Intensive Care Medicine Flashcards

A 58-year-old patient with septic shock is on norepinephrine 0.4 mcg/kg/min. Despite adequate fluid resuscitation, MAP remains 58 mmHg. Vasopressin is added at 0.03 U/min. Four hours later, the patient develops digital ischaemia and worsening lactic acidosis. Which pathophysiological mechanism best explains the refractory vasodilatory shock in this context?

Answer: Excessive nitric oxide synthase activation leading to cyclic GMP-mediated vascular smooth muscle relaxation unresponsive to vasopressors

In refractory vasodilatory shock, excessive inducible nitric oxide synthase (iNOS) activation — driven by cytokines — produces massive nitric oxide (NO) accumulation. NO activates guanylate cyclase, raising intracellular cGMP, which activates protein kinase G to phosphorylate myosin light-chain kinase and opens ATP-sensitive K⁺ channels, causing profound vascular smooth muscle relaxation. This mechanism can become refractory to both catecholamines and vasopressin. While relative adrenal insufficiency (option A) is a recognised complication of sepsis, it does not directly explain the primary refractory mechanism. V1a downregulation (option B) is not a well-established clinical phenomenon at standard vasopressin doses. Option D describes a different clinical entity.

During prone positioning of a patient with severe ARDS (P/F ratio 68), the ICU team notes that after 16 hours prone, oxygenation has improved (P/F 180) but the patient develops a new pressure injury over the right cheek and anterior superior iliac spine. Repositioning to supine is being considered. According to current evidence, which statement regarding proning duration and outcomes is MOST accurate?

Answer: Prone positioning reduces 28-day mortality primarily by homogenising ventilation-perfusion matching and reducing ventilator-induced lung injury

The PROSEVA trial demonstrated a 28-day mortality benefit of prolonged prone positioning (≥16 hours/session) in severe ARDS. The mechanism is dual: prone positioning redistributes perfusion more uniformly, reducing V/Q mismatch, and critically, it homogenises tidal volume distribution — reducing overdistension of dorsal (previously non-dependent) units and recruiting previously dependent (dorsal) atelectatic regions. This homogenisation reduces cyclic atelectrauma and stress/strain heterogeneity, directly mitigating VILI. Option A is incorrect — shorter sessions have not demonstrated non-inferiority. Option B describes the PROSEVA discontinuation criterion but does not explain the mechanism of mortality reduction. Option D is not evidence-based; multiple prone cycles are often required.

A 44-year-old woman is admitted to the ICU following a witnessed out-of-hospital cardiac arrest (OHCA) with an initial shockable rhythm. ROSC was achieved after 18 minutes. She is comatose and is commenced on targeted temperature management (TTM) at 36°C. On Day 2, EEG shows burst suppression with a suppression ratio of 75%. Which prognostication approach is most consistent with current ERC-ESICM guidelines for post-cardiac arrest care?

Answer: Prognostication should be deferred until at least 72 hours after normothermia is achieved, combining multimodal assessment including clinical, electrophysiological, biochemical, and neuroimaging findings

ERC-ESICM guidelines (2021) mandate a multimodal prognostication strategy, with no single test sufficient for a poor outcome prediction. Crucially, prognostication must be delayed until at least 72 hours after return to normothermia to mitigate the confounding effects of TTM, sedation, and metabolic disturbances. The recommended multimodal approach combines: (1) clinical examination (pupillary and corneal reflexes, motor response), (2) EEG (presence/absence of background continuity, reactivity), (3) SSEPs (bilateral absent N20), (4) serum biomarkers (NSE at 48–72h with lab-specific cut-offs), and (5) neuroimaging (CT/MRI for grey-white matter ratio or DWI changes). Burst suppression alone (option A) is not sufficient. Absent N20 at 24h (option C) is too early and must be part of a multimodal assessment. NSE alone (option D) is not a standalone predictor.

A 67-year-old man with known cirrhosis (Child-Pugh C) is admitted with hepatorenal syndrome type 1 (HRS-AKI). Serum creatinine has risen from 88 to 320 µmol/L over 48 hours despite 1.5 g/kg/day albumin infusion for 48 hours and discontinuation of diuretics. Which pharmacological treatment has the strongest evidence for improving short-term renal function and acting as a bridge to liver transplantation in this scenario?

Answer: Terlipressin plus albumin (goal: MAP increase ≥10 mmHg)

Terlipressin — a synthetic vasopressin analogue with preferential V1a receptor agonism on splanchnic vasculature — in combination with albumin is the most robustly evidence-based treatment for HRS-AKI (type 1). Multiple RCTs and meta-analyses, including the CONFIRM trial (2021), demonstrated that terlipressin + albumin significantly improves renal function reversal (defined as creatinine <133 µmol/L) and is superior to placebo + albumin. The mechanism involves splanchnic vasoconstriction, reducing portal hypertension-driven systemic vasodilation, restoring effective circulating volume, and improving renal perfusion pressure. Norepinephrine (option B) is an acceptable alternative in ICU but has weaker evidence. Midodrine + octreotide (option C) has modest evidence, primarily in less severe HRS, and is not first-line for HRS-AKI. N-acetylcysteine (option D) has no established role in HRS-AKI.

A 52-year-old ICU patient on mechanical ventilation develops refractory hypoxaemia. High-resolution CT shows diffuse bilateral ground-glass opacities. Bronchoalveolar lavage reveals haemosiderin-laden macrophages (>20%), and serum anti-GBM antibodies are positive. Renal function shows creatinine 380 µmol/L with red cell casts on urinalysis. Which combination of treatments is MOST appropriate as immediate induction therapy?

Answer: High-dose methylprednisolone, cyclophosphamide, and urgent plasmapheresis

Anti-GBM disease (Goodpasture syndrome) with both pulmonary haemorrhage and rapidly progressive glomerulonephritis (RPGN) requires immediate aggressive immunosuppression and plasmapheresis. The standard induction regimen is: (1) high-dose methylprednisolone (1g/day IV × 3 days, then oral prednisolone), (2) oral cyclophosphamide (2 mg/kg/day), and (3) daily plasmapheresis (4L exchanges with FFP or albumin) for 14 days or until anti-GBM antibodies are undetectable. Plasmapheresis is critical as it rapidly removes circulating pathogenic anti-GBM antibodies. In pulmonary haemorrhage, FFP is preferred over albumin replacement during plasmapheresis to replete clotting factors. Rituximab (option B) has no established evidence in anti-GBM disease and monotherapy is inappropriate given the severity. MMF (option C) is not used in anti-GBM induction — cyclophosphamide is standard. IVIG (option D) has no role in this condition.

A 70-year-old patient with New York Heart Association Class III heart failure (EF 25%) develops cardiogenic shock with a cardiac index of 1.6 L/min/m² and a pulmonary capillary wedge pressure of 28 mmHg. Dopamine is started at 10 mcg/kg/min. Six hours later, the patient develops new atrial fibrillation with rapid ventricular response and the cardiac index drops to 1.3 L/min/m². Which statement about the use of dopamine in cardiogenic shock is MOST consistent with current evidence and pharmacology?

Answer: Dopamine at >5 mcg/kg/min has a predominantly alpha-1 adrenergic effect, and its beta-1 activity increases myocardial oxygen demand, predisposing to arrhythmias — switching to norepinephrine reduces arrhythmia risk

The SOAP II trial (De Backer et al., NEJM 2010) demonstrated that dopamine — compared to norepinephrine — was associated with a significantly higher rate of arrhythmic events (primarily atrial fibrillation) in patients with cardiogenic shock. At doses >5–10 mcg/kg/min, dopamine has prominent beta-1 adrenergic effects that increase heart rate and myocardial oxygen demand, and also stimulates norepinephrine release from sympathetic terminals. This combination predisposes to tachyarrhythmias. Current guidelines (ESC 2021) recommend norepinephrine over dopamine in cardiogenic shock due to lower arrhythmia risk. Option B is incorrect — 'renal dose' dopaminergic effects are physiologically negligible at 10 mcg/kg/min relative to adrenergic activity. Option C is dangerous — escalating dopamine in the context of new AF would worsen haemodynamic compromise. Option D ignores the causative pharmacological relationship.