Management of Heart Failure in Dogs

Chapter 176


Management of Heart Failure in Dogs




Heart failure (HF) is very common in dogs, and this section of Current Veterinary Therapy (and the accompanying digital version) offers a detailed consideration of the different congenital and acquired heart diseases responsible for this clinical syndrome. This chapter focuses on canine HF, beginning with an overview, describing methods for staging the severity of heart disease, and then discussing the authors’ specific approaches for management of patients with chronic HF. The chapter concludes with a consideration of some special but relevant issues related to HF: namely, an approach to management of respiratory signs in dogs with heart disease, initial hospital treatment of acute congestive heart failure (CHF) and cardiogenic shock, and the treatment of heart rhythm disturbances in the setting of HF.



Overview of Heart Failure


The term heart failure describes the situation in which the heart, despite normal to increased venous pressures, cannot maintain a cardiac output or arterial blood pressure (BP) sufficient to satisfy the perfusion demands of the tissues. From a pathophysiologic perspective the initial event in the syndrome of HF is arterial underfilling, triggered by systolic or diastolic dysfunction of the heart. Initially, inadequate tissue perfusion is apparent only during exercise; therefore early signs of HF may be subtle or go unrecognized. However, eventually venous pressures increase to support or augment cardiac filling. This situation contrasts sharply with most cases of shock, in which a reduced cardiac output is due mostly to decreased venous pressures and reduced cardiac filling. The elevated venous pressures associated with a failing heart increase capillary hydrostatic pressure and lead to more obvious clinical signs of CHF.


Physiologic control systems coordinate an array of vascular, neurologic, and endocrine responses involving the heart, blood vessels, kidney, lung, and central nervous system. These systems maintain blood volume, arterial and venous pressures, heart rate, cardiac output, and ventilation at levels sufficient to meet metabolic needs at rest, with exercise, and during other times of stress. HF triggers a cascade of these compensatory events, all focused on refilling the arterial tree and restoring BP toward normal. These physiologic controls predominately activate vasoconstrictor and sodium-retaining systems, attenuate vasodilator and natriuretic systems, and stimulate tissue mediators of inflammation. Prominent features of these compensations include (1) arterial and venous constriction mediated by the sympathetic, renin-angiotensin, vasopressin, and vascular endothelial systems; (2) redistribution of blood flow away from the skin, gut, kidneys, and skeletal muscle; (3) sodium and water retention mediated by altered renal blood flow; release of norepinephrine, aldosterone, and vasopressin; and inhibition of natriuretic hormones; (4) activation of inflammatory and growth-promoting systems that include fetal gene programs in the cardiac muscle cells and apoptosis.


If the cause of decreased cardiac output and arterial BP is rapidly reversible, activation of these systems is transient, and no permanent harm is apparent. However, when continually activated to support cardiac output and arterial BP, these compensations become maladaptive, persisting at the expense of structural and functional damage to blood vessels and cardiac muscle (hypertrophy, interstitial remodeling, and fibrosis), renal function, and skeletal muscle. These compensations also support the circulation, which makes many heart diseases difficult to diagnose until they have caused extensive cardiac remodeling and damage. However, the progression of heart disease and pump dysfunction triggers a spiral of increasing dependence on neurohormonal activity to maintain normal arterial BP and flow and eventually may lead to overt CHF. This is the stage most often managed by practicing veterinarians.


Clinical signs of CHF traditionally were classified as “forward” or “backward.” So-called forward HF produces signs of low cardiac output and inadequate tissue perfusion that include weakness, lethargy, and prerenal azotemia. Backward HF identifies the inability of the heart to drain blood from the venous system. The resultant increases in venous pressures induce lung or tissue congestion or the development of body cavity effusions and also may impair renal and abdominal organ function. Clinical signs include tachypnea, dyspnea, and cough from pulmonary edema or pleural effusion. Additionally, jugular venous distention, hepatomegaly, and ascites are observed when the right side of the heart has failed. Metabolic disturbances in HF include weight loss, especially of muscle mass (cardiac cachexia), azotemia, and possibly insulin resistance. Although hemodynamic changes may explain the acutely life-threatening clinical signs of HF, morbidity and mortality in patients with chronic HF appear to be related strongly to the tissue effects of the accentuated neurohormonal and cytokine-mediated compensations that develop in response to the reduced output of the failing heart.


Most causes of canine HF cannot be reversed with the exceptions of pericardial effusions, some congenital heart defects, and sustained cardiac arrhythmias. Accordingly, drug therapy represents the major therapeutic method for treating HF in dogs. The treatment of acute HF is focused on identifying and correcting life-threatening hemodynamic derangements. The long-term treatment of HF is aimed at maintaining hemodynamic gains while modulating and blunting the maladaptive compensatory responses to protect tissues and prolong life while minimizing clinical signs.



Classifications of Heart Disease and Heart Failure


HF is not a specific disease but a clinical syndrome, precipitated by a definable cardiac lesion and characterized by hemodynamic, renal, neurohormonal, and proinflammatory abnormalities. Causes of heart disease can be classified anatomically, morphologically, etiologically, and by predominant pathophysiologic disturbances. Although these classifications are not always necessary, they do focus the clinician on the correct diagnosis and inform the prognosis and therapy. Additionally, the functional status of the patient, relative to the heart disease, helps to organize the optimal management approach (see the following section on functional classifications).


The anatomic location and morphology of the lesions that characterize the heart disease should be identified before a diagnosis of HF is accepted. The abnormalities can include structural heart lesions such as a thickened mitral valve as well as secondary responses evident in the cardiac chambers such as atrial or ventricular dilatation and hypertrophy. Anatomic and morphologic lesions, which often are verified in patients by echocardiography, can be classified simply by location and pathologic features.


For example, heart diseases can be described as pericardial diseases (idiopathic pericardial hemorrhage, pericarditis, and hemopericardium associated with hemangiosarcoma, chemodectoma, and mesothelioma), myocardial diseases (dilated cardiomyopathy [DCM], right ventricular cardiomyopathy, myocarditis), valvular diseases (congenital malformations, degenerative disease, infective endocarditis), intracardiac or extracardiac shunts (atrial septal defect, ventricular septal defect, patent ductus arteriosus), and vascular diseases (systemic hypertension, pulmonary hypertension, heartworm disease).


The cause of cardiac disease may be obvious or uncertain, and without doubt some disorders are primary or idiopathic; however, the underlying cause often can be identified. Etiologic categories include malformations, degeneration, metabolic and endocrine disorders, nutritional diseases, infections, immune-mediated diseases, ischemia, inherited/genetic diseases, tumors, trauma, and toxins.


Pathophysiologic disturbances of heart function usually are identified in patients with cardiac failure. These include valvular regurgitation (mitral and tricuspid valvular regurgitation), valvular stenosis (subaortic or pulmonic stenosis), intracardiac or extracardiac shunting, and heart rhythm disturbances (e.g., atrial fibrillation and ventricular tachycardia). Additionally, the basic mechanism by which the ventricle fails can be labeled as systolic HF or diastolic HF, although both abnormalities often are present to varying degrees. Systolic dysfunction indicates ineffective cardiac contraction because of myocardial or valvular dysfunction. Typical examples are DCM and chronic mitral regurgitation (MR). Diastolic dysfunction means that the heart cannot fill unless atrial or venous pressures are increased and suggests impaired myocardial relaxation, increased ventricular chamber stiffness, or both conditions. Examples include concentric hypertrophy associated with aortic stenosis or untreated systemic hypertension. Additionally, pericardial diseases compress or constrain the ventricles, also leading to diastolic HF. Finally, cardiac arrhythmias usually compromise both filling and pumping of the heart.


The clinician often classifies CHF as right-sided, left-sided, or biventricular. In some cases, right-sided CHF is a consequence of the pulmonary hypertension caused by severe left-sided heart disease. Most patients with HF experience clinical signs related to limited cardiac output, such as reduced exercise capacity. With left-sided CHF respiratory signs tend to dominate the clinical picture related to pulmonary congestion, with or without pleural effusion. Right-sided CHF in dogs is characterized by ascites (with or without pleural effusion). Biventricular CHF is most common in cases of left-sided heart disease complicated by either pulmonary hypertension or atrial fibrillation. Some dogs with DCM also have signs of biventricular HF. Finally, a small subset of dogs exhibit clinical signs of both forward and backward HF along with profound hypotension and biochemical markers of hypoperfusion (e.g., lactic acidosis). These cases are classified as cardiogenic shock.


These diagnostic categorizations are reviewed because the clinician’s first step in treating cardiac failure involves identifying the underlying cardiac lesion(s) and the “heart disease” responsible for CHF. Therapy is predicated on these anatomic, morphologic, etiologic, and functional diagnoses. In the authors’ experience, the most common mistake made when treating HF in practice is the use of “appropriate” HF therapy in a dog with clinical signs attributable to primary airway or lung disease. This error can be avoided by remembering that HF is not a disease but a consequence of a cardiac disorder that requires appropriate delineation.



Functional Classifications


The clinical signs of CHF are similar regardless of the underlying cardiac disease. Similarly, classification systems that grade the severity of HF or stage patients with heart disease are largely independent of anatomic or etiologic diagnoses.


A number of functional classifications of heart disease and heart failure have been applied to animals. These include the symptom-based classifications of the New York Heart Association (NYHA) and modifications of the scheme originally proposed by the International Small Animal Cardiac Health Council (ISACHC). The newer American College of Cardiology (ACC)/American Heart Association (AHA) classification scheme has been modified recently for dogs by an American College of Veterinary Internal Medicine (ACVIM) consensus panel. Each system provides a framework for discussing the clinical signs in patients with HF and a semiquantitative method for comparing these signs and, to some extent, estimating the need for various therapies.



Classifications Based on Clinical Signs


The first two systems assume that heart disease is present and that any functional impairment can be summarized as follows:



• NYHA/ISACHC class I: No clinical signs are evident at exercise or at rest.


    Notes: The modified ISACHC system subcategories include class IA (heart disease without cardiomegaly) and ISACHC class IB (heart disease with associated cardiomegaly).


• NYHA/ISACHC class II: There is mild functional limitation with clinical signs or limitations evident only with exercise or activity. There are no clinical signs at rest.


• NYHA class III: There is moderate functional impairment with clinical signs developing with mild exercise. The patient is comfortable only at rest.


    Note: There is no specific ISACHC classification comparable to NYHA class III.


• NYHA class IV/ISACHC class III: Severe functional limitations with clinical signs that are evident during exercise and at rest.


    Notes: ISACHC subclass IIIA indicates that home therapy for HF is possible; ISACHC subclass IIIB indicates that hospitalization is needed.


Although some animals with heart disease follow an orderly progression through functional classes, both the NYHA and ISACHC schemes allow an animal to move freely in both directions, for example, from class I to IV (or IIIB) following a dietary salt load, ruptured chordae tendineae, or hemodynamically significant arrhythmia, and then back from class IV to class II following successful medical management of CHF.



Modified ACC/AHA Classification


As an improvement on the clinical signs–based systems, the ACC and the AHA developed a staging system that emphasizes the progressive nature of most underlying diseases. This scheme was adapted for canine use in the report of the ACVIM consensus panel on the diagnosis and treatment of valvular heart disease (Atkins et al, 2009). This scheme can be summarized as follows:



• Stage A: Patients are at high risk of the development of HF but without apparent structural abnormality at the present time.


    Examples: Cavalier King Charles spaniels, boxers, and Doberman pinschers, as well as other dogs belonging to breeds, families, or demographic groups known to be predisposed to heart disease.


• Stage B: Patients have a structural abnormality but have never demonstrated any (client-recognized) symptoms or clinical signs of HF. Stage B1 includes dogs with normal heart size based on evaluation of radiographs (and, optimally, echocardiographic findings). Stage B2 includes dogs with evidence of cardiomegaly and ventricular remodeling.


    Examples: An asymptomatic dog with a murmur of MR; an apparently healthy Doberman pinscher with systolic myocardial dysfunction and left ventricular dilatation on echocardiography.


• Stage C: Patients have a structural abnormality and current or previous clinical signs of HF.


    Examples: This stage includes all patients that have experienced an episode of clinical HF. Importantly, most dogs with cardiac disease remain in this stage despite improvement of their clinical signs with standard medical and dietary therapy for CHF.


• Stage D: Patients have clinical signs of CHF that are refractory to standard treatments.


    Examples: In human patients this stage includes those receiving standard dosages of diuretics, angiotensin-converting enzyme (ACE) inhibitors, β-blockers, and digoxin; in veterinary medicine, “standard therapy” for canine CHF (as discussed in detail later) includes usual dosages of furosemide, spironolactone, an ACE inhibitor, and pimobendan.


This staging emphasizes the progressive structural abnormalities that underlie the pathogenesis of HF. The system is meant to encourage a program of management and education that supports early detection and screening for heart disease and provides a loosely defined “stepped” plan of treatment intensification that may be applied as heart disease progresses. This staging system further departs from the NYHA and ISACHC functional classifications in that a patient can still progress suddenly from stage B to stage D but the entire path cannot be traveled in reverse.


This modified ACC/AHA staging system is more analogous to the standard clinical classification of cancer; that is, the screening and identification of patients that are known to be at risk of disease (stage A); the identification and treatment of patients with in situ disease (stage B); and the identification and treatment of patients with established (stage C) or widespread (stage D) disease. The main limitation of the ACC/AHA system is the categorization of dogs in which CHF first manifests as an acute condition requiring aggressive short-term treatment that may include hospital management and intravenous or other nonstandard therapies; such a patient would be classified as stage D, but the patient’s condition actually may be stabilized back to stage C.



Management of Heart Failure in Dogs


Considering what we know regarding the origin, pathogenesis, progression, and response to therapy of the common acquired heart diseases of dogs (valvular heart disease and DCM), a practical therapeutic framework for managing HF in dogs should include diagnostic, treatment, and educational plans specific for each stage of heart disease and HF. Management plans should consider the natural history of the disease and carefully weigh what is known regarding the potential benefits and risks of each medication, and their combination, when used in a specific clinical setting. Using the ABCD classification just reviewed, a framework can be advanced for treatment of canine heart disease. Specific recommendations are offered in the following sections, with chronic MR and DCM used to illustrate the key issues. More details about cardiovascular drugs, including a table of common dosages, are provided in Chapter 175 and in the Appendix. The balance of the chapter offers specific management approaches to canine HF. Further details about degenerative valvular disease and canine cardiomyopathies can be found in other chapters in this section of the book.



Stage A: Dogs at Risk of Heart Disease


Stage A classification indicates that the dog is at risk of heart disease but currently has no clinical signs. Cavalier King Charles spaniels, dachshunds, and other small breeds at increased risk of development of chronic valvular heart disease should be screened by thorough cardiac auscultation. In otherwise healthy animals, the absence of a systolic click or the typical murmur of mitral valve regurgitation (a systolic murmur heard best over the left cardiac apex) adequately rules out significant degenerative valvular disease. Repeated annual screenings are indicated. If results of a screening examination are positive for valvular disease, then the classification is stage B. It should be emphasized that auscultation is an appropriate screening examination for degenerative valvular heart disease. However, if the clinician is interested in screening for preclinical DCM or arrhythmogenic right ventricular cardiomyopathy, different examinations (e.g., echocardiography or Holter ECG monitoring) are required.



Stage B: Asymptomatic Canine Heart Disease


Stage B is a “prefailure” state which indicates that cardiac disease is present in an otherwise asymptomatic dog. A typical case example is a mature small-breed dog in which a holosystolic murmur of MR is auscultated over the left apex. In this case the heart disease almost certainly is degenerative (myxomatous) valvular disease (i.e., endocardiosis). The workup should start with acquisition of high-quality lateral and dorsoventral (or ventrodorsal) thoracic radiographs. Objective quantitation of heart size using a vertebral heart size is useful at this stage because most dogs that develop clinical signs of CHF in the future will demonstrate a marked increase in heart size. In contrast, dogs coughing from primary airway or lung disease often exhibit little change in cardiac size compared with the previous examination. This approach not only provides a baseline for assessing progressive heart disease but also improves future differentiation of cardiac causes from primary respiratory causes of cough or dyspnea. Radiographs are especially helpful when an effort is made to obtain serial studies with similar positioning and exposure technique.


Depending on availability and client acceptance, a two-dimensional echocardiogram, optimally with Doppler studies, should be obtained to confirm the presence and severity of the valvular disease (presumably) responsible for the murmur. Echocardiography also is indicated in dogs younger than 6 years of age to rule out the possibility of congenital heart disease. Older dogs should be screened for systemic hypertension that might be caused by chronic kidney disease or Cushing’s disease because high BP can worsen the severity of MR. Again, other clinical scenarios would suggest different diagnostic tests, especially for assessment of an asymptomatic dog at high risk of cardiomyopathy. In these patients, serial echocardiography and ECG have higher priorities in the cardiac workup.




Stage B2


If either radiography or echocardiography reveals obvious cardiomegaly, the patient would be classified as having stage B2 disease. Treatment of dogs in this stage certainly is controversial, and therapeutic recommendations are different depending on whether the heart disease is chronic MR from valvular degeneration or preclinical DCM. Clients should be educated regarding the presence of significant heart disease and different treatment options discussed within the context of available evidence on prevention of CHF, quality of life, and long-term prognosis. Additionally, the cost of therapy and monitoring should be addressed. There are a number of therapeutic possibilities for dogs with stage B2 cardiac disease, and these are now considered.


ACE inhibitors such as enalapril and benazepril are controversial therapies at this stage in dogs with degenerative valvular disease. Two randomized, prospective, blinded clinical trials have yielded results considered negative and inconclusive. One study did show a possible benefit equivalent to an approximately 3-month extension of time before the onset of HF during a 3-year treatment period. Therefore the authors do not recommend an ACE inhibitor for dogs with MR and only mild cardiomegaly. The authors do start ACE inhibitor treatment in the following situations: (1) when moderate to severe cardiomegaly is present based on vertebral heart size obtained via echocardiography or radiography; (2) when a significant increment in cardiac size has been observed compared with the previous examination (e.g., an increase in vertebral heart size of >0.5); or (3) when there is definitive evidence of systemic hypertension. This recommendation would be tempered in those countries in which low-cost generic ACE inhibitors cannot be prescribed to dogs because the cost : benefit ratio might be quite high in these locations.


In dogs with clearly documented preclinical DCM, the authors recommend a full dosage of enalapril (0.5 mg/kg q12h PO), benazepril, or other ACE inhibitor as cardioprotection based on the results of one open-label prospective study as well as experimental evidence of cardiac muscle protection conferred by this drug class. Similarly, the authors consider larger-breed dogs (>20 kg) with chronic MR to be at risk of progressive left ventricular myocardial dysfunction and treat these patients the same way those with DCM are treated; that is, an ACE inhibitor is prescribed for these patients when there is evidence of cardiac remodeling or impaired left ventricular systolic function.


β-Adrenergic blockers such as atenolol, bisoprolol, metoprolol, or carvedilol are even more controversial for treatment of stage B heart disease. Recently a multicenter prospective clinical trial of bisoprolol was stopped due to apparent lack of efficacy in delaying the onset of clinical HF. Accordingly, the authors do not recommend use of a β-blocker in small-breed dogs with stage B MR. Some evidence from studies of experimentally induced mitral valve disease in dogs suggests a potential cardioprotective benefit in larger-breed dogs (>20 kg) with MR. In the setting of significant left ventricular remodeling or impaired left ventricular systolic function in a large-breed dog with MR a β-blocker (carvedilol, metoprolol, or atenolol) can be considered, but such therapy is empiric. A similar approach is taken in dogs with preclinical (occult) DCM. Owing to the negative inotropic effects of this class of drugs, the clinician should appreciate the risk of precipitating CHF in dogs with impaired left ventricular systolic function.


Whether or not to use inotropic drugs still is unresolved. Digoxin is not recommended by the authors or by the ACVIM consensus panel at this stage of disease based on a lack of any clinical trial evidence. Similarly, pimobendan is not recommended for this stage of disease in smaller-breed dogs with MR. A clinical trial (Evaluating Pimobendan In Cardiomegaly [EPIC]) currently is under way in dogs with advanced stage B2 MR (with an end point of prevention of CHF), but results are not likely until after 2014. The use of pimobendan in preclinical DCM also is controversial, but a recent multicenter study of Doberman pinschers with preclinical DCM (Pimobendan Randomised Occult DCM Trial to Evaluate Clinical Symptoms and Time to Heart Failure [PROTECT]; Summerfield et al, 2012) did demonstrate a significant benefit for the primary end points of delaying the onset of CHF and all-cause mortality. Accordingly, in Doberman pinschers with well-defined DCM (including left ventricular dilatation) use of pimobendan can be justified. Whether this approach can be generalized to other breeds with preclinical DCM, however, cannot be determined from this study. Until there are further data for other breeds with preclinical DCM, the routine use of pimobendan to treat a lower than normal ejection fraction in a dog with no clinical signs cannot be advocated; accordingly, the authors suggest that a cardiologist be consulted in these cases.


Spironolactone is not recommended by the authors for stage B2 disease in dogs with MR until further studies are conducted. Because there are theoretical advantages to treatment with aldosterone receptor antagonists in preclinical stage B2 cardiomyopathy, some cardiologists prescribe spironolactone empirically, especially where it is available in a generic formulation.


Nutraceuticals have been discussed frequently for the early treatment of heart disease in dogs; however, there are no trial data to recommend taurine, l-carnitine, coenzyme Q10, omega-3 fatty acid–containing fish oils, pomegranate extracts, hawthorn berry, or other holistic therapies except in very specific conditions of known dietary or metabolic deficiencies. None of these supplements is recommended by the authors for this stage of valvular heart disease. In cases of preclinical DCM the diet and the breed should be considered carefully because dietary or metabolic deficiencies of taurine and of l-carnitine have been reported on occasion. In addition, some special diets (vegan diets, exclusively lamb and rice diets) have been reported to be deficient in these micronutrients.


Sodium (salt)–restricted diets could be of potential benefit because there is evidence of abnormal sodium handling in animals with experimental valvular insufficiency before the onset of CHF. However, from a practical standpoint, sodium restriction is unlikely to be important at this stage of disease unless extremely high-sodium meals or treats are consumed by a dog on the verge of developing CHF. Some sodium-restricted diets (especially the renal diets) are relatively low in protein, and these may not be helpful to the cardiac patient. Many senior diets are controlled in sodium and include appropriate protein content for cardiac disease. See Chapter 168 for more details.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Management of Heart Failure in Dogs

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