AS7.1-5 | Intensive Care Management — Graded Quiz

Correct. The closed-model ICU, where a dedicated intensivist team manages all aspects of critical illness rather than separate subspecialists handling individual organs, consistently demonstrates better outcomes. The key advantage is simultaneous management of multiorgan interactions (e.g., managing the interplay between ventilator settings, haemodynamic support, and renal perfusion in one decision-making framework).

Closed-model ICU (dedicated intensivist, multidisciplinary team) reduces ICU mortality vs open/consultative model. The benefit is integrative, simultaneous multiorgan management — a single team that sees the whole patient, not individual organ-specific consultants.

Incorrect. The evidence base for dedicated ICU teams centres on the closed-model versus open-model comparison, showing reduced mortality with 24-hour intensivist on-site cover and integrated multidisciplinary management. It is the simultaneous management of multiorgan interactions — not pharmacological knowledge or investigation costs — that is the mechanistic advantage.

Correct. COPD with acute hypercapnoeic respiratory failure (pH 7.22, confused, PaCO2 78) meets ICU admission criteria for respiratory support. However, the advance directive must be respected. The appropriate response is ICU admission for a time-limited trial of NIV — a non-invasive intervention that does not violate the DNIV directive — with the agreement that if NIV fails and the patient deteriorates, invasive ventilation will not be escalated. This balances the reversibility of the acute exacerbation against patient autonomy.

ICU triage integrates clinical criteria (acute organ failure, reversibility) with patient goals of care. An advance directive limits the ceiling of treatment, not the floor — a DNIV patient may still benefit from and be admitted for NIV as a time-limited trial.

Incorrect. Confusion from hypercapnoea does not invalidate a previously stated advance directive. Refusing ICU admission entirely ignores the potential reversibility with NIV. The discharge option is dangerously under-escalated for a patient with pH 7.22 and GCS 12.

Correct. GCS 10 with eye opening to voice, purposeful movement (localising, M5), and apparent awareness in an overdose patient who is now 48 hours post-ingestion represents meaningful neurological recovery. The emergence from sedation combined with agitation towards the ETT is a strong cue to reassess the need for mechanical ventilation. If oxygenation, ventilatory effort, haemodynamics, and airway reflexes are adequate, a spontaneous breathing trial should be performed and extubation planned rather than resuming deep sedation.

Daily sedation holds and spontaneous breathing trials (SBT) are the standard approach to minimise ventilator days. Agitation towards the ETT in a recovering patient is a signal to assess extubation readiness, not an indication for more sedation.

Incorrect. Re-sedating an improving overdose patient delays extubation and increases ventilator-associated complications. Physical restraint without addressing the root cause (unnecessary intubation) is not appropriate. A CT brain is not indicated without neurological signs or trauma history in a drug overdose with improving GCS.

Correct. The relationship between peak and plateau pressure diagnoses the site of the problem: high Ppeak WITH high Pplat = reduced lung/chest wall compliance (ARDS, pneumothorax, pleural effusion, abdominal distension, main stem intubation). High Ppeak WITH normal Pplat = increased airway resistance (bronchospasm, secretions, kinked ETT). Pplat >30 cmH2O mandates tidal volume reduction (target 4–6 mL/kg IBW) to prevent barotrauma.

Peak pressure = resistance + compliance components. Plateau pressure (end-inspiratory pause) isolates compliance. Pplat >30 cmH2O = barotrauma risk; reduce tidal volume and investigate lung/chest wall compliance causes immediately.

Incorrect. The key is the Ppeak–Pplat relationship: if Pplat is also high (>30 cmH2O), the problem is compliance, not resistance. Bronchodilators address airway resistance. A Pplat of 38 cmH2O is dangerously high and requires immediate tidal volume reduction and compliance investigation.

Correct. In cardiogenic shock, low cardiac output means tissues extract more oxygen from the blood (as delivery falls), resulting in a low ScvO2 (<65% is abnormal; <50% is severely depressed). The combination of low MAP, low ScvO2, and high lactate despite inotropic support indicates severely impaired oxygen delivery from pump failure. Normal ScvO2 is 65–70%; in distributive (septic) shock it may be paradoxically high (>75%) due to peripheral shunting.

ScvO2 interprets oxygen delivery–demand balance: low (<65%) = high extraction = low output or high demand; high (>75%) in shock = distributive (septic) with impaired extraction. Post-MI cardiogenic shock classically shows low ScvO2 + high lactate.

Incorrect. Distributive shock has high ScvO2 (peripheral shunting prevents extraction), not low. Hypovolaemia alone does not explain the clinical context of post-MI cardiogenic shock with the observed ScvO2 pattern. Normal ScvO2 in compensated heart failure is >65%.

Correct. In obstructive airways disease (asthma, COPD), the expiratory phase is prolonged. When the ventilator delivers the next breath before expiration is complete, gas is trapped, generating auto-PEEP (intrinsic PEEP). This is diagnosed by the flow-time waveform not returning to zero. Consequences: hyperinflation, increased plateau pressure, reduced venous return, and risk of barotrauma. Management: reduce respiratory rate (allow more time for expiration), increase the I:E ratio (longer expiratory time), consider permissive hypercapnoea.

Auto-PEEP in obstructive disease: diagnose by expiratory flow not returning to zero between breaths. Treat by reducing respiratory rate and extending expiratory time (adjust I:E ratio). Permissive hypercapnoea is acceptable to avoid barotrauma in severe asthma.

Incorrect. VILI is not directly diagnosed from the flow waveform. PE causes oxygenation failure and elevated capnograph gradient, not a characteristic expiratory flow pattern. Cuff leak presents as tidal volume discrepancy and audible leak, not expiratory flow pattern.

Correct. A sudden unexplained fall in EtCO2 in a ventilated patient with unchanged ventilator settings should trigger urgent consideration of a large pulmonary embolism. PE causes acute obstruction of pulmonary arteries, converting previously perfused alveoli into dead space (ventilated but no longer perfused). CO2 is no longer washed out from the affected lung regions, so EtCO2 drops even as SpO2 may remain transiently preserved by unaffected lung. This widened PaCO2–EtCO2 gradient (normally <5 mmHg) is the haemodynamic monitoring signature of acute dead-space increase.

Sudden unexplained EtCO2 drop in a ventilated patient = PE until proven otherwise. Mechanism: acute dead-space from pulmonary arterial obstruction widens the PaCO2–EtCO2 gradient. Confirm with ABG (increased PaCO2–EtCO2 gradient) and CT pulmonary angiogram.

Incorrect. Oesophageal intubation would show EtCO2 near zero from the start (or a rapid decay), not a sudden drop in a previously stable ventilated patient, and SpO2 would fall quickly. Hypoventilation raises EtCO2, not lowers it. Metabolic acidosis causes compensatory hyperventilation, which can lower EtCO2, but not as an abrupt isolated drop.

Correct. While the GCS 8-or-below rule is a general threshold, clinical context overrides rigid thresholds. Hepatic encephalopathy Grade III routinely progresses rapidly to Grade IV (deep coma, completely unresponsive). Acute liver failure patients are coagulopathic, making emergency intubation in the context of vomiting and aspiration extremely hazardous. The standard recommendation is to intubate electively at Grade III before deterioration, not wait for Grade IV emergency conditions.

In hepatic encephalopathy, elective intubation at Grade III is preferred over waiting for Grade IV — because deterioration is rapid, coagulopathy makes emergency intubation high-risk, and the GCS 8 threshold is a guideline, not an absolute cutpoint. Always integrate trajectory and context.

Incorrect. The GCS 8-threshold is a guide, not an absolute law — clinical trajectory and context are paramount. In a patient with acute liver failure, waiting for GCS to fall further before securing the airway risks a dangerous emergency intubation. A supraglottic airway is not a definitive airway in a patient at high aspiration risk.

Correct. ICU admission criteria exist precisely to allocate a scarce, expensive, and potentially harmful resource (invasive monitoring, nosocomial infection risk, ICU psychosis) to those who will benefit most. Criteria include: actual or threatened single/multiorgan failure, monitoring needs that cannot be met elsewhere, or specific interventions only available in the ICU. Physiologically stable post-operative patients who can be managed on surgical wards or high-dependency units should not occupy ICU beds.

ICU triage is ethically and clinically guided: admit when benefit outweighs risk and the patient meets threshold criteria (organ failure, monitoring need, or ICU-only intervention). Routine prophylactic ICU admission is not supported — it misallocates resources and exposes stable patients to ICU-specific harms.

Incorrect. The argument is clinical, not financial. Stable post-operative patients do not meet organ-failure or monitoring threshold criteria for ICU admission, and ICU admission carries its own risks (nosocomial infections, ICU delirium, resource constraints that disadvantage other critical patients). The guiding principle is benefit-to-harm ratio and evidence-based triage criteria.

Correct. The ABG shows a respiratory acidosis (high PaCO2 58 mmHg, low pH 7.28) with adequate oxygenation (PaO2 88 on FiO2 0.6). The tidal volume is already at lung-protective range (6 mL/kg). The safest way to increase CO2 clearance (minute ventilation = rate × tidal volume) without worsening barotrauma is to increase respiratory rate. Increasing tidal volume would violate lung-protective strategy.

Minute ventilation = rate × tidal volume. To increase CO2 clearance in a patient on lung-protective ventilation (tidal volume already at 6 mL/kg), increase respiratory rate rather than tidal volume. Sodium bicarbonate does not fix respiratory acidosis.

Incorrect. FiO2 increase is not indicated — oxygenation is adequate at PaO2 88 mmHg. Sodium bicarbonate treats metabolic acidosis, not respiratory acidosis (the problem is CO2 retention, not bicarbonate loss). Increasing tidal volume beyond 6 mL/kg IBW violates lung-protective strategy and risks barotrauma/volutrauma.