Clinical meaning
The body maintains arterial pH within a narrow range (7.35-7.45) through three compensatory mechanisms. Chemical buffers respond within seconds: the bicarbonate buffer system (H2CO3 ↔ H+ + HCO3-) is the most important extracellular buffer; phosphate and protein buffers operate intracellularly. Respiratory compensation acts within minutes to hours: central chemoreceptors in the medulla and peripheral chemoreceptors in the carotid/aortic bodies detect pH/PCO2 changes and adjust ventilation (hypoventilation retains CO2 to compensate metabolic alkalosis; hyperventilation eliminates CO2 to compensate metabolic acidosis). Renal compensation takes 3-5 days for full effect: proximal tubule reabsorbs filtered HCO3-, distal tubule secretes H+ and generates new HCO3-. Compensation adjusts the ratio of HCO3- to PCO2 toward normal but NEVER fully normalizes pH (except in chronic respiratory alkalosis).
Diagnosis & workup
Diagnostics & workup: - Arterial blood gas (ABG): pH (7.35-7.45), PCO2 (35-45 mmHg), HCO3- (22-26 mEq/L), PaO2 (80-100 mmHg) - Systematic ABG interpretation: 1) Identify acidemia (pH <7.35) or alkalemia (pH >7.45); 2) Determine primary disorder (metabolic or respiratory); 3) Assess compensation (expected vs actual); 4) Calculate anion gap if metabolic acidosis - Anion gap = Na+ - (Cl- + HCO3-); normal 8-12; elevated gap = acid accumulation (MUDPILES); normal gap = HCO3- loss - Expected compensation formulas: Metabolic acidosis → Winter's formula: expected PCO2 = 1.5(HCO3-) + 8 ± 2; Metabolic alkalosis → PCO2 rises ~0.7 for each 1 mEq/L rise in HCO3-; Acute respiratory acidosis → HCO3- rises 1 per 10 mmHg PCO2 rise; Chronic respiratory acidosis → HCO3- rises 3.5 per 10 mmHg PCO2 rise - Delta-delta ratio for elevated AG acidosis: Δgap/ΔHCO3-; <1 = concurrent non-gap acidosis; 1-2 = pure AG acidosis; >2 = concurrent metabolic alkalosis - Venous blood gas: adequate for pH and HCO3- screening; less reliable for PCO2 and PaO2