UKMLA ABG Interpretation Algorithm: Five-Step Method

Arterial blood gases are one of the three investigations the UKMLA tests in every specialty. They appear in respiratory failure stems, DKA stems, poisoning stems, shock stems, sepsis stems, and post-operative stems. Candidates who approach an ABG with a consistent five-step algorithm convert them from a pattern-recognition lottery into routine arithmetic.

This pillar is designed as a standalone reference. Section 3 through 7 is the algorithm itself; sections 9–12 are the four primary acid-base disorders; section 14 walks ten worked cases representative of AKT-style stems. If you only have twenty minutes before the exam, re-read sections 3, 7, and 14.

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1. Why ABG is a UKMLA favourite across specialties

ABGs test integrated physiology, clinical reasoning, and numerical fluency in one stem. The GMC content map explicitly lists them across:

• Respiratory — asthma, COPD, PE, pulmonary oedema.
• Endocrine — DKA, HHS, adrenal crisis.
• Nephrology — AKI, CKD, electrolyte disorders.
• Toxicology — salicylate, methanol, ethylene glycol.
• Gastroenterology — ALF, pancreatitis with ARDS, ischaemic bowel.
• Cardiology — cardiogenic shock, cardiac arrest.

The pattern across these specialties is the same: combine pH, CO₂, HCO₃⁻, anion gap, and A–a gradient to identify the disorder, then map it to a cause.

For respiratory-specific ABG use in breathlessness and asthma, see our UKMLA Respiratory Masterclass. For electrolyte and renal acid-base, see our UKMLA Renal & Electrolyte Emergencies pillar.

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2. When is an ABG actually indicated? (VBG vs ABG)

True ABG indications:

• Need for accurate PaO₂ (respiratory failure assessment, oxygenation target titration, home O₂ eligibility).
• Need for accurate A–a gradient — PE, ARDS, pulmonary oedema evaluation.
• Carboxyhaemoglobin / methaemoglobinaemia measurement (though many analysers accept VBG).
• Severe shock where mixed venous may diverge from arterial.

VBG is usually sufficient:

• Acid-base and metabolic assessment — pH and HCO₃⁻ differ by <0.03 and <1 mmol/L respectively from arterial.
• DKA management — VBG pH and bicarbonate monitoring per JBDS.
• Lactate.
• Electrolytes and glucose (point-of-care).

VBG limitation: PvCO₂ is ~5 mmHg higher than PaCO₂ and PvO₂ does not reflect oxygenation. If a question hinges on oxygenation or A–a gradient, choose ABG.

Technique and sample handling errors to recognise:

• Air bubble → falsely high PaO₂, low PaCO₂.
• Delayed analysis → falling pH, rising CO₂ (ongoing metabolism).
• Sampling a clenched-fist patient → falsely high lactate from forearm ischaemia.
• Allen's test before radial puncture — collateral ulnar circulation.

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3. Step 1 — pH: acidaemic vs alkalaemic

Normal arterial pH range: 7.35–7.45.

• pH <7.35 = acidaemia.
• pH >7.45 = alkalaemia.
• pH 7.35–7.45 with abnormal CO₂/HCO₃⁻ = fully compensated disorder — or a mixed disorder cancelling out.

Commit this rule: the pH tells you the net effect, not the cause. A normal pH with deranged CO₂ and bicarbonate is never "normal" — it is compensated or mixed.

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4. Step 2 — pCO₂: respiratory contribution

Normal PaCO₂: 4.7–6.0 kPa (35–45 mmHg).

• PaCO₂ >6.0 kPa = respiratory acidosis contribution. If primary, pH low.
• PaCO₂ <4.7 kPa = respiratory alkalosis contribution. If primary, pH high.

Interpret with pH direction:

CO₂ moves with the pH in respiratory disorders; opposite to pH in metabolic disorders with compensation.

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5. Step 3 — HCO₃⁻: metabolic contribution

Normal bicarbonate: 22–26 mmol/L.

• HCO₃⁻ <22 = metabolic acidosis contribution.
• HCO₃⁻ >26 = metabolic alkalosis contribution.

Combine with CO₂ and pH to name the disorder:

Base excess (BE) gives the same metabolic information as bicarbonate — BE <−2 = metabolic acidosis contribution; BE >+2 = metabolic alkalosis.

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6. Step 4 — compensation: full, partial, none

Compensation in the opposite system never fully normalises pH. If pH is fully normal (7.40) with deranged CO₂ and HCO₃⁻, suspect a mixed disorder.

Compensation direction:

• Metabolic acidosis → hyperventilation lowers CO₂ (Kussmaul breathing).
• Metabolic alkalosis → hypoventilation raises CO₂ (modest — limited by hypoxia drive).
• Respiratory acidosis → renal retention of HCO₃⁻ (slow: 3–5 days for full compensation; acute retention minimal).
• Respiratory alkalosis → renal excretion of HCO₃⁻ (slow).

Compensation rules (worth memorising for AKT/PSA level questions):

If observed compensation differs from expected → mixed disorder.

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7. Step 5 — anion gap: HAGMA vs NAGMA

Anion gap = (Na⁺ + K⁺) − (Cl⁻ + HCO₃⁻)

Some use Na⁺ alone in the numerator, giving a slightly lower reference. Use the formula your lab uses. Normal 10–18 mmol/L (with K⁺) or 8–16 mmol/L (without K⁺).

Only calculate the anion gap in metabolic acidosis.

High Anion Gap Metabolic Acidosis (HAGMA) — MUDPILES:

• Methanol.
• Uraemia.
• Diabetic ketoacidosis (also alcoholic ketoacidosis, starvation).
• Paracetamol / Paraldehyde / Propylene glycol.
• Iron, Isoniazid.
• Lactic acidosis (sepsis, shock, metformin, ischaemic bowel, seizures).
• Ethylene glycol.
• Salicylates.

Normal Anion Gap Metabolic Acidosis (NAGMA) — USED CAR:

• Ureterostomy / small bowel fistula.
• Small bowel fistula.
• Excess saline (hyperchloraemic acidosis from 0.9% NaCl resuscitation).
• Diarrhoea.
• Carbonic anhydrase inhibitors (acetazolamide).
• Addison's disease.
• Renal tubular acidosis (types 1, 2, 4).

Delta ratio (for HAGMA patients — spots mixed disorders):

• Δratio = (anion gap − 12) ÷ (24 − HCO₃⁻).
• <0.4 — pure NAGMA (HAGMA corrected + another process).
• 0.4–1 — HAGMA + NAGMA.
• 1–2 — pure HAGMA.

• 2 — HAGMA + metabolic alkalosis.

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8. A–a gradient calculation and interpretation

A–a gradient = PAO₂ − PaO₂

PAO₂ = (FiO₂ × (760 − 47)) − (PaCO₂/0.8) [mmHg units]

Simplified room-air approximation (kPa): PAO₂ ≈ 20 − (PaCO₂ × 1.25).

A–a gradient = PAO₂ − PaO₂.

Normal A–a gradient:

• Young adult ≈ <2 kPa (15 mmHg).
• Age-adjusted upper limit ≈ (age ÷ 4) + 1 kPa.

Interpretation:

A widened A–a gradient with normal or low CO₂ is classic for PE — pair with a Wells score calculation as covered in the UKMLA Respiratory Masterclass.

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9. Respiratory acidosis — causes and clinical correlation

Pattern: pH ↓, PaCO₂ ↑, HCO₃⁻ normal (acute) or ↑ (chronic compensation).

Causes:

Key clinical markers:

• Acute (pH ↓↓, HCO₃⁻ normal): minutes to hours — patient usually distressed, tachypnoeic or agonal.
• Chronic (pH near normal, HCO₃⁻ ↑↑): COPD, obesity hypoventilation — compensated over days.

Acute-on-chronic: pH <7.35 + PaCO₂ much higher than expected from chronic baseline — decompensation. Consider NIV if Type 2 respiratory failure (PaCO₂ >6, pH <7.35) and appropriate.

Oxygen titration in COPD: aim 88–92%, use 24% or 28% Venturi mask, recheck ABG at 30–60 min. Over-oxygenation worsens Type 2 failure via V/Q mismatch, lost hypoxic vasoconstriction, Haldane effect, and reduced respiratory drive.

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10. Respiratory alkalosis

Pattern: pH ↑, PaCO₂ ↓, HCO₃⁻ normal (acute) or ↓ (chronic compensation).

Causes (the "CHAMPS" framework):

• CNS disease (stroke, meningitis, tumour).
• Hypoxia (PE, high altitude, CHF early).
• Anxiety / panic / pain.
• Mechanical ventilation (iatrogenic).
• Pregnancy (progesterone).
• Salicylate toxicity (early stage — respiratory alkalosis, then HAGMA later).

Clinical features:

• Paraesthesia (perioral, fingertips) — due to hypocalcaemia (alkalosis shifts calcium onto albumin).
• Tetany, carpopedal spasm.
• Lightheadedness, syncope.

Management: identify and treat cause. Rebreathing into a paper bag for panic-associated hyperventilation only after excluding organic causes (PE, MI, DKA). A PE stem + hyperventilation must not be "rebreathing" — that is a classic distractor.

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11. Metabolic acidosis — HAGMA vs NAGMA

Pattern: pH ↓, HCO₃⁻ ↓, PaCO₂ ↓ (respiratory compensation).

HAGMA — most common UKMLA causes:

• DKA — hyperglycaemia + ketones + acidosis. Triad confirmed with glucose >11, ketones ≥3, pH <7.3 or HCO₃⁻ <15. Management per Endocrinology pillar.
• Lactic acidosis — sepsis, shock, tissue hypoperfusion, metformin (especially in renal impairment), mesenteric ischaemia. Always consider mesenteric ischaemia in elderly + pain out of proportion.
• Uraemic acidosis — CKD 4/5, acute uraemia.
• Salicylate overdose — early respiratory alkalosis (direct medullary stimulation) then HAGMA (mitochondrial uncoupling).
• Toxic alcohols — methanol (visual disturbance, blindness), ethylene glycol (oxalate crystals in urine), propylene glycol (lorazepam infusions).
• Paracetamol overdose (late) — with fulminant hepatic failure.

NAGMA — most common UKMLA causes:

• Diarrhoea (commonest) — bicarbonate loss.
• Renal tubular acidosis — Type 1 (distal, stones, hypokalaemia), Type 2 (proximal, Fanconi syndrome), Type 4 (hyperkalaemia, DM/Addison's).
• Large-volume 0.9% NaCl resuscitation — hyperchloraemic acidosis.
• Acetazolamide.
• Addison's (also HAGMA in severe).

Management principles:

• Treat the cause (insulin + fluids in DKA, fluids + antibiotics in sepsis, dialysis in uraemia, N-acetylcysteine in paracetamol, fomepizole or ethanol in methanol/ethylene glycol).
• Bicarbonate therapy — reserved for pH <7.0 or hyperchloraemic acidosis. Avoid in DKA (paradoxical CSF acidosis).
• Potassium — monitor and replace early (acidosis drives K⁺ out of cells; correction drops it).

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12. Metabolic alkalosis

Pattern: pH ↑, HCO₃⁻ ↑, PaCO₂ ↑ (respiratory compensation).

Causes:

• Vomiting, NG suction — loss of gastric H⁺, volume contraction.
• Diuretics (loop, thiazide) — volume contraction + distal H⁺ loss + K⁺ loss.
• Primary hyperaldosteronism (Conn's), Cushing's, Liddle's — mineralocorticoid excess.
• Excess bicarbonate / alkali ingestion.
• Milk-alkali syndrome.
• Hypokalaemia (any cause) — intracellular H⁺ shift.

Chloride-responsive vs chloride-resistant (urinary Cl⁻ differentiates):

• Urine Cl⁻ <20 — chloride-responsive (vomiting, NG suction, diuretic-off). Responds to saline + K⁺ replacement.
• Urine Cl⁻ >20 — chloride-resistant (mineralocorticoid excess, Bartter's, Gitelman's, diuretic-on). Saline unhelpful; address cause.

Clinical features: neuromuscular irritability (like respiratory alkalosis), worsening hypokalaemia, hypocalcaemia, hypomagnesaemia, arrhythmias.

Management: correct volume (0.9% saline if chloride-responsive), replace K⁺ and Mg²⁺, treat cause. Rarely IV acetazolamide for refractory alkalosis.

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13. Mixed disorders — spotting and interpreting

Mixed disorders are common in sick patients and frequently appear as AKT distractors.

Spot a mixed disorder when:

• pH is normal but CO₂ and HCO₃⁻ are both markedly deranged in opposite directions.
• Compensation differs from the expected Winter's or compensation rule.
• Delta ratio <0.4 or >2 (HAGMA with another process).

Common mixed patterns:

Exam trap: a vomiting DKA patient may have near-normal pH despite being critically unwell — the HAGMA and metabolic alkalosis mask each other. Always calculate the anion gap.

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14. Ten clinical case ABGs worked through

Case 1 — 24 yr asthma exacerbation, RR 40:

• pH 7.48, PaCO₂ 3.5 kPa, HCO₃⁻ 22, PaO₂ 10, lactate 1.2.
• Respiratory alkalosis due to hyperventilation — expected in acute asthma.
• Red flag: if CO₂ rises into normal range (4.7+) in severe asthma = fatiguing — intubation consideration.

Case 2 — 68 yr COPD exacerbation on 24% O₂:

• pH 7.26, PaCO₂ 10.5 kPa, HCO₃⁻ 32, PaO₂ 8.2.
• Acute-on-chronic respiratory acidosis — HCO₃⁻ raised (chronic retention), but pH <7.35 and CO₂ higher than expected.
• Management: NIV (BiPAP) — T2RF with pH <7.35.

Case 3 — 18 yr T1DM, unwell 2 days, Kussmaul breathing:

• pH 7.14, PaCO₂ 2.0 kPa, HCO₃⁻ 6, glucose 28, ketones 5.1, Na 132, K 5.0, Cl 96, anion gap 30.
• HAGMA with partial respiratory compensation — DKA.
• Delta ratio = (30−12) / (24−6) = 18/18 = 1.0 → pure HAGMA.
• Management: JBDS protocol — 1 L saline over 1 h, fixed-rate insulin 0.1 units/kg/h, potassium replacement once <5.5, hourly ketones + VBG.

Case 4 — 85 yr post-op with post-hernia ileus, 3 days vomiting:

• pH 7.52, PaCO₂ 6.1 kPa, HCO₃⁻ 34, K 3.0, Cl 88, urine Cl 10.
• Chloride-responsive metabolic alkalosis — NG/vomiting + volume contraction.
• Management: 0.9% saline + K⁺ replacement.

Case 5 — 70 yr hypotensive, RR 30, distended abdomen, elderly:

• pH 7.22, PaCO₂ 3.2 kPa, HCO₃⁻ 10, lactate 8.6, Cr 180.
• HAGMA with respiratory compensation — lactic acidosis, think mesenteric ischaemia.
• Management: urgent CT angiography, surgical review, resuscitation.

Case 6 — 28 yr taken paracetamol + aspirin 6 h ago:

• pH 7.50, PaCO₂ 3.0 kPa, HCO₃⁻ 18, Na 138, Cl 100, anion gap 20.
• Respiratory alkalosis + HAGMA (mixed) — salicylate toxicity.
• Management: activated charcoal if <1 h, IV sodium bicarbonate (urine alkalinisation), check levels; dialysis if severe.

Case 7 — 60 yr obese, day 2 post-op, saturation 88% on air:

• pH 7.33, PaCO₂ 7.6 kPa, HCO₃⁻ 29, PaO₂ 7.8, A–a gradient 4.5 kPa.
• Acute respiratory acidosis with widened A–a gradient — atelectasis ± pneumonia; consider PE given post-op context.
• Management: CTPA + chest physio, oxygen titration, early mobilisation.

Case 8 — 75 yr CKD4, hyperkalaemia clinic:

• pH 7.30, PaCO₂ 4.8 kPa, HCO₃⁻ 18, Na 138, Cl 108, anion gap 12, K 6.8, Cr 450.
• NAGMA — renal tubular dysfunction (RTA 4).
• Management: hyperkalaemia ladder (see nephrology pillar); oral sodium bicarbonate long-term.

Case 9 — 40 yr found collapsed, dilated pupils, visual loss:

• pH 7.10, PaCO₂ 3.5 kPa, HCO₃⁻ 8, anion gap 26, glucose 6, lactate 2.
• HAGMA — toxic alcohol (methanol).
• Management: fomepizole (or ethanol drip), bicarbonate, folinic acid, dialysis.

Case 10 — 55 yr pneumonia + sepsis + vomiting:

• pH 7.40, PaCO₂ 4.2 kPa, HCO₃⁻ 22, lactate 4, Na 138, Cl 95, anion gap 25.
• Normal pH, deranged values → mixed: HAGMA (lactate) + metabolic alkalosis (vomiting).
• Delta ratio = (25−12) / (24−22) = 13/2 = 6.5 → HAGMA + alkalosis.
• Management: sepsis six + antiemetics + volume correction.

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15. Common exam traps and edge cases

Trap 1 — normal pH, deranged CO₂ and HCO₃⁻. Always ask: is this compensation or is it a mixed disorder? Compare to expected compensation rules.

Trap 2 — salicylate overdose. Always mixed — respiratory alkalosis (early medullary stimulation) + HAGMA (uncoupling). Pure respiratory alkalosis ≠ salicylate overdose alone.

Trap 3 — post-cardiac arrest ABG. Always mixed acidosis — respiratory (CO₂ retention during arrest) + metabolic (lactate from hypoperfusion).

Trap 4 — DKA with vomiting or diuretic. Anion gap is diagnostic — don't be misled by near-normal pH.

Trap 5 — excess 0.9% saline resuscitation. Hyperchloraemic NAGMA — common on post-op and sepsis wards. Does not mean resuscitation failed; may mean fluid choice needs revisiting (Plasma-Lyte / Hartmann's).

Trap 6 — peripheral cyanosis with normal SpO₂. Methaemoglobinaemia (nitrate, dapsone, topical anaesthetic) — SpO₂ falsely normal (~85%), MetHb on co-oximetry, treat with methylene blue.

Trap 7 — "normal" ABG with raised lactate in elderly abdominal pain. Mesenteric ischaemia. Surgery, not observation.

Trap 8 — COPD patient becoming somnolent on oxygen. Over-oxygenation has caused CO₂ narcosis. Reduce FiO₂ to target 88–92%, ABG, consider NIV.

Trap 9 — venous gas misread as arterial. A VBG with PCO₂ 7.5 in a patient who looks well → possibly normal venous sample. Don't intubate on a single VBG.

Trap 10 — exercising patient with lactate 4. Not pathological. Lactate rises with exertion, seizures, β-agonists. Interpret in context.

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Exam technique — the 60-second ABG read

On exam day, read every ABG in this order:

1. pH — acidaemia, alkalaemia, or compensated/mixed?
2. PaCO₂ — direction relative to pH.
3. HCO₃⁻ — direction relative to pH.
4. Compensation check — matches expected rules?
5. Anion gap — if metabolic acidosis, calculate. HAGMA → MUDPILES search. NAGMA → USED CAR search.
6. A–a gradient — if oxygenation question or respiratory alkalosis with hypoxia (PE).
7. Bind to clinical context — the stem drives the final answer.

Finish every ABG by naming the disorder, the likely cause, and the next management step. That is the template the UKMLA wants.

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Summary — five reflexes that win ABG SBAs

1. Algorithm first, never pattern-match raw numbers. pH → CO₂ → HCO₃⁻ → compensation → anion gap → A–a gradient.
2. Calculate the anion gap on every metabolic acidosis. HAGMA vs NAGMA decides half the management.
3. Mixed disorders hide in normal pH. Use the delta ratio to uncover them.
4. A widened A–a gradient with normal or low CO₂ points to PE until proven otherwise.
5. Acute-on-chronic respiratory acidosis with pH <7.35 = NIV decision point. Target 88–92% SpO₂ in COPD.

Pair this pillar with the UKMLA Respiratory Masterclass for respiratory failure integration, the UKMLA Endocrinology Masterclass for DKA/HHS, the UKMLA Renal & Electrolyte Emergencies pillar for acid-base in AKI, and the UKMLA Emergency Presentations pillar for sepsis and peri-arrest integration. ABG marks are won by algorithm fluency — drill the five steps until they fire automatically.