The purpose of this study is to examine the hemodynamics of the pulmonary circulation and the potential role of pulmonary blood flow in the pathogenesis of cardiogenic pulmonary edema. To do so, the pulmonary circulation was isolated and controlled such that, within a closed circuit, pulmonary blood flow and left atrial pressure (LAP) could be regulated independently: the first by a constant flow pump, the second by a variable height reservoir. The effect of pulmonary blood flow on pulmonary artery pressure and intravascular blood volume was then determined at different LAPs. Contrary to our expectations, the results indicate that (1) pulmonary vascular resistance does not change appreciably as flow increases, (2) the microcirculation comprises the major capacitance vessels of the lung, and (3) increased pulmonary flow in the normal lung causes little change in intravascular pulmonary blood volume, whereas, by contrast, major changes in pulmonary blood volume occur as LAP rises. Next, the effect of pulmonary blood flow on edema formation in the lungs was examined. Below a critical level of LAP (15 mm Hg in these experiments), pulmonary blood flow up to 5 L/min did not produce pulmonary edema. Above this level, however, such an effect was clear. Thus, at an LAP of 20 mm Hg, edema did not develop if pulmonary flow was low (0.7 L/min) but did if flow was increased to 2 L/min. As well, if the LAP was 17.5 mm Hg and pulmonary flow 3.5 L/min, severe pulmonary edema also resulted.
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Cardiology and Cardiovascular Medicine