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Heart Failure, Chronic
Jeffrey Shih, MD
David DeNofrio, MD
image BASICS
  • Heart failure (HF) is the condition resulting from inability of the heart to fill and/or pump blood sufficiently to meet tissue metabolic needs. Alternatively, HF may occur when adequate cardiac output can be achieved only at the expense of elevated filling pressures. It is the principal complication of heart disease.
  • HF is the preferred term over congestive heart failure because patients are not always congested (fluid overloaded).
  • HF may involve the left heart, the right heart, or be biventricular. The New York Heart Association (NYHA) classification is a subjective grading scale used for classifying patients with HF: NYHA I: asymptomatic; NYHA II: symptomatic with moderate exertion; NYHA III: symptomatic with mild exertion and may limit activities of daily living; NYHA IV: symptomatic at rest. For acute HF, see “Heart Failure, Acutely Decompensated.”
The annual direct and indirect cost of HF in the United States is ~$34.4 billion.
In the United States, 550,000 new cases diagnosed annually with >250,000 deaths per year.
  • ˜5.7 million people in the United States have HF; <1% in those age <50 years, increasing to 10% of those age >80 years
  • Primarily a disease of the elderly; 75% of hospital admissions for HF are for persons >65 years of age.
Two physiologic components explain most of the clinical findings of HF and result in classifications of patients in four general categories:
  • HF with reduced ejection fraction (HFrEF) or systolic HF: an inotropic abnormality, often due to myocardial infarction (MI) or dilated cardiomyopathy, resulting in diminished systolic emptying (ejection fraction [EF] ≤40%)
  • HF with preserved ejection fraction (HFpEF) or diastolic HF: a compliance abnormality, often due to hypertensive cardiomyopathy, in which the ventricular relaxation is impaired (EF ≥50%)
  • Borderline HFpEF (EF 41-49%): mild systolic dysfunction but clinically behaves like HFpEF
  • Improved HFpEF (EF >40%): previously HFrEF but with improvement in systolic function
  • Patients with systolic dysfunction may also have diastolic dysfunction.
  • Most common etiologies: coronary artery disease (CAD)/MI and hypertension (HTN)
  • Myocarditis and cardiomyopathy (CM): alcoholic, viral, long-standing HTN, drugs (e.g., chemotherapeutic agents), muscular dystrophy, infiltrative (e.g., amyloidosis, sarcoidosis), postpartum state, infectious (e.g., Chagas disease, HIV), hypertrophic CM (HCM), inherited familial dilated CM, left ventricular noncompaction
  • Valvular and vascular abnormalities: any valvular stenosis or regurgitation, rheumatic heart; renal artery stenosis, usually bilateral, may cause recurrent “flash” pulmonary edema, especially in setting of severe chronic HTN
  • Chronic lung disease and pulmonary HTN (cor pulmonale)
  • Iatrogenic volume overload (requires extreme overload in patients with normal hearts and kidneys)
  • Arrhythmias (atrial fibrillation and other tachyarrhythmias, high-grade heart block)
  • Miscellaneous: high-output states: hyperthyroidism, anemia; cardiac depressants (&bgr;-blocker overdose), stress-induced
  • Idiopathic: 20-50% of idiopathic dilated cardiomyopathies are familial.
  • HF is progressive—manifested by the remodeling (altered heart geometry) process.
Multiple genetic abnormalities responsible for a variety of phenotypes have been identified (HCM, arrhythmogenic right ventricular [RV] dysplasia, left ventricular [LV] noncompaction, dilated CM). Consider genetic screening for first-degree relatives of HCM and arrhythmogenic RV dysplasia.
For development of HF: CAD/MI, HTN (80% of cases of HF in the United States caused by either CAD or HTN), valvular heart disease, diabetes mellitus, cardiotoxic medications (e.g., anthracyclines, tyrosine-kinase inhibitors, TNF-&agr; inhibitors), obesity, older age
Control HTN and other risk factors. Thiazide diuretics and angiotensin-converting enzyme inhibitors (ACE-I) are superior to other agents in preventing development of HF.
Sudden cardiac death and progressive pump failure are the leading causes of death. Most patients have >5 comorbid medical conditions and take >5 medications.
  • Increased filling pressures: rales (crackles) and sometimes wheezing, peripheral edema, S3 gallop, hepatomegaly, jugular venous distension, hepatojugular reflux, ascites
  • Remodeling: enlarged or displaced point of maximal impulse
  • Poor cardiac output: hypotension, pulsus alternans, tachycardia, narrow pulse pressure, cool extremities, cyanosis
Simple dependent edema, pulmonary embolism, exertional asthma, cardiac ischemia, asthma/COPD, constrictive pericarditis, nephrotic syndrome, cirrhosis, venous occlusive disease with subsequent peripheral edema, high-output states: anemia, sepsis, hyperthyroidism, lymphedema, tamponade
Diagnosis should be primarily clinical, with laboratory data as adjunctive and indicative of complications.
Initial Tests (lab, imaging)
  • &bgr;-type natriuretic peptide (BNP) and N-type pro-BNP (NT-BNP) helpful in the acute setting to differentiate the cause of dyspnea (BNP <100 essentially rules out HF; most dyspneic patients with HF have a BNP >400) (1)[A]. Other, non-HF conditions, such as pulmonary embolism, renal failure, and acute coronary syndromes, may cause elevated BNP. Obesity may lower BNP levels. The use of BNP-guided therapy in chronic HF and acutely decompensated HF is not well-established.
  • Lab findings include respiratory alkalosis, mild azotemia, decreased ESR, proteinuria (usually < 1 g/day), elevated creatinine (cardiorenal syndrome), dilutional hyponatremia (poor prognosis), hyperuricemia, and hyperbilirubinemia.
  • Chest x-ray (changes lag clinical symptoms by up to 6 hours): increased heart size, vascular redistribution (cephalization) with “butterfly” pattern of pulmonary edema, interstitial and alveolar edema, Kerley B lines, and pleural effusions. Findings of pulmonary edema may be absent in long-standing HF.
Diagnostic Procedures/Other
Determination of left ventricular ejection fraction (LVEF) is critical to proper diagnosis and management:
  • Echocardiogram is the most useful test to determine LVEF, RV function, diastolic dysfunction, ventricular size, wall thickness, and valvular abnormalities. May be repeated if change suspected in underlying cardiac status
  • Nuclear imaging to estimate ventricular sizes, assess for ischemia or infarction and systolic function
  • Cardiac MRI can be considered in select circumstances: suspicion of cardiac sarcoidosis, arrhythmogenic RV CM, acute myocarditis, amyloidosis, and hemochromatosis. It is also useful for differentiating restrictive CM and constrictive pericarditis.
  • Cardiac catheterization is important for excluding CAD as an etiology in the setting of risk factors.
  • Endomyocardial biopsy should not be performed routinely, only in special circumstances (e.g., suspected giant cell myocarditis) that may change therapy (1)[C].
Test Interpretation
Cardiac pathology depends on underlying etiology.
Correct and treat risk factors for HF. The treatment of chronic HF is focused on improving hemodynamics, relieving symptoms, and blocking the neurohormonal response to hopefully improve survival.
Diuretics are used initially in fluid overload acute HF. The addition of ACE-I and aldosterone antagonists can be added at any time. Once acute HF is stabilized, a &bgr;-blocker should be started. Avoid nonsteroidal anti-inflammatory drugs (NSAIDs), which markedly worsen HF. Avoid use of diltiazem and verapamil in patients with systolic dysfunction as they may increase mortality and have negative inotropic effects.
First Line
  • ACE-I: used to decrease afterload. Shown to increase survival, improve symptoms and overall

    exercise capacity in patients in all NYHA classifications; benefit greatest for patients with systolic dysfunction and post-MI. Number needed to treat (NNT) ˜25 per year for mortality. All ACE-I considered equally effective. Initiate at low doses and titrate as tolerated to target doses.
  • Angiotensin receptor blockers (ARBs) are indicated for those who are intolerant to ACE-I. They are probably slightly less effective than ACE-I. Avoid combination of ACE-I and ARB.
  • &bgr;-Blockers: used in systolic or diastolic HF (Note: initiate in hemodynamically stable/compensated patients at low dose and titrate upward slowly); NNT = 25 for mortality. Mortality decreased in systolic HF. Evidence for titration to heart rate rather than specific dose (1)[A].
    • Carvedilol: 3.125 mg PO BID to a target of 25 mg PO BID; metoprolol succinate extended release: 12.5 mg/day PO to a target of 200 mg/day PO or bisoprolol 1.25 to 10 mg once daily (currently not FDA approved for the treatment of HF)
  • Diuretics are helpful to manage volume overload/reduce preload.
    • Furosemide (Lasix): 20 to 320 mg/day IV/IM/PO divided dose; bumetanide (Bumex): 0.5 mg to 10 mg/day IV/PO divided dose; torsemide (Demadex): 10 to 200 mg/day PO divided dose (1)[C]
    • Metolazone (Zaroxolyn): 2.5 to 20 mg/day PO divided dose; hydrochlorothiazide: 12.5 to 100 mg/day PO divided dose; chlorothiazide (Diuril): 250 to 2,000 mg/day IV/PO divided dose
    • Spironolactone, eplerenone (improve mortality when added to standard therapy in NYHA class II-IV + EF <35%): spironolactone 12.5 to 25 mg/day PO; maximum 50 mg/day PO; eplerenone 25 to 50 mg/day. Caution regarding hyperkalemia and chronic kidney disease (CKD) (1)[A]
  • Digoxin reduces symptoms but has not clearly shown any positive effect on mortality: In patients with preserved renal function (creatinine clearance >50 mL/min), the recommended dose is 0.125 mg/day. Levels lower than used for atrial fibrillation are effective and safer (1)[B].
  • The combination of hydralazine (75 mg/day divided BID or TID) and isosorbide dinitrate (40 mg QID) is effective for African Americans (1)[A] or if unable to take ACE-I or an ARB (1)[B].
  • Ivabradine (Corlanor) is FDA approved to reduce hospitalization from worsening HF based on the SHIFT trial (2). Ivabradine is contraindicated in ADHF, hypotension (<90/50 mm Hg), severe hepatic impairment, pacemaker-dependence, bradyarrhythmias, or strong CYP3A4 inhibitors. It should not be administered to patients that are currently in atrial fibrillation and should be discontinued if atrial fibrillation develops (2)[A].
  • Sacubitril/valsartan (Entresto) was approved by the FDA in July of 2015. It is indicated to reduce the risk of CV death and HF hospitalizations in patients with NYHA class II-IV symptoms due to HFrEF based on the PARADIGM HF trial. This medication is used in place of an ACE inhibitor or ARB and in conjunction with other HF therapies (3)[A].
  • Anticoagulation is not recommended in patients with HFrEF unless there are other indications such as atrial fibrillation, cardioembolism, or intracardiac thrombus (4)[A].
  • In diastolic HF, no medical therapy has improved survival (1,5)[A]. ARBs and spironolactone can be used to potentially reduce hospitalizations (1)[A], (6)[B].
Device therapy including implantable cardioverter defibrillators (ICD) and cardiac resynchronization therapy (CRT) shown to improve outcomes
  • CRT is recommended for patients in sinus rhythm with a QRS width ≥150 ms due to left bundle branch block (LBBB) and LVEF ≤35% and persistent mild to moderate HF (NYHA II-III) despite optimal medical therapy. CRT may be considered for ambulatory NYHA class IV patients in sinus rhythm with a QRS width ≥150 ms, LBBB, and LVEF ≤35% (1)[A].
  • CRT may be considered for patients with LVEF ≤35%, sinus rhythm, QRS width ≥150 ms, non-LBBB pattern, and NYHA III or ambulatory NYHA IV symptoms (1)[A].
  • CRT may also be considered for patients with a QRS width between 120 and 150 ms, LBBB, LVEF ≤35%, and persistent mild to severe HF (NYHA II-IV) despite optimal medical therapy (1)[B].
  • ICDs are recommended for primary prevention in patients with nonischemic CM and ischemic CM who are at least 40 days post-MI; LVEF ≤35%, NYHA class II or III HF (1)[A], or LVEF ≤30%, NYHA I HF (1)[B]; and on optimal medical therapy and >1 year estimated survival. Generally not indicated in American Heart Association (AHA) stage D (end-stage) HF
  • CRT is recommended in patients with reduced LVEF and chronic RV pacing or with bradyarrhythmias and an anticipated need for a pacemaker (7)[A].
  • Heart valve surgery if defective heart valve is responsible; mitral valve repair especially helpful if mitral regurgitation is the primary issue and not functional.
  • Advanced therapies such as cardiac transplantation and LV assist device (LVAD) implantation can be considered in patients with HF refractory to conventional medical/device therapies without other disqualifying medical and psychosocial conditions. Cardiac transplantation is generally considered for patients ≤70 years old with a predicted 1-year survival worse than that afforded by transplantation. Indications for LVAD implantation are generally similar to cardiac transplantation but are evolving.
Admission Criteria/Initial Stabilization
  • See “Heart Failure, Acutely Decompensated.”
  • Admit patients with hemodynamic/respiratory compromise, hypoxia/hypoxemia, change in mental status, acute renal insufficiency, significant volume overload, and significant electrolyte abnormalities (e.g., hyponatremia).
Discharge Criteria
Subjective improvement, euvolemia on clinical assessment, resting heart rate (HR) < 100 bpm, systolic BP >80 mm Hg, HF outpatient education performed
  • Critical patient education performed at all outpatient and inpatient physician visits
  • Rapid office follow-up (1 to 2 weeks) after hospitalization.
Patient Monitoring
Home health monitoring by specially trained nurses have both been shown to decrease frequency of hospitalizations. Readmissions remain problematic.
Reduce sodium load (<1.5 to 2 g/day). Optimal level is unknown.
AHA: www.americanheart.org
After diagnosis: 1-year survival ˜75%, 5-year survival <50%, and 10-year survival <25%
1. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):e147-e239.
2. Swedberg K, Komajda M, Böhm M, et al. Ivabradine and outcomes in chronic heart failure (SHIFT): a randomised placebo-controlled study. Lancet. 2010;376(9744):875-885.
3. McMurray JJ, Packer M, Desai AS, et al. Angiotensinneprilysin inhibition versus enalapril in heart failure. N Engl J Med. 2014;371(11):993-1004.
4. Homma S, Thompson JL, Pullicino PM, et al. Warfarin and aspirin in patients with heart failure and sinus rhythm. N Engl J Med. 2012;366(20):1859-1869.
5. Massie BM, Carson PE, McMurray JJ, et al. Irbesartan in patients with heart failure and preserved ejection fraction. N Engl J Med. 2008;359(23):2456-2467.
6. Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.
7. Curtis AB, Worley SJ, Adamson PB, et al. Biventricular pacing for atrioventricular block and systolic dysfunction. N Engl J Med. 2013;368(17):1585-1593.
Additional Reading
Nohria A, Lewis E, Stevenson LW. Medical management of advanced heart failure. JAMA. 2002;287(5):628-640.
See Also
Algorithms: Congestive Heart Failure: Differential Diagnosis
  • I50.9 Heart failure, unspecified
  • I50.1 Left ventricular failure
  • I50.22 Chronic systolic (congestive) heart failure
Clinical Pearls
  • Have patients weigh themselves daily and report weight gains of >2 lb in a day or 5 lb above dry weight.
  • &bgr;-Blockers, ACE-I, and aldosterone antagonists are the core medications for management of chronic HF.
  • Consider referral for biventricular pacing in patients with LBBB and ICD in those with low EF.
  • Refer to an HF specialist if frequently hospitalized.