Etiology and Predisposing Factors
The causes of hyperthermia are divided into three main groups:
- High ambient temperature. This may include climatic conditions (heat waves, intense sun exposure) or technological/iatrogenic factors (improper incubator settings for newborns, delivery of overheated gas mixtures during mechanical ventilation).
- Reduced heat dissipation. This 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, or high ambient humidity.
- Uncoupling of oxidation and phosphorylation. Mitochondrial processes are disrupted by exogenous factors (calcium channel blockers, 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 features (imperfect thermoregulation in newborns), comorbid conditions (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 near the upper limit of normal.
Heat dissipation mechanisms change 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. Sweat evaporation becomes the primary mechanism. Sweat glands secrete kinins (bradykinin, kallidin), which cause potent vasodilation and enhance sweating.
The cardiovascular system responds with tachycardia, increased cardiac output, and elevated systolic blood pressure. Blood flow becomes 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 potent stressor. The sympathoadrenal and hypothalamic-pituitary systems are activated, releasing catecholamines, glucocorticoids, and thyroid hormones into the bloodstream.
Due to hyperventilation, hypocapnia and respiratory alkalosis initially occur. However, as tissue hypoxia worsens, alkalosis is quickly 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 thermal load is not reduced, thermoregulatory mechanisms fail. Temperature reaches 41–43 °C. The most crucial clinical marker of transition to this stage is the cessation of sweating (skin becomes dry and hot).
Severe circulatory failure develops: stroke volume and diastolic blood pressure drop, and microcirculation is impaired. A risk of multiple organ dysfunction syndrome (MODS) emerges.
Key pathological processes:
- "Desert disease" syndrome: critical hypohydration with a 9–10% loss of body fluid.
- Endogenous intoxication: accumulation of cytotoxic middle molecules in plasma (peptides, heat shock proteins).
- Membrane damage: activation of free radical reactions destroys cells (marked by an increase in diene conjugates).
- Endocrine gland exhaustion: development of adrenal and thyroid insufficiency, leading to collapse.
Without emergency care, the patient falls into hyperthermic coma (cerebral edema, petechial hemorrhages, visceral organ dystrophy) and dies from ventricular fibrillation or respiratory arrest.