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Heart Failure, Chronic

Afsha Rais, MD, Mohamad Elzaim, MD and Niyomi De Silva, MD Reviewed 06/2022

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  • Heart failure (HF) results from inability of the heart to fill and/or pump blood sufficiently to meet tissue metabolic needs. 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. For acute HF, see “Heart Failure, Acutely Decompensated.”

  • HF is the preferred term over congestive HF as patients are not always congested (fluid overloaded). HF may involve the left heart, the right heart, or be biventricular. It is progressive—manifested by the remodeling (altered heart geometry) process.

  • The New York Heart Association (NYHA) classification is a subjective grading scale used for classifying a patient's functional status: 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.

  • The American Heart Association (AHA)/American College of Cardiology (ACC) stages are a system to delineate the progression of HF: stage A: at risk for HF, no structural disease; stage B: structural disease, no HF symptoms; stage C: structural disease, HF symptoms; stage D: end-stage disease. 


HF accounts for close to 1 million hospitalizations a year with 25% readmitted within 30 days. The annual direct and indirect cost of HF in the United States is ~$34.4 billion. 


In the United States, 550,000 new cases are diagnosed annually with >250,000 deaths/year. 


  • An estimated 23 million individuals have HF worldwide. ~6.5 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 in four general categories: 
  • HF with reduced ejection fraction (HFrEF) or systolic HF: an inotropic abnormality, often from myocardial infarction (MI) or dilated cardiomyopathy (CM), resulting in diminished systolic emptying (ejection fraction [EF] ≤40%)

  • HF with preserved EF (HFpEF) or diastolic HF: a compliance abnormality, often due to hypertensive CM, in which the ventricular relaxation is impaired (EF ≥50%)

  • Borderline HFpEF (EF 41–49%): mild systolic dysfunction, clinically behaves like HFpEF

  • Improved HFpEF (EF >40%): previously HFrEF, with improvement in systolic function

Most common etiologies: coronary artery disease (CAD)/MI and hypertension (HTN). Others: 
  • Myocarditis and CM: alcoholic, viral, drugs, muscular dystrophy, infiltrative (e.g., amyloidosis, sarcoidosis), postpartum , infectious (e.g., Chagas disease, HIV), hypertrophic CM (HCM), inherited familial dilated CM

  • Valvular and vascular abnormalities: valvular stenosis or regurgitation, rheumatic heart; renal artery stenosis, usually bilateral, may cause recurrent “flash” pulmonary edema.

  • Chronic lung disease and pulmonary HTN

  • Arrhythmias (atrial fibrillation and other tachyarrhythmias, high-grade heart block, frequent PVCs)

  • Other: high-output states: hyperthyroidism, anemia; cardiac depressants (β-blocker overdose), stress induced; Iatrogenic volume overload (extreme overload in patients with normal hearts and kidneys); Idiopathic: 20–50% of idiopathic dilated CM are familial.


Multiple genetic abnormalities responsible for a variety of phenotypes have been identified. Consider genetic screening for first-degree relatives of HCM and arrhythmogenic RV dysplasia. 


CAD/MI, HTN, valvular heart disease, diabetes, cardiotoxic medications, obesity, older age 


Control HTN and other risk factors. 



  • Dyspnea on exertion: cardinal sign of left-sided HF. Deteriorating exercise capacity: easy fatigued, general weakness

  • Nocturnal nonproductive cough, orthopnea, and paroxysmal nocturnal dyspnea; sometimes frothy or pink sputum. Wheezing, especially nocturnal, in absence of history of asthma or infection (cardiac asthma); Cheyne-Stokes respirations

  • Anorexia and/or fullness or dull pain in right upper quadrant (hepatic congestion). Nausea and poor appetite may indicate advanced HF.


  • Increased filling pressures: rales and sometimes wheezing, peripheral edema, S3 gallop, hepatomegaly, jugular venous distention, 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/chronic obstructive pulmonary disorder, constrictive pericarditis, nephrotic syndrome, cirrhosis, venous occlusive disease 


Diagnosis should be primarily clinical, with laboratory data as adjunctive and indicative of complications. 

Initial Tests (lab, imaging)

  • β-Type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-BNP): helpful in acute setting to differentiate the cause of dyspnea ( <100 essentially rules out HF). A BNP level in those with risk factors for developing HF or with structural heart disease but no symptoms of HF can help predict the development of symptomatic HF (1)[A]. Pulmonary embolism, renal failure, and acute coronary syndromes may elevate BNP.  Sacubitril/valsartan can raise BNP levels but has less impact on NT-proBNP levels. Obesity may lower BNP levels. The use of BNP-guided therapy in chronic HF and acutely decompensated HF is not well established, although a predischarge BNP can predict risk of readmission and survival (1)[A]. 

  • Lab findings: respiratory alkalosis, azotemia, decreased erythrocyte sedimentation rate, proteinuria, elevated creatinine (cardiorenal syndrome), dilutional hyponatremia (poor prognosis), hyperbilirubinemia.

  • Chest x-ray (changes lag clinical symptoms): 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

  • Echocardiogram: most useful test to determine LVEF, which is critical for proper diagnosis and management of HF, as well as RV function, diastolic dysfunction, ventricular size, wall thickness, and valvular abnormalities; repeated if change suspected in underlying cardiac status.

  • Other tests: Nuclear imaging to estimate ventricular size, assess for ischemia or infarction, amyloidosis, and systolic function. Cardiac MRI in select circumstances: suspicion of cardiac sarcoidosis, arrhythmogenic RV CM, acute myocarditis, amyloidosis, and hemochromatosis. Cardiac catheterization is important for excluding CAD as an etiology in the setting of risk factors. Endomyocardial biopsy only in special circumstances (e.g., suspected giant cell myocarditis)



Treatment is focused on improving hemodynamics, relieving symptoms, and blocking the neurohormonal response to improve survival. 


Diuretics and nitrates are used in acute HF management. ACE-I and aldosterone antagonists (especially for HFrEF) can be added at any time. β-blocker should be started once acute HF resolved. Avoid nonsteroidal anti-inflammatory drugs (NSAIDs), which worsen HF. Avoid the use of diltiazem and verapamil with systolic dysfunction due to increase mortality and negative inotropic effects. 

First Line

  • ACE-I: used to decrease afterload, increase survival, improve symptoms, and exercise capacity 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-Is are considered equally effective. Initiate at low doses and titrate as tolerated to target doses.

  • Angiotensin receptor blockers (ARBs): indicated if intolerant to ACE-Is. Avoid combination of ACE-I and ARB.

  • β-Blockers: used in systolic or diastolic HF; Initiate in hemodynamically stable/compensated patients at low dose and titrate upward slowly.); NNT = 25/year for mortality. Mortality decreased in systolic HF; evidence for titration to heart rate (HR) rather than specific dose.

  • Sacubitril/valsartan (Entresto): an angiotensin receptor and neprilysin inhibitor (ARNI), shown to reduce the risk of CV death and HF hospitalizations in patients with HFrEF. Recommended dose: 24/26mg or 49/51mg PO BID to a target of 97/103 PO BID. Patients with HFrEF and NYHA class II and III who tolerate an ACE-I or ARB with CrCl >30, replacement by an ARNI is recommended to reduce morbidity and mortality (NNT to prevent one CV death over 3.5 years: 31). ACE-Is should be discontinued at least 36 hours prior to starting ARNIs. Most common adverse effects: hypotension, angioedema, renal insufficiency​​​​​​

  • Serum glucose cotransporter-2 (SGLT-2) inhibitors, Dapagliflozin and Empagliflozin, medications used for type 2 diabetes mellitus, showed improvement in worsening HF or CV death in patients with EF≤40% and NYHA II/IV, irrespective of diabetes, and may decrease overall death (NNT 50 to 60/year) based on randomized clinical trials, DAPA-HF and EMPEROR-Reduced. Recommended dose for both is 10 mg PO daily. Based on evidence, FDA approved the use of SGLT-2 inhibitors for the treatment of HFrEF. Adverse effects: urogenital infections, ketoacidosis, reduced blood pressure, enhanced diuresis  (2)[A]​

  • Vericiguat, a guanylate cyclase simulator, shown to reduce the risk of death from CV causes or hospitalization for HF with a hazard ration of 0.9 (95% CI 0.82–0.98). FDA approved in patients with an EF≤45%, recent HF hospitalization, or need for IV diuretics based on the VICTORIA trial  (1)[B]

  • Diuretics are helpful to manage volume overload/reduce preload.

  • Digoxin: reduces symptoms, without positive effect on mortality. In patients with preserved renal function (CrCl >50 mL/min), the recommended dose is 0.125mg/day.

  • Combination of isosorbide dinitrate and hydralazine  (20 mg/37.5mg PO TID) is effective for improving survival and reducing hospitalizations in African Americans and can be used if the patient is unable to take an ACE-I/ARB.

  • Ivabradine (Corlanor) can be considered in NYHA II and III HF, EF ≤35%, on maximally tolerated β-blockers with HR >70 to reduce hospitalization  (1)[B]. Contraindication: ADHF, hypotension (<90/50 mm Hg), severe hepatic impairment, pacemaker–dependence, bradyarrhythmias, or strong CYP3A4 inhibitors. Do not administered to patients currently in atrial fibrillation (AF) and discontinued if AF develops.

  • In HFpEF, no therapy has improved survival. ARBs and spironolactone can be used to potentially reduce hospitalizations (1)[A].


Device therapy including implantable cardioverter-defibrillators (ICDs) and cardiac resynchronization therapy (CRT) are shown to improve outcomes. 
  • CRT recommendation: sinus rhythm with a QRS width ≥150 ms due to left bundle branch block (LBBB), LVEF ≤35%, persistent mild to moderate HF despite goal directed medical therapy (GDMT), reduced LVEF and chronic RV pacing or with bradyarrhythmias and an anticipated need for a pacemaker.

  • CRT consideration: LVEF ≤35%, sinus rhythm, QRS width >150 ms, non-LBBB pattern, and NYHA II or ambulatory NYHA IV symptoms. If QRS width >150 ms due to LBBB pattern, consider CRT in ambulatory NYHA class IV patients. If QRS width is between 120 and 150 ms with LBBB pattern, consider CRT in NYHA II to IV, despite GDMT.

  • ICDs recommendation: primary prevention in patients with nonischemic and ischemic CM, at least 40 days post-MI; LVEF ≤35%, NYHA class II or III HF, or LVEF ≤30%, NYHA I HF; and on optimal medical therapy and >1 year estimated survival; generally not indicated in end-stage HF


  • Heart valve surgery for defective heart valve; mitral valve repair if mitral regurgitation (MR) 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. Cardiac transplantation: considered for patients ≤70 years old with a predicted 1-year survival worse than that afforded by transplantation. ILVAD implantation indications are similar but evolving.


  • Admission: hemodynamic/respiratory compromise, mental status change, acute renal injury, significant volume overload, electrolyte abnormalities (e.g. hyponatremia).

  • Discharge: subjective improvement, euvolemia on assessment, improved vitals, , outpatient education performed



Close outpatient follow-up after hospitalization to decrease frequency of readmission 


Reduce sodium load. Optimal level unknown 



After diagnosis: 1-year survival ~75%, 5-year survival <50%, and 10-year survival <25% 


Sudden death, progressive pump failure 


Yancy  CW, Jessup  M, Bozkurt  B, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation.  2017;136(6):e137–e161. [View Abstract on OvidMedline]
Cardoso R, Graffunder FP, Ternes CMP, et al. SGLT2 inhibitors decrease cardiovascular death and heart failure hospitalizations in patients with heart failure: A systematic review and meta-analysis. EClinicalMedicine. 2021 Jun 5;36:100933.


Maddox TM, Januzzi JL Jr, Allen LA, et al. 2021 Update to the 2017 ACC Expert Consensus Decision Pathway for Optimization of Heart Failure Treatment: Answers to the 10 Pivotal Issues About Heart Failure with Reduced Ejection Fraction: A Report of the American College of Cardiology Solution Set Oversight COmmittee. J Am Coll Cardiol. 2021 Feb 16;77(6):772-810.  


Algorithm: Congestive Heart Failure: Differential Diagnosis 



  • I50.9 Heart failure, unspecified

  • I50.1 Left ventricular failure

  • I50.22 Chronic systolic (congestive) heart failure

  • I50.32 Chronic diastolic (congestive) heart failure

  • I50.42 Chronic combined systolic and diastolic hrt fail


  • 48447003 chronic heart failure (disorder)

  • 111283005 Chronic left-sided heart failure (disorder)

  • 10335000 Chronic right-sided heart failure (disorder)

  • 88805009 Chronic congestive heart failure

  • 424404003 decompensated chronic heart failure (disorder)

  • 441481004 Chronic systolic heart failure

  • 441530006 Chronic diastolic heart failure

  • 153941000119100 Chronic combined systolic and diastolic heart failure (disorder)


  • Have patients weigh themselves and report weight gains of >2lb in a day or 5lb above dry weight.

  • β-Blockers, ACE-I, and aldosterone antagonists are the core medications for management.