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Q1: The systematic approach (2 min)
"A nurse shows you this gas: pH 7.30, PaCO2 30, HCO3 15. Talk me through your interpretation."[1]
- Step 1 pH: 7.30 — acidaemia (under 7.35).
- Step 2 Primary: HCO3 low (15) and PaCO2 low (30) — both moved the same way; HCO3 is the driver, so primary metabolic acidosis with respiratory compensation.
- Step 3 Compensation: Winter — expected PaCO2 = 1.5 x 15 + 8 = 30.5 (range 28.5 to 32.5). Measured 30 is within band — appropriate, a simple disorder.
- Step 4 Anion gap: need Na and Cl. If Na 140, Cl 105: AG = 140 minus (105 + 15) = 20 — high-gap. Then delta ratio to exclude a second process.
- Step 5 Treat the cause — high-gap acidosis: work up DKA (glucose, ketones), lactic (sepsis, shock), toxins (salicylate, toxic alcohol), uraemia.
If the examiner pushes: "What if PaCO2 were 40?" — that is higher than expected, so a concurrent respiratory acidosis (mixed).[1]
Q2: Anion gap and delta ratio (2 min)
"Calculate the anion gap. What is the delta ratio and when do you use it?"[1]
- AG = Na minus (Cl + HCO3). Normal 8 to 12.[4]
- Correct for albumin: the normal AG falls by ~2.5 for every 10 g/L below 40. So a patient with albumin 20 has an expected AG of ~3 — a "normal" AG of 8 is actually high for them.
- Delta ratio = (AG minus 12) / (24 minus HCO3). It compares the rise in AG to the fall in bicarbonate.
- Under 0.4 — additional normal-gap (hyperchloraemic) acidosis (e.g. diarrhoea + a high-gap process).
- 0.4 to 0.8 — mixed high-gap + nongap.
- Around 1 — pure high-gap metabolic acidosis (each HCO3 consumed generates one unmeasured anion).
- Over 2 — additional metabolic alkalosis (the HCO3 did not fall as expected because an alkali process is raising it; e.g. vomiting + DKA).
The delta ratio is how you unmask a mixed disorder hidden by a "normal-looking" HCO3.[1]
Q3: DKA and bicarbonate (3 min)
"A patient in DKA has pH 6.9. Do you give bicarbonate?"[4]
- No, not routinely. Standard DKA management: IV fluids, insulin 0.1 unit/kg/h, potassium replacement, treat the trigger. Insulin stops ketogenesis and the ketoanions (beta-hydroxybutyrate, acetoacetate) are metabolised to bicarbonate, so the pH corrects itself.[4]
- Bicarbonate in DKA has been associated with delayed ketone clearance, hypokalaemia, paradoxical CNS acidosis, and cerebral oedema in children — no proven mortality benefit.[4]
- Reserve bicarbonate for pH under 6.9 WITH haemodynamic instability — even this is debated.[4]
- Always correct potassium before/with insulin: if K under 3.3, hold insulin and give K first (insulin drives K into cells and can precipitate dangerous hypokalaemia).
Q4: Salicylate and mixed disorders (2 min)
"Why does aspirin overdose give a mixed disorder, and how do you treat it?"[1]
- Respiratory alkalosis — salicylates directly stimulate the medullary respiratory centre.
- High-anion-gap metabolic acidosis — uncoupling of oxidative phosphorylation and Krebs-cycle inhibition raise lactate and ketones.
- The net is a mixed respiratory alkalosis + high-gap metabolic acidosis; the pH may look deceptively near-normal because two processes cancel.
- Treatment: activated charcoal if recent ingestion; urinary alkalinisation with sodium bicarbonate to keep urine pH 7.5 to 8.0 (traps salicylate as the ionised salt, preventing tubular reabsorption); haemodialysis for level over 100 mg/dL (acute), over 60 to 70 (chronic), severe acidosis, encephalopathy, or renal failure.[1]
Q5: Compensation rules and chronic CO2 retainers (2 min)
"Give me the four compensation rules. A COPD patient has PaCO2 70, HCO3 36 — is that appropriately compensated?"[1]
- Metabolic acidosis (Winter): PaCO2 = 1.5 x HCO3 + 8 (plus or minus 2).[1]
- Metabolic alkalosis: PaCO2 = 0.7 x HCO3 + 20 (plus or minus 5); or rises ~0.6 per 1 mmol/L rise in HCO3.
- Respiratory acidosis, acute: HCO3 rises 1 per 10 mmHg rise in PaCO2.
- Respiratory acidosis, chronic: HCO3 rises 4 per 10 mmHg rise in PaCO2 (renal compensation over days).
- For PaCO2 70 (30 above normal): chronic compensation gives HCO3 rise of 4 x 3 = 12, so expected HCO3 = 24 + 12 = 36. Matches — appropriately compensated chronic respiratory acidosis (typical of a stable COPD patient).
- Oxygen target in chronic CO2 retainers: 88 to 92% — over-oxygenation worsens hypercapnia via V/Q mismatch and the Haldane effect (CO2 displaced from haemoglobin by O2). Consider NIV if decompensating.
References4ShowHide
- [1]Adrogué HJ, Madias NE Management of life-threatening acid-base disorders. First of two parts N Engl J Med, 1998.PMID 9414329
- [2]Wrenn K The delta (delta) gap: an approach to mixed acid-base disorders Ann Emerg Med, 1990.PMID 2240729
- [3]Figge J, Jabor A, Kazda A, et al. Anion gap and hypoalbuminemia Crit Care Med, 1998.PMID 9824071
- [4]Jaber S, Paugam C, Futier E, et al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial Lancet, 2018.PMID 29910040