Patent ductus arteriosus
Patent ductus arteriosus (PDA) is a congenital heart defect wherein a neonate's ductus arteriosus fails to close after birth. Symptoms are uncommon but in the first year of life include increased work of breathing and poor weight gain. With age, the PDA may lead to congestive heart failure if left uncorrected.
Etiology
A patent ductus arteriosus can be idiopathic (i.e. without an identifiable cause), or secondary to another condition. Some common contributing factors in humans include: - Premature infants - Congenital rubella syndrome - Chromosomal abnormalities such as Down Syndrome.
Normal ductus arteriosus closure
In the developing fetus, the ductus arteriosus (DA) is the vascular connection between the pulmonary artery and the aortic arch that allows most of the blood from the right ventricle to bypass the fetus' fluid-filled compressed lungs. During fetal development, this shunt protects the right ventricle from pumping against the high resistance in the lungs, which can lead to right ventricular failure if the DA closes in-utero.
When the newborn takes its first breath, the lungs open and pulmonary vascular resistance decreases. After birth, the lungs release bradykinin to constrict the smooth muscle wall of the DA and reduce bloodflow through the DA as it narrows and completely closes, usually within the first few weeks of life. In most newborns with a patent ductus arteriosus the blood flow is reversed from that of in utero flow, ie. the blood flow is from the higher pressure aorta to the now lower pressure pulmonary arteries.
In normal newborns, the DA is substantially closed within 12-24 hours after birth, and is completely sealed after three weeks. The primary stimulus for the closure of the ductus is the increase in neonatal blood oxygen content. Withdrawal from maternal circulating maternal prostaglandins also contributes to ductal closure. The residual scar tissue from the fibrotic remnants of DA, called the ligamentum arteriosum, remains in the normal adult heart.