Heart Failure

Also known as: Congestive cardiac failure, CCF

Heart failure is a clinical syndrome resulting from structural or functional impairment of ventricular filling or ejection, causing a constellation of symptoms and signs from inadequate cardiac output and venous congestion.

It is classified by ejection fraction: heart failure with reduced ejection fraction (HFrEF, ejection fraction 40% or below), heart failure with mildly reduced ejection fraction (HFmrEF, 41 to 49%), and heart failure with preserved ejection fraction (HFpEF, 50% or above, where the underlying problem is impaired diastolic relaxation and filling rather than reduced contractility).

This classification matters considerably, since the strongest evidence for pharmacological therapy has traditionally applied to HFrEF, though the evidence base for HFmrEF and HFpEF has expanded substantially in recent years.

Functional status is graded using the New York Heart Association (NYHA) classification, from class I (no symptom limitation) through class IV (symptoms at rest), which is used both to communicate severity and to guide certain treatment and device decisions.

This entry addresses the diagnosis and long term management of chronic heart failure; acute decompensation and its emergency management are covered in the separate Acute Heart Failure entry.

Common symptoms include exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, and reduced exercise tolerance. Fluid retention causes peripheral edema, abdominal distension from ascites, and weight gain.

Examination findings include a raised jugular venous pressure, bibasal crackles, a third heart sound (S3 gallop, reflecting rapid ventricular filling in a non-compliant or volume overloaded ventricle), a displaced apex beat from cardiomegaly, and peripheral edema. Signs of poor perfusion in more advanced disease include cool peripheries and a narrow pulse pressure.

Natriuretic peptides, either BNP or NT-proBNP, are a useful first-line test, since a normal or low level has a high negative predictive value and helps exclude heart failure as the cause of a patient's dyspnea. Levels must be interpreted with caution, as renal impairment tends to falsely elevate them, while obesity tends to falsely lower them.

Echocardiography is the key investigation for confirming diagnosis, since it establishes ejection fraction and therefore the heart failure category, identifies valvular disease, and assesses diastolic function. ECG is performed in all patients, looking for evidence of prior infarction, arrhythmia (particularly atrial fibrillation), and conduction abnormality (a broad QRS may indicate candidacy for cardiac resynchronization therapy).

CXR may show cardiomegaly and pulmonary venous congestion. Bloods should include FBC, renal function and electrolytes (both as a baseline and because renal function guides diuretic and ACE inhibitor dosing), LFTs, and thyroid function, since thyroid dysfunction is a reversible contributor to heart failure symptoms that should not be missed. Coronary angiography or non-invasive coronary imaging is considered where an ischemic cause is suspected, since revascularization may be part of management.

Differentials include chronic obstructive pulmonary disease and other causes of chronic dyspnea, anemia, and hypothyroidism, all of which can mimic or coexist with heart failure and should be actively excluded or addressed.

Heart failure with reduced ejection fraction is managed with the so called four pillars of guideline directed medical therapy, which are now typically introduced and up titrated in parallel rather than in the traditional strict sequence, given evidence that earlier combination therapy improves outcomes.

An ACE inhibitor or angiotensin receptor blocker, or, preferably, an angiotensin receptor neprilysin inhibitor (sacubitril valsartan) once the patient is established on standard therapy, forms one pillar. A beta blocker, started at a low dose once the patient is euvolemic and titrated upward as tolerated, forms the second pillar. A mineralocorticoid receptor antagonist, either spironolactone or eplerenone, forms the third pillar, requiring monitoring of potassium and renal function given the hyperkalemia risk, particularly in combination with an ACE inhibitor or ARB. An SGLT2 inhibitor, such as dapagliflozin or empagliflozin, forms the fourth pillar, with benefit demonstrated across the ejection fraction spectrum including HFpEF, independent of diabetes status.

Diuretics, typically loop diuretics such as furosemide, are used for symptomatic control of congestion, titrated to the lowest dose that maintains euvolemia, but do not independently improve mortality and are not one of the four pillars in that sense.

Additional therapies are layered on for specific situations: ivabradine for patients remaining symptomatic with a heart rate above 70 despite beta blockade and in sinus rhythm; hydralazine combined with a nitrate, particularly beneficial in patients of African descent according to trial evidence; and digoxin for symptom control, particularly useful where atrial fibrillation coexists.

Device therapy is considered once patients are optimized on medical therapy for a sufficient period to reassess ejection fraction. An implantable cardioverter defibrillator is considered for primary prevention of sudden cardiac death in patients with an ejection fraction persistently at or below 35%. Cardiac resynchronization therapy is considered for patients with a similarly reduced ejection fraction and a broad QRS complex, typically left bundle branch block morphology, since resynchronizing ventricular contraction improves both symptoms and survival in this group.

Heart failure with preserved ejection fraction management has historically had a narrower evidence base, but SGLT2 inhibitors now have clear benefit in this group and are considered standard therapy. Diuretics remain the mainstay for congestive symptom control. Management otherwise focuses heavily on treating underlying contributors and comorbidities, particularly hypertension, atrial fibrillation, obesity, and coronary artery disease, since these are frequently the primary drivers of the diastolic dysfunction underlying HFpEF.

General measures across all heart failure categories include sodium and fluid intake moderation, regular weight monitoring to detect early fluid accumulation, structured exercise rehabilitation (which improves symptoms and quality of life despite intuitive concerns), vaccination (influenza and pneumococcal), and patient education on recognizing early decompensation.

Advanced heart failure, refractory to optimized medical and device therapy, warrants assessment for mechanical circulatory support or cardiac transplantation in appropriate candidates.

Referral: cardiology for all new heart failure diagnoses, for confirmation, optimization of guideline directed therapy, and device assessment; heart failure and transplant services for advanced, refractory disease.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Rheumatic Fever

Also known as: Acute rheumatic fever

Rheumatic fever is a delayed, autoimmune complication of group A Streptococcus (Streptococcus pyogenes) pharyngitis, occurring roughly two to four weeks after the initial throat infection.

It results from molecular mimicry, in which antibodies raised against streptococcal antigens cross react with host tissue in the heart, joints, skin, and central nervous system.

It remains a major cause of acquired heart disease in children and young adults in low and middle income settings, where access to prompt treatment of streptococcal pharyngitis is limited.

Recurrent episodes cause cumulative valvular damage, and it is this valvular scarring, known as rheumatic heart disease, that carries the long term morbidity and mortality burden.

Diagnosis is guided by the Jones criteria, which separate major and minor manifestations.

The major criteria are carditis (endocarditis, myocarditis, or pericarditis, often presenting as a new murmur, particularly mitral regurgitation), polyarthritis (classically migratory, affecting large joints), Sydenham chorea (involuntary, irregular movements, often delayed in onset by weeks to months after the preceding infection), erythema marginatum (a evanescent, pink, serpiginous rash with central clearing, typically on the trunk and proximal limbs), and subcutaneous nodules (firm, painless, over extensor surfaces and bony prominences).
The minor criteria include fever, arthralgia (which cannot be counted alongside polyarthritis as a major criterion in the same patient), elevated inflammatory markers (ESR or CRP), and a prolonged PR interval on ECG.

Diagnosis requires evidence of a preceding group A streptococcal infection, together with either two major criteria, or one major plus two minor criteria. A separate, lower threshold applies for recurrent episodes in a patient with known prior rheumatic fever.

Evidence of preceding streptococcal infection is sought through a positive throat culture or rapid antigen test (though these are frequently negative by the time rheumatic fever manifests, given the delay after the original infection), or, more usefully at this stage, elevated or rising anti-streptolysin O (ASOT) or anti-DNase B titres.

Inflammatory markers (ESR and CRP) support the diagnosis as minor criteria and help track disease activity.

ECG is essential, looking for a prolonged PR interval and any arrhythmia.

Echocardiography is required in all suspected cases, both to confirm carditis (which may be subclinical, detected only on echocardiography without an audible murmur) and to assess the severity of any valvular involvement, most commonly mitral regurgitation, less commonly aortic regurgitation.

Differentials include septic arthritis, reactive arthritis, juvenile idiopathic arthritis, systemic lupus erythematosus, viral myocarditis, and infective endocarditis, particularly when carditis is the presenting feature.

Eradication of the streptococcal infection is essential even if throat culture is now negative, using a single dose of intramuscular benzathine penicillin, or oral phenoxymethylpenicillin for ten days if intramuscular treatment is not feasible.

Anti-inflammatory treatment follows separately. Arthritis and fever generally respond well to high dose aspirin or another NSAID (naproxen is a commonly used alternative), continued until symptoms and inflammatory markers settle.

Moderate to severe carditis, particularly with heart failure, is treated with corticosteroids, though evidence for a mortality or long term valvular benefit is limited and steroids are used mainly for symptomatic and hemodynamic control in this context.

Heart failure arising from severe carditis is managed with standard heart failure therapy alongside the anti-inflammatory treatment above (see Heart Failure entry).

Sydenham chorea, when mild, may only require reassurance and supportive care; more significant chorea is treated with carbamazepine or sodium valproate, with antipsychotics reserved for severe, refractory cases.

Secondary prophylaxis is the cornerstone of long term management, given the markedly increased risk of recurrent rheumatic fever and progressive valvular damage with each subsequent episode.

Regular intramuscular benzathine penicillin, typically every three to four weeks, is continued for a minimum duration determined by the presence and severity of carditis: at least five years or until age twenty one for rheumatic fever without carditis, at least ten years or until age twenty five for rheumatic fever with carditis but no residual valvular disease, and lifelong for those with established valvular disease.

Referral: cardiology for all confirmed or suspected carditis, given the need for echocardiographic assessment and monitoring of valvular disease; neurology for significant chorea.

Heart Failure

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management