Hypoxic pulmonary vasoconstriction: clinical implications.

Fetal origin of HPV HPV originates in the fetus [3]. Vasomotor tone can be detected in the human fetal pulmonary circulation in the last trimester of pregnancy [4]. HPV contributes significantly to the high pulmonary vascular resistance (PVR) in the fetus (only 10–15% of right ventricular outflow goes to the lungs) [5], mainly because pulmonary artery and alveolar fluid oxygen tension (PO2) levels are considerably lower (18 mmHg) than they are after birth; also, the fetal pulmonary arteries are more muscularised (this regresses in the neonatal period). The low PO2 in the fetal pulmonary artery, versus that in the fetal aorta, is due to “streaming” in the right ventricle, whereby oxygen-poor blood from the tissues enters via the superior vena cava and is directed to the pulmonary circulation; oxygen-enriched blood (via the placental vein) enters from the inferior vena cava and passes into the left ventricle via the foramen ovale.