By definition, the acute respiratory distress syndrome is associated with diffuse cellular infiltration and proteinaceous edema. It is generally believed that the widespread injury that characterizes acute respiratory distress syndrome is a process that is launched almost synchronously throughout the lung, caused by blood-borne mediators of inflammation, voluminous aspiration, or inhalation of noxious gases or infective inoculums. Relatively little attention has been paid to the possibility that inflammatory lung injury may sometimes begin focally and propagate sequentially via the airway network, generalizing as mobile liquids carry their damaging products mouthward from distal to proximal. Were this true, modifications of ventilatory pattern and positioning aimed at geographic containment of the injury process could help prevent generalization and limit disease severity. This seldom-considered mechanism for extending lung injury might further justify implementation of low tidal volume/high positive end-expiratory pressure ventilatory strategies, as well as encourage additional lung protective measures that logically stem from simple mechanics.