Synopsis
Identify primary and mixed metabolic acidosis systematically, distinguish high-gap from bicarbonate-loss mechanisms and treat the time-critical cause.
- Confirm the primary process from pH, bicarbonate and carbon dioxide: metabolic acidosis lowers bicarbonate, while appropriate respiratory compensation lowers carbon dioxide rather than normalising pH completely.
- Calculate anion gap as sodium minus chloride plus bicarbonate using values from the same sample; a raised gap signals unmeasured anions but a normal gap does not mean mild disease.
- Low albumin lowers the expected anion gap, so correct or interpret the gap for albumin in critical illness before dismissing lactate, ketones, renal acids or toxins.
- Common high-gap causes are lactic acidosis, ketoacidosis, advanced renal failure and toxic ingestion; common normal-gap causes are diarrhoea, renal tubular acidosis, saline chloride load and carbonic-anhydrase inhibition.
- Compare measured carbon dioxide with expected respiratory compensation; a higher value indicates superimposed respiratory acidosis and impending ventilatory failure, while a lower value indicates additional respiratory alkalosis.
- A venous gas is usually sufficient for pH and bicarbonate trends, but arterial sampling is required when accurate oxygenation or a precise arterial carbon dioxide assessment changes respiratory management.
- Treat the mechanism—restore perfusion, control sepsis, give the DKA pathway, reverse toxin exposure, stop gastrointestinal loss or arrange dialysis—rather than treating pH as an isolated target.
- Intravenous sodium bicarbonate is not routine for every low pH; use it for a defined indication under senior guidance because sodium load, carbon dioxide generation, hypocalcaemia and overshoot can harm.
Key red flags
Deep rapid breathing reflects respiratory carbon dioxide clearance; slowing respiration, exhaustion or reduced consciousness during severe acidosis signals impending decompensation.
Hypotension, mottling, delayed refill, oliguria and altered mentation suggest impaired perfusion, but sepsis-associated lactate can rise before overt pressure collapse.
Polyuria, dehydration, vomiting, abdominal pain and acetone breath with ketonaemia indicates diabetic, alcoholic or starvation ketoacidosis requiring contextual separation.
Tinnitus, vomiting, tachypnoea, fever, confusion or unexplained mixed respiratory alkalosis and high-gap acidosis raises salicylate poisoning and needs urgent toxicology advice.
Investigation priorities
Confirm acidemia, quantify bicarbonate and carbon dioxide and identify respiratory compensation or a mixed disorder.
Management branches
A gas shows low pH, low bicarbonate or an unexpected carbon dioxide concentration.
- Confirm sampling context, pH and primary bicarbonate reduction, then compare carbon dioxide with expected compensation to identify respiratory failure or additional respiratory alkalosis.
- Calculate an albumin-aware anion gap from the matching chemistry sample and measure lactate, ketones and renal indices directly rather than relying on a mnemonic alone.
- Use delta comparison and clinical history to identify combined high-gap, chloride-associated and alkalotic processes, documenting uncertainty and the next test.