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The umbilical vein, not the ductus arteriosus, becomes the ligamentum teres (also known as the round ligament of the liver) after birth. The umbilical vein is responsible for carrying oxygenated blood from the placenta to the fetus, and its obliteration occurs after the cessation of placental blood flow.

The foramen ovale, a fetal shunt located in the interatrial septum, forms the fossa ovalis after birth. The functional closure of the foramen ovale occurs almost immediately due to the increased left atrial pressure and decreased right atrial pressure, with anatomical closure typically completed over several weeks to months.

If the ductus arteriosus remains patent after birth, it results in a condition called patent ductus arteriosus (PDA), which is a congenital heart defect, not a normal physiological outcome. A patent ductus arteriosus leads to left-to-right shunting of blood, causing pulmonary overcirculation and potentially heart failure, rather than supporting normal pulmonary circulation. Its closure is essential for establishing independent pulmonary circulation.

A significant decrease in systemic vascular resistance is incorrect. As explained, the removal of the low-resistance placental circuit leads to an increase in systemic vascular resistance, not a decrease. This increase is crucial for elevating systemic blood pressure and facilitating the postnatal circulatory changes.

A dramatic increase in pulmonary vascular resistance (PVR) is incorrect. In fetal life, PVR is high due to the unexpanded, fluid-filled lungs and hypoxic pulmonary vasoconstriction. At birth, with the first breaths and the expansion of the lungs, oxygen tension in the alveoli increases dramatically. This rise in oxygen tension, along with mechanical expansion, causes a rapid and dramatic decrease in pulmonary vascular resistance, allowing for a significant increase in pulmonary blood flow.

A decrease in aortic pressure is incorrect. Following the clamping of the umbilical cord and the resultant increase in systemic vascular resistance, there is an immediate and substantial increase in aortic pressure. This rise in systemic pressure is vital for reversing the pressure gradients across fetal shunts (like the foramen ovale and ductus arteriosus) and establishing the adult pattern of circulation.

Prostaglandin E2 maintains fetal circulation by keeping the ductus arteriosus patent. Increased levels do not reduce PVR; in fact, decreased prostaglandin levels after birth contribute to ductal closure. High prostaglandin E2 sustains high PVR in utero by promoting vasoconstriction in the pulmonary bed.

Clamping of the umbilical cord increases systemic vascular resistance, not pulmonary vascular resistance. While it redirects blood flow away from the placenta, it does not directly cause the drop in PVR. The decrease in PVR depends on alveolar oxygenation and mechanical expansion, not cord clamping.

Closure of the ductus arteriosus is a consequence of increased oxygen and decreased prostaglandins after PVR drops. It follows PVR changes rather than causes them. Its closure helps establish adult circulation patterns but is not the initiating event for PVR reduction.