Figure 2.

Slow flow pressure-volume loops and time tracings from a study patient with acute respiratory distress syndrome. (A) Pressure-volume loop of study patient. There was no flow or volume increase until roughly 7.5 cmH₂O airway pressure. In order to generate flow, the airway opening pressure must be greater than the pressure within the lungs which appears to be roughly 7–7.5 cmH₂O. This pressure within the lungs appears to be secondary to elevated pleural pressures; (B) in the same patient wave forms were recorded with zero PEEP which shows that during end-expiratory occlusion, the PEEPi is roughly 7.5 cmH₂O, secondary to elevated esophageal pressure of roughly 9.5 cmH₂O causing airway collapse. Patient had normal lungs at baseline without COPD or asthma with normal resistance.