Bovis ISSN 2398-2993

Patent ductus arteriosus

Synonym(s): PDA, congenital heart disorder

Contributor(s): Louise Cox-O’Shea , Gayle Hallowell

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  • Cause: fetal communication between aorta and pulmonary artery fails to close at birth.
  • Signs:
    • Spectrum from no clinical signs to left-sided congestive heart failure.
    • Continuous, waxing and waning - 'machinery murmur' (pathognomonic), but becomes systolic as animals age.
  • Diagnosis: clinical signs, ultrasonography.
  • Treatment: none currently practical in cattle.
  • Prognosis: poor.



  • During fetal life the ductus arteriosus connects the pulmonary artery to the aorta allowing blood from the right ventricle to bypass the constricted pulmonary circulation and go directly to the placenta. At this stage blood flows from right to left.
  • At birth the lungs inflate and there is a dramatic decrease in pulmonary resistance, at the same time as an increase in systemic resistance and elimination of placental flow. Blood now flows preferentially to the lungs and flow in the ductus is from left to right.
  • Over the first few days of life the ductus closes in response to several factors including increased oxygen tension and changing prostaglandin levels; this occurs in the first 3-4 days.
  • Until complete anatomic closure occurs the ductus can re-open if the calf develops Hypoxemia Hypoxemia and pulmonary hypertension.
  • Patent ductus artieriosus (PDAs) therefore remain open either because of failure of anatomic closure or because other defects result in abnormal pressures, blood flow or oxygen tensions, such as neonatal high altitude disease, sepsis, Neonatal ARDS.


  • The ductus arteriosus, a normal fetal vessel, fails to close in the first hours or days after birth    →   conduit between the descending aorta and the pulmonary trunk.


  • Pulmonary vascular resistance is much lower than systemic vascular resistance so: 
    • Left to right shunt (aorta to pulmonary artery)    →     increased flow through pulmonary vasculature    →     increased return to left heart    →     volume overload of left heart    →     chronic left-sided CHF CHF.
  • Dilation and eccentric hypertrophy of left atrium/ventricle can result in rare circumstances, mitral regurgitation (MR) due to stretching of the mitral annulus.
  • MR as a consequence is much rarer than in other species because cattle have a solid supporting framework between the atria and ventricles that is initially made of cartilage and then ossifies. 


  • Right-to-left shunt.
  • Pulmonary hypertension    →   due to retention of fetal type pulmonary vasculature and/or massive pulmonary overcirculation with a left-right shunt resulting in reactive hypertension (a left-to-right shunt typical of PDA)    →   pulmonary overcirculation    →   pulmonary hypertension (as Eisenmenger's physiology)    →    right-left shunt.


  • Depends on presence of other congenital abnormalities.


  • This is an extremely rare condition in cattle and as such there are insufficient publications to identify breed and gender predispositions.
    • One group of animals with an increased prevalence are cattle born at altitude with high altitude disease and increased pulmonary artery pressures. 


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMed Resource.
  • Summerfield N J & Holt D E (2005) Patent ductus arteriosus ligation and pulmonary artery banding in a kitten. J Am Anim Hosp Assoc 41, pp 113-116.
  • Lee B H & Kim W G (2004) A case of patent ductus arteriosus in a holstein calf. J. Vet Sci (1), pp 83-84 PubMed.
  • Schneider M & Hildebrant N (2003) Transvenous embolization of the patent ductus arteriosus with detachable coils in 2 cats. J Vet Intern Med 17, pp 349-353 PubMed.
  •  Prescott J R R, Slater J D & Jackson P G (1997) Patent ductus arteriosus in an 11- month- old heifer. Veterinary Record 140 pp 430-431 PubMed.
  • Allen D G (1982) Patent ductus arteriosus in a cat. Can Vet J 23, pp 22-23 PubMed.
  • Jones C L & Buchanan J W (1981) Patent ductus arteriosus: anatomy and surgery in a cat. JAVMA 179, pp 364-369 PubMed.