Atrial Fibrillation (AF)

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Atrial fibrillation (AF) is a cardiac arrhythmia characterised by disorganised electrical activity within the atria resulting in ineffective atrial contraction and irregular ventricular contraction.

AF is the most common cardiac arrhythmia in adults. The prevalence of AF increases with age, particularly over 65 years, such that 10% of over 85-year-olds have atrial fibrillation.1

AF can be categorised as either paroxysmal, persistent or permanent:2

  • Paroxysmal: episodes last >30 seconds but <7 days and are self-terminating but recurrent
  • Persistent: episodes last less than or more than seven days but require electrical or chemical cardioversion
  • Permanent: episodes fail to terminate with cardioversion OR a terminated episode that relapses within 24 hours OR long-standing AF (usually >1 year) in which cardioversion has not been indicated or attempted
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The cardiac conduction system

Before understanding the pathophysiology of AF, it is important to understand the normal cardiac conduction system.

Cardiac electrical impulses are first generated in the sinoatrial node (SAN) which is found in the right atrium. The rate at which these impulses are generated is under the influence of the autonomic nervous system. The sympathetic branch of the nervous system increases the rate of impulse generation from the SAN whereas the parasympathetic branch decreases the rate of impulse generation.

The electrical impulses travel through the atria causing atrial contraction and to the atrioventricular node (AVN) which lies between the atria and ventricles. The AVN briefly delays the impulse which then travels through the Bundle of His, down the left and right bundle branches and finally to the Purkinje fibres resulting in ventricular contraction.

The electrical conduction system of the heart
Figure 1. The electrical conduction system of the heart.3

For more information, see the Geeky Medics guide to the cardiac conduction system.

Pathophysiology of atrial fibrillation

AF is a type of supraventricular cardiac arrhythmia meaning the origin of the arrhythmia arises from above the ventricles.

The arrhythmia often originates from left atrial myocytes which extend as sleeves around the pulmonary veins.2 Atrial ectopics from the pulmonary veins trigger micro re-entry circuits in the atria causing chaotic electrical activity and sustained AF.Β 

Conditions including hypertension or mitral regurgitation cause the atria to stretch which changes their electrical properties increasing the substrate for AF. The combination of trigger and substrate leads to an increased likelihood that an atrial ectopic triggers AF and the atria sustain it. AF begets AF as AF causes the atria to dilate and increases AF substrate.

The resulting chaotic electrical activity is intermittently conducted through the AVN which gives rise to the characteristic irregularly irregular ventricular rate seen in AF.

In AF, the ventricular rate is very variable and depends on the speed of AVN conduction. Young patients with slick AV nodes are often very symptomatic and tachycardic.

The presence of chaotic electrical activity within the atria also results in ineffective atrial contraction. The consequence of this is blood stasis within the atria which increases the chance of thrombosis (Virchow’s triad) and subsequently embolic complications including transient ischaemic attacks (TIA), stroke and systemic embolisation.

Causes of atrial fibrillation

Numerous conditions/risk factors can increase the substrate and or triggers for AF. Typically, the mechanism is that they cause the atria to stretch. It is important to address these conditions/risk factors to improve prognosis and maintenance of sinus rhythm if a rhythm control strategy is intended.

AF is most commonly associated with:2

  • Hypertension
  • Obesity
  • Alcohol

Other causes of AF can be split into cardiac and non-cardiac causes.2

Cardiac causes of atrial fibrillation

Cardiac causes include:

  • Heart failure (e.g. secondary to myocardial infarction)
  • Structural pathology (e.g. valve stenosis or valve regurgitation)
  • Congenital heart disease
  • Atrial or ventricular dilation
  • Atrial or ventricular hypertrophy
  • Pre-excitation syndromes (e.g. Wolff-Parkinson-White syndrome)
  • Sick sinus syndrome
  • Inflammatory conditions (e.g. pericarditis or myocarditis)
  • Infiltrative conditions (e.g. amyloidosis)

Non-cardiac causes of atrial fibrillation

Non-cardiac causes include:

  • Acute infection
  • Electrolyte imbalances (e.g. hypokalaemia or hyponatraemia)
  • Pulmonary embolism
  • Thyrotoxicosis or hypothyroidism
  • Diabetes mellitus

Risk factors

As well as the causes of AF discussed above, the following risk factors are associated with an increased likelihood of developing AF:2,4

  • Male sex
  • Caucasian ethnicity
  • Increasing age
  • Alcohol
  • Cigarette smoking
  • Obesity
  • Co-morbidities (e.g. chronic kidney disease and obstructive sleep apnoea)

Caffeine intake is not typically a risk factor although it is often blamed for palpitations.

Clinical features


In some patients, AF can be asymptomatic, even when causing tachycardia and therefore may be an incidental finding during a clinical examination or when performing a 12-lead electrocardiogram (ECG).

Increasingly, AF is identified via patient-initiated monitoring (e.g. Apple watches).Β 

Typical symptoms of AF include:2

  • Breathlessness
  • Chest discomfort
  • Palpitations
  • Light-headedness
  • Reduced exercise tolerance
  • Syncope: due to bradycardia, particular in paroxysmal AF when sinus rhythm is restored because the SAN can take a few seconds to wake up

It is also important to remember that a transient ischaemic attack or stroke can be the presenting feature of AF. For this reason, it is essential that patients presenting with symptoms or signs of a TIA or stroke are also asked about the features of AF.

Other important areas to cover in the history include:

  • Presence of pre-existing cardiac disease
  • Past medical history of cardiac disease as well as non-cardiac conditions (e.g. diabetes, thyroid disease, malignancy)
  • Medications (e.g. thyroxine)
  • Social history (e.g. alcohol abuse, smoking, obesity)

Clinical examination

In the context of suspected AF, a thorough cardiovascular examination is necessary.

Typical clinical findings in atrial fibrillation include:

  • Irregularly irregular pulse when palpating either the radial or carotid arteries or auscultating at the apex.
  • Radial-apical deficit: this is important to assess because each ventricular contraction may not be sufficiently strong enough to transmit a pulse to the radial artery and palpating only the radial artery can miss tachycardia.

Some patients may have co-existing heart failure. Typical clinical findings of heart failure include:

  • Raised jugular venous pressure
  • Added heart sounds on chest auscultation (e.g. gallop rhythm)
  • Crackles on chest auscultation
  • Ankle swelling

Differential diagnoses

Possible differential diagnoses in the context of suspected AF include:2

  • Other supraventricular tachycardias: atrial flutter, atrial extrasystoles, multifocal atrial tachycardia, sinus tachycardia
  • Ventricular ectopics


Bedside investigations

Relevant bedside investigations in the context of suspected AF include:

  • Basic observations (vital signs): to assess for haemodynamic instability suggested by tachycardia, hypotension and cool peripheries.
  • 12-lead ECG: this is the diagnostic investigation for AF. Typical features of AF on an ECG include tachycardia (particularly in new-onset; as aforementioned heart rate depends on the rate of AVN conduction), irregularly irregular rhythm, absent P-waves, fibrillation waves (best seen in lead II and V1 and often confused with atrial flutter waves) and a chaotic (noisy) baseline.
  • Ambulatory ECG: this may be considered for patients with suspected paroxysmal AF to capture a symptomatic episode for diagnostic purposes. It can also be considered to assess the rate in persistent and/or permanent AF once a patient has been established on treatment. Ambulatory monitoring can be achieved using a 24-hour ECG monitor, a cardiac event recorder or a 7-day Holter monitor or in patients with infrequent symptoms an implantable loop recorder.
Atrial fibrillation on a 12-lead ECG
Figure 2. Atrial fibrillation on a 12-lead ECG.5

Laboratory investigations

Relevant laboratory investigations in the context of suspected AF include:

  • Full blood count: to assess for a reversible cause such as acute infection (e.g. suggested by raised white cell count)
  • Urea & electrolytes: to assess for a reversible cause such as hypokalaemia or hyponatraemia
  • Liver function tests: to establish baseline hepatic function before giving anticoagulant drugs
  • Thyroid function tests: to assess for thyroid dysfunction. Raised T4 and low TSH levels indicate hyperthyroidism
  • CRP: to assess for a reversible cause such as acute infection. Raised CRP is suggestive of underlying infection
  • Clotting screen: to establish a baseline coagulation status before giving anticoagulant drugs
  • BNP: can be considered to assess for underlying heart failure but should be interpreted with caution based on the patient’s clinical presentation. AF in itself can cause a raised BNP without evidence of heart failure.


Relevant imaging investigations in the context of suspected AF include:

  • Echocardiogram: a transthoracic echo is used to assess for underlying structural or valvular disease and or left ventricular systolic dysfunction. NICE only recommends performing an echocardiogram if the result is likely to alter management for example AF could be the presenting feature of a cardiac condition such as a cardiomyopathy/valvular pathology.
  • Chest X-ray: to assess for changes associated with heart failure (e.g., alveolar oedema, Kerley B-lines, cardiomegaly, upper lobe diversion, pleural effusion, fluid in the lung fissures)


The European Society of Cardiology states that the following criteria must be met for a diagnosis of AF to be made:4

  • A standard 12-lead ECG recording or a single-lead ECG recording of β‰₯30 seconds showing a heart rhythm of no discernible repeating P-waves AND
  • Irregular RR intervals


Immediate management

The first step is to carry out an ABCDE assessment to identify any adverse features. Adverse features are defined by the Resuscitation Council as any symptoms or signs of shock, syncope, myocardial ischaemia or heart failure. If any of these features are present, synchronised direct current cardioversion should be delivered.

For more information, see the Geeky Medics guide to the acute management of atrial fibrillation.Β 

Ongoing management

Anticoagulation is the primary consideration for AF patients. Following this, the management of AF can broadly be split into rhythm control and rate control.

For most patients, the choice is based on symptoms and the likelihood of maintaining sinus rhythm. There is no clear prognostic benefit to restoring sinus rhythm. However, management of modifiable AF risk factors is essential for overall patient health and improves the chance of maintaining sinus rhythm.

If symptoms are not controlled in primary care NICE recommends prompt referral to a specialist who can offer invasive treatment.

Rhythm control

New-onset AF

Rhythm control is an appropriate strategy for patients presenting with new-onset AF (defined as <48 hours).Β 

The majority (varies depending on study e.g. 69%) of patients will spontaneously cardiovert within 48 hours and delayed cardioversion has been shown to be non-inferior to early cardioversion at four weeks (91% sinus rhythm vs 94%).7

Electrical cardioversion is achieved by sedating/anaesthetising the patient and applying defibrillation pads to the patient’s chest and delivering synchronised DC cardioversion.

Pharmacological cardioversion is achieved by using either flecainide or amiodarone.

Flecainide is a class 1c antiarrhythmic drug that blocks sodium channels within the heart and thereby raises the threshold for depolarisation. It should not be used in patients with evidence of structural or ischaemic heart disease because of the risk of sudden cardiac death. Flecainide can be given orally or intravenously.

Amiodarone is a class 3 antiarrhythmic drug that blocks potassium channels within the heart and thereby prolongs the refractory period of the myocardium. It can be used in patients with evidence of structural heart disease. Amiodarone may prolong the QT interval and should be avoided in patients with QT prolongation.

Side effects of amiodarone include life-threatening lung fibrosis (acute and chronic fibrosis can occur with the first dose), liver failure, photosensitivity, hyper/hypothyroidism, neuropathy and visual deficits. Amiodarone can be given orally or intravenously; however special precautions are needed when given intravenously (follow a local protocol) because extravasation can cause serious skin necrosis.

Therapeutic anticoagulation is required for 4-6 weeks prior to and 4 weeks post either electrical or pharmacological cardioversion unless the onset of AF is within the last 48 hours, and it is a single isolated episode of AF.

Non-acute AF

Rhythm control is an appropriate strategy for patients presenting with non-acute AF who have ongoing symptoms despite adequate rate control, or for patients whom a rate control strategy has not been successful.

Electrical cardioversion is achieved by applying defibrillation pads to the patient’s chest and delivering synchronised DC cardioversion. This should however be delayed until the patient has received adequate anticoagulation (i.e. from the day the direct-acting oral anticoagulant is started or when INR is 2 if using Warfarin) for at least 4-6 weeks.

Amiodarone can be given for 4 weeks prior to electrical cardioversion and continued for 12 months following electrical cardioversion to maintain sinus rhythm.

If it is not appropriate to wait for adequate anticoagulation, transoesophageal echocardiography-guided cardioversion can be used to confirm the absence of a thrombus and deliver cardioversion.

Beta-blockers (e.g. bisoprolol) are the first-line drug for long-term rhythm control.

Amiodarone is the most effective anti-arrhythmic drug, but it requires regular lung, liver and thyroid monitoring and should only be prescribed by a specialist.

Rate control

Rate control is an appropriate strategy for the following groups:

  • Patients presenting with AF onset <48 hours or >48 hours
  • Patients whose AF does not have a reversible cause
  • Patients who do not have heart failure thought to be caused primarily by AF
  • Patients for whom rhythm control would not be more suitable based on clinical judgment

Pharmacological options for rate control include:

  • Beta-blockers (e.g. bisoprolol)
  • Rate-limiting calcium channel blockers (e.g. verapamil or diltiazem): appropriate for patients with good left ventricular function
  • Digoxin: for patients who do little or no exercise or if other rate-control drugs are contraindicated. It can also be used as second-line therapy when a patient is already taking the maximum tolerated dose of a beta-blocker or rate-limiting calcium channel blocker.

Paroxysmal AF

In patients with paroxysmal AF and minimal symptoms, or if symptoms are caused by a known precipitant (e.g. alcohol), a β€˜no drug treatment’ or β€˜pill-in-the-pocket strategy’ can be used.

If there is a clear precipitant for the paroxysm then this should be avoided where possible.

Class 1c antiarrhythmic drugs are used for the β€˜pill-in-the-pocket strategy’ (e.g. flecainide and propafenone). These medications can be taken regularly or as required when a patient experiences a paroxysm of AF.

The risk of structural heart disease increases with age and flecainide should be used with caution/specialist advice in older patients.

The following criteria must be met before a patient can be started on the β€˜pill-in-the-pocket strategy’.

  • Have a history of infrequent symptomatic episodes of AF AND
  • Have no history of left ventricular dysfunction, valvular or ischaemic heart disease AND
  • Have a systolic blood pressure >100mmHg and a resting heart rate of >70bpm AND
  • Are able to understand how to, and when to, take the medication

If paroxysmal AF is not controlled with the β€˜pill-in-the-pocket strategy’ regular flecainide can be considered. Failing this pulmonary vein ablation or the pace and ablate strategy can be considered.


The risk of thromboembolic complications is higher in patients with AF due to blood stasis within the heart resulting in an increased likelihood of thrombus formation. For this reason, anticoagulation must be considered for patients with AF to reduce their risk of TIA and stroke.

The CHA2DS2VASc toolΒ (Table 1) can be used to assess a patient’s risk of stroke in AF. It comprises eight components which when added together guide the decision of whether to offer a patient anticoagulation therapy.2

Table 1. The CHA2DS2VASc tool

Component Score

Congestive heart failure/ left ventricular dysfunction


Hypertension (β‰₯140mmHg systolic and/or β‰₯90mmHg diastolic)


Age β‰₯75 years






Vascular disease e.g., previous myocardial infarction or peripheral arterial disease


Age 65-74 years


Sex category female


The total CHA2DS2VASc score can then be used to decide whether to start anticoagulation therapy (Table 2).

Table 2. Interpretation of the CHA2DS2VASc score

CHA2DS2VASc score Action

Men & women with a score of β‰₯2

Offer anticoagulation

Men with a score of β‰₯1

Consider anticoagulation

Women with a score of 1 just for sex category

Do not offer anticoagulation

Men with a score of 0

Do not offer anticoagulation

If it is decided that a patient should be started on anticoagulation therapy, a choice of either a direct-acting oral anticoagulant (DOACs) or a vitamin K antagonist such as warfarin should be offered.

DOACs are the first-line option. Examples of DOACs include apixaban, rivaroxaban, edoxaban and dabigatran. Apixaban, rivaroxaban and edoxaban inhibit factor Xa within the clotting cascade and thereby prevent thrombus formation. Dabigatran works by inhibiting the action of thrombin and therefore thrombus formation.

Warfarin is a vitamin K antagonist. Clotting factors 10, 9, 7 and 2 are vitamin K dependent factors meaning they require vitamin K for activation. Therefore, if the action of vitamin K is antagonised these factors will not be activated and hence thrombus formation is inhibited.

For more information on warfarin, see the Geeky Medics guides to warfarin prescribing and warfarin counselling.Β 

Assessing the risk of bleeding

The ORBIT tool (recently recommended by NICE, previously HAS-BLED was used) can be used alongside the CHA2DS2VASc score to help guide decisions regarding anticoagulation.

The ORBIT tool comprises six components which are used to identify patients at high risk of bleeding (Table 3).2

Table 3. The ORBIT tool.

Score 2 points Score 1 point


  • Haemoglobin of <130g/L OR
  • Haematocrit <40%

Aged >74 years


  • Haemoglobin of <120g/L OR
  • Haematocrit <36%

eGFR <60ml/min/1.73m2

History of bleeding (e.g. previous GI bleed)

Treated with antiplatelet medication

The ORBIT score can then be used to categorise whether a patient is at low, medium or high risk of bleeding (Table 4).Β 

Table 4. Interpretation of the ORBIT score.Β 

ORBIT score Bleeding risk







Following the restoration of sinus rhythm, there will always be a risk of recurrence of AF.Β  The decision to stop anticoagulation, after the minimum 4-week period of post cardioversion anticoagulation, should be based upon a patient’s CHA2DS2VASc score, ORBIT score and individual preferences.

Invasive management of AF

Invasive management should be considered for patients in whom drug treatment has been unsuccessful or is unsuitable or not tolerated.

Left atrial ablation

This involves creating small scars within the myocardium of the left atrium to block abnormal electrical signals and restore sinus rhythm.

Left atrial ablation is a complex procedure with the risk of serious complications. However, in significantly symptomatic patients the quality-of-life benefits can be profound.

Most AF ablations are performed percutaneously via the femoral veins to access the right atrium. Once the ablation catheter reaches the right atrium a trans-septal puncture is performed so that the left atrium can be accessed, and ablation can take place.

Pace and ablate strategy

This strategy involves pacemaker insertion followed by ablation of the AVN leaving the pacemaker in control of the ventricular rate.

This is a good strategy for patients with poorly controlled AF despite maximum medical treatment who are unlikely to be suitable for ablation or successful DC cardioversion.

This strategy does leave the patient in AF and irreversibly dependent on the pacemaker, but it ensures the rate is controlled and can be beneficial when other strategies have failed. In heart failure patients this approach has shown prognostic benefit.8

Patients with paroxysmal AF are often tachycardic in AF and relatively bradycardic in sinus rhythm, particularly with rate/rhythm control drugs. Often a pacemaker is implanted which then allows a free hand with rate control medications.

Atrial flutter

Atrial flutter is a highly organised electrical circuit typically within the right atrium that is commonly confused with AF. Flutter waves are seen on the ECG and there is often a heart rate of 150bpm.

Atrial flutter often leads to AF because it causes the atria to stretch leading to the development of a substrate for AF.

Atrial flutter requires anticoagulation and rate control/cardioversion as per AF. Atrial flutter can often be cured by performing a relatively simple, low risk, ablation procedure in the right atrium. A successful atrial flutter ablation does not prevent a patient from developing AF.


A diagnosis of atrial fibrillation approximately doubles age-adjusted mortality. The increase in mortality may be attributed to the presence of risk factors (blood pressure, obesity), side effects of treatments and/or direct complications of AF.

Numerous studies have shown restoration of sinus rhythm does not improve prognosis over rate control except for the small CASTLE-AF study in heart failure patients.9

Complications of AF include:2

  • Thromboembolic events: TIA and ischaemic stroke/systemic embolism
  • Tachycardia-induced cardiomyopathy
  • Decompensation of pre-existing cardiac disease: heart failure, valvular disease
  • Cardiac ischaemia can be associated with poorly controlled AF with the high ventricular rate leading to angina and type 2 myocardial infarction

Key points

  • AF is a cardiac arrhythmia characterised by disorganised electrical activity within the atria which results in ineffective atrial contraction and irregular ventricular contraction.
  • It is most commonly associated with hypertension, obesity and alcohol.
  • AF can be asymptomatic, however, common presenting symptoms include breathlessness, chest discomfort, palpitations, dizziness, syncope and reduced exercise tolerance.
  • The most common finding on clinical examination is an irregularly irregular pulse when palpating the radial or carotid pulse.
  • Common ECG findings include irregular RR intervals and absent P-waves.
  • The mainstay of management of AF is consideration of anticoagulation and either a rhythm or rate-control strategy based predominantly on symptoms.
  • Rhythm-control can be achieved either electrically or pharmacologically whereas rate-control is achieved by using drugs such as beta-blockers, rate-limiting calcium channel blockers and Digoxin.
  • Management of modifiable risk factors (e.g. alcohol, obesity) and comorbidities (e.g. hypertension) is particularly important to improve symptoms, prognosis and successful maintenance of sinus rhythm if a rhythm control strategy is considered.
  • For most patients restoring sinus rhythm is a symptomatic treatment and does not reduce the complications of AF which include thromboembolic events such as TIA and stroke, heart failure and tachycardia-induced cardiomyopathy.


Dr Matt Jackson

Consultant Cardiologist

Dr Will Nicolson

Consultant Cardiologist

Honorary Associate Professor of Cardiology


Dr Chris Jefferies


  1. Benjamin, E.J., Muntner, P., Alonso, A., Bittencourt, M.S., Callaway, C.W., Carson, A.P., Chamberlain, A.M., Chang, A.R., Cheng, S., Das, S.R. and Delling, F.N., 2019. Heart disease and stroke statisticsβ€”2019 update: a report from the American Heart Association. Available from: [LINK]
  2. NICE. Atrial Fibrillation. Published May 2021. Available from: [LINK]
  3. Wikipedia. Conduction system of the heart. Published April 2010. Available from: [LINK]
  4. European Society of Cardiology. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS): The Task Force for the diagnosis and management of atrial fibrillation of the European Society of Cardiology (ESC) Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Published February 2021. Available from: [LINK]
  5. Wikipedia. ECG of Atrial Fibrillation. Published November 2020. Available from: [LINK]
  6. NICE. Atrial Fibrillation: diagnosis and management. Published April 2021. Available from: [LINK]
  7. 7. Pluymaekers, N.A., Dudink, E.A., Luermans, J.G., Meeder, J.G., Lenderink, T., Widdershoven, J., Bucx, J.J., Rienstra, M., Kamp, O., Van Opstal, J.M. and Alings, M., 2019. Early or delayed cardioversion in recent-onset atrial fibrillation.Β New England Journal of Medicine,Β 380(16), pp.1499-1508. Available from: [LINK]
  8. Brignole, M., Pentimalli, F., Palmisano, P., Landolina, M., Quartieri, F., Occhetta, E., CalΓ², L., Mascia, G., Mont, L., Vernooy, K. and van Dijk, V., 2021. AV junction ablation and cardiac resynchronization for patients with permanent atrial fibrillation and narrow QRS: the APAF-CRT mortality trial.Β European Heart Journal,Β 42(46), pp.4731-4739. Available from: [LINK]
  9. Marrouche, N.F., Brachmann, J., Andresen, D., Siebels, J., Boersma, L., Jordaens, L., Merkely, B., Pokushalov, E., Sanders, P., Proff, J. and Schunkert, H., 2018. Catheter ablation for atrial fibrillation with heart failure.Β New England Journal of Medicine,Β 378(5), pp.417-427. Available from: [LINK]


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