Health Articles

Congenital Heart Defects - Patent Ductus Arteriosus (PDA)

by Vickie Halstead, RN, CCRN, CEN, CVNS, LNC

This is the second article in a series addressing cardiac diseases in dogs, with an emphasis on diseases that more commonly afflict Bichons Frises. Refer to the first article in the series while you read this article, “Introduction to Canine Cardiac Disease”, which can be found on this web site: This second article includes information on diseases that are present at birth (congenital), so these puppies are born with malformations of the heart or great blood vessels. Bichons are listed as being predisposed to Patent Ductus Arteriosus (PDA), the most common canine congenital cardiac defect, so this article is primarily devoted to this defect.



Cardiac disease in dogs is prevalent, accounting for about 11% of dogs seen by veterinarians. At least 3 million dogs examined by veterinarians in the US have acquired heart disease and may be in heart failure. Acquired heart diseases, both inherited and obtained from influences outside the body such as infections, will be addressed in successive articles.


Clinical Signs of Heart Failure

Cardiac diseases eventually lead to heart failure, AKA congestive heart failure (CHF), which is defined as failure of the heart as a pump, meaning the heart is unable to supply the body and organs with sufficient flow of oxygen-rich blood. This inefficiency is due to weakened muscles in the ventricles, the pumping chambers of the heart, causing backup of blood into the cardiovascular system. Despite many compensatory mechanisms in the heart and body that preserve the balance short term, in time the stress on the heart takes its toll. Initially, clinical signs of CHF are mild, vague, and easy to overlook. As time passes more blood backs up into the lungs causing exercise intolerance, loss of appetite, rapid respirations, and frequent coughing. Blood also backs up into the venous system causing engorged neck veins, liver enlargement, and swelling in the abdomen and legs. Without adequate blood flow, organs in the body malfunction and eventually fail, thus causing more severe clinical signs, such as kidney failure.

Heart murmurs detected during a veterinary exam are the hallmark of most cardiac diseases and may be detected before any clinical signs are present, therefore the importance of that yearly exam and the first puppy exam before leaving the breeder. Other clinical signs of heart failure that may be detected due to inadequate blood flow to the body include slow capillary refill in the gums (it takes longer than 2 seconds for the gums to regain the pink color after pressing with a finger), weak and rapid pulses, cardiac rhythm irregularities (arrhythmias), fainting episodes that may appear to be a seizure, and cyanosis (blue tint) in the white part of the eyes or gums.

Dogs and humans can be born with several cardiac structural defects including tetralogy of Fallot (4 distinct structural defects), holes between the chambers in the heart called septal defects (ASD, VSD), narrowing of the outflow tract of the left ventricle called subaortic stenosis (SAS), and persistent fetal circulation (patent ductus arteriosis, or PDA).


Pathophysiology of Patent Ductus Arteriosus (PDA)

While in the uterus the fetus obtains oxygen from the mother’s blood via the placenta and umbilical cord, instead of breathing it in through the lungs. There is a communication between the 2 major blood vessels that conduct blood out of the ventricles, the pulmonary artery (carries blood to the lungs) and the aorta (carries blood to the body and organs), which allows most of the blood to bypass the lungs that are not being used. Shortly after birth, once the lungs are expanded, the connection between the aorta and pulmonary artery, the ductus arteriosus, closes. If it remains open (patent) blood is shunted through it from the high-pressure aorta to the low-pressure pulmonary artery. The result is excessive blood flow to the lungs, which places a burden on both ventricles that eventually fail.

Diagram obtained from

Key: IVC = inferior vena cava, SVC = superior vena cava, RA = right atrium, RV = right ventricle, PA = pulmonary artery, LA = left atrium, LV = left ventricle, AO = aorta, and black arrow = shunting of blood through the PDA


Diagnosis of PDA

A puppy born with PDA may appear normal for a few weeks, except that it may be the first to tire while playing and the smallest puppy in the litter. Upon auscultation, there will be a loud, continuous murmur. Murmurs are graded on a scale of I to V, with grade I being very soft and grade V being very loud, and can even be palpated on the chest wall. Eventually the puppy will develop clinical signs of heart failure. The diagnosis can be confirmed by ultrasound, x-ray to visualize the congested lungs and enlarged heart, and electrocardiogram that reflects changes in the ventricles.


Treatment of PDA

At the age of 2-3 months, before significant heart failure develops, surgery is indicated to correct the defect, without which 60% will die within one year. Surgery, which is very successful, consists of opening the chest from the left side through the ribs (thoracotomy) and tying off the patent ductus. Prognosis for surviving surgery is 90%, and is excellent for a normal life if surgery is completed early.


Breeding Advice

PDA is believed to be polygenic, caused by more than one pair of genes, so random in nature. The affected dog and its parents should not be bred, plus littermates should only be used for breeding after careful screening. According to Dr. Jerold Bell in his discussion of polygenic diseases (see link below to his article), “If there are multiple generations of normalcy in the breadth of the pedigree, then you can have some confidence that there are less liability genes being carried.” He defines liability genes as, “a number of genes must combine to cross a threshold and produce an affected dog”.



Diseases of the Heart by Charles K. Friedberg
“Matters of the Heart” by Mara Bovsun. AKC Gazette, October, 2005
“Facts on Canine Cardiac Health” by Kevin Schargen. AKC Gazette, March, 2005
OFA web sites: