In utero fetal circulation is different from adult circulation in 4 primary ways:
- Umbilical venous blood bypasses the liver by way of the ductus venosus
- Blood is shunted from right atrium to left atrium through the foramen ovale
- Blood ejected from the right ventricle bypasses the lungs by traveling through the ductus arteriosus and into the systemic circulation
- Blood travels back to the placenta by way of the umbilical artery
The high pulmonary vascular resistance (PVR) of the fetus is responsible for the shunting of blood away from the lungs and through the foramen ovale and ductus arteriosus. As the alveoli are first exposed to oxygen after birth, the PVR decreases resulting in increased flow in the adult circulatory pattern, and eventual closure of the foramen ovale and ductus arteriosus.
There are 3 main categories of etiologies of persistent fetal circulation (PFC) in the newborn:
- Congenital heart defect
Any congenital heart defect which results in elevated pulmonary artery or RV pressures will have PFC in order to allow adequate cardiac output. The effect this will be R –> L shunt and cyanosis.
- Primary PFC
Hypertrophy and increased muscularization of the walls of the pulmonary vessels results in persistently elevated PVR. Poor prognosis.
- Secondary PFC
Most commonly seen in infants with lung disease, where hypoxia and acidosis leads to pulmonary vasoconstriction and persistently elevated PVR. Causes include:
- Meconium aspiration (most common)
- Hyaline membrane disease
- Diaphragmatic Hernia
- Sepsis syndrome (often related to GBS, listeria, E Coli, H influenzae B)
- Pulmonary embolism
Defined by: Pablo Kollmar, MD