Pathophysiology and Therapy of Heart Failure

Chapter 15 Pathophysiology and Therapy of Heart Failure



Keith N. Strickland



INTRODUCTION



Definitions


• Heart disease is any structural (microscopic or macroscopic) abnormality of the heart that may or may not result in heart failure.

• Heart failure is the pathophysiologic state that occurs when the heart is unable to function at a level commensurate with the requirements of the metabolizing tissues or can only do so at elevated filling pressures.

• Preload is the degree of muscle fiber stretch just prior to contraction. This correlates to the volume of blood within the ventricle just prior to contraction (cardiac preload, venous return)

• Afterload is the load against which a muscle exerts its contractile force. Cardiac afterload refers to the blood pressure the ventricle must overcome in order to eject blood.


Overview


• The function of the cardiovascular system is to maintain normal arterial blood pressure and flow (cardiac output) while maintaining normal venous and capillary pressures during rest and exercise. This function is necessary to provide adequate blood flow for oxygen and nutrient delivery to vital tissues (such as the brain, the heart, and the kidneys) as well as for the removal of metabolic waste products from these tissues.

• Heart failure results in a reduction in the previously described functions of the cardiovascular system. If blood pressure and cardiac output are not maintained, or if venous and capillary pressures are markedly increased, then death can occur within hours to weeks (depending on the severity of the abnormality). Heart failure can be associated with systolic or diastolic dysfunction.


HEART FAILURE



Pathophysiology


Our understanding of the progression from asymptomatic heart disease to symptomatic heart failure has changed from the traditional concept of biomechanical dysfunction to a concept emphasizing neuroendocrine dysfunction secondary to chronic biomechanical dysfunction.


• The current model embodies the idea that some cardiac damage or dysfunction results in chronically altered hemodynamics that lead to activation of neurohumoral mechanisms designed to promote cardiac function and tissue perfusion. Chronic activation of these compensatory mechanisms leads to progressive cardiovascular dysfunction culminating in life-threatening congestive heart failure (CHF) low-output failure or sudden death.

• Cardiac dysfunction that leads to the clinical syndrome of heart failure can be subdivided into systolic and diastolic dysfunction. Systolic dysfunction occurs when the ability of the heart to pump blood in a forward direction is impaired. Components of systolic function include myocardial contractility, valvular competence, preload, afterload, and heart rate.


Phases of Heart Failure


• Phase 1: Cardiac Injury

• Phase 2: Compensatory mechanisms

• Phase 3: Cardiac failure with clinical signs of cardiac dysfunction


Key Points


• CHF occurs when cardiac diastolic filling pressures result in elevated venous and capillary hydrostatic pressures with subsequent edema formation. Therapy for CHF is directed toward reducing cardiac diastolic filling pressures so that edema fluid can be mobilized.

• Low-output failure occurs when cardiac function does not produce adequate cardiac output to maintain blood pressure and tissue perfusion.


Myocardial Failure


• Impaired contractility may occur with primary heart disease (idiopathic dilated cardiomyopathy [DCM]) or secondary heart disease.
• Chronic heart disease of varying causes may mimic primary cardiomyopathy. Systolic failure following chronic overload may be secondary to chronic valvular insufficiency and left-to-right shunting lesions, such as patent ductus arteriosus or ventricular septal defect.

• Nutritional deficiencies, such as taurine deficiency, have been recognized as a cause of myocardial failure in the cat, and have been associated with DCM in certain breeds of dogs (American Cocker Spaniels, Golden Retrievers, Dalmatians, Boxers, Welsh Corgis, Newfoundlands). Myocardial deficiency of L-carnitine has been reported in Boxers and Doberman Pinschers.

• Metabolic cardiomyopathies include feline hyperthyroidism, canine hypothyroidism, and chronic uremia.

• Toxic cardiomyopathy: doxorubicin-induced DCM

• Infiltrative cardiomyopathy: neoplastic (e.g., lymphosarcoma), amyloidosis


Valvular Insufficiency


• Valvular insufficiency is one of the most common causes of systolic dysfunction encountered in veterinary medicine. Incompetency of an atrioventricular valve (endocardiosis, endocarditis, congenital malformation) allows retrograde ejection (regurgitation) of blood into the corresponding atrium during systole, reducing forward flow and decreasing cardiac output. Severe regurgitation also increases atrial and ventricular filling pressures, with the risk of CHF.

• Valvular insufficiency can be primary (myxomatous degeneration) or secondary (associated with other conditions that alter valvular function such as ventricular hypertrophy, ischemia, etc.).


Excessive Afterload


• Normally, an abrupt increase in afterload causes a positive inotropic effect (Anrep effect). However, when the hemodynamic overload is severe or chronic, myocardial contractility may be depressed. Chronically increased afterload leads to a reduction in the rate of ejection and the amount of blood ejected at any given preload, and increased myocardial oxygen consumption with the risk of ischemic damage.

• Pulmonary/systemic hypertension or ventricular outflow obstructions (aortic or pulmonic stenosis) are examples of clinically significant causes of increased afterload.


Inadequate Preload


• In cases in which inadequate preload is the primary hemodynamic abnormality (such as cardiac tamponade), the reduction in preload decreases stroke volume and cardiac output. Normally, the reduced preload may be compensated for by systemic mechanisms that result in increased venous return and ventricular end-diastolic volume; however, significant pericardial effusion obstructs venous inflow and limits the end-diastolic volume, precluding the circulatory system from fully compensating for the reduced cardiac output.


Diastolic Dysfunction


• Diastolic dysfunction may result in heart failure. Indeed, most cases of overt heart failure have some degree of diastolic dysfunction. Adequate ventricular filling is dependent on several factors:
• Ventricular relaxation

• Ventricular elasticity (change in muscle length for a change in force)

• Ventricular compliance (change in ventricular volume for a given change in pressure).

• Ventricular relaxation may be decreased in several diseases or disorders (e.g., idiopathic hypertrophic cardiomyopathy, ischemia).

• Ventricular compliance may be reduced when elevated filling pressure are required. This change can be associated with:
• Volume overloading

• An increase in muscle mass or wall thickness, as with myocardial concentric hypertrophy

• A decrease in ventricular distensibility (usually associated with extrinsic compression of the heart)

• Diseases that result in myocardial fibrosis (e.g., restrictive cardiomyopathy, ischemic heart disease) also cause a decrease in ventricular compliance.

• Diastolic dysfunction may increase ventricular end-diastolic pressure, which is then transmitted to the corresponding atrium and the venous system. Elevation in venous and capillary pressures may result in interstitial and alveolar pulmonary edema or ascites through hydrostatic factors.


COMPENSATORY MECHANISMS IN CHRONIC HEART FAILURE



Frank-Starling Mechanism


• The Frank-Starling mechanism is an adaptive mechanism by which an increase in preload enhances cardiac performance. Venous return determines the preload of the ventricle. Physiologic increases in ventricular end-diastolic volume are associated with increases in myocardial fiber length. This allows the sarcomere to function near the upper limit of its maximal length (optimal length), where it is able to generate the maximal amount of force during contraction.

• To better understand the role of the Frank-Starling mechanism, consider the hemodynamic changes associated with exercise. Cardiac output is increased during exercise through the following mechanisms: (1) increased heart rate and contractility through increased sympathetic nervous system (SNS) activity, (2) increased venous return (preload) with a more vigorous contraction (Frank-Starling mechanism), and (3) reduced afterload associated with reduced peripheral vascular resistance. In this way cardiac performance is enhanced during exercise in the absence of heart failure. In the presence of heart failure, cardiac output and ventricular performance may be maintained within normal limits at rest only because the ventricular end-diastolic fiber length and the preload are elevated (ventricular performance is maintained through the Frank-Starling mechanism).

• In the failing heart, these factors that normally help increase cardiac output during exercise are chronically active and cause increased preload and ventricular end-diastolic pressures (especially in a noncompliant, dilated ventricle), with the threat of edema formation. Exercise drives the ventricle along the flat portion of the ventricular performance curve, where increases in ventricular volume and diastolic pressure do not increase ventricular performance.


Renin-Angiotension-Aldosterone System


• The renin-angiotensin-aldosterone system (RAAS) is a complex neurohormonal compensatory system that functions to maintain relatively normal blood pressure and tissue perfusion when cardiac output is reduced. Reduced renal perfusion detected by renal baroreceptors results in release of renin (Figure 15-1). Other factors causing release of renin include decreased sodium delivery to the macula densa, and SNS stimulation of beta-1 adrenoceptors in the juxtaglomerular apparatus of the kidney. Renin initiates a cascade resulting in the formation of angiotensin II, a potent vasoconstrictor. Angiotensin II also causes activation of the SNS, increases synthesis and release of aldosterone from the zona glomerulosa of the adrenal cortex and release of antidiuretic hormone.

• Aldosterone causes sodium retention in the distal renal tubules to promote fluid retention. Aldosterone also promotes fibrosis of the myocardium and vascular smooth muscle.

• The RAAS can be subdivided into:
• Systemic or renal RAAS

• Tissue RAAS

• The tissue RAAS (brain, vascular, and myocardial tissues) can generate angiotensin II independently of the circulating RAAS.

• Angiotensin II stimulates the release of growth factors that promote remodeling of the vessels and myocardium. Vascular remodeling (smooth muscle cell growth and hyperplasia, hypertrophy, and apoptosis; cytokine activation; myocyte and vascular wall fibrosis) results in decreased vascular responsiveness to alterations in blood flow, decreased vascular compliance, and increased afterload. Angiotensin II also causes pathologic ventricular hypertrophy, exerts cytotoxic effects resulting in myocardial necrosis and loss of myocardial contractile mass with resultant cardiac dysfunction.


Sympathetic Nervous System Activation



Sympathetic Nervous System Activation


• The autonomic nervous system plays a crucial role in the compensation of heart failure. The activity of the SNS is increased in part by baroreflex-mediated parasympathetic withdrawal, as well as by activation by the RAAS. Early activation of the SNS helps to maintain cardiac output, blood pressure, and tissue perfusion by increasing venous return to the heart (vasoconstriction of the splanchnic vessels), vasoconstriction of other various vascular beds, and positive inotropic and chronotropic cardiac effects. Activation of the SNS early in heart failure is beneficial, but becomes maladaptive when chronically activated (Figure 15-2).

image

Figure 15-1 RAA cascade. Reduced renal perfusion is the primary stimulus for renin release, which leads to activation of the angiotensin-aldosterone system. RAAS activation results in sodium and water retention and peripheral vasoconstriction.


image

Figure 15-3 Drawings of the left heart from a dog with severe mitral regurgitation before and after administration of an afterload reducing agent. Note that forward flow (out the aorta) increases with afterload reduction because of the reduction in systemic vascular resistance. LV, Left ventricle; LA, left atrium.


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Figure 15-2 Effect of compensatory sympathetic system in response to a reduction in blood pressure. Decreased systemic blood pressure results in activation of the sympathetic nervous system and a cascade of consequences which are deleterious in the long term.



Sympathetic Desensitization:


• Chronic activation of the SNS is associated with elevated levels of plasma norepinephrine (NE), cardiac NE depletion, down-regulation and desensitization of beta-1 adrenergic receptors, and abnormal baroreflex function. Plasma NE levels appear to be increased because of a combination of increased release of NE from adrenergic nerve endings and reduced uptake of NE by adrenergic nerve endings. The depletion of myocardial NE (serum NE levels increase and myocardial levels decrease) probably represents the depletion of the neurotransmitter in adrenergic nerve endings.
• The down-regulation of beta-1 adrenergic receptors occurs relatively soon (24 to 72 hours) after the initial SNS activation, making it progressively more difficult for the SNS to counter impaired contractility.

• Chronic activation of the SNS also overloads the heart by increasing venous return (to a heart that is already volume-overloaded), by increasing myocardial oxygen consumption (by increasing heart rate and volume overloading of the heart) and by damaging the myocardium, creating a substrate for arrhythmogenesis.


Myocardial Hypertrophy


Myocardial hypertrophy occurs as a compensatory mechanism directed toward normalizing cardiac output, wall tension, and filling pressures. The hemodynamic load imposed on the heart (either volume or pressure overloading) determines the type of hypertrophy (eccentric vs. concentric). Chronic activation of the RAAS and the SNS produces pathologic changes (remodeling) within the ventricular myocardium, which contribute to cardiac dysfunction. The result can be myocardial failure with low-output signs or elevated filling pressures with the risk of CHF.


• Eccentric myocardial hypertrophy (or volume-overload hypertrophy) occurs with heart disease as a compensatory mechanism to allow the ventricle to pump a relatively normal amount of blood in spite of abnormal systolic function. Eccentric hypertrophy is characterized by chamber dilation, a response to the increase in blood volume and venous return associated with activation of the RAAS and SNS. More specifically, the increased venous return is secondary to sodium (aldosterone effect) and water (antidiuretic hormone/vasopressin effect) retention as well as to venoconstriction of the splanchnic vascular bed (RAAS and SNS effect). Chronic heart failure represents a nonosmotic (mediated by SNS and RAAS, instead of osmotic hypertonic) stimulus for antidiuretic hormone release from the hypothalamus. Antidiuretic hormone probably plays a limited role in the pathogenesis of CHF. However, chronic volume overload causes an increase in diastolic wall stress, and this leads to replication of sarcomeres in series, elongation of myocytes, and ventricular dilation.

• Concentric myocardial hypertrophy (or pressure-overload hypertrophy) is characterized by thickening of the ventricular walls in response to increased systolic wall stress, and occurs as a compensatory mechanism to normalize systolic wall tension. Increased systolic wall stress stimulates the replication of sarcomeres in parallel, increasing myocardium thickness and thereby normalizing systolic wall stress (via the La Place relationship, wall tension = pressure × radius/wall thickness). The increase in thickness of the ventricular wall compensates for the increased systolic wall stress in a pressure-overloaded ventricle. If the compensatory concentric hypertrophy is inadequate and the systolic wall stress is increased, then afterload-mismatch and decompensation occur. Interestingly, when significant eccentric hypertrophy occurs in a volume-overloaded ventricle, systolic wall tension is increased secondary to the increase in ventricular diameter. Therefore, both eccentric and some degree of concentric hypertrophy are present in severely volume-overloaded ventricles.

Key Points


In the syndrome of heart failure, changes in ventricular mass and geometry are a culmination of compensatory hypertrophy (in response to pressure or volume overload) and pathologic hypertrophy (in response to activation of the RAAS and SNS).


• These compensatory mechanisms require days to weeks to become fully activated. If the cardiac dysfunction is acute and severe, then the compensatory mechanisms do not have sufficient time to become fully activated (with the exception of the SNS, which is immediately activated).
• For example, most dogs with idiopathic DCM have insidious, progressive cardiac dysfunction that worsens over a period of years, therefore allowing the compensatory mechanisms to become fully activated. Although these dogs have compensated heart failure chronically, at some point they may acutely decompensate, mimicking an acute disease process.

• Conversely, a dog with a peracute disease syndrome (such as a very rapid supraventricular tachyarrhythmia like atrial fibrillation) may develop heart failure without activating compensatory mechanisms other than the SNS.


Additional Compensatory Mechanisms/Neuroendocrine Mechanisms


• Endothelins, a vasoactive family of peptides that are released from endothelial cells, play an important role in the regulation of vascular tone and blood pressure. Endothelin-1 is a strong, vasoconstrictive agent with inotropic and mitogenic actions; it is a strong stimulus for activation of the RAAS and SNS. Additionally, Endothelin-1 may play an important role in the pathogenesis of pulmonary hypertension.

• Natriuretic peptides are regulators of salt and water homeostasis and blood pressure control with potential value as diagnostic and prognostic markers in patients with CHF. Natriuretic peptide levels are elevated in many disease conditions resulting in expanded fluid volume (such as DCM and chronic valvular insufficiency in dogs, and cardiomyopathy in cats).

• Atrial, brain, and C-type natriuretic peptides have been identified (ANP, BNP, and CNP, respectively)

• BNP is primarily produced in the atria and is released in response to atrial stretch resulting in natriuresis, diuresis, and balanced vasodilation.

• Natriuretic peptides antagonize the RAAS and SNS, inhibit release of antidiuretic hormone, prevent myocardial fibrosis, and modulate cell growth and myocardial hypertrophy.

• Circulating natriuretic peptide levels may be used to differentiate between symptoms associated with cardiac disease and from symptoms associated with primary pulmonary disease. Lack of elevated BNP levels does not support a diagnosis of symptomatic heart failure.

• Inflammatory and immune mediators such as tumor necrosis factor alpha, interleukins (IL-1, IL-2, and IL-6), nuclear factor-kappa-B, and reactive oxygen species are thought to play a role in the progression of heart failure. The “cytokine hypothesis” suggests that heart failure progresses because cytokine pathways are activated in response to cardiac dysfunction and exert negative effects on the cardiovascular system.


Course of Events: Compensatory Mechanisms


• Reduced cardiac output leads to decreased tissue perfusion

• Activation of baroreceptors in kidney, carotid arteries, aorta, and heart results in SNS activation and parasympathetic nervous system withdrawal

• SNS activation (positive inotropic and chronotropic activity, vasoconstriction to increase venous return and maintain blood pressure, stimulation of antidiuretic hormone and renin)

• RAAS activation associated with the reduced renal perfusion, decreased sodium delivery to the macula densa, and SNS activation

• Renal sodium and water retention to increase blood volume and, therefore, venous return to the heart

• Myocardial hypertrophy (dilation of the affected atrium and ventricle) to maintain relatively normal cardiac output and systolic wall tension while preventing diastolic filling pressures from rising

• Stretch-induced release of atrial natriuretic factor serves to facilitate sodium excretion. The effects of this factor are quickly negated owing to degradation by neutral endopeptidases and the effects of overstimulation of the RAAS and SNS.

• Initially, these mechanisms allow the body to compensate for the decreased cardiac output by increasing blood volume and blood pressure. However, with chronicity, the compensatory mechanisms are maladaptive and facilitate progression of heart failure.

• Overstimulation of inflammatory/immune mediators (tumor necrosis factor–alpha, IL-1, IL-2, IL-6, reactive oxygen species) exert deleterious effects on the heart and circulation.

• The sustained effects of the SNS and RAAS continue to increase the workload of the heart by increasing blood volume and venous return to a heart that has maximized its ability to compensate by eccentric hypertrophy. Ventricular filling pressures begin to increase, with the threat of edema formation. The onset of edema formation is variable, depending on the severity and onset of ventricular dysfunction. Dogs with cardiomyopathy may have mild edema for days to weeks and only show minimal clinical signs, such as tachypnea and exercise intolerance.


TYPES OF HEART FAILURE



Myocardial Failure


• Myocardial failure is associated with decreases in contractility. It can be associated with:
• Primary myocardial disease (idiopathic DCM)

• Secondary myocardial diseases (chronic congenital and valvular heart disease, thyrotoxicosis, taurine deficiency, infectious/inflammatory and infiltrative diseases)

• Myocardial failure causes systolic dysfunction and activation of compensatory mechanisms which increase sodium and water retention to increase venous return to the heart. The ventricles must obtain a larger end-diastolic dimension to maintain a relatively normal total stroke volume (TSV). As the myocardial function deteriorates (as noted by a decrease in fractional shortening and a decrease in ejection fraction), the ventricles progressively enlarge so that the TSV is maintained, even though the percentage of blood being ejected is decreasing. Severe left ventricular dilation causes distortion and dilation of the mitral valve annulus, resulting in mitral regurgitation (MR) and further volume overloading of the left ventricle.

• Once the compensatory limits are reached, further increases in blood volume (associated with sodium and water retention) and venous return cause an increase in cardiac filling pressures, with threat of CHF development.


Volume Overload


• Volume overload is associated with two common causes of heart failure:
• Valvular insufficiency

• Shunts


Atrioventricular Valvular Insufficiency


• Atrioventricular valvular insufficiency can result from:
• Degenerative valvular disease

• Valvular endocarditis

• Congenital valvular dysplasia

• Chamber dilation

• Valvular insufficiency may result in systolic dysfunction and activation of compensatory mechanisms which maintain cardiac output and tissue perfusion by vasoconstriction and fluid retention. As with impaired contractility, valvular insufficiency forces the ventricle to achieve larger end-diastolic dimensions to compensate for the decrease in forward stroke volume. The difference between volume overloading secondary to impaired contractility (DCM) and valvular insufficiency (MR) is associated with the changes in TSV (end-diastolic volume minus end-systolic volume). In MR without myocardial failure, TSV is increased to compensate for the amount of blood leaking through the incompetent valve. The end-diastolic volume increases, but the end-systolic volume remains normal (evidence of normal contractility), thereby resulting in an increased TSV. With impaired contractility, TSV is normal or decreased (depending on the stage of the disease) because both end-diastolic and end-systolic volumes have increased. End-diastolic volumes increase to compensate for the increased end-systolic volumes, reflecting impaired contractility.

• Shunts such as patent ductus arteriosus, ventricular septal defect, and arteriovenous fistula are similar to valvular leaks in that the heart increases TSV to compensate for the reduction in forward flow.


Pressure Overload


• Lesions that cause increased intraventricular systolic pressures usually do not cause CHF because the heart is usually able to compensate for the increased intraventricular systolic pressures with concentric hypertrophy (La Place principle), and the ventricular systolic function remains relatively normal. Only when the obstruction to flow is severe (critical stenosis) or acute does pressure overload result in myocardial failure and heart failure. More commonly, CHF occurs when there is a concurrent valvular insufficiency (e.g., pulmonic stenosis with tricuspid regurgitation, subvalvular aortic stenosis with MR or aortic regurgitation, pulmonary hypertension with tricuspid regurgitation).

• Alternatively, sudden death may occur in dogs with severe (noncritical) congenital subvalvular aortic stenosis or possibly valvular pulmonic stenosis. When the ventricle is severely hypertrophied, coronary perfusion is impaired, and regions of the myocardium (especially the papillary muscles and subendocardial regions) are at risk of hypoxia. Myocardial hypoxia can result in impaired contractility as well as ventricular tachyarrhythmias which may degenerate into ventricular fibrillation, leading to sudden cardiac death.


Decreased Ventricular Compliance or Abnormal Ventricular Relaxation


• In idiopathic hypertrophic cardiomyopathy, the increase in ventricular or septal wall thickness is associated with decreased ventricular compliance (increased ventricular stiffness). Myocardial or endocardial fibrosis (restrictive cardiomyopathy) can also increase ventricular stiffness.

• Decreased ventricular compliance and abnormal ventricular relaxation may result in elevated diastolic intraventricular pressures (filling pressures), even though the ventricular diastolic volume is not increased. During the course of diastole, for any increase in preload, there is an abnormal increase in intraventricular pressure. Over time, the corresponding atrium dilates to compensate for the elevated filling pressure. Once compensatory dilation of the atrium has reached its limit, further elevation of the ventricular filling pressure results in the development of edema (or pleural effusion in cats).

• Pericardial disease with cardiac tamponade is the clinical syndrome in which there is compression of the heart by fluid within the pericardial space (pericardial effusion), resulting in signs of right-heart failure and low-output failure. Elevation of intracardiac pressure, progressive limitation of ventricular diastolic filling, and reduction of stroke volume and cardiac output characterize cardiac tamponade. The clinical course depends on the size and rate of accumulation of the effusion, and the compliance of the pericardial sac.
• Acute tamponade is usually associated with an acute hemorrhage from a neoplastic lesion, such as hemangiosarcoma, but may also be associated with rupture of the left atrium secondary to chronic severe MR. As the effusion accumulates, intrapericardial pressures increase and eventually exceed the diastolic pressures in the right atrium and ventricle, thereby restricting the venous inflow to the right heart. The restriction of venous return causes a reduction in right ventricular cardiac output, pulmonary blood flow, and left-sided venous return that is associated with a reduction in left ventricular stroke volume and cardiac output, and signs of low-output heart failure.

• Chronic tamponade associated with the slow accumulation of pericardial effusion differs from acute tamponade in that the body has time to compensate for the impediment of cardiac inflow, secondary reduction in stroke volume, and cardiac output. Although compensation may somewhat normalize cardiac output, signs of right-sided CHF are often present (jugular distention and ascites).


CLINICAL DESCRIPTIONS OF HEART FAILURE


• CHF is the accumulation of fluid in tissues associated with increased capillary hydrostatic pressures and elevated diastolic intra-atrial and intraventricular pressures. Diseases that cause diastolic or systolic dysfunction are capable of increasing cardiac filling pressures, leading to CHF.

• Low-output failure can be defined as poor cardiac output, resulting in reduced tissue perfusion and inadequate tissue oxygenation. Generally, the term low-output failure is used to describe clinical scenarios in which cardiac output is dramatically reduced by end-stage, primary, systolic dysfunction.

• Right-sided heart failure may result when the right atrium or right ventricle develops elevated filling pressures associated with valvular insufficiency, pericardial disease, outflow tract obstruction, or pulmonary hypertension. Volume and pressure overloading of the right ventricle can cause hepatic congestion accompanied by ascites, pleural effusion, and, rarely, peripheral subcutaneous edema. These diseases may also reduce the forward flow of blood into the pulmonary circulation and the left heart, resulting in reduced stroke volume, cardiac output and, possibly, signs of low-output heart failure.

• Left-sided heart failure may result when the left side of the heart develops elevated filling pressures associated most commonly with valvular insufficiency, impaired contractility, or diastolic dysfunction. Elevated left ventricular filling pressures are transmitted to the left atrium and pulmonary venous and capillary beds, with the threat of fluid accumulation in the interstitial and alveolar spaces (pulmonary edema). In dogs, pleural effusion may develop when biventricular or right ventricular failure is present. Cats may develop pleural effusion with pure left-sided heart failure apparently because the visceral pleural lymphatics drain into the pulmonary venous circulation. Pulmonary venous hypertension creates a functional obstruction, thereby restricting the ability of the lymphatics to maintain a normal amount of fluid in the pleural space.


DIAGNOSIS OF HEART FAILURE



Key Points


• The diagnosis of CHF is considered to be a multimodal diagnosis, based on a careful history, physical examination, and ancillary diagnostics including electrocardiography, thoracic radiography, and echocardiography.

• Good quality thoracic radiographs should always be obtained.

• Exclude diseases that mimic CHF (e.g., chronic broncho-interstitial disease is often present in patients with cardiac disease).


History


• A complete medical history is important to establish the clinical course of the presenting complaint, as well as the presence of concurrent diseases that may complicate heart disease.

• Coughing, tachypnea, dyspnea (respiratory distress), exercise intolerance, lethargy, and weakness are common complaints of clients with pets with symptomatic heart disease or heart failure. Additionally, pets with heart failure may have a history of inappetence, weight loss, and syncope.
• Coughing is a very common historical finding in dogs with heart failure, especially those with chronic MR. In this scenario, a cough reflex is associated with left atrial compression of the left mainstem bronchus. Alternatively, dogs with severe alveolar pulmonary edema may also cough. It is important to be cognizant that other, noncardiac diseases may also cause coughing, and that coughing is not specific for heart failure. Diseases such as tracheal collapse and chronic pulmonary disease also cause coughing and may occur concurrently with heart disease.

• Tachypnea (increased respiratory rate) is a common sign of heart failure. Tachypnea can be caused by many nonpathologic mechanisms and is often overlooked by the client and the clinician. Left-sided CHF with interstitial pulmonary edema causes stimulation of receptors within the pulmonary interstitium that reflexively increase the respiratory rate. The increase in respiratory rate can occur with or without the presence of hypoxia. Because of this concept, the resting respiratory rate may be used effectively to monitor the status of patients with left-sided CHF. The normal resting respiratory rate for most small animals is usually below 30 to 35 breaths per minute. Typically, trends of increasing resting respiratory rate indicate progressive decompensation of left-sided heart failure and the need for cardiac medication adjustments (i.e., an increase in furosemide dosage or frequency of administration).

• Dyspnea (perception of difficult breathing) usually accompanies severe heart failure that has resulted in pulmonary edema or pleural effusion. Dyspnea is exacerbated by exercise in patients capable of exercising.

• Orthopnea (difficult breathing during recumbency) may occur before dyspnea. Often, the client may recognize orthopnea because the patient is reluctant to lie down or because the patient has difficulty breathing when it is lying down.

• Nocturnal coughing or dyspnea typically occurs after the patient has been recumbent for some time. It is not specific for left-sided CHF.

• Exercise intolerance may be a very early sign of heart failure in animals that are active; however, it may be difficult to identify in animals that are inactive. Reduced tolerance for exercise results because cardiac function is abnormal, and the metabolic demands of tissues (especially the working muscles) are not met, leading to hypoxia, lactic acidemia, muscle weakness, and fatigue.

• Abdominal distention secondary to ascites may be associated with right-sided or biventricular failure and must be differentiated from effusions associated with other conditions, such as hypoproteinemia, liver disease, and abdominal neoplasia. Evaluation of the jugular and abdominal subcutaneous veins may aid in determining that ascites is associated with right-sided CHF. With right-sided heart failure, these vessels are often distended and engorged.


Cardiovascular Physical Examination Findings



Murmur


• A cardiovascular murmur is a series of auditory vibrations associated with turbulent (nonlaminar) blood flow and, occasionally, with vibrating valve leaflets. When blood flow velocities are supraphysiologic (i.e., higher than normal physiologic velocities), or when blood viscosity is reduced (e.g., with anemia), blood flow tends to be nonlaminar and turbulent. Nonlaminar blood flow generates acoustic energy that vibrates the structures within the heart or the associated vessel(s). The intensity (loudness), timing in the cardiac cycle, frequency (pitch), configuration (shape), quality, duration, location, and direction of radiation of the sound created by the blood flow are important characteristics of cardiac murmurs.
• The intensity of the murmur refers to the loudness of the murmur and is graded on a scale from 1 to 6 (1 being the least audible murmur, and 6 being the loudest).

• The timing is defined as being systolic, diastolic, or continuous.

• The configuration of the murmur refers to the shape of the sound created by the abnormal blood flow, and is described as being either a plateau (regurgitant murmur) or a crescendo-decrescendo (ejection murmur) sound.

• A cardiac murmur is present in many dogs with heart failure, but the presence of a cardiac murmur is not specific for heart failure.


Cardiac Rhythm Disturbances


• Arrhythmias are relatively common in animals with heart failure.
• Atrial fibrillation is a common supraventricular arrhythmia present in some dogs with DCM and chronic MR secondary to primary valve disease, as well as in cats with cardiomyopathy.

• Ventricular tachyarrhythmias may be present in dogs with heart failure or with extracardiac disease, such as thoracic trauma, splenic disease, and gastric dilatation-volvulus. Ventricular arrhythmias are especially common in boxers and Doberman pinschers with cardiomyopathy.

• Bradyarrhythmias such as third-degree (complete) atrioventricular block may cause signs of reduced cardiac output (lethargy, weakness, and exercise intolerance) and, occasionally, CHF.

• Gallop sounds are abnormal heart sounds in dogs and cats that are often associated with heart failure. A third heart sound (S3) gallop occurs just after the second heart sound (S2) during the rapid diastolic phase of ventricular filling. An S3 gallop occurs commonly in dogs with heart failure associated with volume overload, particularly dogs with DCM. During early diastolic filling, blood rushes out of the atrium into a noncompliant ventricle, which then vibrates, resulting in a low-frequency sound just after S2. A fourth heart sound (S4) gallop occurs just before the first heart sound (S1) and is associated with atrial contraction. Ventricular filling in late diastole associated with atrial contraction vibrates the noncompliant ventricle, creating a low-frequency sound just before S1 and the onset of systole. S4 gallop are commonly auscultated in cats with hypertrophic or restrictive cardiomyopathy. Summation gallops (S3 and S4) may occur during periods of tachycardia.


Diagnostics



Electrocardiography


• Electrocardiography is used to detect cardiac rhythm disturbances, chamber enlargement, or conduction abnormalities that may be associated with cardiac disease. Electrocardiographic abnormalities are not specific for heart failure and therefore should not be used to determine the presence of heart failure. Furthermore, a normal electrocardiogram does not rule out the possibility of severe heart disease with secondary chamber enlargement.


Thoracic Radiography


• Thoracic radiography is important in the evaluation of patients with suspected heart disease or CHF. In general, with respect to heart disease and heart failure, three questions should be answered when evaluating a thoracic radiograph:
• Is cardiomegaly present? If so, which side of the heart is affected?

• What is the pulmonary vascular pattern (e.g., normal, undercirculated, overcirculated, venous distention, or arterial distention)?

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Aug 15, 2016 | Posted by in SMALL ANIMAL | Comments Off on Pathophysiology and Therapy of Heart Failure

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