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HEMODYNAMIC AND ALVEOLAR PROTEIN STUDIES IN NONCARDIAC PULMONARY EDEMA
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1977
Year
Acute Lung InjuryMm HgPulmonary Alveolar ProteinosisCardiac DilationSepsisPublic HealthCardiologyAssisted CirculationPulmonary CirculationPulmonary MedicinePulmonary Vascular DiseasePulmonary EmbolismProtein ContentPulmonary Arterial HypertensionCardiovascular DiseasePulmonary PhysiologyLung MechanicsMedicineEmergency Medicine
Hemodynamic data were obtained within 15 hours of admission in 11 previously healthy patients (20 to 51 years of age, 7 men and 4 women) who had developed transient, reversible pulmonary edema without cardiac dilation in association with near-death from freshwater drowning (2 cases), pentobarbital overdose, heroin overdose (2 cases), smoke inhalation, chest trauma, sepsis (2 cases), pancreatitis, or prolonged abdominal surgery with suspected sepsis. Using a balloon-tipped flow-directed catheter, the pulmonary artery systolic/diastolic pressures (in mm Hg) were 25/12, 22/9, 31/11, 26/15, 20/10, 35/15, 40/15, 32/18, 20/10, 24/10, and 20/7; the corresponding pulmonary capillary wedge pressures (in mm Hg) were 8, 9, 6, 14, 6, 6, 15, 15, 10, 10, and 5, respectively. Plasma colloidal osmotic pressures measured in the latter 5 cases were 26, 18, 18, 18, and 15 mm Hg, respectively. In addition, the protein content of the alveolar fluid was 5.1, 3.4, 4.0, and 7.1 g per 100 ml in 4 patients. The concentration and distribution of the protein in plasma and alveolar fluid were very similar. These findings provide strong efidence that altered capillary permeability is responsible for the pulmonary edema.