The Journal of Thoracic and Cardiovascular Surgery, Vol 87, 130-135, Copyright © 1984 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Pulmonary blood flow. A potential factor in the pathogenesis of pulmonary edema
A Sniderman, T Burdon, J Homan and TA Salerno
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.
