Etiology

• 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 to go directly to the placenta. At this stage blood flows from right (pulmonary artery) to left (descending aorta).
• At birth the lungs inflate and there is a dramatic decrease in pulmonary resistance, at the same time as an increase in systemic vascular 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 days of life in a normal foal. Until complete anatomic closure occurs the ductus can re-open if the foal develops hypoxemia and pulmonary hypertension.
• PDAs therefore remain open either because of failure of anatomic closure or because other defects result in abnormal pressures, blood flow or oxygen tensions.

Pathophysiology

• The PDA allows blood to pass from the high pressure aorta, to the relatively low pressure pulmonary artery.
• This leads to overcirculation of the lungs.
• If the ductus is large there will be volume overload of the left side of the heart.
• In many cases the horse will progress to left-sided heart failure.
• In the presence of severe pulmonary hypertension, blood can flow through the PDA from pulmonary artery to aorta, and lead to differential cyanosis, that is the caudal portion of the body receives non-oxygenated blood whereas the cranial part of the body receives oxygenated blood.

Timecourse

• Depends on presence of other congenital abnormalities.