Congestive Heart Failure (CHF)

I. Congestive Heart Failure (CHF)
A. Definition
Congestive heart failure (CHF) is the inability of the heart, working at normal or elevated filling pressure, to pump enough blood to meet the oxygen requirements of the body tissues. CHF should never be considered a diagnosis. Rather, it is a syndrome resulting from many diseases that interfere with cardiac function. In acting as a muscular pump, the heart does only two things: it contracts (systole) and it relaxes (diastole). Therefore, heart failure can result from only two broad abnormalities—systolic dysfunction and diastolic dysfunction.
B. Etiology
1. Systolic dysfunction. Systole is governed by three cardiac properties: contractility—the ability of myocardium to generate force, afterload—the force against which the heart must contract, and preload—the sarcomere stretch before contraction.
a. Decreased contractility. Most cases of CHF occur when an insult to the myocardium reduces its ability to generate force, thereby reducing its contractility.
(1) Myocardial infarction (MI). In MI, a portion of the myocardium undergoes necrosis and can no longer generate force, resulting in weakening of the ventricle. If extensive areas of the myocardium are infarcted, CHF results.
(2) Valvular heart disease results in stenosis or regurgitation of the cardiac valves, which places a pressure or volume overload, respectively, on the ventricles. Initially, compensatory mechanisms [see I B 1 c] accommodate these overloads and maintain normal cardiac output at acceptable filling pressures. However, eventually these mechanisms fail and heart failure ensues.
(3) Hypertension. Hypertension may contribute to either systolic or diastolic dysfunction.
(4) Cardiomyopathies are diseases that directly injure the myocardium.
(a) Toxic. Substances directly toxic to the myocardium (e.g., ethanol and catecholamines) may damage its force-generating ability. Prolonged exposure to these agents may lead to the development of CHF.
(b) Idiopathic. When the contractile function of the myocardium fails in the absence of a known etiology, a viral cause often is implied but frequently cannot be proven. Other clinical presentations, including peripartum cardiomyopathy, are of unknown etiology.
(c) Infiltrative. Infiltration of the myocardium by a variety of substances (e.g., amyloid) may reduce contractility.
b. Increased afterload. Increasing the afterload makes it harder for the ventricular muscle fibers to shorten, thereby reducing cardiac output. Afterload can be quantified by calculating the systolic force on the myocardium using the Laplace equation for stress:
Stress = (pressure أ— radius)/(2 أ— thickness)
Thus, disease states that increase either the systolic pressure (hypertension, aortic stenosis) or chamber radius (dilated cardiomyopathy, valvular regurgitation) increase afterload unless the wall thickness increases proportionately.
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c. Compensatory mechanisms develop in response to the ventricular pressure and volume overload that accompany decreased contractility.
(1) The Frank-Starling mechanism is activated when reduced ventricular emptying results in more volume retained in the ventricles at the end of systole, which leads to a greater volume at the end of diastole. Increased end-diastolic volume increases sarcomere stretch (preload), which increases the number of systolic actin–myosin cross-bridges that develop. The greater number of cross-bridges increases the strength of contraction.
(2) Cardiac hypertrophy provides additional muscle mass to bear the burden of various overloads.
(3) Adrenergic stimulation by endogenous catecholamines increases the inotropic state.
2. Diastolic dysfunction. Diastole is governed by active and passive properties. Active relaxation occurs early in diastole as calcium is pumped out of the myocardium, resulting in the near cessation of actin–myosin cross-bridge interaction. Passive filling occurs as the mitral valve opens, allowing the blood stored in the atria to fill the ventricles.
a. Abnormalities in active relaxation. Active relaxation is impaired when there is delay in calcium reuptake at the beginning of diastole.
b. Abnormalities of passive filling. Passive relaxation is impaired when the myocardium is stiffer than normal. Stiffness is defined as a change in pressure (خ”P) per unit change in volume (خ”V), or خ”P/خ”V. When stiffness is increased, any change in volume requires or causes a greater increase in pressure. Thus, to fill the heart to an adequate volume, high filling pressure occurs, which in turn leads to pulmonary and systemic congestion. Increased passive stiffness of the ventricles occurs when concentric hypertrophy causes the chamber wall to be thicker than normal, as might occur in hypertension or when the myocardium is infiltrated by abnormal substances such as amyloid.
3. The neurohumoral hypothesis of heart failure. Heart failure leads to the persistent activation of many neurohumoral systems and hormones, including the renin-angiotensin-aldosterone system, the adrenergic nervous system, inflammatory cytokines, endothelin, and vasopressin. Although once thought of as compensatory, persistent overactivation of these agents is cardiotoxic, in turn leading to a progressive decline in cardiac function. Thus, blockade of these systems should be beneficial in treating CHF.
C. Types of Heart Failure
1. High-output failure is characterized by cardiac output that may be several times higher than normal but still is not adequate to maintain tissue perfusion needs or, if adequate, is maintained with a higher-than-normal filling pressure. A classic example of high-output failure is chronic severe anemia, which causes reduced oxygen-carrying capacity. In chronic severe anemia, the following occurs:
a. Compensation is provided by increased forward cardiac output, which is facilitated by cardiac enlargement, decreased total peripheral resistance, and increased venous return to the heart. This causes a volume overload of ventricles.
b. Eventually the demands on the heart lead to cardiac failure; cardiac output, although high, still is not adequate to meet the circulatory demands placed on the heart by the anemia. Some other causes of high-output failure include arteriovenous fistula, beriberi, and thyrotoxicosis.
2. Left-sided failure indicates that the left ventricle is the failing chamber. A disease that primarily affects the left ventricle (e.g., MI) may reduce its contractile force, whereas the right ventricle continues to pump normally. Thus, left ventricular failure can occur without right ventricular failure.
3. Right-sided failure indicates that the right ventricle has failed, either as a result of left ventricular failure or in isolation from the left ventricle.
a. The most common cause of right ventricular failure is left ventricular failure. When left ventricular failure occurs, the filling pressure in the left ventricle becomes elevated, increasing the workload of the right ventricle (the chamber responsible for filling the left ventricle). Thus overtaxed, the right ventricle eventually fails also.

b. The right ventricle also may fail in isolation from the left ventricle. In the presence of chronic obstructive pulmonary disease (COPD), increased pulmonary vascular resistance develops as a result of architectural changes in the lungs. The higher pulmonary vascular resistance produces a pressure overload on the right ventricle, which leads to increased right ventricular work and eventual failure. Pulmonary embolism and primary pulmonary hypertension are some other causes of right-sided failure.
D. Clinical features
1. Symptoms
a. Dyspnea is the most frequently encountered symptom of CHF.
(1) The feeling of breathlessness is caused by vascular congestion, which reduces pulmonary oxygenation. In addition, the vascular congestion diminishes lung compliance, increasing the work of breathing, thus adding to the feeling of breathlessness.
(2) Dyspnea also results from reduced cardiac output to the periphery, which triggers the symptom through neurohumoral mechanisms. In the early stages of CHF, dyspnea occurs only with exertion. As heart failure progresses, the amount of exertion required to produce dyspnea becomes progressively less until dyspnea may occur at rest.
b. Orthopnea refers to dyspnea that occurs in the recumbent position and is relieved by elevation of the head. Orthopnea results from volume pooling in the central vasculature during recumbency, which leads to increased cardiac volume and, in turn, to increased left ventricular filling pressure, pulmonary congestion, and the feeling of dyspnea. The physician may gauge the degree of orthopnea by noting the number of pillows the patient uses to sleep. However, it should be recognized that many patients sleep on more than one pillow out of habit, not because of breathlessness. Nocturnal cough, which has the same pathophysiology as orthopnea, may occur together with, or instead of, nocturnal dyspnea.
c. Paroxysmal nocturnal dyspnea is the occurrence of sudden dyspnea that awakens the patient from sleep. Like orthopnea, it occurs during recumbency as a result of pooling in the central vasculature, which increases left ventricular filling pressure. Paroxysmal nocturnal dyspnea may occur in the orthopneic patient who inadvertently slips off the pillows used to elevate the upper body. Usually, the patient awakens from sleep and feels the need to sit upright or to go to an open window for increased ventilation. The symptom usually subsides after the patient has been in the upright position for 5–20 minutes.
d. Nocturia develops in CHF as a result of increased renal blood flow when the patient is recumbent and asleep.
(1) During the day, when the skeletal muscles are active, limited cardiac output is shifted away from the kidney toward the skeletal musculature. The kidney interprets this reduction in blood flow as hypovolemia and becomes sodium avid via activation of the renin–angiotensin system.
(2) At night, when the patient is at rest, cardiac output is shifted toward the kidney, and diuresis ensues.
e. Edema. There are many causes of peripheral edema, several of which are noncardiac. Cardiac edema occurs when the systemic hydrostatic venous pressure is greater than the systemic oncotic venous pressure. Thus, cardiac edema is a sign of right-sided failure; it occurs because of the increased systemic venous pressure that results from right ventricular dysfunction.
2. Physical signs
a. Tachycardia. Increased heart rate occurs in heart failure due to increased release of catecholamines as a compensatory mechanism for maintaining cardiac output in the presence of decreased stroke volume. Catecholamines increase both the force and the rate of cardiac contraction. However, in chronic heart failure, adrenergic downregulation occurs, and heart rates over 100 bpm in the absence of arrhythmia are distinctly unusual.
b. Pulmonary rales. The increased left-ventricular filling pressure associated with CHF is referred to the left atrium and the pulmonary veins. The increased hydrostatic pressure produces transudation of fluid into the alveoli. As air circulates through the alveoli, crackling sounds (rales) are produced. Note that there are multiple causes of pulmonary rales; the mere presence of rales does not necessarily indicate CHF.




c. Cardiac enlargement. As the failing heart relies more and more on the Frank-Starling mechanism, it dilates and may develop eccentric hypertrophy. In the presence of cardiac enlargement, the point of maximal impulse (PMI) of the left ventricle is shifted downward and to the left. This shift is detected during a physical examination with the patient lying supine.
d. Fourth heart sound (S4). Patients in sinus rhythm and heart failure often have an S4 (atrial gallop). The S4 is produced as left atrial systole propels volume into the left ventricle. In CHF, the left ventricle is noncompliant and the S4 probably results from the reverberation of the blood ejected into the left ventricle. In elderly patients, however, an S4 may indicate reduced compliance of a stiff left ventricle as a result of aging rather than heart failure. The S4 also may be heard over the right ventricle in right ventricular failure.
e. Third heart sound (S3). An S3 (ventricular gallop), which occurs early in diastole, probably is the single most reliable sign of left heart failure revealed during physical examination. The S3 occurs during rapid filling of the left ventricle. Increased left atrial pressure (which propels the blood forward with increased force) and noncompliance of the left ventricle are two important factors in the production of this extra sound. Although an S3 is a reliable sign of heart failure in individuals older than age 40, a similar sound is a normal finding in young, healthy athletes.
f. Neck vein distention. The neck veins can be considered manometers attached to the right atrium and, as such, reflect right atrial pressure [ detection of central venous pressure is described online (Online Figure 1-1)].
To estimate central venous pressure in cm H2O, the patient's back is elevated or lowered so the point demarcating the distended from the nondistended portion of the neck vein can be discerned clearly. The vertical height is measured from this point to the manubrium. The average depth of the right atrium inside the chest cavity (5 cm) is added to the height of the neck vein. This sum approximates the right atrial pressure.
Online Figure 1-1 Assessment of jugular venous pressure should be done with the head of the bed at an angle of 30 degrees. The highest level of jugular venous pulsation should be noted and a line or rectangular object extended from this point parallel to the chest wall. Measure the height above the chest wall at the sternal angle and add 5 cm to account for the distance between the right atrium and the chest wall.
g. Hepatic enlargement. Elevated central venous pressure can lead to hepatic congestion, in turn causing hepatomegaly. On occasion, rapid hepatic enlargement may also cause liver tenderness.
h. Edema. Lower extremity and presacral edema occur in right-sided failure as increased venous pressure results in transudation of fluid into these areas. For edema to be attributable to CHF, distended neck veins indicative of elevated right-sided filling pressure also should be present.
i. Ascites. Transudation of fluid into the peritoneal space also may occur as a result of increased systemic venous pressure. When ascites is caused by CHF, the neck veins typically are elevated and the liver is distended from passive congestion.
E. Diagnosis
Management of CHF must focus on the cause of the heart failure, not simply on relieving the symptoms. Although a careful history and physical examination are the most important tools available in arriving at a diagnosis, in many cases a diagnosis may not be reached. In these instances, the following studies often are helpful:
1. The electrocardiogram (ECG) frequently is nonspecific. However, the presence of Q waves helps confirm that MI has been the cause of the CHF.
2. The chest radiograph is useful in demonstrating cardiac chamber enlargement and in documenting congestion in the lungs.
3. The echocardiogram is essential in identifying chamber enlargement and in quantifying left ventricular function and valvular function. The most commonly used descriptor of ventricular function is the ejection fraction. Ejection fractions between 55% and 76% are normal.
4. Doppler interrogation measures the direction and velocity of blood flow. This technique is useful for detecting blood flow moving in an abnormal direction, which is characteristic of valvular regurgitation and intracardiac shunts. In addition, Doppler interrogation can detect and quantify valvular stenoses by measuring how much velocity is necessary to maintain constant blood flow through a stenotic valve.
5. Radionuclide ventriculography is used to measure right and left ventricular ejection fraction. It is an excellent noninvasive procedure to use when it is necessary to quantify precisely the degree of systolic cardiac dysfunction.
6. During cardiac catheterization, intracardiac pressures, chamber size, valvular stenosis, valvular regurgitation, and coronary anatomy can be evaluated. Given the current accuracy of echocardiography, catheterization is performed principally for the evaluation of ischemia.
F. Therapy
1. Etiologic therapy. It is important, when possible, to direct treatment at the etiologic agent of CHF. For example, if aortic stenosis is the cause, aortic valve replacement is the most effective therapy.
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2. Systolic heart failure
a. Therapy shown to enhance survival and delay progression of the disease. Compensation for development of heart failure by increasing the neurohormones responsible for increasing cardiac contractility and heart rate can improve symptoms of heart failure in the short term. However, chronic stimulation leads to cardiac remodeling and decompensation (see I B 3). Blockade of these agents have been shown to reverse remodeling, improve mortality, and delay the progression of heart failure.
(1) Renin-angiotensin system blockade. Angiotensin-converting enzyme (ACE) inhibitors have been shown to have a mortality benefit. Because many vasodilators have failed to improve survival despite reducing afterload, properties of ACE inhibitors other than vasodilation are thought to be operative, namely reversal of remodeling. In patients who develop coughing due to ACE inhibitors, angiotensin receptor blockers (ARBs) may be substituted with similar efficacy. Additional blockade of the renin-angiotensin system, using spironolactone or eplerenone to block the final product of this system, aldosterone, is also beneficial in selected patients.
(2) خ²-Blocking agents. Because stimulation of the خ²-receptor increases the force of cardiac contraction, خ²-agonists have been used in the therapy of end-stage CHF. [See 2 b (3) (b)]. Paradoxically, cautious use of خ²-receptor antagonists has also been effective in reversing the same syndrome. The mechanism of action for this class of agents in the treatment of heart failure stems from protection of the heart from the toxic effects of prolonged exposure to the high levels of circulating catecholamines.




(3) Hydralazine and nitrates. The combination of hydralazine and nitrates used in class II and III heart failure has also been shown to improve mortality by decreasing preload and afterload and improving cardiac output. However, the mortality benefit with ACE-inhibitors is greater.
b. Symptomatic therapy. Although not shown to improve mortality, many drugs can improve the symptoms and morbidity of heart failure.
(1) Reducing afterload. Agents that cause arteriolar dilation reduce impedance of the outflow of blood from the left ventricle. By diminishing resistance to ejection, these agents cause cardiac output to rise because the left ventricle can eject more completely against a lower afterload. The net effect is increased cardiac output without a serious fall in blood pressure leading to symptomatic improvement. Several vasodilators are used in the treatment of CHF to reduce afterload, including ACE inhibitors, nitrates, and hydralazine.
(2) Reducing preload and left ventricular filling pressure. The increased preload resulting from volume retention in the ventricles is a compensatory mechanism that helps increase forward cardiac output by use of the Frank-Starling mechanism; however, an excessive increase in preload is associated with increased left ventricular and right ventricular filling pressures, which is responsible for symptoms of pulmonary and systemic congestion. Judicious reduction in filling pressures without excessive reduction in preload is indicated in the therapy of CHF.
(a) Diuretics reduce renal tubular absorption of sodium and water and increase the clearance of these substances from the body. The result is a reduction in central volume and in cardiac filling pressure.
(b) Vasodilators, which increase the capacity of the systemic venous system, transfer central volume to the periphery, thus reducing central preload and filling pressure. Nitrates and ACE inhibitors are effective preload-reducing vasodilators.
(3) Increasing the contractile state. Contractile dysfunction is the most common mechanism that produces heart failure; therefore, increasing the contractile state may result in symptomatic improvement.
(a) Cardiac glycosides (e.g., digoxin) increase the contractile state by impeding the Na+/K+-ATPase-controlled intracellular pump. This results in the net influx of calcium into the myocardium, which increases contractile strength.
(b) خ²-Adrenergic agonists (catecholamines, e.g., dobutamine) increase contractile function by increasing the production of cyclic adenosine monophosphate (cAMP), which results in greater myocardial calcium release. They are administered as a continuous infusion in end-stage heart failure as a temporizing measure.
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(c) Phosphodiesterase inhibitors (e.g., milrinone) increase contractile function by inhibiting the breakdown of cAMP. Similar to خ²-adrenergic agonists, they are also administered as a continuous intravenous infusion in end-stage heart failure for short-term use.




3. Diastolic heart failure. Unlike systolic heart failure, no medical treatment is available that reduces mortality in diastolic heart failure. Treatment is aimed at symptomatic relief.
a. Diuretics. Diuretics are the mainstay of treatment. By reducing ventricular volume they lower ventricular pressure and reduce the symptoms of congestion. The dosing must be carefully regulated, however, as reduced ventricular volume also lowers stroke volume and cardiac output. The optimum range would be one that prevents excess dyspnea and hepatic congestion but allows for adequate cardiac output.
b. Induction of bradycardia. Slowing the heart rate increases the time available for ventricular filling. خ²-blockers and nondihydropyridine calcium channel blockers (verapamil and diltiazem) are used to cause relative bradycardia.
c. Relief of ischemia. In patients with coronary disease, ischemia impairs the active relaxation phase of diastole by impairing calcium reuptake by the sarcoplasmic reticulum. Thus, standard therapy for angina is also effective in improving diastolic dysfunction. [See III A 5 a (4)].
d. Maintenance of sinus rhythm. The normal atrial “kickâ€‌ afforded by atrial contraction improves the efficiency of ventricular filling that is lost in atrial fibrillation. Thus, every effort should be made to maintain sinus rhythm (see II).
4. Nonpharmacologic therapy
a. Cardiac resynchronization. Many patients with advanced heart failure develop electrical conduction disturbances, including left bundle branch block, which delays the impulse signaling contraction from getting to the left ventricle. This delay discoordinates contraction, in turn causing further reduction in cardiac output. Insertion of a pacemaker to resynchronize contraction in patients with conduction delays improves functional capacity and quality of life and decreases mortality.
b. Physical conditioning. An important adjunct to the medical treatment of CHF, physical conditioning permits the peripheral tissues to use cardiac output more efficiently. Thus, the patient experiences an increase in tolerance to physical activity without an increase in cardiac output.
c. Cardiac transplantation may offer an improved quality of life to selected patients in whom control of CHF is not possible and prognosis is poor. Currently, approximately 75% of patients undergoing cardiac transplantation achieve a 5-year survival rate. The paucity of cardiac donors is the primary factor limiting the use of this therapy. Left ventricular assist devices (LVADs) may provide a bridge to transplantation.
5. Pulmonary edema is the most extreme example of CHF in which profound transudation of fluid into the pulmonary alveoli occurs because of a high left ventricular filling pressure. The result is impaired oxygenation and, if untreated, death. The goal of therapy is to improve oxygenation, to reduce left ventricular filling pressure, and to increase forward cardiac output.
a. Oxygen should be administered by facemask because patients in pulmonary edema are so dyspneic that they breathe primarily through their mouths.
b. Diuretics. Furosemide is likely the single most commonly used medication in the treatment of acute pulmonary edema. This rapid-acting loop diuretic promotes an immediate diuresis in most cases.
c. Morphine sulfate. This opioid reduces patient anxiety, which may help relieve the arterial vasoconstriction often present in acute pulmonary edema. This, in turn, helps increase forward cardiac output. Morphine is also a venodilator; therefore, it reduces central volume and left ventricular filling pressure.
d. Other vasodilators. Nitroglycerine (administered sublingually or intravenously) or nitroprusside (administered intravenously) is often effective in treating pulmonary edema when other therapies fail. Nesiritide, an analog of B-type natriuretic hormone that causes venous and arteriolar vasodilation may also be beneficial. However, the potent vasodilating ability of these drugs requires that blood pressure be monitored constantly during administration to avoid hypotension.
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e. Intravenous positive inotropic agents (dobutamine, milrinone) may be used if peripheral perfusion is compromised. They will help to increase contractility and improve cardiac output and also have some afterload reduction properties that will allow increased forward flow in acute decompensation.
f. Intubation and positive-pressure ventilation. If the patient's oxygenation does not improve rapidly with the previously noted therapies, intubation or positive-pressure ventilation may be necessary to provide mechanical ventilation and improve oxygenation.




g. Invasive hemodynamic monitoring. Most cases of pulmonary edema resolve quickly, making hemodynamic monitoring unnecessary. However, in cases of refractory pulmonary edema with severe cardiac compromise, exact knowledge of intracardiac filling pressure may be useful in guiding therapy. Hemodynamic monitoring via Swan-Ganz catheterization provides this information so that optimal filling pressure and cardiac output may be obtained.