- Clinical science
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 heart disease, diabetes mellitus, and hypertension. These conditions cause ventricular dysfunction with low cardiac output, which results in blood congestion (backward failure) and poor systemic perfusion (forward failure). CHF is classified as either left heart failure (LHF) or right heart failure (RHF), although biventricular (global) CHF is most commonly seen in clinical practice. LHF leads to pulmonary edema and resulting dyspnea, while RHF induces 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 cardiac output and thereby overwhelm the heart. Acute decompensated heart failure (ADHF) may occur as an exacerbation of CHF or be caused by an acute cardiac condition such as myocardial infarction. CHF is diagnosed based on clinical presentation and requires an initial workup to assess disease severity and possible causes. Initial workup includes measurement of brain natriuretic peptide levels, chest x-ray, and an ECG. Management of CHF includes lifestyle modifications and treatment of associated conditions (e.g., hypertension) and comorbidities (e.g., anemia), along with pharmacologic agents that reduce the workload of the heart. ADHF requires hospitalization and more intensive measures, such as hemodialysis.
- Congestive heart failure (CHF): a clinical syndrome in which the heart is unable to pump enough blood to meet the metabolic needs of the body; characterized by ventricular dysfunction that results in low cardiac output
- Systolic dysfunction: CHF with reduced and ejection fraction (EF)
- Diastolic dysfunction: CHF with reduced and preserved ejection fraction
- Right heart failure (RHF): CHF due to right ventricular dysfunction; characterized by
- Left heart failure (LHF): CHF due to left ventricular dysfunction; characterized by
- Biventricular (global) CHF: CHF in which both the left and right ventricle are affected, resulting in simultaneous backward and forward CHF
- Chronic compensated CHF: clinically compensated CHF; the patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable (see “Diagnostics” below)
- Acute decompensated CHF: sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition (e.g., myocardial infarction)
Epidemiological data refers to the US, unless otherwise specified.
Systolic dysfunction (reduced EF)
Diastolic dysfunction (preserved EF)
|Further risk factors|
Underlying mechanism of reduced cardiac output
Systolic ventricular dysfunction (most common) due to:
- Reduced contractility: Damage and loss of myocytes reduce ventricular contractility and stroke volume.
- Increased afterload: increase in mean aortic pressure, outflow obstruction
- Increased preload: ventricular volume overload
- Cardiac arrhythmias
- High-output conditions (see “High-output heart failure” below)
- Diastolic ventricular dysfunction due to:
Consequences of systolic and diastolic dysfunction
- Forward failure: reduced cardiac output → poor organ perfusion → organ dysfunction (e.g., hypotension, renal dysfunction)
- Backward failure
Aim: maintain cardiac output if stroke volume is reduced
- ↑ Adrenergic activity → increase in heart rate, blood pressure, and ventricular contractility
Increase of activity (): activated following decrease in renal perfusion secondary to reduction of stroke volume and cardiac output
- ↑ Angiotensin II secretion → vasoconstriction → ↑ systemic blood pressure → ↑ afterload
- ↑ Aldosterone secretion → ↑ renal Na+ and H2O resorption → ↑ preload
- Brain natriuretic peptide (BNP): ventricular myocyte hormone released in response to increased ventricular filling and stretching
CHF is characterized by reduced cardiac output that results in venous congestion and poor systemic perfusion!
|General features of heart failure|
|Pulmonary symptoms dominate||Symptoms of fluid retention (backward failure) dominate|
| || |
- Definition: heart failure secondary to conditions associated with a high-output state, in which cardiac output is elevated to meet the demands of peripheral tissue oxygenation
- Etiology: conditions that lead to increased cardiac demand (high-output state)
- Symptoms of low-output CHF; particularly tachycardia, tachypnea, low blood pressure, and jugular distention with an audible hum over the internal jugular vein
- Pulsatile tinnitus
- Bounding peripheral pulses
- Laterally displaced apical heart beat
- Midsystolic murmur, S3 gallop (indicates rapid ventricular filling)
- Manage heart failure: symptom relief, hemodynamic stabilization
- Treat underlying condition
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|| |
No limitations of physical activity; no symptoms of CHF
|Class II||Slight limitations of moderate or prolonged physical activity (e.g., symptoms after climbing 2 flights of stairs or heavy lifting); comfortable at rest|
|Class III||Marked limitations of physical activity (symptoms during daily activities like dressing, walking across rooms); comfortable only at rest|
|Class IV||Confined to bed, discomfort during any form of physical activity; symptoms present at rest|
American Heart Association (AHA) Classification (2013)
The AHA classification system classifies patients according to their stage of disease. It takes objective findings (patient history, diagnostic findings) as well as symptoms of CHF into account.
|Stages||Objective assessment||Corresponding NYHA functional class|
|Stage A||No corresponding NYHA class|
|Stage B||Structural damage to the heart (e.g., infarct scars, dilatation, hypertrophy), without signs or symptoms of heart failure||NYHA I|
|Stage C||Structural damage to the heart + signs or symptoms of heart failure||NYHA I, II, III, IV|
|Stage D||Heart failure at its terminal stage||NYHA IV|
Diagnostic approach 
- Medical history, including preexisting conditions and history of alcohol and recreational or prescribed drug use
- Initial evaluation involves a range of routine laboratory tests and a test for BNP level, ECG, and chest x-ray.
- Echocardiography is the gold standard tool for assessing cardiac morphology and function, as well as investigating the underlying cause of CHF.
- Other procedures (exercise testing, angiography) may be required for further investigation.
Initial evaluation 
Elevated BNP and NT-pro BNP
- High levels of BNP in patients with classic symptoms of CHF confirm the diagnosis (high predictive index). 
|CHF unlikely||CHF likely|
|BNP (pg/mL)||< 100||> 500|
|NT-pro BNP (pg/mL)||< 300|| |
- Elevated atrial natriuretic peptide (ANP):
- Complete blood count: may show anemia
- Serum electrolyte levels: hyponatremia → indicates a poor prognosis
- Kidney function tests: ↑ creatinine, ↓ sodium
- Urine analysis: rule out concurrent renal impairment
- Fasting glucose: to screen for diabetes mellitus, which is a common comorbidity
- Fasting lipid profile: to detect dyslipidemia associated with a higher cardiovascular risk
- ECG abnormalities in CHF are common, but are mostly nonspecific and nondiagnostic.
- Signs of left ventricular hypertrophy
- Assessment of prior or concurrent heart conditions
- Signs of pericardial effusion and tamponade: low voltage ECG
- Useful diagnostic tool to evaluate a patient with dyspnea and differentiate CHF from pulmonary disease
- Signs of cardiomegaly
- Assess pulmonary congestion (see )
- Gold standard for evaluating patients with heart failure
- Assess ventricular function and hemodynamics
- Investigate etiology
- Cardiac stress test (exercise tolerance test): to assess the functional impairment due to CHF or other conditions (particularly CHD!)
- Radionuclide ventriculography : indicated to assess left ventricular volume and ejection fraction (LVEF)
Cardiac MRI: particularly useful for assessing cardiac morphology and function
- Cardiac size and volumes, wall thickness, valvular defects, wall motion abnormalities
- (left heart catheterization): indicated to detect/confirm CHD and possible
: if pulmonary hypertension is suspected, to assess the severity of systolic dysfunction, and/or to differentiate between types of shock
- : will be low in decompensated heart failure
- Endomyocardial biopsy: may be performed if a specific diagnosis is suspected in patients with rapidly progressive clinical CHF or in case the results would alter the management of the patient, e.g., in amyloidosis
General measures 
- Lifestyle modifications
- Patient education
- Treat any underlying conditions and contributing comorbidities.
Pharmacologic treatment algorithm
|Drug||NYHA stages||Indications||Contraindications and important side effects||Benefits|
|Diuretics (loop diuretics and thiazide diuretics)||(✓)||(✓)||✓||✓|| |
|ACE inhibitors||✓||✓||✓||✓|| |
|Beta blockers||(✓)||✓||✓||✓|| |
|Aldosterone antagonists||(✓)||✓||✓|| |
|Hydralazine plus nitrate||(✓)||(✓)|| || || |
|(✓)||(✓)||(✓)|| || |
|ARNI (angiotensin receptor-neprilysin inhibitor, e.g., sacubitril)||(✓)||(✓)||(✓)||(✓)|| || |
|Nesiritide (BNP derivative)|
(✓): see “Indications” column for detailed information
Conducting regular blood tests to assess electrolyte levels (potassium and sodium) is mandatory if the patient is on diuretics!
- Worsen renal perfusion (see “Side effects” of )
- Reduce the effect of diuretics
- May trigger acute cardiac decompensation
- Calcium channel blockers (verapamil and diltiazem): negative inotropic effect; worsen symptoms and prognosis
- Thiazolidinediones: promote the progression of CHF (↑ fluid retention and edema) and increase the hospitalization rate
- Moxonidine: increases mortality in CHF with reduced ejection fraction (systolic dysfunction)
- Implantable cardiac defibrillator (ICD): prevents sudden cardiac death
- Cardiac resynchronization therapy (biventricular pacemaker): improves cardiac function
- Coronary revascularization with or may be indicated if CAD is present.
- Valvular surgery if are present
- Ventricular assist devices: may be implanted to support ventricular function; may be indicated for temporary or long-term support (e.g., to bridge time until transplantation) of decompensated CHF
- end-stage CHF: for patients with (NYHA class IV), ejection fraction < 20%, and no other viable treatment options
- (see section below)
- Cardiorenal syndrome
- Stroke; increased risk of arterial thromboembolisms (especially with concurrent atrial fibrillation)
- Cardiac cirrhosis (congestive hepatopathy): Cirrhosis due to chronic hepatic vein congestion in patients with right‑sided heart failure.
- Venous stasis, leg ulcers
We list the most important complications. The selection is not exhaustive.
Cardiac decompensation is the most common reason for hospital admissions and is the most important complication of congestive heart failure.
ADHF typically occurs in patients who have a history of CHF or other cardiac conditions in which an acute cause precipitates the deterioration of cardiac function.
- Exacerbation of congestive heart failure (e.g., through pneumonia, anemia, volume overload, medication noncompliance)
- Acute myocardial infarction
- Atrial fibrillation, severe bradycardia, and other arrhythmias
- Hypertensive crisis
- Pulmonary embolism
- Pericardial tamponade
- Aortic dissection
- Cardiotoxic substances
- Renal failure
- Cardiodepressant medication (e.g., beta blockers, CCBs)
- Rapid exacerbation of symptoms of CHF (see and )
Pulmonary congestion with:
- Acute, severe dyspnea and orthopnea; worse when supine
- Cough (occasionally with frothing, blood-tinged sputum)
- Auscultation of the lungs: rales accompanied by wheezing
- Flash pulmonary edema: rapid, life-threatening accumulation of fluid associated with the risk of acute respiratory distress
- Weakness, fatigue, and cold, clammy skin
- X-ray findings in pulmonary congestion
- Sputum analysis: heart failure cells (hemosiderin-containing cells)
The radiologic signs of pulmonary congestion can be remembered with “ABCDE”: A = Alveolar edema (bat's wings), B = Kerley B lines (interstitial edema), C = Cardiomegaly, D = Dilated prominent pulmonary vessels, and E= Effusions!
Differential diagnosis of pulmonary edema and respiratory distress
- Noncardiogenic pulmonary edema due to ARDS, pulmonary embolism, transfusion-related acute lung injury, high altitude
- Sufficient oxygenation; and ventilation ; assisted ventilation as needed (e.g., CPAP).
- Fluid management:
- Hemodynamic stabilization: dobutamine) (e.g., in case of systolic dysfunction
- Treat the cause of decompensation.
- Hemodialysis if volume overload is symptomatic (pulmonary edema, pleural effusion, ascites) and resistant to treatment
- pulmonary function. may temporarily substitute
- Ventricular assist devices (see “ ” above)
Acute management checklist for heart failure exacerbation 
Hemodynamically stable patients
- Start IV diuretics. 
- Diuretic-naive patients: furosemide or bumetanide
- All others: Start at 1–2 times the patient's usual dose (e.g., furosemide ).
- Monitor response and consider continued bolus or continuous infusion based on response (e.g., urine output, respiratory effort, oxygenation, weight).
- Refractory diuresis
- Start vasodilator if pulmonary edema is present and/or the patient is hypertensive.
- Provide respiratory support.
- Continue home beta blockers and ACE-inhibitor/ARB for patients already on therapy.
Hemodynamically unstable patients (i.e., cardiogenic shock)
- Immediate cardiology consult for consideration of urgent coronary vascularization
- Treat hypoperfusion.
- Consider small fluid bolus (250–500 mL 0.9% NaCl) if there is inadequate preload.
- Consider inotropic support (e.g., dobutamine or milrinone ). 
- If a vasopressor is needed (e.g., persistent shock despite fluids and inotropic support), norepinephrine is generally because it is associated with a lower risk of arrhythmia than other vasopressors.
- Provide respiratory support with positive pressure ventilation, if indicated
- ICU/CCU transfer
- Monitor urine output closely.
- Close monitoring; consider invasive blood pressure monitoring
- Continuous telemetry and pulse oximetry
- Treat concurrent atrial fibrillation (see acute management checklist for atrial fibrillation).
- Fluid restriction: 1.5–2 L/day 
- Sodium restriction: 2 g/day
- Nephrology consult for consideration of ultrafiltration if the patient is not responsive to medical therapy 
- Discontinue/avoid any cardiotoxic medications (e.g., morphine is associated with a higher risk of mortality). 
- Identify and treat the underlying cause (e.g., cardiac ischemia, hypertensive crisis, infection).
- Venous thromboembolism prophylaxis 
- Monitor therapy
- Continuous telemetry while actively diuresing
- Continuous pulse oximetry if hypoxia is present