Water-electrolyte balance and kidneys
The dynamics of water metabolism and renal function are strictly tied to the stages of the febrile reaction. Direct damage to the renal tissue usually does not occur; all shifts are secondary and regulatory in nature.
- First stage (st. incrementi): Hypohydration develops. Due to the activation of sympathoadrenal influences, filtration pressure increases, which enhances diuresis. Additionally, fluid is lost due to increased sweating. Excess ions begin to accumulate in the tissues: $Na^+$, $Ca^{2+}$, $Cl^-$.
- Second stage (st. fastigii): Hyperhydration sets in — the volume of water in the body increases. The body retains water due to the enhanced synthesis and release of corticosteroids (primarily aldosterone) and antidiuretic hormone (ADH). These hormones activate water reabsorption in the renal tubules. Diuresis decreases, while excess ions in the tissues persist.
- Third stage (st. decrementi): The levels of aldosterone and ADH decrease. There is a massive excretion of accumulated ions and water through sharply increased diuresis and profuse sweating.
Nervous and endocrine regulation
The endocrine system acts as a crucial component of adaptation systems as well as a target for pathogenic influences. The synthesis of liberins, ACTH, TSH, and ADH increases. The concentration of glucocorticoids, catecholamines, insulin, and thyroid hormones (triiodothyronine $T_3$ and tetraiodothyronine $T_4$) rises in the blood. The levels of local biologically active substances—kinins, prostaglandins (PG), and leukotrienes—also change.
The nervous system responds functionally to most pyrogens (infectious, non-infectious, leukocyte cytokines) — they do not exert a specific damaging effect on neural structures. Nonspecific clinical manifestations occur:
- Headache, bad mood, and irritability.
- Sleep disturbances (drowsiness or, conversely, poor sleep).
- Confusion, lethargy, and sometimes hallucinations.
- Hypersensitivity of the skin and mucous membranes (hyperesthesia), altered pain sensitivity.
- Impaired reflexes and the development of neuropathies.
Cardiovascular and respiratory systems
Hemodynamics and the external respiration system are reorganized to meet new metabolic needs.
- Cardiovascular system: In the first stage and at the beginning of the second, the effects of the sympathoadrenal, hypothalamic-pituitary-adrenal, and thyroid systems dominate. Tachycardia, hypertensive reactions, and the phenomenon of blood flow centralization occur. Arrhythmias are frequently recorded. In uncomplicated courses, these changes resolve by the end of the second stage (aggravated in complicated cases), and deviations gradually disappear in the third stage.
- Respiration: Due to fluctuations in metabolic intensity, blood pressure deviations, and impaired blood oxygenation, pH drops (acidosis develops) and the partial pressure of carbon dioxide ($pCO_2$) rises. To compensate for this, the volume of alveolar ventilation significantly increases. Respiratory rate and depth may show unidirectional or multidirectional deviations (e.g., increased depth with decreased rate). Gas exchange in the lungs is activated due to increased blood perfusion against the background of blood circulation centralization.
Digestive System
The digestive system is a target for pathogenic factors, but does not participate directly in the mechanisms of fever development. Due to intoxication, the direct influence of high temperature, and the activation of the sympathoadrenal system, a total suppression of functions occurs:
- Appetite decreases (anorexia) and salivation diminishes, causing dry mouth.
- Secretory, motor, and digestive functions of the stomach and intestines are suppressed.
- The production of pancreatic enzymes and bile secretion are inhibited.
The clinical consequences of such dysfunction include impaired food absorption and digestion, flatulence, constipation, as well as possible nausea and vomiting.
Briefly: answers to topical questions
What is the mechanism of blood flow centralization development in the first stage of fever?
The mechanism of blood flow centralization development in the first stage of fever (st. incrementi) is associated with the restriction of heat transfer and the activation of sympathoadrenal influences.
- Neurogenic mechanism: efferent impulses from cold-sensitive neurons of the thermoregulation center activate neurons of the sympathoadrenal system.
- Vascular reaction: increased sympathoadrenal influences cause a generalized spasm of the arterioles of the skin and subcutaneous tissue.
As a result, the blood filling of peripheral vessels decreases, skin temperature drops, and heat loss through radiation, conduction, convection, and evaporation is reduced. Blood flow centralization is listed among the clinical manifestations of cardiovascular changes in fever.
The "hormonal swing" rule for diuresis: in stage I it increases due to the sympathetic system, in stage II it drops due to the peak of aldosterone and ADH (water is retained), and in stage III it sharply rises again due to the decrease in these hormones.
Class and exam questions
Do pyrogens damage the nervous system directly?
No, most infectious and non-infectious pyrogens, as well as cytokines, do not exert a specific destructive effect on neural structures. They provoke only metabolic and functional disorders.
Why does appetite disappear and the mouth dry out during a fever?
This is a consequence of the suppression of the secretory and motor functions of the digestive tract. The main causes are the direct effect of high temperature, intoxication, and hyperactivation of the sympathoadrenal system.
How does the blood gas composition change during a fever?
A decrease in blood pH is observed (acidosis develops) along with an increase in the partial pressure of carbon dioxide ($pCO_2$). This stimulates a compensatory increase in pulmonary ventilation volume.
What else to study on this topic
- Mechanisms of action of primary pyrogenic agents (infectious and non-infectious).
- The role of local biologically active substances (prostaglandins, leukotrienes, kinins) in thermoregulation.
- Pathogenesis of the blood flow centralization phenomenon during elevated body temperature.
- The effect of fever on acid-base balance and the mechanisms of acidosis development.
- Cardiovascular complications in the second stage of fever.
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