What is Heat Stroke?
Heat Stroke can be defined as an extreme hyperthermia with thermoregulatory failure, characterized by serious end stage organ damage with universal involvement of the central nervous system. Although there is no specific vital sign parameters that define heat stroke, a core body temperature greater than 41 degrees C or 40.5 degrees C with anhydrases and an altered mental state is generally accepted as heat stroke.
Heat stroke can be divided into exertional heat stroke and classic heat stroke. Exertional heat stroke is caused by excessive exercise, and is regularly seen in marathon runners and elite athletes who push their bodies past their thermoregulatory ability to respond to the heat produced through muscle movements. Classic heat stroke occurs more commonly in older patients or in patients with underlying illnesses who are exposed to extreme environmental conditions. In these patients, the increased environmental temperature has caused increased stress on an already weakened body system, such as cardiovascular, renal, and thermoregulatory. As a consequence, the increased temperature will cause one or more of these primary body systems to fail.
Heat Stroke Pathophysiology
Initially, with heat stroke, as a person’s core body temperature increases the body attempts to lower the core temperature through renal and splanchnic vasoconstriction with concomitant peripheral vasodilatation causing a substantial fluid shift from the central compartments to the peripheries. This allows heat to be lost via evaporation and convection. This, in turn results in an increased cardiac output of up to 3L/min per degree C and may lead to cardiac failure in patients with limited cardiac reserve.
Eventually the vasoconstriction needed to keep the blood in the peripheries fails, therefore causing cutaneous blood flow to decrease, further decreasing heat loss from the body’s core and increasing hyperthermia. This hyperthermia will then eventually cause cerebral oedema, which results in an increased intracranial pressure (ICP). This increased ICP combined with a decreased mean arterial pressure (MAP) results in a decreased cerebral perfusion pressure (CPP) and cerebral hypoxia, manifesting as central nervous system (CNS) dysfunction.
Sensible perspiration (also known as thermal sweating) is controlled by the thermoregulatory center within the hypothalamus and involves both heat and water loss through the skin. When external or internal temperature rises thermal sweating is produced. Thermal sweating results in a rapid loss of salt and therefore fluid from the body, but because thermoregulation has priority over water and electrolyte balances, sweating will continue until complete dehydration occurs. It is because of this that patients with heatstroke may present with a high temperature and hot but dry skin (anhydrases). Anhydrases is a late finding in heat stroke and is more common in classic heat stroke than in exertional heatstroke.
Tissue Damage and Heat Stroke
Tissue damage during heat stroke is believed to result from uncoupling during oxidative phosphorylation, which occurs when the temperature exceeds 41 degrees C. As energy stores are depleted cell membranes become more permeable and Na influx occurs. This causes an increased use of the Na+-K+ pump requirement to pump Na out of the cells, resulting in a cycle of increased ATP use, increased metabolic rate and therefore further elevation of core body temperature.
Eventually, the Na+K pump fails and as Na flows into the cell at a rate greater than the Na+K pump can remove it, interstitial fluid is drawn into the cell through osmosis, causes the cell to swell and eventually lyse (rupture), releasing a variety of electroyltes and toxins.