CONGESTIVE HEART FAILURE

CONGESTIVE HEART FAILURE

  1. 1
    Current Diagnosis

    • Identify the presence of characteristics associated with left ventricular systolic dysfunction.

    •   Document the degree of left ventricular dysfunction by imaging.

    •   Ascertain clinical volume and perfusion status.

    • Determine the cause of cardiac dysfunction, if possible, with special attention to coronary artery disease.

  2. 2
    Current Therapy

    • Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blocking agents, β-blockers, and aldosterone receptor antagonists improve survival and are integral to the treatment plan.

    • Use nonpharmacologic therapy along with medical therapy. Sodium and fluid restriction, smoking and alcohol cessation, stress reduction and treatment of depression, and exercise and weight loss, all improve symptoms and reduce hospitalization.

    • Treat comorbidities that exacerbate the heart failure state (e.g., hypertension, arrhythmias, sleep-disordered breathing).

    • Consider interventions to treat concomitant structural heart disease, such as coronary revascularization, mitral valve surgery,

    arrhythmia treatment, and cardiac resynchronization therapy.

    • Refer patients with refractory disease early to an advanced heart failure center for implantation of a ventricular assist device or cardiac transplantation.

    • Provide palliative care for patients who are not candidates for advanced heart failure therapy.

    Despite the decrease in the incidence of other circulatory conditions, or perhaps rather because of improvements in the management of related circulatory conditions, heart failure represents the major clinical challenge facing all clinicians who manage patients with cardiac disease today. It continues to be the most common cause of hospitalization for patients older than 65 years of age and results in the expenditure of almost 40 billion dollars annually in the United States. Heart failure is a chronic degenerative disease; if left untreated, it will result in progressively deteriorating functional capacity and premature death. For optimal patient outcome, it must be managed aggressively and proactively.

    This discussion focuses exclusively on heart failure resulting from systolic dysfunction, the management of which has been most extensively studied. However, it is now recognized that diastolic dysfunction, particularly of the left ventricle (LV), is an increasingly common condition, particularly in the elderly, and can result in similar symptoms. The optimal management of this vexing condition has yet to be determined with certainty, although there are ongoing efforts to establish evidence-based approaches to this disease as well.

     

  3. 3
    Definition

    Although heart failure is defined traditionally as a condition in which the heart is unable to pump enough blood to satisfy the metabolic demands of the body, this expression has little direct clinical relevance. On a practical level, heart failure is perhaps better thought of as a condition involving abnormality of cardiac emptying or filling associated with increased intracardiac filling pressures or decreased cardiac output, exercise intolerance, frequent arrhythmias, and early death. The abnormalities in cardiac structure and function typically precede, often by many years, the onset of symptoms. Therefore, to most effectively treat this disease, it is critically important to affirmatively seek out and diagnose cardiac dysfunction before overt symptoms develop.

  4. 4
    History and Physical Examination

    In the United States, the most common cause of cardiac dysfunction is coronary artery disease due to atherosclerotic cardiovascular disease (ASCVD). Because ASCVD is typically a systemic rather than a localized phenomenon, any suggestion of atherosclerotic disease in any vascular bed should prompt a thorough cardiac evaluation as well.

    Exercise intolerance due to dyspnea or fatigue is the most common presenting symptom in patients with heart failure, although other symptoms may also be present, such as orthopnea, paroxysmal nocturnal dyspnea, dependent edema, or palpitations. Many of these symptoms are nonspecific, and a high index of suspicion is necessary to diagnose underlying heart failure. Other historical findings that should heighten the suspicion for underlying heart failure include the presence of predisposing conditions such as hypertension, diabetes mellitus or metabolic syndrome, obesity, prior exposure to known cardiotoxic agents, ASCVD, and a family history of premature ASCVD, documented cardiomyopathy, or unexplained premature death. When such characteristics are present, particularly in concert with other suggestive findings from the history or physical examination, they should prompt a more directed evaluation, including strong consideration of imaging studies to measure cardiac function.

    Physical examination findings are often subtle, especially if the underlying disease has been progressing insidiously for an extended period before presentation, as is often the case. The vital signs may be normal, although the heart rate is frequently elevated due to the compensatory hyperadrenergic state associated with untreated cardiac dysfunction. Tachycardia, especially sinus tachycardia, should always be considered a symptom of underlying systemic disease and should spur further investigation. Chronic arterial hypertension is a frequent cause of heart failure, particularly in non-Caucasian populations; it often persists despite substantial degrees of cardiac dysfunction and should prompt additional cardiac evaluation. Increased central venous pressure may manifest as an elevation in measured jugular venous pressure or as systemic edema; however, the latter symptom is frequently nonspecific, being often seen in older individuals with venous insufficiency, obesity, or sedentary lifestyles. In contrast, visceral edema, when detected, is more specifically associated with increased central venous pressure. The carotid impulse is typically normal, although in patients with severe degrees of LV systolic dysfunction the impulse may be less dynamic than normal. Asymmetrical arterial pulses or bruits suggest systemic atherosclerotic disease, including likely coronary artery disease.

    The presence of pulmonary rales, although classically described in patients with cardiogenic or noncardiogenic intraalveolar pulmonary edema, is typically seen only with new and rapid onset of cardiac dysfunction, the prototype of which is acute myocardial infarction with associated LV dysfunction. The compensatory potential of pulmonary venous and lymphatic drainage is such that more insidious, slowly developing cardiac dysfunction is most often not associated with intraalveolar fluid; for this reason, the lung fields may be clear on auscultation or even on radiographic examination. In patients with disease of longer standing, in whom one or both ventricular chambers has had a chance to dilate, the apical (LV) impulse may be laterally displaced; in more severe degrees of LV dysfunction, it may not be palpable at all.

    The heart sounds are often subtly decreased in intensity due to decreased LV contractile power, but they remain physiologic in the absence of conduction disease. With an acute onset, gallops may be present, particularly an early diastolic sound (S3); however, a slowly dilating dysfunctional heart may retain a substantial degree of compliance, lessening the chance of an audible filling sound even if LV filling pressures are elevated. In more advanced stages of disease, evidence of impaired peripheral or end-organ perfusion may be present, such as jaundice, cool extremities, delayed capillary refill, or decreased intensity of peripheral pulses. These symptoms are typically accompanied by unequivocal symptoms or other suggestive cardiopulmonary signs of cardiac disease.

  5. 5
    Laboratory and Diagnostic Procedures

    The chest radiography and 12-lead electrocardiography are simple, rapid, and low-risk procedures that can frequently add to the initial diagnostic impression. Depending on the degree of cardiac chamber dilation, the radiographic cardiac silhouette may be variably affected. The LV silhouette is most often enlarged in patients with slowly progressive disease, because the LV chamber has had a opportunity to dilate significantly, whereas in instances of acute onset (e.g., acute myocardial infarction without antecedent disease), the LV may appear normal sized. Patients with chronic valvular or coronary atherosclerotic disease may also demonstrate calcification that can be detected on plain chest films. The presence of intraalveolar pulmonary edema typically is easily detected on standard chest radiographs, although pulmonary interstitial edema can be much more subtle and difficult to discern. More commonly, in patients with chronic LV dysfunction and resultant secondary postcapillary pulmonary hypertension, the central pulmonary arteries are dilated and more prominent than normal. However, patients with chronically elevated left atrial pressure may not manifest traditional evidence of decompensated hemodynamics (e.g., pulmonary rales on examination or infiltrative changes on chest radiography), due to increased pulmonary lymphatic capacity and thickened alveolar-capillary interface.

    Many electrocardiographic abnormalities associated with heart failure are nonspecific. Because the most common cause of heart failure is coronary artery disease, any indication of ongoing myocardial ischemia or pattern of prior infarction or injury should prompt further intensive evaluation. The presence of arrhythmias, especially those of ventricular origin, also suggests underlying organic cardiac disease.

    Standard laboratory results are typically nonspecific but in more advanced cases can yield findings of impaired end-organ perfusion, such as elevations in serum urea nitrogen, creatinine, or liver transaminases. Patients with chronic heart failure may also be anemic and may manifest other chemical evidence of malnutrition or chronic disease. However, patients who have progressed to this degree of impairment typically have a host of other symptoms and signs that point unequivocally to a severe heart failure syndrome. More recently, the presence of elevated levels of plasma brain natriuretic peptide has been associated with cardiac disease in patients with dyspnea. This test has gained increasing popularity as an initial diagnostic tool, although its utility in the diagnosis of nondecompensated heart failure remains to be fully elucidated.

    Transthoracic echocardiography has emerged as the most common method of definitively diagnosing LV systolic dysfunction. It is typically available at short notice in most clinical settings and can provide a wealth of structural and functional data in a noninvasive fashion. After the history, physical examination, and standard laboratory studies discussed earlier, echocardiography should be the next diagnostic study performed if cardiac dysfunction is suspected. Although a complete review of the echocardiographic findings typically seen in heart failure is beyond the scope of this discussion, standard studies can establish the diagnosis, provide clues to the underlying etiology, and help guide initial therapy. Moreover, an echocardiographic study obtained at initial diagnosis establishes an important baseline data set to which subsequent studies can be compared to gauge the efficacy of therapy and assist in determining prognosis.

    Once the diagnosis of LV systolic dysfunction has been established, an effort should be made to determine the underlying etiology, because it may dictate therapy. Cardiac catheterization, including coronary angiography and right heart catheterization for hemodynamic assessment, should be strongly considered in all patients with newly diagnosed LV systolic dysfunction, because noncontracting or poorly contracting myocardium, if ischemic or hibernating (viable but hypoperfused), may regain contractile strength after proper revascularization. In addition, hemodynamic data obtained during catheterization can assist in guiding medical and surgical therapy for heart failure; moreover, like other initial imaging studies, it can provide valuable baseline information for future comparison. The use of supplemental catheter-based procedures such as endomyocardial biopsy remains controversial, predominantly because of the risk associated with these procedures and the variable sensitivity of routine endomyocardial biopsy in the diagnosis of infiltrative myocardial processes such as myocarditis. In specific cases in which the index of suspicion for certain infiltrative diseases is particularly high, biopsy may be used to confirm the diagnosis. If this procedure is employed, it is important that a sufficient volume and distribution of specimens be collected to optimize diagnostic yield, and that the procedure be performed by an experienced operator to minimize the risk of complications.

    Provocative testing (e.g., treadmill exercise testing), with or without supplemental imaging modalities such as radionuclide perfusion imaging, is less useful in patients with already established cardiac dysfunction, although the response to exercise testing in a patient with previously undiagnosed heart failure can be revealing. In addition to the likely finding of decreased exercise performance, the blood pressure and heart rate response to increasing exercise demand may be impaired. Further scrutiny (e.g., cardiac catheterization) should follow the demonstration of inducible or fixed myocardial perfusion defects with exercise or of a decreased left ventricular ejection fraction (LVEF). Resting radionuclide ventriculography can also be employed to determine global LV systolic function (LVEF) in patients in whom effective imaging cannot be achieved with echocardiography. Exercise testing with expired gas analysis may be used to determine peak exercise oxygen consumption and has been demonstrated to correlate with prognosis in patients with chronic heart failure. However, its value when measured before optimization of therapy in patients with newly diagnosed heart failure is uncertain.

  6. 6
    Classification

    Patients with heart failure are classified according to their self- described degree of functional impairment and assigned a New York Heart Association (NYHA) functional class (Table 1). Although it is subjective on the part of both the patient and the interviewer, this classification has long been used for gross estimation of functional status. The NYHA class has been reported to correlate with mortality risk, but its ability to discriminate among patients and its relevance in an individual patient over time remains questionable.

    Table 1

    New York Heart Association Functional Classification of Chronic Heart Failure

     

    Class* Symptoms
    I No perceived limitation of physical activity
    II A/B Symptoms with moderate physical exertion
    III A/B Symptoms with low levels of physical exertion (i.e., activities of daily living)
    IV Resting symptoms

    *  Abbreviations: A = early stage; B = late  stage.

    Heart failure can also be classified by evolutionary stage (Table 2), based predominantly on management strategy (pharmacologic, nonpharmacologic, or surgical).

    Table 2

    Stages of Heart Failure

     

    Stage Description                                                                                                Examples
    A High risk for development of HF due to presence of conditions strongly     associated with HF development

    No identified structural or functional abnormalities of the pericardium,    myocardium, or cardiac valves

    No history of signs or symptoms of HF

    Systemic hypertension Coronary artery disease Diabetes mellitus

    Prior cardiac drug therapy Prior alcohol abuse

    Family history of cardiomyopathy

    B Presence of structural heart disease strongly associated with HF development

    No history of signs or symptoms of HF

    LV hypertrophy or fibrosis LV dilation or dysfunction

    Asymptomatic valvular heart disease Previous  myocardial infarction

    C Current or prior symptoms of HF with underlying structural heart disease Dyspnea or fatigue from LV systolic dysfunction
    Asymptomatic patient undergoing treatment for prior     symptoms of HF
    D Advanced structural heart disease and marked symptoms of HF at rest     despite maximal medical therapy

    Requirement  for  specialized interventions

    Frequent HF hospitalizations and cannot be discharged

    In hospital awaiting heart transplantation Home continuous inotropic or mechanical support

    In hospice setting for HF management

    Abbreviations: HF = heart failure; LV = left  ventricular.

  7. 7
    Management of Heart Failure

    Nonpharmacologic Therapy

    Nonpharmacologic heart failure therapy reduces symptoms and improves functional capacity and quality of life. It is vital to provide ongoing patient and family education about dietary restrictions, avoidance of unhealthy behaviors, stress reduction, and energy conservation. Participation in an exercise program to combat deconditioning and promote weight loss improves functional capacity. Close outpatient monitoring, including a heart failure disease management program, improves compliance and reduces hospitalization. Identification and treatment of sleep-disordered breathing, present in as many as 40% of patients with heart failure, can dramatically improve symptoms.

    Pharmacologic Therapy

    Angiotensin-converting enzyme (ACE) inhibitors and selected β- blockers have been shown in randomized clinical trials to improve symptoms and survival in patients with LV systolic dysfunction and are the cornerstones of medical therapy for heart failure. Angiotensin receptor blocking agents, or the combination of hydralazine (Apresoline)1 and a nitrate, provide similar (but not superior) benefit in patients with contraindications to use of ACE inhibitors. Digoxin (Lanoxin) provides no survival benefit but improves symptoms and hemodynamics in patients with atrial fibrillation and in those patients who remain symptomatic on optimal doses of vasodilators and may also decrease risk for hospitalization. Diuretics provide symptomatic relief if volume overload is present. Antialdosterone agents should be prescribed for all patients with symptomatic LV dysfunction after acute myocardial infarction. For all other heart failure patients, spironolactone was previously reserved for those who remained symptomatic despite optimal doses of vasodilator and β-blocker therapy, but new data suggests that all symptomatic patients benefit from antialdosterone therapy (NYHA functional class II-IV symptoms). Antiarrhythmics should be used only for symptomatic atrial or ventricular arrhythmias, because they may be proarrhythmic. Table 3 describes the use of various medications in patients with heart failure.

    Table 3

    Heart Failure Medications

    Abbreviations: ACEI = angiotensin-converting enzyme inhibitor; NYHA = New York Heart Association.

    1  Not FDA approved for this indication.

    Parenteral agents for heart failure, including dobutamine (Dobutrex), milrinone (Primacor), and nesiritide (Natrecor), are used primarily in the inpatient setting to treat acutely decompensated heart failure and are beyond the scope of this discussion. However, it should be noted that intravenous inotropic agents (dobutamine, milrinone) have been shown in uncontrolled trials to improve symptoms and quality of life but to increase mortality. Therefore, they should be used only for short periods, at the lowest possible doses, and in a monitored setting. Short-term inpatient use of nesiritide also improves symptoms.

    Device Therapy

    Implantable cardioverter-defibrillators (ICDs) have been shown in randomized clinical trials to improve survival in heart failure patients with ischemic or nonischemic cardiomyopathy. Indications for implantation are an LVEF of less than 30% and mild-to-moderate symptoms of heart failure in a patient whose anticipated survival exceeds 1 year or ischemic cardiomyopathy and an LVEF of less than 35% regardless of symptoms.

    Cardiac resynchronization therapy, with or without implantation of a cardioverter-defibrillator, has been shown in randomized clinical trials to improve symptoms and survival in selected heart failure patients when added to optimal medical heart failure therapy. One third of heart failure patients with low LVEF and moderate to severe symptoms have ventricular dyssynchronous contraction, which is associated with increased mortality. Indications for cardiac resynchronization therapy include an LVEF lower than 35%, NYHA functional class II-IV symptoms, and a QRS duration of greater than 120 msec, which is a marker for ventricular dyssynchrony.

    Therapy for Advanced Heart Failure

    Patients with heart failure that has become refractory to medical and resynchronization therapy should be referred to an advanced heart failure center experienced in the surgical treatment of heart failure.

    Surgical therapies improve symptoms and survival and are now considered the standard of care for heart failure patients in whom standard medical therapy has failed.

    Heart transplantation is the only definitive surgical therapy for advanced heart failure, but alternative surgical approaches include coronary revascularization, valve surgery, LV reconstruction, and the use of ventricular assist devices. In patients with ischemic cardiomyopathy and hibernating myocardium, coronary revascularization improves LV function, functional capacity, and survival, compared with medical therapy. Mitral valve repair or replacement can improve symptoms in selected patients. Ventricular reconstruction may benefit patients with LV aneurysms or recurrent ventricular arrhythmias.

    Left ventricular assist devices are implantable pumps that work in parallel with the native heart to provide short-term mechanical circulatory support in patients who are expected to recover heart function (e.g., patients with myocarditis, after acute myocardial infarction, after coronary artery bypass grafting) and in patients awaiting heart transplantation. In addition, these devices are approved as a permanent alternative to transplantation (destination therapy) in patients for whom heart transplantation is not an option. Early identification and referral of patients who might benefit from these therapies is essential for the best surgical outcomes.

  8. 8
    Common Management Errors

    Heart failure management errors result in increased hospitalizations and mortality. ACE inhibitors remain underused, despite evidence from clinical trials in more than 10,000 patients. Although Losartan (Cozaar)1 is commonly used for the patient who cannot tolerate ACE inhibitors, only two members of the angiotensin receptor blocker class, valsartan (Diovan) and candesartan (Atacand), have been shown in clinical trials to provide benefit. The combination of hydralazine (Apresoline)1 and isosorbide dinitrate (Isordil Titradose)1 is also underused, despite evidence that these drugs improve exercise tolerance and survival.

    Only three β-blockers, metoprolol succinate (Toprol XL), carvedilol (Coreg), and bisoprolol (Zebeta),1 have been shown in trials to improve symptoms and survival in heart failure patients. Metoprolol tartrate (Lopressor)1 and atenolol (Tenormin)1 are commonly used as substitutes, even though there are no data supporting their use. β- Blockers are commonly started too early in the course of heart failure, when the patient is experiencing decompensation and fluid overload, and lead to further decompensation. Care should be taken to fully optimize volume status and unloading agents (e.g., vasodilators), before initiating and titrating β-blockers.

    Patients may receive drugs that worsen the heart failure state, such as first-generation calcium channel blockers, nonsteroidal antiinflammatory drugs, cyclooxygenase 2 inhibitors, and antiarrhythmic drugs. Intravenous inotropic therapy or nesiritide (Natrecor) may be used when the patient would be better served by optimization of his or her oral heart failure regimen. Patients are commonly overdiuresed, which results in symptomatic hypotension and makes initiation and titration of vasodilators and β-blockers difficult.

    Many physicians fail to utilize nonpharmacologic therapies as an adjunct to drug therapy. In addition, lack of education and close follow-up can undermine the best medical regimen. Physicians also commonly fail to refer patients who need advanced heart failure therapy, or refer them too late, when end-organ damage is irreversible.

  9. 9
    References

    Bardy G.H., Lee K.L., Mark D.B., et al. Amiodarone or an implantable cardioverter defibrillator for congestive heart failure. N Engl J Med. 2005;352:225–237.

    Cleland J.G., Daubert J.C., Erdmann E., et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005;352:1539–1549.

    Cohn J.N., Archibald D.G., Ziesche S., et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure: Results of a Veterans Administration Cooperative Study. N Engl J Med. 1986;314:1547–1552.

    Cohn J.N., Johnson G., Ziesche S., et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med. 1991;325:303–310.

    The Digitalis Investigation Group. Effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med.

    1997;336:525–533.

    Hunt S.A., Abraham W.T., Chin M.H., et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). Developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation; endorsed by the Heart Rhythm Society. Circulation. 2005;112:e154–235.

    International Registry for Heart and Lung Transplantation (ISHLT Registry). Available at: https://www.ishlt.org/registries/heartLungRegistry.asp. July 16, 2015 Accessed.

    Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF). Effect of metoprolol CR/XL in chronic heart failure. Lancet. 1999;353:2001–2007.

    Moss A.J., et al. Cardic resynchronization therapy for the prevention of heart failure events. N Engl J Med.

    2009;361:1329–1338.

    Packer M., Bristow M.R., Cohn J.N., et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group. N Engl J Med. 1996;334:1349–1355.

    Pitt B., Zannad F., Remme W.J., et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999;341:709–717.

    Rose E.A., Gelijns A.C., Moskowitz A.J., et al. Long-term mechanical left ventricular assistance for end-stage heart failure. N Engl J Med. 2001;345:1435–1443.

    The SOLVD Investigators. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med. 1992;327:685–691.

    Zannad F., et al. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med. 2011;364:11–21.

    1  Not FDA approved for this  indication.

    1  Not FDA approved for this  indication.

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