Patent ductus arteriosus (PDA) is a common congenital heart defect in dogs, and it occurs less commonly in cats. Persistence of a normal fetal structure (ductus arteriosus) after birth allows for shunting of blood from the descending aorta to the pulmonary artery, leading to volume overload and subsequently left heart failure. A continuous murmur heard at the left base and bounding pulses are classic changes on physical examination. Thoracic radiograph findings may support patent ductus arteriosus, although definitive diagnosis is generally obtained with echocardiography and angiography.
Pathophysiology of Patent Ductus Arteriosus in Animals
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 systemic and pulmonary circulations. Inflation of the lungs and remodeling of the fetal pulmonary vasculature allow 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, which becomes 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 and neck results in pink mucous membranes cranially, while delivery of hypoxemic blood caudally results in cyanotic mucous membranes caudally (vulva and 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.
Patent ductus arteriosus
Patent ductus arteriosus viewed from the left. Illustration by Dr. Gheorghe Constantinescu.
Clinical Findings of Patent Ductus Arteriosus in Animals
In animals with a left-to-right patent ductus arteriosus, 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, an aortic ductus diverticulum (ductal bump), and possible presence of pulmonary edema. Echocardiography is valuable in excluding concurrent congenital cardiac defects as well as documenting abnormal blood flow typical of 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.
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. Cardiac auscultation may reveal a right-side systolic murmur (tricuspid regurgitation), split S2, and a soft diastolic murmur (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 possible arrhythmias. Right ventricular enlargement, pulmonary artery dilatation, and a ductal bump may be noted on radiographs.
Diagnosis is typically made by echocardiography, which reveals abnormalities associated with pulmonary hypertension (right ventricular dilatation and hypertrophy, septal flattening, pulmonary artery dilatation). Contrast echocardiography using agitated saline (bubble study) helps to confirm the diagnosis. After the injection of agitated saline into a peripheral vein, hyperechoic microbubbles can be seen within the abdominal aorta.
Treatment of Patent Ductus Arteriosus in Animals
Occlusion of the patent ductus arteriosus, either by device occlusion (Amplatz canine ductal occluder, ACDO) or surgical ligation
Treatment of CHF (pulmonary edema) if present
Because of the high risk of CHF early in life for animals with a PDA, timely closure is generally recommended. There are two major treatment options for PDA closure: interventional transvenous occlusion and surgical ligation. Catheter-based transvenous occlusion is minimally invasive and involves placement of an occlusion device through a peripheral vessel (most commonly the femoral artery). The Amplatz canine ductal occluder (ACDO) is used most often and is highly successful with minimal complications. Transcatheter coil closure and placement of a vascular plug have also been described. The major limitations to a transcatheter approach are ductal size and patient size. Surgical ligation of the ductus is highly successful and considered most often for small dogs and cats. If present, CHF should be medically managed before anesthesia and surgery are performed.
Occlusion or ligation of the ductus is contraindicated with reverse PDA due to the risk of worsening pulmonary hypertension and right heart failure. Therapy in these cases focuses on medical management of pulmonary hypertension and control of polycythemia through periodic phlebotomy. Closure can be considered if treatment of pulmonary hypertension leads to flow reversal (left-to-right flow). Longterm prognosis for reverse PDA is guarded to poor.
Patent ductus arteriosus (PDA) is a common congenital disease in dogs, and it also occurs in cats.
A loud, continuous, left basilar heart murmur and bounding femoral pulses are classically found on physical examination.
Left heart failure (pulmonary edema) is the most common sequelae of PDA, commonly occurring within the first year of life.
Treatment (interventional device occlusion or surgical ligation) before the onset of clinical signs is associated with an excellent prognosis.
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