Patent ductus arteriosus (PDA) is one of the more common congenital cardiac defects, representing up to 10% of congenital heart defects. It is caused by a non-regressed communication between the pulmonary artery and the descending thoracic aorta when the normal physiological closure of the fetal ductus fails to occur. If left untreated, it has an estimated mortality of 1.8% per year in adulthood. This persistent vessel causes left-to-right shunting to an extent determined by both the calibre of the PDA and also the pulmonary vascular resistance. The murmur is due to the movement of blood, continuously from a high pressure vessel to a low pressure vessel. Hence the intensity of the murmur will be based upon the pressure differences between the two vessels.

Clinical findings:

  • Collapsing pulse (in large defects)
  • Thrusting apex beat due to volume overload (in large defects)
  • Continuous machinery murmur heard best at the end of systole
  • Radiation to the clavicle and to the back
  • Can also have an associated thrill
  • Large defects left untreated may over time lead to pulmonary hypertension (RV heave, loud P2), right heart failure (raised JVP, peripheral oedema) and Eisenmenger’s syndrome (clubbing and cyanosis).

Patent ductus arteriosus (PDA) is primarily confirmed with echocardiogram or cardiac MRI.

In adults, a small PDA tends to be an incidental finding, however even in small asymptomatic PDAs there is an increased risk of endocarditis if left untreated. Diagnosis of PDA is primarily confirmed with echocardiogram or cardiac MRI.

ECG changes

  • Normal in small PDA
  • Left atrial dilatation (large PDA)
  • Left ventricular strain (large PDA)


In neonates, treatment is with intravenous indomethacin. The mainstay of treatment of a PDA in adults is either catheter closure or surgical ligation, which entails a thoracotomy.