Managing End Stage Canine Heart Failure: Canine Hospice Care
ACVIM 2008
Sonya G. Gordon, DVM, DVSc, DACVIM (Cardiology); Risa Roland, DVM, DACVIM (Cardiology)
College Station, TX, USA; Yonkers, NY, USA

Introduction

Most dogs with heart failure (HF) 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 HF and navigation through this terminal stage represents one of the biggest challenges of HF therapy.

Hospice care can be defined as the provision of palliative and supportive care for terminally ill patients and their families. This definition underlines the fact that navigation of the terminal stage of HF involves palliation of the patient's clinical signs as well as support and guidance of the client. The authors' typically inform the client early in the management of HF that they will act as an advocate of both the patient and client as long as their best interests are similar, however when these interests diverge the authors' inform the client that as a veterinarian their first responsibility is to the patient. This helps develop a solid doctor client relationship, which is necessary for future discussions regarding quality of life, an important part of managing terminally ill patients. Ultimately, most clients in consultation with their attending veterinarians elect euthanasia when hospice care is unable to adequately palliate clinical signs. The authors' quality of life discussions focus on four categories, 1) can the patient breathe comfortably on room air, 2) does the patient enjoy his meals, 3) does the patient enjoy interactions with the client and family, 4) can the patient get around enough to do his business with dignity and rest comfortably. Thus the authors' approach to hospice care is to listen carefully to the client and optimize therapy in an effort to palliate specific clinical signs through scheduled and unscheduled re-evaluations. When complaints suggestive of decompensation develop such as respiratory embarrassment (e.g., cough, dyspnea, tachypnea), gastrointestinal embarrassment (e.g., inappetence, anorexia, diarrhea) or weakness, exercise intolerance, collapse or syncope the authors' use a methodical approach to determine the likely underlying reason for the complaint and develop a therapeutic plan to address the complaint and then follow-up with the client to determine the level of success of the intervention. Many follow-up evaluations include phone or email 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 patients at this stage of disease. A friend once told me that how you end a relationship is as important as how you start it. This statement is very true for veterinarians that manage patients with end-stage HF and for clients learning to accept the inevitable.

It is important to remember that HF is progressive and medications that were well tolerated at any one time point may lead to or potentiate clinical signs at a later stage. For example: dogs with HF typically tolerate afterload reduction with a combination of agents such as ACEI and pimobendan, but if the patient 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 HF initially may not optimally palliate clinical signs in the end-stages and thus part of management of end-stage HF involves re-evaluation of existing therapies as well as the introduction of new therapies and all efforts are done to palliate specific clinical signs. The following are common categories of client complaints reported in end-stage HF patients and can be used as a framework for a clinical approach to managing end-stage canine HF. This framework focuses on the contribution of progressive HF to the development of clinical signs , however dogs with HF can develop other significant non-cardiac diseases and attending clinicians should keep this in mind and give these considerations due diligence when appropriate.

Anorexia & Inappetence

In the authors experience inappetence leading to anorexia and requisite progressive weight loss represents one of the most common and significant client complaints in advanced canine HF patients. Appetite and perceived food enjoyment is often described as one of the most important quality of life assessments. The most common causes of inappetence and anorexia in chronic HF dogs include: azotemia, pulmonary edema, ascites, medication related, gastrointestinal ulceration, dietary indiscretion, and lastly may be behavioral or unrelated to their cardiovascular disease.

Clinically significant azotemia (azotemia leading to loss of appetite) may be secondary to progression of primary renal insufficiency and or progressive reductions in cardiac output (CO). ****Progressive reductions in CO may be related to any combination the following: arrhythmias, severe pulmonary hypertension (PH), progressive pump failure, pericardial effusion (rarely hemodynamically significant when it is due to HF), and overzealous diuresis or afterload reduction. Diagnostic tests that may be useful to confirm or refute a differential diagnosis (DDx) of reduced CO leading to clinically significant azotemia causing loss of appetite include: a relative tachycardia on physical exam, a moderately increased BUN and creatinine suggesting at least a component of pre-renal azotemia in combination with systemic hypotension (patient specific but typically systolic blood pressure < 105 mmHg) and or markers of poor perfusion such as low venous oxygen tension (<26 mmHg) and elevated blood lactate. A PCV and total solids (TS) may help differentiate overzealous diuresis leading to hypovolemia from other caused of reduced CO. Suspicion of an underlying etiology of hypovolemia in the absence of signs of congestion (pulmonary edema) warrants temporary discontinuation of diuretics (skip 1-5 doses or more) and or lowering the diuretic dose. The use of sub-cutaneous fluids is contraindicated. Oral syringing of water or judicious IV fluids (1 to 1.5 x maintenance) while monitoring resting respiration rate may be employed in severe cases. In the authors' experience, temporary discontinuation of oral diuretics is typically adequate to regain euvolemia. Upon confirmation of low CO unrelated to hypovolemia attempts should be made to identify the etiology. Significant arrhythmias can usually be ruled out on auscultation but if an arrhythmia is heard or suspected and 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 PH or pericardial effusion as well as progressive pump failure (especially when compared to previous studies). Pericardial effusion causing tamponade may require pericardiocentesis (very rare when due to HF). *If moderate to severe PH is documented and suspected of contributing to low CO the etiology for the PH should be investigated (rule out: heart worm, Cushing's, pulmonary thromboembolism) but chronic valve disease (CVD) is one of the most common underlying etiologies for PH. Regardless of the PH etiology dogs with severe PH may benefit from the addition of sildenafil (1-3 mg/kg BID). Addition therapies for PH should be guided by the underlying etiology. Progressive pump failure and PH may be palliated by increasing the dosing frequency of pimobendan from BID to TID (0.25-.3 mg/kg TID). Lastly overzealous afterload reduction can be considered by exclusion of other causes of low CO. Significant pulmonary edema (enough to lead to anorexia or inappetence) will also result in signs of respiratory distress (see following section for treatment). **Clinically significant ascites (abdominal distention) secondary to HF confirms a diagnosis of elevated right heart pressures and leads to passive gastrointestinal (GI) congestion which can lead to absorption and motility issues. In addition, significant ascites can lead to respiratory distress and discomfort which can indirectly lead to anorexia and or inappetence (see following section for treatment). Some HF medications may alter taste in some dogs or have adverse central effects on appetite such as digoxin. Typically this is noticed upon initiation of the medication and in the case of digoxin may even occur when blood levels are within the therapeutic range. Other therapies, particularly antiarrhythmics (e.g., amiodarone, mexiletine) may cause increases in liver enzymes which can contribute to loss of appetite. The bodies of HF patients are under stress, suffer from chronic reductions in CO +/- 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 is frequently a consequence and potentially a cause of anorexia and inappetence. Many dogs with advanced HF are fed a variety of food because owners want to 'treat them special' and because most of these patients 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 and the authors' use a variety of approaches including; separating the feeding and the pill giving both temporally and by administering individual. That is the person who feeds never administers medication. The authors' have also had some success with novel food presentations such as home made diets. Behavioral etiologies should only be considered 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. The authors always evaluate the potential contribution of periodontal disease to loss of appetite. Even in patients with advanced HF tooth extractions (with appropriate precautions and client consent) may be necessary to improve quality of life. In milder to moderate forms of periodontal disease an antibiotic course may be beneficial. However, some dogs in HF have no obvious cardiovascular or non-cardiovascular cause for inappetence. In these patients the authors' have tried low dose corticosteroids and other appetite stimulants in combination with basic GI supportive care such as pepcid +/- 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 & Tachypnea

Progressive, incessant life limiting cough with or without tachypnea or dyspnea is a common complaint in advanced canine HF, particularly in dogs with CVD. Other common non-cardiogenic etiologies for cough such as collapsing trachea (CT) and chronic obstructive pulmonary disease (COPD) should be considered as co-morbidities contributing to cough, particularly in small breed older dogs with CVD. The most common causes of cardiovascular related cough in dogs with HF include pulmonary edema (DCM & CVD) and left atrial enlargement causing left mainstem bronchus compression (CVD). Additionally, given the incidence of CT and COPD in small breed dogs combination therapy is often necessary to optimize palliation of chronic cough in dogs with CVD. Cardiogenic causes for progressive dyspnea and tachypnea without significant cough is typically associated with pulmonary edema, pulmonary hypertension (especially in dogs with CVD), 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 HF even right HF.

Cough and dyspnea or tachypnea due to refractory pulmonary edema can be confirmed with thoracic radiographs. In difficult cases determination of serum NT-proBNP may help confirm the diagnosis. Refractory pulmonary edema should be managed through optimal reduction in plasma volume to achieve euvolemia. Renal function (BUN, creatinine), systemic BP 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 rennin angiotensin aldosterone system (RAAS), dietary sodium restriction, and tolerable afterload reduction +/- inotropic support. In dogs receiving sub maximal doses of furosemide the dose/dosing frequency can be increased. Maximal chronic oral doses are 4-5 mg/kg PO TID. In dogs receiving maximal oral doses the route of administration could be changed to sub cutaneous injections for one or all daily doses. Alternatively, a rescue diuretic could be added such as hydrochlorothiazide (HCZ). *When HCZ 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 etc.) are potentiated due to sequential nephron blockade. Thus to minimize unwanted side-effects the authors' use the following plan when a thiazide diuretic is initiated; the furosemide dose is decreased by approximately 50% 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 HCZ is initiated at 2mg/kg BID. Overtime as the need for diuresis increases the furosemide dose is then up titrated. Venodilation using agents like topical nitroglycerine have no use in the chronic setting. In patients 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 predominant 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 are often more palatable. ***Finally, in normotensive patients 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 BP, heart rate and renal parameters should be frequent (q 3-5 days) during up-titration. Finally, a combination of additional inotropy and afterload reduction may be recruited by increasing the doing 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 and response should be evaluated to guide additional alterations.

Dyspnea and tachypnea due to PH can be presumed in dogs whose degree of dyspnea is worse than expected based on severity of radiographic infiltrates and degree of elevation in serum NT-proBNP concentration. PH can frequently be confirmed with a Doppler echocardiogram. Many dogs with advanced CVD develop secondary PH and the requisite clinical signs such as respiratory embarrassment, exercise intolerance and collapse with exercise. Other DDx for PH should be ruled out (*see previous section). Regardless of PH etiology, patients with dyspnea due to PH 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 also 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 is often required and well tolerated in the management of chronic right HF. If the patient is eating and the frequency of abdominocentesis in not more than once every 10-14 days, typically albumin levels will remain in the normal range. The authors' clinical goal is to use diuretics to the limit the frequency of abdominocentesis to q 4-6 weeks. Many dogs with chronic right HF ultimately require triple diuretic therapy. A dog with a prior diagnosis of right HF due to DCM or CVD is typically receiving a combination of pimobendan (0.25-0.3 mg/kg PO BID), ACEI (0.5 mg/kg PO BID), spironolactone (2mg/kg PO BID) and furosemide (1-5 mg/kg PO BID to TID). Once the dose of furosemide required to minimize abdominocentesis frequency is 4-5mg/kg PO TID, the addition of a third diuretic may be useful. The authors 3rd or rescue diuretic of choice in advanced right (refractory ascites) and left HF (refractory pulmonary edema) is HCZ (*see preceding section on initiation of HCZ). When 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. In the author's experience most patients feel great following abdominocentesis, when this fails to occur it represents an ominous prognosis sign that is typically recognized by the client. If right HF is a new finding further diagnostics such as an echocardiogram may be useful to determine the etiology and guide more specific therapies when indicated. For example dogs that develop severe PH often develop right HF 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 sings in canine HF, 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 CVD. Severe cough in the absence of dyspnea and tachypnea is typically related to left mainstem bronchial compression (LMBC) alone or in combination CT and or COPD. Clinically significant cough can be defined as a cough that based on frequency and or severity limits the dogs and or clients ability to sleep and enjoy normal activities. When managing chronic cough it is important to grade the severity of the cough with the client because many of these coughs cannot be cured. The clinical goal in many cases is a reduction in the coughs frequency and or severity to a tolerable level, i.e., one that does not impair the dogs and or clients ability to sleep and enjoy normal activities. Poor client communication regarding the ultimate goal of cough palliation leads to unrealistic expectations on the part of the client and dooms us to failure. Patients with LMBC may benefit from mild increases (25%) in diuretic dose. If they are normotensive then additional afterload reduction may be useful (see preceding section ***). 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 CT and or COPD may benefit from therapies such as bronchodilator, short courses of antibiotics, a tapering course of corticosteroids, cough suppressants, environmental modification and weight loss.

Lethargy, Weakness, Exercise Intolerance, Collapse & Syncope

This grouping of clinical signs may be related to cardiac or extra-cardiac causes. Cardiac causes typically involve etiologies that lead to reductions in CO or electrolyte derangements secondary to diuretic use. Specific etiologies of reduced CO and approaches to diagnosis and therapy were discussed in preceding sections. Hypokalemia should always be ruled out in dogs with HF receiving diuretics that present for lethargy, weakness or exercise intolerance. Important extra cardiac causes to consider in older dogs (dogs that get HF) include musculoskeletal diseases such as degenerative joint disease and neurological diseases such as inter vertebral disc disease and intracranial disease. Thus a thorough history, orthopedic and neurologic examination should be performed on all HF patients presented for a complaint of lethargy, weakness, exercise intolerance, collapse or syncope. Palliation of extra cardiac diseases must be done with caution in an old dog receiving combination HF therapy. Suggestions based on the authors' experience were discussed in preceding sections and the proceedings of the previous talk entitled "Canine Heart Failure Management: Polypharmacy Pitfalls".

Diarrhea & Soft Stool

Diarrhea and stool issues are present in some end stage HF dogs and are in general poorly tolerated by clients. They are typically related to a combinations or factors including: passive GI congestion due to right HF, poor GI perfusion due to left forward HF, stress of chronic illness and iatrogenic dietary indiscretion. In combination these factors can lead to ulceration and motility issues. Therapies targeting the underlying causes are discussed in the preceding sections. Palliative therapies used by the authors' involve increasing the fiber content in the diet by using Metamucil biscuits or pumpkin and basic GI protectants.

References

1.  Gordon SG, Kittleson MD in Small Animal Clinical Pharmacology 2nd edition. Saunders Elsevier, Edinburg 2008. pp. 380-457.

2.  Roland RM, Gordon SG. Canine Heart Failure Management: Polypharmacy Pitfalls. ACVIM 2008 Forum Proceedings.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Sonya Gordon, DVM, DVSc, DACVIM (Cardiology)
Texas A&M University
College Station, TX

Risa Roland, DVM, DACVIM (Cardiology)
College Station, TX


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