A neonate born at 34 weeks is found to have a patent ductus arteriosus (PDA). Physiologically, the ductus arteriosus normally closes soon after birth primarily because of:

• A Elevated PaO2 causing smooth muscle contraction in the DA wall
• B Fall in prostaglandin E2 levels after placental separation
• C Increased pulmonary vascular resistance causing left-to-right shunt reversal
• D Both A and B — oxygen constricts DA wall and PGE2 falls after cord clamping ✓

Explanation

The ductus arteriosus remains patent in fetal life due to low oxygen tension (fetal PaO2 ~25–30 mmHg) and high circulating PGE2 from the placenta, both of which relax DA smooth muscle. After birth, two simultaneous events promote DA closure: the rise in PaO2 with the first breath directly constricts DA smooth muscle (via oxygen-sensitive potassium channels), and the loss of placental PGE2 after cord clamping removes the vasodilatory stimulus. Indomethacin (a PGE inhibitor) exploits this mechanism therapeutically.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.