Posts Tagged ‘Heart failure’

Patent Ductus Arteriosus, also known as PDA, is a congenital heart defect that can be found in any breed or species of animal including humans. When I graduated from veterinary school in 1960 we were taught about this condition but very few, if any, veterinarians were prepared to do thoracic surgery to attempt a correction.

One of the most helpful things I learned, after graduating from veterinary school, was that most clients wouldn’t talk to me when I had a stethoscope in my ears. It was a perfect time to think about what I had observed and how to communicate with the client.

While I was in school Dr. Smith lectured to our class about heart murmurs, including the continuous murmur associated with a PDA. I remember him standing at the lectern making a very particular noise, mimicking this murmur. The sound was “whoosh, whoosh, whoosh, whoosh.” I never heard the murmur in an animal while still in school but the first time I did hear the murmur it sounded exactly like the noise Dr. Smith made while leaning into the microphone in the lecture hall. The condition can also be detected by feeling the animal’s pulse detecting what is described as a water -hammer or continuous pulse.

When trying to explain this condition to a client, or to students while I’m teaching, I resort to a sketch where I draw a rough outline of the heart with the aorta coming off the left ventricle and supplying the body with arterialized blood and the pulmonary artery coming off the right ventricle going to the lungs so carbon dioxide can be expelled from the blood and oxygen taken on.

Before any mammal is born the lungs haven’t inflated yet, the fetus doesn’t need blood to go the lungs. There’s an opening between the pulmonary artery and the aorta so the blood can cross over into the aorta because until the lungs are inflated the pressure in the pulmonary artery is higher than the pressure in the aorta. The blood crosses over through a structure called the ductus arteriosus.

As soon as the newborn takes a couple of breaths the alveoli, the little air sacs in the lungs, open and the blood vessels that surround each alveolus also open. The resistance to blood flow into the lungs is reduced and the blood pressure in the pulmonary artery drops below the blood pressure in the aorta. This causes the aortic side of the ductus arteriosus to close since the ductus is more of a slit than a tube. So normally the ductus closes shortly after the animal starts breathing. Unfortunately sometimes, for reasons not yet completely understood, the ductus stays open. When that happens, it’s called a patent ductus arteriosus. Since the pressure in the aorta is higher than the pressure in the pulmonary artery, the blood leaks continuously through the opening. With each heartbeat, the pressure increases in the aorta and that causes the leak to be greater.

When we listen to the heart of a normal animal it makes a noise that sounds like; lub dub . . . lub dub . . . lub dub.” A continuous murmur makes the whoosh, whoosh, whoosh sound as the pressure and blood flow into the pulmonary artery increase with each beat while the blood flows continuously surging with the beating heart.

The defect causes both the left and right sides of the heart to work harder and harder. The heart enlarges and finally it fails. Since my time in practice veterinary medicine has made enormous advances. We now have board certified veterinary surgeons capable of performing the relatively simple surgery to tie off the patent ductus. We also have board certified veterinary cardiologists who, if they make the diagnosis early enough, can use a catheter system to deliver a plug to the ductus and correct the problem without surgery. The key to a successful outcome is early diagnosis before the animal goes into heart failure and that means a thorough physical examination by your veterinarian for your new pet while it is still young.

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Cardio” obviously pertains to the heart, “myo” pertains to muscle and “pathy” signifies pathology or abnormality. Therefore, cardiomyopathy is pathology or abnormality of the heart muscle. We describe two kinds of cardiomyopathy; hypertrophic and dilated. Both types occur because of genetic mutations in one or more of the various proteins that comprise the heart muscle.

A study published in 1993 in the American Journal of Cardiology compared lesions found in 38 humans, 51 cats and 10 dogs that died of spontaneous hypertrophic cardiomyopathy. The authors of the paper discovered almost identical changes in all of the subjects.

Hypertrophic cardiomyopathy results in an increase in the volume of the heart muscle. As the muscle, usually that of the left ventricle, the chamber of the heart responsible for pumping blood out into the body, is forced to work harder it becomes thicker. As this happens the muscle also becomes stiffer, less compliant, and the result is that the ventricle is less able to relax and fill with blood during the resting phase between beats, called diastole. Eventually the left ventricle cannot fill enough to pump enough blood to meet the metabolic demands of the body and the resulting condition is “heart failure”. These same changes can also occur in the right ventricle, the heart chamber responsible for pumping blood to the lungs. Sometimes both chambers are afflicted. The results are left heart failure, right heart failure or total heart failure. Hypertrophic cardiomyopathy seems to be particularly prevalent in Maine Coon, Maine Coon crossbreds and Ragdoll cats.

The other type of cardiomyopathy, dilated, is the yang of hypertrophic’s yin. The myocardium dilates and becomes thinner rather than thicker. This condition is also most often a genetic defect and thought to be an autoimmune disease as are Lou Gehrig’s disease, Cohn’s disease, lupus, and many others. The myocardium stretches and becomes weaker over time. Eventually the affected heart chamber(s) stretch to the point where the beating muscle looses strength. When it contracts it can no longer expel enough blood and heart failure occurs. Again, either the left, right or both ventricles can be affected. Large breeds of dogs, especially Irish Wolfhounds and Doberman Pinschers, seem to be the most afflicted by this condition but it has been found in German Shepherds, Boxers, and English Cocker Spaniels, mixed breeds and occasionally other breeds. For unknown reasons dilated cardiomyopathy kills males 2-3 times more commonly than it does females.

Genetic lesions resulting in myocardial changes closely resembling cardiomyopathy have been reported in Polled Hereford cattle, mustached tamarinds (monkeys) and pygmy sperm whales. Cardiomyopathies can also develop as the result of persistent rapid heart rate, high blood pressure, either systemic or pulmonary, diseases of the outflow valves of either the right or left ventricles (aortic or pulmonary valves), following treatment with certain chemotherapeutic agents, following obstruction of the coronary arteries, and after exposure to a host of toxic substances.

If your pet shows signs of lethargy, labored breathing, decreased levels of activity and tiring easily take it to your veterinarian for a checkup. The earlier a heart condition is caught the more successful the treatment and/or management is.

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