Skip to main content
MedVellum
QuestionsVideosPricing

MedVellum

Fellowship exam preparation across every specialty: source-verified topics, questions in every format, and videos.

Product

  • Specialties
  • Questions
  • Videos
  • Topic library
  • Exam tools
  • Pricing

Verification & policy

  • Verified register
  • Editorial policy
  • Privacy
  • Terms

Account

  • Sign in
  • Create account
  • Dashboard
  • Account & billing

© 2026 MedVellum. For education only — not a substitute for clinical judgement.

llms.txtPsychiatry LLM catalogSitemap

LibraryMBBS

MBBS viva

Acid-Base Disorders — Viva

clinicalSource-verified ·
On this page
Study tools

Write your answer

Saved on this device. No marking — you are the marker.

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. [1]Adrogué HJ, Madias NE Management of life-threatening acid-base disorders. First of two parts N Engl J Med, 1998.PMID 9414329
  2. [2]Wrenn K The delta (delta) gap: an approach to mixed acid-base disorders Ann Emerg Med, 1990.PMID 2240729
  3. [3]Figge J, Jabor A, Kazda A, et al. Anion gap and hypoalbuminemia Crit Care Med, 1998.PMID 9824071
  4. [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