pathogenesis of acute respiratory syndrome

The hallmark of acute respiratory distress syndrome (ARDS) is inflammation of the lungs. Early in acute respiratory distress syndrome the pulmonary neutrophils gather in great amounts at the site of inflammation, intraluminal fibrin and platelets also aggregate at the site of inflammation. Injuries from inflammation lead to edema from capillary leaks. This fluid contains plasma proteins that can inactivate the surfactant of the alveoli and cause lack of elasticity with respiration and lead to alveolar collapse. Fibrin clotting then causes obstructed airspaces. The result is decreased respiratory compliance, decreased function, decreased residual volumes, and dead airspace. The end result for the client is ventilation perfusion mismatching, intrapulmonary shunting, and hypoxemia, thrombus, and hypertension, and death.