Association Task Force Statement [16]

Military training or operations in high ambient temperature, humidity, and solar radiation with low air movement. Exercise in a hot environment produces metabolic heat, increased internal body temperature, body water loss as sweat, reduced blood volume, peripheral blood pooling in dilated and compliant skin, loss of splanchnic vasoconstriction, and reduced venous return to the heart

Heat exhaustion is not associated with evidence of organ damage. It occurs when the body cannot sustain cardiac output at a level that is necessary to meet the combined demands of skin blood flow for thermoregulation and blood flow to exercising skeletal muscle

The signs and symptoms include generalized weakness, fatigue, ataxia, dizziness, headache, nausea, vomiting, malaise, hypotension, tachycardia, muscle cramps, hyperventilation and transient alteration of mental status. Sweating may be profuse

Treatment and management details are similar to the above technical report (USARIEM 91–3, 1991). Although patients with heat exhaustion experience rapid clinical recovery, they need at least 24 h of rest and rehydration under medical supervision. Determine the reason for heat exhaustion (e.g., ratio of work-to-rest, water intake, coincident illness, or medication) and develop a plan to avoid similar episodes in the future

Department of the Army Technical Report, heat stress control, heat casualty management [17]

Several lines of evidence suggest that heat exhaustion

Results from peripheral vascular dilation resulting in hypotension and cardiovascular insufficiency. If the air humidity is high, evaporative cooling is impaired, signaling the body to increase skin blood flow that aids nonevaporative heat loss. This explains why heat exhaustion commonly occurs on humid days

Exercise exhaustion may be triggered by some combination of reduced peripheral and central muscle activation, dehydration, depletion of energy stores, or electrolyte imbalance. In hot environments, post-exercise collapse may be due to postural hypotension

It is clinically difficult to distinguish athletes with exhaustion in cool conditions from those who collapse in hot conditions

The signs and symptoms of heat exhaustion are neither specific nor sensitive. During the acute stage, blood pressure is low, the pulse and respiratory rates are elevated, and the patient appears sweaty, pale and ashen. Muscle cramps may or may not exist. In the field, rectal temperature measurement may discriminate between severe heat exhaustion (<40 °C, <104 °F) and heat stroke (>40 °C)

The athlete should be moved to a cool-shaded area, helped to remove excess clothing, placed in a supine position with legs elevated, and monitored (heart rate, blood pressure, rectal temperature, respiratory rate, and central nervous system status). If rectal temperature cannot be measured promptly, empiric cooling therapy should be considered, especially if central nervous symptoms exist. The majority of athletes will resolve collapse within 30 min with leg elevation, oral fluids, and rest. An athlete who does not improve should be transported to an emergency facility.

Oral fluids are preferred for rehydration in athletes who are conscious, able to swallow well, and not losing fluids via vomiting or diarrhea. If blood pressure, pulse, and rectal temperature indicate, i.v. fluids facilitate rapid recovery.

The primary goal of i.v. therapy is intravascular volume

 expansion with saline, to protect organ function and improve blood pressure when signs of shock are observed. The most commonly recommended i.v. fluids are normal saline or 5% dextrose in normal saline. The 5% dextrose provides glucose for cell energy

ACSM Exertional Heat Illness Position Stand [18]

Heat exhaustion is defined as the inability to effectively exercise in the heat, secondary to a combination of cardiovascular insufficiency, hypotension, energy depletion, and central fatigue. This condition manifests with an elevated internal body temperature (usually <40.5 °C) with a high rate or volume of skin blood flow, heavy sweating, and dehydration. This illness most often affects non-acclimatized or dehydrated individuals with a body mass index >27 kg/m2

Heat exhaustion results from a combination of cardiovascular insufficiency, hypotension, energy depletion, and central fatigue

Heat exhaustion may be present if the patient demonstrates excessive fatigue, faints, collapses, or presents with minor cognitive changes (e.g., headache, dizziness, confusion) while performing physical activity. Other signs and symptoms of exertional heat exhaustion may include fatigue, weakness, dizziness, headache, lightheadedness, vomiting, nausea, low blood pressure, and impaired muscle coordination. The NATA strongly recommends that rectal temperature be measured because in cases of heat exhaustion it is usually less than 40.5 °C (105 °F), a characteristic that differentiates it from exertional heat stroke

Cease exercise, move the athlete to a cool-shaded area, remove excess clothing and equipment, elevate legs to promote venous return to the heart, monitor vital signs, and provide fluids

If intravenous fluids are needed or if recovery is eventful and not rapid (≤ 30 min), i.v. fluid should be administered under the care of a physician. If the condition worsens during or after treatment, emergency medical treatment should be activated

NATA Exertional Heat Illness Position Statementb [19]

Note: The above statements are synopses written by the present author. They are not verbatim quotations from original publications

aThis document classifies numerous exertion-related heat illness syndromes as exertional heat illness (EHI). These syndromes form a continuum of multisystem illnesses, which are divided into three levels on the basis of severity: (1) mild EHI, which includes heat exhaustion, mild dehydration, and heat cramps; (2) intermediate EHI, which includes exertional heat injury and mild rhabdomyolysis, renal insufficiency, orthostatic hypotension, heat-related syncope, and reversible electrolyte and metabolic disturbances; and (3) severe EHI, which includes heat stroke, severe rhabdomyolysis, liver necrosis, acute renal failure, cardiovascular collapse, and marked electrolyte or metabolic disturbances

bThis document introduced the illness classification named exertional heat injury, defined as a moderate-to-severe heat illness characterized by organ (e.g., liver, renal) and tissue (e.g., gut, muscle) injury associated with sustained high body temperature resulting from strenuous exercise and environmental heat exposure. Body temperature is usually but not always greater than 40.5 °C (105 °F). Exertional heat injury is distinguished from exertional heat exhaustion and exertional heat stroke (i.e., a medical emergency) involving central nervous system dysfunction manifested as collapse, aggressiveness, irritability, confusion, seizures, and altered consciousness


In September of 1912, Naval Surgeon Charles N. Fiske presented a report to the attendees of the International Congress on Health & Hygiene in Washington, D.C. [20]. His accounts of heat casualties aboard more than 20 US seagoing vessels (1861–1911) demonstrated that the term “heat prostration ” was used sparingly through the year 1877, in reference to both heat exhaustion and heat stroke, without standardized diagnostic criteria. From 1885 forward, the term heat exhaustion was used extensively. Due to the coal-fired boilers that propelled ships during that period, the most common etiology of heat exhaustion involved heavy labor in or near the engine room, high humidity, and extreme temperatures reaching 140–210 °F. In recognition of this remarkably stressful working environment, the US Navy began to modify the below-deck working environment, wall insulation, and air ventilation systems around 1909; also, newly installed oil-burning engines no longer required moving coal by hand, and the work load of sailors was reduced considerably. From 1909 to 1911, the annual rate of heat exhaustion casualties in the US Navy fell by 43%.

Physical exhaustion is vaguely defined as the inability to continue exercise and occurs with strenuous effort in all environments, from cool to hot. As ambient temperature rises above 20 °C (68 °F) and heat stress increases, the time to reach exhaustion decreases [21]. Although the exact mechanism of physical exhaustion has not been discovered, termination of exercise due to exhaustion may result from brain fatigue (i.e., decreased central activation) and subsequently reduced skeletal muscle force output that is influenced by either a whole-body fluid-electrolyte imbalance or depleted energy stores. The H EX that occurs in hot environments may or may not involve the same mechanism as physical exhaustion, but it clearly is more pronounced [18].

Collapse at or near the finish line of an endurance or ultra-endurance event is a common reason for athletes to receive treatment at the medical tent. This benign condition (i.e., a form of exercise-associated collapse) is defined as inability to stand or walk unaided as a result of lightheadedness, dizziness, faintness, or syncope and is confirmed after endurance running by a drop of systolic blood pressure greater than 20 mmHg when moving from a lying to an erect posture [22]. Such exercise-associated collapse occurs in 1.1% of race starters at the finish of cool or mild weather marathons (41–68 °F, 5–20 °C) [23]; in ultramarathon events that involve hours of strenuous upright exercise, the prevalence is considerably greater [23, 24]. The pathophysiology of this exercise-associated collapse (EAC) is believed to involve postural hypotension when a runner finishes [24, 25], due to inactivation of the calf muscle pump, blood pooling in the compliant veins of the lower extremities, reduced atrial filling pressure, and subsequent syncope. Unfortunately, some authorities have interpreted these observations to mean that HEX does not exist as a distinct entity, that the word “heat” is not necessary to describe this condition and extrapolate their observations to mean that the pathophysiology of HEX simply involves postural hypotension [24, 25]. This is unfortunate because (a) the existence of one disorder (i.e., postural hypotension) does not disprove the existence of another; (b) the exertional heat illnesses were not named or classified as heat illnesses because patients were hyperthermic, rather the word heat referred to the environment as a stressor (e.g., heat cramps do not involve a high rectal temperature); and (c) numerous investigators have observed H EX in a variety of scenarios and concluded that H EX is more complex than postural hypotension per se (Table 5.2) [2535]. In the paragraphs below, published reports of HEX cases (see section titled Signs & Symptoms) demonstrate that dizziness, orthostatic rise of heart rate, syncope, and collapse are not universally observed.

Table 5.2

Characteristics of exertional heat exhaustion in diverse scenarios



Signs and symptoms of heat exhaustion



Heat exhaustion that developed across multiple days

as a result of large water-electrolyte losses and inadequate replacement

Below-deck strenuous labor aboard US naval ships with inadequate ventilation, often humid conditions. Long duration work shifts

Not stated, likely because the pathophysiology apparently was not clearly understood

This publication provided the original description of heat exhaustion, distinct from heat stroke (pg. 584) but not distinguished from heat cramps. The symptoms of heat exhaustion included “slight fever” or the subnormal skin temperature of shock, pallor, dull blue or gray-blue skin color, drenching perspiration, weakness of voluntary and involuntary muscles, and embarrassment of circulation and respiration. Skeletal muscle fiber twitching and violent painful cramps of the abdomen, arms, and legs were prominent in some cases

Valid treatment options, from the perspective of today’s knowledge, are not described

Fiske 1913. A 35-year report of sailor heat illnesses that led to casualties and deaths [26]

Hard labor performed by US Navy sailors shoveling in 100 °F and 100% relative humidity. Some engine rooms reported air temperatures exceeding 54 °C (130 °F). Long duration work shifts

The author acknowledged little understanding of the pathophysiology underlying heat exhaustion (i.e., why some men have heat cramps but others do not.

Heat exhaustion patients were prostrated when admitted with cold moist skin, rapid pulse, and no cramps. When the hot ambient conditions of Hawaii were encountered on consecutive days, the conditions below deck were extremely stressful, even for young experienced sailors. The crew felt physically “washed out”

Valid treatment options, from the perspective of today’s knowledge, are not described

Phelps, a summary of heat exhaustion aboard US Navy ships in 1924–1925 [27]

Military activities of UK armed forces in Iraq. The average daily shade temperature for the month of August 1930 was 115 °F (46 °C) with 122 °F (50 °C) maximum, often with low relative humidity. Long duration work shifts each day. No deaths occurred

Environmental heat stress. Metabolic acidosis is presented as a theoretical pathological factor, but little evidence supports this theory

A 1–3 day prodromal period of malaise, weakness of the legs, headache, constipation and small urine volume often is observed in residents, which may not involve direct exposure to the sun. Severe cases involve collapse and circulatory shock; in some, this occurred at night and involved no exercise. The patient is pale, bathed in cold-clammy perspiration, mentally apprehensive, and may be in acute discomfort due to violent cramps of the abdominal and leg muscles. If untreated for hours or days, mild rectal hyperthermia of 101 °F (38.3 °C) can progress to 108 °F (42.2 °C), and coma or convulsions may occur

Preliminary treatment for shock. The effect of i.v. infusion is dramatic in that vomiting and muscle cramps cease. Patients are nearly convalescent within 48 h

Morton, 1932. Military medical report regarding troop activities [28]

In underground mines, the environmental conditions are: 86–96 °F (30–35 °C), a very high relative humidity of 90–96%, and air velocities of 100–250 ft./min (30.5–76.2 m/min). Internal heat production is maintained during 8-h shifts. High relative humidity and temperature discourage sweat evaporation. Miners wear only a pair of shorts and boots. Once on the surface, heat stress is removed. Usually the worker who is engaged in sustained shoveling, although at half his working capacity, suffers heat illness. Older miners are rarely employed underground after the age of 45 years, due to increased incidence of heat illness

The authors include salt-deficiency heat exhaustion, heat cramps, and mixed water-electrolyte depletions in the category named “heat exhaustion” because their etiologies all involve inadequate salt or water replacement after losses (acute or chronic), incurred during labor. Proportionately, the salt imbalance is greater when only water is replaced, and the basic pathology involves extracellular dehydration. No deaths occurred

This publication presented a very comprehensive clinical description of advanced/severe heat exhaustion. Pure water depletion is not seen in this setting because both water and salt are lost in sweat. The signs and symptoms represent salt depletion heat exhaustion and mixed fluid-electrolyte depletions

The average patient body fluid loss was 12% of body weight. Skin turgor and elasticity were markedly decreased and eyeballs were sunken. Skin was cool or cold, often clammy, but at times dry. Nearly all patients confirmed that they had sweat profusely and felt very hot. Collapse during labor was common. Systolic blood pressure was low (80–90 mmHg) and peripheral pulse could not be palpated. In mild or moderate cases, the pulse increased markedly upon standing and the patient fainted. Nausea, vomiting, and weakness were common

Laboratory findings included a low serum Cl conc. (group mean of 86 mEq/L) with normal-to-low Na+ and normal potassium (K+) conc. Hematocrit was elevated. Urine Cl conc. was low in all cases

Electrolyte loss is indisputable. Therapy is designed to provide accurate water and electrolyte replacement, in consideration of the patient’s daily water and salt turnover, relief of muscle cramps, and correction of osmotic imbalance. Extracellular osmolality is reduced, thus i.v. saline is the fastest and best treatment. Normal saline is used for the initial 2 liters of fluid replacement; thereafter, half-normal saline in 5% dextrose is dispensed. Oral fluids may exacerbate vomiting

King and Barry, 1962. Description of workers in deep underground mines of South Africa [29]

A 110.5 kg man performed intermittent high-intensity treadmill running during a research study; 56 min of exercise (57–66% of VO2max) was accomplished during each 100 min heat exposure (days 1–7), except day 8. Although physiological adaptations progressed normally through day 5, heat exhaustion occurred on the eighth day of exercise-heat exposure

Increased cardiovascular strain was evidenced by greater heart rate change (day 1, +71 beats·min−1 and day 8, +96 beats·min−1) and greater plasma volume change (day 1, −10.7% and day 8, −16.2%) post-exercise. Pre-exercise body mass decreased by 3.6 kg from day 1 to day 8 of heat acclimation. Calculations indicated a mild 8-day whole-body Na+ deficit of 3.8 g (166 mEq/8d) and an extracellular volume contraction of 0.72 L

This individual reported no signs or symptoms of heat exhaustion during exercise on days 1–7. Exercise was terminated prematurely only on day 8 and the following symptoms of salt depletion heat exhaustion were observed: vomiting, muscular weakness, fatigue, and abdominal muscle cramps. Heat exhaustion on day 8 was fore-warned by loss of body weight (− 5.4 kg during the 72 h preceding the episode), increased heart rate (days 5–8), and increased rectal temperature (days 7–8) during exercise. Plasma cortisol (i.e., a marker of general body stress) and beta-endorphin (i.e., a sensitive index of heat stress) were elevated on day 8 (twofold and six–ninefold, respectively, above days 1 and 4)

On day 8, investigators moved the participant from the hot laboratory environment to an air-conditioned room. A physician managed his recovery for 48 h post-exercise, including encouragement to increase dietary water and salt intake as tolerated

Armstrong et al., 1988. A case report of monitored heat exhaustion [30]

Religious pilgrims walk across the desert in ambient temperatures that often exceed (113 °F) 45 °C, 50% relative humidity. Hundreds of people, many elderly, succumb to heat illness and are treated at field medical sites along the course

Heat exhaustion patients exhibit hypovolemia and intact mental function with rectal temperature <40 °C. Their hemodynamic changes reflect a hyperdynamic circulation with tachycardia and high cardiac output

Heat exhaustion patients (n = 29) and a control group (n = 31) with no clinical symptoms were assessed via non-invasive echocardiography. Patients demonstrated peripheral vasodilatation

There were no cardiac signs of major hypovolemia in heat exhaustion patients, with a left ventricular size that was only mildly smaller than that of controls, and with no marked collapse of the inferior vena cava. Signs of arterial vasodilatation were reflected in the descending aortic flow, with a higher cardiac output maintained by increased heart rate

Specific treatment options are not described.

Shahid et al., 1999. Heat exhaustion during religious pilgrimage [31]

Heat exhaustion that developed within a single day or event

as a result of water-electrolyte loss and reduced peripheral vascular resistance

Controlled observations of male laborers involved shoveling gravel for 1 h in either a hot environment (dry bulb, 96–98 °F, 35.6–36.7 °C; wet bulb, 94–95 °F, 34.4–35 °C) or a mild environment, then standing upright with arms hanging freely. Pulse rate, respiratory rate, and systolic-diastolic blood pressures were measured

Standing in the mild environment after exercise resulted in no participant collapse. Thus, the observed collapses were truly heat-induced. The most noteworthy differences between these groups were changes in the circulatory system as indicated by pulse rate and blood pressure. The six men who collapsed while standing in the heat exhibited a feeble and slow pulse, a fall in systolic (and often but not invariably diastolic) pressure, and a decrease in pulse pressure (i.e., the difference of systolic minus diastolic). This was a vasovagal form of collapse that likely involved pooling of blood in the extremities and visceral organs. Those men who did not collapse exhibited a high pulse rate, steady blood pressures, and a large pulse pressure, indicative of appropriate physiological responses to upright posture

Of the 36 test participants, only six experienced great distress and collapse. Their syncope was transient and recovery was rapid, once they were removed to a mild environment. The 30 unaffected men stood in the heat without signs or symptoms for 60 min post-exercise. The first signs of syncope were forward bending of the head, closing of the eyes, sighing, absence of body tone, body restlessness, and a verbal request to lean or sit down. At this stage, fainting was imminent. Participants reported weakness, lassitude, nausea, giddiness, and a period of blackness. This is one of the few published studies in which experimental test participants experienced syncope and collapse. This likely occurred because of the requirement to stand for 1 h in the heat

Air movement across the skin is an effective measure to counteract syncope and collapse

Weiner, 1938. Heat collapse research study [32]

Strenuous labor in a deep Australian underground mine (1800 m maximum depth) in hot ambient conditions. Cases of heat exhaustion were reported by telephone; miners were retrieved and transported to a medical center. The heat exhaustion incidence rose in a dose-response manner when ambient conditions reached >33 °C, 91.4 °F dry bulb, >28 °C, 82.4 °F web bulb globe temperature, and <1.5 m/sec air velocity

Heat exhaustion is caused by the inability of the circulatory system to simultaneously supply sufficient blood flow to the skin to achieve heat loss and to supply the vital organs and exercising skeletal muscle. This illness usually is due to hypovolemia resulting from varying degrees of water and salt loss. The urine specific gravity at presentation was strongly correlated with the incidence of heat exhaustion; see Fig 6.1.

A total of 106 miners were included in this study, which spanned 12 months. The incidence of heat exhaustion therefore was 94.2/1000 workers/year. The most commonly observed symptoms were nausea, fatigue, headache, cramps, dizziness and vomiting. Symptom details appear in Table 5.5, which may be compared to Table 5.2

People with heat exhaustion rarely experienced confusion, ataxia, convulsions, or prolonged unconsciousness; the authors noted that these strongly suggest exertional heat stroke

Treatment consisted of either oral fluids or i.v. normal saline, given in an air-conditioned treatment room of the medical center

Donoghue et al., 2000. Heat exhaustion in miners [33]

This brief review paper proposes that heat exhaustion in marathons actually is post-exercise collapse when athletes are fully conscious with no other serious medical conditions, have postural hypotension (blood pressure <100 mm Hg), and low heart rates (<100 beats·min−1). This paper suggests that dehydration is not an important etiological factor in heat exhaustion

Low peripheral vascular resistance is present in patients with heat illness. When high air temperature increases skin temperature, peripheral resistance in blood vessels decreases and cutaneous blood flow increases. Because peripheral resistance provides compensation for upright posture, reduced arterial blood pressure becomes the critical event. Theoretically, this may be accompanied by a vasodilation response in skeletal muscle

Low peripheral vascular resistance may result in postural hypotension, faintness, blacking out, collapse, and weakness with or without vomiting

Lying supine with feet above the level of the head relieves hypotension

Noakes et al., 2007. Marathon runner collapse [25]

This brief review paper considers the causes of marathon collapse related to physical exhaustion, heat exhaustion, and dehydration

During severe exercise-heat stress (i.e., high skin and internal temperatures), cardiac output can decrease below levels observed during exercise in temperate environments. In combination with vasodilated skin and muscle, dehydration accentuates cardiovascular strain. Other factors that may contribute to post-race collapse include reduced skeletal muscle pump activity and an altered cerebrovascular response to orthostatic challenge

Athletes who finish a marathon and collapse are typically fully conscious but are unable to stand without support

Specific treatment options are not described

Kenefick and Sawka, 2007. Marathon runner collapse [34]

Ten healthy men participated in controlled laboratory experiments that evaluated the effects of control (C), partial (P), and full (F) American football uniforms on cardiovascular and thermal responses during mixed mode exercise in a hot, humid environment (33 °C, 91.4 °F; 49% rh). During 19 of 30 trials, participants halted exercise as a result of volitional exhaustion

Seven participants in group C completed the entire 80-min protocol (box lifting and treadmill walking), 3 in P, and 1 in F. Exhaustion occurred during the F and P trials at the same mean internal temperature (39.3 °C, 102.7 °F). Hypotension influenced exhaustion during exercise. Skin temperatures, measured at two sites, were greater during both P and F; this likely reduced peripheral resistance and increased skin blood flow

Systolic blood pressure decreased during box-lifting exercise in the heat. Also, both systolic and diastolic pressures decreased at the end of treadmill walking

Diastolic pressures suggested that cardiac filling decreased as a result of lower pressure during diastole and stroke volume decreased. To maintain cardiac output, the mean final heart rates (C, 164; P, 178; F, 180 beats·min−1) were necessarily high in experiments P and F, indicating great cardiovascular strain at the time of exhaustion. The mean internal temperatures at the end of exercise ranged from 38.7–39.2 °C, 101.7–102.3 °F


Armstrong et al., 2010. Exhaustion during uniformed exercise [35]

Note: The above statements are synopses written by the present author. They are not verbatim quotations from original publications

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Nov 7, 2020 | Posted by in SPORT MEDICINE | Comments Off on Exhaustion

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