Direct demonstration that blood flow through intrapulmonary arteriovenous anastomoses worsens pulmonary gas exchange efficiency

Pulmonary gas exchange efficiency is defined and quantified by the alveolar‐arterial PO 2 difference (AaDO 2 ). Sources of venous admixture (Q VA /Q T ) that increase AaDO 2 are ventilation‐perfusion (V/Q) inequality, diffusion limitation, and shunt (Q S /Q T ). Intravenous infusion of epinephrine (EPI) increases blood flow through intrapulmonary arteriovenous anastomoses (Q IPAVA ) in healthy humans at rest, as detected by saline contrast echocardiography, but whether or not this is a source of shunt remains controversial. We hypothesized that Q IPAVA is a source of shunt, and therefore, AaDO 2 would increase during EPI infusion in healthy humans at rest when Q IPAVA is increased. From baseline to max EPI infusion (320 ng/kg/min), AaDO 2 increased from 4.9 to 9.4 mmHg and Q VA /Q T increased from 2.8 to 3.8% in healthy subjects breathing room air (n=3). We repeated these measurements in the same subjects breathing 40% O 2 which increases alveolar PO 2 and reduces O 2 equilibration time from ~0.6 to <0.2 sec, thereby eliminating Q VA /Q T contributions from diffusion limitation and V/Q inequality, but still allowing for Q IPAVA to occur. From baseline to max EPI infusion breathing 40% O 2 , AaDO 2 increased from 17.3 to 23.7 mmHg and Q S /Q T increased from 4.4 to 5.4%. We conclude that Q IPAVA is a source of shunt, because Q VA /Q T and Q S /Q T both increased by 1% during max EPI infusion. Support: American Heart Association Predoctoral Fellowship