28 INTERPRETING BLOOD GASES
# 29 INTERPRETING BLOOD GASES
ABG interpretation is one of the highest-yield skills in MRCS Part A. A single set of numbers can test physiology, pharmacology, surgical pathology and clinical reasoning at once — but every ABG is solved by the same five-step algorithm. Learn it cold.
Normal values
| Parameter | Normal range |
|---|---|
| pH | 7.35 – 7.45 |
| PaCO₂ | 4.7 – 6.0 kPa (35 – 45 mmHg) |
| PaO₂ (on room air) | 10.5 – 13.5 kPa |
| HCO₃⁻ | 22 – 28 mmol/L |
| Base excess (BE) | −2 to +2 |
| Lactate | < 2 mmol/L |
| Anion gap | 8 – 16 mmol/L |
👩⚕️ The exam uses kPa (mmHg ÷ 7.5 = kPa). Quick check: PaO₂ on room air ≈ FiO₂% − 10, so a healthy patient on air should run ≥ 11 kPa.
The physiology in one line
> pH ∝ HCO₃⁻ / PaCO₂
HCO₃⁻ is controlled by the kidney (slow, days). CO₂ is controlled by the lungs (fast, minutes). Whichever organ caused the problem, the other compensates.
The five-step algorithm
Apply these in order, every time. Do not freelance.
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1. Oxygenation: PaO₂ < 8 → resp failure; CO₂ low/normal = Type I, CO₂ > 6 = Type II
2. pH: < 7.35 acidosis · > 7.45 alkalosis · normal with abnormal CO₂/HCO₃⁻ = compensated or mixed
3. Primary: acidosis + ↑CO₂ = respiratory · acidosis + ↓HCO₃⁻ = metabolic
alkalosis + ↓CO₂ = respiratory · alkalosis + ↑HCO₃⁻ = metabolic
4. Compensation: CO₂ and HCO₃⁻ moving SAME direction = compensating
OPPOSITE directions = mixed disorder
pH normal = full · pH still abnormal = partial (body never overshoots)
5. Anion gap (if metabolic acidosis): AG = Na⁺ − (Cl⁻ + HCO₃⁻)
> 16 = HAGMA (MUDPILES) · normal = NAGMA (HARDUP)
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👩⚕️ The commonest exam error is jumping to "respiratory acidosis" without confirming pH is acidotic. Always start at pH.
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Respiratory acidosis (↑ PaCO₂)
The lungs are failing to blow off CO₂. Anything that hypoventilates:
➡ Airway/lung: COPD, severe asthma, late pneumonia, ARDS
➡ Drive: opioids, sedatives, anaesthesia, raised ICP, brainstem stroke
➡ Pump: Guillain–Barré, myasthenia, MND, flail chest, kyphoscoliosis
Compensation: renal HCO₃⁻ retention over 2–5 days. Chronic COPD = high CO₂ + high HCO₃⁻ + near-normal pH. Acute (post-op opioid) = high CO₂ with normal HCO₃⁻ — kidneys haven't had time.
Respiratory alkalosis (↓ PaCO₂)
➡ Anxiety, pain, hyperventilation
➡ Hypoxia driving tachypnoea — PE is the classic exam trap
➡ Early sepsis, pneumonia
➡ Salicylate poisoning (medullary stimulation — later combines with HAGMA)
➡ Pregnancy, high altitude
Metabolic acidosis (↓ HCO₃⁻)
Either acid is added or bicarbonate is lost — split by the anion gap.
HAGMA — MUDPILES (acid added)
Methanol · Uraemia · DKA · Propylene glycol · Isoniazid/Iron · Lactic acidosis (sepsis, ischaemic bowel, metformin) · Ethylene glycol · Salicylates
NAGMA — HARDUP (HCO₃⁻ lost, replaced by Cl⁻ — "hyperchloraemic acidosis")
Hyperalimentation · Acetazolamide · RTA · Diarrhoea · Ureteric diversion (ileal conduit, ileocystoplasty) · Pancreatic/biliary fistula
👩⚕️ Two surgical NAGMA traps appear repeatedly in MRCS questions: (1) bowel in the urinary tract (ileal conduit, ileocystoplasty — Cl⁻/HCO₃⁻ swap across bowel mucosa) and (2) large-volume 0.9% saline (154 mmol/L Cl⁻ vs plasma ~100 — dumps Cl⁻, dilutes HCO₃⁻).
Compensation: Kussmaul respiration drops CO₂ within minutes (Winters: expected PaCO₂ mmHg ≈ 1.5 × HCO₃⁻ + 8).
Metabolic alkalosis (↑ HCO₃⁻)
➡ Vomiting / high NG output — loss of HCl (the classic surgical cause)
➡ Pyloric stenosis — paediatric prototype: hypochloraemic, hypokalaemic alkalosis
➡ Loop / thiazide diuretics (contraction alkalosis)
➡ Conn's, Cushing's, exogenous steroids
➡ Massive transfusion (citrate → HCO₃⁻), milk–alkali
Vomiting triad: ↓ K⁺, ↓ Cl⁻, ↑ pH. The kidney reabsorbs Na⁺ in exchange for K⁺ and H⁺ to preserve volume — worsening hypokalaemia and producing paradoxical aciduria (acidic urine despite systemic alkalosis).
Respiratory compensation (hypoventilation) is limited — the patient won't tolerate hypoxia.
Mixed disorders
CO₂ and HCO₃⁻ moving in opposite directions from expected compensation = two primary disorders.
➡ Septic shock — respiratory fatigue (↑CO₂) + lactic acidosis (↓HCO₃⁻). Both push pH down. Catastrophic.
➡ Salicylate poisoning — early respiratory alkalosis (medullary stimulation) + later HAGMA (uncoupled oxidative phosphorylation)
➡ Vomiting + DKA — ketones (acidosis) + H⁺ loss (alkalosis)
Type I vs Type II respiratory failure
| Type I | Type II | |
|---|---|---|
| PaO₂ | < 8 kPa | < 8 kPa |
| PaCO₂ | Normal/low | > 6 kPa |
| Problem | Oxygenation (V/Q mismatch) | Ventilation (pump failure) |
| Causes | PE, pneumonia, oedema, ARDS, early asthma | COPD, opioids, NMD, late/exhausted asthma |
| Management | Oxygen | BiPAP, reverse opioids, treat cause |
👩⚕️ Hypoxic post-op COPD patient on 30% O₂ with PaCO₂ 8.5 = Type II respiratory failure. Read the numbers, not the history.
Lactate
➡ < 2 normal · 2–4 tissue hypoperfusion · > 4 severe sepsis / Sepsis-6 trigger
➡ Non-hypoxic causes: metformin, liver failure, salbutamol, seizures, thiamine deficiency
A rising lactate in a post-op patient = ischaemic bowel until proven otherwise.
Anion gap
AG = Na⁺ − (Cl⁻ + HCO₃⁻) — normal 8–16. Represents unmeasured anions (mostly albumin). Added acid (lactate, ketones) widens it; HCO₃⁻ loss with Cl⁻ replacement keeps it normal.
👩⚕️ In a hypoalbuminaemic surgical patient the baseline AG is artificially low — a "normal" 12 may actually be raised. Rough correction: add 2.5 per 10 g/L albumin below 40.
A–a gradient
> A–a gradient = PAO₂ − PaO₂ · on room air: PAO₂ ≈ 20 − (1.25 × PaCO₂) (kPa)
Normal < 2 kPa in the young (roughly (age/4)+4 mmHg).
- Normal gradient with hypoxia = pure hypoventilation (opioids, NMD)
- Raised gradient = V/Q mismatch (PE, pneumonia, ARDS), shunt, diffusion defect
A drowsy patient with PaO₂ 8 and PaCO₂ 9 and a normal A–a gradient is opioid-toxic. The same numbers with a raised gradient mean additional pulmonary pathology.
Compensation rules — at a glance
| Primary disorder | Compensation | Speed |
|---|---|---|
| Respiratory acidosis | ↑ renal HCO₃⁻ retention | Slow (2–5 days) |
| Respiratory alkalosis | ↓ renal HCO₃⁻ retention | Slow (days) |
| Metabolic acidosis | ↑ ventilation (↓ CO₂) | Fast (minutes) |
| Metabolic alkalosis | ↓ ventilation (↑ CO₂) | Limited (hypoxia caps it) |
> Pearl: Respiratory = Renal compensation (slow). Metabolic = respiratory compensation (fast). The body never overshoots — if pH is on the acidotic side, the primary disorder is an acidosis, even if compensation has nearly normalised it.
Central vs peripheral chemoreceptors
| Central | Peripheral | |
|---|---|---|
| Location | Medulla (ventral surface) | Carotid bodies (CN IX), aortic bodies (CN X) |
| Senses | CSF pH (driven by CO₂ across BBB) | PaO₂ mainly; also CO₂, pH |
| Role | Primary minute-to-minute driver | Backup hypoxic drive |
👩⚕️ In chronic CO₂ retainers, central receptors desensitise and the peripheral hypoxic drive dominates. Excessive O₂ abolishes this drive — titrate to SpO₂ 88–92%.
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Test yourself
A patient underwent ileocystoplasty. Creatinine is now high. What is the likely electrolyte disturbance?
- ((Hyperchloraemic acidosis::☑️ Bowel mucosa exchanges urinary Cl⁻ for HCO₃⁻ — classic NAGMA.))
- ((Hypokalaemic metabolic alkalosis::Pattern of vomiting or NG losses, not bowel-in-urinary-tract.))
- ((Hypernatraemic metabolic alkalosis::Ileocystoplasty does not retain Na⁺ or generate alkalosis.))
- ((Hyperkalaemic metabolic acidosis with raised anion gap::Raised AG implies added acid (lactate, ketones), not Cl⁻/HCO₃⁻ swap.))
- ((Respiratory acidosis::A urological procedure has no direct effect on ventilation.))
👩⚕️ Any bowel-in-urinary-tract = hyperchloraemic (non-AG) metabolic acidosis.
After a trauma, a patient received 6 L of normal saline. What will happen?
- ((Hyperchloraemic acidosis::☑️ 0.9% saline has 154 mmol/L Cl⁻ — dilutes HCO₃⁻ and dumps chloride.))
- ((Hyperkalaemic metabolic acidosis with raised AG::Saline has no K⁺ and no organic acid.))
- ((Metabolic alkalosis::Excess Cl⁻ and diluted HCO₃⁻ both drive acidosis.))
- ((Respiratory alkalosis::IV fluid does not change ventilation.))
- ((No acid-base disturbance::6 L is well into volumes that reliably cause measurable acidosis.))
👩⚕️ Why balanced crystalloids (Hartmann's, Plasma-Lyte) are preferred for large-volume resuscitation.
Postoperatively, a patient received 6 L of normal saline. What would her ABG show?
- ((Hyperchloraemic metabolic acidosis::☑️ Non-AG acidosis from Cl⁻ load and HCO₃⁻ dilution.))
- ((Metabolic alkalosis::Saline drives acidosis, never alkalosis.))
- ((Respiratory acidosis::Mechanism is metabolic, not ventilatory.))
- ((Raised anion gap metabolic acidosis::Cl⁻ replaces HCO₃⁻ — gap stays normal.))
- ((Mixed respiratory and metabolic alkalosis::No alkalosis mechanism present.))
A 75-year-old man, smoker for 45 years, is short of breath with widespread wheeze and hyperinflated lungs on CXR. What will an ABG likely reveal?
- ((High PaCO₂, High HCO₃⁻::☑️ Chronic COPD with renal HCO₃⁻ retention — compensated respiratory acidosis.))
- ((Low PaCO₂, Low HCO₃⁻::Chronic respiratory alkalosis pattern (e.g. altitude, chronic hyperventilation).))
- ((Normal PaCO₂, Low HCO₃⁻::Suggests primary metabolic acidosis — no source here.))
- ((High PaCO₂, Low HCO₃⁻::That's a mixed acidosis, not compensation.))
- ((Low PaCO₂, High HCO₃⁻::Physiologically impossible as a primary disorder.))
👩⚕️ Chronic respiratory acidosis = high CO₂ + high HCO₃⁻ + near-normal pH.
What is the expected ABG finding in a patient having a COPD exacerbation?
- ((Respiratory acidosis with a compensatory metabolic alkalosis::☑️ Hypoventilation raises CO₂; chronic renal retention keeps HCO₃⁻ high.))
- ((Metabolic acidosis with respiratory compensation::Needs a source of acid (lactate, ketones) — not the primary problem here.))
- ((Respiratory alkalosis::A failing COPD lung retains CO₂, it does not blow it off.))
- ((Mixed metabolic and respiratory alkalosis::No mechanism for alkalosis in this scenario.))
- ((Uncompensated metabolic acidosis::Primary problem is ventilatory, and HCO₃⁻ is raised not low.))
A man with emphysema on 28% O₂: pH 7.28, PaO₂ 6.2, PaCO₂ 8, HCO₃⁻ 36, BE +5. Interpretation?
- ((Partially compensated respiratory acidosis::☑️ pH still acidotic despite raised HCO₃⁻ — compensation incomplete.))
- ((Fully compensated respiratory acidosis::Would need pH back inside 7.35–7.45.))
- ((Uncompensated respiratory acidosis::HCO₃⁻ 36 with BE +5 shows compensation is well underway.))
- ((Metabolic acidosis with respiratory compensation::Both CO₂ and HCO₃⁻ would be low in that case.))
- ((Mixed respiratory and metabolic alkalosis::pH is acidotic, not alkalotic.))
👩⚕️ Algorithm in 3 seconds: pH 7.28 → acidosis; high CO₂ → respiratory; high HCO₃⁻ → compensating; pH still abnormal → partial.
A COPD patient's ABG shows elevated PCO₂ and elevated HCO₃⁻. Most likely explanation?
- ((Compensated respiratory acidosis::☑️ Primary CO₂ retention with renal HCO₃⁻ retention.))
- ((Compensated metabolic alkalosis::Clinically wrong — COPD's primary lesion is ventilatory, not bicarbonate excess.))
- ((Mixed metabolic and respiratory acidosis::HCO₃⁻ would be low, not high.))
- ((Uncompensated respiratory alkalosis::Requires low CO₂, the opposite of this picture.))
- ((Type 1 respiratory failure::Type 1 has normal/low CO₂; this is Type 2.))
👩⚕️ Same lab values fit two disorders — use clinical context to choose.
A 1-month-old with non-bilious vomiting and pyloric stenosis. What will his ABG show?
- ((Hypochloraemic metabolic alkalosis::☑️ Loss of HCl in vomitus depletes H⁺ and Cl⁻.))
- ((Hyperchloraemic metabolic acidosis::Cl⁻ is being lost, not retained; and H⁺ loss alkalinises.))
- ((Respiratory acidosis::Pyloric stenosis is metabolic, not ventilatory.))
- ((Metabolic acidosis with raised AG::No source of unmeasured anion.))
- ((Respiratory alkalosis::Distress may hyperventilate, but the characteristic finding is metabolic alkalosis.))
👩⚕️ The pyloric stenosis triad: ↓ Cl⁻, ↓ K⁺, ↑ pH — plus paradoxical aciduria.
Which set of electrolyte derangements is expected in severe vomiting?
- ((Hypokalaemic hyponatraemic hypochloraemic metabolic alkalosis::☑️ H⁺, Cl⁻, Na⁺ and K⁺ all lost; renal volume preservation depletes K⁺ further.))
- ((Hyperkalaemic metabolic acidosis::Vomiting causes alkalosis and hypokalaemia, not the reverse.))
- ((Hyperchloraemic metabolic acidosis::Cl⁻ is lost in gastric secretions — hypochloraemic.))
- ((Respiratory acidosis::Vomiting does not impair ventilation.))
- ((Hyperkalaemic metabolic alkalosis::Alkalosis is right, but K⁺ is depleted, not raised.))
A man with septicaemia after perforated appendicitis is hypotensive. ABG: pH 7.26, PaCO₂ 7.2, PaO₂ 7.5, HCO₃⁻ 17. Most likely explanation?
- ((Compensated metabolic acidosis::Then CO₂ would be low from hyperventilation — here it's high.))
- ((Compensated respiratory acidosis::Then HCO₃⁻ would be raised — here it's low.))
- ((Mixed metabolic and respiratory acidosis::☑️ High CO₂ + low HCO₃⁻ = both systems failing.))
- ((Uncompensated metabolic acidosis::Pure metabolic acidosis would drive CO₂ down, not up.))
- ((Uncompensated respiratory acidosis::Pure respiratory acidosis leaves HCO₃⁻ normal, not low.))
👩⚕️ Mixed acidosis = ventilation failure (fatigue) + lactic acidosis (hypoperfusion). Mortality is high — escalate.
A 69-year-old man after anterior resection received 2 mg intrathecal morphine. Drowsy. ABG: pH 7.28, PaCO₂ 8.1, PaO₂ 10.2, BE +2.1, lactate 4. Diagnosis?
- ((Respiratory acidosis::☑️ Opioid-induced hypoventilation with CO₂ retention — naloxone may be needed.))
- ((Metabolic acidosis::Lactate is mildly raised but BE is positive and CO₂ is markedly high.))
- ((Mixed respiratory and metabolic acidosis::Metabolic component is minimal — BE is positive.))
- ((Compensated metabolic alkalosis::pH is acidotic, not alkalotic.))
- ((Type 1 respiratory failure::PaO₂ is 10.2 — not hypoxic. CO₂ is high — Type 2 picture.))
👩⚕️ Intrathecal morphine causes delayed (6–18 h) respiratory depression — monitor accordingly.
A 72-year-old COPD patient with peritonitis. BP 100/60, HR 100. ABG: pH 7.31, PaCO₂ 5.3, BE −3, HCO₃⁻ 17, lactate 5.3. Diagnosis?
- ((Metabolic acidosis due to peritonitis::☑️ Lactic acidosis from sepsis; normal CO₂ in a COPD patient = respiratory compensation.))
- ((Respiratory acidosis from COPD exacerbation::CO₂ is normal — would be high in a COPD exacerbation.))
- ((Compensated respiratory acidosis::Would need raised HCO₃⁻ and CO₂; here both wrong direction.))
- ((Metabolic alkalosis::pH acidotic, HCO₃⁻ low, BE negative — opposite picture.))
- ((Mixed respiratory and metabolic alkalosis::Every parameter points to acidosis.))
👩⚕️ A "normal" CO₂ in a chronic retainer is actually a relatively low CO₂ — they are hyperventilating to compensate.
A 78-year-old COPD patient is confused post-hemicolectomy on 30% O₂. PaO₂ 6.2, PaCO₂ 8.5. Diagnosis?
- ((Severe asthma attack::No bronchospasm or wheeze described, and patient has COPD.))
- ((Emphysema::A chronic diagnosis, not an acute event.))
- ((Pulmonary embolus::PE causes low/normal CO₂ from hyperventilation, not CO₂ this high.))
- ((Type 1 respiratory failure::Type 1 has normal/low CO₂ — this is markedly high.))
- ((Type 2 respiratory failure::☑️ PaO₂ < 8 + PaCO₂ > 6 — ventilation failure from post-op hypoventilation.))
👩⚕️ Type 2 = pump/ventilation failure. Type 1 = gas-exchange/oxygenation failure.
What acid-base status is expected from high nasogastric output?
- ((Metabolic alkalosis::☑️ HCl loss = hypochloraemic alkalosis, same mechanism as vomiting.))
- ((Metabolic acidosis::Loss of H⁺ raises pH, not lowers it.))
- ((Respiratory acidosis::NG drainage is metabolic, not respiratory.))
- ((Respiratory alkalosis::No hyperventilation component.))
- ((No acid-base disturbance::High-output NG losses are measurable on ABG.))
👩⚕️ Replace high NG losses with 0.9% saline + KCl.
Where are the central chemoreceptors that regulate breathing located?
- ((Medulla::☑️ Sense H⁺ in CSF generated by CO₂ crossing the blood-brain barrier.))
- ((Carotid body::Peripheral chemoreceptor — primarily senses PaO₂ (CN IX).))
- ((Aortic arch::Peripheral chemoreceptors (CN X) — not central.))
- ((Pons::Houses the pneumotaxic/apneustic pattern centres, not the chemoreceptors.))
- ((Hypothalamus::Temperature, thirst, hormones — not respiratory chemoreception.))
👩⚕️ Central = CO₂ (via CSF pH). Peripheral = O₂. In chronic CO₂ retainers, hypoxic drive dominates — beware uncontrolled O₂.
Revision summary
➡ Normals: pH 7.35–7.45 · CO₂ 4.7–6.0 · O₂ 10.5–13.5 · HCO₃⁻ 22–28 · BE ±2 · lactate < 2 · AG 8–16
➡ Five-step algorithm: Oxygenation → pH → Primary disorder → Compensation → Anion gap
➡ Respiratory = renal compensation (slow, days). Metabolic = respiratory compensation (fast, minutes). Body never overcompensates.
➡ Type I RF: PaO₂ < 8, CO₂ normal/low — oxygenation failure (PE, pneumonia, oedema)
➡ Type II RF: PaO₂ < 8, CO₂ > 6 — ventilation failure (COPD, opioids, NMD)
➡ HAGMA — MUDPILES: Methanol, Uraemia, DKA, Propylene glycol, Isoniazid/Iron, Lactic, Ethylene glycol, Salicylates
➡ NAGMA — HARDUP: Hyperalimentation, Acetazolamide, RTA, Diarrhoea, Ureteric diversion, Pancreatic fistula
➡ Surgical NAGMA traps: ileocystoplasty / ileal conduit, large-volume 0.9% saline
➡ Vomiting / NG / pyloric stenosis triad: ↓ K⁺, ↓ Cl⁻, ↑ pH (with paradoxical aciduria)
➡ Sepsis: mixed picture — respiratory fatigue (↑CO₂) + lactic acidosis (↓HCO₃⁻)
➡ Lactate: > 2 hypoperfusion, > 4 severe sepsis / Sepsis-6 trigger
➡ Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻). Raised → unmeasured acid added. Normal → HCO₃⁻ lost, Cl⁻ replaced.
➡ A–a gradient: normal in pure hypoventilation (opioids, NMD); raised in V/Q mismatch, shunt, diffusion defect.
➡ Chemoreceptors: Central (medulla) → CO₂ via CSF pH. Peripheral (carotid + aortic bodies) → O₂.