Keys to managing end-stage heart failure - DVM
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Keys to managing end-stage heart failure


DVM360 MAGAZINE

Q: Please provide an updated review on managing end-stage canine heart failure.

A: Drs. Sonya G. Gordon and Risa Roland gave an excellent lecture on managing end-stage canine heart failure and canine hospice care at the 2008 American College of Veterinary Internal Medicine Forum in San Antonio.

Some relevant points in this lecture are provided in this article.

Most dogs with heart failure are stabilized with multimodal therapy, including furosemide, pimobendan and an angiotensin-converting enzyme inhibitor (ACEI). However, despite the best therapy, progressive and often refractory clinical signs develop. This represents the end stage of heart failure, and navigation through it represents one of the biggest challenges of heart-failure therapy.

Most animal owners, in consultation with their attending veterinarians, elect euthanasia when medical therapy is unable to adequately palliate clinical signs of heart failure. When complaints suggestive of early cardiac decompensation develop such as respiratory embarrassment (e.g., cough, dyspnea, tachypnea), gastrointestinal embarrassment (e.g., inappetence, anorexia, diarrhea), exercise intolerance and collapse/syncope, the likely underlying reason for the complaint should be determined and a therapeutic plan developed. It's also necessary to follow up with the owner to determine the level of success with the intervention.

Many follow-up evaluations include telephone or e-mail dialogue in an attempt to minimize hospital re-evaluations. Most re-evaluations and therapeutic plans are carried out on an outpatient basis. Hospitalization should be avoided in animals at the late stages of disease.

It is important to remember that heart failure is progressive, and medications that were historically well-tolerated may lead to, or potentiate, clinical signs at a later stage. For example, dogs with heart failure typically tolerate afterload reduction with a combination of agents such as ACEI and pimobendan, but if the dog develops progressive pump failure leading to clinically significant systemic hypotension, then the degree of afterload reduction may need to be reduced or alternatively the degree of systolic support of the failing ventricle may need to be increased. That is, the combination of agents that palliated the signs of heart failure initially may not optimally palliate clinical signs in the end stages. So, part of management of end-stage heart failure involves re-evaluation of existing therapies as well as the introduction of new therapies. Remember, the goal is to palliate specific clinical signs.

Anorexia and inappetence

Inappetence leading to anorexia and requisite progressive weight loss represents one of the most common and significant complaints in advanced canine heart failure. Appetite and perceived food enjoyment are often described as important assessments to a pet's quality of life. The most common causes of inappetence and anorexia in dogs with chronic heart-failure include azotemia, pulmonary edema, ascites, medication-related, gastrointestinal ulceration, dietary indiscretion, behavioral or those unrelated to cardiovascular disease.

Clinically significant azotemia (azotemia leading to loss of appetite) may be secondary to progression of primary renal disease and/or progressive reductions in cardiac output. Progressive reductions in cardiac output may be related to the following problems: arrhythmias, severe pulmonary hyper- tension, progressive pump failure, pericardial effusion (rarely hemo- dynamically significant when it is due to heart failure), overzealous diuresis or afterload reduction. Diagnostic tests that may be useful to confirm or refute a differential diagnosis of reduced cardiac output leading to clinically significant azotemia causing loss of appetite include a relative tachycardia, a moderately increased BUN and creatinine suggesting at least a component of pre-renal azotemia in combination with systemic hypotension (typically systolic blood pressure <105 mmHg) and/or markers of poor perfusion such as low venous oxygen tension (<26 mmHg) and elevated blood lactate.

PCV and total solids may help differentiate overzealous diuresis leading to hypovolemia from other causes of reduced cardiac output. Suspicion of an underlying cause of hypovolemia in the absence of signs of congestion (pulmonary edema) warrants temporary discontinuation of diuretics (skip one to five doses or more) and/or lowering the diuretic dose. The use of subcutaneous fluids is contraindicated. Oral syringing of water or judicious IV fluids (1 to 1.5 times maintenance) while monitoring resting respiration rate may be employed in severe cases. Temporary discontinuation of oral diuretics is typically adequate to regain euvolemia.

On confirmation of low cardiac output unrelated to hypovolemia, attempts should be made to identify the cause. Significant arrhythmias usually can be ruled out on auscultation, but if an arrhythmia is heard or suspected, ECG and/or Holter (24-hour ambulatory ECG) may be required to guide therapy. Even inappropriate sinus tachycardia (those unrelated to hypovolemia or pain) can be deleterious and may need to be managed with judicious beta-blockade (very low dose titrated to effect) or digoxin. An echocardiogram may be useful to determine the presence and severity of pulmonary hypertension or pericardial effusion as well as progressive pump failure (especially when compared to previous echo studies).

Pericardial effusion causing tamponade may require pericardio- centesis (very uncommon when due to heart failure). If moderate to severe pulmonary hypertension is documented and suspected of contributing to reduced cardiac output, the cause for the pulmonary hyper- tension should be investigated (ruling out heartworm disease, hyperadreno- corticism, pulmonary thrombo- embolism) but chronic valvular disease (CVD) is one of the most common underlying causes for pulmonary hypertension. Regardless of the cause of pulmonary hypertension, dogs with severe pulmonary hypertension may benefit from the addition of sildenafil (1-3 mg/kg BID). Additional therapies for pulmonary hypertension should be guided by the underlying cause. Progressive pump failure and pulmonary hypertension may be palliated by increasing the dosing frequency of pimobendan from BID to TID (0.25-0.3 mg/kg TID).

Overzealous afterload reduction can be considered by exclusion of other causes of low cardiac output. Significant pulmonary edema (enough to lead to anorexia or inappetence) also will result in signs of respiratory distress. Clinically significant ascites (abdominal distention) secondary to heart failure confirms a diagnosis of elevated right-heart pressures and leads to passive gastrointestinal congestion, which can lead to absorption and motility problems. In addition, significant ascites can lead to respiratory distress and discomfort which can indirectly lead to anorexia and/or inappetence.

Some heart-failure medications, such as digoxin, may alter taste in some dogs or have adverse central effects on appetite. Typically, this is noticed on initiation of the medication and in the case of digoxin may even occur when blood levels are within the therapeutic range. Other therapies, particularly anti-arrhythmics, may cause increases in serum liver enzymes which can contribute to loss of appetite.

The bodies of animals with heart failure are under stress, suffer from chronic reductions in cardiac output passive GI congestion and, in combination these factors, may lead to GI stasis and ulceration, both of which can contribute to loss of appetite. Dietary indiscretion frequently is a consequence and potentially a cause of anorexia and inappetence. Many dogs with advanced heart failure are fed a variety of food because owners want to "treat them special" and most of these dogs develop some degree of inappetence. Part of acquired inappetence may be related to food avoidance in dogs that resent receiving medications in food and thus become more and more "picky." It is difficult to treat this problem. A variety of approaches can be used, such as separating the feeding and pill administration, and the person who feeds should never administer medication. Novel food presentations such as homemade diets can be tried.

Behavioral causes should be considered only after ruling out other more obvious causes of loss of appetite. Common non-cardiac causes that may lead to, or contribute to, loss of appetite include severe periodontal disease leading to pain when eating. Even in dogs with advanced heart failure, tooth extractions (with appropriate precautions and owner consent) may be necessary to improve quality of life. In milder to moderate forms of periodontal disease, an antibiotic course may be beneficial.

Some dogs in heart failure have no obvious cardiovascular or non-cardio- vascular cause for inappetence. In these animals, low-dose corticosteroids and other appetite stimulants in combination with basic GI supportive care such as famotidine sucralfate. When possible, multiple therapeutic changes should not be done concurrently, but rather one or two changes made at a time and response should be evaluated to guide additional alterations.

Cough, dyspnea and tachypnea

Progressive, incessant life-limiting cough with or without tachypnea or dyspnea is a common complaint in advanced canine heart failure, particularly in dogs with chronic valvular disease. Other common non-cardiogenic causes for cough are concurrent collapsing trachea and chronic obstructive pulmonary disease (COPD). The most common causes of cardiovascular-related cough in dogs with heart failure include pulmonary edema and left atrial enlargement causing left mainstem bronchus compression.

Given the incidence of collapsing trachea and COPD in small-breed dogs, combination therapy is often necessary to optimize palliation of chronic cough in dogs with chronic valvular disease. Cardiogenic causes for progressive dyspnea and tachypnea without significant cough is typically associated with pulmonary edema, pulmonary hypertension (especially in dogs with chronic valvular disease), and/or severe ascites leading to limited excursion of the diaphragm. Pleural effusion is rarely severe enough to cause dyspnea or tachypnea in dogs with heart failure and even right heart failure.

Cough and dyspnea or tachypnea due to refractory pulmonary edema can be confirmed with thoracic radiographs. Refractory pulmonary edema should be managed through optimal reduction in plasma volume to achieve euvolemia. Renal function (BUN, creatinine), systemic blood pressure and hydration status (PCV, TS) should be evaluated and taken into consideration during formulation of a treatment plan. Strategies employed to regain euvolemia may include increased diuresis, venodilation, maximal inhibition of the renin angiotensin aldosterone system (RAAS), dietary sodium restriction, and tolerable afterload reduction inotropic support.

In dogs receiving submaximal doses of furosemide, the dose and/or dosing frequency can be increased. Maximal chronic oral doses for furosemide are 4-5 mg/kg PO TID. In dogs receiving maximal oral doses, the route of administration could be changed to subcutaneous injections for one or all daily doses. Alternatively, a rescue diuretic could be added, such as hydrochlorothiazide. When hydrochlorothiazide is added to chronic furosemide therapy (with or without spironolactone), diuresis and potential side-effects of diuresis (hypovolemia leading to azotemia, electrolyte abnormalities especially hypokalemia) are potentiated due to sequential nephron blockade. Thus, to minimize unwanted side effects when a thiazide diuretic is initiated, the furosemide dose is decreased by approximately 50 percent and potassium supplementation is initiated. Typically, the furosemide dose is reduced from 4-5 mg/kg PO TID to 3-3.5 mg/kg BID or 2-2.5 mg/kg TID, spironolactone is left at the same dose, and hydrochlorothiazide is initiated at 2 mg/kg BID. Over time, as the need for diuresis increases, the furosemide dose is then titrated up.

Venodilation using agents like topical nitroglycerine have no use in the chronic setting. In animals receiving sub-maximal doses of ACEI, additional RAAS inhibition may be achieved by increasing the dose of enalapril or benazepril to 0.5-0.6 mg/kg BID.

If spironolactone was not already part of the treatment plan, it could be added at this time at a dose between 0.5-2 mg/kg BID. Its beneficial effects in this setting are likely related to its RAAS blockade, not diuresis. Dietary sodium restriction may be useful if tolerated. Homemade sodium-restricted diets often are more palatable.

Finally, in normotensive animals additional afterload reduction may reduce filling pressures and thus reduce pulmonary edema. When adding pure afterload reducers such as amlodipine (0.005-1.0 mg/kg PO SID to BID) or hydralazine (0.25-2 mg/kg PO BID) to a background of ACEI and pimobendan, starting doses should be very low and re-evaluation of blood pressure, heart rate and renal parameters should be frequent (every three to five days) during up-titration.

Finally, a combination of additional inotrope and afterload reduction may be recruited by increasing the frequency of pimobendan to TID from BID.

When possible, multiple therapeutic changes should not be done concurrently but rather one or two changes made at a time. Response should be evaluated to guide additional alterations.

Dyspnea and tachypnea due to pulmonary hypertension can be presumed in dogs whose degree of dyspnea is worse than expected based on severity of radiographic infiltrates. Pulmonary hypertension can frequently be confirmed with a Doppler echo- cardiogram.

Many dogs with advanced chronic valvular disease develop secondary pulmonary hypertension and the requi- site clinical signs such as respiratory embarrassment, exercise intolerance and collapse with exercise. Regardless of the cause of the pulmonary hypertension, animals with dyspnea due to pulmonary hypertension may benefit from increasing the dose of pimobendan from BID to TID and adding sildenafil (1-3 mg/kg BID). Short-term oxygen support may be needed while starting the new medications. Ascites contributing to dyspnea and tachypnea should be removed in total if possible via abdominocentesis, and then diuretics should be used to minimize the speed of recurrence.

Intermittent abdominocentesis often is required and well tolerated in the management of chronic right heart failure. If the animal is eating and the frequency of abdominocentesis is not more than once every 10-14 days, typically albumin levels will remain in the normal range. The clinical goal is to use diuretics to limit the frequency of abdominocentesis to every four to six weeks.

Many dogs with chronic right heart failure ultimately require triple diuretic therapy. A dog with a prior diagnosis of right heart failure due to dilated cardiomyopathy or chronic valvular disease is typically receiving a combination of pimobendan (0.25-0.3 mg/kg PO BID), ACEI (0.5 mg/kg PO BID), spironolactone (2 mg/kg PO BID) and furosemide (1-5 mg/kg PO BID to TID). Once the dose of furosemide required to minimize abdominocentesis frequency is 4-5 mg/kg PO TID, the addition of a third diuretic may be useful. The third or rescue diuretic of choice in advanced right (refractory ascites) and left heart failure (refractory pulmonary edema) is hydrochlorothiazide. When serum albumin levels begin to decline significantly due to progressive loss of appetite and/or increased frequency of abdominocentesis, then there is little left to do clinically. Most animals feel great following abdomino- centesis. When this fails to occur, it represents an ominous prognosis sign that is typically recognized by the owner.

If right heart failure is a new finding, further diagnostics such as an echocardiogram may be useful to determine the cause and guide more specific therapies when indicated. For example, dogs that develop severe pulmonary hypertension often develop right heart failure and may benefit from sildenafil (1-3 mg/kg BID) in addition to palliative intermittent abdominocentesis and optimized diuresis. Pleural effusion is rarely of sufficient severity to cause clinical signs in canine heart failure; however, if it is contributing to clinical signs it should be removed.

Severe "clinically significant" cough is a common complaint in dogs with end-stage chronic valvular disease. Severe cough in the absence of dyspnea and tachypnea is typically related to left mainstem bronchial compression alone or in combination collapsing trachea and/or COPD. Clinically significant cough can be defined as a cough that based on frequency and/or severity limits the dogs and/or owner's ability to sleep and enjoy normal activities.

When managing chronic cough, it is important to grade the severity of the cough (with the owner) because many of these coughs cannot be cured. The clinical goal in many cases is a reduction in the cough frequency and/or severity, i.e., one that does not impair the dog's and/or owner's ability to sleep and enjoy normal activities. Poor owner communication regarding the ultimate goal of cough palliation leads to unrealistic expectations on the part of the owner and dooms us to failure. Animals with left mainstem bronchial compression may benefit from mild increases (25 percent) in diuretic dose. If they are normo- tensive, then additional afterload reduction may be useful. An oral or inhaled bronchodilator may help, and finally a cough suppressant may be employed to achieve and maintain a goal of "tolerable" cough.

Additionally, dogs with concurrent collapsing trachea and/or COPD may benefit from therapies such as broncho- dilator, short courses of antibio- tics, tapering course of corticosteroids, cough suppressants, environmental modification and weight loss.

by Johnny D. Hoskins DVM, PhD, Dipl. ACVIM

Dr. Hoskins is owner of Docu-Tech Services. He is a diplomate of the American College of Veterinary Internal Medicine with specialities in small animal pediatrics. He can be reached at (225) 955-3252, fax: (214) 242-2200 or e-mail:

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Source: DVM360 MAGAZINE,
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