Hyperthermia

1. Hyperthermia MehrdadEsmailian MD. Assistant professor of Emergency Medicine

2. Definition • Elevation of core body temperature above the normal diurnal range of 36ºC to 37.5ºC due to failure of thermoregulation • Hyperthermia is not synonymous with the more common sign of fever, which is induced by cytokine activation during inflammation, and regulated at the level of the hypothalamus

4. Hyperthermia • The most important causes of severe hyperthermia (greater than 40ºC or 104ºF) caused by failure of thermoregulation are: • Heat stroke • Neuroleptic malignant syndrome • Malignant hyperthermia

5. Physiology • Body temperature is maintained within a narrow range by balancing heat load with heat dissipation • Body's heat load results from both metabolic processes and absorption of heat from the environment • As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the ANS to produce sweating and cutaneousvasodilation

6. Physiology • Evaporation is the principal mechanism of heat loss in a hot environment, but this becomes ineffective above a relative humidity of 75% • Other methods of heat dissipation • Radiation- emission of infrared electromagnetic energy • Conduction- direct transfer of heat to an adjacent, cooler object • Convection-direct transfer of heat to convective air currents • These methods cannot efficiently transfer heat when environmental temperature exceeds skin temperature

12. Physiology • Temperature elevation  ↑ O2 consumption and metabolic rate  hyperpnea and tachycardia • Above 42ºC (108ºF), oxidative phosphorylationbecomes uncoupled, and a variety of enzymes cease to function • Hepatocytes, vascular endothelium, and neural tissue are most sensitiveto these effects, but all organs may be involved • As a result, these patients are at risk of multiorgan system failure

13. Heat Regulation • The regulation of body temperature involves three distinct functions: • Thermosensors • Central integrative area • Thermoregulatory effectors

14. Thermosensors • Temperature-sensitive structures are located both peripherally in the skin and centrally in the body • Skin temperature changes, correlate poorly with changes in the rate of heat loss • Thermosensitive neurons are in the preoptic area of the anterior hypothalamus. They are activated when the temperature of the blood circulating through that area exceeds a certain “set point”

15. The skin temperature affects heat loss, since a person resting in a warm environment initiates sweating, even though the core temperature remains constant • In contrast, changes in core temperature are more potent in producing heat-dissipating responses

16. Central Integrative Area • The 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

17. For example, fever, the circadian rhythm of temperature variation, and the 0.5° C difference in rectal temperature after ovulation can be explained by variation of a thermal set-point

18. Thermoregulatory Effectors • Sweating and peripheral vasodilationare 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

19. 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

20. 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 to 2 L/hr of sweat; loss of 4 L/hr for short periods is possible

21. Cooling is best achieved by evaporation from the body surface; sweat that drips from the skin does not cool the body, and sweat evaporated from clothing is considerably less efficient • Each liter of completely evaporated sweat consumes 580 kcal of heat

22. The ability of the environment to evaporate sweat is termed atmospheric cooling powerand varies primarily with humidity, but also with wind velocity • As humidity approaches 100%, evaporative heat loss ceases

23. The vascular response to heat stress is cutaneousvasodilationand 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

24. To maintain blood pressure, cardiac output must increase 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

25. Acclimatization • Definition : 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 in 7 to 14 days. This is characterized by an earlier onset of sweating (at a lower core temperature), increased sweat volume, and lowered sweat electrolyte concentration

26. Acclimatization is hastened by modest salt deprivation and delayed by high dietary salt intake • As acclimatization proceeds, the sweat sodium concentration drops while the volume increases

27. The cardiovascular system plays a major role in both acclimatization and endurance training, largely resulting from an expansion of plasma volume • Heart rate is lower and associated with a higher stroke volume

28. 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

29. The well-conditioned athlete is not necessarily heat acclimatized • To maintain heat and exercise-induced adaptive responses, 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

30. Predisposing Factors • Elderly patients or those with chronic diseases who are taking medications predisposing to heat illness are prone to classic heatstroke during periods of high ambient heat and humidity. Adequate fluid intake is essential. • Elderly patients sometimes dress inappropriately for hot weather; heat loss is maximized by light, loose-fitting garments

31. Exertional heatstroke is most likely to occur in young, healthy people involved in strenuous physical activity, especially if they have not acclimatized • 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, pleasantly flavored fluids

32. 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° C to 15.8° C) • High osmolality inhibits gastric emptying; osmolality of less than 200 mOsm/L is optimal

33. Hydration can be monitored by measuring bodyweight before and after training or athletic competition • An athlete with a loss of 2% to 3% body weight (1.5-2 L in a 70-kg man) should drink extra fluid and be permitted to compete only when within 0.5 to 1 kg (1-2 pounds) of the starting weight on the previous day

34. A weight loss of 5% to 6% represents a moderately severe deficit and usually is associated with intense thirst, scanty urine, tachycardia, and an increase in rectal temperature of about 2° C. Such athletes should be restricted to light workouts after hydration to their normal weight

35. A loss of 7% or more of body weight represents severe water depletion; the athlete should not participate in sports until examined by a physician. 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

36. 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

37. 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

38. 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

39. The body's heat dissipation mechanisms are analogous to the cooling system of an automobile : 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)

41. MINOR HEAT ILLNESS Heat Cramps Heat Edema Heat Syncope Prickly Heat

42. MAJOR HEAT ILLNESS • HEAT EXHAUSTION • HEATSTROKE • Classic • Exertional

43. Heat Cramps • Brief, intermittent, and often severe muscular cramps occurring typically in muscles that are fatigued by heavy work • Heat cramps occur most commonly during the first days of work in a hot environment and develop in persons who produce large amounts of thermal sweat and subsequently drink copious amounts of hypotonic fluid • Heat cramps appear to be related to salt deficiency

44. The most commonly victims : athletes, roofers, steel workers, coal miners, field workers, and boiler operators • Heat cramps tend to occur after exercise when the victim has stopped working and is relaxing. In this respect, they differ from the cramps experienced by athletes during exercise, which tend to last for several minutes, are relieved by massage, and resolve spontaneously

45. Essentials of Diagnosis : • Cramps of most worked muscles • Usually occur after exertion • Copious sweating during exertion • Copious hypotonic fluid replacement during exertion • Hyperventilation not present in cool environment

46. DDs : hyperventilation tetany • Heat cramp victims exhibit hyponatremia, hypochloremia, and low serum sodium and chloride levels • Rhabdomyolysis or resultant renal damage is not present with isolated heat cramps

47. Management • Mild cases without concurrent dehydration may be treated orally with 0.1% to 0.2% salt solution (two to four 10-grain salt tablets [56 to 112 mEq] or ¼ to ½ teaspoon table salt dissolved in a quart of water), which is the general limit of palatability • Severe cases respond rapidly to intravenous isotonic solution (0.9% NaCl) • Salt tablets are gastric irritants and are not recommended

48. Heat Edema • Swollen feet and ankles are often reported by nonacclimatized individuals, especially the elderly, who encounter climatic stresses of tropical and semitropical area • Such individuals often have no underlying cardiac, hepatic, venous, or lymphatic disease. They commonly have assumed rigorous schedules with long periods of sitting or standing

49. The edema is usually minimal, not accompanied by any significant impairment in function, and often resolves after several days of acclimatization

50. It is presumed that hydrostatic pressure and vasodilation of cutaneous vessels, combined with some degree of orthostatic pooling, lead to vascular leak and accumulation of interstitial fluid in the lower extremities • Aldosterone increases in response to the heat stress and perceived central volume deficit