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Congestive Heart Failure

If you’re reading this page, then it is likely that cats and/or dogs are an important part of your family. Do you want to have to assign a dollar value to them if they become sick or injured? That could be the case if you don’t have pet health insurance. Veterinary medicine becoming evermore sophisticated to the point of rivaling human means that pet owners can pay hundreds and even thousands of dollars for their pets health problems. As the bills stack up, uninsured pet owners sometimes must determine how much they are willing to spend on their animal friend. It can be a heartbreaking decision to make. Now, that being said, the question is, how much can pet insurance help with Congestive heart failure is a common disease affecting both dogs and cats. This is a condition where fluid collects within or around the lungs, or in the abdomen, secondary to abnormalities of the cardiopulmonary system. These abnormalities can be congenital, aquired and/or age related. In this article, canine and feline congestive heart failure will be discussed indepthly, complete with clinical signs, diagnosis, prognosis, and treatment options.

In order to acheive a full understanding of the implications of congestive heart failure in dogs and cats, it it first necessary to briefly discuss the heart and lungs, and how they are intimately intertwined, both in anatomical proximity, and as organ systems that ultimately are one in the same – that is, the function of one system, greatly depends on the other. Armed with this information, you will be more able to recognize the signs of canine/feline congestive heart failure, understand why these signs occur, visualize what treatment is geared toward and how it works.

The canine and feline heart heart and lungs are very similar to the human counter part. The hearts consist of left and right upper chambers called atria, and left and right lower chambers called ventricles.

Blood depleted of oxygen enters the right atrium of the heart from the great veins (called vena cava). Once collected in the right atrium, the heart muscles contract and pump this blood through a one way valve into the right ventricle. The heart contracts once again, pumping the blood from the right ventricle into the lungs where the blood picks up oxygen. The now oxygen rich blood from the lungs, following a negative pressure gradient, then collects into the left atrium of the heart. Following yet another heart muscle contraction, the blood is sent to the left ventricle of the heart, where oxygen rich blood is sent out to the body.

Disease of one or more of the one way valves separating the heart chambers, or the heart muscle, leads to disruption in blood flow and back up of blood. In the case of right sided heart muscle or valvular disease, the back up of blood generally occurs in the vena cava. In left sided heart muscle or valvular disease, the back up generally occurs in the lungs.

In the vast majority of cases, the body makes physiological compensations for these anatomical dispruptions of blood flow through the heart and lungs. These physiological compensations include dilation or widening of blood vessels and the anatomical dispruptions of blood flow through the heart and lungs. These physiological compensations include dilation or widening of blood vessels and the heart pumping harder and faster to facilitate the passage of blood through the vessels, organs, and body. Depending on the severity of the anatomical defects, the body can maintain normal function for a time, sometimes for many years.

However, the physiological compensations the body makes to maintain adequate blood circulation, take their toll on the body. The most significant changes occur within the heart. Just like any other muscle in the body, when the heart has to work harder, it enlarges. Muscle enlargement is a welcome change with our skeletal muscles, however, within the heart this is detrimental. The enlargement of the heart muscles lessens the volume capacity of the heart chambers. This leads to less filling and therefore less blood being pumped. It also tends to
exacerbate the initial deformites that led to the heart enlargement. As a result, the heart pumps even harder and faster to move the same volume of blood, which in turn leads to more enlargement. Eventually, once the body and heart compensations can no longer keep up with the diseased cardiovascular system, congestive heart failure results.

Congestive heart failure in dogs and cats has a range of clinical signs. Mild cases of canine and feline congestive heart failure may show only exercise intolerance, a sign that often goes unnoticed by owners. As the disease advances, the patient will often show a chronic, non-productive cough. Eventually the patient may begin to faint periodically, a condition termed syncopal episodes. In the most advanced to end stage scenario, the patient will display markedly labored breathing, may turn blue, or even die acutely.

Diagnosis of congestive heart failure is multifactorial. The dog or cat suspected of having congestive hear failure often has had a life long history of a heart murmur, but this is not always the case. On physical examination, the pet may have “crackley” lung sounds in the case of left sided heart failure and subsequent pulmonary edema. The heart sounds may be muffled from pericardial effusion (fluid around the heart), or a belly distended with free fluid, both of which occur with right sided heart failure.

Chest x-rays typically show enlarged heart and fluid in or around the lungs. On cardiac ultrasound (echocardiogram), the specific defects, valvular deformity, valvular leakage, and cardiac muscle wall thickening can be visulaized and detailed measurements taken. All of this diagnostic information enables the veterinarian to fine tune a treatment strategy, as well as offer prognosis information.

Treatment of congestive heart failure depends on the severity and underlying cause. The goal of therapy is to return the patient into a state of physiological compensation. The one generally universal drug that is used in virtually all cases of canine and feline congestive heart failure is a diuretic, most commonly furosemide. This drug and others like it facilitate the drying out of tissues, helping to decrease fluid in the chest, around the heart, or within the belly. The following drugs will be used, depending on the severity of disease and underlying cause.

Nitroglycerin – Nitro is a vasodilator, serving to quickly open the blood vessels to facilitate the forward flow of blood. It is usually administered as a gel that is applied to the ear, which absorbs quickly to exert its effect. The drug is not used regularly, but reserved for times of full blown crisis.

Enalapril – This is a vasodilator, in a class of drugs called ACE inhibitors. These drugs dilate the vessels to facilitate the flow of blood, as well as decrease the load of the heart.

Diltiazem – This drug is in a class of drugs called calcium channel blockers. They serve to increase the strength of the heart contraction, while decreasing overall heart rate. These drugs increase the flow of blood, while minimizing stress on the heart.

Digoxin – This drug works in a variety of ways to improve the strength of the heart contraction and blood flow, but tends to be reserved only for severe cases, as it is associated with a relatively high incidence of toxicity.

Pimobendan – This drug works by improving cardiac efficiancy by decreasing heart rate, opening up blood vessels, and increasing the strength of the heart’s contraction. Pimobendan is associated with only very rare incidence of toxicity.

Prognosis for congestive heart failure depends on the severity of the disease and the presence of lack of other systemic disease at the time of diagnosis. Best results are attained with careful patient monitoring, frequent bloodwork to make sure that the drugs are not leading to organ toxicity, as well as frequent ultrasounds to look for any changes that may require an augmentation of treatment.


Roger L. Welton, DVM
Founder and Chief Editor,
President, Maybeck Animal Hospital

Article updated 8/18/2012

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