PATHOPHYSIOLOGY



The physiological abnormalities in ARDS, re­gardless of the predisposing event, are associated with an increase in extravascular lung water. Water movement in the lung is governed by vas­cular permeability and the balance of the hydro­static and oncotic pressures across the capillary endothelium as described in the Starling equation . Hydrostatic forces favor fluid filtra­tion, while oncotic pressure promotes reabsorp-tion. Normally, filtration forces dominate and fluid continuously moves from the vascular space into the interstitium. Despite this, extravascular water does not accumulate because the lung lym­phatics effectively remove the filtered fluid and return it to the circulation. However, the capacity of the lymphatic system is limited and if the rate of fluid filtration exceeds its functional capabil­ities water accumulates. Initially, it accumulates in the loose interstitial tissues around the airways, pulmonary arteries, and later the alveolar walls (interstitial edema). This causes increased lung stiffness and dyspnea due to stimulation of lung receptors but rarely produces significant abnor­malities in the arterial blood gases. If the process continues the excess fluid pours into the alveolar space with two consequences: alveolar surface forces are altered, leading to a further reduction in compliance and a decreased lung volume, and the flooded alveoli can no longer be ventilated, thus converting their blood supply into intrapul-monary shunt. Shunt is the major cause of the se­vere hypoxemia characteristic of ARDS .

Two major alterations of the Starling equation are seen clinically. The commonest is an increase in hydrostatic pressure as with cardiogenic pul­monary edema and fluid overload. Edema fluid in this setting has a low protein content and is es­sentially an ultrafiltrate of plasma. In ARDS, fluid accumulation is due to an alteration in alveolar-capillary membrane permeability, which may re­sult from either endothelial or epithelial cell in­jury . The etiology of the injury is oc­casionally clear-cut, as in gastric aspiration or viral pneumonia, but is more commonly elusive and ascribed to complex immunologic or biomonary edema, the presence of low intravascular oncotic pressure increases the rate of fluid tran­sudation in both low- and high-pressure pulmo­nary edema. Similarly, any increase in microvas­cular hydrostatic pressure in the setting of increased capillary permeability dramatically in­creases the rate of fluid filtration.