DOI: 10.1097/01.CCM.0000262546.91365.CA
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Issn Print: 0090-3493
Publication Date: 2007/05/01
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Excerpt
First, the authors demonstrated that different lung-protective ventilation strategies cause reduced venous return and, consequently, a decrease in cardiac performance in normal subjects. Apart from these unfavorable hemodynamic side effects, application of lung-protective ventilation in subjects with normal lungs cannot be recommended due to impaired oxygenation and severe hypercapnia. Currently there is insufficient evidence that lung-protective ventilation strategies should be applied as a preventive technique in patients with normal lungs. Although mechanical ventilation may trigger release of inflammatory mediators in patients with acute respiratory distress syndrome (2), a release of cytokines due to conventional ventilation with high tidal volumes and low positive end-expiratory pressure (PEEP) in patients with normal lungs is mostly related to preexisting damage of lung tissue and systemic inflammatory state (3). This issue was not addressed appropriately by the authors in the study’s title, objectives, or conclusions.
Second, gas exchange was worse during both protective strategies compared with controls. Indeed, lung-protective ventilation strategies are primarily purposed to limit alveolar overdistension and repeat alveolar collapse with the use of small tidal volumes. A key issue in this respect is the choice of an adequate PEEP level (2) that may largely differ from the high PEEP of 10 cm H2O, as it has been used in the present study. Application of high PEEP in healthy subjects has already been shown to result in worse oxygenation (4), as high PEEP prevents atelectasis but also impairs ventilation/perfusion ratio and subsequently increases intrapulmonary shunt (5). Furthermore, high PEEP in normal lungs has also been suggested to cause severe hypercapnia due to alveolar overdistension and decreased respiratory system compliance, an adverse effect also reflected by the authors’ data.
Finally, the observed reduction in cardiac output, systemic oxygenation, and oxygen delivery may have compromised tissue perfusion and metabolism in the periphery. Unfortunately, all variables were measured only once 30 mins after switching to a new ventilation strategy. Changes of hemodynamic variables, however, are most pronounced straight after an increment of mean airway pressure, whereas these variables adapt to increased PEEP level thereafter (6). Therefore, it is particularly important to investigate variables of individual organ perfusion, tissue oxygenation, and biochemistry. Furthermore, brain and cardiac tissue are extremely susceptible to ischemia, and even a few minutes of compromised perfusion can affect metabolic rate of oxygen and tissue integrity. To elucidate the impact of mechanical ventilation on these tissues, the authors should have analyzed regional blood flow or established biomarkers of tissue ischemia.
