ABSTRACT
I. Introduction Fluid management for patients with acute lung injury (ALI) has been an area of uncertainty and controversy for approximately three decades (1-4). Several observational studies have suggested that restricting the quantity of fluid replacement might be beneficial in reducing the extent of pulmonary edema in patients with ALI. On the other hand, there has been concern that a restrictive fluid management strategy might potentiate nonpulmonary organ failure. From a physiologic perspective, although the fundamental mechanism responsible for pulmonary edema formation in ALI can be best explained by an increase in lung vascular permeability, elevation in lung vascular hydrostatic pressures also does result in a greater increase in extravascular lung water (Fig. 1). Short-term experimental studies demonstrated that lowering pulmonary vascular pressure was an effective mechanism for reducing lung edema in models of lung injury. A classic study by Prewitt and coworkers (5) published in 1981 demonstrated that lowering left atrial hydrostatic pressure reduced the quantity of lung edema in short-term studies of oleic acid-induced lung injury in dogs. Also, based on several experimental studies in 1978, Staub provided a convincing physiologic rationale for the likely value of lowering pulmonary vascular pressures in noncardiogenic pulmonary edema (6).
