- Clinical science
Congestive heart failure (CHF) is a clinical syndrome in which the heart is unable to pump enough blood to meet the metabolic needs of the body. The three main causes of heart failure are coronary heart disease, diabetes mellitus, and hypertension. These conditions cause ventricular dysfunction with low cardiac output, which in turn results in congestion of blood (backward failure) and poor systemic perfusion (forward failure). Heart failure is commonly classified as left-sided and right-sided heart failure, although biventricular heart failure is most commonly seen in clinical practice. Left-sided heart failure results in pulmonary edema and associated dyspnea, while right-sided heart failure induces systemic venous congestion that causes symptoms such as pitting edema and hepatomegaly. Biventricular (global) HF presents with clinical features of both left-sided and right-sided failure, as well as general symptoms such as tachycardia, fatigue, and nocturia. In rare cases, high-output HF may occur as a result of conditions with an increased (rather than decreased) cardiac output, which overwhelms the heart. Acute decompensated heart failure (ADHF) may occur as an exacerbation of CHF or be due to an acute cardiac condition such as myocardial infarction. The diagnosis of CHF is based on clinical presentation and requires an initial workup to assess disease severity and possible causes. The initial workup includes measurement of brain natriuretic peptide levels, chest x-ray, and ECG. Management of CHF includes lifestyle modifications, treatment of associated conditions (e.g., hypertension) and comorbidities (e.g., anemia) that would otherwise worsen the symptoms of HF, and additional pharmacologic agents that reduce the workload of the heart. ADHF requires hospitalization and more intensive measures, such as hemodialysis.
- Heart failure (HF): 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: heart failure with reduced stroke volume and ejection fraction
- Diastolic dysfunction: heart failure with reduced stroke volume and preserved ejection fraction
- Right-sided HF: heart failure due to right ventricular dysfunction; characterized by
- Left-sided HF: heart failure due to left ventricular dysfunction; characterized by
- Biventricular HF: heart failure in which both the left and right ventricle are affected, resulting in backward and forward heart failure
- Chronic compensated HF: heart failure that is clinically compensated; the patient is asymptomatic or symptomatic and stable, with echocardiographic signs of HF (see “Diagnostics” below)
- Acute decompensated HF: sudden deterioration of chronic HF or new onset of severe HF due to an acute cardiac condition (e.g., myocardial infarction)
Epidemiological data refers to the US, unless otherwise specified.
|Systolic dysfunction||Diastolic dysfunction|
|Further risk factors|
The three major causes of heart failure are coronary artery disease, hypertension, and diabetes mellitus. Patients typically have multiple risk factors that contribute to the development of HF!
General physiological concepts
Underlying pathomechanism of reduced cardiac output
Systolic ventricular dysfunction (most common) due to:
- Reduced contractility: Damage and loss of myocytes reduces 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:
- Systolic ventricular dysfunction (most common) 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
Compensation mechanisms to 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|
|Clinical features of left-sided heart failure||Clinical features of right-sided heart failure|
|Pulmonary symptoms dominate||Symptoms of fluid retention (backward failure) dominate|
In clinical practice, biventricular heart failure with features of left and right heart failure is more likely than isolated failure of one ventricle!
- 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 an increased cardiac demand (high-output state)
- Symptoms of low-output HF; 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)
- Primarily a clinical diagnosis
- X-ray and echocardiography: cardiomegaly
- Manage heart failure: symptom relief, hemodynamic stabilization
- Treat underlying condition
|NYHA class||Characteristics|| |
Physical exercise capacity or functional capacity measured in Watts
|Cardiac output (CO)|
|Class I|| |
No limitations of physical activity; no symptoms of HF
|> 100 watts||Normal even under stress|
|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||= 100 watts||Adequate with low amount of stress|
|Class III||Marked limitations of physical activity (symptoms during daily activities like dressing, walking across rooms); comfortable only at rest||Up to 50 watts||Reduced under stress|
|Class IV||Confined to bed, discomfort during any form of physical activity; symptoms present at rest||No physical activity possible||Reduced 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 HF 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|
- Medical history, including pre-existing conditions and history of alcohol and recreational or prescribed drug abuse
- Initial evaluation involves laboratory tests 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 HF.
- Other procedures (exercise testing, angiography) may be required for further investigation.
Elevated BNP and NT-pro BNP
- High levels of BNP in patients with classic symptoms of HF confirm the diagnosis (high predictive index).
|HF unlikely||HF likely|
|BNP (pg/mL)||< 100||> 400|
|NT-pro BNP (pg/mL)||< 300|| |
> 450 (patients aged < 50 years)
> 1800 (patients aged > 75 years)
- Elevated atrial natriuretic peptide (ANP):
- Complete blood count
- Urine analysis: rule out concurrent renal impairment
- Investigate causative factors and common comorbidities
- ECG abnormalities in HF 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 HF from pulmonary disease
Signs of cardiomegaly
- Cardiac-to-thoracic width ratio > 0.5
- Boot-shaped heart on PA view (due to left ventricular enlargement)
- Assess pulmonary congestion (See in “Acute decompensated heart failure” below.)
- Gold standard for evaluating patients with heart failure
Assess ventricular function and hemodynamics
- Atrial and ventricular size
- Interventricular septum thickness: > 11 mm (normal 6–11 mm) indicates cardiac hypertrophy
Systolic function: left ventricular ejection fraction
- Normal EF: > 55%
- Slightly reduced EF: 45–54%
- Reduced EF: 30–44%
- Extremely reduced EF: < 30%
- Diastolic function (diastolic filling, ventricle dilation)
- Investigate etiology
- Ultrasound of pleural cavities: sensitive method for detecting pleural effusion (CT may be better for detecting small amounts of fluid)
Ultrasound of large blood vessels
- The volume status of the inferior vena cava is used to assess intravascular volume
- Normal IVC diameter is < 2 cm. It is more important to determine its variation during respiration and the dynamics of the volume status after initiating diuretic treatment, rather than comparing it with normal values.
- Ultrasound of the abdomen
- Cardiac stress test (exercise tolerance test) to assess the functional impairment due to HF 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
- heart catheterization): indicated to detect/confirm CHD and possible (left
; : if pulmonary hypertension; is suspected, to assess the severity of systolic dysfunction; , and/or to differentiate between types of shock
- heart failure: will be low in decompensated
- Lifestyle modifications
- Self-monitoring and symptom recognition
- Daily weight check
- Weight gain > 2 kg within 3 days: consult the doctor
- Monitoring potential side effects (e.g., hypotension caused by ACE inhibitors, hyperkalemia caused by aldosterone-antagonists, sensitivity to sunlight caused by amiodarone)
- Travel restrictions: Include most recent medical record when traveling. Advise against traveling to destinations with limited access to or inadequate health care.
- Patients suffering from symptoms of depression and cognitive dysfunction should also be offered neurological and psychiatric treatment.
- 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||(✓)||✓||✓|| |
|Ivabradine||(✓)||(✓)||(✓)|| || |
|Hydralazine plus nitrate||(✓)||(✓)|| || || |
|Digoxin||(✓)||(✓)||(✓)|| || |
|ARNI (angiotensin receptor-neprilysin inhibitor)|| || |
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 HF (↑ fluid retention and edema) and increase the hospitalization rate
- Moxonidine: increases mortality in HF with reduced ejection fraction (systolic dysfunction)
- Implantable cardiac defibrillator: (ICD): prevents sudden cardiac death
Cardiac resynchronization therapy: (CRT): improves cardiac function
- Indications: HF with EF < 35% and left bundle branch block (intraventricular conduction delay with QRS > 120–150 ms)
- Can be combined with an ICD
- Coronary revascularization with or may be indicated if CHD is present
- Valvular surgery if are present
- Ventricular assist devices: (left-ventricular assist devices, right-ventricular assist devices, or biventricular assist devices): a device that 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 HF
- for patients with end-stage HF (NYHA class IV), ejection fraction < 20%, and no other viable treatment options :
Cardiac decompensation is the most common reason for hospital admissions and is the most important complication of chronic heart failure.
ADHF typically occurs in patients who have a history of chronic HF or other cardiac conditions in which an acute cause precipitates the deterioration of cardiac function.
- Exacerbation of chronic heart failure (e.g., through pneumonia, anemia, volume overload)
- Acute myocardial infarction
- Atrial fibrillation, severe bradycardia, and other arrhythmias
- Hypertensive crisis
- Pulmonary embolism
- Pericardial tamponade
- Aortic dissection
- Cardiotoxic substances
- Renal failure
- Rapid exacerbation of symptoms of HF (see and )
Pulmonary edema 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)
- Indicated if the etiology of the pleural effusion is unclear
- Pleural fluid analysis: effusions are typical of cardiogenic causes.
Differential diagnosis of pulmonary edema and respiratory distress
- Noncardiogenic pulmonary edema due to ARDS, pulmonary embolism, transfusion-related acute lung injury, high altitude
- Symptom relief: ,
- Sufficient oxygenation; and ventilation Assisted ventilation may be required (e.g., CPAP).
- Hemodynamic stabilization: aggressive diuresis (IV furosemide) to reduce volume overload, (e.g., dobutamine)
- 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)
Treatment of acute pulmonary congestion with LMNOP: Lasix® (furosemide), morphine, nitrates, oxygen, (upright) position.
Beta blockers must be used cautiously in decompensated heart failure!
Cardiorenal syndrome is a complication of acute and chronic HF.
- Definition: : a complex syndrome in which renal function progressively declines as a result of severe cardiac dysfunction; occurs in ∼ 20–30% of cases of acute decompensated HF
- Cardiac forward failure → renal hypoperfusion → prerenal kidney failure
- Cardiac backward failure → 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: treat heart failure; manage renal failure (see treatment of )
- Prognosis: : HF with reduced GFR is associated with a poor prognosis; mortality increases by ∼ 15% for every 10 mL/min reduction in estimated GFR.
- Prognosis estimates vary depending on patient characeristics, type and severity of heart disease, medication regimens, and lifestyle changes.
- Prognosis for patients with preserved EFs may be similar or improved compared to those with decreased EFs.
1-year survival according to NYHA stage:
- Stage I: ∼ 95%
- Stage II: ∼ 85%
- Stage III: ∼ 85%
- Stage IV: ∼ 35%