Patent Ductus Arteriosus


Patent ductus arteriosus.svg
Diagram of a cross-section through a heart with PDA


  • The ductus arteriosus is a communication between the pulmonary artery and the aortic arch, distal to the left subclavian artery.
  • A patent ductus arteriosus (PDA) indicates the failure of the fetal ductus arteriosus to close after birth.


  • PDA produces a left to right shunt that leads to increased blood flow to the lungs.
  • The amount of blood that flows through the ductus and the degree of symptoms is determined by the difference in systemic vs. pulmonary vascular resistance, and in the circumference and the length of the PDA.


  • The incidence of PDA has increased dramatically over the last 2 decades due to improved survival of premature infants, especially those < 30 weeks gestation
  • The incidence of an isolated PDA in term infants ranges from 0.03 to 0.08 percent
  • There is a 2:1 female to male predominance
  • Increased incidence in infants born at high altitude compared to sea level 
  • Increased incidence in infants with congenital rubella
  • Having a sibling with a PDA increases the chance of having a PDA by 2-4% 


  • Clinical manifestations of a PDA are determined by:
    • Degree of left to right shunt, which depends on the size and length of the PDA
    • The difference between pulmonary and systemic vascular resistance
  • The murmur of a PDA is described as a medium pitched high-grade continuous murmur heard best at the pulmonic position, with a harsh machinelike quality that often radiates to the left clavicle.
  • The first heart sound is normal but the second heart sound is obscured by a continuous crescendo-decrescendo murmur, which runs from the start of systole to the end of diastole, peaking at the second heart sound.


Listen to the PDA:

Symptoms that parents notice

  • Fast breathing
  • Poor feeding habits
  • Shortness of breath
  • Sweating while feeding
  • Tiring very easily
  • Poor growth

Physical Exam Findings

  • Tachycardia
  • Respiratory problems
  • Continuous machine-like murmur
  • Cardiomegaly
  • Bounding pulses
  • Widened pulse pressure

Differential of continuous murmurs

  • Physical exam should distinguish a PDA from:
    • A venous hum is more located on the right side, and changes with position an local compression
    • Murmurs of systemic AV fistulas are in extracardiac locations
    • Murmurs of coronary artery fistulas are mostly located over the lower precordium
    • Aortopulmonary window often only has a systolic murmur
    • Aortic Stenosis or ventricular septal defect (VSD) with aortic regurgitation has characteristic systolic and diastolic murmurs


  • The diagnosis of a PDA is determined by clinical findings, but is typically confirmed by echocardiography.
  • Chest x-rays and electrocardiograms may be helpful, but are less sensitive and specific than echocardiography.


  • Heart Failure due to cardiac volume overload
    • Infants present with: failure to thrive (FTT), poor feeding, respiratory distress
  • Infective Endocarditis: vegetations accumulate at the pulmonary end of the PDA and shower the lungs with septic emboli
  • Pulmonary Hypertension
    • Presentation: continuous murmur vanishes  a right ventricular impulse is visualized on exam, auscultation reveals a prominent pulmonary ejection sound, a loud single second heart sound, or a Graham Steell murmur


  • If a newborn has a PDA, pharmaceutical treatment is used to encourage closure, primarily with indomethacin or ibuprofen.
  • If the newborn fails to respond to medical management, surgery or cardiac catheterization procedures are recommended.
  • Premature infants with PDAs are at an increased risk for heart failure, which may be treated with diuretics and/or digitalization.
  • Surgery is indicated for infants with heart failure who have failed to respond to medical management and for any child older than 12 months of age.
  • Antibiotic prophylaxis is not recommended in patients with unrepaired PDA unless they develop Eisenmenger syndrome.

Resources for Families


  1. NursePub/UCSF & Mt Zion Nursing Services/Unit Documents/6picu/cardiac defectsbook.pdf
  2. Johns Hopkins University, Helen B. Taussig Children’s Heart Center website:
  3. Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol 2002; 39:1890.
  4. Reller MD, Strickland MJ, Riehle-Colarusso T, et al. Prevalence of congenital heart defects in metropolitan Atlanta, 1998-2005. J Pediatr 2008; 153:807.
  5. Coggins KG, Latour A, Nguyen MS, et al. Metabolism of PGE2 by prostaglandin dehydrogenase is essential for remodeling the ductus arteriosus. Nat Med 2002; 8:91.
  6. Nora JJ. Multifactorial inheritance hypothesis for the etiology of congenital heart diseases. The genetic-environmental interaction. Circulation 1968; 38:604.
  7. Mullins CE. Patent ductus arteriosus. In: The Science and Practice of Pediatric Cardiology, Garson A, Bricker JT, McNamara DG (Eds), Lea & Febiger, Philadelphia 1990. p.1055.


Back to Table of Contents