Introduction
Arterial blood gas (ABG) interpretation is one of the most clinically important skills in acute medicine and a staple of UK OSCE examinations. A blood gas result provides real-time information about oxygenation, ventilation, and acid-base status. Mastering a systematic approach means you will never panic in front of an ABG result — in the exam or on the wards.
Normal ABG Values
| Parameter | Normal Range | What It Measures |
|---|---|---|
| pH | 7.35–7.45 | Acidity/alkalinity of blood |
| PaO₂ | 10–13.3 kPa (75–100 mmHg) | Arterial oxygen partial pressure |
| PaCO₂ | 4.7–6.0 kPa (35–45 mmHg) | Arterial CO₂ — ventilatory control |
| HCO₃⁻ | 22–26 mmol/L | Metabolic bicarbonate buffer |
| Base excess (BE) | -2 to +2 mmol/L | Metabolic contribution to acid-base |
| Lactate | <2.0 mmol/L | Tissue perfusion marker |
Step-by-Step Interpretation
Step 1 — Is the Patient Acidaemic or Alkalaemic?
- pH <7.35 = acidaemia
- pH >7.45 = alkalaemia
- pH 7.35–7.45 = normal (may still have a mixed disorder)
Step 2 — What Is the Primary Respiratory Contribution?
- PaCO₂ >6.0 kPa = respiratory acidosis (hypoventilation, CO₂ retention)
- PaCO₂ <4.7 kPa = respiratory alkalosis (hyperventilation, CO₂ blown off)
Step 3 — What Is the Primary Metabolic Contribution?
- HCO₃⁻ <22 mmol/L or BE <-2 = metabolic acidosis
- HCO₃⁻ >26 mmol/L or BE >+2 = metabolic alkalosis
Step 4 — Is There Compensation?
🧠 Mnemonic
ROME — Direction of Compensation
Respiratory Opposite: in respiratory acidosis, HCO₃⁻ rises (metabolic compensates in opposite direction to CO₂)
Metabolic Equal: in metabolic acidosis, PaCO₂ falls (both pH and PaCO₂ move in the same direction)
In practice: pH and PaCO₂ move in opposite directions in respiratory disorders; pH and HCO₃⁻ move in the same direction in metabolic disorders.
| Primary Disorder | Compensatory Response | Expected Compensation |
|---|---|---|
| Metabolic acidosis | Hyperventilate — lower CO₂ | PaCO₂ ≈ (1.5 × HCO₃⁻) + 8 ± 2 (Winter's formula) |
| Metabolic alkalosis | Hypoventilate — raise CO₂ | PaCO₂ rises 0.5–1 kPa per 3 mmol/L rise in HCO₃⁻ |
| Respiratory acidosis (acute) | Kidneys retain HCO₃⁻ | HCO₃⁻ rises 1 mmol/L per 1.3 kPa rise in PaCO₂ |
| Respiratory acidosis (chronic) | Kidneys retain HCO₃⁻ | HCO₃⁻ rises 3.5 mmol/L per 1.3 kPa rise in PaCO₂ |
| Respiratory alkalosis | Kidneys excrete HCO₃⁻ | HCO₃⁻ falls 2 mmol/L per 1.3 kPa fall in PaCO₂ |
Step 5 — Assess Oxygenation
- PaO₂ <10 kPa on room air = hypoxaemia
- Type 1 respiratory failure: PaO₂ <10 kPa, PaCO₂ normal or low (V/Q mismatch, shunt)
- Type 2 respiratory failure: PaO₂ <10 kPa, PaCO₂ >6.0 kPa (ventilatory failure)
The Four Primary Acid-Base Disorders
Metabolic Acidosis
pH <7.35, HCO₃⁻ <22 mmol/L, PaCO₂ low (Kussmaul breathing).
Always calculate the anion gap (AG):
AG = Na⁺ – (Cl⁻ + HCO₃⁻) — normal is 8–12 mmol/L
| High Anion Gap (HAGMA) | Normal Anion Gap (NAGMA) |
|---|---|
| Mnemonic: MUDPILES | Mnemonic: USED CARP |
| Methanol, Uraemia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates | Ureteral diversion, Saline excess, Extra chloride, Diarrhoea, Carbonic anhydrase inhibitors, Addison's, RTA, Pancreatic fistula |
💎 Clinical Pearl
In DKA, the ABG will show high-AG metabolic acidosis and the dipstick will show ketonuria and glycosuria. Check venous ketones and blood glucose. Severe DKA has pH <7.1, bicarbonate <5 mmol/L, or ketones >6 mmol/L.
Respiratory Acidosis
pH <7.35, PaCO₂ >6.0 kPa, HCO₃⁻ raised (renal compensation — minimal acutely, significant chronically).
Causes: COPD exacerbation, respiratory muscle weakness, central hypoventilation (opioid overdose, brainstem lesion), chest wall deformity, obesity hypoventilation.
⚠️ Red Flag
Acute respiratory acidosis with PaCO₂ >8 kPa and a rising trend is a pre-arrest state. Escalate immediately to a senior clinician or critical care team. Consider NIV/BiPAP in COPD, or intubation in non-COPD ventilatory failure.
Metabolic Alkalosis
pH >7.45, HCO₃⁻ >26 mmol/L, PaCO₂ mildly raised.
Causes: vomiting (loss of HCl), nasogastric suction, diuretics (loss of K⁺ and H⁺), primary hyperaldosteronism, Cushing's syndrome, antacid overuse.
Respiratory Alkalosis
pH >7.45, PaCO₂ <4.7 kPa, HCO₃⁻ low (renal compensation).
Causes: anxiety/hyperventilation, pulmonary embolism (early), altitude, sepsis (early), salicylate poisoning (early), pregnancy, mechanical over-ventilation.
💎 Clinical Pearl
Pulmonary embolism classically presents with a respiratory alkalosis — the patient hyperventilates due to hypoxia and pleuritic pain, blowing off CO₂. A normal ABG does not exclude PE.
Mixed Acid-Base Disorders
When the pH is normal but both PaCO₂ and HCO₃⁻ are abnormal, suspect a mixed disorder.
| Combination | Example Clinical Scenario |
|---|---|
| Metabolic acidosis + respiratory alkalosis | Sepsis (lactic acidosis + hyperventilation) |
| Metabolic alkalosis + respiratory acidosis | COPD + diuretics |
| Metabolic acidosis + metabolic alkalosis | DKA + vomiting |
Worked OSCE Example
ABG result: pH 7.28, PaCO₂ 3.2 kPa, HCO₃⁻ 11 mmol/L, PaO₂ 11.5 kPa, lactate 4.8 mmol/L
- Step 1: pH 7.28 → acidaemia
- Step 2: PaCO₂ 3.2 kPa → low — but pH is acidotic, so this is compensatory
- Step 3: HCO₃⁻ 11 mmol/L → primary metabolic acidosis
- Step 4: Winter's formula: expected PaCO₂ = (1.5 × 11) + 8 = 24.5 mmHg ≈ 3.3 kPa — actual 3.2 kPa → appropriate compensation
- Step 5: PaO₂ 11.5 kPa — borderline normal. Lactate 4.8 → significant hyperlactataemia
Conclusion: Primary high-AG metabolic acidosis with appropriate respiratory compensation and hyperlactataemia — consistent with septic shock. Urgent senior review.
FAQs
"How do I know if compensation is adequate?"
Use Winter's formula for metabolic acidosis (expected PaCO₂ = 1.5 × HCO₃⁻ + 8 ± 2 mmHg). If the actual PaCO₂ matches the expected value, compensation is appropriate. If higher than expected, there is a co-existing respiratory acidosis. If lower, there is a co-existing respiratory alkalosis.
"What does a normal pH with abnormal PaCO₂ and HCO₃⁻ mean?"
It suggests a mixed acid-base disorder where two primary disturbances are cancelling each other out. Calculate the expected compensatory response for each disturbance — if the observed values exceed compensation, a second primary disorder is present.
"How do I calculate the anion gap?"
Anion gap = Na⁺ – (Cl⁻ + HCO₃⁻). Normal is 8–12 mmol/L. Correct for hypoalbuminaemia: add 2.5 mmol/L to the AG for every 10 g/L albumin is below 40 g/L. Low albumin (common in hospitalised patients) masks a true high-AG acidosis if uncorrected.
"What does a raised lactate tell me?"
Lactate >2 mmol/L indicates tissue hypoperfusion, anaerobic metabolism, or impaired lactate clearance. Causes include sepsis, hypovolaemia, cardiac failure, severe anaemia, metformin toxicity, and hepatic failure. Lactate >4 mmol/L in sepsis confirms septic shock.
"Can I interpret an ABG without knowing the clinical context?"
Not safely. The same ABG result means different things in different patients — a PaCO₂ of 7.5 kPa is a chronic retention finding in a stable COPD patient, but a pre-arrest deterioration in a previously well patient with pneumonia. Always interpret ABGs in their full clinical context.
Related Posts
- A–E Assessment OSCE — using ABG findings to guide management of the acutely unwell patient
- Blood Results Interpretation OSCE — lactate, renal function, and metabolic panels to complement ABG interpretation
- Prescribing Safety OSCE — prescribing in acidosis, renal failure, and electrolyte disturbance