Heart failure


Definition & classification

Heart failure is a clinical syndrome that results from an inability of the heart to maintain adequate circulation.

It is a progressive disorder associated with high morbidity and mortality. Prognosis is generally poor; approximately 50% die within five years. 

A wide range of classifications reflects the complexity of the condition.

Classification of HF


The New York Heart Association (NYHA) classifies the symptoms of heart failure as follows:

NYHA classification

Systolic vs Diastolic


  • Reduced left ventricular ejection fraction (LVEF) - the heart is pumping out a reduced proportion of the blood that fills its ventricles during diastole.
  • Results in ventricular dilatation and characteristic eccentric remodelling.


  • Impaired ventricular relaxation or filling
  • Contraction is unaffected and as such the LVEF is preserved.
  • Diastolic heart failure may be called 'heart failure with preserved LVEF'.
  • Ventricular hypertrophy tends to develop and characteristic concentric remodelling may occur.

Cardiac remodelling refers to changes in cardiac size, shape and function in response to cardiac injury or increased load (e.g. exercise). 

Pathological remodelling may occur after conditions such as myocardial infarction or cardiomyopathy.


The aetiology of heart failure is complex. 

Though systemic disease may cause heart failure it will typically do so through one of the pathologies listed below (often cardiomyopathy). The exception are the high-output heart failures which are discussed separately.

1. Vascular

These are the most common causes of heart failure.

  • Ischaemic heart disease (35-40%)
  • Hypertension (15-20%)

2. Muscular

Cardiomyopathy is a common cause of heart failure. Dilated cardiomyopathies are often idiopathic.

  • Dilated cardiomyopathy (30%)
  • Hypertrophic cardiomyopathy
  • Congenital heart disease

3. Valvular

Valvular disease may lead to either acute or chronic heart failure.

  • Stenotic valves
  • Regurgitant valves

4. Electrical

Arrhythmias (abnormalities of normal conduction) may cause acute heart failure through decompensation.

5. High-output

Typically heart failure is caused by a reduced cardiac output. In some cases, however, the cardiac output may be raised but the systemic vascular resistance very low. Causes include:

  • Anaemia
  • Septicaemia
  • Thyrotoxicosis 
  • Liver failure


Stroke volume: the amount of blood pumped out of the heart from each contraction.

Cardiac output: the amount of blood pumped out of the heart in one minute, equivalent to HR x SV.

Preload: stretching of cardiomyocytes at the end of diastole. 

Afterload: pressure or load against which the ventricles must contract.

Inotropy: refers to myocardial contractility (i.e. the force of muscular contractions).

Frank-Starling law

The relationship between ventricular stretching and contractility. Essentially stretching of cardiac muscle (within physiological limits) will increase the force of contraction.

Discovered in the mid-19th century by Otto Frank and Ernest Starling. The ability of the heart to respond to increased venous return by increasing the stroke volume is essential to normal cardiac function. Failure to do so would result in input-output mismatch and pooling of blood in either the systemic or pulmonary circulation.

Frank-Starling Curve

The titles of the axis may vary slightly. Here we display stroke volume (SV) and left ventricular end-diastolic volume (LVEDV) - essentially the preload.

In a normal heart, increased venous pressures lead to increased venous return and raised end diastolic volume (EDV). This increased EDV means an increase in the preload (see definition above), as there is increased stretch on the cardiomyocytes. This increased stretching - an increase in the length of the sarcomere - leads to a more forceful contraction. In turn, this increase in contractility leads to an increase in the stroke volume.

Frank-Starling Curve

Interestingly, the heart does not sit on a single curve, rather it is affected by afterload and the inotropic state.

  • Reduced afterload and increased inotropy - move the curve up and to the left (green)
  • Increased afterload and decreased inotropy - move the curve down and to the right (red).

In effect, venous return governs where on the curve the heart sits while the pre-existing afterload and inotropic environment control which curve it sits on.

In summary, the primary determinants of stroke volume are:

  • Preload
  • Myocardial contractility
  • Afterload

The relationship between increasing preload and increasing stroke volume does not continue unfettered. At a point, increases in preload lead to a depression of contractility and stroke volume - this concept is crucial in understanding heart failure.


As a heart fails the amount of blood left after each contraction increases i.e. the ejection fraction decreases. This increased end-systolic volume (ESV) means the myocardium experiences greater stretch. In a normal heart this would lead to an increase in myocardial contractility by the Frank-Starling principle.

However, in a failing heart, this causes a reduction in stroke volume (and thus cardiac output).

Pathophysiology of heart failure

The body may compensate for this in a number of ways:

  • Increasing preload (increasing venous pressures):
    • Increases EDV compensating for the reduced ejection fraction, thus maintaining cardiac output. 
    • In severe disease, large increases result in pulmonary oedema, ascites and peripheral oedema.
  • Increasing heart rate (a sinus tachycardia):
    • Remember cardiac output = stroke volume x heart rate.

Renin-angiotensin system (RAS):

  • Reduced cardiac output leads to renal hypoperfusion and activation of RAS.
  • Contributes to increased venous pressures, in addition to the retention of sodium and water leading to oedema

Sympathetic system:

  • Reduced cardiac output activates the sympathetic nervous system via baroreceptors.
  • Increases myocardial contractility and heart rate.
  • Chronic activation is detrimental triggering myocyte cell death and further activation of RAS.

Neurohormonal and sympathetic influences in heart failure

To maintain cardiac output, the heart undergoes hypertrophy of the stressed myocardium. This accompanied by other compensatory mechanisms discussed above may mean that patients are asymptomatic at rest. However, physical activity may lead to decompensation and the development of symptoms.

Clinical features

CHF typically manifests with dyspnoea and fatigue (which may limit exercise tolerance) and symptoms associated with fluid retention.


  • Shortness of breath (SOB)
  • Wheeze
  • Fatigue 
  • Weight loss 
  • Paroxysmal nocturnal dyspnoea (SOB and coughing at night)
  • Orthopnoea (positional-related SOB)
  • Ankle swelling


  • Raised JVP
  • Displaced apex
  • Crackles
  • Ankle swelling
  • Heart sounds S3/S4
  • Pulsus alternans (variation in pulse strength)
  • Hepatomegaly
  • Ascites

Clinical features of CHF

Investigations & diagnosis

NICE recommends echocardiography and specialist assessment​ in patients with suspected heart failure. BNP is used to stratify risk in those without previous history of myocardial infarction.

Indications for urgent specialist assessment within 2 weeks:

  • Previous MI
  • Severe symptoms (NYHA IV)
  • Evidence of valvular heart disease or impaired kidney function
  • BNP > 400 pg/mL

B-type natriuretic peptide (BNP) is a protein released by cardiomyocytes in response to excessive stretching. It is used to assess the likelihood of heart failure. Conditions other than heart failure which may raise BNP levels include diabetes, sepsis, old age, hypoxaemia (PE and COPD), kidney disease, and liver cirrhosis.

Diagnosis of CHF


  • Observations
  • Blood pressure
  • ECG
  • Urinalysis


  • FBC - exclude anaemia, infective cause.
  • U&Es - exclude renal failure as a cause of oedema.
  • LFT - exclude liver failure as a cause of oedema.
  • Cholesterol and HbA1c - cardiovascular risk stratification.
  • TFT - exclude thyroid disease.
  • BNP


  • Echocardiogram:
    • Evidence of previous MI
    • Left ventricular strain / hypertrophy
    • Conduction abnormalities / AF
  • CXR:
    • Cardiomegaly (Cardiothoracic ratio > 50% on PA film)
    • Alveolar shadowing oedema
    • Kerley B lines (fluid in septae of secondary lobules)
    • Pleural effusion
    • Upper lobe diversion


  • Cardiac catheterisation
  • Cardiac biopsy
  • 24 hr ECG
  • Lung function tests


Management follows NICE guidance and is based upon the type of heart failure, although there are some general management principles.

Modifiable risk factors:

  • Lifestyle modification and patient education are paramount in treating heart failure.
  • Patients personal needs and values must be taken into account.
  • Offer annual flu and a one-off pneumococcal vaccination.
  • Smoking, alcohol, travel, driving and sexual advice may be needed.


  • Example: Furosemide 20 mg OD
  • Can be started immediately; titrated up or down according to the degree of oedema.
  • Improve symptoms but not mortality.

Management of CHF

LV systolic dysfunction

1. Angiotensin-converting enzyme (ACE) inhibitors:

  • Example: Ramipril 1.25 mg OD
  • Started once the diagnosis is established; improve prognosis and symptoms.
  • Check renal function prior to initiation; repeat tests within 1-2 weeks.
  • Double dose every 2-4 weeks until target dose is achieved (e.g. Ramipril 5 mg BD).

Angiotensin receptor blockers (ARBs) such as losartan may be used in those individuals who have intolerable side effects with ACE inhibitors.

2. Beta-blockers:

  • Example: Bisoprolol 1.25 mg OD
  • Improve prognosis and symptoms.
  • Contra-indicated in severe asthma, COPD, pulmonary oedema, or bradycardia.
  • Double dose every 4 weeks until target dose is achieved (e.g. Bisoprolol 5 mg BD).

If a patient remains symptomatic despite optimal treatment consider adding second-line treatment:

  • Aldosterone antagonist
  • Angiotensin receptor blocker
  • Hydralazine in combination with nitrate
  • Digoxin

Second line treatment of CHF

Preserved LVEF

Insufficient evidence exists for the role of ACE-inhibitors, ARBs, and beta-blockers in heart failure with preserved LVEF. 

  • A loop diuretic (e.g. furosemide) may be given if the patient has symptomatic fluid overload.
  • Specialist input is required if further treatment is necessary.
  • Co-morbidities and underlying causes should be addressed.

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