Fluid management in acute lung injury: Physiologic and clinical principles

The inability to improve the high mortality rate (>40%) of acute respiratory distress syndrome has forced many investigators to focus on the major etiologic event in this syndrome, namely lung edema formation. It is generally accepted that increased permeability of the alveolar epithelial- capillary endothelial barrier is the most prominent abnormality in the lungs during the early stages of this syndrome. This capillary leak is underestimated by the traditionally measured pulmonary capillary wedge pressure (PCWP). A better measure of microvascular pressure is pulmonary capillary pressure (P(c)), which can be estimated by using a conventional pulmonary artery catheter. In healthy individuals, PCWP measuring the left- heart filling pressure is very close to P(c). However, in critically ill patients, the two may drift apart and even move in opposite directions. This may be particularly true when positive end-expiratory pressure is added. Therefore, estimates of the more accurate P(c) should be added to the routine measurements of PCWP. There is a preponderance of evidence that volume administration contributes to edema formation and should be kept to minimal amounts needed to maintain satisfactory left-heart filling pressure. Further, volume infusion not only has no added benefit but also causes elevated right- heart pressure. This exacerbates lung edema formation in acute lung injury as well as in other critical illnesses. Controversy continues regarding the use of colloids versus crystalloids. Although both can be used to achieve the same physiologic end points, a greater volume of crystalloid is needed to accomplish this. The clinical significance of this is uncertain.