Intraoperative one-lung ventilation

INTRODUCTION — 

In most patients requiring mechanical ventilation, both lungs are inflated and deflated together. One-lung ventilation (OLV) refers to mechanical separation of the lungs to allow ventilation of only one lung. OLV is a standard approach to facilitate surgical exposure for thoracic surgeries and may be used to isolate a pathologic lung from a healthy one to prevent soiling or to provide differential ventilation.

This topic will discuss the general principles and physiology of OLV, its management, and its complications. Devices used for OLV, their placement, and comparative performance are reviewed separately. (See "Techniques to achieve lung isolation during general anesthesia".)

INDICATIONS — 

OLV is used either to improve exposure to the surgical field in thoracic surgery or to anatomically isolate one lung from a pathologic process of the other lung [1].

Surgical exposure — A non-ventilated, collapsed lung improves the view of the thoracic cavity and access to structures in the surgical field. OLV is often used during:

●Pulmonary resection, including pneumonectomy, lobectomy, and wedge resection (see "Anesthesia for open pulmonary resection", section on 'Airway control')

●Video-assisted thoracoscopic surgery (VATS), including wedge resection, biopsy, and pleurodesis (see "Anesthesia for video-assisted thoracoscopic surgery (VATS) for pulmonary resection", section on 'Airway management and surgical bronchoscopy')

●Mediastinal surgery (see "Anesthesia for patients with an anterior mediastinal mass", section on 'Airway management')

●Esophageal surgery (see "Anesthesia for esophagectomy and other esophageal surgery", section on 'Considerations for one lung ventilation')

●Thoracic vascular surgery (see "Anesthesia for open descending thoracic aortic surgery", section on 'Induction and airway management')

●Thoracic spine surgery (see "Anesthesia for elective spine surgery in adults", section on 'Airway management')

●Minimally invasive cardiac valve surgery (see "Minimally invasive aortic and mitral valve surgery")

Lung isolation — Lung isolation may be necessary to:

●Avoid cross-contamination from one lung to the other in the following circumstances (see "Techniques to achieve lung isolation during general anesthesia"):

•Pulmonary hemorrhage (see "Evaluation and management of life-threatening hemoptysis")

•Purulent pulmonary secretions

•During whole lung lavage for pulmonary alveolar proteinosis [2] (see "Treatment and prognosis of pulmonary alveolar proteinosis in adults", section on 'Whole lung lavage')

●Decrease pressure or airflow on the side of pathology, as in bronchopleural fistula or unilateral cyst/bullae (see "Bronchopleural fistula in adults" and "Overview of pulmonary resection", section on 'Pulmonary blebs and bullae')

CONTRAINDICATIONS — 

Contraindications to OLV include dependence on bilateral mechanical ventilation. Patients with severe pulmonary disease or prior pulmonary resection may not tolerate OLV; in these cases, selective lobar blockade may be an option.

Placement of a double-lumen endotracheal tube (DLT) may not be technically possible in a patient with an intraluminal airway mass restricting access to the tracheobronchial tree, and may be inadvisable if the intraluminal mass could be dislodged during placement since this could cause complete airway obstruction.

PHYSIOLOGY — 

The clinician using OLV needs to understand the changes in physiology caused by differential ventilation of the two lungs.

During normal two lung ventilation, ventilation and perfusion are well matched anatomically, because dependent portions of the lungs receive both greater blood flow (a result of gravity) and greater ventilation (from gravitational effects on lung compliance). The initiation of OLV stops all ventilation to one lung, which would create a 50 percent right-to-left shunt and relative hypoxemia if perfusion were unchanged. However, the actual shunt fraction is usually only 20 to 30 percent for the following reasons [3]:

●Surgical manipulation of the atelectatic lung obstructs vascular flow to the non-ventilated lung.

●Most patients undergoing thoracic surgery are in the lateral decubitus position. Lateral positioning of the patient leads to a gravitational increase in perfusion to the dependent, ventilated lung. The ventilated dependent lung is within the closed side of the chest and is exposed to the weight of the contralateral hemithorax contents. These factors result in an increase in lung elastance and the power delivered by the mechanical ventilator, even though tidal volume (TV) is reduced during OLV [4].

●Hypoxic pulmonary vasoconstriction (HPV) modulates the blood flow to hypoxic regions of the lungs [5,6]. HPV reduces shunt flow through the nonventilated lung by 40 to 50 percent during OLV, moderating the degree of hypoxemia [7,8]. Alveolar hypoxia triggers the pulmonary vessels to constrict, directing blood away from poorly/nonventilated areas to better-ventilated segments, thereby improving ventilation/perfusion matching. Clinically, HPV is proportional to the degree of local hypoxia, and is triggered primarily in response to an alveolar oxygen tension less than 100 mmHg [8]. The onset of HPV is two-phase with an initial rapid onset phase (minutes) and a delayed phase (hours). When oxygenation and ventilation are re-established, the attenuation of HPV follows a reverse two-phase pattern and may not completely return to normal for several hours [7]. This is an important consideration in the case of bilateral sequential thoracic procedures, such as bilateral wedge resections for lung metastases, in which patients tend to desaturate more during the OLV of the second lung.

A number of anesthetic factors may influence the extent of HPV, some of which may be controlled by the management of the anesthetic.

HPV is potentiated (causing less shunt, improving oxygenation) by [8]:

•Metabolic and respiratory acidosis

•Hypercapnia

•Mild decreased mixed venous oxygenation

•Hyperthermia

HPV is decreased (causing increased shunt, worsening oxygenation) by:

•Metabolic and respiratory alkalosis

•Hypocapnia

•Hypothermia

•Increased left atrial pressure

•Administration of a volatile inhalation anesthetic at a dose >1 minimum alveolar concentration (MAC)

•Hemodilution

IMPROVING DEFLATION OF THE NONVENTILATED LUNG — 

After placement of a lung isolation device to achieve OLV, expedited deflation of the nonventilated lung improves surgical access. One or more of the following maneuvers may help improve collapse of the nonventilated lung (table 1):

●Denitrogenate both lungs by ventilating with either 100 percent oxygen (O₂) or a nitrous oxide (N₂O)/O₂ mixture for several minutes prior to initiating OLV [9]. Replacing the poorly absorbed nitrogen in the nonventilated lung with more soluble O₂ or N₂O will facilitate collapse [10].

●Apply low suction (20 cmH₂O) until the nonventilated lung has collapsed well [11]. Low suction also prevents passive entrainment of air into the nonventilated lung [12].

•With a dual-lumen tube (DLT), low suction is applied via a suction catheter placed into the endotracheal lumen that leads to the nonventilated lung. (See "Techniques to achieve lung isolation during general anesthesia".)

•With a bronchial blocker, low suction is applied via the suction channel lumen. When a bronchial blocker is used, disconnect the anesthetic circuit and allow a prolonged expiration for 20 to 30 seconds, or until the end-tidal carbon dioxide (ETCO₂) falls to zero. Then begin OLV after inflating the cuff of the bronchial blocker under direct vision with the flexible intubating scope [10,13]. (See "Techniques to achieve lung isolation during general anesthesia", section on 'Placement of bronchial blockers'.)

●Use pressure-controlled ventilation during OLV to avoid the peaks in airway pressure that may occur during volume-controlled ventilation (eg, due to surgical manipulation in the chest or patient coughing). This decreases the chance of inadvertent reinflation of the nonventilated lung due to gas being forced past the inflated cuff of the DLT or bronchial blocker device.

LUNG-PROTECTIVE VENTILATION STRATEGIES DURING OLV — 

Thoracic surgery with OLV can result in a spectrum of lung injuries ranging from mild to severe acute respiratory distress syndrome (ARDS) [14-18]. The incidence of clinically overt acute lung injury (ALI) following lung resection generally ranges from 2 to 4 percent [19-22]. However, the incidence is higher after larger resections and is 8 to 12 percent after pneumonectomy [20,23]. Mortality in patients with ALI is approximately 40 percent [8,24]. (See "Ventilator-induced lung injury".)

Protective lung ventilation strategies during controlled ventilation under general anesthesia are used to minimize the risk of lung injury during both two lung ventilation and OLV. These strategies were adapted from approaches used in patients with ARDS in the critical care setting. The goal of protective ventilation is to minimize ventilator-induced lung trauma, inflammation, and injury due to alveolar over-distension and cyclic atelectasis while maintaining adequate oxygenation. Further discussion is available in a separate topic. (See "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia'.)

Low tidal volume (TV) ventilation — During protective OLV, a TV of 4 to 6 mL/kg is used. For comparison, historically, TV of 8 to 10 mL/kg was used during OLV as well as two lung ventilation.

Evidence from randomized trials and meta-analyses suggest that lower TV strategies decrease the risk of postoperative pulmonary complications [25,26]. A 2023 meta-analysis noted that lower TVs of 4 to 7 mL/kg during OLV were associated with a decreased risk of postoperative pulmonary complications (including abnormal chest radiograph, pneumonia atelectasis, infiltrates, pleural effusion, ALI, or ARDS), compared with higher TVs of 8 to 15 mL/kg (odds ratio [OR] 0.50, 95% CI 0.38-0.68; 10 trials with 1076 patients) [25]. Lower TV ventilation was also associated with a significantly higher arterial oxygen tension (PaO₂)/fraction of inspired oxygen (FiO₂) ratio 15 minutes after the start of OLV (mean difference 33.7 mmHg) and at the end of surgery (mean difference 18.59 mmHg), and a lower incidence of arrhythmias (OR 0.58, 95% CI 0.39-0.87). Hospital length of stay (LOS) did not differ [25].

Permissive hypercapnia — Use of low TVs without compensatory increases in respiratory rate (RR) leads to hypercapnia (see "Permissive hypercapnia during mechanical ventilation in adults"). This seems to be well-tolerated, and may be advantageous in OLV.

Hypercapnia potentiates hypoxic pulmonary vasoconstriction (HPV) [27], and causes a rightward shift of the oxyhemoglobin dissociation curve, enhancing oxygen delivery to tissue and thus, potentially improving wound healing and reducing infectious complications [28]. However, the benefits of hypercapnia must be balanced against the potential for increased intracranial pressure, pulmonary hypertension, myocardial depression, and decreased kidney perfusion. Hypercapnia (to 64 mmHg) during OLV was well tolerated in one trial, although it was associated with a 42 percent increase in pulmonary vascular resistance [29]. In two other series with higher levels of hypercapnia, patients tended to require inotropic support [30,31].

Many patients undergoing surgical procedures that require lung isolation OLV have significant preexisting pulmonary disease and may develop a large arterial oxygen tension (PaO₂) to end-tidal carbon dioxide (ETCO₂) gradient during OLV. Once OLV is established, we obtain an arterial blood gas to assess the magnitude of the gradient and to ensure ventilation is sufficient.

Positive end-expiratory pressure (PEEP) level — PEEP of 5 to 10 cmH₂O is typically applied during OLV with low TVs to prevent atelectasis. Details and evidence are discussed in a separate topic. (See "Mechanical ventilation during anesthesia in adults", section on 'Positive end-expiratory pressure' and "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Positive end-expiratory pressure'.)

During OLV, equivalent or improved oxygenation and lower inflammatory markers have been noted with use of PEEP (5 to 10 cmH₂O) with low TV (5 to 7 mL/kg) during OLV, compared with larger TV (9 to 15 mL/kg) without PEEP [32-34]. Use of PEEP also reduces injury from the mechanical stress of repetitive inflation/deflation cycles in the alveoli, which may lead to hypoxia and inflammation [35]. However, excessive PEEP >10 cm H₂O during OLV may shift perfusion away from the ventilated lung, resulting in increased shunt [36,37].

In patients with severe obstructive pulmonary disease (low forced expiratory volume in one second [FEV₁]), extrinsic PEEP should be used with caution. These patients may have high levels of intrinsic auto PEEP, which can cause incomplete expiration and significant air trapping [38-42]. The addition of extrinsic PEEP can worsen alveolar distension, increase pulmonary vascular resistance within the ventilated lung, increase shunting of blood flow to the non-ventilated lung, and worsen hypoxia. (See "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Mechanical ventilation' and "Positive end-expiratory pressure (PEEP)", section on 'Intrinsic (auto) PEEP'.)

During OLV, most patients develop some level of auto-PEEP that is inversely correlated to the severity of coexisting obstructive pulmonary disease [43]. In one trial, either 10 cmH₂O PEEP or no PEEP was employed during OLV; PEEP improved oxygenation and lung compliance only in patients without obstructive disease [38]. In a series of 42 patients having OLV with 10 mL/kg TV, addition of PEEP 5 cmH₂O improved oxygenation in 14 percent and worsened oxygenation in 21 percent, with no change in 65 percent [39]. Patients most likely to benefit were those with normal spirometry and low levels of intrinsic auto-PEEP.

Low airway pressures — Either pressure-controlled ventilation (PCV) or volume-controlled ventilation (VCV) may be selected, with the goal of avoiding high airway pressures and preventing barotrauma. Two crossover studies during OLV demonstrated improved oxygenation and shunt fraction with PCV compared with VCV, especially in patients with poor preoperative lung function [44,45]. This may be because PCV provides a more homogeneous distribution of TV, thus improving oxygenation and dead space ventilation [46]. Two other trials were unable to demonstrate any improvement in oxygenation, although they did have lower airway pressures with PCV [47,48]. (See "Mechanical ventilation during anesthesia in adults", section on 'Modes of intraoperative mechanical ventilation' and "Mechanical ventilation during anesthesia in adults", section on 'Plateau pressure'.)

No prospective trials have demonstrated improved outcomes when ventilation is specifically managed to lower airway pressures. Since plateau airway pressures >35 cmH₂O are associated with pulmonary barotrauma, maintaining plateau inspiratory pressures <30 cmH₂O is a reasonable goal. Two observational studies in patients undergoing OLV found an association between ventilation at higher airway pressures with development of postoperative ALI, but whether this is a causative effect or simply an early marker for lung injury is unclear [19,49]. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)

Oxygen concentration — Patients should be ventilated with the minimum FiO₂ needed to maintain oxygen saturation >90 percent (see "Mechanical ventilation during anesthesia in adults", section on 'Fraction of inspired oxygen'). If desaturation occurs while lower oxygen concentrations are used, increases in FiO₂ should be temporary while measures are taken to remedy the cause of the problem. (See 'Treatment of hypoxemia' below.)

Potentially preventable hyperoxemia and substantial oxygen exposure are common during OLV [50,51]. A high FiO₂ causes absorption atelectasis in the ventilated lung, increasing shunt and worsening oxygenation [52]. Furthermore, hyperoxia produces toxic oxygen free radicals, though the threshold above which oxygen toxicity and acute lung injury occur is unknown [53]. Re-expansion of the collapsed lung after OLV worsens this oxidative stress, resulting in increased vascular permeability and alveolar-capillary membrane edema, while re-expansion using low FiO₂ may mitigate any damage [54]. In one propensity score-weighted analysis that included 2936 patients, 74 percent received median intraoperative FiO₂ >80 percent [51]. This was associated with impaired postoperative oxygenation compared with those who received lower median intraoperative FiO₂ (OR 1.84, 95% CI 1.6-2.1).

MANAGEMENT OF HYPOXEMIA — 

The incidence of hypoxemia (oxygen saturation less than 90 percent) during OLV is approximately 5 percent [3,55]. Most commonly, this results from shunting.

Predicting hypoxemia during OLV — Several factors predict an increased likelihood of hypoxemia during OLV [3,56-59]:

●Low arterial oxygen tension (PaO₂) prior to OLV

●Left-sided ventilation (due to the smaller left lung) compared with right-sided ventilation

●High forced expiratory volume in one second (FEV₁), which results in minimal auto-positive end-expiratory pressure (PEEP) and higher potential for atelectasis

●Body mass index (BMI) >30 kg/m²

●Supine compared with lateral positioning (see 'Physiology' above)

Treatment of hypoxemia — Management of hypoxemia depends on the acuity of the situation. For severe acute hypoxemia, re-expansion of the non-ventilated lung may be necessary. However, since re-expansion of the lung would interfere with the surgical procedure if the onset is gradual, a series of other maneuvers are attempted first.

Episodes that occur suddenly or are associated with oxygen (O₂) saturation <90 percent are particularly concerning. In these situations, immediate treatment includes (table 2) [59]:

●Increasing the fraction of inspired oxygen (FiO₂) to 100 percent.

●Resuming two-lung ventilation temporarily if oxygen saturation does not rapidly rise to >90 percent on 100 percent FiO₂.

Once the oxygen saturation improves, the following additional maneuvers should be performed (table 2):

●Evaluate the position of the lung isolation device (double-lumen endotracheal tube or bronchial blocker). A flexible intubating scope (FIS) should be used to check the lung isolation device and reposition it as necessary. In one large series, lung isolation device malpositioning (often caused by changes in patient position or surgical manipulation) was responsible for 60 percent of hypoxic episodes during OLV [55].

●Suction the ventilated lung. Occlusion of major bronchi by secretions or blood may be diagnosed and suctioned using a FIS. For thick secretions and blood, suction with an endotracheal catheter may be needed.

●Optimize cardiac output. Many patients undergoing surgical procedures requiring OLV have poor cardiopulmonary reserve. Exacerbation of low cardiac output may occur due to hypovolemia, pump failure, or increases in pulmonary vascular resistance due to hypercapnia or dynamic hyperinflation. (See 'Positive end-expiratory pressure (PEEP) level' above.)

If hypoxemia persists after these maneuvers, the use of other ventilation strategies are attempted in the following order:

●Use recruitment maneuvers before, during, and after OLV to re-expand alveoli, improve oxygenation, decrease shunting, and decrease dead space. Such maneuvers include short periods of higher airway pressure and larger tidal volume (TV) to re-expand atelectatic lung tissue [60-66]. However, these recruitment maneuvers can cause lung injury in animal models; therefore, use is weighed against risks of atelectasis [67,68]. (See "Mechanical ventilation during anesthesia in adults", section on 'Recruitment maneuvers'.)

●Increase PEEP to the ventilated lung up to 10 cmH₂O to minimize atelectasis and improve oxygenation, especially if low TVs are being used. Exercise caution in patients with chronic obstructive pulmonary disease (COPD) [63-65,69]. (See 'Positive end-expiratory pressure (PEEP) level' above.)

●Deliver O₂ to the non-ventilated lung

●Insufflate a low flow of O₂ (3 L/min) to the non-ventilated lung via a suction catheter inserted into the lumen of the double-lumen endotracheal tube (DLT) before restarting OLV to decrease the incidence of subsequent hypoxemia. It is unclear if the beneficial effect is primarily due to absorption of the insufflated oxygen, or due to prevention of the passive entrainment of room air into the non-ventilated lung [70].

●Apply O₂ via continuous positive airway pressure (CPAP) 5 to 10 cmH₂O to the nonventilated lung to reduce shunt fraction of the nonventilated lung [71]. The surgeon should be informed before initiating CPAP since this maneuver can cause sudden movement in the surgical field, and the partial inflation of the operative lung worsens surgical exposure.

●Use high-frequency jet ventilation to the nonventilated lung as an alternative to CPAP to improve oxygenation and decrease shunt [72].

●Use partial ventilation of the operative lung:

•Employ selective lobar collapse

•Insufflate O₂/CPAP selectively into the nonoperative lobe(s) of the operative lung via a bronchial blocker or FIS [35]. (See "Techniques to achieve lung isolation during general anesthesia".)

●Intermittently resume two-lung ventilation as needed, although this usually requires interruption of the surgical procedure [59].

●Manually restrict pulmonary blood flow via surgical manipulation to decrease shunting through the non-ventilated lung [73].

●Use nebulized prostacyclin or its derivative iloprost in the ventilated lung to treat hypoxemia during OLV, particularly if a total intravenous anesthesia (TIVA) technique is employed [74]. Inhaled nitric oxide (NO) as a pulmonary vasodilator could theoretically increase perfusion of the ventilated lung and thus minimize shunt, but this agent did not improve oxygenation in clinical trials [75-77].

ANESTHETIC CHOICE — 

There is insufficient evidence that the choice of anesthetic type (inhalation versus intravenous) affects oxygenation during OLV, or the incidence of lung injury; therefore, the decision to use inhalation and/or intravenous anesthetics should be based on standard considerations unrelated to OLV [3]. The impact of thoracic epidural use during general anesthesia on oxygenation and shunt during OLV has been inconsistent, and should not change the management plan. [78-82].

RE-EXPANDING THE NONVENTILATED LUNG — 

Except in the case of pneumonectomy, re-expansion of the nonventilated lung is necessary following completion of the surgical procedure. This is accomplished with a sustained inflation at low levels of positive airway pressure (eg, 20 to 30 cmH₂O for 10 to 15 seconds). Higher pressures (>30 cmH₂O) are avoided due to reduce the risk of acute lung injury or and the risk of new air leaks after pulmonary resection. (See 'Low airway pressures' above.)

Such gently sustained inflations may be repeated to reinflate all atelectatic areas. If pulmonary resection was performed, sustained inflations also allow detection of bronchial air leaks. When feasible, expansion is accomplished with direct observation of the lung in an open chest or on the monitor during video-assisted thoracoscopic surgery (VATS). This ensures gradual but complete recruitment of residual lung tissue with the application of the minimum sustained positive pressure that is necessary.

Subsequently, two lung ventilation is managed with a protective ventilation strategy and the minimum fraction of inspired oxygen (FiO₂) that maintains oxygen saturation >93 percent. (See 'Lung-protective ventilation strategies during OLV' above.)

SUMMARY AND RECOMMENDATIONS

●Indications for OLV – Ventilation of a single lung while allowing the other to collapse is known as one-lung ventilation (OLV). Indications for OLV include (see 'Indications' above):

•Surgical exposure during thoracic surgery

•Isolation of one lung from the other for the treatment of pulmonary pathology

●Contraindications for OLV – Contraindications include dependence on bilateral mechanical ventilation, and intraluminal airway masses that restrict access to the tracheobronchial tree. (See 'Contraindications' above.)

●Physiology of OLV – Physiologic changes caused by differential ventilation of the two lungs include ventilation/perfusion mismatch and hypoxic pulmonary vasoconstriction. (See 'Physiology' above.)

●Deflating the nonventilated lung – After placement of a lung isolation device, expedited deflation of the nonventilated lung to improve surgical access can be achieved by one or more maneuvers (table 1). (See 'Improving deflation of the nonventilated lung' above.)

●Lung-protective ventilation strategies – During OLV, protective ventilation minimizes lung injury while maintaining oxygenation. We suggest using the following combination of ventilation strategies to the ventilated single lung (Grade 2C) (see 'Lung-protective ventilation strategies during OLV' above):

•Low tidal volume (TV) ventilation (4 to 6 mL/kg)

•Permissive hypercapnia is well-tolerated in most patients, and may be advantageous during OLV. However, patients with significant pre-existing pulmonary disease may develop a large arterial oxygen tension (PaO₂) to end-tidal carbon dioxide (ETCO₂) gradient during OLV. An arterial blood gas is obtained once OLV is initiated

•Positive end-expiratory pressure (PEEP; 5 to 10 cmH₂O), except in patients with severe obstructive disease

•Limit airway pressures (plateau inspiratory pressures <30 cmH₂O), or pressure-controlled ventilation

•Lower fraction of inspired oxygen (FiO₂), adjust as needed to maintain oxygen saturation >90 percent

●Management of hypoxemia during OLV – Increase FiO₂ to 100 percent. If this is not effective, temporarily resume two lung ventilation to increase oxygen saturation to >90 percent, and then perform the maneuvers outlined in the table (table 2). (See 'Treatment of hypoxemia' above.)

●Anesthetic choices – Decisions to use inhalation and/or intravenous anesthetics should be based on standard considerations unrelated to OLV. (See 'Anesthetic choice' above.)

Re-expanding the nonventilated lung – Re-expansion is necessary to reinflate all atelectatic areas of the nonventilated lung and detect bronchial air leaks. This is accomplished with a sustained inflation at low levels of positive airway pressure (eg, 20 to 30 cmH₂O for 10 to 15 seconds), which may be repeated for optimal recruitment of lung tissue. Higher pressures (>30 cmH₂O) are avoided due to the risk of exacerbation of acute lung injury or the creation of new air leaks after pulmonary resection. (See 'Re-expanding the nonventilated lung' above.)