Acid –base balance disorders - classification, etiology, adaptive-compensatory mechanisms, pathogenesis.
Physiological context
Normal arterial pH: 7.35–7.45.
Main regulators:
- Buffer systems (bicarbonate, proteins, phosphates).
- Lungs (CO₂ excretion).
- Kidneys (H excretion, bicarbonate reabsorption).
Etiology & Pathogenesis
Metabolic acidosis
Etiology
Increased acid production:
- Diabetic ketoacidosis.
- Lactic acidosis.
Loss of bicarbonate:
- Severe diarrhea.
- Renal tubular acidosis.
Decreased renal acid excretion:
- Chronic kidney failure.
Pathogenesis
Acid accumulation or bicarbonate loss → ↓ HCO₃ → ↓ pH.
Compensation: hyperventilation → ↓ PaCO₂.
Metabolic alkalosis
Etiology
Loss of gastric acid (vomiting, nasogastric suction).
Diuretic therapy (volume depletion → ↑ HCO₃ reabsorption).
Excess bicarbonate intake.
Pathogenesis
↑ HCO₃ or loss of H → ↑ pH.
Compensation: hypoventilation → ↑ PaCO₂.
Respiratory acidosis
Etiology
Hypoventilation:
- Chronic obstructive pulmonary disease (COPD).
- Respiratory center depression (sedatives, CNS injury).
- Neuromuscular disorders (myasthenia gravis, Guillain-Barré).
Pathogenesis
CO₂ retention → ↑ PaCO₂ → formation of carbonic acid → ↓ pH.
Compensation: kidneys ↑ H excretion and ↑ HCO reabsorption (chronic adaptation).
Respiratory alkalosis
Etiology
Hyperventilation:
- Anxiety/panic attacks.
- High altitude.
- Fever, sepsis.
- Salicylate poisoning (early phase).
Pathogenesis
Excess CO₂ loss → ↓ PaCO₂ → ↓ H₂CO₃ → ↑ pH.
Compensation: kidneys ↑ HCO₃ excretion.