Critically evaluate the respiratory and cardiovascular data below, link it with appropriate pathophysiology and discuss the current ICU management, and specifically consider the patient’s experience

Sample Answer

NCL+ Intensive Care Qualification in Specialism

Level 6, Module 1, Assessment 1 – Clinical Scenario

Critical evaluation of respiratory and cardiovascular data, linked pathophysiology and current ICU management (≈1,150–1,220 words)

Brief clinical picture

A 53-year-old, previously well runner collapsed in A&E after a marathon and is now post–return of spontaneous circulation (ROSC) in ICU. Key problems are: mixed acidosis (pH 7.25; PaCO₂ 6.1 kPa; HCO₃⁻ 17 mmol/L; lactate 5.6 mmol/L), hyperkalaemia (K⁺ 6.0 mmol/L), acute kidney injury with very low urine output and tea-coloured urine (suggesting rhabdomyolysis; CK 6100 IU/L, creatinine 201 µmol/L, urea 21 mmol/L), mild thrombocytopenia (platelets 110 × 10⁹/L), hypomagnesaemia (0.6 mmol/L), and ongoing circulatory malperfusion despite numerically acceptable arterial pressure. These findings fit with post-cardiac arrest syndrome plus exertional rhabdomyolysis and pre-renal/ pigment-induced AKI.

Respiratory assessment and pathophysiology

Ventilation/oxygenation. She is on CMV-VC, FiO₂ 0.4, Vₜ 300 mL, RR 20, minute ventilation 6 L/min, PEEP 10 cmH₂O, PIP 16–18 cmH₂O, SpO₂ 99%, PaO₂ 18 kPa. Compliance appears good (low PIP at a PEEP of 10). Oxygenation is more than adequate on 40% oxygen.

Acid–base/PaCO₂. The blood gas shows acidaemia from a mixed disturbance: (1) metabolic acidosis (low HCO₃⁻, raised lactate) and (2) respiratory acidosis (PaCO₂ 6.1 kPa) from insufficient alveolar ventilation relative to metabolic demand. In post-arrest and rhabdomyolysis, lactate rises due to global tissue hypoperfusion and β-adrenergic stimulation; adrenaline can also augment lactate production.

Lung-protective settings. For a 160 cm woman, predicted body weight ≈52 kg; current Vₜ 300 mL is ~5.7 mL/kg, appropriately lung-protective. With PIP <20 and normal oxygenation, there is room to increase minute ventilation safely, preferably by gently raising RR (e.g., toward 22–24) while keeping an eye on auto-PEEP and ensuring plateau pressure remains <30 cmH₂O. This aims to bring PaCO₂ toward ~4.5–5.5 kPa and reduce respiratory contribution to the acidaemia. FiO₂ may be titrated down (e.g., to 0.3–0.35) if SpO₂ and PaO₂ remain well within target, to minimise oxygen toxicity risk. PEEP of 10 is reasonable post-arrest to counter atelectasis; if haemodynamics permit and gas exchange stays stable, a careful step-down to 8 could be tested.