The acute respiratory distress syndrome (ARDS) has been recognized for more
than three decades as a cause of respiratory failure in patients with a va
riety of illnesses. Clinically, it is characterized by pulmonary edema, ref
ractory hypoxemia, diffuse pulmonary infiltrates, and altered lung complian
ce. Pathologically, it is distinguished by infiltration of the lungs with i
nflammatory cells, interstitial and alveolar edema, hyaline membrane format
ion, and ultimately fibrosis. Although we have learned much about the patho
physiology of this inflammatory syndrome since its earliest descriptions, A
RDS continues to claim the lives of 40%-70% of its victims. Many treatment
strategies have been used to prevent or treat ARDS, but thus far the most e
ncouraging strategy to prevent lung injury and improve survival is mechanic
al ventilation with low tidal volumes and high levels of positive end-expir
atory pressure.