Arterial blood gas (ABG) interpretation is one of those bedside skills that feels overwhelming the first time you face an unwell patient in the resuscitation room — and feels almost automatic a year into residency. The trick is not memorising endless rules, but having a reliable framework you apply the same way every single time. This guide walks you through that framework step by step, with worked examples and the common pitfalls that catch out medical students and junior doctors.

This article is intended as an educational reference for medical students, junior doctors and other healthcare professionals studying acid–base physiology. It is not a substitute for clinical judgement, local guidelines or specialist input. Always interpret an ABG in the context of the whole patient.

What an ABG actually measures

A standard arterial blood gas reports four headline values that drive almost every interpretation:

  • pH — the overall acidity of arterial blood (normal range 7.35–7.45).
  • PaCO₂ — the partial pressure of carbon dioxide, the respiratory component (normal 4.7–6.0 kPa or 35–45 mmHg).
  • HCO₃⁻ — bicarbonate, the metabolic component (normal 22–26 mmol/L).
  • PaO₂ — the partial pressure of oxygen, used to assess oxygenation (normal >10.6 kPa or >80 mmHg on room air).

Most analysers also report base excess, lactate, electrolytes and haemoglobin. Useful, but the four values above carry the diagnostic weight.

A 5-step framework for every ABG

Apply these five steps in order. Resist the urge to skip ahead — the order is what protects you from missing mixed disorders.

Step 1 — Look at the pH: acidaemia or alkalaemia?

If pH is below 7.35, the patient is acidaemic. Above 7.45, alkalaemic. A “normal” pH does not exclude a disorder — it may indicate a fully compensated process or two opposing primary disorders cancelling out. Always continue to the next steps even if pH looks normal.

Step 2 — Identify the primary disorder: respiratory or metabolic?

Look at PaCO₂ and HCO₃⁻ and ask which one is moving in the same direction as the pH disturbance:

  • Acidaemia + high PaCO₂ → primary respiratory acidosis (e.g. COPD exacerbation, opioid toxicity).
  • Acidaemia + low HCO₃⁻ → primary metabolic acidosis (e.g. DKA, lactic acidosis, renal failure).
  • Alkalaemia + low PaCO₂ → primary respiratory alkalosis (e.g. pain, anxiety, sepsis, pulmonary embolism).
  • Alkalaemia + high HCO₃⁻ → primary metabolic alkalosis (e.g. vomiting, diuretics).

Step 3 — Assess compensation

The body tries to drag the pH back toward normal by adjusting the other system. Respiratory compensation (changing minute ventilation) happens within minutes; metabolic compensation (renal HCO₃⁻ handling) takes hours to days. A few useful rules of thumb:

  • Acute respiratory acidosis: HCO₃⁻ rises by ~1 mmol/L for every 10 mmHg rise in PaCO₂.
  • Chronic respiratory acidosis: HCO₃⁻ rises by ~3.5 mmol/L for every 10 mmHg rise in PaCO₂.
  • Metabolic acidosis (Winter’s formula): expected PaCO₂ ≈ (1.5 × HCO₃⁻) + 8 ± 2 mmHg.
  • Metabolic alkalosis: expected PaCO₂ ≈ HCO₃⁻ + 15 mmHg.

If the actual compensation differs significantly from the expected, suspect a second, coexisting disorder — a mixed acid–base disturbance.

Step 4 — Calculate the anion gap (in any acidosis)

Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻). Normal is roughly 8–12 mmol/L (correct for albumin in critically ill patients). A raised anion gap metabolic acidosis points you toward a specific differential — the classic mnemonic MUDPILES (Methanol, Uraemia, DKA, Propylene glycol/paraldehyde, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates) is a reasonable starting list. A normal anion gap acidosis points instead toward bicarbonate loss (diarrhoea, renal tubular acidosis).

Step 5 — Assess oxygenation separately

Acid–base and oxygenation are independent problems. Always check PaO₂ and SaO₂ in the context of the patient’s FiO₂. A useful screening calculation is the alveolar–arterial (A–a) gradient — a widened gradient suggests a problem with gas exchange (e.g. pulmonary oedema, PE, pneumonia) rather than pure hypoventilation.

A worked example

A 24-year-old presents with abdominal pain, vomiting, deep rapid breathing and a capillary glucose of 28 mmol/L. Her ABG on room air shows: pH 7.18, PaCO₂ 2.8 kPa (21 mmHg), HCO₃⁻ 8 mmol/L, Na⁺ 138, Cl⁻ 100, PaO₂ 14 kPa.

  1. pH 7.18 → acidaemia.
  2. HCO₃⁻ is low and PaCO₂ is low → primary metabolic acidosis.
  3. Expected PaCO₂ by Winter’s = (1.5 × 8) + 8 = 20 mmHg. Actual 21 mmHg — appropriate respiratory compensation, no second disorder by this rule.
  4. Anion gap = 138 − (100 + 8) = 30 mmol/L → high anion gap. With the clinical picture, this is diabetic ketoacidosis.
  5. PaO₂ 14 kPa on room air — oxygenation is fine.

Diagnosis: high anion gap metabolic acidosis with appropriate respiratory compensation, consistent with DKA.

Common pitfalls

  • Trusting a “normal” pH. Mixed disorders frequently produce a near-normal pH. Always check PaCO₂ and HCO₃⁻ even when the pH looks reassuring.
  • Forgetting to correct the anion gap for albumin in ICU patients — a low albumin can mask a real high-anion-gap acidosis.
  • Confusing acute and chronic respiratory acidosis. A COPD patient with chronically high PaCO₂ has had time to renally compensate and will have a higher HCO₃⁻ baseline.
  • Treating the number, not the patient. An ABG is one data point in a clinical picture. Always integrate it with the history, examination and other investigations.
  • Ignoring the lactate. A rising lactate often precedes overt clinical deterioration in sepsis and shock states.

Practising at the bedside

The fastest way to internalise this framework is to apply it to every ABG you see, even when the answer feels obvious. Over time the five steps collapse into a few seconds of mental arithmetic. If you would like a tool that performs the calculations for you and walks through the differential diagnosis at the bedside, our free ABG Pro app for iPhone and iPad is built around exactly this framework — enter the values, and it returns the primary disorder, expected compensation and a structured differential.

Educational content only. Always confirm clinical decisions with senior colleagues, local guidelines and the full clinical picture.