Respiratory and Thoracic Anesthesia Flashcards

During one-lung ventilation (OLV) for a right pneumonectomy, the patient develops severe hypoxaemia (SpO₂ 78%) despite 100% FiO₂ and PEEP 5 cmH₂O to the dependent lung. Which intervention is MOST likely to improve oxygenation without compromising the surgical field?

Answer: Apply continuous positive airway pressure (CPAP) of 2–5 cmH₂O to the non-dependent (operative) lung

Low-level CPAP (2–5 cmH₂O) applied to the non-dependent operative lung recruits alveoli and allows passive oxygenation across a partially distended lung without full re-expansion, substantially reducing shunt fraction while keeping the surgical field acceptable. Increasing tidal volume risks ventilator-induced lung injury in the dependent lung. HFJV to the dependent lung is not a standard first-line rescue. PA clamping is a surgical manoeuvre appropriate only at the moment of pneumonectomy, not as an anaesthetic intervention for hypoxaemia.

A 58-year-old man with severe COPD (FEV₁ 28% predicted) undergoes left upper lobectomy via VATS. Postoperatively he develops progressive dyspnoea and hypoxaemia. CT shows a large right-sided air space with contralateral mediastinal shift. His peak airway pressure is 42 cmH₂O. What is the MOST likely diagnosis and its mechanism?

Answer: Dynamic hyperinflation (auto-PEEP) causing bilateral gas trapping and haemodynamic compromise

Severe COPD with markedly reduced FEV₁ produces severe expiratory flow limitation. Post-operatively, increased respiratory drive combined with airflow obstruction leads to breath stacking and auto-PEEP. Bilateral gas trapping raises intrathoracic pressure, compresses mediastinal structures (giving a 'shift' appearance on CT) and impairs venous return. High peak airway pressures (>40 cmH₂O) and the clinical context confirm dynamic hyperinflation. A contralateral bronchial stump leak would be exceptionally rare immediately post-VATS lobectomy. Mucus plugging causes atelectasis, not hyperinflation with raised airway pressures. Post-pneumonectomy pulmonary oedema affects the contralateral lung and is not associated with auto-PEEP.

When using a double-lumen tube (DLT) for OLV, fibreoptic bronchoscopy confirms correct initial placement. After repositioning the patient from supine to lateral decubitus, SpO₂ drops and breath sounds are heard bilaterally but with wheeze. What is the MOST probable cause?

Answer: The DLT has migrated proximally, making the bronchial cuff sit above the carina and both lumens now ventilate both lungs

Repositioning from supine to lateral commonly causes proximal migration of a DLT (the tube effectively 'rides up' with gravity and neck/thorax movement). If the bronchial cuff retreats above the carina, both lumens open to both lungs — bilateral breath sounds return, but the loss of lung isolation leads to inadequate surgical conditions and the 'wheeze' may reflect carina stimulation or partial obstruction. Distal migration would cause right upper lobe obstruction (right DLT) or complete right lung exclusion (left DLT), not bilateral sounds. Cuff herniation over the carina causes complete airway obstruction, not bilateral ventilation. Bronchospasm is possible but does not explain bilateral sounds returning after previous successful isolation.

A patient with idiopathic pulmonary arterial hypertension (mPAP 55 mmHg, PVR 12 Wood units) requires urgent thoracotomy for haemoptysis. Intraoperatively, after induction, RV systolic pressure by TOE rises to 90 mmHg and the patient develops hypotension (MAP 52 mmHg). Which combination of interventions is MOST appropriate?

Answer: Norepinephrine infusion, inhaled nitric oxide 20 ppm, and avoidance of hypoxia/hypercarbia/acidosis

In acute RV failure complicating severe PAH, the priority is to: (1) maintain systemic vascular resistance to preserve RV coronary perfusion pressure (norepinephrine); (2) selectively reduce PVR without systemic vasodilation (inhaled NO at 20 ppm achieves this — it is inactivated by haemoglobin before reaching the systemic circulation); and (3) aggressively prevent all triggers of pulmonary vasoconstriction (hypoxia, hypercarbia, acidosis). Volume loading risks RV dilation and septal shift worsening LV output. High PEEP markedly increases PVR. Sodium nitroprusside causes systemic vasodilation, worsening hypotension and RV ischaemia. GTN similarly drops systemic BP. Permissive hypoxia is absolutely contraindicated as it is a powerful pulmonary vasoconstrictor.

During thoracoscopic sympathectomy for hyperhidrosis under general anaesthesia with a laryngeal mask airway (LMA) and spontaneous ventilation, CO₂ is insufflated into the right pleural cavity. The patient's end-tidal CO₂ rises to 68 mmHg and SpO₂ falls to 89%. Which physiological mechanism BEST explains the combination of hypercapnia and hypoxaemia in this scenario?

Answer: CO₂ absorption from the pleural insufflation combined with ipsilateral lung compression creating an intrapulmonary shunt

Pleural CO₂ insufflation for thoracoscopy causes two simultaneous effects: first, CO₂ is absorbed across the pleural membrane directly into the systemic circulation, causing hypercapnia (especially problematic with spontaneous ventilation and an unprotected airway like an LMA that cannot deliver controlled higher minute volumes); second, the ipsilateral lung is compressed by the pneumothorax, converting a ventilated region to one that continues to receive pulmonary blood flow but no ventilation — a true intrapulmonary shunt causing hypoxaemia. Vagal apnoea is rare and does not produce sustained SpO₂ drop. LMA migration would cause a different pattern. CO₂ venous embolism is exceptional in pleural insufflation and would present with cardiovascular collapse.

A 67-year-old woman with a Pancoast tumour involving the T1 nerve root undergoes pre-operative CT-guided biopsy. She develops new ipsilateral ptosis, miosis, and anhidrosis 2 hours later. Which structure was most likely injured during the biopsy, and what is the PRIMARY anaesthetic implication for her subsequent pneumonectomy?

Answer: Injury to the stellate ganglion causing Horner syndrome; careful assessment of contralateral lung reserve is now more critical because the recurrent laryngeal nerve may also be at risk from tumour/biopsy

The stellate ganglion (inferior cervical/first thoracic sympathetic ganglion) lies in close proximity to the apex of the lung and Pancoast tumours. Its injury produces the classic Horner triad: ptosis (superior tarsal muscle), miosis (dilator pupillae), and anhidrosis (ipsilateral facial sweat glands). The primary anaesthetic implication is not haemodynamic (stellate ganglion block produces only modest cardiovascular changes) but rather that the stellate ganglion is anatomically adjacent to the recurrent laryngeal nerve and the brachial plexus — structures that the tumour or biopsy needle may also have compromised. If the contralateral RLN is injured (or the tumour extends), vocal cord palsy on the remaining functional side post-pneumonectomy creates a serious aspiration and ventilation risk. Assessing contralateral cord and lung function is therefore critical. Volatile induction bradycardia is not a recognised consequence of Horner syndrome. Phrenic nerve injury would cause diaphragm elevation, not Horner syndrome.