•Fetal circulation contains hemoglobin F. At a placental PO2 of 30 mmHg, fetal hemoglobin becomes ~70% saturated and maternal hemoglobin (Hgb A) becomes ~50% saturated. The ‘left shift’ of Hgb F, therefore, permits oxygen offloading from mother to baby, but also creates more fetal tissue hypoxia at a given SO2.
•Pulmonary vascular resistance is elevated in the fetal lungs (amniotic fluid-filled), diverting the majority of RV output to the descending aorta via ductus arteriosus. Pulmonary blood flow is only ~7% of combined output, potentially masking lesions that obstruct pulmonary venous return (e.g. TAPVC).
•Only ~10% of cardiac output crosses from the ascending to descending aorta in utero, making this region susceptible to underdevelopment in the setting of left heart obstructive lesions and shunts.
•RV does ~66% of stroke work in utero; LV does ~34%. The DA remains unrestrictive throughout fetal life, such that the RVP=LVP (absent valvar stenosis).
•Fetal myocardium minimally increases stroke volume in response to increased atrial pressure and decreases stroke volume significantly in response to increased afterload.
Within hours of birth, several key factors transition the circulation from fetal to normal postnatal physiology.
•At the first cry, the lungs fill with air (raising alveolar oxygen tension) and fluid is resorbed, lowering pulmonary vascular resistance significantly.
•The umbilical cord is clamped, removing the low resistance placental circuit from the systemic circulation.
•Together, these factors promote pulmonary blood flow (which increases 5X within minutes of birth) and increase arterial oxygenation. PDA flow changes direction, primarily going left to right (aorta to PA) and further increasing PBF. Factors that increase PVR, including lung disease, pulmonary hypoplasia, acidosis, hypoxemia may delay this transition (i.e. persistent fetal circulation).
•The removal of the placenta decreases SBF (and right atrial return) and the decrease in PVR increases PBF (and left atrial return), causing an increase in LAP relative to RAP and PFO closure.
•In term infants without cyanosis, PDA closure typically occurs within 10-15 hours. However, PDA reopening is sometimes achievable with PGE1 infusion within the first 1-2 weeks of life.