DOI: 10.1097/01.CCM.0000262531.65750.BE
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Issn Print: 0090-3493
Publication Date: 2007/05/01
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Excerpt
We agree that conventional ventilation with high tidal volumes and low positive end-expiratory pressure (PEEP) is not a trigger for the release of cytokines in patients with normal lungs. This is stressed in the introduction of our article (1), where we cite the publication by Wrigge et al. (2) (which is also cited by Dr. Meybohm and colleagues), who demonstrated this finding in patients with normal pulmonary function. It was the intention of this study to give a detailed description of the hemodynamic effects of lung-protective ventilation strategies when applied to subjects with normal lungs. Based on the results of our study, the use of those ventilatory strategies in patients with normal lungs cannot be justified. So, not only from the point of view of release of cytokines, but also based on hemodynamic findings, those strategies cannot be recommended. In this context the articles are complementary. We think that this is clearly stated in the final conclusion of the article.
The worsening of gas exchange with lung-protective strategies with higher PEEP levels in animals with normal lungs is indeed hardly surprising. As Dr. Meybohm and colleagues state, an inappropriate PEEP level applied to normal lungs can be responsible for alveolar overdistension and increased pulmonary shunt. Apart from the mechanical effects of PEEP, the decreased oxygenation can also be explained by an increased oxygen extraction by the tissues induced by the deterioration of cardiac output. Therefore, it can be rightly questioned why we applied this higher PEEP level in our animals. We did so because of two reasons. First, in the study of Wrigge et al. (2), where the effects of protective ventilation in patients without previous existing lung injury were studied, the same level of 10 cm H2O was used. Moreover, Su et al. (3) investigated the effect of lung-protective ventilation in the development of subsequent acute lung injury in sheep with septic shock but without lung injury. Also in that study, PEEP of 10 cm H2O was used. Second, we thought that our study could yield the most clinical aid for the physician if we could copy the lung-protective approach (as used in acute respiratory distress syndrome lungs) as close as possible in the ventilatory management of normal lungs. But obviously, we agree that application of 10 cm H2O PEEP in normal lungs is not advisable at all.
Dr. Meybohm and colleagues raise very interesting issues in the last paragraph of their letter. The hemodynamic derangement observed in our experimental animals is without any doubt responsible for significant endangering of tissue perfusion. However, it was beyond the scope of our investigation to determine regional blood flow or tissue ischemia markers. Therefore, in this study, this phenomenon cannot be objectified. In the article by Patel and Singer (4), cardiac output decreased immediately after increasing PEEP and tended to normalize after 15 mins. In our study, there was still an important decreased cardiac output 30 mins after the change in ventilatory mode. This suggests that the decrease in cardiac output immediately after the increase in airway pressure might even have been greater, as in the study by Patel and Singer. More frequent hemodynamic measurements or determination of tissue ischemia markers could provide more definite information concerning this topic.
