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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
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
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.
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
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)
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.
Fluid and salt restriction
Regular exercise can improve patient symptoms and prognosis
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 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.
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.
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.
If heart failure is caused or worsened by surgically correctable conditions, these should be treated appropriately:
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
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. Patient.info. Heart failure. Published November 2018. Available from: [LINK]