In fetal life, blood entering the right heart largely bypasses the nonfunctional lungs through either the foramen ovale or the ductus arteriosus. The ductus arteriosus effectively shunts blood from the pulmonary artery into the descending aorta (right-to-left shunt). At birth, several factors mediate closure of the ductus to separate the systemic and pulmonary circulatory systems. Inflation of the lungs and remodeling of the fetal pulmonary vasculature allows the pulmonary circulation to change from a high-pressure, high-resistance system to a low-pressure, low-resistance system. Closure of the ductus occurs shortly after birth, leading to formation of the ligamentum arteriosum.
Persistence or patency of the ductus with an otherwise normal systemic and pulmonary circulatory system results in significant shunting of blood from the descending aorta to the pulmonary artery (left to right). Because systolic and diastolic aortic pressures normally exceed pulmonary artery pressures, shunting is continuous throughout the cardiac cycle. The result is a continuous murmur and volume overload of the pulmonary arteries and veins, left atrium, and left ventricle. Left atrial and left ventricular dilatation may result in cardiac arrhythmias. Diastolic flow (also called diastolic run-off) through the ductus leads to a decrease in diastolic and mean systemic blood pressures. The widened difference between systolic and diastolic pressures creates an increased pulse pressure and bounding femoral pulses. Chronic volume overload and dilatation of the left-side cardiac chambers usually result in development of left-side CHF in most untreated cases within the first 1–2 years of life. Animals with a small ductus and minimal shunting may reach adulthood, although most affected dogs have evidence of volume overload even at a young age. In some animals with a large PDA, increased pulmonary blood flow may induce pulmonary vasoconstriction and development of pulmonary hypertension. In cases of severe pulmonary hypertension in which pulmonary pressures exceed systemic pressures, blood flow through the ductus can reverse and result in right-to-left shunting. This “reverse PDA” causes disappearance of the classic machinery murmur and results in caudal hypoxemia. Delivery of oxygenated blood to the head/neck results in pink mucous membranes cranially, while delivery of hypoxemic blood caudally results in cyanotic mucous membranes caudally (vulva/prepuce). Differential cyanosis is a characteristic examination finding in animals with reverse PDA. In addition, perfusion of the kidneys with deoxygenated blood causes excessive release of erythropoietin and subsequent polycythemia.
Clinical Findings and Treatment
In animals with a left-to-right PDA, a prominent, continuous, machinery-like murmur is present. The murmur is usually loudest at the left base of the heart and is often associated with a precordial thrill. In some cases, the ductus remains open for several days after birth, so a continuous murmur may be detected during examination of the neonate. Femoral pulses are typically bounding. Most young animals do not demonstrate clinical signs. Those with a large shunt and older animals often have signs of left-side CHF. Electrocardiography frequently demonstrates tall R waves in lead II, indicative of left ventricular enlargement. A spectrum of cardiac arrhythmias may also be seen, including both atrial and ventricular premature complexes. Radiographic abnormalities depend on the size of the ductus and may demonstrate left atrial and left ventricular enlargement, prominent pulmonary vessels, aortic and pulmonic aneurysmal dilatations (ductal bump), and variable degrees of pulmonary edema. Echocardiography is valuable in excluding concurrent congenital cardiac defects, as well as documenting presence of the PDA. Continuous turbulence in the main pulmonary artery is characteristic of a left-to-right shunting PDA. Left ventricular and left atrial dilatation are typically noted, and mild mitral regurgitation may be present secondary to annular dilation.
Because of the high risk of CHF early in life for animals with a PDA, closure is generally recommended. There are two major treatment options for PDA closure: interventional transcatheter occlusion and surgical ligation. Catheter-based occlusion is minimally invasive and typically involves placement of an occlusion device through a peripheral vessel (most commonly the femoral artery). The Amplatz canine ductal occluder is used most often and is highly successful with minimal complications. The use of other occlusion devices such as Gianturco coils and vascular plugs has also been described. The major limitations to a transcatheter approach are ductal size and patient size. Surgical ligation of the ductus is also usually curative and considered most often for small dogs and cats. If present, CHF should be medically managed before anesthesia and surgery are performed.
In animals with a reverse PDA, there is usually a history of lethargy, exercise intolerance, and collapse that relates to severe pulmonary hypertension and venous admixture. Careful examination may reveal differential cyanosis. The second heart sound may be split, and there may be a soft diastolic murmur of pulmonic insufficiency. A continuous murmur is not present, and femoral pulses are not bounding. The finding of polycythemia in a young animal with the above clinical signs should prompt further diagnostic evaluation of the heart. Electrocardiography demonstrates severe right ventricular enlargement and occasional arrhythmias. In reverse PDA, right ventricular enlargement and aneurysmal dilatation of the descending aorta can be noted on radiographs. Echocardiography is indicated in these cases and will demonstrate abnormalities associated with pulmonary hypertension (right ventricular dilatation and hypertrophy, septal flattening, pulmonary artery dilatation). Contrast echocardiography using agitated saline can be used to confirm the diagnosis. After the injection of agitated saline into a peripheral vein, microbubbles will be seen within the right heart, pulmonary artery, and abdominal aorta, suggesting a right-to-left shunt between the pulmonary artery and the aorta. Occlusion or ligation of the ductus is contraindicated with reverse PDA, because this results in an increase in pulmonary hypertension (by causing an increase in flow through the pulmonary arteries), right heart failure, and death. Therapy in these cases involves medical management of pulmonary hypertension and control of polycythemia through periodic phlebotomy. Longterm prognosis is poor.
Last full review/revision August 2015 by Sandra P. Tou, DVM, DACVIM