Chapter 147 Heart Failure in Dogs
Heart failure (HF) is a state wherein the cardiac output is inadequate to meet the perfusion needs of the metabolizing tissues and exercise capacity is limited. The causes of HF in dogs are diverse, but there are stereotypical cardiovascular and systemic responses to impaired cardiac function, regardless of cause. This chapter provides a brief overview of HF; considers the causes and diagnoses of HF in dogs; and reviews treatment plans for management of the cardiac failure patient. The clinical pharmacology and pathophysiologic rationale for drugs used in treatment of HF are detailed in Chapter 146. Management of HF in cats is discussed in the chapter “Cardiomyopathy” (Chapter 150).
Overview
• HF is triggered by a cardiac lesion (or injury) that leads to systolic or diastolic dysfunction of the heart. Decreased cardiac output and blood pressure (often called “arterial underfilling”) are pivotal events that initiate the syndrome of HF.
• The decrease in blood pressure is countered by adaptations of the neuroendocrine system, kidney, heart muscle, and blood vessels.
• There is increased activity of vasoconstrictor and sodium-retaining control systems; attenuation of vasodilator and natriuretic systems; activation of fetal-gene programs within the heart; and increased activity of tissue mediators that lead to myocardial and vascular hypertrophy, fibrosis, and inflammation.
• The well-compensated cardiac patient often maintains basal (resting) cardiac output and blood pressure within the normal range. This is achieved through vasoconstriction, mild volume expansion, and redistribution of blood flow.
• Vasoconstriction is a prominent feature of HF and is mediated by sympathetic nervous system activation, the renin-angiotensin system, release of arginine vasopressin, and local endothelial mediators such as endothelin. These systems represent therapeutic targets for both current and for future drug developments.
• The excess sodium and water retention characteristic of the syndrome of congestive heart failure (CHF) is mediated by sympathetic stimulation that alters renal blood flow, the release of aldosterone and vasopressin, and inhibition of natriuretic hormones that are released from the stretched heart. The need for diuretics and dietary sodium restriction in CHF stems from activation of these compensatory responses.
• The heart itself changes in structure and function in a process called cardiac remodeling. As heart disease progresses there is increasing dependence on myocardial hypertrophy, cardiac dilatation, and heart rate to maintain cardiac output. At the same time, structural alterations in the intercellular matrix of collagen and connective tissue impair the filling and pumping functions of the myocardium. Key mediators of cardiac injury include norepinephrine, angiotensin II, aldosterone, and pro-inflammatory cytokines. The increased use of “cardioprotective” drugs in HF are aimed at blunting these mediators and the tissue damage caused by them.
• Despite the effectiveness of these combined compensations for maintaining arterial blood pressure, these systems become increasingly maladaptive. This concept is central to the progression and the treatment of HF.
• Compensatory mechanisms activated in advanced heart disease are so effective that clinical signs of cardiac failure may be evident only with exercise when pulmonary venous pressure increases and perfusion of skeletal muscles becomes limited.
• Decreases in cardiac output, systemic arterial blood pressure (ABP), and tissue perfusion develop, accompanied by increases in systemic and pulmonary vascular resistances.
• Inadequate tissue perfusion contributes to exercise intolerance, azotemia, and metabolic disturbances such metabolic acidosis.
• Elevations in pulmonary arterial, venous, and capillary hydrostatic pressures lead to clinical signs of CHF.
• While hemodynamics may explain many clinical signs, morbidity and mortality of HF are related strongly to the tissue effects of accentuated neurohormonal and cytokine activities that develop in response to the failing heart.
Etiology
Classification
• The morphologic or anatomic diagnosis refers to the lesions one might observe during gross or microscopic examination of the heart or blood vessels (Table 147-1). It is also helpful to classify CV diseases relative to the anatomic components of the system affected; this is often included into the anatomic diagnosis as follows: pericardial diseases; myocardial diseases; valvular and endocardial diseases; disorders of the impulse forming and conduction system (arrhythmias); and vascular diseases.
• The etiologic diagnosis indicates the putative cause of cardiovascular disease and includes genetic disorders and errors of metabolism (Table 147-2). A sub-classification of the etiologic diagnosis includes general designations of “congenital” heart disease and “acquired” heart disease.
• The physiologic diagnosis represents the disruption in cardiovascular function that results from cardiovascular disease, including the clinical signs observed in the patient. This diagnosis can be general or relatively specific. For example, contractility failure, hemodynamic overloads, diastolic failure, and arrhythmia are considered general pathophysiologic mechanisms for reduced cardiac output and heart failure. Examples of more specific cardiovascular diagnoses include syncope, valvular regurgitation, left to right shunt, and cardiac murmur (Table 147-3).
Table 147-1 OVERVIEW OF MORPHOLOGIC/ANATOMIC DIAGNOSES
Developmental disorder or malformation
Vascular change: congestion, edema, hemorrhage, thrombosis, infarction
Apoptosis (programmed cell death)
Disruptive defects such as trauma
Table 147-2 OVERVIEW OF ETIOLOGIC DIAGNOSES
D = developmental disorders; degenerative lesions
A = anomalies, autonomic dysfunction, anemia
N = neoplasia or nutritional disorder
I = infectious, inflammatory, ischemic, immune, iatrogenic and idiopathic diseases
Causes
• Mitral and tricuspid valvular endocardiosis, which is characterized by progressive and chronic atrioventricular valve degeneration often with valve prolapse and ruptured mitral valve chordae tendineae. Atrial arrhythmias, left mainstem bronchial compression, CHF, left atrial rupture, and systemic hypertension may complicate the picture.
• Dilated cardiomyopathy, which is a primary myocardial disorder of progressive contractility failure leading to heart failure. Often associated with cardiac arrhythmias such as atrial fibrillation and ventricular tachycardia; the condition is “idiopathic” but certainly genetically predisposed in many dogs. Sudden death is common.
• Pericardial effusion causing cardiac tamponade (impaired filling of the heart from compression) is under-recognized. The main causes in dogs are idiopathic pericardial hemorrhage in young dogs and cardiac tumors (e.g., hemangiosarcoma, chemodectoma, and mesothelioma) in older dogs.
• Systemic hypertension is most often secondary to chronic glomerular or renal tubular disease, Cushing’s disease, or uncommon tumors such as pheochromocytoma. Essential or idiopathic disease is also recognized. Target organs in hypertension include the brain, eyes, heart, and kidneys.
• Pulmonary hypertension with right-sided heart failure is most often due to the preventable disorder dirofilariasis, but also can be secondary to chronic left heart failure or severe bronchopulmonary disease; some cases are idiopathic.
• Arrhythmias can be recognized that are unassociated with overt structural heart disease such as cardiomyopathy. These primary disorders of electrical impulse formation or impulse conduction include sinus node dysfunction (sick sinus syndrome), lone atrial fibrillation, atrioventricular blocks, and arrhythmogenic cardiomyopathy, such as arrhythmogenic right ventricular cardiomyopathy in the Boxer or English bulldog, or sustained reentrant supraventricular tachyarrhythmias in Labrador retrievers.
• Bacterial endocarditis (infection of the cardiac valves) is relatively uncommon in dogs but may lead to a variable clinical syndrome that includes bacteremia, systemic inflammation (fever, leukocytosis), constitutional illness (depression, anorexia, shivering), metastatic infection (brain, kidneys, bone), immunologic phenomena (polyarthritis, glomerulonephritis), thromboembolic disease, and cardiac injury (valvular regurgitation, arrhythmias, CHF).
• Malformations or congenital heart diseases in dogs represent about 5% to 10% of patients seen in cardiology referral practices. Congenital heart defects are recognized in most cases by detection of a murmur during the puppy vaccination sequence. Malformations are definitively diagnosed by echocardiography with Doppler studies. Optimal management should involve a clinician experienced in congenital heart disease.
The most important of the canine congenital heart defects include the following:
• Aortic stenosis (generally subvalvular AS)—A subvalvular narrowing of the left ventricular outflow tract, leading to pressure overload of the left ventricle. Outcomes in severe disease include exercise intolerance, syncope, sudden death, and congestive heart failure. Dogs are at higher risk for bacterial endocarditis.
• Patent ductus arteriosus—The persistence of the fetal ductus arteriosus leading to a left-to-right shunt and volume overload of the left ventricle. Untreated cases are likely to die from left-sided CHF.
• Pulmonic stenosis—A subvalvular, valvular, or supravalvular narrowing of the right ventricular outflow tract, leading to pressure overload of the right ventricle. Outcomes in severe disease include exercise intolerance, syncope, sudden death, right-to-left shunting across a septal defect or foramen ovale, and right-sided congestive heart failure.
• Mitral valve malformation—Dysplasia of the mitral valve that can lead to progressive left-sided volume overload, atrial fibrillation, or CHF. Rarely the lesion causes mitral stenosis.
• Tricuspid valve malformation—Dysplasia of the tricuspid valve that can lead to progressive right-sided volume overload, atrial fibrillation, or right-sided CHF. Rarely, the lesion causes tricuspid stenosis.
• Ventricular septal defect (VSD)—A persistent opening between the ventricular cavities; clinical significance depends on the size of the defect.
• Tetralogy of Fallot—A large VSD, pulmonary stenosis, right ventricular hypertrophy, and dextropositioned aorta. A cause of cyanosis from right-to-left shunting but rarely leads to CHF.
DIAGNOSIS
History and Clinical Signs
• The history of clinical signs in heart disease is variable. Many patients have no overt clinical signs until CHF develops. No historical sign is specific for HF.
• Signs of low cardiac output, such as exercise intolerance or syncope may be observed, but are subtle and may be overlooked by dog owners.
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