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Congestive Heart Failure

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Last Update: September 19, 2022.

Continuing Education Activity

Heart failure is a complex clinical syndrome in which the heart cannot pump enough blood to meet the body's requirements. It results from any disorder that impairs ventricular filling or ejection of blood to the systemic circulation. Patients usually present with fatigue and dyspnea, reduced exercise tolerance, and fluid retention (pulmonary and peripheral edema). This activity reviews the evaluation and management of congestive heart failure and highlights the role of the healthcare team in improving care for patients with this condition.


  • Review the pathophysiology of congestive heart failure.
  • Describe the diagnostic approach to patients presenting with clinical features of congestive heart failure.
  • Outline the management of congestive heart failure.
  • Explain the importance of collaboration and communication among the interprofessional team to educate the patients on the importance of medication compliance to improve outcomes for those with congestive heart failure.
Access free multiple choice questions on this topic.


Heart failure is a complex clinical syndrome that results from a functional or structural heart disorder impairing ventricular filling or ejection of blood to the systemic circulation. It is by definition a failure to meet the systemic demands of circulation. Heart failure remains a highly prevalent disorder worldwide with a high morbidity and mortality rate. It has an estimated prevalence of 26 million people worldwide and contributes to increased healthcare costs worldwide.[1] Multiple different diseases can cause heart failure. The etiology of heart failure varies the treatment plan to some degree; however, most of the treatment recommendations are based on the presence of heart failure alone, regardless of the cause.

Classification of heart failure is based on symptoms and calculated left ventricular ejection fraction (LVEF). Heart failure due to left ventricular dysfunction is categorized into heart failure with reduced ejection fraction (HFrEF), heart failure with preserved ejection fraction (HFpEF), and heart failure with mid-range ejection fraction (HFmrEF). The latter may consist of mixed left ventricular dysfunction (a combination of systolic and diastolic heart failure). The definition of HFrEF has varied among different studies and guidelines but is generally defined as an ejection fraction (EF) of less than 40%. Heart failure with preserved ejection fraction (HFpEF) is generally defined as heart failure with an EF of greater than 50%. HFmrEF is defined as heart failure with an EF of 40% to 50%.[2]

Heart failure can severely decrease the functional capacity of a patient and increase mortality risk. It is imperative to diagnose and effectively treat the disease to prevent recurrent hospitalizations, improve quality of life, and enhance patient outcomes. The treatment of heart failure requires a multifaceted approach involving patient education, optimal medical regimen to improve cardiac contractility, and prevention/limitation of exacerbations. An interprofessional team approach is warranted to optimize patient care.


Congestive heart failure is caused by structural abnormalities of the heart, functional abnormalities, and other triggering factors. Historically, an overwhelming majority of the cases were due to coronary artery disease and myocardial infarction. Over time, coronary artery disease and diabetes mellitus have become the predominant predisposing factors for heart failure. Other structural causes of congestive heart failure (CHF) include hypertension, valvular heart disease, uncontrolled arrhythmia, myocarditis, and congenital heart disease. Diastolic heart failure with impaired ventricular filling can be caused by restrictive cardiomyopathies and constrictive pericarditis, in addition to the etiologies identified above.[3]

It is important to identify etiologies of decompensated heart failure, as they contribute to most of the morbidity and mortality associated with the disease. The most common cause of decompensated congestive heart failure is inappropriate drug treatment, dietary sodium restriction, and decreased physical activity. Uncontrolled hypertension is the second most common cause of decompensated heart failure.[4] Uncontrolled tachyarrhythmias in patients with underlying congestive heart failure can promptly lead to CHF exacerbations.

Another group of diseases associated with "congestive heart failure" leads to high-output cardiac failure. This, by definition, is not an impairment in cardiac function but a failure of the heart to meet the increased systemic demands due to extracardiac diseases. Common etiologies of this type of congestive heart failure include severe anemia, thyrotoxicosis, obesity, nutritional deficiencies (thiamine deficiency, etc.), and pregnancy.[5]

The above-mentioned list of etiologies is not an all-inclusive list but a broad categorization of various etiologies. 


Approximately 6.2 million people in the United States had clinically manifested heart failure from 2013 to 2016.[6] By some reports, the incidence rate has plateaued; however, the prevalence increases as more patients receive therapy. This has not translated to improved quality of life or a decrease in the number of hospitalizations for patients with heart failure. According to the Global Health Data Exchange registry, the current worldwide prevalence of CHF is 64.34 million cases. This translates to 9.91 million years lost due to disability (YLDs) and 346.17 billion US dollars in healthcare expenditure. Age is a major determinant of HF. Regardless of the cause or the definition used to classify patients with heart failure (HF), the prevalence of HF increases steeply with age. The registry also notes a predilection for race with a 25% higher prevalence of HF in patients of African-American descent than Caucasians. According to the American Heart Association, heart failure is still the primary cause of hospitalization in the elderly population and accounts for 8.5% of cardiovascular-related deaths in the United States.[7] The report states a higher incidence and prevalence of heart failure among African Americans, Hispanic Americans, Native Americans, and recent immigrants from developing nations. According to the Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM program), the prevalence of HF is relatively greater in younger patients, which was attributed to obesity as the cause.[8] The incidence of heart failure in men doubles with each 10-year age increase after the age of 65, whereas in women, for the same age cohort, the incidence triples.[7]

International statistics regarding the epidemiology of HF are similar to those of the United States. The incidence increases dramatically with age, and metabolic risk factors along with a sedentary lifestyle are major risk factors. Ischemic cardiomyopathy, along with hypertension, is a major cause of HF in developing countries.[9] The notable difference based on a review of small cohort studies from these nations is a higher prevalence of isolated right heart failure. The theoretical cause of this is thought to be due to the higher prevalence of tuberculous, pericardial disease, and lung disease. There is a lack of robust data to verify these claims.


The adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance. 

In the initial stages of congestive heart failure, cardiac physiology attempts to adapt via several compensatory mechanisms to maintain cardiac output and meet the systemic demands. These include the Frank-Starling mechanism, changes in myocyte regeneration, myocardial hypertrophy, and myocardial hypercontractility. With increased wall stress, the myocardium attempts to compensate via eccentric remodeling, which further worsens the loading conditions and wall stress.[10]

A decrease in cardiac output stimulates the neuroendocrine system with a release of epinephrine, norepinephrine, endothelin-1 (ET-1), and vasopressin. They cause vasoconstriction leading to increased afterload. There is an increase in cyclic adenosine monophosphate (cAMP), which causes an increase in cytosolic calcium in the myocytes. This increases myocardial contractility and further prevents myocardial relaxation. 

An increase in afterload and myocardial contractility with impaired myocardial relaxation leads to increased myocardial oxygen demand. This paradoxical need for increased cardiac output to meet myocardial demand eventually leads to myocardial cell death and apoptosis. As apoptosis continues, a decrease in cardiac output with increased demand leads to a perpetuating cycle of increased neurohumoral stimulation and maladaptive hemodynamic and myocardial responses.[10]

A decrease in cardiac output also stimulates the renin-angiotensin-aldosterone system (RAAS), leading to increased salt and water retention, along with increased vasoconstriction. This further fuels the maladaptive mechanisms in the heart and cause progressive heart failure. In addition to this, the RAAS system releases angiotensin II, which has been shown to increase myocardial cellular hypertrophy and interstitial fibrosis. This maladaptive function of angiotensin II has been shown to increase myocardial remodeling.[11]

In HFpEF, there is a decrease in myocardial relaxation and an increase in the stiffness of the ventricle due to an increase in ventricular afterload. This perpetuates a similar maladaptive hemodynamic compensation and leads to progressive heart failure.[12]

History and Physical

The diagnosis and classification of heart failure are primarily based on the presence/severity of symptoms and physical exam findings. It is imperative to obtain a detailed history of symptoms, underlying medical conditions, and functional capacity/exercise tolerance to adequately treat the patient. The most commonly reported symptom is shortness of breath. Further qualification of this symptom is essential to help elucidate potential causes of heart failure and to determine the plan of care for the patient. Shortness of breath must further be classified to determine if it is related to exertion, positional changes (orthopnea), and whether it is acute or chronic. Other commonly reported symptoms of HF include chest pain, palpitations, anorexia, and fatigue. Some patients may present with a recumbent cough which may be due to orthopnea.

Physical examination of patients with heart failure requires a comprehensive assessment. The general appearance of patients with severe, chronic heart failure or those with acutely decompensated heart failure will include anxiety, diaphoresis, and poor nutritional status. The classical finding of pulmonary rales translates to heart failure of moderate to severe intensity. Wheezing may be present in acute decompensated heart failure. As the severity of pulmonary congestion increases, frothy and blood-tinged sputum may be seen. It is important to note that the absence of rales does not exclude pulmonary congestion. Jugular venous distention is another classical finding which must be assessed in all patients with HF. A paradoxical increase in jugular venous distention with respiration (Kussmaul sign) may be seen. In patients with elevated left-sided filling pressures, hepatojugular reflux (distention of the jugular vein after applying pressure over the liver with the patient lying at a 45° angle) will be seen. Peripheral edema is present in severe heart failure and will be seen if a substantial degree of volume overload is present.[13]

Cardiac findings in patients with HF include S3 gallop, pulsus alternans, and accentuation of P2. An S3 gallop is the most significant and early finding associated with HF.[14] In decompensated dilated cardiomyopathy, mitral and tricuspid regurgitation murmurs will be noted. 

Framingham Diagnostic Criteria for Heart Failure

The commonly used Framingham Diagnostic Criteria for Heart Failure requires the presence of 2 major criteria or 1 major and 2 minor criteria to make the diagnosis of heart failure. This diagnostic tool is highly sensitive for the diagnosis of heart failure but has a relatively low specificity. The Framingham Diagnostic criteria are as follows:.[13]

Major Criteria

  • Acute pulmonary edema
  • Cardiomegaly
  • Hepatojugular reflex
  • Neck vein distention
  • Paroxysmal nocturnal dyspnea or orthopnea
  • Pulmonary rales
  • Third heart sound (S3 Gallop)
  • Weight loss of 4.5 kg or more in 5 days in response to treatment
  • Central venous pressure greater than 16 cm of water
  • Radiographic cardiomegaly

Minor Criteria

  • Ankle edema
  • Dyspnea on exertion
  • Hepatomegaly
  • Nocturnal cough
  • Pleural effusion
  • Tachycardia (heart rate greater than 120 beats per minute)
  • A decrease in vital capacity by one third the maximal value recorded

New York Heart Association Functional Classification

Based on symptoms, the patients can be classified using the New York Heart Association (NYHA) functional classification as follows: [11]

  • Class I: Symptom onset with more than ordinary level of activity
  • Class II: Symptom onset with an ordinary level of activity
  • Class III: Symptom onset with minimal activity
    • Class IIIa: No dyspnea at rest
    • Class IIIb: Recent onset of dyspnea at rest
  • Class IV: Symptoms at rest


A comprehensive laboratory analysis, including assessment for anemia, iron deficiency, renal dysfunction, and liver dysfunction, is needed to help elucidate the cause and/or severity of heart failure. Cardiac-specific testing and prognostic factors for HF are outlined below.

Serum sodium levels have prognostic value as predictors of mortality in patients with chronic HF. They also play a role in the prediction of short-term mortality for patients admitted with decompensated heart failure. The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) trial demonstrated a significantly increased risk of in-hospital mortality as well as 30-day mortality in patients with HF who presented with hyponatremia. The mean serum sodium for patients enrolled in the study was 134 mEq/L. The highest mortality risk was seen in patients in the lowest quintile of serum sodium levels on presentation.[15] 

Serum B-type natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) levels can aid in differentiating cardiac from noncardiac causes of dyspnea in patients with ambiguous presentations. BNP is an independent predictor of increased left ventricular end-diastolic pressure, and it is used for assessing mortality risk in patients with heart failure. BNP levels correlate with New York Heart Association (NYHA) classification, and the utility is primarily as a marker to assess treatment efficacy. According to the American Heart Association (AHA) and the American College of Cardiology (ACC) recommendations from 2013 and 2017, predischarge natriuretic peptide levels are strong predictors of the risk of death and hospital readmission in patients with HF. In patients with true clinical presentation of HF, natriuretic peptides should not be used to drive treatment plans. It is important to remember that BNP and NT-proBNP levels can be elevated in patients with renal dysfunction, atrial fibrillation, and in older patients. Conversely, BNP levels can be falsely low in patients with obesity, hypothyroidism, and advanced heart failure (due to myocardial fibrosis).[16][17]

Chest radiographs are used to assess the degree of pulmonary congestion and cardiac contour (to determine the presence of cardiomegaly). Findings indicative of congestive heart failure on chest radiographs include enlarged cardiac silhouette, edema at the lung bases, and vascular congestion. In florid heart failure, Kerley B lines may be seen on chest radiographs. The absence of these findings in patients with clinical features of HF does not rule out CHF.[13]

Echocardiography is the most commonly used test for the diagnosis of HF. It can assess for systolic and diastolic dysfunction and help elucidate the presence of focal wall motion abnormalities or valvular pathology. Traditional 2D transcutaneous echocardiography is the most commonly utilized form of testing. However, in patients with severe obesity, pregnancy, or mechanical ventilation, it may be difficult to obtain adequate acoustic windows. Transesophageal echocardiography (TEE) is an alternative for these patients. Adequate rate control in patients with tachyarrhythmias is necessary to obtain adequate echocardiographic images.[13]

Computed tomography (CT) and magnetic resonance imaging (MRI) in patients with HF are used principally for the diagnosis of congenital cardiac abnormalities. Cardiac MRI is also the gold standard test for evaluating right ventricular (RV) function.[18]

Radionuclide multiple-gated acquisition (MUGA) scan is a reliable imaging technique for the evaluation of left ventricular (LV) and right ventricular (RV) function. MUGA scan is, in fact, the most accurate scan to assess for ejection fraction (EF) and is used in patients when there is a disparity of EF measurements from other studies.[19]

Electrocardiogram (ECG)-gated myocardial perfusion imaging is another diagnostic tool for assessing the EF, regional wall motion, and regional wall thickening. EF measurement with this study may be affected in patients with an irregular heart rate, low count density, and extracardiac radiotracer uptake. ECG-gated images are also useful in recognizing artifactual defects seen on SPECT imaging, such as breast tissue and diaphragmatic attenuation.[19]

Iobenguane scanning is scintigraphic imaging using iobenguane I-123 injection. It has been used for cardiac risk stratification in patients with New York Heart Association (NYHA) class II to III and an LVEF of 35% or less. Iobenguane I-123 is a norepinephrine analog. The test can show the amount of norepinephrine uptake in the cardiac sympathetic nervous system. Improved reuptake of norepinephrine is associated with a better prognosis.[20]

Other tests used in evaluating patients with HF include cardiac catheterization, stress testing, and electrocardiograms. However, they are used in patients with HF to determine the underlying cause of the disease. They do not play any specific role in the diagnosis of HF or its prognostication. In patients with severe systolic CHF, abnormalities of the electrocardiogram (ECG) are certain. However, in patients with HFpEF, the ECG may be normal. 

Treatment / Management

The goal of therapy for chronic CHF is to improve symptom management and quality of life, decrease hospitalizations, and decrease overall mortality associated with this disease. The goal of pharmacologic therapy is to give all indicated agents rather than single agents because the aggregate effect of these therapies is better than monotherapy from any of the agents. 

The primary combination therapy for HFrEF includes diuretics, a renin-angiotensin system inhibitor (such as an angiotensin receptor neprilysin inhibitor (ARNI), angiotensin-converting enzyme (ACE) inhibitor, or angiotensin II receptor blockers (ARB)), and a beta-blocker. The combination of hydralazine and nitrate is an alternative to an angiotensin system blocker for primary therapy if ACE inhibitor, ARNI, and ARB therapies are contraindicated. The nitrate and hydralazine combination is also indicated to reduce mortality and morbidity in African American patients with symptomatic HFrEF, currently receiving optimal medical therapy.[21] The combination therapy of ARB-ARNI significantly reduced cardiovascular death and HF hospitalizations when compared to ACE inhibitors alone.[22] 

Mineralocorticoid receptor antagonists such as spironolactone or eplerenone are indicated in patients with NYHA functional class II to IV and an LVEF of less than or equal to 35%. They are also indicated in patients with symptomatic HF after a myocardial infarction (MI) and an LVEF of less than 40%. However, in patients with recent MI and a low EF without symptoms of HF, these medications did not show any benefit.[23]

Ivabradine selectively inhibits the funny current (I-f) in the sinoatrial node. According to the AHA/ACC, ivabradine is indicated in patients with persistently symptomatic HF and an EF of less than or equal to 35% in sinus rhythm. The resting heart rate should be greater than 70 beats/min despite goal-directed beta-blocker therapy.[24]

Vericiguat is an agent that stimulates the intracellular receptor for endogenous NO, which is a potent vasodilator. It was recently approved by the FDA in 2021 to reduce the risk of mortality and HF hospitalizations in adults admitted with HF exacerbation who have chronic symptomatic HF and an EF of less than 45%.[25]

Digoxin may be considered in symptomatic patients in sinus rhythm despite adequate goal-directed therapy to reduce the all-cause rate of hospitalizations, but its role is limited.

An implantable cardioverter-defibrillator (ICD) is indicated for primary prevention of sudden cardiac death in patients with HF who have an LVEF of less than or equal to 35% and an NYHA functional class of II to III while on goal-directed medical therapy. It is also indicated if a patient has NYHA functional class II and an EF of less than or equal to 30% on adequate medical therapy.[26]

Cardiac resynchronization therapy (CRT) with biventricular pacing is indicated in patients with HFrEF and an NYHA functional class of II to IV with an LVEF less than or equal to 35% and QRS duration of greater than 150 ms.[26] According to the European Society of Cardiology (ESC), CRT is not recommended in patients with a QRS duration of less than 130 ms as multiple studies have shown potential harm. The ESC recommends CRT for patients with non-left bundle branch block (LBBB) morphology who meet the criteria for CRT; however, the ACC/AHA guidelines limit it to those with LBBB morphology on ECG. There is ongoing debate as to whether QRS morphology versus QRS duration should be the primary determinant for the selection of CRT.[16]

In patients with refractory HF, despite optimized pharmacologic therapy, intravenous vasodilator therapy and intravenous inotropes have been considered in the past. However, according to the AHA/ACC 2013 and 2017 guidelines, this should be restricted to palliative symptom relief in patients with end-stage disease who cannot get relief with standard medical therapy.[16]

In patients with HFpEF, none of the current therapies have a definitive improvement in mortality or hospitalization. However, medical management with the above therapies is indicated.[27]

Patients with progressive HF or those with acute, severe refractory HF may be considered for heart transplantation. 

It is also important to address potential triggers for HF exacerbation once the diagnosis of HF is made. Drugs that should be avoided in patients with HF include nonsteroidal anti-inflammatory drugs (NSAIDs), calcium channel blockers (CCBs) except vasoselective CCBs, and most antiarrhythmic drugs (except those in class III).[28]

Differential Diagnosis

Diseases that may present with clinical features of volume overload and/or dyspnea are in the differential for HF. These include:

  • Acute renal failure
  • Acute respiratory distress syndrome (ARDS)
  • Cirrhosis
  • Pulmonary fibrosis
  • Nephrotic syndrome
  • Pulmonary embolism (PE)


ACC/AHA Heart Failure Stages [16]

  • Stage A: Patients at high risk for HF but have no symptoms or structural heart disease
  • Stage B: Patients have structural heart disease but are asymptomatic
  • Stage C: Patients have structural heart disease plus symptoms
  • Stage D: Patients have refractory HF that requires modified interventions

Management Recommendations by ACC/AHA According to HF Stages [16]

  • Stage A: Reduction of risk factors and aggressive treatment of comorbidities
  • Stage B: Aggressive risk factor reduction and treatment with an angiotensin-converting enzyme inhibitor/angiotensin-receptor blocker (ACEI/ARB) and/or beta-blocker.
  • Stage C: Combination goal-directed therapy with ACEI/ARBs or angiotensin receptor–neprilysin inhibitors (ARNIs), beta-blockers, and loop diuretics for fluid retention. The most recent AHA/ACC update from 2017 added a class IIa recommendation for ivabradine in patients with stage C HF.[28]
  • Stage D: Goal-directed medical therapies indicated for stage C and consideration for heart transplantation. In patients with advanced disease and decreased life expectancy, palliative care discussions and advance directive planning should be considered. 


According to the Centers for Disease Control and Prevention (CDC), in December 2015, the rate for heart failure-related deaths decreased from 103.1 deaths per 100,000 population in 2000 to 89.5 in 2009 but subsequently increased to 96.9 in 2014. They note that the trend correlates with a shift from coronary heart disease as the underlying cause of heart failure deaths to metabolic diseases and other noncardiac causes of HF such as obesity, diabetes, malignancies, chronic pulmonary diseases, and renal disease. The mortality rate following hospitalization for heart failure is estimated at around 10% at 30 days, 22% at 1 year, and 42% at 5 years. This can increase to greater than 50% for patients with NYHA class IV, stage D heart failure.[29]

Ottawa Heart Failure Risk Score [30]

The Ottawa Heart Failure Risk Score is a useful tool for prognosis determination in patients with HF who present to the emergency department with symptoms of HF. It determines the 14-day risk of mortality, hospital readmission, and acute coronary syndrome in patients who presented to the emergency department with symptoms of HF to help arrive at safe disposition planning. Patients with a score of 0 are considered low risk. A score of 1-2 is considered moderate risk, a score of 3-4 is considered high risk, and a score of 5 or higher is considered very high risk. The scoring criteria are as follows:

One point for each of the following

  • History of stroke or transient ischemic attack
  • Oxygen saturation less than 90%
  • Heart rate greater than 110 beats per minute on the 3-minute walk test
  • Acute ischemic ECG changes 
  • An NT-proBNP level of greater than 5000 ng/L

Two points for each of the following 

  • Prior history of mechanical ventilation for respiratory distress
  • Heart rate greater than 110 beats/min on presentation
  • Blood urea nitrogen (BUN) greater than 33.6 mg/dl (12 mmol/L)
  • Serum bicarbonate greater level than 35 mg/d


Clinical complications of HF include decreased quality of life, decreased functional capacity, unintentional weight loss (cardiac cachexia), renal dysfunction (cardiorenal disease), and liver dysfunction (hepatic congestion).[31] Adverse cardiac events associated with HF include valvular dysfunction with dilated cardiomyopathy, MI, and ventricular arrhythmias. Sudden cardiac death is a potential complication for patients with HFrEF and requires primary prevention with ICD placement, as discussed above. Complications of the treatment for HF include renal failure, hypotension, and recurrent nosocomial infections due to frequent hospitalizations and central venous access.[32]

Deterrence and Patient Education

Risk factor reduction and aggressive management of comorbid conditions in patients with high-risk HF is key to preventing the associated morbidity and mortality of this disease. In addition to appropriate medical therapy, patients need guidance on self-monitoring of symptoms/signs of heart failure and adopting healthy lifestyle habits such as weight loss, smoking cessation, regular exercise, and alcohol cessation. These strategies can help prevent the development of HF in patients at high risk for the disease and slow the progression in those who are already diagnosed with it. Recent data suggests that in high-risk patients with diabetes mellitus type 2, sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of heart failure in patients with coronary artery disease. It also noted a decrease in hospitalizations and other adverse cardiovascular events with the use of SGLT2 inhibitors in this group of patients.[33]

The ACC/AHA and ESC recommend patient education to facilitate self-care and compliance. Close supervision, including surveillance by the patient and family, home-based visits, telephone support, and/or remote monitoring, is recommended by both of these associations to prevent adverse outcomes and progression of the disease. Dietary sodium restriction to 2-3 g/day and fluid restriction to 2 L/day are recommended if patients have hyponatremia and evidence of volume overload despite medical therapy. Patients require frequent in-depth education and re-evaluation to ensure they can adhere to the recommendations to have optimal outcomes.[16][26]

Pearls and Other Issues

Summary of Recommendations for Pharmacotherapy in HF by the 2013 ACC/AHA Guideline Update [16] [28]

Class I Recommendations

  • Evidence-based specific beta-blockers (carvedilol, bisoprolol, and metoprolol succinate) with one of the following:
    • Angiotensin-converting enzyme inhibitors (ACEIs) 
    • Angiotensin receptor blockers (ARBs) 
    • Angiotensin receptor–neprilysin inhibitor (ARNI) 
  • Chronic symptomatic HFrEF NYHA class II or III, replace an ACEI or ARB with an ARNI

Class IIa

  • Ivabradine for patients with symptomatic HF while on goal-directed medical therapy for chronic HFrEF with LVEF less than or equal to 35% and in sinus rhythm with a heart rate of at least 70 bpm at rest.

Class III

  • ARNI should not be given with or within 36 hours of the last dose of an ACEI or in patients with a history of angioedema

The Heart Failure Society of America (HFSA) Guidelines for Management of Acute Decompensated HF [34]

  • Oral therapy should be continued in most patients with HFrEF and up titrated as needed.
  • Continue angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) and beta-blockers during treatment of acute exacerbations.
  • Only consider withholding beta-blockers in patients hospitalized after a recent beta-blocker initiation.
  • Loop diuretics remain the cornerstone of therapy. (Class I recommendation)
  • Vasodilators (e.g., nitroprusside, nitroglycerin, or nesiritide) can be used as adjuvant therapies in patient with systolic blood pressure above 90 mmHg. 
  • Inotropic agents can be used short-term in patients with hypotension (SBP < 90 mmHg) and the patient is symptomatic from hypotension.

Enhancing Healthcare Team Outcomes

Heart failure is a complex clinical syndrome with high morbidity and mortality. It requires a multifaceted treatment approach, including patient education, pharmacologic management, and surgical interventions to optimize clinical outcomes. Specialty trained HF nurses are essential to the interprofessional team caring for patients with HF. They educate the patient on the importance of lifestyle modifications and medical compliance to help improve morbidity and mortality for the patient. They also educate the patient on symptom and weight management to prevent HF exacerbations and hospital admissions. The HF-trained social worker and case manager can help evaluate the patient in community settings/in-home visits to help the patient adhere to the lifestyle modifications recommended by the medical team. The clinical pharmacists assist the medical providers by reviewing patient medication lists and decreasing potential adverse drug-drug interactions. Primary care medical providers and cardiologists must coordinate care to minimize any adverse outcomes of medical therapy and prevent the progression of this disease. A collaborative interprofessional team can greatly improve the quality of life for patients with HF and decrease mortality.[Level 5]

Review Questions

congestive heart failure


congestive heart failure. Image courtesy S Bhimji MD


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