Current Issue
JUNE 1999 - VOLUME 19 - NUMBER 3
Heart Failure: The Physiologic Basis for Current Therapeutic Concepts
Nancy Albert, MSN, RN, CCRN, CNA
Sponsored by an unrestricted educational grant from Bayer Pharmaceuticals
About the Author
Nancy Albert, MSN, RN, CCRN, CNA Clinical Nurse Specialist, Heart Failure and Cardiac Transplantation
Department of Nurse Education and Research, The Cleveland Clinic Foundation
This article originally appeared in the June 1999 supplement issue of Critical Care Nurse, Vol 19, No. 3 and was sponsored by an unrestricted educational grant from Bayer Pharmaceuticals. Reprint requests: InnoVision Communications, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 515); fax, (949) 362-2022; e-mail, ivcReprint@aol.com.
Heart Failure
Approximately 4.7 million Americans suffer from chronic heart failure,1 about 50% of whom die within 5 years.2 The classic textbook definition of heart failure is the inability of the myocardium to pump sufficient blood to the tissues of the body to meet metabolic needs.3 However, current concepts of the condition also incorporate a syndrome involving many other processes and organs. Of primary importance are the neuroendocrine derangements, particularly those related to the sympathetic nervous system and the renin-angiotensin-aldosterone (RAA) axis.
As a result, today’s therapy for heart failure focuses not only on correcting hemodynamic abnormalities but also on suppressing the neurohormonal forces that appear to be responsible for the progression and perpetuation of the condition.1
To understand the contemporary management of acute heart failure, it is essential to understand not only the functions of the normal heart but also what happens to the heart and to the body as a whole when the heart begins (and continues) to fail. This article reviews the physiological aspects of normal cardiac function and the pathophysiological aspects of heart failure, with an eye toward promoting greater understanding of this condition.
The Normal Pump
The 4 primary determinants of cardiac performance are contractility, preload, afterload, and heart rate.
Contractility
The myocardium is composed of muscle cells, or myocytes, secured within a collagenous interstitium. Two types of cardiac myocytes exist, differentiated by function: those that specialize in generating and propagating electrical impulses (ie, conductivity) and those that specialize in contraction (ie, contractility). The bulk of the myocardium consists of contractile cells that can be considered the working cells of the heart.
Each contractile cell is made up of muscle fibers, which are composed of myofibrils embedded in the basic muscle-cell substance, the sarcoplasm. The myofibrils themselves are composed primarily of filaments of the proteins myosin and actin, which are aligned in parallel and connected by cross-bridges. Interaction of calcium with another protein, troponin, found within the myofibril, produces shortening of the cross-bridges and causes the actin and myosin filaments to slide across one another. As a result, the muscle contracts.
The calcium necessary to induce muscle contraction comes from (1) the interstitial fluid surrounding the cell and (2) special storage sites within the sarcoplasmic reticulum, which is the cytoplasmic network containing the working elements of the muscle cell. The calcium that activates the reaction comes from the storage sites in the sarcoplasmic reticulum. However, the amount of calcium released depends not only on the amount of calcium stored within the reticulum but also on the amount of “trigger” calcium that enters the cell from the extracellular environment. After the muscle contracts, the free calcium is returned to its sarcoplasmic storage sites or is released from the cell as the muscle relaxes to prepare for its next contraction, allowing the heart to function as a pump.
Preload
Ventricular filling at the end of diastole is called preload. Preload depends on the volume of venous return to the heart, which is influenced not only by the actual volume of blood within the venous system but also by venous tone or compliance (ie, the degree of contraction or relaxation in the smooth-muscle walls of the veins). A decrease in venous tone permits blood to pool in the peripheral vessels, thereby decreasing the return of blood to the heart. On the other hand, an increase in venous tone will increase the venous return.
The mechanism of preload can be described as the degree of stretch and pressure in the myocardial wall that is produced by the volume of blood in a ventricle at the end of diastole (ie, ventricular end-diastolic volume and/or pressure). Preload is directly related to the force of myocardial contraction; the greater the degree of stretch (up to a point), the greater the force of contraction. This stretch-strength relationship, known as the Frank-Starling law of the heart, can be easily visualized: Just picture stretching an ordinary rubber band before releasing it to fly across the room.
Another tool for visualizing this relationship is the ventricular function curve by which the relationship of cardiac output and preload can be plotted for various states of contractility (Figure 1).
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Pulmonary arterial wedge pressure and left atrial pressure are indicators of left ventricular preload in the absence of clinical pathological changes in the mitral valve or pulmonary artery vasculature. The index of right ventricular preload is right atrial pressure in the absence of tricuspid valve pathology.
Afterload
The pressure against which the left ventricle ejects its content is termed afterload. Because the heart functions within a closed system, afterload will also influence the amount of blood discharged into the systemic circulation. The greater the afterload, the harder the myocardium will have to pump to overcome the increased resistance it meets.
Like preload, afterload can be described mechanistically as the wall stress or tension that develops in the ventricular myocardial wall during systole. Afterload is determined primarily by arterial tone and the resultant pressure within the arterial system (ie, blood pressure).
An increase in systemic arterial tone produces vasoconstriction with a concomitant increase in blood pressure and afterload, whereas a decrease in arterial tone leads to vascular relaxation with a concomitant decrease in afterload. Systemic vascular resistance is a derived parameter that is influenced by many factors including the amount of blood ejected into the arterial circulation. There is an equation that denotes these interrelationships: SVR = (MAP – RAP)/CO, where SVR indicates systemic vascular resistance; MAP, mean arterial pressure; RAP, right atrial pressure; and CO, cardiac output. Right atrial pressure is the equivalent of the central venous pressure. Pulmonary vascular resistance measures right ventricular afterload. The equation that reflects the hemodynamic interrelationships of right ventricular afterload is the following: PVR = (MPAP – PAWP)/CO, where PVR indicates pulmonary vascular resistance; MPAP, mean pulmonary artery pressure; PAWP, pulmonary arterial wedge pressure; and CO, cardiac output.
A mechanical obstruction, such as a sclerosed heart valve, could also impede the forward flow of blood from the heart. In either case, the end result is the same, namely, that of forcing the myocardium to contract with greater force to push the blood forward.
The ventricular function curve described above can also be used to illustrate the effects of afterload on the efficacy of the heart (Figure 2).
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Heart Rate
Heart rate plays an important role in maintaining adequate cardiac output. When contractility fails or when cardiac output is decreased for any other reason, heart rate will increase to maintain a blood flow sufficient to meet metabolic requirements.
At some point, however, an increased heart rate can become more detrimental than beneficial for 2 reasons, both related to the fact that an increased heart rate reduces the period of diastole.
The first reason is related to the filling of the heart during diastole. Like any pump, the heart can only eject what it contains, and its content is determined largely by the amount of blood that enters during diastole. Increased heart rate resulting in a shortened period of diastole will decrease the amount of blood that fills the ventricles during cardiac relaxation. This reduces the amount of blood available for the next ventricular systole, thereby decreasing stroke volume (the amount of blood ejected with each beat). Subsequently, cardiac output will fall as this compensatory attempt to increase cardiac output eventually fails.
The second reason for the detriment associated with a tachycardia-related shortening of diastole is a negative effect on the myocardial oxygen supply-and-demand ratio. Tachycardia not only increases the oxygen demand of the heart, it limits its oxygen supply at the same time. This limitation occurs because blood enters and flows freely through the coronary arteries mainly during diastole, and tachycardia, as discussed, reduces the period of diastole.
Two factors contribute to the negligible blood flow through coronary arteries during systole. First, forward flow is halted as contracting heart muscle surrounding the coronary vessels compresses them. Second, unlike other arteries in the body, coronary arteries fill during diastole as a result of the location along the aorta where they arise. Coronary openings are located right behind the cusps of the aortic valve, so close to the origin of the aorta from the left ventricle that when the aortic valve opens to let blood flow from the heart into the general circulation, its cusps flap against the coronary artery openings, shutting them off and thus preventing the coronary arteries from filling. The coronary arteries fill as a result of pressure within the aorta when the cusps close during diastole.
Duration of diastole is especially critical in terms of meeting increased demands for oxygen by heart muscle. The heart can meet this increased demand only by increasing coronary flow, because—unlike what is found with other types of muscle—myocardial oxygen extraction is at a maximum even when the heart is resting, leaving little room for reserve. When the period of diastole is decreased, the delivery of oxygen to the heart muscle can be seriously impaired, a problem that is magnified by any increase in oxygen demand. Thus, the oxygen demand of the heart will increase not only as heart rate increases, but also as any of the principal determinants of myocardial performance (ie, force of contraction, preload, afterload) increases, thereby hampering the ability of these measures to continue to improve the function of the heart.
The interactions among the 4 basic determinants of cardiac performance are illustrated in Figure 3.4
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Compensatory Mechanisms in Heart Failure
Any reduction in cardiac performance will automatically be met by a series of compensatory neurohormonal adjustments to help boost the efficacy of the heart and maintain the efficiency and integrity of the circulation. These responses primarily include the following:
• Increased adrenergic (sympathetic nervous system) activity
• Increased RAA system activity
• Increased secretion of vasoconstrictive substances such as vasopressin and endothelin
These responses cause constriction of peripheral blood vessels, thereby increasing afterload; expand intravascular volume, thereby increasing preload; strengthen contractility either directly or via reflex response to the increased afterload and preload; and enlarge cardiac muscle mass, thereby improving myocardial performance, at least for a period (Figure 4). However, continued use of these compensatory mechanisms to support the failing heart eventually becomes detrimental. Increases in preload outstrip the ability of the failing left ventricle to increase cardiac output accordingly. The failing ventricle can no longer meet increases in afterload with corresponding increases in contractility. Increased intravascular volume and pressure cause congestion in the venous beds leading to the affected ventricle(s).
In this setting counterregulatory forces are called into play. Among important physiological mechanisms that modulate excessive neuroendocrine stimulation is the expression of natriuretic peptides by the atrium and ventricle, along with their countervailing vasodilatory and diuretic and/or antiproliferative actions. Eventually, however, even these modulating measures are overcome by continuing neurohormonal activation.
A fundamental knowledge of the physiological basis for these compensatory and counterregulatory events—as well as an understanding of the far-reaching effects they exert on the heart and other organs and structures—is necessary to understand the new directions taken in the management of patients with heart failure (especially systolic dysfunction of the left ventricle).
Increased Adrenergic (Sympathetic) Activity
The sympathetic nervous system, part of the autonomic nervous system, regulates functions (eg, the beating of the heart) considered automatic or not under conscious control. In general, the sympathetic nervous system increases physiological activity, and its effect on the heart is no exception. Heightened sympathetic stimulation will accelerate the heart rate (a positive chronotropic effect) and increase the force of myocardial contraction (a positive inotropic effect). Increased sympathetic stimulation also increases vascular tone, leading to vasoconstriction.
The increase in sympathetic activity observed when the heart progressively fails is a reflex response generated by baroreceptors, or stretch receptors, located primarily in the aortic arch and carotid sinus. When cardiac output is reduced in heart failure, the volume of blood entering the arterial tree is also reduced, lessening the stretch within the vessel walls. Baroreceptors respond to the reduced stretch by sending a message to the vasomotor center of the brain calling for an increase in sympathetic tone in an effort to increase stroke volume.
The sympathetic nervous system exerts its physiological effects via the action of catecholamines such as norepinephrine, a neurotransmitter produced at nerve endings, and epinephrine, a hormone produced by the adrenal medulla. Catecholamines exert their effects at adrenergic receptor sites located on the outer surface of myocardial and vascular smooth-muscle cells.
Alpha and Beta receptors are the 2 main classes of adrenergic receptors. They are subdivided into Alpha1, Alpha2, Beta1, and Beta2 receptors. Beta1 receptors are found in cardiac muscle, whereas Alpha1 and Beta2 receptors are found in vascular smooth muscle.
The effect of adrenergic stimulation of the Beta1 receptors of the heart is straightforward: an increase in chronotropic and inotropic effect. Stimulation of the adrenergic receptors in vascular smooth muscle is more complex, because Alpha1 and Beta2 receptors produce opposite effects. Stimulation of Alpha1 receptors produces vasoconstriction, whereas stimulation of Beta2 receptors causes vasodilation. The predominant effect of sympathetic stimulation on the vasculature is vasoconstriction, primarily because there are more a receptors than there are b receptors. In addition, norepinephrine is significantly more active at a receptor sites than at Beta2 receptor sites.
What happens within a cell after a receptor has been activated by an endogenous chemical substance such as a catecholamine is now well understood. In essence, the substance in question binds to the receptor (why it is also called a ligand), setting in motion a series of signaling mechanisms that eventually culminate in a change in cellular activity and an altered physiological response. First, the stimulated receptor triggers activation of a series of cell membrane-associated proteins leading to the generation of a second messenger substance known as a G protein, which is located on the cytoplasmic face of the plasma membrane. The activated G protein then activates an effector element, usually an enzyme. The activated enzyme increases the intracellular concentration of what is appropriately called a second messenger, which instructs the cell to alter the activity of other enzymes and proteins, thereby effecting the appropriate cellular response.
When a Beta-adrenergic receptor is activated by an endogenous ligand (Figure 5), the stimulated receptor typically activates a G protein designated as the GS protein; the GS protein then activates the effector enzyme adenyl cyclase. In turn adenyl cyclase converts adenosine triphosphate to cyclic adenosine monophosphate (cAMP), the second messenger in this chain of events. cAMP then induces other intracellular changes involving calcium that (with regard to Beta1 receptors in the heart) cause an increase in the rate and force of myocardial contraction and that (with regard to Beta2 receptors in vessel walls) produce vascular relaxation and vasodilation. When stimulation of the receptor stops, the intracellular actions of cAMP end and cAMP itself is rapidly degraded by enzymes called phosphodiesterases.
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Unlike Beta receptors, stimulation of a receptors in vascular smooth muscle decreases the activity of adenyl cyclase, thus decreasing the amount of cAMP. With less cAMP, there is less relaxation of vascular smooth muscle and a greater degree of vasoconstriction. The exact intracellular mechanisms by which Alpha-receptor stimulation produces alterations in a cell’s activity are less well understood than those that occur following Beta-receptor activation.
Patients with heart failure continue to manifest heightened adrenergic activity long after this action has ceased to be useful. Persistently elevated levels of circulating norepinephrine are found in these patients when plasma hormone concentrations are assessed. The prognosis in heart failure varies inversely with the concentration of norepinephrine in the blood.
However, the effect of the neurotransmitter may be modified by down regulation of adrenergic receptors that occurs with chronic sympathetic stimulation. Down regulation can be defined as a decrease in the number and/or responsiveness of the adrenergic receptors and can be viewed as a mixed blessing. Although down regulation reduces the effects of excessive neurohormonal stimulation, it can also deprive the myocardium of adrenergic boosts when sympathetic support is necessary. It is not known whether down regulation of adrenergic receptors improves or adversely affects the natural history of myocardial dysfunction in heart failure.
Role of the RAA System
Just as low blood flow through the aorta and carotid circulations activates the baroreceptor reflexes that stimulate increased adrenergic response, low blood flow through the renal arteries activates the baroreceptor reflex, which stimulates the RAA system to exert its vasoconstrictive and sodium- and water-retaining effects. Activation of the RAA axis can also be induced by sympathetic nervous system stimulation, primarily Beta-receptor stimulation itself, and by sodium depletion.
Release of renin from specialized cells near the nephrons of the kidney called juxtaglomerular cells is the initial step in activating the RAA system. Once in the blood, renin interacts with one inert substance, angiotensinogen, to produce another inert substance, angiotensin I (AI). When circulating AI comes in contact with angiotensin-converting enzyme (ACE), which is found on the interior (endothelial) surface of blood vessel walls, it is converted to the potent vasoconstrictor-pressor substance angiotensin II (AII).
Angiotensin II, like catecholamines, acts at receptor sites on blood vessel walls to induce contraction of vascular smooth muscle and vasoconstriction. The 2 types of AII receptors are AT1 and AT2. Most of the effects of AII are mediated via AT1 receptors. Like catecholamines, AII activates a G protein (although a different G protein) to initiate a series of signaling mechanisms that alter the activity of the cell and cause vascular-muscle contraction and vasoconstriction.
Angiotensin II also stimulates the release of aldosterone from the adrenal cortex. Aldosterone promotes the reabsorption of sodium from urine by the distal renal tubules. Because sodium retention is coupled with water retention, increased aldosterone levels will lead to the expansion of plasma volume and increased preload.
Finally, AII acts via a negative feedback loop to reduce the release of renin from the kidney, thereby curtailing its own production. Angiotensin II is inactivated by angiotensinases into angiotensin III and various peptide fragments.
Other Vasoconstrictive Influences
The roles of the sympathetic nervous system and the RAA axis in the initially adaptive and eventually maladaptive events in cardiac failure have long been understood. However, newer actors that likely contribute to this scenario (eg, vasopressin and endothelin) have been discovered. Like catecholamines and AII, these substances exert their physiological and pathophysiological effects at receptor sites on the surface membranes of various cells.
Vasopressin
Vasopressin is produced by the pituitary gland. Its long-recognized effect on the kidney, that of stimulating the reabsorption of water, is responsible for its other name—antidiuretic hormone. However, vasopressin is known to also exert significant vasoconstrictor effects at doses lower than those needed to provide maximum antidiuretic effect, thereby playing an important role in cardiovascular regulation.
Endothelin
Endothelin, as its name implies, is synthesized primarily by endothelial cells, mainly endothelial cells in blood vessel linings. Its major effect appears to be vasoconstriction in most vascular beds within the body. In addition, endothelins have been found to exert positive inotropic and chronotropic effects on the heart muscle.
Endothelin is now thought to play a significant role in the pathogenesis and perpetuation of heart failure. Not only are plasma endothelin levels elevated in heart failure, but plasma concentrations correlate directly with cardiac deterioration. In other words, like norepinephrine, the higher the endothelin levels, the worse the cardiac function becomes.
Counterregulatory Influences
Once cardiac output has been restored by the compensatory neurohormonal changes, the body normally produces a number of counterregulatory substances with opposing vasodilatory and/or diuretic effects to restore cardiovascular homeostasis. Natriuretic peptides are among the counterregulatory substances released for this purpose.
Natriuretic Peptides
Natriuretic peptides, primarily atrial natriuretic polypeptide (ANP) and brain natriuretic polypeptide (BNP), are released from the atria and ventricles, respectively, in response to increased wall stress. (BNP was first discovered in porcine brain, hence the misleading nomenclature.) The largely volume-related release of ANP and pressure-related release of BNP, with their vasodilatory, natriuretic/diuretic, and antiproliferative properties, is considered one of the most important counterregulatory responses to the cardiac, vascular, and renal changes induced by neurohormonal stimulation.
Natriuretic peptides bind to cell surface receptors with intrinsic guanylyl cyclase activity. When natriuretic peptides bind to their receptors, guanylyl cyclase activity is enhanced. The action of guanylyl cyclase leads to the accumulation of cyclic guanosine monophosphate that induces smooth muscle cell relaxation and vasodilation.
Molecular Basis of Heart Failure
Remodeling
It is now believed that the progressive nature of myocardial dysfunction observed in chronic left ventricle heart failure has its origin at a molecular level. The basic mechanism of these molecular changes is termed “remodeling” and involves changes in the structure, function, and gene expression of the myocardial cell. Remodeling essentially involves hypertrophy of the ventricular myocytes and regression from an adult to a fetal phenotype (gene makeup), leading to large, genetically abnormal myocardial cells that cannot contract as efficiently as normal cells. In addition, changes also occur in the interstitium, with fibrotic infiltration leading to a stiffened and less compliant myocardial wall.
These hypertrophic changes are not merely the natural muscular growth engendered by increased work, but rather growth that initially helps the heart to maintain circulation. The myocyte hypertrophy accompanying heart failure is associated with an unnatural growth pattern in which there is cellular disorganization leading to, among other things, loss and disruption of contractile elements. Furthermore, these abnormal hypertrophic changes produce myocytes that are lengthened far more significantly than they are widened. These changes eventually render the myocytes, and thus the ventricles, less efficient despite their larger size, causing an increase in wall stress and increased need for oxygen, with an unfavorable change in the oxygen supply-and-demand ratio.
Apoptosis Versus Necrosis
The intracellular changes associated with remodeling cause not only myocardial dysfunction but also the death of myocardial cells at an accelerated rate. The process by which remodeled cells die is called apoptosis. This is 1 of 2 ways in which a cell may die; the other is by necrosis. The 2 processes cause cell death in distinct ways.
Apoptosis can be thought of as preprogrammed death or the normal gradual process by which all cells eventually die. Death by necrosis, on the other hand, generally follows a sudden catastrophic event such as a myocardial infarction (MI).
The causes and internal cellular derangements of apoptosis and necrosis differ. Furthermore, apoptosis generally occurs randomly, affecting cells scattered throughout the myocardium and weakening function throughout the ventricular walls of the heart. Areas of necrotic death are generally localized, typically weakening only a circumscribed area of myocardium. These processes are not mutually exclusive, and an area of necrosis can be superimposed on a myocardium weakened by apoptosis. This phenomenon occurs when an MI worsens the already compromised cardiac function in those with heart failure.
The accelerated death associated with remodeling poses a unique threat to the integrity of myocardial performance. Because cardiac myocytes normally do not divide and reproduce, the cells that die will not be replaced. Premature myocyte loss places an additional burden on the remaining contractile cells, making them work harder, leading to further hypertrophy and remodeling, ultimately resulting in more myocardial deterioration.
Neurohormonal Fuel
This self-perpetuating cycle of cell death and further hypertrophy is fueled by neurohormonal activation, which is called into play by the increased wall stress associated with hypertrophy. Neurohormonally induced vasoconstriction causes further hypertrophy because increased peripheral resistance makes myocardial cells work harder due to increased afterload. In addition, neurohormonal stimulation of the cardiac myocyte has a direct effect in inducing unnatural growth patterns.
Because of the central role that neurohormonal stimulation appears to play in the remodeling process, control of excessive endogenous neurohormonal activity has become one management objective in the treatment of patients with heart failure (ie, ACE inhibitors and b blockers). Of course, correcting hemodynamic abnormalities associated with heart failure continues to be an important part of managing patients who decompensate.
Clinical Classifications
Heart failure may be clinically classified in numerous ways, depending on the severity of symptoms or the predominant underlying pathophysiology. Heart failure may thus be categorized by a subjective scale first introduced by the New York Heart Association, or as systolic or diastolic, high-output or low-output, right-sided or left-sided, or as backward or forward. Although these pathophysiologic classifications are rarely exclusive, they can provide a rational basis for determining appropriate treatment for heart failure.
Functional Classes
The New York Heart Association functional classification system is based on the degree of effort required to cause symptoms. An assignment of class I reflects symptoms with activity that would occur in normal individuals. Class II reflects symptoms with ordinary activities. Class III reflects marked limitations due to symptoms with less than ordinary activities. Class IV failure reflects symptoms at rest and severe limitation in functional activity. This subjective scale is used as a prognostic measure as well as a measure of treatment effectiveness.
Systolic Versus Diastolic Heart Failure
As the term implies, in systolic heart failure, the primary defect is an impaired ability of the heart to contract. The myocardium is weakened, and the resultant impairment of contractility leads to reduced cardiac output and insufficient ventricular emptying. Systolic dysfunction is associated with eccentric hypertrophy and thus increased heart size. Left ventricular ejection fraction (the percentage of blood ejected with contraction) is used to quantify systolic dysfunction. A left ventricular ejection fraction less than 40% signifies systolic failure.
In diastolic heart failure, on the other hand, the ability of the heart to relax is impaired, and the myocardial wall becomes stiff and thickened, impairing the heart’s ability to fill. Diastolic dysfunction is associated with concentric hypertrophy, so heart size remains normal as reflected in a cardiothoracic ratio less than 55% on anterior-posterior chest radiograph.
The 2 conditions are not mutually exclusive; some patients exhibit both abnormalities of emptying and filling. Table 1 lists conditions in which systolic or diastolic failure is observed.
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Low-Output Versus High-Output Failure
Acute heart failure may be caused by a low-output state and is associated with a significantly reduced cardiac output, ie, less than 4 L/min (cardiac index < 2.5 L/min/m2). In patients with low-output failure, cardiac output may be normal at rest but may simply fail to rise sufficiently on exertion.
On rare occasion, high-output failure may occur. In this condition, cardiac output may be within normal range or even elevated but cannot meet increased metabolic needs. Table 2 lists conditions associated with low-output and high-output failure.
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Left-Sided Versus Right-Sided Heart Failure
In the early stages of heart failure, one ventricle is usually affected more than the other (based on heart failure etiology), and clinical presentation will be influenced by the increase in cardiac volume and pressures and/or fluid behind the ventricle that fails first. Thus, in left-sided failure, in which the left ventricle is weakened or overloaded, pulmonary congestion will induce symptoms such as dyspnea or orthopnea. On the other hand, right-sided failure, in which the right ventricle is impaired, will manifest clinically as peripheral edema, congestive hepatomegaly, and systemic venous distention.
However, evidence of localization of excess fluid often fades, especially as heart failure progresses, and patients present with signs and symptoms that may be attributable to failure of either or both ventricles. One reason is that left ventricular failure causes secondary pulmonary hypertension, leading to the failure of the right ventricle over time. Indeed, isolated right-sided failure is rare and usually seen secondary to left-sided failure. However, right-sided failure can occur without a failing left heart from such conditions as right ventricular infarction, pulmonary or
tricuspid valvular disease, primary pulmonary hypertension, a large pulmonary infarction, and septal defects.
Backward Versus Forward Heart Failure
The concept of backward heart failure focuses on the inability of the ventricle to eject its contents, leading to elevated filling pressures, subsequent venous congestion, and pulmonary congestion. The concept of forward failure, on the other hand, focuses on decreased cardiac output and inadequate tissue perfusion. Rarely does either condition exist independent of the other; both are usually present to some degree.
Acute Versus Chronic Heart Failure
The onset of heart failure may be acute, as after an MI, or gradual, as when the condition slips into a chronic state, in general secondary to the slow structural changes occurring in the stressed myocardium. The gradual process by which chronic heart failure develops includes the progression of compensatory mechanisms discussed above: a decrease in contractility, neuroendocrine activation, increased afterload, increased preload, and, eventually, ventricular remodeling.
These compensatory mechanisms help patients to carry out activities of daily living without continuous respiratory distress. In addition, medications such as ACE inhibitors and diuretics help to keep patients relatively asymptomatic. The compensatory mechanisms may occur at a rapid rate (though this is uncommon), and patients may progress to end-stage chronic heart failure within months.
A patient who has been living with heart failure relatively without symptoms may suddenly decompensate. Acute decompensation may be either a recurrent problem in a patient previously diagnosed with heart failure or the first clinical evidence of the gradual compensatory process described above. The causes of acute decompensation in a patient previously diagnosed with heart failure are numerous and varied and include the following: increased exertion or intensified emotion; incautious salt intake; fluid indiscretion; noncompliance with (or failure of) medications; sudden increase in metabolic demand related to, for example, fever or anemia; concomitant valve disease; and acute MI.
Although chronic heart failure can usually be managed on an outpatient basis, hospitalization is recommended for patients with acute onset of severe or long-suffering clinical manifestations of acute exacerbation of chronic failure. Management of the hospitalized patient with acute heart failure and the role of the critical care nurse in providing this care are the focus of part 2 of this supplement.
References
1. ACC/AHA Task Force Report. Guidelines for the evaluation and management of heart failure. J Am Coll Cardiol. 1995;26:1376-1398.
2. Katzung BG, Parmley WW. Cardiac glycosides and other drugs used in congestive heart failure. In: Katzung BG, ed. Basic and Clinical Pharmacology. 7th ed. Stamford, Conn: Appleton & Lange; 1998:197-215.
3. Smith TW. Heart failure. In: Wyngaarden JB, Smith LH, Bennett JC, eds. Cecil Textbook of Medicine. Philadelphia, Pa: Saunders; 1992:187-207.
4. Braunwald E. Normal and abnormal myocardial function. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:1278-1286.
Additional References
1. Packer M, Cohn JN. Consensus recommendations for the management of chronic heart failure. Am J Cardiol. 1999;83(2A):1A-38A.
2. Pathophysiology of congestive heart failure. Part 2. In: Hosenpud JD, Greenberg BH, eds. Congestive Heart Failure. New York, NY: Springer-Verlag; 1994:chap 2-11.
3. Albert N. Advanced systolic heart failure: emerging pathophysiology and current management. Prog Cardiovasc Nurs. 1998;13(3):14-30.
4. Background and current concepts. Section 1. In: Mills RM, Young JB, eds. Practical Approaches to the Treatment of Heart Failure. Baltimore, Md: Williams & Wilkins; 1998.
5. Francis GS. Pathophysiology of the heart failure clinical syndrome. In: Topol EJ, ed. Textbook of Cardiovascular Medicine. 1st ed. Philadelphia, Pa: Lippincott-Raven; 1998:chap 79.