The lung's alveolar–capillary structure normally provides a large surface for gas exchange and a tight barrier between alveolar gas and pulmonary capillary blood. Diffuse damage to the alveolar region occurs in the acute or exudative phase of acute lung injury and ARDS (Figure 2). This damage involves both the endothelial and epithelial surfaces and disrupts the lung's barrier function, flooding alveolar spaces with fluid, inactivating surfactant, causing inflammation, and producing severe gas exchange abnormalities and loss of lung compliance. These events are reflected in the presence of bilateral infiltrates, which are indistinguishable by conventional radiology from cardiogenic pulmonary edema (11). Computed tomography of the chest often demonstrates heterogeneous areas of consolidation and atelectasis, predominantly in the dependent lung (12–13), although areas of apparent sparing may still show inflammation. Pathologic findings consist of diffuse alveolar damage, including capillary injury, and areas of exposed alveolar epithelial basement membrane (14–16). The alveolar spaces are lined with hyaline membranes and are filled with protein-rich edema fluid and inflammatory cells. The interstitial spaces, alveolar ducts, small vessels, and capillaries also contain macrophages, neutrophils, and erythrocytes.