 The patent ductus arteriosus is an example of an acyanotic heart defect. You'll recall from embryology that the ductus arteriosus is a shunt in fetal circulation from the pulmonary artery to the aorta. You'll see over here on the right side an example of a patent ductus arteriosus. Again, it's connecting the pulmonary artery and the aorta here. This is an acyanotic heart defect again because in a newborn the aorta is a much higher pressure vessel compared to the pulmonary artery so blood will flow down the pressure gradient from the aorta into the pulmonary artery here. Again, blood in the aorta is already oxygenated and oxygenated blood is still flowing into systemic circulation so there shouldn't be a cyanosis at presentation. We expect these defects to close usually within 24 hours of delivery and if they don't that's when we call them a patent ductus arteriosus. High yield association here is with congenital rubella so mothers that are infected with rubella during pregnancy they run the risk of having a child with a patent ductus arteriosus as well as some of the other features of congenital rubella syndrome. These patients on physical exam will have a continuous machine like murmur and what does continuous mean? That means it's a murmur that's present in both systole and diastole so if you ever have a question stem about a murmur present in both systole and diastole or you have a question where you have to put on the headphones and listen to a murmur and you hear it in both systole and diastole chances are it's caused by a PDA. Another physiology point you should be aware of here is the effect of a PDA on diastolic blood pressure. There will actually be a drop in the diastolic blood pressure in the setting of a PDA because again blood is being pulled away from the aorta into the pulmonary artery and it happens that happens preferentially during diastole and as a result of this decreased diastolic blood pressure will have an increased pulse pressure as well. And again we'll evaluate these patients with echo and it's particularly important in a patent ductus arteriosus patient because if the patient has another comorbid structural heart defect for example a transition of the great vessels or tetralgia flow that we'll mention in another video they might be dependent on the PDA to oxygenate their blood that may be the only connection between the right side and the left side of the heart so if you assume that it needs to be closed you may cut off the patient's only access to their pulmonary circulation and that brings us to the treatment so how do we treat these patients if we are confident that there's no comorbid structural heart defect we can treat these patients with indomethicin which is the NSAID and that should close the patent ductus arteriosus and if we note another heart defect that requires the PDA to be open we can maintain that PDA keep it open by administering prostaglandin E1 and a kind of pharmacology tie in here is something that could help you remember the treatment here so NSAIDs like indomethicin block the the production of prostaglandins thus they would close the patent ductus arteriosus whereas prostaglandins themselves will keep it open