Current Concepts

Current Concepts in the Management of Congestive Heart Failure

Heart failure is often the outcome for a variety of diseases in cats and dogs, with the exceptions of congenital disease (e.g., PDA) or certain acquired diseases, like taurine deficiency and idiopathic pericarditis.There is no cure for heart failure, therefore, treatment is determined by improving  clinical signs and improving the quality of life. Treatment options may vary based on the underlying type of disease (e.g., hypertrophic cardiomyopathy versus chronic valvular disease) and it may be more essential to treat the body’s response to the failing heart rather than the appearance of the heart itself.

Verifying congestive heart failure (CHF) has been done by historical and physical findings, as well as, thoracic radiographs (Figure 1), NT-proBNP testing and echocardiography. CHF is treated with a combination of diuretics, an angiotensin-converting enzyme inhibitor, pimobendan, and dietary management.

Angiotensin-Converting-Enzyme Inhibitors: Angiotensin-converting-enzyme (ACE) inhibitors are commonly used in the management of CHF. The use of inhibitors is based  on the knowledge that the renin-angiotensin-aldosterone axis is stimulated in dogs and cats with CHF. Administration of ACE inhibitors reduces the fluid retention and vasoconstriction that accompany CHF, resulting in improved clinical signs and a longer survival. ACE inhibitors may also alter the progressive cardiac enlargement and remodeling associated with most forms of heart disease, although trials in dogs with asymptomatic mitral regurgitation and cats with asymptomatic hypertrophic cardiomyopathy failed to show a clear delay in the progression of cardiac disease. In general, our usual clinical practice is to initiate ACE inhibitors in asymptomatic animals once moderate to marked left atrial enlargement is present, and in virtually all animals once CHF has developed. Use of ACE inhibitors in animals with minimal atrial enlargement is of marginal benefit, unless there is concurrent systemic hypertension or proteinuria. Once CHF has developed, administration of an ACE inhibitor twice-a-day is recommended ,and serial evaluation of renal values and electrolytes is appropriate.

Furosemide – Diuretic administration is typically reserved for dogs and cats with congestive heart failure. Administration before the onset of CHF can cause adverse neuroendocrine stimulation, and is often thought to be counterproductive. Once CHF has developed, furosemide is the most commonly used diuretic, and the dose is adjusted in each individual animal based on clinical signs. When respiratory rates rise due to congestion (typically above 30-40 breaths per minute at rest or during sleep) the dose of furosemide is increased. When clinical signs of congestion are well controlled, then the dose may be reduced in 15% to 25% increments, especially if electrolyte disturbance, dehydration or pre-renal azotemia develop. The goal is to find the “lowest possible dose of furosemide” that controls signs of congestion, although most animals with CHF need to stay on at least some dose of diuretic indefinitely to prevent recurrence of congestion and avoid a costly emergency visit for worsening CHF. Renal function and electrolytes should be checked before initiation of diuretics, and recheck values should be obtained five to ten days after starting therapy. Once a stable dose of cardiac medications is achieved ,then renal values should be rechecked every two to three months. In most instances, canine patients are given 1-2 mg/kg q 12 h for mild CHF (Figure 1a). In many cats, pulmonary edema can be controlled with 6.25 mg/cat q 24-48 hours for chronic therapy, however, in cats with pleural effusion that has required thoracocentesis, a higher dose of furosemide is often required, typically ≥ 6.25 mg/cat q 12 hours. When a dose of 2.2 mg/kg twice a day is exceeded during chronic therapy, we start to consider development of diuretic resistance and typically add spironolactone or other diuretics into the mix. Alternatively in refractory cases, use of injectable furosemide can restore a diuresis in some animals. We have also had some success adding torsemide into the drug regimen for animals with refractory CHF with a starting dose of 0.2 to 0.3 mg/kg q 24 hours.

Pimobendan – Pimobendan is a calcium sensitizing drug that acts as a positive inotrope. Pimobendan also acts as a phosphodiesterase inhibitor which accounts for the drug’s vasodilation properties. It has been studied in dogs with chronic valvular disease, and in dogs with dilated cardiomyopathy, and the drug appears to improve clinical signs and prolong survival when used after the onset of CHF. In most veterinary studies, dogs treated with pimobendan have fared as well, or better than dogs treated with ACE inhibitors. Pimobendan is also associated with a low side effect profile, and we have not recognized repeatable side effects in dogs, other than rare GI upset or excitability, and the side effects do not appear to be associated with any negative impact on the animal’s well being. In cats there are concerns that the drug may be poorly tolerated in hypertrophic cardiomyopathy, especially in cats with hypertrophy of the septum that leads to left ventricular outflow tract obstruction (Figure 2). We have used pimobendan in cats with HCM, although we generally avoid the drug in cats with documented LV outflow obstruction. The drug is only approved for use in dogs with active CHF and the role for this drug in pre-CHF situations is unclear at this point in time. Currently we are withholding pimobendan until CHF is present or at least some signs of cardiac disease (e.g., exercise intolerance or cough with marked left atrial enlargement) are evident. The usual dose for pimobendan is 0.25 to 0.3 mg/kg q 12 hours. We sometimes use higher doses (off-label) for advanced refractory CHF.

Dietary Modifications – Moderate dietary sodium restriction is recommended in earlier stages of heart disease and heart failure, although more severe sodium restriction may be needed as CHF advances. A variety of diets account for reduced sodium requirements and some have more specific modifications which are desirable for heart disease such as supplemental fish oil or taurine supplementation. Many dogs get a considerable amount of calories and sodium from treats and people food, these are the “easiest” sources of sodium to control early in the management of CHF and we routinely counsel owners to avoid high sodium treats and people foods. Diets with lower sodium content and treats that are lower in sodium can be found at the following web sites: http://www.tufts.edu/vet/heartsmart/ OR http://www.tufts.edu/vet/heartsmart/resources/treats_for_dogs_with_heart_disease.pdf.

Protein restriction should be avoided as these diets may contribute to muscle loss and cardiac cachexia seen commonly as CHF advances; many renal diets have inadequate protein and renal diets should generally not be recommended for dogs and cats with CHF. Similarly, geriatric diets vary widely in their sodium content so the suggestion to “just feed a geriatric diet” is not recommended as some of these diets contain too much sodium.

When should I do a re-check exam, and what should I do?

We routinely recommend re-evaluation of the patient with a chemistry profile to check renal function and electrolytes 5 to 10 days after initiation, or alteration of cardiac medications. Physical examination, packed cell volume, total protein, blood pressure, follow-up thoracic radiographs, follow-up electrocardiography in animals with arrhythmia, and historical reports from the owner are all useful in trying to assess response to therapies. Blood pressure should be obtained in animals that are weak, lethargic or anorexic and drug doses may require reduction if the systolic blood pressure is < 100-110 mm Hg. Serum digoxin levels should be obtained, ideally 8 hours post-pill, approximately seven to ten days after initiation of the medication; post-pill values of 0.8 to 1.2 ng/ml are recommended. If drug doses or types are adjusted then a subsequent recheck is recommended in seven to ten days.

Once cardiac medication doses are stabilized, and the animal is eating and breathing well, the next re-check visit should be scheduled for two to three months. At this time, a physical examination with chemistry profile should be performed as well. Finally, six-months after initial diagnosis ,the author recommends a follow up examination with echocardiogram to examine changes in the appearance of the heart, or other alterations which might dictate a need for change in therapy.

Figure 1a: Right lateral thoracic radiographic projection of a 7-year-old Cavalier King Charles Spaniel with chronic valvular disease resulting in left atrial enlargement and mild left-sided congestive heart failure. Heart failure was well controlled on standard doses of furosemide, pimobendan, and an ACE inhibitor.

Figure 1a: Right lateral thoracic radiographic projection of a 7-year-old Cavalier King Charles Spaniel with chronic valvular disease resulting in left atrial enlargement and mild left-sided congestive heart failure. Heart failure was well controlled on standard doses of furosemide, pimobendan, and an ACE inhibitor.

Figure 1b: Right lateral thoracic radiograph from the same dog taken 9 months later. Severe generalized cardiomegaly is now present resulting in severe mainstem bronchial compression and recurrent CHF. At this stage of advanced CHF the dog had developed diuretic resistance and required several medications, including injectable furosemide and an increased dose of pimobendan, to manage congestive signs.

Figure 1b: Right lateral thoracic radiograph from the same dog taken 9 months later. Severe generalized cardiomegaly is now present resulting in severe mainstem bronchial compression and recurrent CHF. At this stage of advanced CHF the dog had developed diuretic resistance and required several medications, including injectable furosemide and an increased dose of pimobendan, to manage congestive signs.

Figure 2: Right parasternal long axis echocardiographic loop from a cat with severe hypertrophic cardiomyopathy showing dynamic left ventricular outflow tract obstruction resulting from septal hypertrophy and systolic anterior motion (SAM) of the mitral valve.