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HEAT EMERGENCIES
by
Ann Dye, RN MSN

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Heat Illness

A. Thermoregulation

1. ATP - about 50% of the energy in food becomes heat during ATP production.

2. Metabolic rate - the factors that affect metabolic rate are: exercise, thyroid hormone, male sex hormone, fever, sleep, age, sympathetic stimulation, growth hormone, climate, malnutrition.

3. Heat loss - radiation, conduction to air (convection), and conduction to objects - (these apply as long as skin temperature is greater than the temperature of the surroundings); evaporation.

4. Hypothalamic and/or spinal cord integrative mechanisms - vasodilatation, sweating, decrease in heat production, set point - complex and not completely understood.

5. Behavioral control - "Mad Dogs and Englishmen go out in the Midday Sun" (Noel Coward)

  • Adaptive behaviors:
            Conserving activity or sheltering during periods of increased heat stress, e.g., "The Siesta", Nocturnal Activity;

    Increasing fluid intake;

    Water play (water conducts heat thirty times greater than air).
  • Adaptive clothing:
            "Sombrero" means shade (=/> 10º cooler in shade);

            loose flowing gowns conserve evaporative loss of sweat, protect from direct sun injury, and insulate without trapping heat, e.g., arab dress,

        "summerwear" shorts & tank tops permit greater exposure increasing evaporative, convective, and radiant loss of heat, but increase risk of direct sun injury and dehydration.
  • Adaptive personal environment:

            Sod or adobe dwellings (other insulation);

            Porches, patios, breezeways, fans;

            Air conditioning (rate of temperature drop determined by maximum number of "British Thermal Units" of heat for which equipment is rated). Air conditioning and refrigeration equipment do not  "make things colder" but instead "removes the warm and puts it somewhere else"; the resulting    dehumidification of ambient air may also increase one's efficiency in losing heat by evaporation.   ("It's not the heat, ---it's the humidity!)"

B. Heat acclimatization - requires two or more weeks for maximal development

1. Cardiovascular adaptations - increased maximal cardiac output, decrease peak heart rate, increased stroke volume

2. Endocrine adaptations - activation of renin-angiotensin system, aldosterone production may be decreased, growth hormone release - causes salt and water retention, increased ACTH, norepinephrine ---- see reduction in exercised induced levels, ADH release

3. Sweat volume and composition - decreased Na and Cl concentration and increased volume of sweat produced

4. Renal response - renal plasma flow falls, GFR falls then rises by about 20%, inability to maximally concentrate urine

5. Body fluid composition - increase in volumes of plasma, extracellular fluid volume and total body water content; excretion of Na into urine with Na conservation by sweat glands; hypokalemia

C. Heat illnesses

1. Heat syncope - orthostatic dizziness or syncope when no other cause is apparent; more common in persons with heart disease or in patients on diuretics

2. Heat edema - slight dependent edema; common in unacclimatized persons

3. Heat tetany - persons exposed to heated air may hyperventilate enough to develop acute respiratory alkalosis; may see circumoral paresthesias

4. Heat cramps - mechanism unknown but hyponatremia appears to be the cause

a. Predisposing factors - able to produce sweat in large quantities due to acclimatized state; consumption of adequate amounts of water to replace sweat losses; failure to replace NaCl losses

b. Precipitating factors - exhaustive work, hemodilution, cooling the muscles involved in work

c. Treatment - promptly relieved with 0.1% saline solution by mouth or IV Normal Saline 

5. Heat exhaustion (prostration) - most common clinical disorder resulting from work in high temperature; may be divided into two forms - dehydration and salt depletion. Pure forms are rare - most cases involve mixed water and salt depletion. Fluid and electrolyte replacement should be based on lab results and vital signs.

Dehydration - classically occurs when the supply of water is limited. Symptoms include: oliguria, intense thirst, fatigue, weakness, anxiety, and impaired judgement. CNS symptoms include hyperventilation, paresthesias, tetany, agitation, hysteria and muscle incoordination. May see delirium, fever, and coma. If untreated, may end in heat stroke.

Treatment - controlled water administration. Water should be given orally if the patient is awake and not vomiting. If the patient has orthostatic hypotension, hypotonic saline should be given. If the patient is not orthostatic but cannot take fluids by mouth, use D5W. When the serum Na drops to 150 mEq/L, hypotonic saline may be substituted. Avoid hyperglycemia and hypokalemia.

Salt depletion - occurs when large volumes of sweat are replaced by adequate water but inadequate salt. It differs from heat cramps in that it is accompanied by systemic symptoms and tends to occur in unacclimatized persons. Symptoms include profound weakness, fatigue, severe frontal headache, giddiness, anorexia, nausea, vomiting, diarrhea, skeletal muscle cramps, hypotension and tachycardia.

Treatment - easier than for dehydration. Salted liquids by mouth, if possible;NS intravenously, if not.

6. Heat stroke - least common of the heat illnesses but almost always fatal unless promptly recognized and treated. The urban, elderly poor are the most common victims of heat stroke. Characterized by a body temperature above 40.6º C. Predisposing factors: salt and water depletion, infection, fever following immunization, lack of acclimatization, obesity, drugs, fatigue. Predisposing diseases: cardiovascular disease, diabetes mellitus, malnutrition, acute or chronic alcoholism, hyperthyroidism, impaired sweat production, and potassium deficiency. May be divided into two forms: classic and exertional.

a. Classic - occurs after several days of temperatures above 37.0º C or somewhat lower temperatures but with high relative humidity. Active perspiration is continuous but eventually fails and body temperature rises sharply. The first symptom may be sudden collapse. In 80% of cases onset is sudden and the patient becomes delirious, comatose or may have a seizure. In the other 20% of cases the patient may have weakness, dizziness, nausea, syncope, or frontal headache prior to collapse. Muscle cramps are unusual. Patients progress to coma. Hot and dry skin is usual but sweating may persist.

b. Exertional - seen in association with events that increase endogenous heat production. In the U.S. the majority of cases occur in competitive long distance runners, football players and military recruits. Sustained physical exertion commonly precedes heat stroke. The overzealous administration of salt supplements with insufficient water intake can be lethal. Core temperature may in fact not exceed 40.6º C and be fatal, while in classic heat stroke, patients whose core temperature measured 43.7º C have survived without sequelae. Unless cooled rapidly there may be widespread necrosis of many body tissues. Thrombocytopenia, prolonged PT and PTT are seen and DIC is marked. Hypotension or shock occur commonly. In severe cases, acute pulmonary edema has been observed. Evidence of rhabdomyolysis exists in virtually all cases. Severe hypoglycemia may occur. Death commonly occurs as a result of acute hyperkalemia following a seizure or as a result of extensive rhabdomyolysis with acute renal failure. Exertional heat stroke and rhabdomyolysis in women is extremely rare.

c. Treatment - Delay in cooling probably represents the single most important factor leading to death or disability in those who survive. Delay is due either to failure to make the diagnosis, failure to appreciate the seriousness of the problem, or lack of proper cooling facilities. As in all cases, the ABC's are the first priority. Immersion in ice water or evaporative cooling using large circulating fans and skin wetting are the most effective cooling methods. Cooling measures should stop when the core temperature reaches 39º - 40º C. The body temperature will normally continue to fall. Cooling normally restores the BP by cutaneous vasoconstriction. Large amounts of IV fluid should be avoided initially; pulmonary edema is common. Fluid boluses are used with careful monitoring of CVP and urine output. The use of alpha-adrenergic drugs such as norepinephrine are not recommended. Check glucose and replace with D50% if indicated; more common in exertional heat stroke. If rhabdomyolysis is severe, the patient may have hyperkalemia and myoglobinuria which may lead to acute renal failure, shock, and necrosis of the diaphragm with respiratory failure. Hyperthermia may recur in 3-4 hours and cooling measures must be repeated. Some patients lose their ability to sweat for several weeks and need to be watched closely.


c.f., also,"Research Applied to Clinical Practice: Geriatric Thermoregulation"

"Heat Emergencies"
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is a webarticle by Ann Dye, RN MSN
©Ann Dye, RN MSN
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