CICM Second Part Exam Practice SAQs 08102020

As prepared by Chris Nickson, here are the practice written questions from a recent CICM Second Part exam practice session at The Alfred ICU, with recommended reading from Critical Care Compendium and other FOAM sources:


Discuss vasoplegia in ICU patients, including the underlying mechanisms and consideration of treatment options. (100%)

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Possible approach to answering this very big question:



  • No consensus definition
  • Characterised by
    • Decreased SVR
    • due to arteriolar dilatation
    • due to decreased vascular smooth muscle (VSM) constriction
    • normal or hyperdynamic cardiac function (however cardiac dysfunction can co-exist with vasoplegia)
  • May or may not involve vasoplegic shock (distributive shock), characterised by hyperfusion (high lactate carries worse prognosis)
  • Often associated with relative hypovolaemia from increased venous capacitance and capillary leak
  • Has multifactorial causes, is common in ICU, and is associated with morbidity and mortality


  • Contractile state of VSM is primarily determined by intracellular calcium, which is affected by ATP-sensitive K channels that determine depolarisation state
  • Factors affecting vascular smooth muscle contractility are:
      • Sympathetic nervous system
      • Endocrine
        • Glucocorticoids
        • Catecholamines
        • Thyroid hormones
        • Vasopressin
      • Endothelial secretions
        • NO
        • PGI2
        • ET1
      • Metabolites
        • Acidemia
        • Hypoxia
        • ROS
      • Autacoids
        • 5HT
        • Prostaglandins
        • TXA2
  • These processes are dysregulated in pathological states by cytokine cascades triggered by DAMPS (damage-associated molecular patterns, e.g. HSPs, nucleic acids) and PAMPS (pathogen-associated molecular patters, e.g. LPS) that bind PRR (pattern recognition receptors, e.g. Toll-like receptors), as well as other mechanisms PAMPS – sepsis
    • PAMPS and DAMPS – post-op, post-bypass, post-arrest, transfusion, pancreatitis
    • DAMPS – burns, trauma, any other cause of shock
    • Other – GA, epidural, neurogenic, anaphylaxis, vasodilatory drugs and toxins


  • Seek and treat underlying cause
    • E.g. antibiotics for infection, stop vasodilatory drugs
  • Determine appropriate MAP target
    • E.g. >65 mmHg for septic shock (SSC guidelines) and most patients
    • Can individualise to patient (but evidence lacking)
      • E.g. tolerate MAP >60 if no shock, otherwise well and likely short-lived cause to prevent SEs/ complications of vasopressors
      • E.g. higher DBP target if known CAD to ensure coronary perfusion
      • E.g. MAP 80 may be preferred in neurogenic shock from spinal cord injury
  • Correct hypovolaemia and metabolic state
    • E.g. up to 30 mL/kg IBW for septic shock
    • Consider HCO3/ RRT for severe acidemia (controversial, unclear thresholds)
    • O2 therapy to targt SpO2 92-96% in most patients
    • Thiamine if suspected deficiency or hyperlactemia
    • Calcium if hypocalcemia
  • Noradrenaline is usual first line agent (e.g. supported by SSC guidelines)
    • Alpha >> beta effects
      • Increased SVR -> increased DBP & MAP, drives perfusion
      • Increased venous tone -> preload
    • If possible, avoid:
      • pure alpha agonists (e.g. phenylephrine, midodrine, metaraminol)
        • Worse outcomes in septic shock
        • Less “ventriculo-arterial matching”
        • Acceptable if low dose, likely short-term, and cause is pure vasodilation (e.g. peri-operative)
      • Epinephrine
        • Increased lactate and heart rate
        • Acceptable alternative in low resource settings or inotropic effect required
      • Dopamine
        • Increased dysrhythmias
  • Second line agents are vasopressin and hydrocortisone
    • Useful if:
      • Apparent catecholamine resistance
      • Avoid side effects of high dose single agent (e.g. catecholamines)
    • Vasopressin
      • Early use may be beneficial in some settings (e.g. VANCS trial for cardiac surgery; if coexistent pulmonary hypertension as has less pulmonary vascular constriction) but unclear evidence in septic shock
    • Hydrocortisone
      • Likely decreases NO/ NOS in VSM
      • ADRENAL study showed decreased vasopressor duration in septic shock
  • Refractory vasoplegia
    • Exclude/ treat other causes of shock
    • Consider “NO antagonists” (improve vasoplegia but evidence is lacking for improved outcomes)
      • Methylene blue (CI: serotonin syndrome, G6PD deficiency)
      • Hydroxcobalamin
  • Future/ experimental agents include:
    • Angiotensin (ATHOS3 trial)
    • Ascorbic acid
    • Adrenomedullin


Outline the specific therapies used in the management of:

a) phaeochromocytoma (25%)

b) myxoedema coma (25%)

c) hypercalcaemia (25%)

d) carcinoid syndrome (25%)

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(a) List the thresholds for platelet transfusion in ICU patients (30%)

(b) Describe and interpret this non-contrast CT head image (20%)

c) Suggest a cause of the hemostatic abnormailty, and appropriate therapy, for each of the TEG profiles a) to f) shown below:  (50%)

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You can access all the previous practice questions since 2014 here:
See this link on INTENSIVE for exam resources:

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