Heart failure



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

Heart failure (HF) is a clinical syndrome with multiple aetiologies. It is commonly secondary to ischaemic heart disease or hypertensive heart disease. The condition is characterised by progressive shortness of breath, fatigue and fluid overload. Unfortunately, HF is a progressive disorder associated with high morbidity and mortality. Prognosis is generally poor; approximately 50% die within five years.

There are many different ways to classify heart failure, which reflex the complexity of the condition:

  • Acute versus chronic
  • Right-sided versus left-sided
  • Systolic (HFrEF) versus diastolic (HFpEF)
  • High output versus low output

Heart failure classification

Acute vs chronic

Acute heart failure is characterised by a rapid onset of symptoms and/or signs of heart failure that is usually life-threatening. Acute heart failure requires urgent evaluation and treatment. The most common causes of acute heart failure include acute myocardial dysfunction (ischaemic, inflammatory), acute valvular, pericardial tamponade. Acute heart failure may present suddenly with cardiogenic shock or subacutely with decompensation of chronic heart failure.

Chronic heart failure is due to progressive cardiac dysfunction from structural and/or functional cardiac abnormalities. There is a reduction in cardiac output and/or elevated intracardiac pressure at rest or on stress. Chronic heart failure is usually precipitated by conditions that affect the muscle (e.g. cardiomyopathy), vessels (e.g. ischaemic heart disease), valves (e.g. aortic stenosis), or conduction (e.g. atrial fibrillation). Chronic heart failure is characterised by progressive symptoms with episodes of acute deterioration.

Systolic vs diastolic

Systolic heart failure refers to a reduction in the left ventricular ejection fraction (LVEF). In other words, the heart is pumping out a reduced proportion of the blood that fills its ventricles during diastole. The increase in blood at the end of systole leads to ventricular stretch, dilatation, and eccentric remodelling.

Diastolic heart failure refers to impaired ventricular relaxation or filling. The contraction during systole is unaffected, which means the LVEF is preserved. This leads to the term heart failure with preserved ejection fraction or HFpEF. Ventricular hypertrophy tends to develop and diastolic heart failure is characterised by concentric remodelling.

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 type of remodelling may predispose to systolic or diastolic heart failure.

Right vs left

Left-sided heart failure may be caused by a wide range of conditions. It is the most common form of heart failure that is associated with a reduced or preserved pumping function of the left ventricle. Advanced left-sided heart failure commonly causes right-sided failure due to increased intrathoracic pressure and pulmonary hypertension. The combination of left and right failure is known as congestive cardiac failure.

Right-sided heart failure commonly occurs as a result of advanced left-sided failure. Primary right-sided heart failure is uncommon and broadly related to three categories:

  • Pulmonary hypertension
  • Pulmonary/Tricuspid valve disease
  • Pericardial disease

Pulmonary hypertension may occur secondary to left-sided heart disease, primary pulmonary hypertension or significant pulmonary disease (e.g. COPD).

High output vs low output

The traditional concept of heart failure is a low output state as the heart cannot maintain an adequate cardiac output to meet the demands of the body. This results in increased systemic vascular resistance in an attempt to maintain mean arterial pressure. Clinically, patients have a weak pulse, cool peripheries and low blood pressure.

In high output failure there is a high cardiac output (i.e. > 8L/min). The heart is unable to meet the increased demand for perfusion despite normal cardiac function. The problem is with reduced systemic vascular resistance, often due to diffuse arteriole vasodilatation or shunting (transfer of blood from arteries to veins bypassing the capillary beds that increase venous flow and overloads the heart). It is generally due to states of increased metabolic demand (e.g. hyperthyroidism), reduced vascular resistance (e.g. thiamine deficiency, sepsis) or significant shunting (e.g. large arteriovenosu fistula).

The exact mechanisms leading to high output failure are usually specific to the underlying cause.


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


There are a number of key terms to be aware of to better understand heart 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

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 in failure

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 pathogenesis of heart failure is complex and follows from mechanisms that result in a failure of cardiac output.

To understand heart failure, we briefly have to review what makes up our mean arterial pressure (i.e. our blood pressure).

Mean arterial pressure

Mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle. It can be calculated as follows:

MAP = diastolic blood pressure + 1/3rd of the pulse pressure

Pulse pressure is the difference between systolic and diastolic blood pressure.

MAP is dependent on the cardiac output and systemic vascular resistance

  • Cardiac output: the amount of blood pumped out the heart each minute. Measured in litres per minute (L/min).
  • Systemic vascular resistance: resistance to blood flow offered by all of the systemic vasculatures, excluding the pulmonary vasculature.

Cardiac output is determined by heart rate x stroke volume:

  • Heart rate: number of times the heart beats each minute
  • Stroke volume: the amount of blood pumped by the left ventricle with each contraction

Systemic vascular resistance is determined by factors that alter vessel size:

  • Vasodilatation: reduced vascular resistance
  • Vasoconstriction: increased vascular resistance


Stroke volume

Stroke volume is the amount of blood pumped out of the left ventricle in one contraction. It can be calculated as the end-diastolic volume (i.e. the amount of blood left in the ventricle at the end of diastole) minus the end-systolic volume (i.e. the amount of blood left in the ventricle at the end of systole).

Several factors can influence the stroke volume and thus the cardiac output.

  • Preload: stretching of cardiomyocytes at the end of diastole.
  • Afterload: pressure or load against which the ventricles must contract.
  • Contractility (Inotropy): refers to myocardial contractility (i.e. the force of muscular contractions)

Preload is influenced by venous return and filling time:

  • Venous return: increased venous return increases the preload and thus stretch on the cardiomyocytes
  • Filling time: a longer filling time in diastole increases the blood within the ventricle

Afterload is influenced by vascular resistance and valvular disease

  • Vascular resistance: vasoconstriction increases the pressure the heart has the pump against decreasing SV
  • Valvular disease: stenotic valves increases the pressure the heart has to pump against decreasing SV

Contractility is influenced by myocardial strength and the autonomic nervous system

  • Muscular function: increased muscular bulk (e.g. hypertrophy) is a physiological and pathological response to increase SV
  • Autonomic nervous system: innervation from the parasympathetic and sympathetic nervous systems alter the strength of contraction

Stroke volume

The failing heart

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). This is because the relationship between cardiomyocyte stretch and contractility cannot continue unfettered. There is a physiological limit. This concept is crucial in understanding heart failure.

Frank-starling - failing heart

Beyond the physiological limit. Increases in preload have a negative effect on stroke volume.

Compensatory mechanisms

The body may compensate for the decrease in cardiac output in a number of ways. However, in a failing heart, these compensatory mechanisms are actually detrimental and contribute to the development of symptoms.

  • Increasing preload (increasing venous pressures):
    • Increases end-diastolic volume (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
  • Activation of the renin-angiotensin-aldosterone system (RAAS)
  • Sympathetic nervous system activation

The RAAS is activated due to renal hypoperfusion from the reduced cardiac output. This contributes to increased venous pressures through vasoconstriction and there is retention of water and sodium that contributes to oedema. Continued decreases in cardiac output activate the sympathetic nervous system via baroreceptors. This increases myocardial contractility and heart rate. Chronic activation is detrimental triggering myocyte death and further activation of the RAAS.

We can observe this relationship between the failing heart and these compensatory mechanisms in the diagram below.

Physiology of 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 signs associated with fluid retention.


  • Shortness of breath (SOB)
  • Wheeze
  • Fatigue
  • Weight loss
  • Paroxysmal nocturnal dyspnoea
  • Orthopnoea
  • Ankle swelling


  • Raised JVP
  • Displaced apex
  • Crackles
  • Ankle swelling
  • Heart sounds S3/S4
  • Pulsus alternans
  • Hepatomegaly
  • Ascites

Clinical features of heart failure


NICE recommends echocardiography and specialist assessment​ in patients with suspected heart failure based on BNP.

In patients with suspected heart failure, the first step is taking a detailed history and performing a clinical examination. The next step is measuring a BNP, which is used to risk stratify patients and determine the urgency of referral. At this point, an ECG should be performed in all patients. Consideration should be made regarding further blood tests, chest radiograph, urinalysis and lung function testing (if alternative diagnosis is suspected). However, it is reasonable to await the BNP result.


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. It has an excellent negative predictive value, which means it is good at excluding heart failure. A negative test should warrant investigation into others causes of the patients symptoms.

The BNP, along with a detailed history and examination and other relevant investigations, may be used to decide who to refer for further assessment:

Diagnosis of heart failure


A transthoracic echocardiography (TTE) is the main investigation for the confirmation of heart failure. It should be completed in patients with an elevated BNP. A TTE may still be warranted, regardless of BNP, if clinical examination reveals a murmur or the ECG is abnormal for example.

The main determinant of an TTE is to look at the ejection fraction of the heart. This helps to differentiate suspected heart failure into three groups:

  • Heart failure with reduced ejection fraction (HFrEF): LVEF <40%
  • Heart failure with minimally reduced ejection fraction (HFmrEF): LVEF 40-49%
  • Heart failure with preserved ejection fraction (HFpEF): LVEF ≥50%

NOTE: additional echo criteria are used to help diagnose HFpEF or 'diastolic heart failure'. These are broadly based on ventricular thickness, chamber size and other features


The New York Heart Association (NYHA) classifies the symptoms of heart failure.

The NYHA system classifies the severity of heart failure based on symptoms. It helps determine how functionally impaired an individual is due to heart failure. It is also used to guide justification for certain treatments in heart failure (e.g. devices).

New York Heart Association (NYHA) classification


Investigations are essential to determine the aetiology, complications associated with heart failure and modifiable risk factors.


  • 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 MRI:
    • May be used when transthoracic echo is non-diagnostic
    • May be used to determine the aetiology of heart failure (e.g. ischaemic versus non-ischaemic in dilated cardiomyopathy)

Heart failure on CXR

Heart failure on CXR demonstrating cardiomegaly, upper lobe diversion and Kerley-B lines

Image courtesy of Dr Roberto Schubert and Radiopaedia


  • Coronary angiogram: used for diagnostic and therapeutic purposes to diagnose/treat coronary artery disease
  • Right heart catheterisation: reserved for the investigation of right-sided heart failure
  • 24 hr ECG: if an arrhythmia is suspected
  • Lung function tests: to exclude alternative pathology impacting on symptoms (e.g. breathlessness)


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 if the patient has symptomatic fluid overload; titrated up or down according to the degree of oedema.
  • Improve symptoms but not mortality.

The BNP, along with a detailed history and examination and other relevant investigations may be used to decide who to refer for further assessment.

LV systolic dysfunction

ACE inhibitors and beta blockers are the mainstay of management.

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).

3. Mineralocorticoid receptor antagonists (MRA):

  • Example: Eplerenone 25 mg OD
  • May be added to ACE and beta-blocker if symptoms persist.
  • Contra-indicated in hyperkalaemia, hyponatraemia, acute kidney injury.
  • Increase dose to 50 mg as tolerated within four weeks of initiation.

Second line management of heart failure

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

  • Ivabradine
  • Sacubitril/valsartan: ARB with new neprilysin inhibitor, which prevents breakdown of natriuretic peptides.
  • Hydralazine in combination with nitrate
  • Digoxin

NOTE: these second-line agents should be prescribed following specialist assessment by a clinician that manages heart failure.

If a patient remains symptomatic despite optimal treatment consider intervention of device in selected patients:

  • Implantable cardiac defibrillator (ICD): important for primary and secondary prevention of sudden cardiac death (specific indications).
  • Cardiac resynchronisation therapy (CRT): biventricular pacing, which is indicated in certain patients with HFrEF (i.e. ≤ 35%) & prolonged QRS (i.e. ≥ 130 ms). Usually receive combined device with defibrillator.
  • Percutaneous coronary intervention (PCI): patients with ischaemic heart disease may be offered revascularisation therapy if indicated.
  • Cardiac transplant: highly specialised procedure for certain patient groups with heart failure.

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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