Healthy human lungs are normally the sites of fluid and solute filtration across the pulmonary capillary endothelium. Unlike other organs, the filtrate in the lungs is confined anatomically within adjacent interstitial spaces, through which it moves by a built-in pressure gradient from its site of formation to its site of removal through pulmonary lymphatic channels. The quantity of fluid filtered and its protein content depend on the transvascular hydrostatic and protein osmotic (colloid) pressure differences, and the leakiness of the endothelial barrier to water and protein. Lymphatic drainage can increase several-fold, which means that pulmonary edema-defined as an increase in extravascular water content of the lungs-cannot occur until the rate of fluid filtration exceeds the rate of lymphatic removal. Two main types of pulmonary edema are recognized: first, cardiogenic (or hydrostatic) pulmonary edema from, as the name implies, an elevated pulmonary capillary pressure from left-sided heart failure; second, noncardiogenic (increased permeability) pulmonary edema from injury to the endothelial and (usually) epithelial barriers. Owing to their fundamental differences, each occurs in distinct clinical conditions, requires separate therapy, and has a different prognosis.