Congestive Heart Failure in the Dog

Filed Under: Dogs, Diseases

Is your dog sleeping more than usual? Is your small dog suddenly coughing, especially after that nap or following the least bit of exertion? Has your dog had problems with his dental health in the past? Then your pet could be suffering from congestive heart failure which is a leading cause of death in older, especially smaller breeds of dogs.

Congestive heart failure (CHF) is traditionally defined as a functional failure of the left side of the heart and the activation of neurologic and hormonal mechanisms that result in pulmonary edema (accumulation of fluid in the lungs). The most common cause of CHF is mitral valve regurgitation secondary to valve degeneration (deterioration) from vegetative endocardiosis. Vegetative Endocardiosis is the inflammation and remodeling of the heart lining and valves secondary to bacterial contamination in the bloodstream (septicemia). The presence of a heart murmur typically precedes the presence of clinical signs of heart failure by years.

Typical clinical signs of CHF include a moist cough, anorexia (poor appetite), exercise intolerance, respiratory distress, tachypnea (rapid, shallow breaths), cyanosis (blue mucous membranes due to a lack of oxygen), and in rare cases, syncope (fainting). The cough is typically seen more after resting or at night initially. On auscultation of the chest pulmonary (lung) crackles may be heard. The strength of the blood pulse or variation in pulse quality may assist in the diagnosis of heart failure. Under normal conditions the mucous membranes (gum color) are pink in the dog, and if pressure is applied to the gum it will initially blanch (appear white or pale) followed by a return to the original pink color in one to two seconds, a phenomenon called capillary refill time or CRT. A CRT that is greater then 2 seconds may be indicative of a cardiac problem. Pale or cyanotic mucous membranes may indicate severely reduced cardiac output. Radiography and echocardiography may be used to demonstrate heart changes.

Heart failure occurs due to three separate mechanisms: (1) myocardial failure (2) volume or pressure overload and (3) compliance failure. These three mechanisms originally help the heart keep up with the demands of the circulatory system.

The cardiac cycle consists of a period of relaxation called diastole followed by a period of contraction called systole.

Myocardial failure occurs when the myocardium or heart muscle can no longer keep up with the demand to pump blood. Muscle fibers have an extensive endoplasmic reticulum which is called the sarcoplasmic reticulum in muscle tissue. This sarcoplasmic reticulum makes calcium available to the muscle during systole. Muscle contraction will continue as long as the calcium ions are present in high enough concentration within the sarcoplasmic fluid. A continually active calcium pump is located in the walls of the sarcoplasmic reticulum that pumps calcium ions back out of the sarcoplasmic fluid and back into the reticulum once used. When the sarcoplasmic reticulum does not function at an optimum level less calcium is available to the muscle for contraction. An elevation of intracellular calcium (calcium level within the cell) during diastole causes the heart chamber not to fill adequately because the muscle does not adequately relax.

Volume overload occurs when the left ventricle becomes enlarged to accommodate a greater volume of blood to keep up with the demand on the system. This change temporarily allows the impaired heart to eject more blood. This compensation mechanism thereby increases the normal stroke volume (amount of blood per contraction) despite the heart’s inability to contract normally.

Ventricular compliance is determined by the volume, thickness, and general tissue composition of the chamber walls of the heart. Compliance failure occurs when the ventricles cannot distend enough during the relaxation part of the cycle to adequately fill the chamber with blood.

Regardless of the cause of the heart failure, other body mechanisms, hormonal and neurologic, will then become activated to overcome the decrease in heart output. A decrease in the heart output will cause a decrease in arterial blood pressure. The decrease in pressure is detected by baroreceptors which in turn activate the sympathetic nervous system. Activation of the sympathetic nervous system causes an increase in the heart rate and causes vasoconstriction to peripheral body areas (the body’s extremities). This activation causes the cardiac output to increase to a level that will adequately maintain circulatory stability.

The kidneys will receive approximately 1/3 of the body’s blood flow at any given time. When the renal (kidney) blood flow is decreased, renal function in turn is decreased and will be seen clinically as prerenal azotemia (a build-up of blood ammonia levels). This decrease in blood pressure or the amount of blood being delivered to the kidneys causes a release of the hormone prorenin which is later cleaved to renin. The release of renin causes the activation of the renin-angiotension-aldosterone system, or RAAS. The purpose of the RAAS is to increase arterial blood pressure. This is accomplished by promoting sodium and water retention in an effort to conserve circulating fluid volume.

Normal left arterial pressure is 4 to 12 mm of mercury. When the pressure exceeds the critical level of 23 mm of mercury then pulmonary edema (fluid collection in the lungs) will be a consequence.

With heart failure, the sympathetic tone increases when the renin-angiotension system is activated. As a consequence, the heart pumps faster and more vigorously. The blood supply to the extremities is vasoconstricted to maintain perfusion pressure. The renin-angiotension system makes the kidneys retain sodium which increases the plasma volume, making the forward cardiac output increase.

With heart failure, four areas should be addressed to improve cardiac output: optimize filling by relaxing the heart or slowing it down, address arrhythmias (abnormalities in the heart beat), unload the ventricle and make the ventricle pump more vigorously. Various treatments to address these issues follow:

Furosemide is the diuretic most commonly used to treat heart failure. It is not indicated unless you have edema. Furosemide diminishes fluid buildup and drops venous blood pressure, which is the driving force for the development of edema. The primary problem with furosemide usage is that it wastes stores of potassium within the body, resulting in electrolyte abnormalities. Spironolactone is a diuretic that spares potassium in the body and may be used as a substitute for furosemide, although it is typically more expensive.

Enalapril and benazepril are two common ACE inhibitors used to treat heart failure. The have been shown to prolong survival time in dogs with valvular heart disease. The use of Enalapril before the development of clinical disease has been shown to give a significant 10.6 months improvement in CHF-free survival time. Enalapril is excreted primarily by the kidneys while benazepril is excreted primarily by the liver.

Amlodipine treatment reduces mitral valve regurgitation in dogs, and the administration of felodipine adds to the proven benefits of enalapril treatment in humans with CHF. Amlodipine treatment may activate the RAAS through its vasodilatory affect on renal arterioles, and therefore its use should be accompanied by ACE inhibition.

Pimobendan, whose trade name is Vetmedin® and is currently manufactured by Boehringer Ingelheim Vetmedica, is a relatively new drug in the U.S. for the treatment of canine heart failure. It is already the drug of choice for dogs with dilated cardiomyopathy or valvular disease that have gone into heart failure. Pimobendan increases myocardial contractility primarily by increasing troponin C’s sensitivity to calcium and by off-loading the heart with peripherally vasodilating vessels through its inhibition of phosphodiesterase (PDE) III. The nonselective inhibition of PDE may also palliate signs of pulmonary hypertension. It is the first positive inotrope and vasodilator (inodilator) licensed for use in dogs. In general it is considered to be well- tolerated, safe, and efficacious in dogs with heart failure. Researchers at Texas A&M have demonstrated that treatment of congestive heart failure with pimobendan, Enalapril and Furosemide resulted in a median survival rate of 18 months for congestive heart failure secondary to chronic valve disease, with many pets surviving beyond 2 years of treatment.

Digoxin, a cardiac glycoside, is used routinely in congestive heart failure due to its inotropic effects, and because it can suppress the renin-angiotension system and reset the autonomic tone and baroreceptors. The problem with digoxin is that it usually does not slow the heart rate adequately and you almost always have to add another drug to control the ventricular response rate. Most veterinarians have exchanged digoxin for pimobendan. In severe and unresponsive cases digoxin may be used with pimobendan to gain further benefit. Both drugs, pimobendan and digoxin work by different mechanisms and the combination may have beneficial effects in unresponsive cases and in end-stage congestive heart failure.

Lidocaine is the drug most commonly used to treat ventricular arrhythmias (abnormal heart beats).

Sotalol is an excellent drug for the chronic management of ventricular tachycardia (rapid heart rate) in dogs.

Calcium-channel blockers are similar to ß-blockers in that they are negative inotropes, which means that they decrease contractility of the heart. In the treatment of congestive heart failure it is often necessary to exchange the decrease in contractility for control of the heart rate.

Sildenafil, presently marketed under the trademark Viagra®, and available from Pfizer, reduces calcium release form intracellular muscle stores and thereby improves smooth-muscle relaxation, which in turn allows for arterial dilation. In patients with debilitating pulmonary hypertension (PHT), sildenafil has been shown to decrease the severity of PHT, including those caused by left-sided congestive heart failure. This drug is now being added as an adjunct to traditional pulmonary hypertension therapy at a dose of 1-3 mg/kg, 2 to 4 times daily.

Low potassium levels will decrease the efficacy of class I antiarrhythmics (drugs to control abnormal heart beats), predisposes dogs to arrhythmias, leads to weakness and will increase the likeliness of digitalis intoxication.

The median survival time for dogs with valvular disease, with appropriate treatment, has increased from 1 to 2 years.

Preliminary research from Purdue University demonstrates that there is a link between oral and heart health in the dog. This direct correlation has already been demonstrated in the human field. Heart failure, in many instances, may be prevented by improved oral health. The gums are very vascular and dental tarter is loaded with bacteria. As a consequence of the close association between the gums and tarter small groups of bacteria may break off entering the blood stream, thereby resulting in a septicemia. The bacteria, once in the blood stream, may colonize the heart valves, typically the mitral valve, resulting in vegetative endocarditis. Vegetative endocarditis leads to the remodeling of the heart valve, thereby affecting its function. The end result of the remodeling is congestive heart failure. Congestive heart failure secondary to vegetative endocarditis may be a completely preventable disease by practicing impeccable oral hygiene. Congestive heart failure is a leading cause of death, and is especially prevalent in small breed of dogs.


Atkins, Clarke and Bruce Keene et al. “Results of the Veterinary Enalapril Trial to prove Reduction in onset of Heart Failure in dogs chronically Treated with Enalapril alone for Compensated naturally occurring Mitral Valve Insufficiency.” JAVMA, Vol. 231, No. 7. October 1, 2007. Pp. 1061-1069.

Basilio, Paul. “Understanding Heart Failure.” Veterinary Forum. January 2008. P. 16-17. Vol. 30(2). February 2008. Pp.79-90.

Erling, Peter and Elisa Mazzaferro. Left-Sided Congestive Heart Failure in Dogs: Treatment and Monitoring of Emergency Patients. Compendium Continuing Education for Veterinarians.

Guyton, Arthur. Textbook of Medical Physiology. W.B. Saunders Co. 5th Edition. 1976. Pp. 130-175.

Hoskins, Johnny. “Cardiac Therapy: New Treatments Modalities Emerge.”. DVM. August 2006. Pp. 10S-13S.

“Research Links Oral, Heart Disease in Dogs.” DVM Newsmagazine. November 2007. P. 14.

Yin, Sophia. “Cardiology update: Canine Heart Failure.” Veterinary Forum. February 2008. Pp. 48-49.

Topics: heart failure

Symptoms: cough, decreased appetite, fainting

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