Patent ductus arteriosus (PDA’s) represent up to 10% of the congenital heart defects in children. The male to female ratio differs in the literature with a male predominance (1:3) to female predominance (1:2). If left untreated, it has an estimated mortality of 1.8% per year in adulthood.

In adults, it tends to be an incidental finding. However, even in small PDAs which are asymptomatic there is an increased risk of endocarditis if left untreated.

PDA is primarily confirmed with echocardiogram or cardiac MRI.  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.  It is one of the more common congenital cardiac defects.

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.  In some patients this leads to potentially large flows between the systemic and pulmonary circulations.  As a consequence blood flow through the lungs may become excessive and lead to pulmonary engorgement.  PDA’s can also lead to Eisenmenger’s syndrome.

ECG changes

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


In infants, treatment is with intravenous indomethacin – however, this is never used in adults.  The mainstay of treatment of a PDA is either catheter closure or surgical ligation, which entails a thoracotomy.