Fetal to Neonatal Circulatory Transition

Expansion

Before birth: pulmonary vascular resistance is high (fluid-filled, hypoxic lungs) and systemic resistance is low (the low-resistance placenta), so blood is shunted right to left away from the lungs.

At birth, two changes reverse this:

1. First breath - lungs inflate, alveolar oxygen rises, hypoxic pulmonary vasoconstriction is released, and pulmonary resistance falls sharply
2. Cord clamping - the low-resistance placenta is removed, so systemic resistance rises

Consequences:

• Pulmonary blood flow rises, so left atrial pressure exceeds right atrial pressure and the flap of the foramen ovale is pressed shut; it seals over months
• The ductus arteriosus constricts in response to rising oxygen and falling prostaglandin E2, functionally closing within 24 to 48 hours
• The ductus venosus closes as umbilical flow ceases

Failure to make this transition, from hypoxia, acidosis or sepsis, leaves pulmonary resistance high and gives persistent pulmonary hypertension of the newborn, with continued right to left shunting. Prostaglandin E1 is used to keep the duct open in duct-dependent congenital heart disease.