Continuing Education Activity

Heart failure (HF), also known as congestive heart failure (CHF), is a complex clinical syndrome characterized by the heart's inability to pump blood effectively due to structural or functional impairments. The most common cause of HF is ischemic heart disease, but other factors, such as hypertension, valvular disease, and myocarditis, also contribute to its development.

HF is classified based on left ventricular ejection fraction (LVEF) and clinical staging. Common symptoms of HF include shortness of breath, fatigue, fluid retention, and edema. This course explores the complexities surrounding HF's extensive etiologies, assessment, classification, and staging. This activity for healthcare professionals is designed to enhance the learner's competence in identifying HF, performing the recommended multifaceted evaluation, and implementing an appropriate interprofessional approach when managing this condition, which is essential to improve patient outcomes and quality of life.

Objectives:

• Evaluate clinical presentation and apply the staging and classification systems of heart failure.

• Assess the etiology of heart failure using clinical assessment and appropriate diagnostic tests. 

• Develop a management plan for patients with heart failure based on their clinical stage and investigations.

• Collaborate with interprofessional healthcare teams, including cardiologists, nurses, physiotherapists, and pharmacists, to ensure coordinated and comprehensive care for heart failure patients.

Introduction

Heart failure (HF), as defined by the American College of Cardiology (ACC) and the American Heart Association (AHA), is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. HF is a common disorder worldwide with a high morbidity and mortality rate. With an estimated prevalence of 26 million people worldwide, CHF contributes to increased healthcare costs, reduces functional capacity, and significantly affects quality of life. Accurately diagnosing and effectively treating the disease is essential to prevent recurrent hospitalizations, decrease morbidity and mortality, and enhance patient outcomes.[1] 

The etiology of HF is variable and extensive. Ischemic heart disease is the leading cause of HF. The general management of HF aims to relieve systemic and pulmonary congestion and stabilize hemodynamic status, regardless of the cause. The treatment of HF requires a multifaceted approach involving patient education, optimal medication administration, and decreasing acute exacerbations. Per the recent ACC/AHA guidelines for HF 2022, patients with HF are classified based on left ventricle ejection fraction (LVEF), whereas clinical and laboratory parameters are integrated to stage patients. The New York Heart Association (NYHA) classification stratifies and defines the functional capacity and severity of HF symptoms. This system is subjectively determined by clinicians and is widely used in clinical practice to direct therapy. Management of patients depends on the classification and staging of the disease.[1]

The following parameters are used to classify HF based on LVEF:

• HF with reduced ejection fraction (HFrEF): LV EF ≤40% 
• HF with mildly reduced ejection fraction: LVEF 41% to 49% and evidence of HF (spontaneous or provokable elevated cardiac biomarkers or elevated filling pressures)
• HF with preserved ejection fraction (HFpEF): LVEF ≥50% and evidence of HF (spontaneous or provokable elevated cardiac biomarkers or elevated filling pressures) 
• HF with improved ejection fraction: LV EF >40%, with previously documented LV EF ≤40% [1]

The ACC/AHA Stages of HF are as follows: 

• Stage A: At risk for HF. No current or past symptoms, structural heart disease, or evidence of elevated cardiac biomarkers, but risk factors are present. Risk factors include hypertension, diabetes, metabolic syndrome, cardiotoxic medications, or having a genetic variant for cardiomyopathy. 
• Stage B: Pre-HF. Patients have no signs or symptoms of HF but have risk factors and structural heart disease, evidence of elevated filling pressures (by invasive or noninvasive assessment), or persistently elevated cardiomarkers in the absence of other reasons for elevated markers, like chronic kidney disease or myocarditis. 
• Stage C: Symptomatic HF. Patients with current or past history of HF symptoms. 
• Stage D: Advanced HF. Patients with refractory symptoms that interfere with daily life or recurrent hospitalization despite targeted guideline-directed medical therapy.

For stage C and stage D HF patients, the following NYHA classification of HF symptoms should be used:

• 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 III a: No dyspnea at rest
• Class III b: Recent onset of dyspnea at rest
• Class IV: Symptoms at rest [2]

Etiology

Heart Failure Etiologies

The etiologies of HF are extensive, though coronary artery disease (CAD) causing ischemic heart disease is the most common cause. Every attempt should be made to identify causative factors to help guide treatment strategies. The etiologies can be broadly classified as intrinsic heart disease and pathologies that are infiltrative, congenital, valvular, myocarditis-related, high-output failure, and secondary to systemic disease.[3][4] These classifications have significant overlap.

The 4 most common etiologies responsible for about two-thirds of HF cases are ischemic heart disease, chronic obstructive pulmonary disease (COPD), hypertensive heart disease, and rheumatic heart disease. Higher-income countries have higher rates of ischemic heart disease and COPD; lower-income countries have higher rates of hypertensive heart disease, cardiomyopathy, rheumatic heart disease, and myocarditis.

Ischemic heart disease

Ischemic heart disease is by far the most common cause of HF worldwide. Ischemia leads to a lack of blood flow to heart muscles, reducing the EF. Incidence is increasing in developing countries as they adopt a more Western diet and lifestyle, and improved medical care decreases the infectious burden in these countries (myocarditis is often infection-related.)

Valvular heart disease

Valvular heart disease is another common intrinsic heart condition that can cause HF. Rheumatic heart disease is the most common cause of valvular heart disease in children and young adults worldwide. It is caused by an immune response to group A Streptococcus and primarily causes mitral and aortic stenosis.[5] Age-related degeneration is the most common overall cause of valvular disease, and the aortic valve is the most commonly affected. Women are more likely to experience mitral valve rheumatic heart disease or mitral valve prolapse, while men are more likely to suffer from aortic valve diseases such as regurgitation or stenosis. Endocarditis is also more common in men. 

Hypertension

Hypertension causes HF even in the absence of CAD or ischemic heart disease. High blood pressure causes mechanical stress by increased afterload and neurohormonal changes that increase ventricular mass.[3] Hypertension is also strongly associated with other comorbidities for HF development, and aggressively treating hypertension is shown to lower the incidence of HF.[3] 

Cardiomyopathy

Cardiomyopathy is a heterogeneous group of diseases characterized by enlarged ventricles with impaired function not related to secondary causes such as ischemic heart disease, valvular heart disease, hypertension, or congenital heart disease. The most common types of cardiomyopathies are hypertrophic, dilated, restrictive, arrhythmogenic right ventricular, and left ventricular noncompaction.[6] In addition to CHF, cardiomyopathy can present as arrhythmia or sudden cardiac death, further compelling the identification of underlying disorders.

Many of these conditions have a genetic basis, and a detailed family history of sudden cardiac death, especially in first-degree relatives older than 35 years, should be taken. Over 50 identified genes contribute to the development of dilated cardiomyopathy alone. Genetic determinants have variable phenotypic expression, and many nongenetic factors also affect the clinical symptoms. Some of these factors include diabetes, toxic exposure, or pregnancy. Fabry disease is a rare glycogen storage disease that can cause CHF symptoms through a hypertrophic cardiomyopathy pattern.[3][6] 

Inflammatory cardiomyopathy

Inflammatory cardiomyopathy is defined by myocarditis along with ventricular remodeling and cardiac dysfunction. The most common cause is viral infection. Other etiologies are bacterial, fungal, or protozoal infections; toxic substances or drugs; and immune-mediated diseases. Chagas disease is caused by Trypanosoma cruzi, which is endemic in Latin America and commonly causes myocarditis, cardiomyopathy, and CHF. Other viral causes of myocarditis and inflammatory cardiomyopathy include adenoviruses, enteroviruses, herpes virus 6, Epstein-Barr virus, and cytomegalovirus. Viruses can also activate autoimmune myocarditis, including HIV, hepatitis C virus, influenzas A and B, and coronaviruses (including COVID-19). When associated with CHF, these conditions tend to have a poor prognosis.[7]

Infiltrative cardiomyopathies 

Infiltrative cardiomyopathies cause a restrictive cardiomyopathy pattern (similar to the genetically determined restrictive cardiomyopathy variant), which is notable for normal ventricular systolic function but with diastolic dysfunction and restrictive left ventricular (LV) and right ventricular (RV) filling dynamics. This is often associated with a high E/A ratio showing increased early filling and delayed late filling.[6][8] 

Cardiac amyloidosis results from misfolded protein deposits in the heart; this leads to cardiomyocyte separation, cellular toxicity, and tissue stiffness. Patients are preload dependent and are prone to symptomatic hypotension. Currently, tamifidis is the only medication known to prevent cardiac amyloidosis. It prevents, but does not reverse, amyloid deposition. Its high cost is also a limiting factor.[1][9]

Sarcoidosis is an acquired cardiomyopathy characterized by conduction defects and arrhythmias caused by the formation of granulomas. The most common cardiac manifestation is CHF. Due to the associated conduction abnormalities, beta-blockers must be used with caution.

Cardiac hemochromatosis is present in 15% to 20% of patients with hereditary hemochromatosis. This condition initially presents with a restrictive pattern but develops into biventricular systolic dysfunction.[8] Patients with restrictive cardiomyopathy physiology can develop hypotension when treated with traditional CHF medications due to preload dependence, so caution should be used to avoid systemic hypoperfusion.[10] 

Takotsubo or stress-induced cardiomyopathy

Takotsubo or stress-induced cardiomyopathy (colloquially broken-heart syndrome) is an underrecognized cause of HF, which causes transient left-ventricular wall abnormalities that are not localized to a specific vascular territory. It has several proposed pathophysiologic mechanisms, including coronary vasospasm, microcirculatory dysfunction, and increased sympathetic nervous system activation. This condition is treated with medications typical for HF with the addition of antithrombotic medications in certain clinical situations with wall motion abnormalities. Recognized cases increased significantly during the COVID-19 epidemic.[11][12][13]

Peripartum cardiomyopathy

Peripartum cardiomyopathy is a significant cause of maternal mortality. During pregnancy, cardiac output is increased by 20% to 30% due to increased heart rate and stroke volume. It presents with CHF due to LV systolic dysfunction during late pregnancy, postpartum, or up to several months after delivery. There is likely an underlying genetic component, and it is more common in women with advanced maternal age, Black race, and multifetal pregnancies. If wall motion abnormalities are present, anticoagulation is essential due to the hypercoagulable state caused by pregnancy. Recovery is variable by global region and inversely correlates with lowered EF.[14]

Obesity

Obesity is a leading cause of CHF in patients younger than 40 years, according to the "Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity" (the CHARM study). The "obesity paradox" described elsewhere has significant study flaws and is derived from older data. Up to 10% of CHF cases are thought to be attributable to obesity alone. Patients with obesity are more likely to have HFpEF, possibly secondary to adipose-produced cytokines, eg, IL-1b, IL-8, and TNFα. Adipose tissue also degrades natriuretic peptides.[15][16][17]

Tachycardia and arrhythmia

Tachycardia and arrhythmia can induce a low-output CHF state. Dilation of all cardiac chambers and preservation or thinning of biventricular wall thickness is usually noted. Electrophysiologic changes accompany this, including prolonged duration and decreased amplitude of action potentials in the myocytes. All of these factors induce the typical neurohormonal response causing CHF. With rate control, these changes are often reversible due to myocardial hibernation.[18]

Thyrotoxicosis

Thyrotoxicosis is a rare cause of HF despite initiating a hyperdynamic circulatory state. This may be partially due to activation of the renin-angiotensin-aldosterone axis, causing sodium and water retention, as well as upregulation of erythropoietin-stimulating agent, both of which will cause increased blood volume. Sustained tachycardia with or without atrial fibrillation can also cause CHF.[19]

High-output cardiac failure

High-output cardiac failure can be associated with thiamine deficiency, which is a rare condition found primarily among patients who are elderly, homeless, or have alcohol abuse disorder. Thiamine deficiency causes decreased ATP production with an accumulation of adenosine, which causes systemic vasodilation. This leads to lowered systemic vascular resistance and increased cardiac output. This evolves to weakened myocardium and decreased EF. Diuretic use can also cause urinary thiamine loss, further compounding the situation.[20][21] 

Other common causes of high-output cardiac failure are obesity, liver disease, and arteriovenous shunts. The causative physiologic changes are decreased afterload (ie, systemic vascular resistance) and increased metabolism. These can often present with preserved EF, pulmonary congestion, increased filling pressures, and elevated natriuretic peptides.[22][23]

Epidemiology

The global magnitude of the disease cannot be accurately assessed given the significant differences in geographical distribution, assessment methods, lack of imaging modalities, and nonadherence to the uniform staging and diagnosis of the disease. Approximately 1.2 million hospitalizations were due to CHF in 2017, with an increase in the percentage of patients with HFpEF compared to HFrEF.[1] By some reports, the incidence rate has plateaued; however, the prevalence increases as more patients receive therapy. Moreover, treatment has not translated to improved quality of life or a decrease in the number of hospitalizations for patients with CHF. 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 and 346.17 billion United States dollars in healthcare expenditure.[24] 

Age is a major determinant of HF. Regardless of the cause or the definition used to classify patients with HF, the prevalence of HF increases steeply with age. The Framingham Heart Study showed CHF prevalence to be 8 per 1000 males aged 50 to 59 years, with an increase to 66 per 1000 males aged 80 to 89.[25] The incidence of HF 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. Men have higher rates of heart disease and CHF than women worldwide.[26][3]

The global registry also notes a predilection for a race with a 25% higher prevalence of HF in Black patients than in White patients. HF is still the primary cause of hospitalization in the elderly population and accounts for 8.5% of cardiovascular-related deaths in the United States.[26] International statistics regarding the epidemiology of HF are similar. The incidence increases dramatically with age, metabolic risk factors, and a sedentary lifestyle. Ischemic cardiomyopathy and hypertension are significant causes of HF in developing countries.[27] A notable difference based on a review of small cohort studies from these nations is a higher prevalence of isolated right HF. The theoretical cause of this is thought to be due to the higher prevalence of tuberculous, pericardial, and lung diseases; however, robust data to verify these claims are lacking.

Pathophysiology

HF is a progressive disease. Any acute insult to cardiac structure or acute alteration secondary to genetic mutation, cardiac tissue infiltration, ischemia, valvular heart disease, myocarditis, or acute myocardial injury may initiate the compensatory mechanism, which, once exhausted, results in maladaptation. In the initial stages of CHF, several compensatory mechanisms attempt to maintain cardiac output and meet the systemic demands. The chronic activation of the sympathetic nervous system results in reduced beta-receptor responsiveness and adrenaline stores. This results in changes in myocyte regeneration, myocardial hypertrophy, and myocardial hypercontractility.[28] The increased sympathetic drive also results in the activation of the renin-angiotensin-aldosterone system (RAAS) system, systemic vasoconstriction, and sodium retention.[28][29] In addition, the RAAS system releases angiotensin II, which has been shown to increase myocardial cellular hypertrophy and interstitial fibrosis, contributing to myocardial remodeling.[2]

A decrease in cardiac output stimulates the neuroendocrine system by releasing epinephrine, norepinephrine, endothelin-1 (ET-1), and vasopressin. These mediators cause vasoconstriction, leading to increased afterload. Cyclic adenosine monophosphate (cAMP) increases, which causes an increase in cytosolic calcium in the myocytes. This increases myocardial contractility and further prevents myocardial relaxation. Increased afterload and myocardial contractility, combined with impaired myocardial relaxation, increase 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.[29] The loss of myocytes decreases EF (cardiac contractility), which leads to incomplete LV emptying. Increased LV volume and pressure cause pulmonary congestion.[30] Renal hypoperfusion causes the release of antidiuretic hormone, further potentiating sodium and water retention. Increased central venous and intraabdominal pressure causes reduced renal blood flow, further decreasing GFR.[31]

Decompensated CHF is characterized by peripheral vasoconstriction and increased preload delivery to the overburdened heart. The natriuretic peptides BNP and ANP are secreted but are ineffective in counteracting the excess sodium and water retention.[31] Neprilysin is an enzyme that breaks down several hormones, including BNP, ANP, and bradykinin; it targets several novel therapeutics. Neprilysin is always used with an angiotensin receptor blocker because it increases angiotensin II levels, and when administered with an ACE inhibitor, it causes significant angioedema.[32][33]

Causes of CHF are split about equally between HFrEF and HFpEF but require different treatment plans. In HFpEF, myocardial relaxation decreases, and the stiffness of the ventricle increases due to an increase in ventricular afterload. This perpetuates a similar maladaptive hemodynamic compensation and leads to progressive HF. Patients with HFpEF tend to be older, female, and hypertensive. Atrial fibrillation and anemia are also more likely comorbid conditions. Some evidence has demonstrated that the prognosis is worse than those with HFrEF. However, appropriate targets may not have been identified for optimal therapeutic interventions.[34][35]

History and Physical

Clinical History

The diagnosis and classification of HF are primarily based on the presence and severity of symptoms and physical exam findings. A detailed history of symptoms, underlying medical conditions, and functional capacity is imperative to treat the patient adequately.

Acute CHF presents primarily with signs of congestion and may also present with organ hypoperfusion or cardiogenic shock.[36] The most commonly reported symptom is shortness of breath. This must be classified as exertional, positional (orthopnea), and acute or chronic. Other commonly reported symptoms of CHF include chest pain, anorexia, and exertional fatigue. Anorexia is due to hepatic congestion, bowel edema, and reduced blood flow to splanchnic circulation. Some patients may present with a recumbent cough due to orthopnea. Patients may also experience abdominal discomfort due to hepatic congestion or ascites. Patients with arrhythmias can present with palpitations, presyncope, or syncope. Another symptom that increases morbidity is edema, especially of the lower extremities. This can limit mobility and balance; total body water and weight increases of >20 lbs are not uncommon. 

While patients with acute HF present with overt respiratory distress, orthopnea, and paroxysmal nocturnal dyspnea, patients with chronic heart failure tend to curtail their physical activity; hence, symptoms may be obscured. Identifying triggers of acute decompensation, including recent infection, noncompliance with cardiac medications, use of NSAIDs, or increased salt intake, is essential.

Physical Examination Findings

The findings on physical examination vary with the stage and acuity of the disease. Patients may have isolated symptoms of left-sided HF, right-sided HF, or a combination of both. The general appearance of patients with severe CHF or those with acutely decompensated HF includes anxiety, diaphoresis, tachycardia, and tachypnea. Patients with chronic decompensated HF can appear cachexic. On chest examination, 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. Notably, the absence of rales does not exclude pulmonary congestion. Jugular venous distention is another classical finding that must be assessed in all patients with HF. In patients with elevated left-sided filling pressures, hepatojugular reflux (sustained increase in JVP of >4 cm after applying pressure over the liver with the patient lying at a 45° angle) is often seen.

Patients with stage D HF may show signs of poor perfusion, including hypotension, reduced capillary refill, cold extremities, poor mentation, and reduced urine output. There may be pulsus alternans (an alternating weak and strong pulse), suggestive of severe ventricular dysfunction. The pulse can be irregular in the presence of atrial fibrillation or ectopic beats. Some degree of peripheral edema is present with most HF.[37] Weight gain is another method for assessing volume retention, and precise daily weights can be a useful monitoring tool. 

Precordial findings in patients with HF include an S3 gallop, or displaced apex beat (dilated heart). There may be murmurs of associated valvular lesions such as the pan-systolic murmur of mitral regurgitation or tricuspid regurgitation, systolic ejection murmur of aortic stenosis, or early diastolic murmur of aortic regurgitation. Patients with pulmonary hypertension may have palpable or loud P2 or parasternal heave. Patients with congenital heart disease may also have associated clubbing, cyanosis, and splitting of the second heart sound. An S3 gallop is the most significant and early finding associated with HF.[38] Patients with hypertensive heart disease may have an S4 or loud A2. Patients with HF with preserved EF may have an S4 gallop related to ventricular noncompliance.

Framingham Clinical Diagnostic Criteria for Heart Failure

The commonly used Framingham Diagnostic Criteria for Heart Failure require the presence of 2 major criteria or 1 major and 2 minor criteria to make the diagnosis. This clinical diagnostic tool is highly sensitive for the diagnosis of HF but has a relatively low specificity. The Framingham Diagnostic criteria are as follows:[37]

The major criteria of HF include:

• Acute pulmonary edema
• Cardiomegaly
• Hepatojugular reflex
• Neck vein distention
• Paroxysmal nocturnal dyspnea or orthopnea
• Pulmonary rales
• Third heart sound (S3 Gallop)

The minor criteria of HF include:

• Ankle edema
• Dyspnea on exertion
• Hepatomegaly
• Nocturnal cough
• Pleural effusion
• Tachycardia (heart rate >120 beats per minute) [37]

Evaluation

A comprehensive assessment is required when evaluating a patient with HF. This includes a complete blood count and iron, renal, and liver profiles. Patients require further investigations after the basic metabolic and blood panel, depending on the etiology and clinical stage.[1]

Laboratory Studies

Laboratory investigations recommended in patients with HF include:

• Complete blood count (CBC): A CBC may suggest anemia or leukocytosis suggestive of an infection triggering CHF. 
• Renal profile: A complete renal profile is necessary for all patients with HF. It indicates the degree of renal injury associated with HF and guides medication choice. Determining a patient's baseline renal function before initiating medications, including renin-angiotensin-aldosterone (RAAS) inhibitors, sodium-glucose transporter-2 (SGLT-2) inhibitors, or diuretics, is essential. Serum sodium level has prognostic value as a predictor of mortality in patients with chronic HF. "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.[39]
• Live enzymes: An assessment of liver function is usually performed. Hepatic congestion secondary to HF may result in elevated gamma-glutamyl transferase levels, aspartate aminotransferase (AST), and alanine aminotransferase (ALT).[40]
• Urine studies: Urine studies can be useful in diagnosis. If amyloidosis is suspected, urine and serum electrophoresis and monoclonal light chain assays should be performed. Bone scintigraphy can be performed if clinical suspicion is high despite negative testing for light chains.[1] 
• Serum B-type natriuretic peptide (BNP): BNP or N-terminal pro-BNP (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 is used to assess mortality risk in patients with HF. BNP levels correlate with NYHA classification, and the utility is primarily used as a marker to evaluate treatment efficacy. NT-ProBNP is the chemically inert N-terminal fragment of BNP and has a longer half-life. The ratio of NT-ProBNP/BNP varies depending on underlying comorbidities and may be a useful tool in the future.[41] In patients with a clear clinical presentation of HF, natriuretic peptides should not be used to drive treatment plans. Clinicians should remember that BNP and NT-ProBNP levels can be elevated in patients with renal dysfunction, atrial fibrillation, and older patients. Conversely, BNP levels can be falsely low in patients with obesity, hypothyroidism, and advanced HF (due to myocardial fibrosis).
• Cardiac enzymes: Troponin-I or T suggests ongoing myocardial injury when persistently elevated and predicts adverse outcomes and mortality. 

Additional Diagnostic Studies

Electrocardiogram

An electrocardiogram (ECG) may show evidence of prior infarction, chamber enlargement, intraventricular conduction delay, or arrhythmia. This study may also give clues to specific etiologies. A low voltage and pseudo infarction pattern of ECG is seen in cardiac amyloidosis. An epsilon wave is seen in ARVC. ECG also suggests the presence of ventricular desynchrony, with a QRS duration of more than 120 msec, predicting the patient's response to device therapy for HF. 

Chest radiographs

Chest radiographs are used to assess the degree of pulmonary congestion and cardiac contour (to determine the presence of cardiomegaly). Findings indicative of CHF on chest radiographs include enlarged cardiac silhouette, edema at the lung bases, and vascular congestion (see Image. Congestive Heart Failure, Radiograph). In florid HF, Kerley B lines may be seen on chest radiographs. The absence of these findings in patients with a suggestive clinical presentation does not rule out CHF.[37]

Echocardiography

Echocardiography is the initial modality of choice in patients with suspected HF and is a readily available bedside tool. It quantifies right and left ventricular function, denotes structural abnormalities in cardiac chambers and valves, and helps visualize focal wall motion abnormalities. However, in patients with severe obesity, pregnancy, or mechanical ventilation, it may be challenging to obtain adequate acoustic windows. 

Transesophageal echocardiography (TEE) is an alternative for these patients. To obtain adequate echocardiographic images, adequate rate control is necessary in patients with tachyarrhythmias.[37] In patients with severe LV dysfunction, M-mode echocardiography may show increased left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD), decreased fractional shortening, increased E-point septal separation, or B-bump or notching of the mitral valve. 

Cardiac catheterization

Cardiac catheterization is often required for diagnosing ischemic cardiomyopathy and can be helpful in accurately evaluating intracardiac pressures, eg, left ventricular end-diastolic or pulmonary artery pressures.

Computed tomography

Computed tomography (CT) may be used for the assessment of coronary artery disease in a young patient with ventricular dysfunction (older patients are likely to have baseline calcifications). CT may also be used in patients with congenital heart diseases causing HF. Cardiac CT may help detect tumors causing HF. CT may also be used to evaluate stent patency and graft. 

Myocardial perfusion imaging

SPECT-myocardial perfusion imaging helps define the presence of ischemia in patients with newly diagnosed left ventricular dysfunction and not undergoing coronary angiography. This study is particularly useful for assessing CAD in patients with no history of ischemia but elevated troponin. ECG-gated myocardial perfusion imaging evaluates LVEF, 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 valuable for recognizing artifactual defects seen on SPECT imaging, eg, breast tissue and diaphragmatic attenuation.[42]

Cardiac magnetic resonance imaging

Cardiac magnetic resonance imaging has evolved as an essential tool when a discrepancy exists between the clinical stage of the disease and echocardiographic findings. It helps with the precise evaluation of volume, chamber sizes, and ventricular function. Cardiac magnetic resonance imaging also assesses the stage of valvular heart disease in detail. Cardiac magnetic resonance imaging (MRI) also helps evaluate complex congenital heart diseases. The tool can also be used for noninvasive assessment of conditions, eg, myocarditis, dilated cardiomyopathy, infiltrative cardiomyopathy, or arrhythmogenic right ventricular dysplasia.[43]

Radionuclide multiple-gated acquisition scan 

A radionuclide multiple-gated acquisition (MUGA) scan is a reliable imaging technique for evaluating EF and is used in patients when a disparity of EF measurements from other studies is noted.[42]

Noninvasive stress imaging 

Noninvasive stress imaging includes stress echocardiography, stress cardiac MRI, and SPECT imaging. These studies can be used to assess the benefit of coronary revascularization in patients with ischemic cardiomyopathy. 

Genetic testing

Genetic testing is indicated for identifying genetic variants causing cardiomyopathies, eg, Titin, laminin A or C, myosin heavy chain, and cardiac troponin-T mutations.[44]

Treatment / Management

The goal of therapy for chronic HF is to improve symptoms and quality of life, decrease hospitalizations, and improve cardiac mortality. Pharmacologic treatment aims to control symptoms and to initiate and escalate drugs that reduce mortality and morbidity in HF.[1] Management for the respective stages of HF is outlined by the American College of Cardiology and the American Heart Association.[1]

Stage A Heart Failure Management

The recommended treatment for stage A (at-risk for HF) HF include:

• In patients with hypertension, guideline-directed medical therapy (GDMT) should be used for the management of hypertension.
• In patients with type 2 diabetes, SGLT-2 inhibitors are indicated to reduce HF hospitalizations. 
• Lifestyle modifications, including healthy eating, physical activity, maintaining a normal weight, and avoidance of smoking, are indicated.
• Prognostication scores are recommended for patients with HF to estimate the risk of future HF events.[45] Examples include the Framingham Heart Failure Risk Score (1999), Health ABC Heart Failure Score (2008), ARIC Risk Score (2012), and PCP-HF score (2019). 
• Optimal management of cardiovascular diseases in patients known to have CAD should be implemented.
• Patients at risk for HF due to exposure to cardiotoxic medications (eg, chemotherapy) should be managed with an interprofessional approach.
• Natriuretic peptide screening and periodic evaluation should be performed. 

Stage B Heart Failure Management

Management of Stage B (pre-HF) is focused on preventing clinical HF and reducing mortality and adverse cardiovascular events, including:

• For patients with LVEF ≤40%, angiotensin-converting enzyme inhibitors (ACEI) should be used to prevent clinical HF and for mortality reduction. 
• For patients with LVEF ≤40% and evidence of prior or recent acute coronary syndrome or myocardial infarction, the use of a statin and beta-blocker is recommended for reduction of mortality, CHF, and adverse cardiovascular events. 
• For patients with LVEF ≤30% and receiving optimal medical therapy, with NYHA-class I and an expectation of meaningful survival of more than 1 year, a primary prevention ICD is recommended.
• Beta-blockers are recommended for patients with LVEF ≤40%, irrespective of the etiology, to prevent symptomatic HF.
• For patients with LVEF ≤50%, the use of thiazolidinediones and non-dihydropyridine calcium channel blockers increases the risk of adverse outcomes and HF hospitalizations, so they should be avoided. 
• Valve repair, replacement, or interventions have associated guidelines for asymptomatic valvular heart disease. 
• Patients with congenital heart disease also have associated guidelines.

Stage C Heart Failure Management

The recommended treatment for stage C (HF) includes:

• Interprofessional management is indicated for improving self-care and mortality of patients with HF.
• Patient education and social support are required for optimal management.
• Vaccination against respiratory illnesses is effective in reducing mortality. 
• Screening patients for frailty, depression, low literacy, low social support, and resource and transport logistics during healthcare encounters is reasonable.
• A low-sodium diet is recommended.
• Exercise training is effective in improving functional class and quality of life.
• For patients with congestion, diuretics improve symptoms and reduce HF progression.
• A thiazide diuretic (such as metolazone) should be added only to patients who do not respond well to a moderate or high dose of loop diuretics.
• For patients with HFrEF, an ARNI is recommended to reduce mortality and morbidity. ARNI should not be given to patients who are intolerant of ACEI, and an angiotensin receptor blocker (ARB) should be substituted. For patients unable to take an ARNI due to economic factors, an ACEI or ARB is indicated. ARNI should not be used within 36 hours of the last dose of ACEI. Switching to ARNI is recommended for patients tolerating ACEI/ARB well, as it has a high economic value. As with ACEI, ARNI should not be given to patients with a history of angioedema. 
• For patients with HFrEF, using the beta-blockers carvedilol, bisoprolol, or sustained-release metoprolol effectively reduces mortality and hospitalization.
• MRA is recommended for patients with HFrEF, NYHA class II to IV, an eGFR of >30 mL/min/1.73 m², and a serum potassium of <5.0 mEq/L. However, MRA is harmful for patients with a serum potassium of >5.0 mEq/L. 
• For patients with HFrEF, the use of SGLT-2 inhibitors is recommended to reduce mortality and HF hospitalization, irrespective of the diabetes status. 
• For African American patients with HFrEF and NYHA class III to IV who are already receiving optimal medical therapy, the addition of a combination of hydralazine and nitrate is recommended to reduce morbidity and mortality. This is of high economic value. 
• For patients with HFrEF and intolerance to RAASI or in whom RAASI is contraindicated due to renal insufficiency, the use of a combination of hydralazine and nitrate might be effective. 
• Titrating medications aggressively to achieve desired outcomes is recommended. This can be done as frequently as 1 to 2 weeks as tolerated. 
• Ivabradine can be useful in patients on optimal medical therapy with a heart rate of more than 70 bpm, providing mortality benefits and reducing HF hospitalization. 
• Digoxin may be considered in symptomatic patients with sinus rhythm despite adequate goal-directed therapy to reduce the all-cause rate of hospitalizations, but its role is limited.
• In patients with HFrEF and recent HF, an oral soluble guanylate cyclase stimulator (Vericiguat) might be useful in reducing mortality and HF hospitalization. Vericiguat is a soluble guanylate cyclase stimulator that stimulates the intracellular receptor for endogenous nitric oxide, a potent vasodilator. It also improves cardiac contractility.[46][47]
• Device therapy
• An implantable cardioverter-defibrillator (ICD) is indicated for primary prevention of sudden cardiac death in patients with HF who have an LVEF of ≤35% and an NYHA functional class of II to III while on goal-directed medical therapy. An ICD is also indicated if a patient has NYHA functional class I and an EF of ≤30% on adequate medical therapy.
• Cardiac resynchronization therapy (CRT) with biventricular pacing is recommended in patients with HFrEF and an NYHA functional class of II to III or ambulatory class IV with an LVEF ≤35%, QRS duration ≥150 ms, and sinus rhythm with left bundle branch block (LBBB) morphology. It can also be considered in non-LBBB morphology and QRS ≥150 ms.
• Revascularization is indicated in selected patients with coronary artery disease and HFrEF while on GDMT.
• Valvular heart disease interventions such as transcatheter edge-to-edge mitral valve repair or mitral valve surgery might be beneficial for patients with HF and on GDMT.

Stage D Heart Failure Management

The recommended treatment for stage D (advanced HF) includes:

• Referral to an HF specialist is indicated.
• It is reasonable to utilize inotropic support and device therapy in patients awaiting mechanical cardiac support or transplants. Inotropic support alone can be used in patients not eligible for a transplant or mechanical cardiac support. 
• Mechanical cardiac support, eg, a durable left ventricle assist device (LVAD) or ECMO, can be beneficial as a bridge to transplant.
• For highly selected patients, cardiac transplant is indicated to improve survival and quality of life.
• Shared decision-making should determine the goals of care. This includes considering comorbid conditions, frailty, and socio-economic support. Palliative care should be offered as indicated after shared decision-making. 

Differential Diagnosis

Differential diagnoses for HF include:

• Valvular heart diseases
• Renal failure
• Acute respiratory distress
• Pulmonary fibrosis
• Nephrotic syndrome
• Pulmonary embolism
• Pericardial diseases
• Cirrhosis

Staging

The ACC/AHA stages of HF are as follows: 

• Stage A: At risk for HF. No current or past symptoms, structural heart disease, or evidence of elevated cardiac biomarkers, but risk factors are present. Risk factors include hypertension, diabetes, metabolic syndrome, cardiotoxic medications, or having a genetic variant for cardiomyopathy. 
• Stage B: Pre-HF. Patients have no signs or symptoms of HF but have risk factors and structural heart disease, evidence of elevated filling pressures (by invasive or noninvasive assessment), or persistently elevated cardiomarkers in the absence of other reasons for elevated markers, like chronic kidney disease or myocarditis. 
• Stage C: Symptomatic HF. Patients with current or past history of HF symptoms. 
• Stage D: Advanced HF. Patients with refractory symptoms that interfere with daily life or recurrent hospitalization despite targeted guideline-directed medical therapy.

Prognosis

According to the Centers for Disease Control and Prevention (CDC), in December 2015, the rate of HF-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. The report noted that the trend correlates with a shift from coronary heart disease as the underlying cause of HF deaths to metabolic diseases and other noncardiac causes of HF, including obesity, diabetes, malignancies, chronic pulmonary diseases, and renal disease. The mortality rate following hospitalization for HF is estimated at around 10% at 30 days, 22% at 1 year, and 42% at 5 years. This can increase to >50% for patients with stage D HF.[48]

Ottawa Heart Failure Risk Score

The Ottawa Heart Failure Risk Score is a useful tool for determining prognosis in patients presenting to the emergency department with HF.[49] This score is used to determine the 14-day mortality risk, hospital readmission, and acute coronary syndrome to help arrive at safe disposition planning. Patients with a score of 0 are considered low risk. A score of 1 to 2 is considered moderate risk, a score of 3 to 4 is considered high risk, and a score of 5 or higher is considered very high risk.

Each of the following criteria is given 1 point if present:

• History of stroke or transient ischemic attack
• Oxygen saturation <90%
• Heart rate >110 bpm on the 3-minute walk test
• Acute ischemic ECG changes 
• An NT-ProBNP level of >5000 ng/L

Each of the following criteria is given 2 points if present: 

• Prior history of mechanical ventilation for respiratory distress
• Heart rate >110 bpm on presentation
• Blood urea nitrogen (BUN) >33.6 mg/dL (12 mmol/L)
• Serum bicarbonate level >35 mg/d

Complications

Complications of HF include:

• Reduced quality of life
• Arrhythmia and sudden cardiac death
• Cardiac cachexia
• Cardiorenal disease
• Liver dysfunction
• Functional valvular insufficiencies (eg, functional MR or TR)
• Mural thrombi and risk of thromboembolism (brain, kidney, lung, major limb vessels)
• Recurrent hospitalizations and nosocomial infection
• Mortality

Consultations

The consultation type depends on the disease stage and the intended management strategy. Commonly consulted specialists include:

• Heart failure specialist
• Interventional cardiologist (to address structural heart disease percutaneously)
• Cardiac electrophysiologist (device therapy)
• Cardiac surgeon (for CABG, VHD, or mechanical cardiac support)
• Cardiac imaging specialist
• Cardiac transplant specialist for stage D patients
• Cardiac rehabilitation physiotherapist
• Dietician
• Palliative care (if aligned with the goal of care)

Deterrence and Patient Education

Risk factor reduction and aggressive management of comorbid conditions are crucial to reducing morbidity and mortality associated with HF. In addition to compliance with medications, patients need guidance on self-monitoring of symptoms of HF and avoiding the triggers of HF. 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. Patient education is necessary to facilitate self-care and compliance. Close supervision, including surveillance by the patient and family, home-based visits, telephone support, and remote monitoring, is recommended. Socioeconomic support is pivotal in the appropriate management of the disease.[1] Patients require close clinical follow-up to assess volume status, effects of drug therapy, and escalation of care as indicated. 

Enhancing Healthcare Team Outcomes

HF is a complex clinical syndrome with high morbidity and mortality, necessitating an interprofessional approach to optimize patient-centered care and outcomes. Physicians, including clinical cardiologists, interventionalists, electrophysiologists, HF specialists, and cardiac imaging specialists, collaborate to diagnose, manage, and treat HF using evidence-based medical and procedural interventions. Advanced practitioners, such as HF nurse practitioners, play a crucial role in ongoing patient assessment, medication titration, and patient education to improve adherence to guideline-directed therapy. Specialty-trained HF nurses are vital in educating patients on lifestyle modifications, symptom recognition, and weight management to prevent exacerbations and reduce hospital admissions. Physical therapists help improve functional capacity and promote safe activity levels, while HF-trained social workers and case managers assess patients in community settings or through home visits to facilitate adherence to care plans and address social determinants of health that may impact disease management.

Effective interprofessional communication and care coordination are essential to enhancing patient safety, team performance, and long-term outcomes in HF management. Structured communication strategies, such as interdisciplinary rounds and shared electronic health records, ensure seamless information exchange among clinicians. Clinical pharmacists work closely with physicians and nurses to review patient medication lists, optimize pharmacologic therapy, and prevent adverse drug-drug interactions, thereby improving medication safety. Collaboration between primary care clinicians and cardiologists helps ensure continuity of care, minimize adverse effects of medical therapy, and slow disease progression. A well-coordinated, team-based approach significantly improves the quality of life for HF patients by integrating medical, pharmacologic, and lifestyle interventions while reducing hospitalizations and mortality.