Description
- Four primary disturbances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis
- Kidney's role: generates/reabsorbs bicarbonate and excretes fixed acid (as ammonium) - renal disease is both a cause and a victim of acid-base disturbance
Epidemiology
- Metabolic acidosis near-universal by CKD stage 4-5
- Mixed disorders common in critically ill patients - always check all three (pH, pCO2, HCO3-) together
Aetiopathogenesis
Metabolic acidosis - by anion gap
- AG = Na+ - (Cl- + HCO3-), normal ~8-12 (correct for albumin: add 2.5 per 10 g/L below 40)
- Raised AG: MUDPILES - Methanol, Uraemia, DKA, Propylene glycol/Paraldehyde, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates
- Normal AG (hyperchloraemic): GI bicarbonate loss (diarrhoea), renal tubular acidosis (type 1 distal, type 2 proximal, type 4 with hyperkalaemia + hypoaldosteronism), early CKD, acetazolamide
- Delta ratio (change in AG / change in HCO3-) identifies a mixed picture: <1 = concurrent normal-AG acidosis, >2 = concurrent metabolic alkalosis
Metabolic alkalosis
- Chloride-responsive (urine Cl- <20) - vomiting, NG losses, diuretics (contraction alkalosis)
- Chloride-resistant (urine Cl- >20) - mineralocorticoid excess, severe hypokalaemia, Bartter/Gitelman
Respiratory acidosis/alkalosis
- Acidosis - hypoventilation (COPD, opioid overdose, neuromuscular weakness, obesity hypoventilation)
- Alkalosis - hyperventilation (anxiety, pain, sepsis, salicylate toxicity early, pregnancy is physiologically mildly alkalotic)
Diagnosis
Systematic approach
1. Check pH - acidaemia or alkalaemia
2. Identify primary disturbance (which of pCO2/HCO3- moved in the direction explaining the pH)
3. Calculate expected compensation (Winter's formula for metabolic acidosis: expected pCO2 = 1.5 x HCO3- + 8 +/-2) - compensation outside the expected range = a second primary disorder
4. Calculate anion gap if metabolic acidosis present
5. Delta ratio if raised AG, to detect a co-existing normal-AG process
Key numbers
- Lactate >2 mmol/L - hyperlactataemia; >4 - significant, correlates with mortality in sepsis
- Salicylate toxicity - classic mixed picture: respiratory alkalosis (direct medullary stimulation) + high-AG metabolic acidosis
Management
Metabolic acidosis
- Treat the cause (insulin for DKA, dialysis for uraemia/toxin, fluids + treat sepsis for lactic acidosis)
- CKD-associated chronic acidosis - oral sodium bicarbonate if serum HCO3- persistently <22 mmol/L - slows CKD progression and reduces muscle wasting
- Severe acidaemia (pH <7.1-7.2) with haemodynamic compromise - cautious IV bicarbonate is reasonable, though evidence for outcome benefit is limited outside severe cases/hyperkalaemia
Metabolic alkalosis
- Chloride-responsive - IV normal saline + correct K+ - resolves once volume/chloride restored
- Chloride-resistant - treat underlying mineralocorticoid excess; potassium-sparing diuretic if Bartter/Gitelman
Respiratory disturbances
- Treat the underlying respiratory/ventilatory driver; NIV or intubation for severe respiratory acidosis with failure to compensate
Associations
- Chronic metabolic acidosis - muscle wasting, bone demineralisation (buffering), accelerated CKD progression
- Respiratory acidosis - cor pulmonale if chronic (COPD)
- Severe acidaemia - reduced cardiac contractility, arrhythmia, RAAS/catecholamine resistance
Natural history & complications
- Acute severe acid-base derangement - treat the primary process; the derangement itself resolves as the cause is corrected
- Chronic metabolic acidosis in CKD - progressive if untreated, improved with bicarbonate supplementation
- Always re-check gas/electrolytes after treatment - compensation and correction should be monitored, not assumed
Study aid only. These notes are written with the help of AI. Not for guiding clinical decisions.