I now have comprehensive material from Miller's, Morgan & Mikhail's, and Barash's to write a thorough 10-mark answer. Let me compile it.
One-Lung Ventilation (OLV)
Sources: Miller's Anesthesia 10e, Morgan & Mikhail's Clinical Anesthesiology 7e, Barash's Clinical Anesthesia 9e
Definition
One-lung ventilation (OLV) is a technique in which only one lung is ventilated while the other is intentionally allowed to collapse, primarily to facilitate thoracic surgery. The non-ventilated lung is deliberately deflated but continues to be perfused, creating an obligatory right-to-left intrapulmonary shunt.
Indications
Divided into absolute and relative:
Absolute (Lung Isolation)
- Protection from contamination - massive hemoptysis, lung abscess, empyema (to prevent spillage to the healthy lung)
- Control of distribution of ventilation - bronchopleural fistula, bronchopleural cutaneous fistula, unilateral cyst/bullae, major bronchial disruption
- Unilateral bronchopulmonary lavage (e.g., pulmonary alveolar proteinosis)
- Video-assisted thoracoscopic surgery (VATS)
Relative (Lung Separation for Surgical Exposure)
| Priority | Examples |
|---|
| High priority | Thoracic aortic aneurysm, pneumonectomy, lung volume reduction, upper lobectomy, minimally invasive cardiac surgery |
| Low priority | Esophageal surgery, middle/lower lobectomies, mediastinal mass resection, thymectomy, bilateral sympathectomies |
Key distinction: Lung isolation (protects against cross-contamination) requires DLT; lung separation (surgical exposure) can use either DLT or bronchial blockers.
- Barash's Clinical Anesthesia 9e, p. 3173
Physiology of OLV
Two-Lung vs One-Lung Ventilation
During two-lung ventilation:
- Nondependent lung: 40% of blood flow; dependent lung: 60%
- PaO2 ~400 mmHg; Qs/Qt ~10%
During OLV (lateral decubitus):
- Nondependent (collapsed) lung: ~22.5%; dependent lung: ~77.5%
- PaO2 falls to ~150 mmHg; Qs/Qt rises to ~27.5%
The increase in Qs/Qt (intrapulmonary shunt) from ~10% to ~27.5% is the fundamental cause of hypoxemia during OLV.
Two Main Causes of Impaired Oxygenation During OLV
- Persisting blood flow through the non-ventilated (nondependent) lung → obligatory shunt
- Development of atelectasis in the dependent (ventilated) lung → additional local shunt and low V/Q areas
- Miller's Anesthesia 10e, p. 1321
Role of Hypoxic Pulmonary Vasoconstriction (HPV)
HPV is a compensatory mechanism that reduces blood flow to the non-ventilated lung, limiting the degree of shunt. Without HPV, OLV would result in a shunt fraction of ~35-40%; with HPV it is typically 20-30%. HPV reduces blood flow to the nondependent collapsed lung by ~50%.
Factors that INHIBIT HPV (worsen oxygenation):
- Pulmonary hypertension
- Hypocapnia, alkalosis
- Increased cardiac output; increased mixed venous PO2
- Hypothermia
- Vasodilators: nitroglycerin, nitroprusside, nitric oxide
- Phosphodiesterase inhibitors (milrinone, enoximone)
- Beta-adrenergic agonists
- Calcium channel blockers
- Inhalation anesthetics (volatile agents at >1 MAC)
Factors that decrease blood flow to the VENTILATED (dependent) lung (also worsen hypoxemia):
- High mean airway pressures (excessive PEEP, hyperventilation, high PIP)
- Low FiO2 in the ventilated lung (triggers HPV in ventilated lung)
- Vasoconstrictors (greater effect on normoxic than hypoxic vessels)
- Intrinsic PEEP from inadequate expiratory time
- Morgan & Mikhail's Clinical Anesthesiology 7e, p. 1024
Techniques for Achieving OLV
Four techniques are available:
1. Double-Lumen Endobronchial Tube (DLT) - Most Commonly Used
- Two bonded endotracheal tubes: one lumen enters a mainstem bronchus, one ends in the distal trachea
- Two cuffs: a proximal tracheal cuff and a distal bronchial cuff
- Left-sided DLT preferred in most situations (longer left mainstem bronchus; safer margin from carina)
- Right-sided DLT used when: left pneumonectomy, left-sided tracheobronchial disruption, left mainstem stenosis, left-sided tumor at the carina
- Sizes: 35, 37, 39, 41 Fr (generally 39-41 Fr for men; 35-37 Fr for women)
- Fiberoptic bronchoscopy is the gold standard for confirming position
- Advantages: reliable, fast placement, allows suctioning, CPAP/PEEP to either lung independently
- Disadvantage: larger tube, more airway trauma, higher rate of hoarseness (44% vs 17% with blockers)
2. Bronchial Blockers
- Single-lumen ETT + balloon-tipped blocker (e.g., Arndt, Cohen, EZ-blocker)
- Useful in: difficult airway, tracheostomy patients, existing ETT
- Disadvantage: unreliable seal (not suitable for true lung isolation/protection), difficult suctioning, slower collapse, higher dislodgement risk
3. Mainstem Intubation with Single-Lumen ETT
- Conventional ETT advanced into a mainstem bronchus
- Simplest but least versatile; limited to emergencies
4. Tubeless Techniques
- For select VATS procedures; no intubation; relies on spontaneous ventilation
- Barash's Clinical Anesthesia 9e, pp. 3175-3186
Management of OLV: Lung-Protective Ventilation Strategy
The focus has shifted from merely preventing hypoxemia to preventing acute lung injury (ALI) - which occurs in 2.5% of all resections and up to 7.9% post-pneumonectomy, with ~40% mortality/major morbidity.
Recommended ventilation parameters during OLV:
| Parameter | Target |
|---|
| Tidal volume | 4-5 mL/kg predicted body weight (NOT the same as two-lung TV) |
| FiO2 | Start at 1.0; can reduce to 50-80% if saturations are adequate |
| Plateau pressure | <25 cmH2O |
| Peak airway pressure | <35 cmH2O |
| PEEP | Titrated to optimal compliance in ventilated lung |
| Ventilatory mode | Pressure-controlled ventilation preferred (limits peak pressures, more homogenous gas distribution) |
Pre-OLV preparation:
- Before commencing OLV, ventilate with 100% O2 to de-nitrogenate the operative lung (nitrogen's low blood-gas solubility delays collapse)
- Perform a recruitment maneuver on the dependent lung immediately after starting OLV (sustain 20 cmH2O for 15-20 seconds) to clear atelectasis that developed during two-lung anesthesia
- Morgan & Mikhail's Clinical Anesthesiology 7e, pp. 1045-1046
Management of Hypoxemia During OLV
Target: SpO2 ≥90% (PaO2 >60 mmHg). In patients with CAD, cerebrovascular disease, or anemia, maintain a higher threshold.
Stepwise management (escalating):
| Step | Action |
|---|
| 1 | Check DLT/blocker position with FOB - surgical manipulation may dislodge it; suction both lumens |
| 2 | Increase FiO2 to 1.0 |
| 3 | Optimize cardiac output - ensure no IVC compression by surgeon; stop vasodilators; reduce volatile agent to ≤1 MAC |
| 4 | Recruitment maneuver of the ventilated lung (20 cmH2O for 15-20 sec; causes transient worsening before improvement) |
| 5 | Apply PEEP to the ventilated lung (avoid in emphysematous patients - risk of intrinsic PEEP) |
| 6 | Apply CPAP 1-2 cmH2O to the non-ventilated lung (first do a recruitment maneuver on it) |
| 7 | Apneic oxygen insufflation to non-ventilated lung |
| 8 | Partial ventilation of non-ventilated lung (intermittent PPV, small tidal volumes, selective lobar collapse) |
| 9 | Pharmacologic: almitrine (potentiates HPV; improves PaO2 without altering PAP or CO) + inhaled NO to ventilated lung |
| 10 | Ask surgeon to clamp ipsilateral pulmonary artery |
| 11 | Resume two-lung ventilation (if severe/precipitous desaturation) |
| Last resort | Venovenous ECMO |
- Miller's Anesthesia 10e, pp. 7212-7213; Morgan & Mikhail's 7e, pp. 1046-1047
Lung Injury Mechanisms During OLV
Both lungs are at risk:
- Dependent (ventilated) lung: hyperperfusion (77.5% of cardiac output) + ventilator-induced lung injury (VILI) from large tidal volumes and high pressures
- Non-dependent (collapsed) lung: ischemia-reperfusion injury + direct surgical trauma
This is why lung-protective ventilation is so critical - tidal volumes >8 mL/kg used historically (same as two-lung TV) are now strongly discouraged.
Pharmacological Adjuncts
- Almitrine (IV pulmonary vasoconstrictor): potentiates HPV in non-ventilated lung; at low doses does not increase PA pressure or reduce CO; best used in combination with inhaled NO
- Inhaled NO (pulmonary vasodilator): when given to ventilated lung, increases blood flow to already-ventilated areas; minimal effect alone but synergistic with almitrine
- Volatile anesthetics: inhibit HPV at >1 MAC; use ≤1 MAC or switch to TIVA (propofol) if hypoxemia is refractory
- Miller's Anesthesia 10e, p. 1322
Monitoring During OLV
- SpO2 (continuous)
- Arterial line for serial ABGs - especially for permissive hypercapnia monitoring
- End-tidal CO2: useful as a trend monitor but arterial-to-end-tidal CO2 gradient is unpredictable and increases during OLV due to dead space ventilation
- Peak/plateau airway pressures: continuous monitoring to limit VILI
- Periodic fiberoptic bronchoscopy to confirm DLT position, especially after patient repositioning
Postoperative Considerations
- Operative lung is reinflated gradually to PIP <30 cmH2O to avoid disruption of staple lines
- During reinflation, clamping the dependent lung lumen prevents overdistention
- V/Q matching may take time to normalize; expect impaired oxygenation early postoperatively
- Pain control (thoracic epidural, paravertebral block) is essential to prevent splinting and atelectasis
Summary table for exam:
| Feature | Key Point |
|---|
| Shunt fraction during OLV | ~27.5% (up from 10%) |
| Key compensatory mechanism | HPV (reduces non-ventilated lung flow by 50%) |
| Best technique for lung isolation | Left-sided DLT confirmed with FOB |
| Tidal volume during OLV | 4-5 mL/kg IBW |
| First step for hypoxemia | Check DLT position with FOB |
| Best pharmacologic combo | Almitrine + inhaled NO |
| ALI incidence post-pneumonectomy | 7.9%; mortality 40% |
| Acceptable SpO2 lower limit | ≥90% (PaO2 >60 mmHg) |