Congestive heart failure (CHF) is a clinical condition in which the heart is unable to pump enough blood to meet the metabolic needs of the body because of pathological changes in the myocardium. The three main causes of CHF are coronary artery disease, diabetes mellitus, and hypertension. These conditions cause ventricular dysfunction with low cardiac output, which results in blood congestion and poor systemic perfusion. CHF is classified as either left heart failure (LHF) or right heart failure (RHF), while a combination of both is called biventricular or global CHF. LHF leads to pulmonary edema and consequent dyspnea, while RHF leads to systemic venous congestion that causes symptoms such as pitting edema, jugular venous distension, and hepatomegaly. Biventricular CHF manifests with clinical features of both RHF and LHF, as well as general symptoms such as tachycardia, fatigue, and nocturia. In rare cases, high-output CHF may occur as a result of conditions that increase metabolic demands, leading to an increased cardiac output that eventually overwhelms the heart. CHF is diagnosed based on clinical presentation and requires an initial workup to assess the severity of the disease and determine the possible causes. Initial workup includes measurement of brain natriuretic peptide levels, chest x-ray, ECG, and an echocardiogram. Management of CHF includes lifestyle modifications and treatment of associated conditions (e.g., hypertension) and comorbidities (e.g., anemia), along with pharmacological agents that reduce the workload of the heart. Acute heart failure may occur as an exacerbation of CHF (acute decompensated heart failure) or be caused by an acute cardiac condition such as myocardial infarction (see “Acute heart failure”).
- Congestive heart failure (CHF)
- Heart failure with reduced ejection fraction (HFrEF, systolic HF)
- Heart failure with preserved ejection fraction (HFpEF, diastolic HF)
- Right heart failure (RHF)
- Left heart failure (LHF)
- Biventricular (global) CHF
- Chronic compensated CHF: a clinically compensated type of CHF in which the patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable 
- Acute decompensated CHF: sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition (e.g., myocardial infarction)
- 1–2% of the population in the US (∼ 5.7 million individuals) has CHF. 
- The incidence is higher among African Americans and Hispanics . 
- Incidence increases with age: ∼ 10% of individuals > 60 years old are affected. 
- Systolic heart disease is the most common form of CHF overall.
Epidemiological data refers to the US, unless otherwise specified.
|Etiology of CHF |
Systolic dysfunction (reduced EF)
Diastolic dysfunction (preserved EF)
|Further risk factors|
American Heart Association (AHA) classification (2013) 
The AHA classification system categorizes patients according to the stage of disease based on an objective assessment of clinical features and diagnostic findings.
|Stages||Objective assessment||Corresponding NYHA functional class|
|Stage A|| |
|Stage B|| |
|Stage C|| |
|Stage D|| || |
NYHA functional classification 
The NYHA (New York Heart Association) functional classification system is used to assess the patient's functional capacities (i.e., limitations of physical activity and symptoms) and has prognostic value.
|Class I|| |
|Class II|| |
|Class III|| |
|Class IV|| |
Underlying mechanism of reduced cardiac output
Systolic ventricular dysfunction (most common) due to:
- Reduced contractility: damage and loss of myocytes (e.g., following myocardial infarction, CAD, DCM)
- Increased afterload: increase in mean aortic pressure, outflow obstruction (e.g., arterial hypertension, aortic stenosis)
- Increased preload: ventricular volume overload (e.g., backflow into the left ventricle caused by aortic insufficiency)
- Cardiac arrhythmias
- High-output conditions (see “” below)
Diastolic ventricular dysfunction due to:
- Decreased ventricular compliance: increased stiffness or impaired relaxation of the ventricle (e.g., in long-standing arterial hypertension, constrictive pericarditis, pericardial tamponade) → reduced ventricular filling and increased diastolic pressure → decreased cardiac output
- Increased afterload: increase in pulmonary artery pressure (e.g., pulmonary hypertension)
- Increased preload: ventricular volume overload (e.g., tricuspid valve regurgitation, left-to-right shunt)
Consequences of systolic and diastolic dysfunction
- Systolic dysfunction: reduced cardiac output → poor organ perfusion → organ dysfunction (e.g., hypotension, renal dysfunction)
- Increased left-ventricular volume and pressure → backup of blood into lungs → increased pulmonary capillary pressure → → orthopnea
- Reduced cardiac output → systemic venous congestion → edema and progressive congestion of internal organs
- Nutmeg liver: the macroscopic appearance of the liver which resembles a nutmeg seed due to ischemia and fatty degeneration from hepatic venous congestion
- Increased adrenergic activity: : increase in heart rate, blood pressure, and ventricular contractility
- Increase of activity (RAAS): activated following decrease in renal perfusion secondary to reduction of stroke volume and cardiac output
- Secretion of brain natriuretic peptide (BNP)
General features of heart failure
Clinical features of left-sided heart failure
Symptoms of pulmonary congestion
- Dyspnea , orthopnea
- Pulmonary edema
- Paroxysmal nocturnal dyspnea
- Cardiac asthma
- Physical examination findings 
Clinical features of right-sided heart failure
- Symptoms of fluid retention and increased CVP
Physical examination findings
- Jugular venous distention: visible swelling of the jugular veins due to an increase in CVP and venous congestion
- Kussmaul sign
- Hepatosplenomegaly: may result in cardiac cirrhosis and ascites
- Hepatojugular reflux: jugular venous congestion induced by exerting manual pressure over the patient's liver → ↑ right heart volume overload → inability of the right heart to pump additional blood → visible jugular venous distention that persists for several seconds
Subtypes and variants
High-output heart failure
- Definition: heart failure secondary to conditions associated with a high-output state, in which cardiac output is elevated to meet the peripheral tissue oxygen demands
- Etiology: conditions that lead to an increased cardiac demand (high-output state) 
- Clinical features
Heart failure management
- Symptom relief
- Hemodynamic stabilization
- Treatment of the underlying condition
- Heart failure management
- All patients: Establish the diagnosis with routine laboratory studies, cardiac biomarkers, ECG, chest x-ray, and echocardiogram.
- If CHF is confirmed, investigate for:
Routine laboratory studies 
- CBC; : Screen for anemia and infection.
- Liver chemistries: Elevations, particularly of the cholestatic enzymes, can indicate hepatic venous congestion. 
- Inflammatory markers: ↑ CRP can indicate acute infection or inflammation
- Fasting lipid studies: Elevated cholesterol is a common finding.
- TSH: potentially signs of hyperthyroidism 
Cardiac biomarkers 
Natriuretic peptides (NP): BNP or NT-proBNP (NT-proBNP is a precursor of BNP; either can be used, as long as the correct values are used for interpretation) 
- To establish the diagnosis of CHF (alongside echocardiography)
- Evaluation of prognosis and disease severity (e.g., level at admission and predischarge)
- Findings and interpretation (see “Natriuretic peptide levels in the diagnosis of heart failure” for cutoff values in acute heart failure)
- High levels in patients with classic symptoms of CHF confirm the diagnosis (high predictive index).
- High levels at discharge and no decrease during hospitalizations may signal worse outcomes.
- Raised NPs are seen in a multitude of conditions (e.g., renal impairment, ACS, effects of pharmacotherapy).
- Obesity and flash pulmonary edema can lead to normal or decreased NP levels. 
- Cardiac troponin T or I
- Every patient with suspected new-onset HF (best initial imaging test to assess cardiac structure and function) 
- Changes in clinical features in patients receiving treatment (monitoring)
- Evaluation for device therapy
- Features of heart failure
- Evidence of complications 
- Underlying causes, including:
Chest x-ray 
- Indication: acute, new-onset, or suspected heart failure
- Changes to cardiac silhouette
- X-ray findings of pulmonary congestion
- Signs of concurrent heart conditions, including:
Electrocardiogram (ECG) 
ECG abnormalities in CHF are common but mostly nonspecific.
- Signs of left ventricular hypertrophy 
- Signs of concurrent heart conditions
Additional studies 
The following tests are not always part of the standard workup for heart failure but can be helpful when there is diagnostic uncertainty and to evaluate for underlying causes. For details on the evaluation for myocardial ischemia see “Diagnostics” in “Coronary artery disease”.
Advanced cardiac imaging
- Cardiac MRI
- Radionuclide ventriculography: used to assess LVEF and volume if other imaging modalities are inadequate or contraindicated 
- PET myocardial perfusion imaging: alternative noninvasive workup for suspected coronary artery disease
- Left heart catheterization or coronary angiogram: identification and treatment of coronary artery disease
- Right heart catheterization 
- Endomyocardial biopsy: indicated if there is ongoing diagnostic uncertainty in rapidly progressive disease or to confirm the diagnosis of infiltrative heart disease 
- Blood pressure monitoring: Consider in patients with suspected hypertension.
- ECG monitoring: Consider in suspected paroxysmal atrial fibrillation or other underlying arrhythmias.
- All patients
- Assess for evidence of decompensation and treat if present (see “Treatment” in “Acute decompensated heart failure”).
- Advise regular exercise and lifestyle modifications; consider cardiac rehabilitation. 
- Treat associated conditions, e.g., hypertension, dyslipidemia, and diabetes.
- Start medical treatment based on heart failure staging.
- Refer to cardiology for regular follow-up.
- Options for patients refractory to first-line medical therapy
General measures 
- Cessation of smoking, alcohol consumption, and recreational drug use
- Weight loss 
- Immunization: and
Making sure that the patient understands the pathophysiological basis of the disease improves the effectiveness of treatment and quality of life.
- Diet and fluid restriction 
Self-monitoring and symptom recognition
- Daily weight check: Patients with a weight gain of > 4–5 lbs (> 2 kg) within 3 days should consult a doctor.
- Patients may be counseled to independently adjust their diuretic dose if there is weight gain and advised that this needs regular review by a heart failure specialist to avoid overtreatment with diuretics. 
- Recognition of symptoms of worsening heart failure
- Monitoring of potential medication side effects
- Awareness of travel precautions: e.g., carrying a copy of medical records and avoiding destinations with limited healthcare 
Treatment of comorbid conditions
The following conditions may worsen the symptoms of heart failure and accelerate progression.
- Hypertension: Treat with a target systolic BP of < 130.
- Dyslipidemia: Start statins to keep lipids within the normal range.
- Iron deficiency: Screen for and start iron replacement in patients with NYHA class II and III symptoms and iron deficiency. 
- Obstructive sleep apnea: Consider nocturnal continuous positive airway pressure (CPAP) therapy. 
- Atrial fibrillation: Start either rate or rhythm control and consider anticoagulation. 
- Coronary artery disease: Consider coronary revascularization if there is concomitant ischemic heart disease.
Avoidance of drugs that may worsen CHF 
- Most antiarrhythmic agents
- Calcium channel blockers (except amlodipine)
- Thiazolidinediones (e.g., pioglitazone)
- Inhalation anesthetics
- Cautious selection of antidepressants due to numerous interactions and adverse effects when used with HF drugs (SSRIs may be used judiciously) 
Medical treatment of heart failure
Initial therapy 
- Treatment is based on the stage of heart failure.
- Additional therapies are added to the baseline medications as symptoms worsen.
- From stage B onward, device therapy can be considered alongside medical therapy.
- Start all new medications at the lowest recommended dose and slowly titrate up to the target dose where applicable.
- The following table deals predominantly with the management of HFrEF; there is a paucity of evidence supporting best practice in HFpEF.
- For modifications in pregnancy and lactation see “Use of heart failure medications in pregnancy and lactation.”
|Initial medical treatment of heart failure |
|Treatment of cardiovascular risk factors|
|Beta blockers|| || |
|Stage C (additions)|
|Loop diuretics and thiazide diuretics|
|Isosorbide dinitrate (ISDN) and hydralazine|
|Angiotensin receptor-neprilysin inhibitors (ARNIs)|| |
|Stage D (additions)|
Conducting regular blood tests to assess electrolyte levels (K+ and Na+) is mandatory if the patient is taking diuretics.
Therapy for refractory symptoms
Consider adding the following drugs if patients are adherent and have persistent symptoms despite maximum tolerated doses of first-line medical therapy. Invasive interventions may also be considered.
|Additional medical treatment options for heart failure|
|Digoxin|| || |
|If channel inhibitor (Ivabradine)|
Patients with CHF are at risk of sudden cardiac death (SCD) from arrhythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF) and heart failure may be worsened by cardiac dyssynchrony. Devices may only pace or have both pacing and defibrillator functions. 
Implantable cardioverter defibrillator (ICD): consist of a pulse generator and leads that can sense VF or VT and deliver a shock to restore sinus rhythm. 
- Patients with CHF are at risk of sudden cardiac death (SCD) from arrhythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF).
- Indications in heart failure 
- HFrEF with expected survival of > 1 year if, despite receiving optimized medical therapy for 3–6 months, the following criteria are still met:
- Patients who have previously had sustained VT or a cardiac arrest secondary to VF or VT 
Cardiac resynchronization therapy (CRT): leads in the RA, RV, and coronary sinus (which lies adjacent to the LV) pace the heart in a coordinated manner.
- Benefits include:
- Indications: The criteria below apply to patients with stage C HFrEF with an LVEF ≤ 35% on optimized medical therapy and an expected survival of > 1 year. 
Management of end-stage heart failure
- Cardiac transplant is the only cure for end-stage heart failure; however, the majority of patients are not candidates.
- Refer patients who are not candidates for transplant to palliative care.
- Patients referred for transplant typically require bridging measures, including inotropic and mechanical circulatory support.
- Inotropic support
Mechanical circulatory support (MCS)
- Invasive devices used to support ventricular function
- May be short-term (days to weeks) or long-term (months to years)
- Short-term devices include intraaortic balloon pump and venoarterial extracorporeal membrane oxygenation.
- Long-term devices include ventricular assist devices, e.g., left-ventricular assist device. 
- Acute decompensated heart failure (see “Acute heart failure”)
- Cardiorenal syndrome
- Cardiac arrhythmias
- Central sleep apnea
- Cardiogenic shock
- Stroke: due to increased risk of arterial thromboembolisms (especially with concurrent atrial fibrillation)
- Chronic kidney disease
- Cardiac cirrhosis (congestive hepatopathy): cirrhosis due to chronic hepatic vein congestion in patients with
- Venous stasis, leg ulcers
We list the most important complications. The selection is not exhaustive.
- A complex syndrome in which renal function progressively declines as a result of severe cardiac dysfunction 
- Occurs in ∼ 30% of cases of ADHF 
- Systolic dysfunction → reduced cardiac output → renal hypoperfusion → prerenal kidney failure
- Diastolic dysfunction → systemic venous congestion → renal venous congestion → decreased transglomerular pressure gradient → ↓ GFR → worsening kidney function
- RAAS activation → salt and fluid retention → hypertension → hypertensive nephropathy
- Diagnosis: ↓ GFR, ↑ creatinine that cannot be explained by underlying kidney disease 
- Treatment: heart failure and renal failure management (see “ ”)
- Prognosis: : CHF with reduced GFR and high creatinine levels (> 3 mg/dL) is associated with a poor prognosis. 
The prognosis depends on the patient, type and severity of heart disease, medication regimens, and lifestyle changes. The prognosis for patients with preserved EF is similar to or better than for patients with decreased EF. Risk stratification scales may be used to evaluate the prognosis (e.g., CHARM and CORONA risk scores).
- Factors associated with worse prognosis 
1-year survival according to NYHA stage
- Stage I: ∼ 95%
- Stage II: ∼ 85%
- Stage III: ∼ 85%
- Stage IV: ∼ 35%
- One-Minute Telegram 10-2020-2/3: Positive effects of SGLT2 inhibitors in patients with heart failure regardless of diabetes status
- One-Minute Telegram 8-2020-3/3: For some patients with heart failure, more pills mean better outcomes, study finds
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