Increased cardiac output, not pulmonary artery systolic pressure, increases blood flow through intrapulmonary arteriovenous anastomoses and impairs pulmonary gas exchange efficiency (717.2)

Abstract

Sources of venous admixture (QVA/QT) that impair pulmonary gas exchange efficiency, defined by an increased alveolar‐arterial PO2 difference (AaDO2), are ventilation‐perfusion inequality (VA/Q), diffusion limitation, and shunt. Blood flow through intrapulmonary arteriovenous anastomoses (QIPAVA) increases QVA/QT and the AaDO2. However, it is unclear whether increased cardiac output (QT) or pulmonary artery systolic pressure (PASP) cause the increase in QIPAVA. We hypothesized that an increase in QT alone would increase QIPAVA resulting in an increased AaDO2 at rest breathing room air and 40% O2 to prevent contributions from diffusion and VA/Q. Epinephrine, i.v. at 320 ng/kg/min (EPI), and low dose epinephrine (80 ng/kg/min) combined with 2 mg of atropine (EPI+ATR) were used in healthy human subjects (n=5) to increase QT. When breathing either room air or 40% O2, EPI and EPI+ATR increased QT, (measured by acetylene uptake) from 7.8±1.0 to 13.3±3.4 L/min. Only EPI significantly increased PASP (to 54±14 mmHg), measured with ultrasound, but not with EPI+ATR (to 39±5 mmHg). However, EPI and EPI+ATR, breathing either room air or 40% O2 resulted in equal QIPAVA detected with saline contrast echocardiography. Furthermore, with EPI and EPI+ATR, the AaDO2 increased significantly when breathing either room air or 40% O2. Consistent with our data above, the calculated QVA/QT required to account for the entire AaDO2 was 2.4±0.4% with EPI and EPI+ATR, breathing either room air or 40% O2. We conclude that increased QT alone significantly increases QIPAVA and AaDO2 in healthy humans.Grant Funding Source: Supported by: Department of Defense #W81XWH‐10‐2‐0114, AHA Predoctoral Fellowship