High pulmonary vascular resistance after birth: I. Pathophysiologic considerations and etiologic classification.
The clinical syndrome known as persistent fetal circulation, or persistent pulmonary hypertension of the newborn, is characterized by maintenance of a high pulmonary vascular resistance after birth. The small pulmonary arteries of the fetus have a thick muscular medial layer; they are very reactive, being actively constricted by the low PO2 levels normally present during fetal life. The pulmonary vascular smooth muscle layer is hypertrophied in conditions that result in chronic fetal hypoxia, or a maintained increase in pulmonary arterial pressure. Normally, pulmonary vasodilation occurs rapidly after birth, partly related to physical expansion with gas, but mainly due to the increased PO2 associated with ventilation with air. Based on these developmental considerations, the factors responsible for an increased pulmonary vascular resistance after birth may be classified in three main groups: (A) Acute vasoconstriction due to postnatal hypoxia and aggravated by acidemia; (B) Prenatal increase in pulmonary vascular smooth muscle development; and (C) Decreased cross sectional area of the pulmonary vascular bed due to inadequate numbers of vessels. The various mechanisms that may promote these responses are presented.
D000818:Animals; D001794:Blood Pressure; D001809:Blood Viscosity; D005260:Female; D005312:Fetal Blood / Q000502:physiology; D005311:Fetal Hypoxia / Q000150:complications; D005333:Fetus / Q000502:physiology; D006330:Heart Defects, Congenital / Q000150:complications; D006801:Humans; D007231:Infant, Newborn; D008168:Lung / Q000196:embryology; D010547:Persistent Fetal Circulation Syndrome / Q000209:etiology / Q000503:physiopathology*; D011247:Pregnancy; D011652:Pulmonary Circulation; D051381:Rats; D014655:Vascular Resistance; D014661:Vasoconstriction