Last updated on April 4, 2019 at 10:56
The body’s defence against heat includes:
- Skin vasodilation – increases heat loss by allowing heat to conduct away from the skin, increasing conduction
- Sweating – as the sweat evaporates heat is lost by evaporative cooling
- Arrector pili muscles relax – the flat hairs on the skin increase air flow around skin, increasing convection
The sympathetic nervous system is activated. As the cardiac output increases the skin vasodilation will be more effective in losing heat.
The warm-defence is different between people who live in warmer and colder countries. Those that live in warmer countries are better adapted and sweat less than a non-adapted individual would under the same circumstances.
The humidity of the air is important in the warm-defence. The higher the humidity the harder it is for sweat to evaporate, meaning that sweating is less effective in causing heat loss.
As described in topic 22 would the BMR by itself cause the body temperature to increase by 1°C every hour. From this it’s easy to understand that normal heat loss is very important in preventing hyperthermia.
Disorders of warm-defence
Any condition that causes decreased sweating (anhidrosis) will dramatically decrease the body’s defence against heat. This can be due to peripheral neuropathy, congenital dysplasia of sweat glands or Sjögren’s syndrome for example. Dehydration will decrease the sweat capacity. Elderly usually have decreased sweat capacity.
Cardiovascular diseases, especially chronic heart failure, decreases the body’s ability to increase the cardiac output in response to heat. Dehydration will also decrease this ability.
Drugs that induce peripheral vasoconstriction can also impair the skin vasodilation response. These drugs include antihistamines, atropine and sympathomimetics.
Circulatory disorders of heat stress
These disorders may develop in simple heat stress, without the presence of real hyperthermia.
Heat syncope refers to syncope that occurs due to heat. As the skin vasodilates will blood pool in the skin. This causes less blood to be available for the brain, potentially causing syncope. Salt and water loss during sweating contributes to this picture. Heat syncope is mainly a danger in orthostatic position. Assuming a supine position usually resolves this.
Heat decompensation is the cardiac decompensation that may occur in sub-compensated heart failure patients during exposure to heat. As the skin vasodilation warrants an increased cardiac output will this cause decompensation in these patients. Signs of forward-failure develop as blood is redirected to the skin rather than splanchnic organs. Decreased muscle perfusion may cause patient to fall.
There is no loss of consciousness, but there is mental impairment, often in the form of confusion. Assuming a supine position does not cure these symptoms. The decompensation itself reduces the warm-defence. Increased body temperature decreases myocardial contractility.
Ischaemic heart disease, like AMI or angina pectoris, develop more easily during heat stress. While the work of the heart increases due to the sympathetic activation the coronary circulation will not be elevated, due to the maldistribution of cardiac output.
Arrhythmias may develop because of hypokalaemia, which develops due to hypovolaemia and secondary hyperaldosteronism.
Salt/water disorders of heat stress
Sweat is a hypoosmolar fluid, meaning that it contains more water than salt. Continuous sweating eventually causes hyperosmolarity. The sweating capacity of healthy people may reach up to 3 litre/hour, which shows that hypovolaemia may occur quickly.
Water-depletion type heat exhaustion occurs when people exposed to heat stress don’t replace the fluid they lose after sweating excessively. Severe thirst, hypovolaemia and hyperosmolarity occurs. The thirst will trigger most people to replenish fluids, however the sensation of thirst is reduced in elderly. In this population hypovolaemic shock may develop. The acute hypertonicity may cause deterioration of the mental state. As hypovolaemia develops the capacity to sweat will decrease, which may cause hyperthermia to develop.
Salt-depletion type heat exhaustion occurs when people exposed to heat stress replace their lost fluid by drinking pure water (or hypoosmolar fluids), so that they don’t replace the lost salt. This causes hypoosmolarity and hyponatraemia, in contrast with the other type of heat exhaustion. The hypoosmolarity causes fluid to move from the extracellular space into the intracellular space, worsening the hypovolaemia. Hyponatraemia and hypoosmolarity can cause muscle cramps, nausea and vomiting.
Hyperthermia refers to the elevated body temperature above the normal. In contrast with fever, where the body temperature is also elevated, is the set point temperature in the case of hyperthermia normal (37°C). The temperature is elevated in hyperthermia because there is an increase in heat load and/or decrease in heat loss. In contrast to hypothermia the tissue oxygen need increases in hyperthermia.
The heat load may originate from external sources or may be produced in the body.
The heat load doesn’t need to be very much elevated to develop hyperthermia; as described earlier is continuous heat loss essential to prevent body temperature from rising. Any disorder of warm-defence may cause hyperthermia. Elderly or alcoholics in warm environments are typical people at risk for developing hyperthermia.
Hyperthermia has many effects on the body:
- Direct effects of the increased temperature
- Elevated temperature causes proteins to denaturate and precipitate
- Elevated temperature causes cell membranes to have higher Ca2+-permeability
- Secondary effects due to circulatory changes
- Skin vasodilation causes maldistribution of CO away from internal organs
- Excessive sweating may cause hypovolaemia and hypertonicity
Tissues all over the body are damaged due to the increased oxygen demand, hypovolaemia, maldistribution, denaturation of proteins and changes in the cell membranes. Brain oedema develops, which may cause CNS damage, altered mental state or even coma. Distributive or hypovolaemic shock may develop. Dead cells release potassium, potentially causing hyperkalaemia.
35. Cold-defense and cold-induced disorders
37. Heat stroke and malignant hyperthermia