One-lung ventilation and methods of improving oxygenation

Published on 07/02/2015 by admin

Filed under Anesthesiology

Last modified 22/04/2025

Print this page

This article have been viewed 1245 times

One-lung ventilation and methods of improving oxygenation

Michael J. Murray, MD, PhD and Sarang S. Koushik, MD

One-lung ventilation (OLV) is achieved through a double-lumen tracheal tube, through a single-lumen tracheal tube advanced into either the right or left mainstem bronchus, or by advancing a bronchial blocker though a single-lumen tracheal tube into one of the mainstem bronchi. Multiple indications for OLV are noted in Table 158-1.

Table 158-1

Indications for One-Lung Ventilation

Absolute	Relative
Video-assisted thoracoscopy Protective isolation (infection, hemorrhage) Differential ventilation (bronchopleural fistula) Pulmonary alveolar lavage	Surgery on thoracic aorta or esophagus Pneumonectomy or lobar resection*

^*If one-lung ventilation is used, the surgical incision can be smaller because the deflation of the nondependent lung enables the surgeon to have better surgical access without a large thoracotomy incision.

Mechanism of hypoxia

The lateral decubitus position is often necessary to perform various thoracic operations and for some cardiac surgical procedures. When patients are in the lateral position, their dependent lung is often underventilated because it is compressed by the abdominal contents and by the mediastinum. The nondependent lung is relatively overventilated because its compliance is increased, particularly when the corresponding hemithorax is opened. Conversely, because of gravity, the dependent lung is well perfused, whereas the nondependent lung is underperfused. Because of the mismatch of perfusion to ventilation, hypoxemia is common in patients operated upon in the lateral decubitus position. Once ventilation to the nondependent lung ceases and the dependent lung is the only lung being ventilated (as occurs with OLV), the nondependent lung becomes atelectatic and the ventilation-perfusion ratio approaches 0, creating a transpulmonary shunt through the upper lung. The degree of hypoxemia correlates with the degree of the shunt. Because CO₂ is 20 times more diffusible than O₂ in the lung, ventilation through the dependent lung removes sufficient CO₂ so that hypercarbia is rarely seen.

Factors affecting oxygenation during one-lung ventilation

Many factors may affect oxygenation during OLV. Normally, when part of a lung is not ventilated (e.g., atelectasis, edema), “hypoxic” pulmonary vasoconstriction (HPV) restricts flow to the affected alveoli. HPV is of greatest benefit when 30% to 70% of the alveoli in a region contain a hypoxic gas mixture or are collapsed. Many factors blunt HPV and contribute to the development of hypoxemia, even when the patient is ventilated with 100% O₂. Most systemic vasodilators (e.g., nitroglycerin, nitroprusside, calcium channel blockers, and many β₂-receptor agonists) inhibit HPV. With the exception of N₂O, the inhalation anesthetic agents also inhibit HPV but not to such an extent as to be clinically relevant. Anything that increases pulmonary arterial pressure—volume overload, elevated left atrial pressure, pulmonary embolism, vasoconstriction in the pulmonary vasculature caused by drugs (dopamine, epinephrine, phenylephrine, and other vasoconstrictors that preferentially constrict normoxic lung vessels and defeat the HPV mechanism), or hypocarbia—will decrease flow through the dependent lung and increase the shunt through the nondependent lung. Hypocapnia directly inhibits HPV, but during OLV this can be achieved only through hyperventilation of the dependent lung, leading to increased airway pressure and increased pulmonary vascular resistance (PVR) in the ventilated lung, which redirects blood flow into the nondependent lung, thereby worsening the shunt.

Although HPV is responsible for most of the redistribution of blood flow away from the nonventilated lung, compression of the nonventilated lung may further reduce blood flow in the nonventilated lung.

Preoperative and intraoperative condition of the dependent lung

The PVR of the dependent lung determines the ability of that lung to accept redistributed blood flow from the nondependent lung. Preexisting pulmonary hypertension (i.e., high PVR in the dependent lung) interferes with the ability of HPV to redistribute flow to the dependent lung. Clinical conditions that may increase PVR in the dependent lung include low inspired O₂ tension and hypothermia. Maintaining the patient in the lateral decubitus position for long periods of time may cause a pericapillary transudate in the dependent lung, collapsing alveoli and increasing PVR in the dependent lung.

Methods to attenuate hypoxemia during one-lung ventilation

An FIO₂ of 1.0 protects against hypoxemia and has been associated with PaO₂ values between 150 and 250 mm Hg during OLV. A high FIO₂ also promotes vasodilation in the dependent lung to accept blood flow redistribution from the hypoxic nondependent lung. However, a high FIO₂ may lead to absorption atelectasis or O₂ toxicity, and in patients who have been previously treated with bleomycin, a high FIO₂ may induce lung injury. The risks and benefits of high FIO₂ should be assessed on a case-by-case basis.

The dependent lung should initially be ventilated with a tidal volume of 6 to 8 mL/kg at a rate sufficient to maintain the PaCO₂ at 40 mm Hg or less. Tidal volumes below 6 mL/kg may lead to increased atelectasis in the dependent lung. The patient’s respiratory rate should be adjusted to maintain the PaCO₂ at approximately 40 mm Hg.

Despite these efforts, patients may still develop hypoxemia, and, when hypoxemia occurs, routine issues and problems such as an FIO₂ of less than 1.0, a kinked or occluded (with secretions or blood) tracheal tube, or malposition of the tracheal tube must be addressed. If the hypoxemia is thought to be secondary to OLV, the treatment is controversial, evidenced by a letter sent to program directors of anesthesia residencies by the American Board of Anesthesiology (ABA) stating that individuals taking the written examination for ABA certification were marking the incorrect answer for treating hypoxemia during OLV. Examinees were choosing continuous positive airway pressure (CPAP) to the nondependent lung first and then applying positive end-expiratory pressure (PEEP) to the dependent lung if CPAP failed to correct the hypoxemia. The ABA, presumably based on the Seventh Edition of Miller’s Anesthesia (the previous six editions advised using CPAP first, followed by PEEP), had scored the correct answer as PEEP to the dependent lung first, followed by CPAP to the nondependent lung second. However, animal studies from the early 1990s and clinical experience have validated the concept that, in patients who develop hypoxemia during OLV, CPAP to the nondependent lung is the most effective way to increase PaO₂. CPAP at 5 to 10 cm H₂O maintains the patency of alveoli that have not already collapsed in the nondependent lung, drawing blood flow from already collapsed alveoli, allowing some gas exchange to occur in the nondependent lung.

If CPAP to the nondependent lung fails to reverse the hypoxemia, then PEEP of 5 to 10 cm H₂O to the dependent lung should be applied. PEEP to the dependent lung should not be tried first because it may compress small interalveolar vessels, increasing PVR, shunting more blood to the nondependent lung, and ultimately decreasing PaO₂ even more.

The only circumstance in which CPAP to the nondependent lung does not work is if the nondependent lung is completely collapsed (a very uncommon situation; i.e., all alveoli in the nondependent lung are collapsed); in this case, 5 to 10 cm H₂O pressure will not expand these alveoli (it takes ∼30 cm H₂O pressure to open alveoli if all are collapsed), and the hypoxia will persist. PEEP applied to the lower lung, by increasing functional residual capacity in that lung, may, to the extent that it optimizes the ventilation-perfusion ratio in the lower (dependent) lung, attenuate some of the hypoxemia.

If neither CPAP nor PEEP improves the hypoxemia, then the anesthesia provider should communicate with the surgeon to advise him or her of the degree of the patient’s desaturation and what has been tried to resolve the problem. If the surgical procedure involves removal of a lobe of lung—or is a pneumonectomy—and the surgeon is in a position to ligate the pulmonary vessels supplying the lung tissue to be resected, the surgeon might decide to do so expeditiously because this will decrease the shunt. If ligation of the pulmonary vasculature is not an option for whatever reason, then the surgeon should pause while the anesthesia provider ventilates both lungs, applying enough CPAP to the nondependent lung to reexpand that lung; the hypoxia should resolve. The nondependent lung is again allowed to collapse, and the operation continues until the hypoxemia progresses to the point that the upper lung must again be reexpanded and ventilated.

Miscellaneous causes of hypoxemia

As mentioned previously, various other causes of hypoxemia during OLV must be considered and ruled out when one is implementing the algorithm outlined earlier, including failure of the O₂ supply, or malfunction of the tracheal tube in the dependent lung because of malposition or blockage of the lumen by secretions or blood.

Related

Fausts Anesthesiology Review Expert Consult 4e