Respiratory and Thoracic Anesthesia Flashcards

During one-lung ventilation (OLV) for a left pneumonectomy, the patient's SpO₂ drops to 88% despite FiO₂ 1.0 and PEEP 5 cmH₂O to the dependent lung. Fibreoptic bronchoscopy confirms correct DLT position. Which intervention is most likely to improve oxygenation with the least haemodynamic compromise?

Answer: Request surgical clamping of the pulmonary artery on the operative side

During pneumonectomy, early surgical ligation or clamping of the ipsilateral pulmonary artery eliminates blood flow to the non-ventilated lung, abolishing the intrapulmonary shunt (Qs/Qt) that is causing hypoxaemia. This is the most definitive and haemodynamically well-tolerated manoeuvre at this stage of the procedure. CPAP to the operative lung (Option A) is the first-line intervention in lobectomy/non-resection thoracic cases but cannot be used once the chest is open and the lung is collapsed for pneumonectomy without obstructing the surgical field; moreover it may not be feasible with an open pleura. Increasing tidal volume risks ventilator-induced lung injury (VILI) and worsens hypercapnia without reliably improving oxygenation when shunt fraction is very high. High-frequency jet ventilation of the non-dependent lung would re-expand it, conflicting with the surgical field.

A 58-year-old patient with severe COPD (FEV₁ 32% predicted, RV/TLC 68%) is undergoing right lower lobectomy under general anaesthesia with OLV. After 45 minutes of OLV the airway pressure alarm triggers. Plateau pressure rises from 28 to 41 cmH₂O while peak pressure rises from 34 to 52 cmH₂O. SpO₂ remains 96%, HR 110, BP 140/85. The DLT position is confirmed. What is the most likely explanation?

Answer: Dynamic hyperinflation with auto-PEEP in the ventilated lung

The hallmark of dynamic hyperinflation (air trapping / auto-PEEP) is a proportional rise in both peak and plateau pressures with maintained SpO₂ and haemodynamic stability — the lung is simply over-distended, not obstructed at a single point. Severe COPD with high RV/TLC ratio indicates severely impaired expiratory flow; during OLV the single ventilated lung must handle the entire minute ventilation with even less time for exhalation relative to inspiration, accelerating gas trapping. Management includes prolonging expiratory time (I:E 1:4 or longer), reducing respiratory rate, and allowing permissive hypercapnia. Tension pneumothorax would produce haemodynamic collapse and tracheal deviation. A mucous plug would raise peak pressure more than plateau. DLT cuff herniation would be identified by bronchoscopy and present with sudden complete airway obstruction rather than a gradual pressure rise.

Which of the following correctly describes the hypoxic pulmonary vasoconstriction (HPV) response during one-lung ventilation and its interaction with anaesthetic agents?

Answer: Almitrine bismesilate potentiates HPV in the non-ventilated lung but is no longer available in most countries due to peripheral neuropathy

Almitrine bismesilate is a specific pharmacological potentiator of HPV that diverts blood flow away from the collapsed non-ventilated lung, improving V/Q matching and PaO₂ during OLV. It was used clinically in France and some European centres but was withdrawn from most markets because of dose-dependent peripheral sensory neuropathy with long-term use. This combination of mechanism and toxicity is a classic EDAIC exam point. Option A is incorrect: propofol TIVA does NOT abolish HPV (intravenous agents preserve HPV), whereas volatile agents cause dose-dependent HPV inhibition — this is the key pharmacological difference. Option B is partially correct in that ≤1 MAC volatile agents have modest HPV inhibition, but this is still clinically significant and is not 'negligible.' Option D is incorrect: hypercapnia and hypoxia both POTENTIATE HPV (not reverse it) via shared intracellular pathways.

A patient undergoes video-assisted thoracoscopic surgery (VATS) lobectomy in the lateral decubitus position. The anaesthetist uses a size 39F left-sided double-lumen tube. After repositioning from supine to lateral decubitus, the surgeon reports incomplete lung collapse. Fibreoptic bronchoscopy through the tracheal lumen reveals the tracheal cuff is positioned 1 cm above the carina with no endobronchial herniation. What is the most appropriate next step?

Answer: Apply suction to the bronchial lumen of the DLT

When a bronchoscopically confirmed well-positioned DLT fails to achieve adequate lung collapse, applying suction (negative pressure) to the bronchial lumen of the operative (non-ventilated) lung actively evacuates residual gas and dramatically accelerates lung deflation. This is the recommended manoeuvre before repositioning the tube. The DLT position described (tracheal cuff 1 cm above carina, no cuff herniation) is actually ideal — withdrawing would risk losing bronchial seal; advancing risks right upper lobe obstruction on the ventilated side. Switching to a right-sided DLT is technically more difficult, associated with a higher failure rate, and is not indicated when left-sided isolation is the goal and tube position is confirmed correct.

A 44-year-old patient with a large anterior mediastinal mass (5 × 7 cm) is scheduled for mediastinoscopy under general anaesthesia. Preoperative CT shows >50% tracheal cross-sectional area compression at the level of the carina. The patient is symptomatic when supine. Which of the following is the safest induction strategy?

Answer: Inhalational induction with sevoflurane maintaining spontaneous ventilation, with the patient semi-recumbent or in lateral position, and rigid bronchoscopy on standby

Anterior mediastinal masses with significant (>50%) tracheal compression and positional symptoms represent one of the highest-risk scenarios in thoracic anaesthesia. Loss of spontaneous ventilation and muscle tone at induction can cause complete airway collapse (the mass compresses the trachea when thoracic muscle tone is lost), leading to 'can't intubate, can't oxygenate' cardiac arrest. The gold-standard approach is inhalational induction with sevoflurane in a semi-upright or lateral decubitus position, preserving spontaneous ventilation throughout, with rigid bronchoscopy and an experienced bronchoscopist immediately available to stent the airway open if collapse occurs. RSI abolishes spontaneous breathing and muscle tone, which is contraindicated. Awake fibreoptic intubation addresses vocal cord/upper airway issues but does not protect against tracheal or carinal collapse distal to the tube tip. Pre-bypass is reserved for cases where collapse is judged inevitable or where less invasive strategies have failed — not used routinely for all >50% compression cases.

During thoracic epidural anaesthesia for post-thoracotomy analgesia, a patient develops profound hypotension (BP 72/40 mmHg), bradycardia (HR 42 bpm), and paradoxical mydriasis (dilated pupils) 20 minutes after a bolus of 0.5% bupivacaine 8 ml through a T4–T5 epidural catheter. SpO₂ is 95% on 4 L/min O₂. What is the most likely mechanism and correct immediate treatment?

Answer: Intravascular injection of bupivacaine causing direct myocardial sodium-channel blockade; treat with 20% lipid emulsion IV bolus

The clinical picture — rapid onset of cardiovascular collapse with bradycardia, hypotension, and mydriasis after a bolus dose through a presumably correct epidural catheter — represents local anaesthetic systemic toxicity (LAST) from unrecognised intravascular injection of bupivacaine. Bupivacaine is particularly cardiotoxic because it blocks cardiac sodium channels in a use-dependent manner and dissociates very slowly ('fast-in, slow-out'), causing refractory arrhythmias and myocardial depression. Mydriasis (not miosis) due to sympathetic dominance is a key differentiating sign — high spinal and epidural spread cause miosis through interruption of the cervical sympathetic chain. The AAGBI/ESRA guideline treatment is immediate 20% intralipid emulsion (1.5 ml/kg bolus then infusion), vasopressors, and preparation for CPR. Option C (sympathectomy at T1–T4) could explain bradycardia and hypotension but not mydriasis, and would not produce this acute severity with a 8 ml dose at T4–T5. Option D (epidural haematoma) presents subacutely with back pain and neurological deficit, not acute cardiovascular collapse.