Heat stroke and death as a result of illnesses relating to the body’s inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (i.e. prickly heat), heat cramps, and tetany, as well as heat syncope and heat exhaustion. Heatstroke is the most severe form of the heat-related illnesses and is defined as a body temperature higher than 41°C (106°F) associated with neurologic dysfunction.
Heatstroke EHS= Exertional heatstroke generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment.
Heatstroke NEHS=Non-Exertional Heatstroke more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons. Classic NEHS occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years. Both types of heatstroke are associated with a high morbidity and mortality, especially when therapy is delayed.
Body Condition: The human body can maintain a constant body temperature by balancing heat gain with heat loss in-balance. When heat gain overwhelms the body’s mechanisms of heat loss, the body temperature rises, and a major heat illness ensues. Excessive heat de-natures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death. The exact temperature at which cardiovascular collapse occurs varies among individuals because coexisting disease, drugs, and other factors may contribute to or delay organ dysfunction. Full recovery has been observed in patients with temperatures as high as 46°C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106°F or 41°C generally are catastrophic and require immediate aggressive treatment and care.
Temperature can be acquired by a number of different mechanisms. At rest, basal metabolic processes produce approximately 100 kcal of heat per hour or 1 kcal/kg/h. These reactions can raise the body temperature by 1.1°C/h if the heat dissipating mechanisms are nonfunctional. Strenuous physical activity can increase heat production more than 10-fold to levels exceeding 1000 kcal/h. Fevers, shivering, convulsions, sympathomimetic drugs, heaty food staff, hot drinks, chillies and many other conditions and food staff can increase heat production, thereby increasing body heat.
Your body also can get heat from the environment through some of the same mechanisms involved in heat dissipation, including conduction, convection, and radiation. These mechanisms occur at the level of the skin and require a properly functioning skin surface, sweat glands, and autonomic nervous system, but they also may be manipulated by behavioral responses. Conduction refers to the transfer of heat between 2 surfaces with differing temperatures that are in direct contact. Convection refers to the transfer of heat between the body’s surface and a gas or fluid with a differing temperature. Radiation refers to the transfer of heat in the form of electromagnetic waves between the body and its surroundings. The efficacy of radiation as a means of heat transfer depends on the angle of the sun, the season, and the presence of clouds, among other factors. During summer, lying down in the sun can result in a heat gain of up to 150 kcal/h. Staying in any hot and stuffy can also increases the heat in the body. Always try to stay in an well aired or air-conditional area to reduce heat from your body.
Physiologicaly, heat gain is counteracted by a commensurate heat loss. This is orchestrated by the hypothalamus, which functions as a thermostat, guiding the body through mechanisms of heat production or heat dissipation, thereby maintaining the body temperature at a constant physiologic range. In a simplified model, thermo sensors located in the skin, muscles, and spinal cord send information regarding the core body temperature to the anterior hypothalamus, where the information is processed and appropriate physiologic and behavioral responses are generated. Physiologic responses to heat include an increase in the blood flow to the skin (as much as 8 L/min), which is the major heat-dissipating organ; dilatation of the peripheral venous system; and stimulation of the eccrine sweat glands to produce more sweat.
When the heat is drying up your organs, the skin can transfer heat to the environment through conduction, convection, radiation, and evaporation. Radiation is the most important mechanism of heat transfer at rest in temperate climates, accounting for 65% of heat dissipation, and it can be modulated by clothing. At high ambient temperatures, conduction becomes the least important of the 4 mechanisms, while evaporation, which refers to the conversion of a liquid to a gaseous phase, becomes the most effective mechanism of heat loss.
Evaporation as a mechanism of heat loss depends on the condition of the skin and sweat glands, the function of the lung, ambient temperature, humidity, air movement, and whether or not the person is acclimated to the high temperatures. For example, evaporation does not occur when the ambient humidity exceeds 75% and is less effective in individuals who are not acclimated. Nonacclimated individuals can only produce 1 L of sweat per hour, which only dispels 580 kcal of heat per hour, whereas acclimated individuals can produce 2-3 L of sweat per hour and can dissipate as much as 1740 kcal of heat per hour through evaporation. Acclimatization to hot environments usually occurs over 7-10 days and enables individuals to reduce the heat at which sweating begins, increase sweat production, and increase the capacity of the sweat glands to reabsorb sweat sodium, thereby increasing the efficiency of heat dissipation.
During heat gain exceeds heat loss, the body temperature rises. Classic heatstroke occurs in individuals who lack the capacity to modulate the environment ( infants, elderly individuals, individuals who are chronically ill). Furthermore, elderly persons and patients with diminished cardiovascular reserves are unable to generate and cope with the physiologic responses to heat stress and, therefore, are at risk of heatstroke. Patients with skin diseases and those taking medications that interfere with sweating also are at increased risk for heatstroke because they are unable to dissipate heat adequately. Additionally, the redistribution of blood flow to the periphery, coupled with the loss of fluids and electrolytes in sweat, place a tremendous burden on the heart, which ultimately may fail to maintain an adequate cardiac output, leading to additional morbidity and mortality.
Areas that interfere with heat dissipation include an inadequate intravascular volume, cardiovascular dysfunction, and abnormal skin. Additionally, high ambient temperatures, high ambient humidity, and many drugs can interfere with heat dissipation, resulting in a major heat illness. Similarly, hypothalamic dysfunction may alter temperature regulation and may result in an unchecked rise in temperature and heat illness. During these conditions
In the US: According to the National Centers for Health Statistics (NCHS), 7046 deaths were attributed to excessive heat exposure from 1979-1997, or an average of 371 deaths occurred per year. Heatstroke and deaths from excessive heat exposure are more common during summers with prolonged heat waves. During the heat wave of 1980 (a record year for heat), 1700 deaths were attributed to heat, compared to only 148 deaths attributed to heat the previous year. Persons older than 65 years accounted for at least 44% of cases. The numbers published by the NCHS are believed to grossly underestimate the true incidence of heat-related deaths because death rates from other causes (e.g, cardiovascular disease, stroke, kidney failure, dihydration, respiratory disease, etc, etc) also increase during the summer, and especially during heat waves.
Internationally: Heatstroke is uncommon in subtropical climates. The condition is recognized increasingly in countries that experience heat waves rarely (e.g. Japan), and it commonly affects people who undertake a pilgrimage to Mecca, especially when the pilgrims arrive from a cold environment. In 1998, one of the worst heat waves to strike India in 50 years resulted in more than 2600 deaths in 10 weeks. Unofficial reports described the number of deaths as almost double that figure.
Race and country: With the same risk factors and under the same environmental conditions, heatstroke affects all races equally. However, because of differences in social advantages, the annual death rate due to environmental conditions is more than 3 times higher in blacks than in whites.
Genatal: With the same risk factors and under the same environmental conditions, heatstroke affects both genders equally. However, because of gender differences in the workforce, the annual death rate due to environmental conditions is 2 times higher in men than in women.
Age: Infants, children, and elderly persons have a higher incidence of heatstroke than young, healthy adults.
Babies and children are at risk for heat illness due to inefficient sweating, a higher metabolic rate, and their inability to care for themselves and control their environment. Old persons also are at increased risk for heat-related illnesses because of their limited cardiovascular reserves, preexisting illness, and use of many medications that may affect their volume status or sweating ability. In addition, elderly people who are unable to care for themselves are at increased risk for heatstroke, presumably because of their inability to control their environment. EHS is the second most common cause of death among high school athletes, surpassed only by spinal cord injury. Unacclimatization is a major risk factor for EHS in young adults.
Heatstroke is defined typically as hyperthermia exceeding 41°C and anhidrosis associated with an altered sensorium. However, when a patient is allowed to cool down prior to measurement of the temperature....
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