Is the ICU Fellowship (CICM) library medical advice?

No. Content is educational examination preparation with cited sources. It is not a substitute for clinical judgement or local guidelines.

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Browse topics, short-answer / written formats, cases, and vivas under /s/icu.

Fellowship exam preparation

ICU Fellowship (CICM)

The Australian College of Intensive Care Medicine Fellowship — written SAQs and an oral of hot cases and cross-table vivas. Every claim anchored to a PubMed-verified source.

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Intensive care bedside with ventilator and monitors — Plate — fellowship exam preparationMedVellum Press

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Four ways through ICU — one evidence base.

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Curriculum domains with PubMed-verified evidence.

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SAQs

Second- and First-Part SAQs with model answers.

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Cases

Long case, short case, and bedside hot case.

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Vivas

Data, imaging, equipment, and communication vivas.

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★ High yield

GI & nutrition / surgical

Abdominal Sepsis & Peritonitis — Source Control, SBP & the Polymicrobial

The peritonitis is the inflammation of the peritoneum, usually from the intra-abdominal infection; the abdominal sepsis is the sepsis from the intra-abdominal source. The three types: the primary (the spontaneous bacterial peritonitis — the SBP in the cirrhosis and the ascites, the monomicrobial, the ascitic PMN over 250 cells per cubic mm, the cefotaxime plus the albumin), the secondary (the GI perforation or the ischaemia, the polymicrobial — the Gram-negative and the anaerobes, the source control plus the antibiotics), and the tertiary (the persistent or the recurrent after 48 hours of the failed initial treatment, the resistant — the Enterococcus, the Candida, the MDR organisms). The diagnosis: the peritonism (the rigid abdomen, the guarding, the rebound), the CT (the gold standard — the free gas, the fluid, the source), the lactate, the cultures. The management: the Sepsis-6 bundle, the broad antibiotics (the piperacillin-tazobactam ± the vancomycin ± the antifungal, or the ceftriaxone plus the metronidazole or the meropenem), the duration 4 to 7 days after the source control, and the SOURCE CONTROL (the surgery or the IR — the drainage, the debridement, the repair) — the definitive; the delayed source control worsens the mortality.

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★ High yield

Trauma

Abdominal Trauma — Blunt, Penetrating, FAST & Non-Operative Management

The abdominal trauma: the blunt (the solid organ — the spleen, the liver; the hollow viscus — the small bowel, the colon; the mesenteric) and the penetrating (the stab, the gunshot). The FAST scan (the bedside — the free fluid in the 4 views) — the rapid triage. The CT with the IV contrast (the stable patient — the grading). The laparotomy indications: the peritonitis, the hypotension unresponsive, the penetrating with the peritonitis, the evisceration. The non-operative management (the NOM) for the blunt solid organ (the spleen, the liver) if the haemodynamically stable. The angioembolisation for the contrast extravasation (the blush). The damage-control laparotomy (the physiological extremis — the open abdomen, the packing, the planned re-operation).

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Environmental emergencies

Accidental Hypothermia

The accidental hypothermia — the core below 35 degrees C. The severity (the mild 32 to 35, the moderate 28 to 32, the severe below 28). The clinical (the shivering → the bradycardia, the decreased the LOC, the loss of shivering, the Osborn / J waves, the VF / the asystole). The rewarming (the passive, the active the external, the active the internal — the ECMO for the severe). The handle gently (the cold heart irritable). The NOT the dead until the warm and the dead. The drugs the extended intervals (the below 30).

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★ High yield

Renal/Metabolic

Acid-base disorders in the ICU

Acid-base interpretation is fundamental to ICU practice. Use a disciplined 9-step algorithm: (1) pH (acidaemia/alkalaemia); (2) primary process (PaCO2 vs HCO3); (3) expected compensation (Winter formula); (4) A-a gradient; (5) anion gap (albumin-corrected); (6) delta gap; (7) osmolar gap; (8) lactate; (9) clinical correlation. High-AG acidosis = GOLDMARK (glycols, oxoproline, L- and D-lactate, methanol, aspirin, renal failure, ketoacidosis). Normal-AG = hyperchloraemic (diarrhoea, RTA, saline). Metabolic alkalosis: urine chloride separates saline-responsive from resistant. Chronic respiratory acidosis: classic rules have HCO3 rising 3.5 mmol/L per 10 mmHg; human COPD data suggest more. Treat the cause, not the number — BICAR-ICU found no overall benefit from sodium bicarbonate in severe acidaemia (pH at or under 7.20) with more hypernatraemia and metabolic alkalosis, though the AKI subgroup fared better.

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★ High yield

Acid–base

Acid–Base Physiology and Blood-Gas Interpretation

Acid–base homeostasis is the chemistry of the hydrogen ion, and its disturbances are among the commonest and most informative derangements in critical illness. This topic builds the examiner's framework on four ideas. First, the physiology — the bicarbonate buffer system described by Henderson and Hasselbalch, and the more complete Stewart view in which pH is set by the carbon dioxide tension, the strong ion difference (largely sodium minus chloride) and the total concentration of weak acids (albumin and phosphate). Second, a systematic method for reading a blood gas — the pH, the pattern (metabolic versus respiratory), the appropriateness of compensation, the anion gap and the delta-delta, and the osmolar gap when a toxin is suspected. Third, the clinical disorders — the high anion-gap and normal anion-gap acidoses (lactic acidosis, ketoacidosis, the toxic alcohols, and renal tubular acidosis), the metabolic alkaloses, and the respiratory acid–base disturbances. Fourth, the evidence that has reshaped management — the SMART and SALT-ED trials showing balanced crystalloids modestly outperform saline, BICAR-ICU showing bicarbonate confers no overall benefit in severe acidaemia (with a signal in the acute-kidney-injury subgroup), and the principles of treating the cause rather than the number. Built entirely on these verified landmark trials.

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Cardiovascular

Acute aortic dissection and acute aortic syndrome

Acute aortic dissection is a tear in the aortic intima allowing blood to enter the media, creating a false lumen. Stanford classification: Type A involves the ascending aorta (surgical emergency — mortality 1-2%/h, surgical repair). Type B involves only the descending aorta (medical management — BP control, TEVAR for complicated). Presentation: tearing chest/back pain, pulse deficit, BP differential (20 mmHg between arms), widened mediastinum on CXR, new aortic regurgitation murmur, neurological deficit, syncope. Diagnosis: CT angiography (gold standard — intimal flap, true/false lumen), transoesophageal echo in the unstable patient, CXR widened mediastinum as a clue. Management: Type A = emergency surgery (BP control first — beta-blocker before vasodilator, target SBP 100-120 HR 60-80); Type B = medical (IV beta-blocker first — labetalol/esmolol — reduce dP/dt, target SBP 100-120), TEVAR if complicated (malperfusion, rupture, rapid expansion — ADSORB/INSTEAD trials). Acute aortic syndrome also includes intramural haematoma (IMH) and penetrating atherosclerotic ulcer (PAU). Complications: malperfusion (coronary/cerebral/mesenteric/renal/spinal), cardiac tamponade, rupture. DeBakey classification refines anatomy (I = ascending + beyond, II = ascending only, III = descending only).

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Topics carry the clinical spine. SAQs, cases, and vivas force the same knowledge into the formats you will sit. Claims are written for examiners — and cited for trust.

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