Patent ductus arteriosus (PDA)
At birth, mammals must adapt from living in a fluid environment (the amniotic fluid in the mother's uterus) where they acquire oxygen through the mother's blood, to breathing air and acquiring oxygen through their own lungs. The ductus arteriosus is very important in the adaptation process. The ductus arteriosus is a normal, small communicating blood vessel beside the heart, connecting the pulmonary artery (which carries blood to the lungs) and the aorta (which carries blood to the rest of the body). Before birth, most of the blood from the fetal heart bypasses the fetal lungs via the ductus arteriosus. At birth, the blood supply from the mother is terminated when the umbilical cord is cut, the dog (or other mammal) begins breathing on its own, and blood flow through the ductus arteriosus is no longer necessary. Within a few days, the ductus shrinks and closes off completely.
Where the ductus arteriosus does not close within 24-48 hours after birth, the dog is left with a patent ductus arteriosus (PDA). PDA causes unnecessary recirculation of blood through the heart, greatly increasing the workload of the heart and potentially causing terminal heart failure in time if the PDA is not closed via surgery. The extent to which a PDA affects any given dog depends on the degree of patency, or size, of the ductus.
There is a sex-linked genetic predisposition for PDA: females are three times more likely to be affected than males, and PDA occurs disproportionately more often in specific breeds (see below), further indicating a genetic basis for the disorder. The exact lesion is hypoplasia of the smooth muscle of the wall of the ductus arteriosus; therefore, medications that cause ductal contraction (as used in children) are ineffective for PDA in dogs because the muscle tissue is missing from the wall of the ductus arteriosus.
With very few exceptions, PDA causes such a significant increase in the workload of the heart that without surgery, it causes congestive heart failure before a normal lifespan -- and often in the first year or two of life. Therefore, a suspicion of PDA requires confirmation (see below) and treatment via surgery. Dogs never "outgrow" a PDA, and most dogs are fully asymptomatic when they have it: PDA causes no symptoms until very late in its course, when permanent damage to the heart has occurred.
The speed and degree of damage caused by PDA varies, depending on the magnitude of the defect. This cannot be known from physical examination alone; tests are needed to identify the size of the PDA (larger is worse) and the corresponding impact on the heart and the rest of the body's circulation.
Most commonly with PDA, there is a shunt from the left to the right side of the heart, with blood from the higher pressure aorta continuously shunted to the main pulmonary artery. This means an increased volume of blood to the lungs which results in fluid accumulation in the lung tissue (pulmonary edema) and volume overload of the left heart. Left unchecked, these consequences may lead to life-threatening overt symptoms such as breathlessness/very laboured breathing due to poor oxygenation, severely reduced tolerance of exercise, and even fainting or collapsing.
Much less commonly (about 2% of PDA cases), there is a right-to-left shunt. This may be the case from birth, or it may develop because the PDA is so large that the pressure in the lungs, and resultant resistance to this pressure, markedly increase. In effect, the circulation is the same as when the dog was a fetus - that is, some of the blood leaving the right side of the heart bypasses the lungs entirely. This results in circulation of poorly oxygenated blood. Dogs with right-to-left shunting PDA classically have weakness or collapse of the hindlegs associated with exercise: they slow down and sit mid-walk and are reluctant to start again, but eventually do, only to slow down and sit again as the poorly-oxygenated hindlegs become weak and cramped.
Usually a PDA is first suspected when the veterinarian hears a telltale type of heart murmur -the "machinery," or "washing-machine" continuous heart murmur- with the stethoscope when examining a dog during puppyhood as part of a routine appointment for vaccinations. Much less commonly the heart murmur may go unnoticed until later, when overt symptoms emerge, as described above. Either way, any suspicion of PDA warrants confirmation, which requires thoracic radiographs (X-rays of the chest) and an echocardiogram (also called cardiac ultrasound, or sonogram of the heart). These tests identify the PDA itself, its secondary effects on the heart and lungs, and any concurrent, unrelated heart defects that sometimes can be masked by PDA and help to determine whether a dog is a good surgical candidate for PDA repair.
Surgery is recommended for all dogs with PDA, except the few (2%) that have right-to-left shunting and therefore, no heart murmur. Historically, surgery consisted of an operation under general anesthesia involving thoracotomy (open-chest, closed-heart procedure) to ligate the ductus and close it permanently with stitches. Nowadays, a minimally invasive procedure has replaced this approach in a majority of cases. The catheter-based approach, called deployment of an Amplatzer canine ductal occluder, involves passage of a self-expanding double-umbrella-shaped plug that closes the ductus from within. Like angioplasty in a person, this procedure does not require opening the chest, but rather is performed by passing a catheter through the femoral vein (in the groin) or jugular vein (in the neck).
When surgery is performed early and successfully, the long-term outlook for a normal life is generally excellent. That is, surgery performed when there is only a murmur and the puppy feels well has the greatest chance of success: changes in the heart caused by the PDA can return to normal and there may be no permanent damage at all.
Where there are overt symptoms, the treatment of choice remains surgery because the underlying problem must be corrected. The degree of secondary damage to the heart is highly variable and often can only be known in hindsight: the surgery must be performed and a recheck 6-8 weeks post-operatively reveals the degree of improvement and expected long-term outlook (i.e., whether medications will need to be given, whether a normal lifespan may be expeted, etc.).
The problems associated with the far less common right-to-left shunt are managed without surgery. Treatment includes mild exercise restriction (avoiding vigorous or prolonged activity) and avoidance of stress. Medications, and/or periodic bloodletting (phlebotomy) can help improve circulation in these cases.
- MURMUR: classically, a continuous "machinery" -type murmur that generally is loudest very cranially on the left side of the chest: in the axilla, over the 2nd or 3rd intercostal space. Failure to listen sufficiently cranially (deep in the left axilla) or sufficiently completely (ending the auscultation prematurely if the pup is whining, sniffing, or moving) is the most common reason for failure to diagnose patent ductus arteriosus early. There is no murmur in cases of right-to-left shunting PDA.
- ELECTROCARDIOGRAM: signs of left atrial enlargement, and dramatic left ventricular dilation and hypertrophy (markedly tall R waves) are common but may overlap with normal in many cases. Signs of right ventricular hypertrophy (right axis deviation) are common with right-to-left shunting PDA.
- RADIOGRAPHS: varying degrees of pulmonary overcirculation, left atrial and ventricular enlargement (may be extreme), and possibly focal dilation of the descending aorta and main pulmonary artery are typical. Evidence of right ventricular hypertrophy may occur with right-to-left shunting PDAs.
- ECHOCARDIOGRAPHY: left atrial and ventricular dilation with preserved or increased contractility; with careful evaluation, the ductus itself can usually be demonstrated in the left or right cranial short-axis views. Doppler evaluation invariably demonstrates turbulent blood flow in the proximal pulmonary artery in left-to-right shunting PDAs.
- OTHER: signs of pulmonary edema and left-sided heart failure may be present when PDA has been left undiagnosed/untreated, leading to decompensation. With the rare, right-to-left shunting PDAs, unoxygenated blood directly from the pulmonary artery mixes with oxygenated blood in the descending aorta, causing hindlimb weakness and differential cyanosis (cyanosis afffects the caudal half of the body but not the cranial half); desaturated arterial blood perfusing the kidneys causes renal hypoxia, erythropoietin excess, polycythemia, and hyperviscosity, and the packed cell volume often exceeds 65 per cent.
Dogs in whom PDA has been diagnosed, with or without surgical correction, should not be used for breeding. Their parents should not be bred either, and siblings should only be used after careful screening. If any affected offspring are born, breeding of the parents should be discontinued.
FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.
Oyama MA, Sisson DD, Thomas WP, Bonagura, JD. Congenital heart disease. In Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine, 7th ed (St. Louis, MO: Saunders Elsevier, 2010) pp. 1250-1298.
Buchanan JW. Patent ductus arteriosus. In Cote E, ed. Clinical Veterinary Advisor: Dogs and Cats (St. Louis, MO: Mosby Elsevier, 2011) pp. 843-845.
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