Acid-Base Physiology

Quick Answer

Acid-base balance maintains arterial pH 7.35-7.45 through chemical buffering, respiratory compensation, and renal regulation. pH: Negative logarithm of [H⁺]; normal [H⁺] 40 nEq/L (35-45); pH 7.40 = [H⁺] 40 nEq/L; pH changes 0.01 = [H⁺] changes 1 nEq/L in opposite direction. Buffers: Bicarbonate (HCO₃⁻, most important extracellular buffer, 24 mmol/L, pKa 6.1), proteins (intracellular, haemoglobin most important), phosphate (intracellular and urine). Henderson-Hasselbalch equation: pH = 6.1 + log([HCO₃⁻]/(0.03×PaCO₂)); relates pH, HCO₃⁻, and PaCO₂; simplified: [H⁺] = 24×(PaCO₂/[HCO₃⁻]). Metabolic acidosis: Gain of acid or loss of HCO₃⁻; anion gap (Na⁺ − [Cl⁻ + HCO₃⁻]) normal 8-12 mEq/L; high anion gap (MUDPILES—Methanol, Uraemia, DKA, Paraldehyde, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates); normal anion gap (hyperchloraemic—GI losses, RTA, dilutional). Metabolic alkalosis: Loss of acid (vomiting, NG suction) or gain of HCO₃⁻; chloride responsive (urine Cl⁻ <20, responds to NaCl) vs. chloride resistant (urine Cl⁻ >20, mineralocorticoid excess). Respiratory acidosis: CO₂ retention (hypoventilation); acute (1 mmHg PaCO₂ ↑ = 0.8 mEq/L HCO₃⁻ ↑); chronic (1 mmHg PaCO₂ ↑ = 3.5 mEq/L HCO₃⁻ ↑, renal compensation over 3-5 days). Respiratory alkalosis: CO₂ washout (hyperventilation); acute (1 mmHg PaCO₂ ↓ = 0.2 mEq/L HCO₃⁻ ↓); chronic (1 mmHg PaCO₂ ↓ = 0.4 mEq/L HCO₃⁻ ↓). Compensation: Never fully corrects pH to normal; expected compensation predictable (Winter's formula for metabolic acidosis: expected PaCO₂ = (1.5×[HCO₃⁻]) + 8 ± 2; if measured PaCO₂ different, mixed disorder). Anaesthetic causes: Lactic acidosis (hypoperfusion, sepsis, seizures), respiratory acidosis (opioids, residual NMB, airway obstruction), dilutional acidosis (large volumes 0.9% saline—hyperchloraemic). Treatment: Treat underlying cause; bicarbonate rarely indicated (pH <7.1 with hemodynamic compromise); THAM (tris-hydroxymethyl aminomethane) alternative buffer; hyperventilation for acute respiratory acidosis; correct volume/electrolytes for metabolic alkalosis. Indigenous populations: Higher rates of renal disease and diabetes (DKA risk); careful acid-base monitoring essential. [1-10]