## Pathophysiology of Patent Ductus Arteriosus ### Normal Ductus Closure **Key Point:** The ductus arteriosus is a normal fetal structure that allows right-to-left shunting. After birth, increased oxygen tension and decreased prostaglandin E2 levels trigger functional closure within 24–48 hours, followed by anatomical closure (ligamentum arteriosum) over weeks to months. ### PDA Hemodynamics **Key Point:** In PDA, the patent vessel allows left-to-right shunting (aorta → pulmonary artery) because systemic pressure exceeds pulmonary pressure. This increases pulmonary blood flow (Qp:Qs > 1) and causes: - Left atrial volume overload - Left ventricular volume overload and eccentric hypertrophy (NOT concentric) - Eventual left heart dilatation and dysfunction if untreated ### Auscultatory Finding **High-Yield:** The continuous 'machinery' or 'Gibson' murmur is pathognomonic for PDA. It: - Begins in systole and continues through S2 into diastole - Is best heard at the left infraclavicular region (left subclavian area) - Reflects continuous flow from high-pressure aorta to low-pressure pulmonary artery throughout the cardiac cycle ### Risk Factors for PDA **Clinical Pearl:** PDA risk factors include: - Prematurity (most common) - Maternal rubella infection in first trimester - Maternal alcohol use - Maternal anticonvulsant use - **NOT maternal indomethacin use** — indomethacin actually *promotes* ductus closure and is used therapeutically to close PDA in premature infants | Risk Factor | Effect on PDA | | --- | --- | | Prematurity | ↑ Risk (immature closure mechanism) | | Maternal rubella (1st trimester) | ↑ Risk (teratogenic) | | Maternal alcohol | ↑ Risk | | Maternal indomethacin | ↓ Risk (promotes closure) | | Maternal NSAIDs | ↓ Risk (promote closure) | **Warning:** Maternal indomethacin is *protective* against PDA, not causative. This is a common NEET PG trap — students confuse the therapeutic use of indomethacin in neonates (to close PDA) with a causative role in pregnancy.
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