Concept of acid-base balance and pH
Acid-base balance (ABB) reflects the balance between hydrogen protons (H⁺) and hydroxyl ions (OH⁻) in biological fluids. Acids in the body release H⁺ upon dissociation, and bases release OH⁻. The integral indicator of this balance is pH — the negative decadic logarithm of the hydrogen ion concentration.
An inverse relationship follows from the pH formula: the higher the H⁺ concentration, the lower the pH value, and vice versa. This is fundamentally important for interpreting ABB shifts. The normal pH of arterial blood is 7.35–7.45. This value is a strict constant of homeostasis: a deviation of even hundredths (e.g., 7.33 or 7.46) is already regarded as pathology.
pH affects enzyme activity, all types of metabolism (protein, lipid, carbohydrate), the ability of hemoglobin to bind oxygen, water-electrolyte balance, the permeability of biological membranes, and the intensity of redox reactions. Therefore, correcting a patient's ABB is an urgent task.
Acidosis and alkalosis: general concepts
Acidosis is a condition in which an excess of hydrogen protons occurs in the body, and the pH drops below 7.35 (from the English acid). Alkalosis is a condition with an excess of bases (HCO₃⁻ and other OH-containing particles) in which the pH exceeds 7.45.
According to pathogenesis, both conditions are divided into gas (respiratory) forms, associated with changes in the partial pressure of CO₂, and non-gas (metabolic) forms, caused by disturbances in H⁺ and HCO₃⁻ metabolism.
Respiratory acidosis
The main sign of gas acidosis is an increase in the partial pressure of carbon dioxide (pCO₂) in arterial blood above normal (normal is 38–42 mm Hg) — a condition of hypercapnia. The connection with H⁺ is explained by the reaction: CO₂ + H₂O under the action of carbonic anhydrase turns into H₂CO₃, which dissociates into H⁺ and HCO₃⁻. The accumulation of CO₂ naturally increases the H⁺ concentration.
Main causes:
- Alveolar hypoventilation — airway obstruction, depression of the respiratory center, neuromuscular transmission disorders.
- Inhalation of air with an excessive CO₂ content (prolonged stay in a tightly closed room).
- Increased endogenous CO₂ production during the intensification of tissue respiration and the Krebs cycle.
Clinical example: a foreign body entering the trachea causes hypoventilation, CO₂ accumulation, a drop in pH, and the development of gas acidosis.
Respiratory alkalosis
Gas alkalosis develops with a decrease in pCO₂ in arterial blood — hypocapnia. The causes are the opposite of those in gas acidosis:
- Alveolar hyperventilation of any genesis.
- Exogenous hypobaric hypoxia (high-altitude ascent): O₂ deficiency causes shortness of breath, during which CO₂ is actively eliminated.
- Drug-induced stimulation of the respiratory center.
- Inadequate mechanical ventilation mode.
Example: during surgery with mechanical ventilation due to excessive ventilation, pCO₂ decreases, pH rises to 7.47 and above — gas alkalosis forms.
Non-gas (metabolic) acidosis
Unlike gas acidosis, in metabolic acidosis, the concentrations of H⁺ and HCO₃⁻ are key, rather than CO₂. Causes:
- Exogenous intake of acids (ingestion of acid-containing substances through the gastrointestinal tract).
- Endogenous accumulation of H⁺ due to metabolic disorders (e.g., lactic acidosis, ketoacidosis).
- Decreased renal excretion of H⁺ in kidney diseases.
- Excessive losses of HCO₃⁻ (via the kidneys or gastrointestinal tract), disrupting the buffer balance.
Clinical example: in a patient with diabetes mellitus, due to glucose deficiency in cells, aerobic glycolysis is disrupted, and lactate accumulates. A pH of 7.3 and hyperlactatemia are registered — typical non-gas acidosis.
Non-gas (metabolic) alkalosis
The condition is characterized by an increase in HCO₃⁻ and/or loss of H⁺ with normal or moderately altered pCO₂. It develops due to:
- Excessive intake of bicarbonate from outside (infusions, intake of alkalis).
- Decreased renal excretion of HCO₃⁻.
- Direct loss of H⁺ by the body.
A classic example is repeated untamable vomiting in traumatic brain injury: a significant amount of H⁺ is lost with the gastric contents, and the pH shifts to the alkaline side. The level of lactic acid remains normal, which confirms the non-metabolic, but rather "loss-related" origin of alkalosis.
Compensation of ABB disorders
Gas and non-gas forms of ABB disorders are interconnected through buffer and physiological compensation mechanisms. Gas acidosis is partially compensated by the development of non-gas alkalosis (renal retention of HCO₃⁻), and gas alkalosis by non-gas acidosis (increased bicarbonate excretion). Similarly, metabolic disorders are compensated by changes in pulmonary ventilation. These mechanisms are aimed at keeping pH within physiological limits.
Key points
- The normal pH of arterial blood is 7.35–7.45; this is a strict constant of homeostasis.
- The more H⁺, the lower the pH (inverse logarithmic relationship).
- Acidosis is an excess of H⁺ (pH < 7.35); alkalosis is an excess of bases (pH > 7.45).
- Gas acidosis is caused by hypercapnia during alveolar hypoventilation.
- Gas alkalosis is associated with hypocapnia during hyperventilation, hypoxia, and inadequate mechanical ventilation.
- Non-gas acidosis is caused by the accumulation of H⁺ or the loss of HCO₃⁻ (an example is lactic acidosis in diabetes mellitus).
- Non-gas alkalosis develops with the loss of H⁺ (vomiting) or an excess of HCO₃⁻.
- Gas and metabolic ABB disorders are mutually compensated by renal and respiratory mechanisms.