Synopsis
Read an arterial blood gas in a fixed clinical sequence, recognise ventilatory failure and mixed acid-base disease, and act on the cause rather than treating a number in isolation.
- Record the inspired oxygen, device, time and clinical state before interpreting PaO2; an oxygen tension without FiO2 is incomplete information.
- Use one sequence: pH, PaCO2, bicarbonate/base excess, compensation, oxygenation, lactate, then electrolytes and clinical cause.
- Acidaemia is pH below 7.35 and alkalaemia above 7.45; decide which component moves in the direction that explains the pH.
- A high PaCO2 drives respiratory acidosis; a low PaCO2 drives respiratory alkalosis. A low bicarbonate drives metabolic acidosis; a high bicarbonate drives metabolic alkalosis.
- Compensation does not normally overshoot the pH. A near-normal pH with clearly abnormal PaCO2 and bicarbonate may represent compensation or two opposing primary disorders.
- Type 1 respiratory failure is hypoxaemia without hypercapnia; type 2 includes hypercapnia and usually reflects inadequate alveolar ventilation.
- For most acutely ill adults target SpO2 94-98%; if at risk of hypercapnic respiratory failure use 88-92% pending blood gases, unless a patient-specific target applies.
- In COPD, persistent pH below 7.35 with PaCO2 above 6.5 kPa despite optimal initial treatment is a standard trigger to consider NIV; do not delay escalation when the trajectory is adverse.
- An anion gap helps organise metabolic acidosis: calculate Na - (Cl + HCO3), interpret against the laboratory range and consider albumin because hypoalbuminaemia lowers the expected gap.