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Patent ductus arteriosus (PDA) is a congenital heart defect wherein a child’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. In older children or adults the PDA may lead to congestive heart failure if left uncorrected.
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 newborn infants 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 fall in circulating maternal prostaglandins contributes to this. The residual scar tissue from the fibrotic remnants of DA, called the ligamentum arteriosum, remains in the normal adult heart.
Patent ductus arteriosus, or PDA, is a heart condition that is normal but reverses soon after birth. In a persistent PDA, there is an irregular transmission of blood between two of the most important arteries in close proximity to the heart. Although the ductus arteriosus normally seals off within a few days, in PDA, the newborn’s ductus arteriosus does not close, but remains patent. PDA is common in infants with persistent respiratory problems such as hypoxia, and has a high occurrence in premature children. In hypoxic newborns, too little oxygen reaches the lungs to produce sufficient levels of bradykinin and subsequent closing of the DA. Premature children are more likely to be hypoxic and thus have PDA because of their underdeveloped heart and lungs.
A patent ductus arteriosus allows that portion of the oxygenated blood from the left heart to flow back to the lungs (following the pressure gradient from the higher pressure aorta to the pulmonary arteries). If this shunt amount is substantial, the infant becomes short of breath because there is not only the normal amount of unoxygenated blood that has returned from the body to go to the lungs but in addition there is the amount shunted through the PDA. The infant’s work of breathing is increased, using up more calories and often interfering with feeding in infancy. This condition as a constellation of findings is called congestive heart failure.
In some cases, such as in transposition of the great vessels (the pulmonary artery and the aorta), a PDA may need to remain open. In this cardiovascular condition, the PDA is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the patent ductus arteriosus open.
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