Increased cardiac output increases shunt: role of pulmonary edema and perfusion.
In low-pressure pulmonary edema increased cardiac output (QT) increases shunt (Qs/QT); we tested whether the mechanism is an increase in extravascular lung water in turn mediated by the accompanying increase in microvascular pressure. In six pentobarbital sodium-anesthetized dogs ventilated with O2 we administered oleic acid into the right atrium. From base line to 2 h post-oleic acid we measured concurrent significant increases in Qs/QT (6-29%, O2 technique) and extravascular thermal volume (ETV, 2.6-7.1 ml/g dry intravascular blood-free lung wt, thermal-green dye indicator technique) that were stable by 90 min. Then, bilateral femoral arteriovenous fistulas were opened and closed in 30-min periods to cause reversible increases in QT and associated Qs/QT. When fistulas were open the time-averaged QT increased from 5.1 to 6.9 min (P less than 0.05), the simultaneous Qs/QT rose from 30.7 to 38.4% (P less than 0.05), but ETV did not increase. We conclude that increasing lung edema does not account for our rise in Qs/QT when QT increased.
D000818:Animals; D001164:Arteriovenous Fistula / Q000503:physiopathology; D002302:Cardiac Output; D004285:Dogs; D005263:Femoral Artery; D005268:Femoral Vein; D007201:Indicator Dilution Techniques; D019301:Oleic Acid; D009829:Oleic Acids; D011652:Pulmonary Circulation; D011653:Pulmonary Diffusing Capacity; D011654:Pulmonary Edema / Q000139:chemically induced / Q000503:physiopathology*; D013997:Time Factors; D014692:Ventilation-Perfusion Ratio
D009829:Oleic Acids; D019301:Oleic Acid