Heart Failure in Dogs and Cats

The pulmonary capillaries and veins drain into the left atrium. Left atrial pressure increases as left heart diseases worsen (eg, from regurgitant blood flow and increased circulating blood volume). An increase in left atrial pressure is transmitted backward to the pulmonary veins and pulmonary capillaries. Increased pulmonary capillary hydrostatic pressure causes fluid to leak out of the capillaries (transudation), first into the lung interstitium and then into the alveoli as the pressure increase becomes more severe. Simply put, pulmonary edema develops and becomes worse as heart failure progresses. In animals, the first result is tachypnea, and dyspnea follows. Most owners do not notice the tachypnea, so they do not seek veterinary attention until dyspnea is present. For this reason, the onset of the heart failure often appears acute when, in fact, it is chronic.

Dyspnea is usually apparent in the exam room. Tachypnea due to pulmonary edema or pleural effusion, however, is commonly masked by panting in dogs. Consequently, it is often advantageous to send a nondyspneic dog home to have the owner count the dog's sleeping respiratory rate (SRR) to detect tachypnea. The owner must be taught how to count respiratory (breathing) rate and then count the rate preferably while the dog is sound asleep and in a cool environment. A normal dog has an SRR of < 30 breaths/minute, so a rate greater than that is abnormally high and the dog is tachypneic. If the SRR is elevated, a trial administration of furosemide is indicated. If the SRR decreases appreciably after furosemide administration, cardiogenic pulmonary edema can be diagnosed.

Some dogs and a few cats will cough with cardiogenic pulmonary edema. In all species, however, cough is much more commonly associated with primary lung disease than with cardiogenic pulmonary edema. Coughing is always present in dogs with chronic bronchitis, and chronic bronchitis is the most common cause of a chronic cough, especially in small breeds. Even in a smaller, old dog with a loud left apical systolic murmur, if dyspnea is not present, a cough is most likely due to chronic bronchitis, not to pulmonary edema.

Animals with heart failure may also be exercise intolerant, because of lower-than-normal cardiac output during exercise and/or hypoxemia, which is due to pulmonary edema or pleural effusion. Exercise intolerance is rarely a complaint presented with cats, because they usually do not exercise. Even in dogs, however, most true exercise intolerance (fatigue with marked tachypnea or dyspnea) is due to respiratory failure (ie, hypoxemia) rather than heart failure, or due to an unwillingness to exercise because of other conditions, such as orthopedic disease or obesity.

In cats, congestive heart failure (CHF) also commonly manifests as pleural effusion. The pleural effusion may be a modified transudate, pseudochylous effusion, or chylous effusion in cats with left heart failure. A small volume of pericardial effusion can also be evident in cats with heart failure and is generally of no hemodynamic consequence (pericardiocentesis is not required). Cats also often stop eating and may stop drinking when in heart failure.

A severe decrease in cardiac output results in cold extremities (paws, ears) and can lead to total body hypothermia, especially in cats. Although syncope is not a clinical sign of heart failure, it may also be noted in dogs with cardiogenic pulmonary edema, especially in small-breed dogs with chronic valvular disease. In many instances, the cause is unknown. However, syncope often improves once pulmonary edema is treated. In some cases it is associated with coughing and is most likely a vagally mediated event. Syncope is frightening to the owner, but sudden death is rare unless associated with dilated cardiomyopathy or subaortic stenosis.

Congestive heart failure, dog, radiograph

Image

Courtesy of Dr. Mark D. Kittleson.

The diagnosis of CHF (cardiogenic pulmonary edema) in dogs is typically based on radiographic evaluation. However, the inability to take a radiograph during a deep inspiration--unlike in human patients who can respond to this instruction-- is a diagnostic obstacle. Consequently, the caudodorsal lung fields on a lateral radiograph, where cardiogenic pulmonary edema is usually identified, often have an interstitial density that is either mistaken for pulmonary edema or hides pulmonary edema. This problem is exacerbated in older dogs. Most cases of severe pulmonary edema in dogs can be identified radiographically; mild to moderate edema, however, is more difficult to identify. In dogs with less severe edema, it is often beneficial to send the dog home (if it is stable) to have the owner count the dog's SRR.

All dogs with pulmonary edema have an increased SRR (are tachypneic). Dogs with respiratory disease/failure, however, can also have an increased SRR. Therefore, once an increased SRR is documented, the dog should be started on furosemide at a dosage of at least 2 mg/kg, PO, every 12 hours. If the SRR decreases, then the diagnosis of left heart failure is confirmed. The same can be done in cats for both pulmonary edema and pleural effusion. All healthy cats have an SRR of < 40 breaths/minute; in most, the SRR is < 30 breaths/minute. Once the diagnosis is established, the owner should continue to count the SRR daily and titrate the furosemide dosage to keep the SRR within the normal range. In dogs thought to be in an impending stage of heart failure (large left atrium but no pulmonary edema), the owner can also be instructed to count the SRR daily to weekly in an attempt to identify heart failure at an early stage. Owners should also always be instructed to keep a log and bring it with them at each recheck.

Chronic bronchitis, dog, radiograph

Image

Courtesy of Dr. Mark D. Kittleson.

The following 10 guidelines for distinguishing CHF from chronic bronchitis in dogs may be helpful:

1. Heart failure occurs only when severe, overwhelming heart disease is present. Mild, moderate, and even fairly severe heart disease does not result in heart failure. When chronic CHF is present, the left atrium is usually severely enlarged and always at least moderately enlarged.

2. In dogs with acute chordal rupture leading to acute CHF, the left atrium may not be enlarged, because it has not had time to become enlarged. These cases are uncommon but do occur. Chordal rupture should be suspected only when the onset of clinical signs is acute.

3. Murmur intensity is a poor index of the severity of mitral regurgitation in dogs, except in the case of a soft (grades 1–2) murmur. A soft murmur is almost always associated with mild mitral regurgitation. However, a loud murmur is not necessarily associated with severe disease or left heart failure.

4. Diagnosing cardiogenic pulmonary edema by radiographic evaluation is not easy. Often, pulmonary edema cannot be accurately diagnosed by radiographic evaluation. If there is no clear and obvious marked (severe) left atrial enlargement and clear pulmonary edema (especially in the dorsocaudal lung fields), further workup is necessary. If dyspneic, supportive treatment (furosemide, oxygen insufflation) should be instituted before the workup continues.

5. The sleeping respiratory rate (SRR) is a useful clinical metric. Any dog that has pulmonary edema will have tachypnea (increased respiratory rate). Therefore, if the respiratory rate in the exam room is normal (< 30 breaths/minute), pulmonary edema is not present. However, since many dogs are excited or stressed in the exam room, an elevated respiratory rate on examination may not be representative of the patient's true respiratory status. In such cases, as long as the dog does not appear to have fulminant clear-cut CHF, the patient should be sent home to have the owner count the SRR.

6. If the patient has an elevated SRR (ie, > 30 breaths/minute), the next step is a trial administration of furosemide. A decrease in SRR after appropriate furosemide treatment is reasonable confirmation that the dog has CHF (cardiogenic pulmonary edema). If the SRR does not decrease, the furosemide dosage may be too low, or the dog may have primary lung disease instead.

7. Most dogs with a cough and a heart murmur are not in heart failure; coughing is more commonly due to chronic bronchitis. Notably, just because a cough improves with furosemide treatment does not mean the dog has cardiogenic pulmonary edema; furosemide is a bronchodilator, so coughing will often decrease or resolve after furosemide administration in dogs with chronic bronchitis.

8. CHF cannot be diagnosed by echocardiography, because this modality cannot detect pulmonary edema. The echocardiogram is useful only for identifying findings that are compatible with CHF (eg, severely enlarged left atrium, ruptured chordae tendineae). A veterinary cardiologist can estimate the amount of left atrial pressure that might increase the probability that a dog has pulmonary edema; even that, however, is not proof.

9. Heart failure is a progressive disease.  So, if a dog has had a cough for months without change and the dog is not receiving furosemide, the cough is very unlikely to be due to heart failure. Similarly, a patient that has been on the same dosage of furosemide for many months (maybe even years) and is still alive is not in heart failure. Heart failure inevitably progresses, requiring a higher and higher dosage of furosemide over time.

10. Loud, coarse crackles (the only type usually detected on examination) are much more common with chronic bronchitis than with pulmonary edema, and they are due to the mucus in the airways popping with respiration. Crackles in a small-breed dog that is coughing and is not dyspneic in the exam room is virtually diagnostic of chronic bronchitis.

The right atrium receives systemic and cardiac venous and lymphatic drainage via the cranial and caudal venae cavae and the coronary sinus. Right atrial pressure increases as right heart disease worsens as a result of diseases such as tricuspid valve insufficiency and pulmonary hypertension. Clinical signs of right heart failure include jugular venous distention, hepatomegaly, pleural effusion, pericardial effusion, ascites, and peripheral edema. Dogs and cats are more likely to develop ascites (although right heart failure is uncommon in cats).

Also see Diuretics in the chapter "Systemic Pharmacotherapeutics of the Cardiovascular System" and the table Commonly Used Cardiovascular Drugs and Dosages for dosages of drugs mentioned below.

Loop diuretics are the single most effective agents for treating CHF in animals. They decrease edema and effusion primarily by decreasing circulating blood volume. They act by inhibiting the Na⁺/K⁺/2 Cl^– cotransporter in the thick ascending loop of Henle. The result is increased renal sodium and chloride excretion, with subsequent sodium and free water loss.

Furosemide is the most widely used loop diuretic. Adverse effects observed with furosemide administration are generally related to dehydration from volume depletion, decreased cardiac output and glomerular filtration rate (GFR), and electrolyte and acid-base abnormalities. Less common adverse effects include vomiting, pancreatitis, and idiosyncratic deafness with rapid intravenous administration. Animals with preexisting renal disease are more likely to develop adverse effects. Renal values should be monitored at the start of diuretic treatment (on initiation and at least 1 week later), and they should be reassessed at least every 3–6 months during chronic administration. Many animals develop mild to moderate prerenal azotemia (usually with a greater increase in BUN than in creatinine), which is generally tolerated, as long as they are eating and drinking adequately.

Torsemide is a newer loop diuretic that has better and more consistent bioavailability (better and more consistent GI absorption), has longer-lasting action (so it can be administered less frequently), and is more potent (requiring a lower dosage) than furosemide. Although it has not been in use as long as furosemide has, torsemide can be useful in the management of refractory heart failure in which furosemide resistance has been documented or when furosemide is not tolerated.

Thiazide diuretics (hydrochlorothiazide, chlorothiazide) decrease sodium resorption in the distal convoluted tubule. This action increases sodium and water delivery to the collecting ducts, and subsequently hydrogen and potassium excretion. Although the thiazides are relatively weak diuretics, they exert a synergistic effect when administered with loop diuretics and can cause profound electrolyte abnormalities (particularly hypokalemia) and dehydration when administered in combination, if not used judiciously. Thiazide diuretics are generally reserved for cases in which resistance to furosemide has developed.

Potassium-sparing diuretics (spironolactone, eplerenone, triamterente, amiloride) are the weakest of the diuretic class, exhibiting little to sometimes undetectable diuretic effect at standard dosages, especially when used alone in healthy dogs. Although they may produce more diuresis in a dog in heart failure, they should never be relied on to produce diuresis in cases of heart failure. They should also never be used to replace a loop diuretic; they are used only as adjunctive (add-on) agents.

Also see Positive Inotropes in the chapter "Systemic Pharmacotherapeutics of the Cardiovascular System."

Pimobendan is a novel inodilator (inotropic drug and vasodilator) that was approved by the FDA in 2007 for use in dogs with CHF related to atrioventricular valve insufficiency or dilated cardiomyopathy (DCM). It is classified as a calcium sensitizer and a phosphodiesterase (PDE) III inhibitor. The combination of increased inotropy (contractility) and mildly decreased afterload results in improved cardiac output and decreased cardiac filling (diastolic) pressures in dogs in heart failure that is due to either mitral regurgitation or DCM. Clinical improvements evident with pimobendan include better quality of life, better clinical scores, and a longer survival time. The inotropic effect of pimobendan is substantially greater than that observed with digoxin, and pimobendan has supplanted digoxin for inotropic support in CHF in dogs.

There is ongoing debate regarding the use of pimobendan in cats. Pimobendan is not approved for use in cats. While one retrospective case-controlled study has suggested clinical benefit in cats with heart failure due to cardiomyopathy,(1) the only prospective, blinded and placebo-controlled study demonstrated no benefit in cats with hypertrophic cardiomyopathy.(2) Therefore, the routine use of pimobendan in cats is probably not warranted; however, if a cat is no longer responding to conventional heart failure drug treatment, pimobendan (1.25 mg/kg per cat, PO, every 12 hours) may be tried.

Sympathomimetic amines (eg, dobutamine, dopamine) improve contractility and cardiac output via β-adrenergic agonist effects and can be valuable in the acute management of cardiogenic shock or CHF secondary to myocardial failure in dogs and cats. Because they increase myocardial contractility and relaxation, they also increase myocardial oxygen consumption. Inotropes also decrease the myocardial depolarization threshold, increase heart rate, and increase conduction velocity, all of which predispose the animal to cardiac arrhythmias.

Dobutamine is administered intravenously as a continuous-rate infusion. Starting at a lower dosage with up-titration every 15–30 minutes as required is recommended. Concurrent ECG monitoring is strongly recommended, and if arrhythmias worsen, the dosage of dobutamine should be decreased or dobutamine should be discontinued. Because dobutamine increases conduction through the atrioventricular node, additional caution is advised in atrial fibrillation. Dobutamine may preferentially increase myocardial blood flow, as compared with dopamine, which tends to increase renal and mesenteric flow. Dobutamine also tends to cause less tachycardia than dopamine does. Dopamine is also administered as a continuous-rate infusion with gradual up-titration of the dose, to effect. Both dopamine and dobutamine may cause GI upset. These agents are less commonly used in cats, although the same general treatment strategy may be followed; however, treatment should start at more conservative infusion dosages (~1 mcg/kg per minute) for both dobutamine and dopamine.

Milrinone, a PDE III inhibitor, decreases the degradation of cyclic AMP and produces effects similar to those of sympathomimetic amines. These agents are generally reserved for animals with severe refractory myocardial failure, because their use is associated with a greater risk of mortality than that observed with the sympathomimetic amines. Because they do not depend on beta-receptor stimulation, PDE III inhibitors are unaffected by beta-receptor downregulation or uncoupling that may occur with progressive cardiac disease, and they may be useful in patients refractory to sympathomimetic amine treatment. Vasodilation is an added benefit of PDE III inhibition. Adverse effects noted with PDE III inhibitors include tachycardia, tachyarrhythmias, thrombocytopenia, GI upset, and hypotension at higher dosages. Milrinone is administered as an initial loading dose followed by constant-rate infusion.

The digitalis glycosides (eg, digoxin, digitoxin) are relatively weak positive inotropes that increase vagal tone to the heart, have a narrow therapeutic range, and are associated with many more adverse effects than pimobendan. Digitoxin is no longer commercially available. Although used only infrequently for its inotropic effects since the introduction of pimobendan, digoxin still plays an important role in managing cardiac disease, particularly atrial fibrillation or supraventricular tachycardia with concurrent CHF, because it is the only available pharmacologic agent that slows AV nodal conduction without concurrent negative inotropic effects. (For a complete discussion, see Cardiac Glycosides in the chapter "Systemic Pharmacotherapeutics of the Cardiovascular System".)

In order to avoid toxic effects, digoxin dosing begins conservatively; adequate serum concentration is not achieved until the second day of administration. Serum digoxin concentration should be checked 4–7 days after initiation of treatment, 6–8 hours after the last dose is given. The therapeutic serum concentration is 0.5–2 ng/mL. Dosage adjustments should be based on the animal’s serum digoxin concentration and clinical response, aiming for the lowest effective dose for each patient. If digoxin is used in cats, it may be started at one-fourth of a 0.125-mg tablet every third day for cats < 5 kg and every other day for cats > 5 kg. Some larger cats may ultimately tolerate dosages as high as one-fourth of a 0.125-mg tablet per day.

Adverse effects of digoxin are increasingly likely at higher serum concentrations and generally occur in the following order: GI (anorexia, vomiting), cardiac (bradycardia, atrioventricular [AV] block, premature ventricular contractions), and CNS derangements. Because of its ability to slow electrical conduction as well as increase intracellular calcium, digoxin can cause almost any cardiac arrhythmia, and it is contraindicated in cases of AV block, appreciable bradycardia, and rapid ventricular tachycardia. If adverse effects are noted or if the serum concentration is in the toxic range, the drug should be temporarily discontinued (usually for at least 1–2 days) and the dosage subsequently decreased by at least 50%.

Also see Angiotensin-converting Enzyme Inhibitors in the chapter "Systemic Pharmacotherapeutics of the Cardiovascular System" and the table Commonly Used Cardiovascular Drugs and Dosages for dosages of drugs mentioned below.

Angiotensin-converting enzyme (ACE) inhibitors competitively inhibit ACE, one of the enzymes that converts angiotensin I to angiotensin II, thereby blunting the increase in systemic vascular resistance, hypertrophy, and aldosterone release that is due to angiotensin II. ACE inhibitors are mild, balanced vasodilators. Additional potential benefits include a decrease in left ventricular filling pressure, which reduces pulmonary vascular pressure and, therefore, pulmonary edema. The beneficial effects of ACE inhibitors are thought to be due primarily to neurohormonal modulation, in addition to hemodynamic benefits.

Once in heart failure, the effect of ACE inhibitors is generally one of mild, but transient, clinical improvement. Although a trend toward prolonged survival has been documented in some studies, the benefits of ACE inhibitors for patients in heart failure are negligible overall. Aldosterone breakthrough, in which the plasma aldosterone concentration initially decreases and then increases again after weeks of ACE inhibitor administration, is common in dogs.

The role of ACE inhibitor treatment before the onset of CHF remains controversial. However, a recent analysis of the available clinical trials in dogs concluded they were of little to no benefit in prolonging the time to onset of heart failure in dogs with mitral regurgitation.(1)  Studies of ACE inhibition in cats in CHF are limited, and none have shown a true statistical benefit of ACE inhibition over standard diuretic treatment alone; nonetheless, many cardiologists do prescribe an ACE inhibitor in addition to appropriate background treatment for cats with CHF. ACE inhibitors are not effective for treatment of occult hypertrophic cardiomyopathy.

The primary serious adverse effect of ACE inhibition is a decreased GFR and resultant azotemia. Anorexia, vomiting, and lethargy (uremia) may occur, so owners should be warned to watch for these clinical signs after ACE inhibitor treatment is initiated. Renal function values (BUN, creatinine) should be measured before administration of an ACE inhibitor begins, again 3–7 days later, and periodically thereafter.

Enalapril is the only approved ACE inhibitor in the US for dogs with CHF. Other ACE inhibitors used for treatment of heart failure in dogs include benazepril, captopril, ramipril, and lisinopril.

Also see Vasoactive Drugs in the chapter "Systemic Pharmacotherapeutics of the Cardiovascular System."

Vasodilators exert a positive effect in CHF by dilating either arterioles or veins and thereby decreasing resistance to blood flow. Nitrates (sodium nitroprusside, nitroglycerin ointment, isosorbide dinitrate) increase nitric oxide production to induce endothelial smooth muscle relaxation. Sodium nitroprusside is the most clinically useful nitrate: it is a potent mixed vasodilator, acting on both the arterial and venous systems. The combination of sodium nitroprusside and dobutamine may be especially useful in cases of cardiogenic shock and severe pulmonary edema. Although sodium nitroprusside dramatically and acutely decreases preload and afterload, its use is limited by the need for close monitoring and administration as a constant-rate infusion; concurrent blood pressure monitoring is recommended. However, since the duration of its effect is very short (1–2 minutes), any resultant hypotension should dissipate quickly once the infusion is stopped. Prolonged administration (> 16 hours) increases the risk of cyanide toxicosis (see the package insert).

If nitroprusside therapy treatment is unavailable or undesired, nitroglycerin ointment or isosorbide dinitrate might be can be administered transdermally. Clinical impact on the patient may be only mild to negligible with these drugs but they are still used as adjunct vasodilators on occasion. Nitroglycerin is absorbed transcutaneously by the person administering the drug, so gloves must be worn during administration.

Hydralazine is a potent systemic arteriolar vasodilator typically reserved for dogs with mitral regurgitation due to myxomatous mitral valve degeneration that are refractory to conventional treatment, or for dogs in acute CHF due to ruptured mitral chordae tendineae when nitroprusside is unavailable. Hydralazine is presumed to act by producing vasodilatory prostaglandins. It may decrease systemic vascular resistance by up to 50%. This decrease in resistance results in the left ventricle pumping more blood forward through the systemic vasculature and less blood backward through the incompetent mitral valve into the left atrium, thereby decreasing left atrial and pulmonary capillary pressures and the development of pulmonary edema. This oral drug is effective within 30 minutes, peaks in 1–3 hours, and maintains that peak for 11–13 hours. Approximately 90% of dogs respond to a dosage of 2 mg/kg PO every 12 hours, after progressive dose increases from 0.5-1mg/kg PO. Approximately 30% of dogs vomit after receiving hydralazine; the drug generally needs to be discontinued in these cases.

Amlodipine is a calcium channel blocker with only peripheral vascular effects (no cardiac effects). It produces a moderate to marked vasodilatory effect on systemic arterioles. Its actions are very similar to those of hydralazine (decreased mitral regurgitation and pulmonary edema), but without the adverse effects of vomiting and tachycardia. Amlodipine has a relatively slow onset of action; its effects take 1–2 days to be noticeable. It is typically reserved for dogs with heart failure due to mitral regurgitation that is refractory to conventional heart failure drug treatment, or for dogs and cats with moderate to severe systemic hypertension. Adverse effects are generally related to hypotension and are uncommon when up-titration is gradual. Gingival hyperplasia can occur in some dogs administered amlodipine, often necessitating discontinuation of the drug.

Phosphodiesterase type 5 (PDE5) inhibitors (eg, sildenafil, tadalafil) are used to relax the smooth muscle in pulmonary arterioles. PDE5 inhibitors are used in the treatment of moderate to severe pulmonary arterial hypertension. Studies in dogs have demonstrated modest clinical improvement (decrease or cessation of syncope, improved right heart failure), despite only minimal detectable improvement in pulmonary artery pressures. Anecdotally, PDE5 inhibitors seem to provide the most notable clinical benefit to animals with syncope secondary to pulmonary hypertension, and also with right-to-left shunting cardiac defects. Adverse effects are uncommon but may include GI upset and hypotensive-related effects; PDE5 inhibitors should never be administered concurrently with nitrates.

"Beta-blockers" exert a sympatholytic effect by virtue of their beta-adrenergic receptor antagonism. Drugs in this class (eg, metoprolol, propranalol, atenolol), can dramatically improve myocardial function in humans with DCM and heart failure, but these results have not been replicated in client-owned dogs with DCM. Dogs with experimentally induced heart failure have shown measurable improvements in cardiac performance after administration of metoprolol; however, these were models of ischemic cardiomyopathy, which is a rare cause of DCM in dogs. Large dogs (> 20 kg) with experimentally induced mitral regurgitation also have had lesser decreases in contractility over time when administered atenolol as compared with placebo.

Beta-blockers are commonly administered to cats with hypertrophic cardiomyopathy, primarily to decrease systolic anterior motion of the mitral valve. Current evidence suggests that the administration of beta-blockers does not result in clinical improvement or prolonged survival in cats with HCM. However, no study has examined only cats with severe systolic anterior motion of the mitral valve, so such treatment is generally still recommended for that subset of cats. Atenolol (6.25–12.5 mg/cat, PO, every 12 hours) is the beta-blocker most commonly used in cats.

Important metabolic changes may occur in animals with heart failure. Upregulation of the RAAS leads to increased plasma volume, largely mediated by increased sodium retention. “Cardiac cachexia” due to proinflammatory cytokines is common in patients with cardiac insufficiency or failure. When possible, the body condition of cardiac patients should be maintained by nutritional supplementation, as weight loss is associated with a poorer prognosis in patients with CHF. In some patients, deficiencies of certain nutrients (eg, taurine, carnitine) have been shown to cause DCM. Decreased concentrations of circulating fatty acids have been documented in humans and dogs with heart failure. The overall nutritional goals in the management of animals with heart failure should therefore include supplying adequate calories, modulating the production of proinflammatory cytokines, managing sodium balance, and supplementing nutrients that may be deficient.

The concept that sodium restriction decreases circulating plasma volume and preload is well established. However, sodium restriction is known to activate the RAAS, and there is continued debate as to the role of sodium restriction in animals, especially those with asymptomatic cardiac disease or mild to moderate CHF. In contrast, moderate to severe sodium restriction may be indicated in animals with severe CHF, especially in those refractory to drug treatment. It is also important to counsel owners to avoid foods and treats with high sodium content, because an acutely high sodium load (as can occur in animals fed human snacks or table foods such as ham) may precipitate CHF in animals with compensated heart disease. For animals in mild to moderate heart failure, moderate sodium restriction (50–80 mg/100 kcal) might be tried if the dog or cat will readily eat such a diet. In animals with severe refractory CHF, more aggressive sodium restriction (< 50 mg/100 kcal) may be tried. Sodium restriction is particularly challenging in patients with cardiac cachexia, because lower-sodium foods are often less palatable. In general, maintaining adequate caloric intake is more important than restricting sodium.

Supplementation with omega-3 fatty acids has been shown to have multiple benefits in humans with CHF, and may have antiarrhythmic benefits in dogs as well. Omega-3 fatty acids may decrease circulating inflammatory cytokine concentrations and seem to improve appetite in some dogs with cardiac cachexia. Daily doses of eicosapentaenoic acid (40 mg/kg) or docosahexaenoic acid (25 mg/kg) can be tried.

Taurine supplementation is indicated in animals with documented taurine deficiency and DCM. The incidence of DCM has declined dramatically in cats since taurine deficiency was identified as a primary cause in the late 1980s. Taurine deficiency is still documented in some cats with DCM that are fed noncommercial diets (especially chicken, dog food, and vegetarian diets) and rarely a commercial cat food diet. Supplementation at 250 mg, PO, every 12 hours, can be started in cats while awaiting results of plasma and whole-blood taurine concentrations.

Dogs are able to synthesize more endogenous taurine than cats, and dogs do not have obligatory loss in bile, so deficiency is less common. However, Cocker Spaniels with DCM uniformly have a low plasma taurine concentration and respond to taurine or taurine-carnitine supplementation. Newfoundlands are predisposed to taurine deficiency, especially when fed lamb and rice or high-fiber, low-protein/low-taurine diets. Rarely, dogs of other breeds with DCM (mostly breeds not usually thought of as being predisposed to developing DCM) will be taurine-deficient/responsive.

Whole-blood and plasma taurine concentrations should be obtained in any dog suspected of having a taurine-deficient cardiomyopathy, and supplementation can be started at 500–1,000 mg, PO, every 8–12 hours, while awaiting results. Clinical improvement occurs within weeks of starting taurine supplementation in cats or dogs with DCM due to taurine deficiency. Echocardiographic improvement takes longer (2–3 months).

-Carnitine plays an important role in fatty acid metabolism and energy production. Carnitine deficiency has been documented in one family of Boxers, and myocardial carnitine deficiency is common in dogs with DCM; however, most likely this deficiency is a result of cardiomyopathy, not the cause, in these dogs. Carnitine has been supplemented in other breeds with DCM, but with little success. Diagnosis of carnitine deficiency is difficult and requires an endomyocardial biopsy. Supplementation is also expensive, and given our limited knowledge of the role that carnitine plays in canine cardiomyopathy, supplementation is not routinely recommended.

Coenzyme Q is involved with mitochondrial energy production and possesses general antioxidant properties. Anecdotal benefits of supplementation in humans and dogs with DCM have been reported; however, well-controlled studies are lacking, and reports are conflicting.

Grain-free diets made by small (boutique) dog food manufacturers are suspected of causing DCM in some dogs. A careful diet history should be obtained for any dog with DCM, but especially for those that do not have a breed predisposition for DCM (eg, any small-breed dog). Lentils, peas, and possibly potatoes are common ingredients in the implicated diets. Taurine deficiency does not appear to be a factor, except possibly in Golden Retrievers, so sending blood to a lab for taurine analysis is usually not indicated. If DCM is diagnosed in a dog on an implicated diet (see FDA Investigation into Potential Link between Certain Diets and Canine Dilated Cardiomyopathy), the diet should be changed. Most veterinarians also supplement with taurine. In some dogs, myocardial function improves over ~6 months; some dogs show no improvement.

The presence of pulmonary edema in animals with CHF increases the alveolar-arterial diffusion distance and disturbs ventilation/perfusion matching. Supplemental oxygen administration increases the alveolar-arterial diffusion gradient and thus increases arterial oxygen content. Oxygen may be administered via oxygen cage, flow-by method (least preferred), nasal cannula, or oxygen collar (constructed by covering the ventral 50%–75% of an Elizabethan collar with plastic wrap and taping oxygen tubing along the ventral aspect of the collar). The oxygen cage is the least stressful for the animal but is expensive, because high flows of oxygen are required to achieve a therapeutic concentration (> 40% inspired oxygen). The oxygen collar has the potential to achieve a very high concentration of inspired oxygen (as much as 80%); however, light sedation may be required to increase patient tolerance.

Pleural effusion decreases ventilatory capacity and should always be excluded as the cause of dyspnea in animals in heart failure, especially cats. Ultrasonography is the best method for ruling out pleural effusion. If ultrasonography is unavailable, radiography is an option; however, extreme care must be taken to avoid stressing the animal (especially cats), because stress in a dyspneic animal can result in death. If radiography is not possible, diagnostic thoracocentesis is an option. In cats, thoracocentesis can often be done in the examination room using a butterfly catheter with the cat in sternal recumbency. If fluid is present, as much of the fluid as possible should be removed. Thoracocentesis is the most effective treatment in animals with respiratory distress due to an appreciable volume of effusion. Again, however, caution should be taken in particularly stressed animals, which may require pretreatment with oxygen and light sedation. Diuretic treatment is ineffective at acutely resolving a large volume of pleural effusion.

Ascites may produce abdominal discomfort and worsen dyspnea by decreasing available lung capacity in animals in right heart failure. Abdominocentesis should be performed at the time of initial diagnosis of right heart failure if the ascites is severe. In animals with recurrent ascites refractory to diuretic treatment, abdominocentesis may be performed every 1–4 weeks to improve patient comfort and quality of life. Every attempt should be made to remove all or as much fluid as possible on each visit to prolong the time between repeat abdominocenteses.

Also see for information on antithrombotics as treatment in cats with heart disease.

Bronchodilators (eg, theophylline, terbutaline) are generally reserved for animals with chronic airway disease, which is common in older small-breed dogs. Caution should be taken in animals with CHF, especially with tachyarrhythmias, because of the sympathomimetic effects of these agents. In dogs with cardiovascular disease and syncope, theophylline has been used for its positive chronotropic effects, with some success.

Cough suppressants generally should not be used if a cough is due to cardiogenic pulmonary edema, but if clinically necessary, common antitussive agents used for dogs with cardiac disease include butorphanol (0.05–0.3 mg/kg, PO, every 8 hours) and hydrocodone (0.22 mg/kg, PO, every 8–12 hours).

Anxiolytics may be used for some animals with severe respiratory distress secondary to CHF; morphine, butorphanol or acepromazine are commonly used medications for this purpose.