I read with interest the article titled “Intraoperative Tidal Volume as a Risk Factor for Respiratory Failure after Pneumonectomy” by Fernández-Pérez et al.  1This is an important article because the traditional approach to one-lung ventilation has been to deliver 10–12 ml/kg tidal volume.2As the authors pointed out, two previous studies reported that high intraoperative airway pressures during one-lung ventilation were associated with postoperative acute lung injury.3,4The study by Fernández-Pérez et al.  1showed that larger tidal volumes were associated with a higher risk of postoperative respiratory failure. However, the largest tidal volume recorded on the chart was used in the analysis. This would most likely have been during two-lung ventilation, even if the tidal volume had been reduced during one-lung ventilation. If the tidal volume is not adjusted when initiating one-lung ventilation, the airway pressure will increase due to reduced compliance. It is possible that the ventilator will not deliver the full tidal volume, and then the largest recorded tidal volume would be the two-lung tidal volume. Data were missing in more than 20% of the cases in this study, but it may still have been useful to examine what data were available, because this is the critical time period, and apparently there still would have been more than 100 cases to analyze. It would be important to follow up this study with either a prospective, randomized study using different tidal volumes during one-lung ventilation or even a retrospective study in which the tidal volumes can be definitely correlated with one-lung ventilation.

The authors stated that their most interesting finding was the association of both large tidal volume and greater fluid administration with postoperative respiratory failure. This makes sense in that the larger fluid administration can lead to pulmonary edema, once there is a capillary leak from a ventilator-induced injury. The authors hypothesized that the larger tidal volumes might have led to hypotension, which “forced” the anesthesiologists to administer more fluid. Although it is possible that resulting hypotension could have been treated with fluid, an alternative would have been infusion of a vasoconstrictor, such as phenylephrine. A more likely possibility is simply that the anesthesiologist who does not limit the tidal volumes or airway pressures during one-lung ventilation is less likely to be vigilant in limiting fluid administration. I do not understand, based on their data, how the authors concluded that even brief exposure to such ventilator settings could cause the postoperative complications.

Mount Sinai Medical Center, New York, New York. steve.neustein@msnyuhealth.org

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