Pathogenesis of Tissue Hypoxia
Against the background of respiratory alkalosis, oxygen deprivation of tissues naturally develops. This process is caused by several pathophysiological mechanisms simultaneously:
- Bohr Effect: There is a sharp increase in the affinity of hemoglobin (Hb) for oxygen. Dissociation of oxyhemoglobin (HbO2) becomes difficult, causing tissues to receive insufficient oxygen.
- Metabolic Block: The carboxylation of pyruvic acid is disrupted (transition of pyruvate to oxaloacetate followed by reduction to malate).
- Inhibition of Glycolysis: If the partial pressure of carbon dioxide (pCO2) drops to critical values (15–18 mm Hg), glycolytic enzymes lose their activity.
- Circulatory Insufficiency: This exacerbates the overall picture of oxygen delivery to cells.
Electrolyte Disturbances and Their Consequences
The shift of pH to the alkaline side forces the body to look for ways of compensation, which inevitably impacts the electrolyte balance.
The main problem is hypokalemia. To compensate for the shortage of protons in the blood, hydrogen ions (H+) leave the cells, and potassium (K+) is actively pumped inward in their place.
Clinically, this manifests as severe disorders:
- Muscle Weakness: Patients suffer from hypodynamia, intestinal paresis, and even skeletal muscle paralysis.
- Cardiac Abnormalities: Potassium deficiency affects the cardiac conduction system, causing extrasystoles and paroxysmal tachycardia.
Hyperventilation tetany deserves special attention. It occurs due to a decrease in potassium concentration in the extracellular fluid (it binds to albumins) and a critical drop in the level of ionized calcium (Ca2+). During alkalosis, plasma proteins begin to actively bind calcium, sharply reducing its free, physiologically active fraction.
Compensatory Mechanisms
The body's strategic goal in eliminating alkalosis is to decrease the concentration of bicarbonate (HCO3-) and increase the level of pCO2 (and consequently carbonic acid H2CO3). Two lines of defense are activated for this.
Urgent mechanisms (aimed at rapidly lowering pH):
- Pulmonary Hypoventilation: Retention of carbon dioxide.
- Activation of Glycolysis: Enhanced production of acidic products such as lactate.
- Ion Exchange: Intracellular chloride (Cl-) enters the blood in exchange for bicarbonate, which enters the cell, reducing the alkaline reserve of plasma.
- Engagement of Buffer Systems: Cellular and extracellular buffers operate (protein, hemoglobin, phosphate, bicarbonate).
Long-term mechanisms (implemented by the kidneys):
- Decreased secretion of hydrogen ions into the urine (inhibition of acidogenesis).
- Reduction in the synthesis and excretion of ammonium ions (NH4+).
- Enhanced dumping of alkaline phosphates (Na2HPO4).
- Accelerated excretion of potassium (loss of this ion is a frequent companion to alkalosis).
Clinical Context and Associated Pathologies
This condition is considered one of the most frequent and dangerous forms of acid-base imbalance.
In clinical practice, it often occurs against the background of severe systemic disorders. These include:
- Organ Failure: Cardiac, renal, or hepatic.
- Various Types of Hypoxia.
- Depletion of Buffer Systems: Occurs with massive blood loss or pronounced hypoproteinemia.
In addition, with the insufficiency of physiological mechanisms, the neutralization and excretion of excess fixed acids may be impaired, which further complicates the picture of metabolic processes in the body.