Heart Failure in Dogs

Table 147-4 COMMON CANINE DISEASES

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Chapter 147 Heart Failure in Dogs

John D. Bonagura, Bruce Keene

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

Heart failure is a not a specific disease but a pathophysiologic disorder. Some of the key abnormalities of this condition are summarized below, and the pathophysiologic rationale for using particular cardiovascular drugs is summarized in Chapter 146. The reader is directed to other textbooks for a detailed review of pathophysiology of HF.

• 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.
• With worsening cardiac function hemodynamic abnormalities become prominent.
• 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.
• Chronic therapy of CHF is aimed at modulating and countering these responses to minimize clinical signs of CHF, protect tissues, and prolong life.

Etiology

Next in this chapter we will consider the key causes of heart disease in dogs, as well as an overview of cardiac disease classification and applicable diagnostic studies. The following are salient points regarding cardiac diagnosis and the clinical workup.

Classification

Identifying the predominant form and cause of heart disease and classifying the pathophysiologic mechanism of cardiac failure allows the clinician to direct appropriate therapy and render a more accurate prognosis. Cardiac diagnoses can be classified in a number of ways.

• 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

Inflammation

Degeneration

Necrosis

Apoptosis (programmed cell death)

Hypertrophy

Neoplasia

Disruptive defects such as trauma

These lesions may be encountered in the pericardium, myocardium, endocardium-valves, conduction system, or blood vessels of the heart or circulation.

Table 147-2 OVERVIEW OF ETIOLOGIC DIAGNOSES

D = developmental disorders; degenerative lesions

A = anomalies, autonomic dysfunction, anemia

M = metabolic diseases (endocrine diseases, electrolyte disturbances, renal failure), mechanical problems (such as a foreign body)

N = neoplasia or nutritional disorder

I = infectious, inflammatory, ischemic, immune, iatrogenic and idiopathic diseases

T = tumor, trauma or toxin

Table 147-3 OVERVIEW AND DEFINITION OF PHYSIOLOGIC CV DIAGNOSES

Arrhythmia (dysrhythmia)—disorder of electrical impulse formation or conduction leading to an abnormal heart rate or rhythm.

Bradyarrhythmia—a cardiac arrhythmia characterized by a slow heart rate as with sinus bradycardia, sinus arrest, atrial standstill, or atrioventricular block.

Cardiac murmur: functional—a prolonged audible vibration associated with blood flow in the heart or great vessels but unrelated to structural heart disease (also termed physiologic or innocent murmur); functional murmurs are often caused by anemia, fever, thyrotoxicosis, elevated sympathetic tone, or protracted bradycardia.

Cardiac murmur: organic—audible vibration associated with abnormal blood flow in the heart or great vessels associated with structure disease; these murmurs typically indicate pathology affecting the heart valves or a congenital shunt.

Congestive heart failure—an advanced pathophysiologic state of heart failure characterized by renal sodium retention, elevated venous pressures, and fluid accumulation in the lung, subcutaneous tissues, or body cavities.

Contractility failure—a general mechanism of ventricular dysfunction; see myocardial failure.

Diastolic heart failure (diastolic dysfunction)—impairment of ventricular diastolic filling or distensibility as with concentric hypertrophy of the ventricle or pericardial disease; the ventricle must be filled by higher than normal filling (venous and atrial) pressures.

Heart failure—a pathophysiologic state caused by systolic or diastolic failure of the heart and characterized by neurohormonal activation and inadequate cardiac output relative to exercise and tissue perfusion demands.

Hemodynamic overload—a condition characterized by increased demand on the ventricle to pump a greater stroke volume or a higher pressure than normal; typically these are subdivided into volume overloads and pressure overloads (see the following).

Hypertension—elevated systemic arterial blood pressure; in dogs systolic values exceeding 160 mm Hg are suspicious and those >180 mm Hg are considered elevated

Hypotension—reduced systemic arterial blood pressure; when systolic ABP is <90 mm Hg, clinically significant hypotension is possible.

Myocardial failure—loss of ventricular myocardial contractility leading to systolic dysfunction as with dilated cardiomyopathy or chronic volume or pressure overload.

Pressure overload—condition wherein the ventricular systolic (pumping) pressure must be higher than normal to eject the stroke volume; usually associated with hypertension or obstruction to ejection as with aortic stenosis.

Pulmonary hypertension—elevated pulmonary arterial blood pressure generally caused by left-sided heart failure, pulmonary vascular or parenchymal disease, or marked increase in pulmonary blood flow (without concomitant decline in pulmonary vascular resistance).

Shock—an acute, life-threatening disorder characterized by diminished tissue perfusion, impaired oxygen delivery, altered metabolism, and tissue injury; various causes of shock include cardiogenic shock (from profound heart failure), hypovolemic shock (from fluid loss or hemorrhage), and distributive shock (excessive vasodilation secondary to sepsis, anaphylaxis, or spinal injury).

Shunting: left-to-right—abnormal flow of blood from the systemic to the pulmonary circulation as with ventricular septal defect or patent ductus arteriosus.

Shunting: right-to-right—abnormal flow of blood from the pulmonary to the systemic circulation as with tetralogy of Fallot or PDA with elevated pulmonary vascular resistance.

Sudden cardiac death—cardiac arrest due to asystole or ventricular fibrillation.

Syncope—sudden loss of consciousness and postural tone caused by reduced cardiac output, excessive vasodilation, or both.

Systolic heart failure (systolic dysfunction)—impairment of ventricular systolic pumping that limits stroke volume and cardiac output; typical of dilated cardiomyopathy, severe valvular heart diseases, and myocardial failure due to chronic volume or pressure overloads.

Tachyarrhythmia—a cardiac arrhythmia generally characterized by a fast heart rate, as with sinus tachycardia, atrial tachycardia/flutter/fibrillation, supraventricular re-entrant tachycardia, and ventricular tachycardia.

Valvular regurgitation—incompetency or insufficiency of the valve permitting backflow of blood during systole (mitral, tricuspid valves) or diastole (aortic, pulmonic valves).

Valvular stenosis—narrowing and obstruction to flow across a valve (or adjacent tissue) during systole (aortic, pulmonic valves) or diastole (mitral, tricuspid valves).

Volume overload—condition wherein the ventricular systolic (pumping) volume is higher than normal; usually associated with a left-to-right shunt, a regurgitant heart valve, or chronic bradycardia.

Causes

The most important causes of canine heart disease involve a limited number of acquired disorders and a handful of important congenital heart defects. These conditions, as well as usual diagnostic findings, are summarized in Table 147-4 and in other chapters across this section. The most important acquired cardiac disorders responsible for HF in dogs are:

• 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.
• The peritoneopericardial diaphragmatic hernia is an uncommon pericardial defect in puppies.

Key Point

The most important reasons for CHF in dogs are degenerative valvular disease, dilated cardiomyopathy, pericardial diseases, and heartworm heart disease. These conditions can be complicated by systemic hypertension, pulmonary hypertension, and arrhythmias such as atrial fibrillation or ventricular tachycardia.

DIAGNOSIS

History and Clinical Signs

The diagnosis of heart disease involves a systematic examination that begins with consideration of species, age, breed, and sex.

There are obvious risks for cardiovascular disease relative to these factors. Young animals will be suspected of congenital heart disease; mature animals of acquired, degenerative, and neoplastic diseases. There are dozens of genetic breed predispositions to cardiovascular diseases. These tend to be tabulated in standard reference textbooks and are described in other chapters within this volume.

• 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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  4. Otitis Media and Otitis Interna

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Heart Failure in Dogs

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