Patent Ductus Arteriosus (PDA): Pathophysiology, Murmur, and Management

A patent ductus arteriosus (PDA) is persistent patency of the fetal ductus arteriosus beyond the neonatal period.

Normal Physiology

• Fetal life: Ductus shunts oxygenated blood from pulmonary artery → aorta (bypasses fluid-filled lungs). Prostaglandin E₂ maintains patency.
• After birth: Lung inflation → ↑PO₂ → prostaglandin drop → functional closure by 24–48 h; anatomic closure by 2–3 weeks.

PDA Pathophysiology

• Left-to-right shunt: Aorta (high pressure) → pulmonary artery (low pressure).
• Volume overload: ↑ pulmonary blood flow → pulmonary hypertension (if large/untreated) → Eisenmenger reversal (right-to-left shunt, cyanosis).
• Left heart volume overload → LA/LV dilation → heart failure.

Clinical Features

• Continuous "machinery" murmur: Best at left upper sternal border/left infraclavicular. Systolic + diastolic components.
• Wide pulse pressure (bounding pulses) from diastolic runoff.
• Failure to thrive, recurrent respiratory infections, exercise intolerance.
• Preterm infants: apnea, ventilator dependence, IVH, NEC.

Diagnosis

• Echo: ductal size, shunt direction/magnitude, PA pressure, LA/LV dimensions.
• CXR: cardiomegaly, pulmonary overcirculation.
• ECG: LVH ± RVH.

Treatment

• Preterm infants: IV ibuprofen or indomethacin (COX inhibition → closure). Surgery if failed/contraindicated.
• Term infants/children/adults: Transcatheter device closure (Amplatzer) — preferred. Surgical ligation if anatomy unsuitable.
• Asymptomatic small PDA: Monitor; may close spontaneously in infancy.

Untreated large PDA leads to irreversible pulmonary vascular disease. Early closure normalizes life expectancy.