patent ductus arteriosus

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Patent Ductus Arteriosus



Patent ductus arteriosus (PDA) is a heart defect that occurs when the ductus arteriosus (the temporary fetal blood vessel that connects the aorta and the pulmonary artery) does not close at birth.


The ductus arteriosus is a temporary fetal blood vessel that connects the aorta and the pulmonary artery before birth. The ductus arteriosus should be present and open before birth while the fetus is developing in the uterus. Since oxygen and nutrients are received from the placenta and the umbilical cord instead of the lungs, the ductus arteriosus acts as a"short cut" that allows blood to bypass the deflated lungs and go straight out to the body. After birth, when the lungs are needed to add oxygen to the blood, the ductus arteriosus normally closes. The closure of the ductus arteriosus ensures that blood goes to the lungs to pick up oxygen before going out to the body. Closure of the ductus arteriosus usually occurs at birth as levels of certain chemicals, called prostagladins, change and the lungs fill with air. If the ductus arteriosus closes correctly, the blood pumped from the heart goes to the lungs, back into the heart, and then out to the body through the aorta. The blood returning from the lungs and moving out of the aorta carries oxygen to the cells of the body.
In some infants, the ductus arteriosus remains open (or patent) and the resulting heart defect is known as patent ductus arteriosus. In most cases, a small PDA does not result in physical symptoms. If the PDA is larger, health complications may occur.
In an average individual's body, the power of blood being pumped by the heart and other forces leads to a certain level of pressure between the heart and lungs. The pressure between the heart and lungs of an individual affected by PDA causes some of the oxygenated blood that should go out to the body (through the aorta) to return back through the PDA into the pulmonary artery. The pulmonary artery takes the blood immediately back to the lungs. The recycling of the already oxygenated blood forces the heart to work harder as it tries to supply enough oxygenated blood to the body. In this case, usually the left side of the heart grows larger as it works harder and must contain all of the extra blood moving back into the heart. This is know as a left-to-right or aortic-pulmonary shunt.
As noted, the size of the PDA determines how much harder the heart has to work and how much bigger the heart becomes. If the PDA is large, the bottom left side of the heart is forced to pump twice as much blood because it must supply enough blood to recycle back to the lungs and move out to the body. As the heart responds to the increased demands for more oxygenated blood by pumping harder, the pulmonary artery has to change in size and shape in order to adapt to the increased amount and force of the blood. In some cases, the increase in size and shape changes the pressure in the pulmonary artery and lungs. If the pressure in the lungs is higher than that of the heart and body, blood returning to the heart will take the short cut back into the aorta from the pulmonary artery through the PDA instead of going to the lungs. This backward flowing of blood does not carry much oxygen. If blood without much oxygen is being delivered to the body, the legs and toes will turn blue or cyanotic. This is called a shunt reversal.
When a PDA results in a large amount of blood being cycled in the wrong order, either through a left-to-right shunt or shunt reversal, the overworked, enlarged heart may stop working (congestive heart failure) and the lungs can become filled with too much fluid (pulmonary edema). At this time, there is also an increased risk for a bacterial infection that can inflame the lining of the heart (endocarditis). These three complications are very serious.
PDA is a very common heart defect. Though an exact incidence of PDA is difficult to determine, one review in 1990 found that approximately 8% of live births were found to be affected by PDA. PDA can occur in full-term infants, but it seen most frequently in preterm infants, infants born at a high altitude, and babies whose mothers were affected by the German measles (rubella) during pregnancy. PDA is two to three times more common in females than males. PDA occurs in individuals of every ethnic origin and does not occur more frequently in any one country or ethnic population.

Causes and symptoms

PDA can be a result of an environmental exposure before birth, inheriting a specific changed or mutated gene or genes, a symptom of a genetic syndrome, or be caused by a combination of genetic and environmental factors (multifactorial).
Environmental exposures that can increase the chance for a baby to be affected by PDA include fetal exposure to rubella before birth, preterm delivery, and birth at a high altitude location.
PDA can be an inherited condition running in families as isolated PDA or part of a genetic syndrome. In either case, there are specific gene changes or mutations which lead to a defect in the elastic tissue forming the walls of the ductus arteriosus. The genes causing isolated PDA have not been identified, but it is known that PDA can be inherited through a family in an autosomal dominant pattern or an autosomal recessive pattern.
Every person has approximately 30,000 genes, which tell our bodies how to grow and develop correctly. Each gene is present in pairs since one is inherited from our mother, and one is inherited from our father. In an autosomal dominant condition, only one specific changed or mutated copy of the gene for PDA is necessary for a person to have PDA. If a parent has an autosomal dominant form of PDA, there is a 50% chance for each child to have the same or similar condition.
PDA can also be inherited in an autosomal recessive manner. A recessive condition occurs when a child receives two changed or mutated copies of the gene for a particular condition, such as PDA (one copy from each parent). Individuals with a single changed or mutated copy of a gene for a recessive condition, are known as "carriers," and have no health problems related to the condition. In fact, each of us carries between five and 10 genes for harmful, recessive conditions. However, when two people who each carry a changed or mutated copy of the same gene for a recessive condition meet, there is a chance, with each pregnancy, for the child to inherit the two changed or mutated copies from each parent. In this case, the child would have PDA. For two known carriers, there is a 25% risk with each child to have a child with PDA, a 50% chance to have a child who is a carrier, and a 25% chance to have a child who is neither affected nor a carrier.
Most cases of PDA occur as the result of multifactorial inheritance which is caused by the combination of genetic factors and environmental factors. The
Patent ductus arteriosus (PDA) is the failure of the ductus arteriosus to close after birth, allowing blood to inappropriately flow from the aorta into the pulmonary artery.
Patent ductus arteriosus (PDA) is the failure of the ductus arteriosus to close after birth, allowing blood to inappropriately flow from the aorta into the pulmonary artery.
(Illustration by Electronic Illustrators Group.)
combined factors lead to isolated defects in the elastic tissue forming the walls of the ductus arteriosus. Family studies can provide different recurrence risks depending on the family member affected by multifactorial PDA. If an individual is affected by isolated, multifactorial PDA, they have a 2-4% chance of having a child affected by PDA. If a couple has one child with isolated, multifactorial PDA, there is a 3% chance that another of their children could be affected by PDA. If a couple has two children affected by isolated, multifactorial PDA, there is a 10-25% chance that they could have another child affected by PDA.
Unless a specific pattern of inheritance, preterm delivery, or known exposure is found through the examination of a detailed pregnancy and family history, the multifactorial family studies are used to estimated the possible risk of recurrence of PDA in a family.
The main sign of PDA is a constant heart murmur that sounds like the hum of a refrigerator or other machinery. This murmur is usually heard by the doctor using a stethoscope. Otherwise, there are no specific symptoms of PDA, unless the ductus arteriosus size is large. Children and adults with a large ductus arteriosus can show difficulty in breathing during moderate physical exercise, an enlarged heart, and failure to gain weight. In some cases, heart failure and pulmonary congestion can indicate a PDA.


Diagnosis is most often made by detecting the characteristic "machinery" heart murmur heard by a doctor through a stethoscope. Tests such as a chest x ray, echocardiograph, and ECG are used to support the initial diagnosis. Other indications of PDA include failure to gain weight, frequent chest infections, heavy breathing during mild physical exertion, congestive heart failure, and pulmonary edema. Prenatal ultrasounds are unable to detect PDA because the heart defect does not occur until the time of birth.


The treatment and management of PDA depends upon the size of the PDA and symptoms being experienced by the affected individual. In some cases, a PDA can correct itself in the first months of life. In preterm infants experiencing symptoms, the first step in correcting a PDA is treatment through medications such as indomethacin. In preterm infants whose PDA is not closed through medication, full term infants affected by PDA, and adults, surgery is an option for closing the ductus arteriosus. In 2000 and 2001, medicine has developed and reviewed alternatives to surgical closure such as interventional cardiac catheterization and video-assisted thorascopic surgical repair. A cardiologist can help individuals determine the best method for treatment based on their physical symptoms and medical history.


Adults and children can survive with a small opening remaining in the ductus arteriosus. Treatment, including surgery, of a larger PDA is usually successful and frequently occurs without complications. Proper treatment allows children and adults to lead normal lives.



Jaworski, Anna Marie, editor. The Heart of a Mother. Temple, Texas: Baby Hearts Press, 1999.


CHASER (Congenital Heart Anomalies Support, Education, and Resources). 2112 North Wilkins Rd., Swanton, OH 43558. (419) 825-5575. 〈∼hfmth006/chaser〉.
Kids with Heart. 1578 Careful Dr., Green Bay, WI 54304. (800) 538-5390.∼kdswhrt.


Berger, Sheri. The Congenital Heart Defects Resource Page. January 6, 2000. 〈∼hfmth006/chaser/〉.
"Congenital Cardiovascular Disease." American Heart Association 2000. 〈〉.
"Heart Disorders." Family Village. March 24, 2000. 〈〉.

Key terms

Aorta — The main artery located above the heart which pumps oxygenated blood out into the body. Many congenital heart defects affect the aorta.
Catheterization — The process of inserting a hollow tube into a body cavity or blood vessel.
Ductus arteriosus — The temporary channel or blood vessel between the aorta and pulmonary artery in the fetus.
Echocardiograph — A record of the internal structures of the heart obtained from beams of ultrasonic waves directed through the wall of the chest.
Electrocardiogram (ECG, EKG) — A test used to measure electrical impulses coming from the heart in order to gain information about its structure or function.
Endocarditis — A dangerous infection of the heart valves caused by certain bacteria.
Oxygenated blood — Blood carrying oxygen through the body.
Pulmonary artery — An artery that carries blood from the heart to the lungs.
Pulmonary edema — A problem caused when fluid backs up into the veins of the lungs. Increased pressure in these veins forces fluid out of the vein and into the air spaces (alveoli). This interferes with the exchange of oxygen and carbon dioxide in the alveoli.


 [duk´tus] (pl. duc´tus) (L.)
ductus arterio´sus a fetal blood vessel that joins the aorta and pulmonary artery.
ductus de´ferens the excretory duct of the testis, which joins the excretory duct of the seminal vesicle to form the ejaculatory duct; called also vas deferens.
patent ductus arteriosus see patent ductus arteriosus.
ductus veno´sus a major blood channel that develops through the embryonic liver from the left umbilical vein to the inferior vena cava.


1. open, unobstructed, or not closed.
2. apparent, evident.
patent ductus arteriosus abnormal persistence of an open lumen in the ductus arteriosus, between the aorta and the pulmonary artery, after birth. The ductus arteriosus is open during prenatal life, allowing most of the blood of the fetus to bypass the lungs, but normally this channel closes shortly after birth and changes into a fibrous cord called the ligamentum arteriosum. When it remains open, it places special burdens on the left ventricle, since much of the ventricular output is being shunted from the aorta into the pulmonary artery. The condition may coexist with other congenital malformations.

The symptoms of patent ductus arteriosus are usually so slight that they are not noticed until the child is older and more active. He then begins to experience dyspnea on exertion. If the ductus is large there may be retardation of growth. Pulmonary congestion may result from poor left ventricular function. The heart compensates through hypertrophy and dilation.

Treatment is surgical ligation of the open ductus, preferably when the child is from 4 to 10 years of age. Prognosis, when the condition is not accompanied by other congenital heart defects, is excellent.

The ductus may remain open in as many as 10 per cent of preterm infants, especially those under 1500 grams. If the shunt across the ductus is large, heart failure can occur and surgical repair may be necessary. Investigators into the effects of the prostaglandins have reported that closure of a patent ductus arteriosus can be produced in preterm infants by administration of an inhibitor of prostaglandin formation. Conversely, in neonates suffering from severe complex congenital heart defects in which an open ductus arteriosus could be beneficial, injections of prostaglandins have been used to keep the channel open.
Patent ductus arteriosus. The shunt is from aorta to pulmonary artery. From Betz et al., 1994.

duc·tus ar·te·ri·o·sus

a fetal vessel connecting the left pulmonary artery with the descending aorta; in the first 2 months after birth, it normally changes into a fibrous cord, the ligamentum arteriosum; persistent postnatal patentcy is a correctable cardiovascular handicap.

patent ductus arteriosus (PDA)

an abnormal opening between the pulmonary artery and the aorta caused by failure of the fetal ductus arteriosus to close after birth. It is seen primarily in premature infants. The defect allows blood from the aorta to flow into the pulmonary artery and recirculate through the lungs, where it is reoxygenated and returned to the left atrium and left ventricle, placing an increased workload on the left side of the heart and causing increased pulmonary vascular congestion and resistance. Clinical manifestations include cardiomegaly, especially of the left atrium and left ventricle; dilated ascending aorta; bounding pulses resulting from increased systolic pressure; tachycardia; and a typical machinery-like murmur that is heard during all of systole and most of diastole. Characteristic auscultatory and radiological findings are sufficient to confirm diagnosis so that cardiac catheterization is not necessary. Correction is delayed until the child is old enough to tolerate surgery and until spontaneous closure, which sometimes occurs. Untreated complications include congestive heart failure, pulmonary vascular disease, calcification of the ductal site, and infective endocarditis. See also congenital cardiac anomaly.
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Patent ductus arteriosus

patent ductus arteriosus

PDA Cardiology An acyanotic congenital heart disease–CHD characterized by postpartum persistence of a ductus arteriosus–a fetal vessel that connects the pulmonary artery–PA to the aorta in utero, bypassing the unexpanded lungs–which normally closes soon after birth; PDA accounts for 10% of cases of CHD;1/3 of Pts with nontreated PDAs die of heart failure, pulmonary HTN or endoarteritis by age 40 Risk PDA is more common in pregnancies with persistent perinatal hypoxia, maternal rubella, prematurity and high altitude Heart sounds Normal 1st HS, machinery murmur in 2nd left anterior IC space after 1st HS, peaking at beginning of 2nd; it declines during diastole EKG Asymptomatic if small; large PDAs with major L→R shunting have left atrial and LV hypertrophy Clinical SOB, DOE, palpitations, Rt heart failure, paradoxic embolism, recurrent pneumonia, small shunts are asymptomatic, ↑ risk of infective endocarditis and septic pulmonary embolism; moderate shunts appear in later childhood with fatigue; large shunts may cause LV failure Diagnosis Catheterization to localize ASDs Imaging CXR-lung plethora, proximal PA dilatation, prominent ascending aorta; pulmonary HTN with RV hypertrophy; 2D echocardiography demonstrates PDA, Doppler studies demonstrate continuous flow through pulmonary trunk; catheterization and angiography quantify severity of shunt and vascular resistance Management Ligation; once severe pulmonary vascular obstructive disease develops, repair is contraindicated. See Congenital heart disease.

pa·tent duc·tus ar·te·ri·o·sus

(pātĕnt dŭktŭs ahr-tērē-ōsŭs)
A condition in which the normal channel between the pulmonary artery and the aorta fails to close at birth. In fetal circulation, the blood bypasses the pulmonary circuit because oxygen and carbon dioxide are exchanged through the placenta. After birth, this channel normally closes in response to expansion of the lungs.

patent ductus arteriosus

A congenital heart defect in which the ductus arteriosus, which, during fetal life allows blood to bypass the lungs, fails to close at or soon after birth. The ductus arteriosus lies between the AORTA and the PULMONARY ARTERY. Persistent patency is often of minor degree. The result of a widely patent ductus may be inadequate oxygenation of the blood with breathlessness and strain on the heart which has to work harder than normal to provide an adequately oxygenated circulation. Treatment, if necessary, is initiated by use of the drug indomethacin (indometacin). If this fails, the abnormally retained connection may be tied off.

pa·tent duc·tus ar·te·ri·o·sus

(pātĕnt dŭktŭs ahr-tērē-ōsŭs)
A condition in which the normal channel between the pulmonary artery and the aorta fails to close at birth.

patent ductus arteriosus (ahrtēr´ ēōsis),

n a congenital heart defect in which the passage between the aorta and the pulmonary artery is open, allowing blood to pool back into the lungs, causing the heart to work harder than necessary.