Heat stroke pathophysiology
|
Heat stroke Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Heat stroke pathophysiology On the Web |
|
American Roentgen Ray Society Images of Heat stroke pathophysiology |
|
Risk calculators and risk factors for Heat stroke pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]
Overview
Pathophysiology
Heat stress means perceived discomfort and physiologic strains during heat exposure. A series of physiologic events occur to adapt heat. These events include thermoregulation (with acclimatization), an acute-phase response, and production of heatshock proteins. If these sequence of actions fails to prevents body from high temperature, heat stress progresses to heat stroke.
Thermoregulation
The core body temperature is set to 37 °C. Thermoregulatory center is located in hypothalamus, every 1 °C in body temperature activates the peripheral and central receptors to maintain core body temperature at 37 °C.(1,29) Increase in the peripheral body temperature will activate sympathetic response through thermoregulatory action of hypothalamus to deliver more blood flow by vasodilation of surface cutaneous veins. This increase in blood flow will cause sweating. The elevated blood temperature will cause tachycardia, increase in cardiac output, and increase in minute ventilation. (1,31,32,33)Blood shift from internal organs to the skin may cause decreased visceral perfusion and predispose them to ischemia. Increased sweating will cause loss of salt and water up to 2 liters per hour. Therefore, dehydration may worsen thermoregulation. (33,34)
Acclimatization
The process of body adaptation to heat which, might take up to 3 weeks is called acclimatization. Acclimatization, involves enhancement of cardiovascular performance, activation of the renin–angiotensin– aldosterone axis, salt conservation by the sweat glands and kidneys, an increase in the capacity to secrete sweat, expansion of plasma volume, an increase in the glomerular filtration rate, and an increase in the ability to resist exertional rhabdomyolysis.(35)
Acute-Phase Response
Endothelial cells, leukocytes, and epithelial cells incorporate a variety of cytokines (mainly nterleukin-1 and nterleukin-6) to protect against tissue injury and promote repair. A similar event occur in sepsis.(55)
Heat-Shock Response
Heat-shock proteins are secreted in response to heat to protect cells from injury. Heat-shock proteins bind to proteins and act as chaperons to prevent them from denaturation. (15,16,58,56)
Pathogenesis
Microscopic findings
Severe heat stroke causes vascular congestion and/or hemorrhage, thrombi, increased inflammatory cells, and disruption of architecture in many internal organs including: liver, jejunum, spleen, lungs, and kidneys. Angiotelectasis, congestion, and thickening of the lung matrix are another pathological findings.