Metabolic Acidosis

Metabolic acidosis is a primary reduction in serum bicarbonate producing a fall in pH, compensated by an increase in alveolar ventilation that lowers PaCO₂.

The first and most useful step in assessment is calculating the anion gap, because it separates two entirely different differential diagnoses:

• Raised anion gap acidosis results from added unmeasured acid, and is usefully remembered as GOLD MARK: Glycols (ethylene glycol, propylene glycol), Oxoproline (chronic paracetamol use), L-lactate, D-lactate, Methanol, Aspirin (salicylates), Renal failure, Ketoacidosis
• Normal anion gap (hyperchloraemic) acidosis results from bicarbonate loss or impaired renal acid excretion, principally diarrhoea, renal tubular acidosis, and saline loading

Severity is driven less by the pH itself than by the underlying cause and the patient's ability to compensate; a patient with a pH of 7.2 from ketoacidosis and one with the same pH from cardiogenic shock have very different trajectories.

• Blood gas confirming low pH and low bicarbonate, with a low PaCO₂ if respiratory compensation is intact
• Assess compensation using Winter's formula: expected PaCO₂ ≈ (1.5 × HCO₃) + 8 ± 2. A PaCO₂ higher than predicted indicates a coexisting respiratory acidosis: often a tiring patient who can no longer sustain the work of breathing, which is an ominous finding. A PaCO₂ lower than predicted indicates a coexisting respiratory alkalosis
• Anion gap: Na − (Cl + HCO₃), corrected for albumin
• Delta ratio (change in anion gap divided by change in bicarbonate) identifies mixed disorders: a ratio below 1 suggests a coexisting normal anion gap acidosis, and above 2 a coexisting metabolic alkalosis
• Directed investigations by suspected cause: lactate, glucose and ketones, renal function, salicylate and paracetamol levels, osmolar gap if toxic alcohol ingestion is possible, creatine kinase, and urinary anion gap if the gap is normal
• Review the drug and fluid chart, including metformin, and the volume of saline given
• In a normal anion gap acidosis, proceed as in the hyperchloraemic acidosis entry

• Treat the underlying cause, which is almost always the definitive intervention: insulin and fluid for ketoacidosis, restoration of perfusion for lactic acidosis, antidote and dialysis for toxic alcohols, dialysis for uraemic acidosis, and rehydration for diarrhoeal losses
• Bicarbonate is not routinely given, and its role remains genuinely contested. It is generally reserved for severe acidaemia (pH below approximately 7.1), for normal anion gap acidosis where bicarbonate has genuinely been lost, and for specific indications such as hyperkalaemia with acidosis, salicylate poisoning (where alkalinisation is therapeutic in its own right), and tricyclic antidepressant toxicity
• The arguments against routine bicarbonate are substantive: it generates CO₂ which can worsen intracellular acidosis if ventilation is fixed, causes hypokalaemia and hypocalcaemia, produces sodium and volume loading, and shifts the oxygen dissociation curve. In diabetic ketoacidosis and lactic acidosis specifically, it has not been shown to improve outcomes
• Support ventilation where respiratory compensation is failing. A rising or normalising PaCO₂ in a severely acidotic patient signals exhaustion and impending respiratory arrest, and is an indication for urgent critical care review rather than reassurance
• Correct potassium, anticipating that it falls as acidosis is corrected and potassium shifts back into cells, this is the same dynamic seen in diabetic ketoacidosis management
• Monitor gas, electrolytes and lactate serially to confirm the trajectory rather than relying on a single set

Referral: critical care for severe acidosis, haemodynamic instability, or failing compensation; nephrology for dialysis; toxicology for suspected poisoning.