title: Human pulmonary vascular and venous compliances are reduced before and during left-sided heart failure.
abstract: Human pulmonary vascular and venous compliances were measured in 41 patients with or without left-sided heart failure. Two methods were used. Method 1 was based on analysis of pulmonary capillary wedge (PCW) pressure tracings according to Cv,PCW = (SF/100)(0.075PCW + 0.90)SV/[(v - d)PCW + 1], where Cv,PCW is compliance of pulmonary venous system, SF is systolic fraction of pulmonary venous flow [related to pulmonary capillary wedge pressure (PCW) as SF = 82 - 2.01PCW], (v - d)PCW is pulse pressure in PCW position, and SV is stroke volume. The (0.075PCW + 0.90) term equals k", i.e., systolic run-off ratio. Method 2 was used to measure to pulmonary vascular volume-pressure (V-P) relationship and pulmonary vascular compliance (Cvasc) and is based on measurement of pulmonary blood volume (PBV) and its increase with passive elevation of the legs to calculate Cvasc. Assuming the proportion of blood entering pulmonary venous system (in increase of PBV) during passive leg elevation to be 0.8, pulmonary venous compliance (Cv,PBV) was calculated as Cv,PBV = 0.8Cvasc. Cv,PCW correlated fairly closely with Cv,PBV (r = 0.81, coefficient of variation = 31%). This fair agreement between two independent methods suggests strongly that both methods may be valid, although other interpretations are possible. Cv,PCW, Cvasc, and Cv,PBV decreased going from New York Heart Association class I to classes II and III. When PBV was plotted vs. PCW, average V-P line for class II patients was flatter and shifted downward to the right compared with that for class I. This suggests pulmonary vasoconstriction as well as other factors. Average V-P line for class III patients is flatter but not displaced compared with that for class II. Another previously reported series of 50 patients, most of whom had ischemic heart disease, are included in this study.
authors.affiliation: Second Department of Medicine, Gifu University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Hirakawa
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: K
authors.initials: K
authors.lastname: Gotoh
authors.forename: H
authors.initials: H
authors.lastname: Ito
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: Y
authors.initials: Y
authors.lastname: Ohsumi
authors.forename: Y
authors.initials: Y
authors.lastname: Yagi
authors.forename: Y
authors.initials: Y
authors.lastname: Terashima
authors.forename: H
authors.initials: H
authors.lastname: Fujiwara
authors.forename: K
authors.initials: K
authors.lastname: Nagashima
mesh_terms: D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D011651:Pulmonary Artery / Q000502:physiology; D011652:Pulmonary Circulation / Q000502:physiology*; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology*; D014661:Vasoconstriction / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology