To the Editor:
The results of the study of management of one-lung ventilation by Blank et al.1 suggest that adequate positive end-expiratory pressure (PEEP) is an important factor in reducing pulmonary complications. Blank et al.1 provide an excellent discussion of the mechanical mechanisms and implications. I suggest an alternative or additional possible explanation of the beneficial effects of PEEP. The ventilated lung is subjected to increased blood flow, and this hyperemia may create additional shear stress, resulting in damage to the endothelial glycocalyx, which can then result in clinically significant respiratory complications.2–4 Studies support the concept that increased pulmonary blood flow may induce lung injury or aggravate a preexisting injury state.5–9 PEEP to the ventilated lung may reduce this hyperemia and hence reduce complications. Lower tidal volumes and the resultant reduced inspiratory pressure may result in more hyperemia, thus offsetting any potential beneficial effect of the expected reduced volutrauma. If we find a way to protect the glycocalyx or otherwise reduce the hyperemia to the ventilated lung, it is possible that lower tidal volumes may have a net beneficial effect. Larger tidal volumes to the ventilated lung may increase inspiratory pressure, resulting in less hyperemia and less damage to the glycocalyx, but damage from volutrauma could still occur.
Unfortunately, this hypothesis creates a clinical dilemma. Reducing blood flow by the application of PEEP to the ventilated lung may result in a greater shunt with potential desaturation. Applying continuous positive airway pressure (CPAP) to the operative lung to treat desaturation may not be as much of a problem. While the percentage of blood flow to the ventilated lung may increase, thus reducing shunt, it is unclear if there is an absolute increased blood flow to the ventilated lung as a result of the CPAP; the CPAP may just reduce blood flow to the operative lung with no change in blood flow to the ventilated lung.
This hypothesis is consistent with their results. Blank et al.1 found that low tidal volume and low PEEP, conditions that would be expected to increase blood flow to the ventilated lung, are associated with increased pulmonary complications. In the presence of PEEP, which would be expected to decrease blood flow to the operative lung, low tidal volume ventilation is protective.
The concept of pulmonary hyperemia being a cause of pulmonary complications is also consistent with the observations that pulmonary complication rates increase with increased amounts of pulmonary resection. For a given cardiac output, hyperemia may occur because of the reduced pulmonary vascular bed. In the most extreme case of a pneumonectomy, hyperemia would be expected to be maximal and complication rates are the highest; pulmonary edema may result from hyperemia-induced damage to the glycocalyx.
Further studies that incorporate measures of pulmonary blood flow would be helpful. Additional studies should also evaluate carbon dioxide management. Hypercarbia causes pulmonary artery vasoconstriction, which may reduce hyperemia, would require less minute ventilation, thus reducing the risk of volu- or barotrauma while trying to normalize the partial pressure of carbon dioxide, and may by itself be pneumoprotective. Permissive hypercarbia also permits lower respiratory rates, thus reducing the risk of potentially damaging air trapping.
The author declares no competing interests.