ICU · Acid–base
Acid–Base Physiology and Blood-Gas Interpretation
Also known as Acid-base · Blood gas interpretation · Metabolic acidosis · Metabolic alkalosis · Stewart approach · Strong ion difference · Anion gap
Acid–base homeostasis is the chemistry of the hydrogen ion, and its disturbances are among the commonest and most informative derangements in critical illness. This topic builds the examiner's framework on four ideas. First, the physiology — the bicarbonate buffer system described by Henderson and Hasselbalch, and the more complete Stewart view in which pH is set by the carbon dioxide tension, the strong ion difference (largely sodium minus chloride) and the total concentration of weak acids (albumin and phosphate). Second, a systematic method for reading a blood gas — the pH, the pattern (metabolic versus respiratory), the appropriateness of compensation, the anion gap and the delta-delta, and the osmolar gap when a toxin is suspected. Third, the clinical disorders — the high anion-gap and normal anion-gap acidoses (lactic acidosis, ketoacidosis, the toxic alcohols, and renal tubular acidosis), the metabolic alkaloses, and the respiratory acid–base disturbances. Fourth, the evidence that has reshaped management — the SMART and SALT-ED trials showing balanced crystalloids modestly outperform saline, BICAR-ICU showing bicarbonate confers no overall benefit in severe acidaemia (with a signal in the acute-kidney-injury subgroup), and the principles of treating the cause rather than the number. Built entirely on these verified landmark trials.
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Red flags
- A high anion-gap metabolic acidosis with a simultaneously elevated osmolar gap is a toxic alcohol poisoning (methanol or ethylene glycol) until proven otherwise — fomepizole and haemodialysis are time-critical, because the parent alcohol is non-toxic and the damage is done by its metabolites
- Severe metabolic acidaemia (pH at or below 7.20) is not itself an indication for sodium bicarbonate outside the peri-arrest or hyperkalaemic setting — BICAR-ICU found no overall outcome benefit, and bicarbonate can worsen intracellular acidosis, raise the sodium load and aggravate hypercapnia
- A 'normal' anion gap does not exclude a high anion-gap acidosis when albumin is low — the observed gap must be corrected upwards for hypoalbuminaemia, or a life-threatening lactic or toxic acidosis will be missed
- Persistent metabolic alkalosis in the ventilated patient delays weaning by suppressing respiratory drive and shifting the oxyhaemoglobin curve leftwards — it is most often iatrogenic (diuretics, nasogastric losses, citrate from transfusion) and is corrected by treating the cause and giving chloride
- Do not interpret a single blood-gas value in isolation — the trend, the mixed or combined disorder revealed by the delta-delta, and the clinical context together determine the diagnosis and the response to treatment
Meet the patient
A 47-year-old man is brought to the emergency department confused and ataxic, found unconscious beside an empty antifreeze bottle. He is breathing hard. The gas reads pH 7.18, PaCO₂ 18 mmHg, HCO₃⁻ 7 mmol/L; the sodium is 142, the chloride 102, and the urine shows envelope-shaped crystals.[6]
The two questions that decide his next hour decide every toxic gas you will ever see: what is the gap? — the anion gap and the osmolar gap read together — and what is generating the acid? — the metabolite, not the parent alcohol. Hold those two questions and the management — fomepizole, cofactors, dialysis — slots into place behind them.[6]
References23ShowHide
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