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Hemodynamic Characterization of Patients with Severe Emphysema

Pulmonary and Critical Care Divisions, Long Island Jewish Medical Center, Long Island Campus for the Albert Einstein College of Medicine, New Hyde Park, New York; St. Louis University School of Medicine, St. Louis, Missouri; Temple University School of Medicine, Philadelphia, Pennsylvania; and Johns Hopkins Medical Institutions, Baltimore, Maryland

Correspondence and requests for reprints should be addressed to Steven M. Scharf, M.D., Ph.D., Pulmonary and Critical Care Division, University of Maryland Baltimore, 685 West Baltimore St., MSTF 800, Baltimore, MD 21201-1192. E-mail: sscharf{at}medicine.umaryland.edu

In 120 patients with severe emphysema evaluated for participation in the National Emphysema Treatment Trial, pulmonary hemodynamics and ventricular function were assessed. Pulmonary function tests were (%predicted): FEV₁ = 27%; residual volume = 224.6%; diffusion capacity = 26.7%. In 90.8% of patients, end-expiratory pulmonary artery mean pressure was > 20 mm Hg; in 61.4%, end-expiratory wedge pressure was > 12 mm Hg. Cardiac index was normal. Mean pulmonary artery pressure correlated inversely with arterial PO₂, and severity of emphysema, and directly with wedge pressure. Multiple stepwise regression revealed that arterial PO₂ was not an independent predictor of mean pulmonary artery pressure. No correlation was found between indices of emphysema severity and PA pressures. Diastolic ventricular pressures were increased without evidence of systolic dysfunction. We conclude that (1) elevations of pulmonary vascular pressures are common, (2) pulmonary hypertension may be related to factors other than hypoxia, (3) pulmonary hypertension does not impair resting systemic O₂ delivery, and (4) elevated cardiac diastolic pressures do not represent systolic dysfunction.

Key Words: emphysema • pulmonary hypertension • cardiovascular function

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