American Review of Respiratory Disease

When normal lungs are ventilated with large tidal volumes (Vt) and end-inspired pressures (Pei), surfactant is depleted and pulmonary edema develops. Both effects are diminished by positive end-expiratory pressure (PEEP). We reasoned that ventilation with large Vt-low PEEP would similarly increase edema following acute lung injury. To test this hypothesis, we ventilated dogs 1 h after hydrochloric acid (HCl) induced pulmonary edema with a large Vt (30 ml/kg) and low PEEP (3 cm H2O) (large Vt-low PEEP) and compared their results with dogs ventilated with a smaller Vt (15 ml/kg) and 12 cm H2O PEEP (small Vt-high PEEP). The small Vt was the smallest that maintained eucapnia in our preparation; the large Vt was chosen to match Pei and end-inspired lung volume. Pulmonary capillary wedge transmural pressure (Ppwtm) was kept at 8 mm Hg in both groups. Five hours after injury, the median lung wet weight to body weight ratio (WW/BW) was 25 g/kg higher in the large Vt-low PEEP group than in the small Vt-high PEEP group (p < 0.05). Venous admixture (Qva/Qt) was similarly greater in the large Vt-low PEEP group (49.8 versus 23.5%) (p < 0.05). We conclude that small Vt-high PEEP is a better mode of ventilating acute lung injury than large Vt-low PEEP because edema accumulation is less and venous admixture is less. These advantages did not result from differences in Pei, end-inspiratory lung volume, or preload (Ppwtm). We speculate that in acute lung injury, PEEP protects against surfactant depletion and that large Vt-low PEEP augments transfer of fluid from vessels to alveoli and thereby increases edema.


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