Acid-base balance disorders: acidosis, alkalosis, and Astrup parameters

Regulation of acid-base balance

Acid-base balance (ABB) is determined by the ratio of H⁺ and OH^- ion concentrations. An increase in proton concentration shifts the environment to the acidic side, while an increase in hydroxyl ions shifts it to the alkaline side. Normally, arterial blood pH is 7.35–7.45, and its maintenance is ensured by two levels of regulation: chemical (buffer systems) and physiological (lungs and kidneys).

Body buffer systems

A buffer is a mixture of substances that prevents a pH shift upon the addition of an acid or a base. The main buffer systems:

• Bicarbonate buffer — weak carbonic acid H₂CO₃ and its salt NaHCO₃; a key extracellular buffer.
• Phosphate buffer — a mixture of NaH₂PO₄ and Na₂HPO₄; works predominantly inside cells and in urine.
• Protein buffer — amphoteric properties of proteins due to amino groups (–NH₂, alkaline) and carboxyl groups (–COOH, acidic).
• Hemoglobin buffer — operates in erythrocytes, the most important buffer of whole blood.

Physiological compensation mechanisms

External respiration system regulates pH through the elimination of CO₂: hyperventilation decreases paCO₂ and shifts pH to the alkaline side, hypoventilation does the opposite.

Kidneys implement three mechanisms:

• alteration of bicarbonate HCO₃^- reabsorption in the tubules;
• acidogenesis — secretion of protons into the tubular lumen;
• ammoniogenesis — secretion of ammonium ions NH₄⁺, which allows the excretion of acids without excessive urine acidification.

Astrup acid-base parameters

• pH — normal range 7.35–7.45.
• paCO₂ — partial pressure of carbon dioxide, about 40 mmHg; reflects the respiratory component.
• SB (Standard Bicarbonate) — standard plasma bicarbonate measured under standard oxygen saturation conditions.
• BB (Buffer Base) — the sum of all blood buffer bases.
• BE (Base Excess) — buffer base shift; the difference between actual and normal BB.
• Titratable acidity of urine (TA) — determined by titrating daily urine with NaOH to pH 7.4; characterizes the ability of the kidneys to excrete free protons.
• Urine NH₄⁺ concentration — reflects the intensity of ammoniogenesis.

Acidosis: respiratory and non-respiratory

Acidosis occurs with an excess of hydrogen ions. According to compensation, compensated (pH 7.35–7.4) and uncompensated (pH below 7.35) variants are distinguished.

Respiratory acidosis develops with a primary increase in paCO₂ — hypercapnia due to hypoventilation, bronchial obstruction, or depression of the respiratory center. Compensatorily, the kidneys increase bicarbonate reabsorption, increasing SB.

Non-respiratory acidoses are divided into:

• Metabolic — accumulation of organic acids (lactate, ketone bodies) in hypoxia, diabetes mellitus, starvation; characterized by an increased anion gap.
• Renal excretory — renal tubular acidosis: decreased H⁺ secretion and HCO₃^- reabsorption, a drop in TA and NH₄⁺; provoked by hemolysis, a number of antibiotics and antiviral agents.
• Intestinal excretory — loss of bicarbonate with intestinal contents in diarrhea, intestinal fistulas.
• Exogenous — intake of acids from the outside (poisoning, infusion of acidic solutions).

In non-respiratory acidosis, SB decreases and paCO₀ drops compensatorily via hyperventilation.

Alkalosis: respiratory and non-respiratory

Respiratory alkalosis forms during hyperventilation and decreased paCO₂ (high-altitude hypoxia, hysteria, mechanical ventilation). Compensatorily, the kidneys reduce HCO₃^- reabsorption, and SB decreases.

Non-respiratory (metabolic) alkalosis occurs with a primary increase in HCO₃^-: excessive intake of alkalis, loss of acidic gastric contents during vomiting, hyperaldosteronism. SB rises, and compensatory hypoventilation increases paCO₂.

Algorithm for assessing simple acid-base disorders

1. Assess pH: below 7.35 — acidosis, above 7.45 — alkalosis.
2. Determine the nature of the disorder by paCO₂:
   • in acidosis, an increase in paCO₂ indicates respiratory, a decrease indicates non-respiratory;
   • in alkalosis, a decrease in paCO₂ is characteristic of respiratory, an increase is characteristic of non-respiratory.
3. Assess SB and BE: their shift confirms the engagement of compensatory mechanisms and helps differentiate an acute process from a chronic one.
4. In non-respiratory acidosis, clarify the subtype based on TA, urine NH₄⁺, anion gap, and clinical context.

Key points

• Normal blood pH is 7.35–7.45; regulation is carried out by buffers, lungs, and kidneys.
• The main buffers are bicarbonate, phosphate, protein, and hemoglobin.
• The kidneys regulate pH through HCO₃^- reabsorption, acidogenesis, and ammoniogenesis.
• The main Astrup acid-base parameters: pH, paCO₂, SB, BB, BE, TA, and urine NH₄⁺.
• Respiratory acidosis is associated with hypercapnia, respiratory alkalosis with hypocapnia.
• Non-respiratory acidoses are divided into metabolic, renal excretory, intestinal, and exogenous.
• Metabolic alkalosis is accompanied by an increase in SB and compensatory hypoventilation.
• Diagnostic algorithm: pH → paCO₂ → SB/BE → clinical data.