VIVAs · 2026A

2026 First Sitting VIVAs

8 VIVA stations from the CICM examiner report for this sitting. Examiner wording, report provenance and reported performance data are preserved.

View 2026A SAQs →

Exam outcomes

52% (43/83)Written pass · MCQ + SAQ
81% (42/52)Oral pass · VIVAs
45.7% (42/92)*Overall pass · CICMWrecks-derived
How passing worked

Written pass: candidates successful in both written components (MCQ + SAQ) and progressing to the oral examination, divided by candidates presenting for the written examination.

Oral pass: candidates successful after the oral component, divided by candidates sitting the oral examination. The First Part oral component consists of VIVAs.

2026A standard setting: the written examination used the Angoff method. The examiner report lists Angoff pass marks of 69.4% for MCQ and 47.95% for SAQ, with marks required to present for the oral of 61.8% and 45.96% respectively; candidates had to meet the required mark in both components. The oral pass mark was determined by borderline regression, with candidates within one standard error below the borderline regression pass mark individually reviewed by the examiner court.

Carry-over: 9 candidates entered the oral component carrying a written pass from a previous sitting.

* Overall pass: a CICMWrecks-derived contextual figure: final successful candidates ÷ (candidates presenting for the written examination + candidates carrying a written pass). It is not a CICM-reported pass percentage.

VIVA stations

2026A

VIVA 1

Respiratory Physiology and Pharmacology
57.7%Successful candidates
11.77Borderline regression pass mark
12.49Average mark
17.00Highest mark
Opening question
Explain how the prone position may affect gas exchange in a healthy adult?
Current · V5 (2025) C8.iii · primary C10.iii C3.iii C3.x C5.ii
Structured examiner prompts 10
  1. Explain how the prone position may affect gas exchange in a healthy adult?
    C8.iii
  2. How might the prone position affect pulmonary vascular resistance?
    C5.iiC8.iii
  3. How might the prone position affect respiratory system compliance?
    C3.iiiC8.iii
  4. How does dynamic compliance compare with static compliance?
    C3.iii
  5. This is a curve for a normal lung depicting work of breathing. How might this curve change with reduced compliance?
    C3.xC3.iii
  6. How might this curve change with increased airway resistance?
    C3.xC3.vi
  7. This is a normal graph of respiratory rate vs work of breathing. What changes would you expect to see for a patient with reduced compliance?
    C3.xC3.iii
  8. What about with asthma?
    C3.xC10.iiiC3.vi
  9. What factors determine how much of an inhaled bronchodilator reaches the target site?
    C10.iii
  10. What is one major advantage and disadvantage of intravenous, rather than inhaled bronchodilator administration?
    C10.iii
Official source: 2026A CICM Examiner Report · page 17

2026A

VIVA 2

Acid Base, Renal Physiology and Pharmacology
38.5%Successful candidates
11.13Borderline regression pass mark
10.88Average mark
18.00Highest mark
Opening question
Describe the abnormalities in the following arterial blood gas.
Current · V5 (2025) G2.i · primary E1.v E3.i G1.iii
Structured examiner prompts 8
  1. Describe the abnormalities in the following arterial blood gas.
    G2.iG1.iv
  2. What is the clinical significance of measuring Base excess versus bicarbonate?
    G2.i
  3. Why is the bicarbonate buffer considered the most important extracellular buffer?
    G1.iii
  4. If you were to give a carbonic anhydrase inhibitor, what effect will this have on the body’s acid base balance?
    E3.iG1.ii
  5. How is bicarbonate handled in the distal tubule?
    E1.vG1.iii
  6. How does spironolactone act on the kidney?
    E3.i
  7. If there was no urinary buffer, what would happen to the body’s acid base balance?
    G1.iii
  8. What is the role of ammonia production in chronic metabolic acidosis?
    E1.vG1.iii
Official source: 2026A CICM Examiner Report · page 18

2026A

VIVA 3

Gastrointestinal Physiology and Pharmacology
50%Successful candidates
11.59Borderline regression pass mark
11.85Average mark
17.00Highest mark
Opening question
How does critical illness predispose to stress ulcer formation?
Current · V5 (2025) J4.i · primary J1.iv J4.ii J4.iii J4.iv
Structured examiner prompts 9
  1. How does critical illness predispose to stress ulcer formation?
    J1.iiJ4.i
  2. Why are Proton Pump Inhibitors used for prevention (of stress ulcer formation)?
    J4.i
  3. What are the adverse consequences of PPI administration?
    J4.iB3.i
  4. What are the mechanisms responsible for a rising urea after an upper GI bleed?
    J1.viE1.v
  5. Why may we use terlipressin to assist in the management of variceal bleeding?
    L2.vJ4.iv
  6. What’s the mechanism of nausea due to a large volume UGI bleed
    J1.iv
  7. Why would you use metoclopramide for this patient?
    J4.iiJ4.iii
  8. How does erythromycin differ as a prokinetic to metoclopramide?
    J4.iii
  9. How does lactulose assist in liver disease?
    J4.iv
Official source: 2026A CICM Examiner Report · page 18

2026A

VIVA 4

Nutrition, Metabolism and Endocrine Physiology and Pharmacology
61.5%Successful candidates
10.23Borderline regression pass mark
11.11Average mark
16.50Highest mark
Opening question
Explain the metabolic response to prolonged fasting (>16 hours).
Current · V5 (2025) K1.iii · primary B3.iii L1.ii L2.iii L2.iv
Structured examiner prompts 8
  1. Explain the metabolic response to prolonged fasting (>16 hours).
    K1.iiiL1.ii
  2. How might the response to fasting differ in a neonate?
    B3.iiiK1.iii
  3. By what mechanism might a non-selective beta-blocker cause hypoglyaemia in a neonate?
    D7.iiiB3.iiiL1.ii
  4. How will the administration of IV adrenaline alter glucose homeostasis?
    D7.iL1.ii
  5. Following a period of starvation, why do electrolytes become deranged with reintroduction of calories?
    K1.iiiF1.v
  6. Explain the physiological consequences of an absence of insulin?
    L1.ii
  7. How is insulin modified so as to alter its duration of action?
    L2.iii
  8. Describe the pharmacodynamic effects of exogenous glucagon.
    L2.iv
Official source: 2026A CICM Examiner Report · page 19

2026A

VIVA 5

Cardiovascular Physiology and Pharmacology
42.3%Successful candidates
10.56Borderline regression pass mark
10.05Average mark
15.50Highest mark
Opening question
Explain the effect of high serum potassium on the ventricular action potential?
Current · V5 (2025) D2.i · primary D6.i D7.iv F1.v
Structured examiner prompts 6
  1. Explain the effect of high serum potassium on the ventricular action potential?
    D2.iF1.v
  2. How is the SA node action potential changed by high serum potassium?
    D2.iF1.v
  3. Relate those changes in the action potential to the changes on the ECG (in hyperK)?
    D6.iD2.iF1.v
  4. How does iv calcium help in this situation?
    F2.iiiF1.v
  5. How does vagal stimulation affect the action potential?
    D2.iH3.iv
  6. How is digoxin toxicity affected by serum potassium level?
    D7.ivF1.v
Official source: 2026A CICM Examiner Report · page 19

2026A

VIVA 6

Pain Physiology and Pharmacology of Local Anaesthetics
63.5%Successful candidates
11.74Borderline regression pass mark
13.05Average mark
17.50Highest mark
Opening question
Describe how a peripheral noxious stimulus is detected and transmitted to the level of the spinal cord.
Current · V5 (2025) H4.i · primary D7.iv H2.v H6.ii Q.i
Structured examiner prompts 10
  1. Describe how a peripheral noxious stimulus is detected and transmitted to the level of the spinal cord.
    H4.i
  2. How is this signal transmitted in the spinal cord?
    H4.i
  3. How can descending pathways from the brain modulate this signal?
    H4.i
  4. The skin around a wound can become abnormally painful. Explain this hyperalgesia and allodynia?
    H4.i
  5. What is the mechanism of action of lignocaine?
    H6.ii
  6. Why are some nerve fibres more susceptible to local anaesthetics?
    H2.vH6.ii
  7. Describe properties of local anaesthetics that determine their onset and duration of action? Can you give some examples?
    H6.iiB1.iiB1.iv
  8. IV Lignocaine can be used to treat arrhythmias. Why do we use lignocaine and not bupivacaine?
    H6.iiD7.iv
  9. What are the cardiovascular features of local anaesthetic systemic toxicity (LAST)?
    H6.ii
  10. What is the antidote for LAST and how does it work?
    Q.iH6.ii
Official source: 2026A CICM Examiner Report · page 19

2026A

VIVA 7

Pharmacokinetics Relevant to ICU
61.5%Successful candidates
11.89Borderline regression pass mark
12.66Average mark
18.00Highest mark
Opening question
The ICU pharmacist tells you that your patient’s phenytoin level is low. Explain why this might happen?
Current · V5 (2025) B1.vi · primary B1.vii B1.viii H6.i H6.iii H6.vi
Structured examiner prompts 8
  1. The ICU pharmacist tells you that your patient’s phenytoin level is low. Explain why this might happen?
    B1.viiiB3.iiiH6.vi
  2. You provide a small dose increase, and the patent demonstrates phenytoin toxicity. Why might this have occurred?
    H6.viB1.iv
  3. Why is a loading dose used for phenytoin to treat seizures?
    B1.iiiH6.vi
  4. Explain the toxic effects of phenytoin relevant to use in the ICU?
    H6.vi
  5. A patient has been on a 3-day infusion of propofol and fentanyl. Explain what happens to the plasma concentrations after the infusions are ceased?
    B1.viB1.viiH6.iH6.iii
  6. What is CSHT and what factors influence fentanyl’s?
    B1.viH6.iii
  7. How does context-sensitive half time differ from elimination half-life, and which is more clinically useful in ICU?
    B1.vi
  8. Explain strategies to mitigate fentanyl’s long CSHT in ICU.
    B1.viH6.iii
Official source: 2026A CICM Examiner Report · page 20

2026A

VIVA 8

Microbial Physiology and Antimicrobial Pharmacology
71.2%Successful candidates
12.20Borderline regression pass mark
13.37Average mark
17.50Highest mark
Opening question
Explain why a continuous infusion of meropenem may be more effective than regular intermittent dosing?
Current · V5 (2025) O2.i · primary B1.vii B3.iii O1.i O2.ii
Structured examiner prompts 10
  1. Explain why a continuous infusion of meropenem may be more effective than regular intermittent dosing?
    B1.viiO2.i
  2. In critical illness we risk underdosing meropenem. Explain what patient and drug factors lead to this.
    B3.iiiO2.i
  3. Why don’t we give gentamicin as a continuous infusion?
    B1.viiO2.i
  4. How are the spectrums of activity different between gentamicin and meropenem?
    O2.i
  5. This is a gram stain (Gram -ve Bacilli image provided). What class of bacteria is demonstrated and why is it that colour?
    O1.i
  6. This organism was cultured from a patient’s urine. Name 4 likely organisms?
    O1.i
  7. This organism is resistant to amoxicillin but is sensitive to meropenem. How is meropenem active over a broader range of bacteria in comparison to amoxicillin?
    O2.iO2.ii
  8. Describe other mechanisms that bacteria may use to evade antibiotics with common examples?
    O2.ii
  9. How can you make an antibiotic more effective if resistance is starting to develop?
    O2.ii
  10. How does the addition of clavulanic acid change the spectrum of amoxicillin?
    O2.iiO2.i
Official source: 2026A CICM Examiner Report · page 20