Pathogenesis of respiratory failure (ARDS) after hemorrhage and trauma: I. Cardiorespiratory patterns preceding the development of ARDS.

To evaluate clinical and physiologic determinants of adult respiratory distress syndrome (ARDS), we studied 152 consecutively monitored patients with trauma and hemorrhage: 60 developed ARDS. The cardiorespiratory patterns of hemorrhage and trauma patients who did not develop ARDS were compared to those who subsequently did develop ARDS, but before the time of their ARDS. Comparisons also were made in the patients with trauma and those with hemorrhage, as well as in those who survived and those who did not. Hemorrhage and trauma patients who developed ARDS had greater reductions in blood volume, red cell mass, PaCO2 and O2 delivery throughout all stages, as well as greater pulmonary vascular resistance index (PVRI) and pH in the early and middle stages. Nonsurvivors of ARDS had greater deficits in blood volume and red cell mass, higher PVRI and pH, as well as lower central venous pressure (CVP), hemoglobin (Hgb), and PaCO2 than did ARDS survivors. Hemorrhage patients had lower blood volume, left ventricular function, O2 delivery and VO2, as well as higher systemic vascular resistance index (SVRI), PVRI, and O2 extraction than either the trauma patients or normal subjects. Description of the temporal cardiorespiratory patterns before the clinical appearance of ARDS showed the progressive appearance of these deficits beginning 36 h before the hypoxemia was observed. The data are consistent with the concept that ARDS after hemorrhage and trauma is preceded by hypovolemia, reduced myocardial performance, inadequate O2 delivery, and inadequate O2 extraction needed to maintain VO2 at the elevated levels demanded by the increased metabolic requirements of the injured patients. Thus, the so-called shock lung is a complication of shock associated with hypovolemia, hypoxemia, and inadequate cardiac compensatory responses to increasesd O2 demands.