Congestive heart failure

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”).

• Heart failure (HF): a complex of signs and symptoms caused by structural or functional impairment of ventricular filling and/or ejection of blood ^[1]
• 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
• Heart failure with reduced ejection fraction (HFrEF, systolic HF): CHF with reduced stroke volume, reduced ejection fraction (EF) (left ventricular EF ≤ 35–40%)
• Heart failure with preserved ejection fraction (HFpEF, diastolic HF): CHF with reduced stroke volume, normal/reduced EDV, and preserved EF (LVEF ≥ 40–50%)
• Right heart failure (RHF): CHF due to right ventricular dysfunction resulting in congestion of blood in the vena cavae and peripheral veins, which increases venous hydrostatic pressure and results in peripheral edema, increased jugular venous pressure, ascites, and hepatomegaly.
• Left heart failure (LHF): CHF due to left ventricular dysfunction resulting in tissue hypoperfusion and increased pulmonary capillary pressure
• Biventricular (global) CHF: CHF in which both the left and right ventricles are affected resulting in the development of both RHF and LHF symptoms
• Chronic compensated CHF: a patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable ^[2]
• Acute decompensated CHF: sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition (e.g., myocardial infarction)

• ∼ 1.9% of the population in the US has CHF (∼ 6.2 million individuals) ^[3]
• The incidence is higher among African Americans and Hispanics. ^[4]
• Incidence increases with age: ∼ 10% of individuals > 60 years old are affected. ^[5]
• Systolic heart disease is the most common form of CHF overall.

Epidemiological data refers to the US, unless otherwise specified.

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 CHF.

American Heart Association (AHA) classification (2013) ^[1]

The AHA classification system categorizes patients according to the stage of disease based on an objective assessment of clinical features and diagnostic findings.

NYHA functional classification ^[1]

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.

Cardiac output, which is stroke volume times heart rate, is determined by three factors: preload, afterload, and ventricular contractility.

Underlying mechanism of reduced cardiac output

• Heart failure with reduced ejection fraction (HFrEF)
  • Reduced contractility → systolic ventricular dysfunction → decreased left ventricular ejection fraction (LVEF) → decreased cardiac output
  • Causes include:
    • Damage and loss of myocytes (e.g., following myocardial infarction, coronary artery disease, dilated cardiomyopathy)
    • Cardiac arrhythmias
    • High-output conditions (see “High-output heart failure” below)
• Heart failure with preserved ejection fraction (HFpEF)
  • Decreased ventricular compliance → diastolic ventricular dysfunction → reduced ventricular filling and increased diastolic pressure → decreased cardiac output (while the left ventricular ejection fraction remains normal)
  • Causes include:
    • Increased stiffness of the ventricle (e.g., long-standing arterial hypertension with ventricular wall hypertrophy, restrictive cardiomyopathy)
    • Impaired relaxation of the ventricle (e.g., constrictive pericarditis, pericardial tamponade)
• Left-sided heart failure (HFrEF and/or HFpEF)
  • Increased left ventricular afterload: increased mean aortic pressure (e.g., arterial hypertension), outflow obstruction (e.g., aortic stenosis)
  • Increased left ventricular preload: left ventricular volume overload (e.g., backflow into the left ventricle caused by aortic insufficiency)
• Right-sided heart failure
  • Increased right ventricular afterload: increase in pulmonary artery pressure (e.g., pulmonary hypertension)
  • Increased right ventricular preload: right ventricular volume overload (e.g., tricuspid valve regurgitation, left-to-right shunt)

Consequences of decompensated heart failure

• Forward failure: reduced cardiac output → poor organ perfusion → organ dysfunction (e.g., hypotension, renal dysfunction)
• Backward failure
  • Left ventricle: increased left-ventricular volumes or pressures → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary edema (presenting with orthopnea) and increased pulmonary artery pressure
  • Right ventricle: increased pulmonary artery pressure → reduced right-sided cardiac output → systemic venous congestion → peripheral edema and progressive congestion of internal organs (e.g., liver, stomach)
  • Nutmeg liver: the macroscopic appearance of the liver which resembles a nutmeg seed due to ischemia and fatty degeneration from hepatic venous congestion

CHF is characterized by reduced cardiac output that results in venous congestion and poor systemic perfusion.

Compensation mechanisms

The compensation mechanisms are meant to maintain the cardiac output when stroke volume is reduced.

• Increased adrenergic activity: : increase in heart rate, blood pressure, and ventricular contractility
• Increase of renin-angiotensin-aldosterone system activity (RAAS): activated following decrease in renal perfusion secondary to reduction of stroke volume and cardiac output
  • ↑ Angiotensin II secretion results in:
    • Peripheral vasoconstriction → ↑ systemic blood pressure → ↑ afterload
    • Vasoconstriction of the efferent arterioles; → ↓ net renal blood flow and ↑ intraglomerular pressure → maintained GFR
  • ↑ Aldosterone secretion → ↑ renal Na⁺ and H₂O resorption → ↑ preload
• Secretion of brain natriuretic peptide (BNP)
  • Definition: ventricular myocyte hormone released in response to increased ventricular filling and stretching
  • Mechanism of action: ↑ intracellular smooth muscle cGMP → vasodilation → hypotension and decreased pulmonary capillary wedge pressure

General features of heart failure

• Nocturia ^[8]
• Fatigue
• Tachycardia, various arrhythmias
• S₃/S₄ gallop on auscultation
• Pulsus alternans
• Cachexia ^[9]

Clinical features of left-sided heart failure

• Symptoms of pulmonary congestion
  • Dyspnea , orthopnea
  • Pulmonary edema
  • Paroxysmal nocturnal dyspnea
    • Nocturnal bouts of coughing and acute shortness of breath
    • Caused by reabsorption of peripheral edema at night → increased venous return
  • Cardiac asthma
    • Increased pressure in the bronchial arteries → airway compression and bronchospasm
    • Symptoms mimic asthma, with shortness of breath, wheezing, and coughing. ^[10]
• Physical examination findings ^[11]
  • Bilateral basilar rales may be audible on auscultation.
  • Laterally displaced apical heart beat (precordial palpation beyond the midclavicular line)
  • Coolness and palor of lower extremities

Clinical features of right-sided heart failure

• Symptoms of fluid retention and increased CVP
  • Peripheral pitting edema: as a result of fluid transudation due to increased venous pressure
  • Hepatic venous congestion symptoms
    • Abdominal pain
    • Jaundice
  • Other symptoms of organ congestion (e.g., nausea, loss of appetite in congestive gastropathy)
• 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

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) ^[12]
  • Physiological causes
    • Pregnancy
    • Fever
    • Exercise
  • Other causes
    • Anemia
    • Systemic arteriovenous fistulas (e.g., Paget disease of bone)
    • Hyperthyroidism
    • Wet beriberi (vitamin B₁ deficiency)
    • Sepsis
    • Multiple myeloma
    • Glomerulonephritis
    • Polycythemia vera
    • Carcinoid heart disease ^[13]
• Clinical features
  • Symptoms of low-output CHF ^[14]
    • Dyspnea, tachypnea
    • Tachycardia
    • Low blood pressure
    • 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
• Diagnostics
  • Primarily a clinical diagnosis
  • X-ray and echocardiography: cardiomegaly
• Treatment
  • Heart failure management
    • Symptom relief
    • Hemodynamic stabilization
  • Treatment of the underlying condition

Approach

• All patients: Establish the diagnosis with routine laboratory studies, cardiac biomarkers, ECG, chest x-ray, and echocardiogram.
• If CHF is confirmed, investigate for:
  • Underlying causes (consider coronary angiogram, chest imaging, and advanced cardiac imaging)
  • Modifiable risk factors (e.g., hypertension, coronary artery disease)

Laboratory studies

Routine laboratory studies ^[1]

• CBC: Screen for anemia and infection.
• BMP
  • Creatinine: normal or ↑
  • Na: normal or ↓ (hyponatremia can indicate a poor prognosis) ^[15]
  • Glucose or HbA1c: may be elevated in diabetes ^[16]
• Liver chemistries: Elevations, particularly of the cholestatic enzymes, can indicate hepatic venous congestion. ^[17][18]
• Inflammatory markers: ↑ CRP can indicate acute infection or inflammation
• Fasting lipid studies: Elevated cholesterol is a common finding.
• TSH: possibly lowered as a sign of hyperthyroidism ^[1]

Cardiac biomarkers ^[1][19]

• 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) ^[20][21]
  • Indications
    • 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. ^[22]
• Cardiac troponin T or I
  • Elevated levels can suggest ischemia but troponins can be elevated in CHF without acute myocardial ischemia. ^[23][24]
  • Potentially helpful for risk stratification ^[19]

Imaging

Transthoracic echocardiogram (TTE)

• Indications
  • Every patient with suspected new-onset HF (best initial imaging test to assess cardiac structure and function) ^[25][26]
  • Changes in clinical features in patients receiving treatment (monitoring)
  • Evaluation for device therapy
• Supportive findings
  • Features of heart failure
    • Left ventricular systolic dysfunction: assessed via LVEF ^[1]
      • HFpEF: normal (50–70%)
      • Borderline HFpEF: (41–49%)
      • HFrEF: reduced (≤ 40%)
    • Diastolic dysfunction ^[27]
    • Pulmonary hypertension and right ventricular dysfunction
    • Pericardial and/or pleural effusion ^[28]
  • Evidence of complications ^[27]
    • Cardiac dyssynchrony
    • Functional mitral regurgitation
    • Left atrial enlargement
  • Underlying causes, including:
    • Regional wall motion abnormalities in coronary artery disease
    • Left ventricular hypertrophy in hypertension
    • Flow abnormalities across heart valves in valvular disease

Chest x-ray ^[1]

• Indication: acute, new-onset, or suspected heart failure
• Findings
  • Changes to cardiac silhouette
    • Enlarged: cardiothoracic width ratio > 0.5 ^[29]
    • Boot-shaped heart on PA view: RV enlargement
    • Signs of pericardial effusion (e.g., water bottle heart)
  • X-ray findings of pulmonary congestion
  • Signs of concurrent heart conditions, including:
    • Valvular calcifications in valvular disease
    • Pericardial calcification in constrictive pericarditis

Electrocardiogram (ECG) ^[30][31]

ECG abnormalities in CHF are common but mostly nonspecific.

• Common findings
  • ECG signs of left ventricular hypertrophy (e.g., positive Sokolow-Lyon index) ^[32]
  • Left axis deviation
  • ST-T abnormalities (e.g., ST depression)
  • P wave abnormalities (e.g., P mitrale)
  • Prolonged QTc interval ^[33]
  • Incomplete or complete left bundle branch block ^[30]
• Signs of concurrent heart conditions
  • Ischemic changes of a previous or acute myocardial infarction (e.g., Q waves or ST elevations)
  • Arrhythmias (e.g., atrial fibrillation, sinus tachycardia or bradycardia)
  • Pericardial effusion (e.g., electrical alternans, low voltage QRS)

Additional studies ^[1]

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
  • Gold standard for assessment of ventricular volume, mass, and ejection fraction ^[25]
  • Indications include:
    • Diagnostic uncertainty following echocardiography
    • Investigation of congenital heart disease or infiltrative processes
    • Determination of myocardial scar burden
• Radionuclide ventriculography: used to assess LVEF and volume if other imaging modalities are inadequate or contraindicated ^[1]
• PET myocardial perfusion imaging: alternative noninvasive workup for suspected coronary artery disease

Other

• Left heart catheterization or coronary angiogram: identification and treatment of coronary artery disease
• Right heart catheterization ^[1]
  • Assessment of right heart function and pulmonary vascular resistance in patients being considered for mechanical circulatory support or transplant
  • Monitoring in cardiogenic shock: SvO₂ will be low in decompensated heart failure. ^[1]
• Endomyocardial biopsy: indicated if there is ongoing diagnostic uncertainty in rapidly progressive disease or to confirm the diagnosis of infiltrative heart disease ^[1]
• Blood pressure monitoring: Consider in patients with suspected hypertension.
• ECG monitoring: Consider in suspected paroxysmal atrial fibrillation or other underlying arrhythmias.

Sputum analysis in patients with pulmonary edema may show heart failure cells (hemosiderin-containing cells).

General measures ^[1]

Lifestyle modifications

These interventions reduce general risk factors that are known to lead to the progression of CHF or other comorbidities (e.g., diabetes mellitus, hypertension).

• Exercise
• Cessation of smoking, alcohol consumption, and recreational drug use
• Weight loss ^[35]
• Immunization: pneumococcal vaccine and seasonal influenza vaccine

Patient/family education

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 ^[1]
  • Salt restriction: ≤ 1.5 g/day in stages A and B, ≤ 3 g/day in stages C and D
  • Avoidance of potassium-rich foods while taking aldosterone antagonists ^[36]
  • Fluid restriction: 1.5–2 L/day in stage D patients who have edema and/or hyponatremia
• 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. ^[37]
  • 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 ^[38][39]

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.
• Diabetes
  • Screen for hyperglycemia and implement gradual glycemic control. ^[25]
  • Consider starting an SGLT2 inhibitor. ^[40]
• Iron deficiency: Screen for and start iron replacement in patients with NYHA class II and III symptoms and iron deficiency. ^[19][41]
• Obstructive sleep apnea: Consider nocturnal continuous positive airway pressure (CPAP) therapy. ^[1][19]
• Atrial fibrillation: Start either rate or rhythm control and consider anticoagulation. ^[1]
• Coronary artery disease: Consider coronary revascularization if there is concomitant ischemic heart disease.

Avoidance of drugs that may worsen CHF ^[1]

• Most antiarrhythmic agents
• Calcium channel blockers (except amlodipine)
• NSAIDs
• 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) ^[42]

Avoid the simultaneous use of nondihydropyridine calcium channel blockers with beta blockers as this can cause complete heart block. ^[43]

Medical treatment of heart failure

Initial therapy ^[1][19]

• 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.”

Drugs that improve prognosis are beta blockers, ACE inhibitors, ARNIs, aldosterone antagonists, and hydralazine with nitrate.

Diuretics and digoxin improve symptoms and significantly reduce the number of hospitalizations.

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.

Invasive interventions

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. ^[46]

• 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. ^[47]
  • 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 ^[1]
    • HFrEF with expected survival of > 1 year if, despite receiving optimized medical therapy for 3–6 months, the following criteria are still met:
      • Stage B with ischemic cardiomyopathy if LVEF is ≤ 30%
      • Stage C with dilated cardiomyopathy (DCM) or ischemic heart disease with an LVEF ≤ 35% and NYHA class II–III symptoms
    • Patients who have previously had sustained VT or a cardiac arrest secondary to VF or VT ^[48]
• 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:
    • Improved ventricular function ^[1][49]
    • Reversal of ventricular remodeling
    • Reduction of secondary mitral regurgitation
  • 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. ^[1]
    • NYHA class I–IV symptoms in sinus rhythm with QRS duration of > 150 ms; (can be either left bundle branch block (LBBB) pattern or non-LBBB pattern)
    • Patients with LVEF ≤ 35% who require pacing for other purposes, e.g., atrial fibrillation, replacement of existing pacemaker

Management of end-stage heart failure

• General principles
  • 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
  • Used as a temporary measure to maintain organ perfusion in patients with cardiogenic shock (see “Acute decompensated heart failure”)
  • In rare cases, may be used for symptom control in patients receiving palliative care ^[1]
• 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. ^[1][50]

• 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
  • A complication of right-sided heart failure characterized by cirrhosis due to chronic hepatic vein congestion.
  • Associated with "nutmeg liver" (diffuse mottling on imaging due to ischemia and fatty degeneration).
• Venous stasis, leg ulcers

We list the most important complications. The selection is not exhaustive.

• Definition
  • A complex syndrome in which renal function progressively declines as a result of severe cardiac dysfunction ^[51]
  • Occurs in ∼ 30% of cases of ADHF ^[52]
• Pathophysiology
  • 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
• Diagnostics: ↓ GFR, ↑ creatinine that cannot be explained by underlying kidney disease ^[53]
• Treatment: heart failure and renal failure management (see “Acute renal injury”)
• Prognosis: : CHF with reduced GFR and high creatinine levels (> 3 mg/dL) is associated with a poor prognosis. ^[53][54]

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 ^[55]
  • Elevated BNP
  • Hyponatremia
  • Systolic BP < 120 mm Hg
  • Diabetes
  • Anemia
  • Weight loss or underweight
  • S₃ heart sound
  • Implantable cardioverter-defibrillator use
  • Frequent hospitalizations due to CHF
• 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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