Etiology and predisposing factors
The causes of hyperthermia are divided into three main groups:
- High environmental temperature. These can be climatic conditions (heat, active insolation) or technogenic/iatrogenic factors (improper incubator settings for newborns, delivery of overheated gas mixtures during mechanical ventilation).
- Decreased heat dissipation. Occurs with primary damage to the hypothalamus (due to hypoxia or trauma), as well as under the influence of external barriers: tight swaddling, heavy clothing, high air humidity.
- Uncoupling of oxidation and phosphorylation. The process in mitochondria is disrupted under the action of exogenous factors (calcium preparations, dicumarol) or endogenous factors (excess catecholamines, thyroid hormones, higher fatty acids), as well as specific proteins—thermogenins. Energy begins to dissipate as heat.
The development of the pathology is facilitated by age-related characteristics (imperfect thermoregulation in newborns), concomitant diseases (obesity, hyperthyroidism), and excessive physical activity.
Compensation (adaptation) stage
In response to overheating, the body triggers a triad of emergency reactions: behavioral (seeking coolness), autonomic (altering heat dissipation), and a stress response. At this stage, body temperature rises but is maintained at the upper limit of normal.
Heat dissipation mechanisms vary depending on the external environment:
- At 30–31 °C skin arterioles dilate, and heat is lost via radiation, convection, and conduction.
- At 32–33 °C and above these pathways are blocked. The main mechanism becomes sweat evaporation. Sweat glands secrete kinins (bradykinin, kallidin), which potently dilate blood vessels and enhance sweating.
The cardiovascular system reacts with tachycardia, an increase in cardiac output, and a rise in systolic blood pressure. Blood flow is centralized. Interestingly, metabolism initially slows down (oxygen consumption decreases), but upon reaching a body temperature of 38–39 °C, metabolic processes sharply accelerate, increasing pulmonary ventilation and $O_2$ utilization.
Metabolic shifts and stress response
Excess heat acts as a severe stressor. The sympathoadrenal and hypothalamo-pituitary systems are activated: catecholamines, glucocorticoids, and thyroid hormones are released into the blood.
Due to pulmonary hyperventilation, hypocapnia and respiratory alkalosis initially occur. However, as tissue hypoxia increases, alkalosis is rapidly replaced by metabolic acidosis. Profuse sweating leads to the loss of water, water-soluble vitamins, and essential ions (Cl⁻, K⁺, Na⁺, Ca²⁺, Mg²⁺). The blood becomes viscous.
Decompensation stage
If the heat load is not reduced, thermoregulation mechanisms fail. The temperature reaches 41–43 °C. The most important clinical marker of transition to this stage is cessation of sweating (the skin becomes dry and hot).
Severe circulatory failure develops: stroke volume and diastolic pressure drop, and microcirculation is impaired. The threat of multiple organ dysfunction syndrome (MODS) arises.
Key pathological processes:
- «Desert sickness» syndrome: critical hypohydration with the loss of 9–10% of body fluid.
- Endogenous intoxication: accumulation of cytotoxic middle molecules (peptides, heat shock proteins) in plasma.
- Membrane damage: activation of free radical reactions destroys cells (marker: increase in diene conjugates).
- Exhaustion of endocrine glands: development of adrenal and thyroid insufficiency, leading to collapse.
Without emergency care, the patient falls into a hyperthermic coma (cerebral edema, petechial hemorrhages, organ dystrophy) and dies from ventricular fibrillation or respiratory arrest.
Briefly: answers to topical questions
Which specific classes of heat shock proteins are synthesized in cells during the development of endogenous intoxication in hyperthermia?
The blood plasma shows an increased content of middle molecules, which include heat shock proteins. Mammals synthesize the following variants of heat shock proteins: HSP20, HSP40, HSP60, HSP70, HSP90.
What are the anatomical and physiological features of thermoregulation in newborns that predispose them to hyperthermia?
The anatomical basis is the immaturity of thermoregulation centers: neurons in the medulla oblongata centers mature only by 3–4 months of life. Consequently, the body temperature of newborns depends on the environment, creating a risk of overheating (transient hyperthermia), which can lead to dysfunction of the respiratory and cardiovascular center neurons. The physiological prerequisite is the predominance of heat dissipation over heat production, as well as the immaturity of both central and peripheral thermoregulation mechanisms.
What is the fundamental difference in the pathogenesis of hyperthermia compared to fever in the context of the thermoregulatory center function?
The fundamental difference lies in the mechanism of participation of the thermoregulatory system in pathogenesis.
| Criterion | Fever | Exogenous hyperthermia |
|---|---|---|
| Key mechanism | Temporary dynamic reconstruction of the thermoregulatory system (shifting of the «set point») | Failure of the body's adaptation mechanisms to the action of exogenous heat |
To memorize the triad of emergency responses to overheating, use the rule «AVS»: A — Autonomic (sweating, vasodilation), V — Behavioral (seeking shade), S — Stress response (release of adaptation hormones).
Class and exam questions
Why does the skin become dry in severe hyperthermia?
Dry skin is a sign of transition to the decompensation stage. Due to the exhaustion of thermoregulation mechanisms and critical fluid loss, sweating stops completely.
How does the acid-base balance change during overheating?
Initially, respiratory alkalosis develops due to rapid breathing. Later, due to impaired microcirculation and tissue hypoxia, acidic metabolic products accumulate, resulting in severe mixed acidosis.
What is «desert sickness» syndrome?
This is a state of profound hypohydration in the decompensation stage, in which the body loses 9–10% of fluid along with vital electrolytes and vitamins.
What else to study on this topic
- The role of kinins (kallidin and bradykinin) in the humoral regulation of sweating
- Mechanisms of uncoupling of oxidation and phosphorylation in mitochondria
- Pathogenesis of middle molecule formation and their cytotoxic effect
- Specific changes in the central nervous system and visceral organs in hyperthermic coma
- Dynamics of oxygen consumption at different stages of the compensation phase
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