Chronic Heart Failure (CHF)

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Chronic heart failure (CHF) is a clinical syndrome resulting in reduced cardiac output as a result of impaired cardiac contraction. Typical clinical symptoms of CHF include shortness of breath, fatigue and ankle swelling.1


Structural Classification

Chronic heart failure can be classified structurally based on left ventricular ejection fraction (LVEF). LVEF is the percentage of blood that enters the left ventricle in diastole that is subsequently pumped out in systole. LVEF is usually measured using transthoracic echocardiography, however, MRI, nuclear medicine scans and transoesophageal echocardiography can also be used.

European Society of Cardiology (ESC) classification:1

  • Heart failure with reduced ejection fraction (HFrEF) = EF <40%
  • Heart failure with preserved ejection fraction (HFpEF) = EF >50%
  • Heart failure with mid-range ejection fraction (HFmrEF) = EF 40-49%*

*HFmrEF is considered a grey area where normal ejection fraction is 50 or more. The definition of normal varies somewhat between experts, but NICE and the ESC guidelines agree on the 40% cut off for reduced vs preserved ejection fraction definitions.1,2


Symptomatic/Functional Classification

The New York Heart Association’s (NYHA) classification system relies on patient symptoms and level of function:3

  • Class I: no symptoms on ordinary physical activity
  • Class II: slight limitation of physical activity by symptoms
  • Class III: less than ordinary activity leads to symptoms
  • Class IV: inability to carry out any activity without symptoms


  • CHF prevalence is 1-2%, rising to 10% in over 70-year-olds4
  • It is increasingly prevalent with increasing age.


The most common causes of heart failure in the UK are coronary heart disease (myocardial infarction), atrial fibrillation, valvular heart disease and hypertension.

Cardiac output (CO) = Heart rate (HR) x Stroke volume (SV)

Stroke volume requires:

  • adequate preload
  • optimal myocardial contractility (Frank-Starling mechanism)
  • decreased afterload

As a result, cardiac output (CO) can be reduced by any of the following (potentially causing CHF):

  • decreased heart rate
  • decreased preload
  • decreased contractility
  • increased afterload


The acronym HIGH-VIS is useful to remember some of the many possible causes of CHF:

  • Hypertension (common cause)
  • Infection/immune – viral (e.g. HIV), bacterial (e.g. sepsis), autoimmune (e.g. lupus, rheumatoid arthritis)
  • Genetic – hypertrophic obstructive cardiomyopathy (HOCM), dilated cardiomyopathy (DCM)
  • Heart attack – ischaemic heart disease (common cause)
  • Volume 0verload – renal failure, nephrotic syndrome, hepatic failure
  • Infiltration – sarcoidosis, amyloidosis, hemochromatosis
  • Structural –  valvular disease, septal defects

Other causes

Endocrine disease

  • Hypothyroidism
  • Hyperthyroidism
  • Diabetes
  • Adrenal insufficiency
  • Cushing’s syndrome


  • Calcium antagonists
  • Anti-arrhythmics
  • Cytotoxic medication
  • Beta-blockers

High-output cardiac failure

Occurs in states where demand exceeds normal cardiac output:

  • Pregnancy
  • Anaemia
  • Sepsis


Presenting Complaint

Patients with CHF typically present with symptoms that have gradually worsened over months to years including:

  • Dyspnoea on exertion
  • Fatigue limiting exercise tolerance (quantify in terms of metres able to be walked)
  • Orthopnoea (patient may be using several pillows to reduce this symptom – important to ask how many to quantify symptom)
  • Paroxysmal nocturnal dyspnoea (PND) – attacks of severe shortness of breath in the night that are relieved by sitting up (pathognomonic for CHF)
  • Nocturnal cough (may also have the typical ‘pink frothy sputum’)
  • Pre-syncope/syncope
  • Reduced appetite


Past Medical History

It is important to ask about conditions associated with CHF which were discussed in the previous section. Ensure you ask about the most common causes of CHF which include:

  • Hypertension
  • Coronary artery disease (e.g. angina, myocardial infarction)
  • Valvular heart disease (e.g. aortic stenosis)



Several medications can cause or worsen CHF:

  • Beta-blockers (in the acute phase – but long term provide prognostic benefit)
  • Calcium antagonists
  • Anti-arrhythmics
  • Cytotoxic medication

Family History

Ask about close relatives with cardiac issues:

  • Cardiomyopathy (e.g. HOCM)
  • Coronary artery disease


Social History

Identify any risk factors for CHF:

  • Smoking history
  • Alcohol history
  • Recreational drugs

Clinical Examination

Cardiovascular examination

  • Tachycardia at rest
  • Hypotension
  • Narrow pulse pressure
  • Raised jugular venous pressure
  • Displaced apex beat (due to left ventricular dilatation)
  • Right ventricular heave
  • Gallop rhythm on auscultation (pathognomic for CHF)
  • Murmurs associated with valvular heart disease (e.g. an ejection systolic murmur in aortic stenosis)
  • Peripheral oedema (sacrum, ankles)

Respiratory examination

  • Tachypnoea
  • Bibasal end-inspiratory crackles and wheeze on auscultation of the lung fields
  • Wheeze
  • Reduced air entry on auscultation with stony dullness on percussion (pleural effusion)

Abdominal examination

  • Tender hepatomegaly
  • Ascites


After a comprehensive history and clinical examination have been performed, the following investigations are recommended by NICE.2


An ECG should be performed in all patients with suspected heart failure:

  • Previous myocardial infarction (e.g. old Q-waves)
  • Arrhythmias (e.g. AV block, atrial fibrillation)

ECG findings associated with heart failure

  • Tachycardia
  • Atrial fibrillation (due to enlarged atria)
  • Left-axis deviation (left ventricular hypertrophy)
  • P wave abnormalities (P.mitrale/P.pulmonale due to atrial enlargement)
  • Prolonged PR interval – AV block
  • Wide QRS complex – ventricular dyssynchrony

A normal ECG makes heart failure very unlikely.1


N-terminal pro-B-type natriuretic peptide (NT-proBNP) should be measured in all patients presenting with symptoms and clinical signs of heart failure. The NT-proBNP result will then inform the type and urgency of further investigations such as echocardiography.

  • NT-proBNP level >2000 ng/L – refer urgently for specialist assessment and transthoracic echocardiography within 2 weeks
  • NT-proBNP level 400-2000ng/L – refer routinely for specialist assessment and transthoracic echocardiography within 6 weeks
  • NT-proBNP level <400 ng/L – heart failure unlikely

Other conditions in which NT-proBNP can be raised

  • Left ventricular hypertrophy
  • Tachycardia
  • Liver cirrhosis
  • Diabetes
  • Acute or chronic renal disease


All patients with suspected chronic heart failure should undergo transthoracic echocardiography, with the urgency determined by their NT-proBNP level as discussed above.

Other Investigations

Further investigations can be useful to identify or rule out various underlying aetiologies.

Blood tests

  • FBC – anaemia
  • U&Es – renal failure, electrolyte abnormalities due to fluid overload (e.g. hyponatraemia)
  • LFTs – hepatic congestion
  • Troponin – if considering recent myocardial infarction
  • Lipids/HbA1c – ischaemic risk profile
  • TFTs – hyperthyroidism/hypothyroidism
  • Cardiomyopathy screen:
    • Serum iron and copper studies (haemochromatosis and Wilson’s disease)
    • Rheumatoid factor, ANCA/ANA, ENA, dsDNA (autoimmune disease)
    • Serum ACE (sarcoidosis)
    • Serum-free light chains (amyloidosis)


  • Glycosuria – diabetes
  • Leukocytes/nitrites – urosepsis
  • Protein/blood – renal failure

Chest X-ray

Patient’s with CHF often have associated changes on chest X-ray including:

  • A – Alveolar oedema (perihilar/bat-wing opacification)
  • B – Kerley B lines (interstitial oedema)
  • C – Cardiomegaly (cardiothoracic ratio >50%)
  • D – Dilated upper lobe vessels
  • E – Effusions (e.g. pleural effusions – blunted costophrenic angles with meniscus sign)
CXR signs of heart failure
Typical CXR signs associated with heart failure 4

Cardiac MRI

Cardiac MRI is the gold standard investigation for assessing ventricular volumes, mass and wall motion. It can also be used with contrast to identify infiltration (e.g. amyloidosis), inflammation (e.g. myocarditis) or scarring (e.g. myocardial infarction). It is typically used when echocardiography has provided inadequate views.5


Treatment aims are to improve function, quality of life, prevent hospitalisation and reduce mortality. CHF onset may be delayed through early risk factor modification and treatment of both precipitants and left ventricular systolic dysfunction.

Lifestyle Advice2

  • Fluid and salt restriction
  • Regular exercise can improve patient symptoms and prognosis
  • Smoking cessation
  • Reduce alcohol intake
  • DVLA restrictions (relevant to those driving large goods vehicles or passenger carrying vehicles)



All patients with chronic heart failure require monitoring including:

  • a clinical assessment of functional capacity, fluid status, cardiac rhythm (minimum of examining the pulse), cognitive status and nutritional status
  • a review of medication, including the need for changes and possible side effects
  • an assessment of renal function

The frequency of monitoring will depend on the clinical status and stability of the patient.


Pharmacological Treatment2

Pharmacological treatment aims to increased cardiac output ­by optimising preload and contractility whilst decreasing afterload. The medications below target the pathological sympathetic response and renin-angiotensin-aldosterone system (RAAS) activation that occurs in CHF.

ACE inhibitors

  • Decrease RAAS activation.
  • All patients with a left ventricular ejection fraction (LVEF) of 40% or less, regardless of symptom severity, should receive an ACE inhibitor unless contraindicated or not tolerated.
  • ACE inhibitors have been shown to improve ventricular function and patient well-being, to reduce mortality and hospital admissions in many large clinical trials and to be indicated in all stages of left ventricular systolic dysfunction (LVSD).
  • Contraindications include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.
  • U&Es should be checked prior to starting treatment and then after 1-2 weeks of treatment.


  • Increase sodium excretion causing diuresis and decreased afterload.
  • Diuretics (e.g. furosemide) should be routinely used for the relief of congestive symptoms and fluid retention
  • Doses should be titrated according to clinical response (renal function should be monitored)


  • Decrease heart rate, myocardium oxygen demand and RAAS activation.
  • Beta-blockers (e.g. bisoprolol) should be used in all patients with symptomatic heart failure and a LVEF of ≤40% (unless contraindicated or not tolerated)
  • They should be initiated in stabilised patients already on diuretics and ACE inhibitors, regardless of whether or not symptoms persist.
  • Contraindications include asthma, 2nd or 3rd degree AV block, sick sinus syndrome and sinus bradycardia.
  • Blood pressure and heart rate need to be monitored carefully when adjusting doses.

Angiotensin-II receptor antagonists (ARBs)

  • Target RAAS activation
  • ARBs (e.g. candesartan and valsartan) are indicated for the treatment of heart failure with reduced ejection fraction in patients who cannot tolerate ACE inhibitors.
  • Patients must have normal serum potassium and adequate renal function to commence an ARB.

Mineralocorticoid/aldosterone receptor antagonists (MRAs)

  • Antagonise aldosterone increasing ­sodium excretion causing diuresis and decreased afterload.
  • A low-dose aldosterone antagonist (e.g. spironolactone or eplerenone) should be considered in all patients unless contraindicated or not tolerated and in the absence of hyperkalaemia and significant renal dysfunction.
  • Measure renal function and U&Es at one week and four weeks after starting/increasing the dose. This should be repeated monthly for the first three months and then at least twice a year on maintenance treatment.


  • Ivabradine inhibits the sinoatrial node, slowing the heart rate of patients in sinus rhythm, increasing stroke volume whilst preserving myocardial contractility.
  • Ivabradine does not slow the ventricular rate in atrial fibrillation.
  • It has been shown to reduce cardiovascular death or hospitalisation for heart failure by 18%.

ARNI (angiotensin receptor and neprilysin inhibitor)

  • ARNI’s increase BNP levels by inhibiting the neprilysin enzyme which breaks down BNP.
  • Higher BNP causes natriuresis/diuresis and therefore decreases afterload.


Non-pharmacological Intervention2

If heart failure is caused or worsened by surgically correctable conditions, these should be treated appropriately:

  • Revasculation (e.g. coronary artery bypass grafting)
  • Valve surgery (e.g. aortic valve replacement)
  • Implantable cardiac defibrillator (ICD) – inserted if EF <30% for prevention of fatal arrhythmia.
  • Cardiac resynchronisation therapy + defibrillator (CRT-D) – a biventricular pacemaker for EF <30% + QRS >130 m/sec to re-synchronise left and right ventricular contraction to improve EF.
  • Cardiac transplantation is rare and strict criteria must be met for consideration.


  • Prognosis is poor on the whole, with approximately 50% of people with heart failure dying within five years of diagnosis.5

Key Points

  • Chronic heart failure (CHF) is a clinical syndrome resulting in reduced cardiac output as a result of impaired cardiac contraction.
  • The most common causes of heart failure in the UK are coronary heart disease (myocardial infarction, atrial fibrillation, heart block) and hypertension.
  • Typical clinical symptoms of CHF include shortness of breath, fatigue and ankle swelling.1
  • Investigations typically required for diagnosis include ECG, NT-proBNP and echocardiography.
  • Management involves a combination of lifestyle advice and pharmacological therapies (and in some cases surgical intervention).
  • Prognosis is poor.


1. European Society of Cardiology. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Published in 2016. Available from [LINK].

2. Chronic heart failure in adults – diagnosis and management; NICE Guidance (Sept 2018). Available from: [LINK]

3. Penn Medicine. Heart Failure Classification – Stages of Heart Failure and Their Treatments. Published in 2014. Available from: [LINK]

4. Mikael Häggström. Public domain. Available from: [LINK]

5. Dr Colin Tidy. Heart failure. Published November 2018. Available from: [LINK]


 Dr Steven Sutcliffe

Consultant Cardiologist


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