One-Lung Ventilation in a Patient with Severe Pulmonary Hypertension

Risk assessment: This is a very high-risk patient. Severe PAH (mPAP 52, PVR 9 WU, NYHA III) with exertional desaturation and a limited 6MWD carries substantial perioperative mortality for thoracic surgery. The key threats:

1. Hypoxemia during OLV - she already has a reduced baseline PaO₂ (62 mmHg on room air) and a compromised pulmonary vascular bed. OLV creates shunt through the non-ventilated lung; her ability to compensate via HPV is impaired by pulmonary vascular disease and by vasodilator therapy (tadalafil, ambrisentan), which can blunt hypoxic pulmonary vasoconstriction and worsen shunt.
2. Acute RV failure - OLV increases pulmonary vascular resistance (atelectasis, hypoxic vasoconstriction, hypercapnia, acidosis, high airway pressures). In a patient with PVR of 9 WU and an already strained RV, any further rise in PVR can precipitate RV ischemia and failure. Hypoxia, hypercapnia, acidosis, and hypotension are all potent pulmonary vasoconstrictors.
3. Lateral decubitus position - the dependent lung receives more perfusion; with the non-dependent (operative) lung down or up, ventilation-perfusion matching changes and can worsen hypoxemia. Positioning also compresses the dependent lung and reduces FRC.
4. Systemic hypotension - RV perfusion depends on systemic diastolic pressure; any drop in SVR (from anesthetics, epidural, or vasodilation) reduces coronary perfusion to the RV and can trigger a downward spiral.

Bottom line: She is at high risk for intraoperative hypoxemia, RV failure, and cardiac arrest. A candid, multidisciplinary discussion (cardiology, pulmonology, thoracic surgery, anesthesia) about risk versus benefit is essential, and the case should be done at a center experienced with PAH.

Anesthetic plan:

• Avoid neuraxial/regional techniques that drop SVR and avoid drugs that increase PVR. Use a balanced general anesthetic with careful titration; consider total intravenous anesthesia to avoid volatile-induced HPV inhibition and myocardial depression, though evidence is mixed - the key is avoiding hypotension and hypercapnia.
• Invasive monitoring: arterial line (ideally pre-induction), central venous access, and consider TEE to assess RV function. Pulmonary artery catheter if available and the team is experienced.
• Maintain sinus rhythm and preload; avoid tachycardia (reduces RV filling) and avoid excessive fluid that distends the RV.
• Ventilation: protective lung ventilation with low tidal volumes (6 mL/kg predicted body weight), PEEP titration to avoid derecruitment, and permissive hypercapnia avoided - keep PaCO₂ near baseline (34 mmHg) because hypercapnia raises PVR. Use the lowest FiO₂ that maintains saturation, but do not compromise oxygenation.
• Hemodynamic goals: maintain SVR with norepinephrine or vasopressin (vasopressin is attractive because it does not increase PVR and preserves RV perfusion). Avoid hypotension. Consider inhaled nitric oxide or epoprostenol if RV failure develops.
• Positioning: careful padding, avoid compression of the dependent lung, and ensure the double-lumen tube is correctly positioned with fiberoptic bronchoscopy.

Response to desaturation during OLV:

1. Increase FiO₂ to 1.0.
2. Check tube position with bronchoscopy (most common cause of sudden desaturation).
3. Apply CPAP (e.g., 2–5 cmH₂O) to the non-dependent (operative) lung and/or PEEP to the dependent lung - titrate carefully, as excessive PEEP can increase PVR.
4. Recruit the dependent lung with gentle recruitment maneuvers.
5. Optimize cardiac output - ensure adequate preload and avoid hypotension; low cardiac output worsens shunt.
6. Reduce shunt by intermittent reinflation of the operative lung if the surgeon can tolerate it.
7. Treat RV failure if present (inhaled pulmonary vasodilators, inotropes, avoid acidosis/hypercapnia).
8. If refractory, communicate with the surgeon about aborting OLV or converting to open approach.

Structuring the conversation:

• Be honest and specific without being fatalistic. Acknowledge that her pulmonary hypertension makes this a high-risk operation and that the team has planned specifically for her risks. Avoid quoting a single mortality number you cannot defend; instead describe the categories of risk (breathing problems, heart strain, need for intensive care).
• Explain the plan in plain language: specialized monitoring (arterial line, possibly TEE), a breathing tube that lets us ventilate one lung, medications to support the heart and circulation, and a planned ICU stay.
• Set expectations for the postoperative course: she will likely remain intubated and sedated initially, and weaning will be gradual.
• Include her in decisions: discuss code status, goals of care, and what matters to her. Document a shared decision.
• Involve the multidisciplinary team (PAH specialist, thoracic surgery, ICU) and consider a palliative care consult for symptom and goals support - not because she is dying, but because it improves communication.

Postoperative concerns:

• RV failure remains the dominant risk; continue pulmonary vasodilators (do not abruptly stop tadalafil/ambrisentan - rebound PAH can be fatal), monitor with echo, and use inhaled vasodilators/inotropes as needed.
• Hypoxemia and atelectasis in the postoperative period; aggressive pulmonary hygiene, early mobilization, incentive spirometry, and possibly NIV.
• Fluid management - avoid volume overload that distends the RV; use goal-directed therapy.
• Pain control - adequate analgesia to allow coughing and ambulation, but avoid techniques that cause hypotension; a carefully titrated thoracic epidural or paravertebral block can be considered with close hemodynamic monitoring.
• Arrhythmias - monitor for AF and other arrhythmias that compromise RV filling.
• VTE prophylaxis and early ambulation.
• Avoid hypoxia, hypercapnia, acidosis, and hypotension in the ICU - the same rules as intraoperatively.