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Thermoregulation Disorders: Hyperthermia and Hypothermia

Hyperthermia et Hypothermia

For medical students2 min readUpdated 2026-10-10

Thermoregulation disorders manifest as shifts in the temperature balance leading to overheating or cooling of the organism. These processes can occur both under the influence of an extreme environment and under the action of endogenous pyrogens, fundamentally changing the intensity of tissue metabolism.

Fever mediatorInterleukin-1 restructures hypothalamic function by exciting cold-sensitive neurons
Adaptation failureProlonged hyperventilation during overheating leads to the development of alkalosis
Core coolingReducing core body temperature to 29–30 °C is critical for cardiac surgery
SpaceflightControlled anabiosis is considered a way to reduce food consumption in space

Mechanism of Microbial Fever Development

Upon the introduction of infectious agents into brain tissues, the production of a specific endogenous pyrogen—interleukin-1 (IL-1)—is activated. This substance directly acts on the thermoregulatory centers in the hypothalamus, causing a functional reorganization:

Key molecular mediators in this chain are arachidonic acid derivatives (primarily group E prostaglandins), as well as adrenocorticotropic hormone (ACTH). As a result, the body begins to perceive its normal temperature as too low and triggers heat production mechanisms.

Hyperthermia and Consequences of Overheating

If the ambient temperature rises above blood temperature, the body begins to heat up passively. Excessive heat enters the organism via heat radiation and conduction.

In response to hyperthermia, compensatory reactions are triggered. Humans experience tachycardia (increased heart rate) and tachypnea (rapid breathing). In animals, such as dogs, cooling occurs via polypnea—very rapid breathing that repeatedly enhances the evaporation of saliva from the surface of the respiratory mucosa.

Prolonged exposure to high temperatures leads to the exhaustion of compensatory mechanisms:

  1. Respiratory alkalosis occurs (a result of marked hyperventilation).
  2. Heat stroke develops, accompanied by deep CNS depression and loss of consciousness.

Artificial Hypothermia in Clinical Practice

Unlike overheating, artificial cooling of the organism is widely used in medicine. Hypothermia implies the targeted reduction of core body temperature to 29–30 °C. The main physiological rationale of the procedure is a drastic slowing down of all metabolic processes in tissues, shifting cells into a state of hypo- and anabiosis.

This technique is indispensable in cardiac surgery: it allows complex operations on a "dry" heart temporarily excluded from the circulation, significantly increasing the permissible ischemia time.

Methods of achieving hypothermia:

V.M. Bakhmetiev's Theory of Anabiosis

The prospects of studying temperature effects are inextricably linked with the doctrine of anabiosis, founded by V.M. Bakhmetiev. The basic idea of the theory is the ability to voluntarily stop and then restart cellular metabolism (following the principle of a mechanical clock pendulum).

Beyond medicine, the control of anabiosis is of colossal interest for astronautics. The implementation of controlled anabiosis technologies in deep space missions will make it possible to drastically reduce the required food supplies.

Mnemonic

To easily remember the action of interleukin-1 in fever, imagine a climate control system: it "turns on the heater" (exciting cold neurons to induce warming) and "turns off the AC" (inhibiting heat neurons).

Frequently asked questions

What stages are distinguished in the pathogenesis of a typical fever?

Three successive stages are distinguished in the pathogenesis of typical fever.

  • Temperature rise (stadium incrementi) — caused by a shift in the ratio between heat production and heat loss.
  • Temperature plateau (stadium fastigii) — the elevated temperature stage.
  • Temperature decline — return of body temperature to the normal range.
Which physical thermoregulation mechanisms are activated in humans during hyperthermia?

At high ambient temperatures, physical thermoregulation mechanisms (heat loss) are activated to dissipate heat.

  • Sudomotor response — sweating and evaporation of moisture from the skin surface.
  • Vasomotor response — vasodilation of skin vessels, increasing heat loss via radiation and convection.
  • Respiratory response — increased intensity of external respiration (tachypnea).
  • Piloerection change — the arrector pili muscle (m. arrector pili) relaxes, and hairs lie flat against the skin.
How does the mechanism of fever fundamentally differ from hyperthermia?

The fundamental difference is that fever is a protective adaptive reaction, whereas hyperthermia is a pathological process resulting from the breakdown of thermoregulatory mechanisms.

CriterionFeverExogenous Hyperthermia
CausePyrogensHigh ambient temperature
Key mechanismTemporary dynamic reorganization of the thermoregulation system (shifting the "set point")Breakdown of the body's adaptation mechanisms to exogenous heat
Diurnal fluctuationsPreservedAbsent
What classes of pyrogens are distinguished according to their origin?

Depending on their origin, pyrogens are divided into two main groups.

  • Primary pyrogens — a heterogeneous group of exogenous or endogenous substances (e.g., lipopolysaccharides) that induce the synthesis of secondary pyrogens.
  • Secondary pyrogens — endogenous cytokines (e.g., interleukin-1) produced by leukocytes under the influence of primary pyrogens, triggering the febrile response.
Why can alkalosis develop during hyperthermia?

In response to overheating, rapid breathing (tachypnea) occurs. Prolonged hyperventilation leads to excessive elimination of carbon dioxide from the blood, shifting the acid-base balance toward the alkaline side.

Why is pharmacological blockade used when cooling a patient?

Exclusively physical cooling with ice causes a powerful protective cold stress reaction in the patient. Drug blockade of the heat production center suppresses this undesirable reaction.

What role do prostaglandins E play in fever?

These arachidonic acid metabolites act as key molecular intermediaries that transmit the pyrogenic signal from interleukin-1 to the hypothalamic neurons.

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