The lung is homogeneously affected by the disease process during the early phase of acute respiratory distress syndrome. This leads to an homogeneous alteration of the vascular permeability. Consequently, the edema accumulates evenly in all lung regions (nongravitational distribution). The increased lung weight, through the transmission of hydrostatic forces, however, causes a collapse of the lung regions along the vertical axes (compression atelectasis). At plateau pressure, the pulmonary units reopen, and during the following expiration they stay open, if the applied positive end-expiratory pressure is adequate. Positive end-expiratory pressure is adequate if it is equal or higher than the hydrostatic forces compressing that unit. Prone position is another maneuver effective in keeping open pulmonary units that were previously collapsed. During late acute respiratory distress syndrome, the compression atelectasis does not exist due to the edema reabsorption, and the lung undergoes structural changes, usually associated with carbon dioxide retention and development of emphysema-like lesions.