Atrial fibrillation (AF) occurs when electrical activity within the atria becomes chaotic and uncoordinated. This results in atrial fibrillation (random twitching rather than an organised contraction) and produces an irregularly irregular pulse.

Overall consequences of AF include:

• Irregularly irregular ventricular contraction pattern
• Tachycardia (increased heart rate)
• Heart failure due to reduced ventricular filling during diastole
• Increased stroke risk

Pathophysiology

Normal cardiac pumping relies on a highly organised conduction system. Under usual conditions, the electrical impulse begins in the sinoatrial (SA) node, the heart’s physiological pacemaker. The SA node is located where the superior vena cava meets the right atrium.

The impulse spreads across the right and left atria, producing atrial contraction and pushing blood into the ventricles. This coordinated atrial depolarisation is represented by the P wave on an ECG.

The signal then travels through the atrioventricular (AV) node, the electrical connection between the atria and ventricles, before passing into the ventricular conduction system, triggering ventricular contraction. Ventricular depolarisation is seen as the QRS complex on an ECG.

In normal function, each P wave precedes a QRS complex, and QRS complexes appear at regular intervals—this is sinus rhythm.

In AF, atrial electrical activity becomes disordered, leading to rapid, irregular, and ineffective atrial activation rather than a coordinated atrial contraction. Because there is no unified atrial depolarisation, P waves are absent on the ECG.

Signals reaching the ventricles via the AV node occur in an unpredictable and often rapid fashion. This produces randomly spaced QRS complexes, meaning the ventricular rhythm is irregularly irregular with no repeating pattern.

Because atrial contraction is ineffective, blood can pool within the atria, encouraging thrombus (clot) formation. A clot forming in the left atrium can embolise to the brain and occlude a cerebral artery, causing an ischaemic stroke. Stroke risk is approximately five times higher in AF (depending on patient-specific risk factors).

Common Causes

Frequent causes of atrial fibrillation can be recalled using “SMITH”:

• S – Sepsis
• M – Mitral valve disease (stenosis or regurgitation)
• I – Ischaemic heart disease
• T – Thyrotoxicosis
• H – Hypertension

Lifestyle triggers worth remembering include alcohol and caffeine.

Presentation

Many people with AF have no symptoms, and the condition is often discovered incidentally. It may also first be identified after a stroke.

When symptomatic, patients may report:

• Palpitations
• Breathlessness
• Dizziness or syncope (loss of consciousness)
• Features of associated conditions (e.g. stroke symptoms, sepsis features, or thyrotoxicosis symptoms)

The hallmark clinical sign is an irregularly irregular pulse. The two key differentials for an irregularly irregular pulse are:

• Atrial fibrillation
• Ventricular ectopics

Ventricular ectopics tend to disappear once the heart rate rises beyond a certain level. Therefore, if the rhythm becomes regular during exercise, this supports ventricular ectopics rather than AF.

Investigations

All patients with an irregularly irregular pulse require an ECG. Typical AF findings are:

• No P waves
• Narrow-complex tachycardia
• Irregularly irregular ventricular rhythm

An echocardiogram may be indicated when evaluating:

• Valvular disease
• Heart failure
• Planned cardioversion

Paroxysmal Atrial Fibrillation

Paroxysmal AF refers to recurrent episodes that start and stop spontaneously, returning to sinus rhythm without intervention. Episodes may last from 30 seconds up to 48 hours.

If a patient has symptoms suggestive of AF but a normal ECG, further testing may include:

• 24-hour Holter (ambulatory) ECG
• Event monitor for 1–2 weeks

Valvular Atrial Fibrillation

Valvular AF refers to AF in the presence of significant mitral stenosis or a mechanical heart valve, implying valve pathology has contributed to AF development.

AF without valve disease, or AF with other valve problems (e.g. mitral regurgitation or aortic stenosis), is classified as non-valvular AF.

The NICE 2021 guidance does not specifically use the term “valvular AF”; instead, it recommends that patients with valvular heart disease be referred to cardiology for further assessment and management.

Core Management Principles

This section follows NICE (2021); use local and national guidance in practice.

AF management has two overarching goals:

1. Rate control or rhythm control
2. Anticoagulation to reduce stroke risk

TOP TIP: The rate/rhythm pathways can become detailed. In reality, most patients end up on a beta blocker (often bisoprolol) for rate control plus a DOAC for anticoagulation. If you only remember one practical treatment pairing, remember that one.

Rate Control

Atrial contraction normally contributes to ventricular filling. In AF, atrial contractions are ineffective, so ventricular filling relies more on passive mechanisms (suction and gravity), which is less efficient.

Higher heart rates shorten diastole, leaving even less time for ventricular filling and reducing cardiac output. Rate control aims to slow the ventricular rate to under 80 bpm at rest, increasing diastolic filling time.

NICE (2021) recommends rate control as first-line for most patients, except when:

• There is a reversible trigger
• AF is new onset within 48 hours
• AF is causing heart failure
• Symptoms persist despite effective rate control

Rate control options

• Beta blocker first-line (e.g. atenolol or bisoprolol)
• Rate-limiting calcium-channel blocker (e.g. diltiazem or verapamil) (not preferred in heart failure)
• Digoxin (only for sedentary patients with persistent AF; requires monitoring and carries toxicity risk)

Rhythm Control

Rhythm control may be considered in the same situations where rate control is not preferred:

• Reversible cause
• AF onset within 48 hours
• AF causing heart failure
• Persistent symptoms despite adequate rate control

The aim is to restore and maintain sinus rhythm, using:

• Cardioversion
• Long-term rhythm-control medication

Cardioversion Options

There are two timing strategies:

• Immediate cardioversion
• Delayed cardioversion

Immediate cardioversion

Used if AF is:

• Present for < 48 hours, or
• Causing life-threatening haemodynamic instability

Immediate cardioversion can be:

• Pharmacological
• Electrical

Pharmacological cardioversion options:

• Flecainide
• Amiodarone (preferred when there is structural heart disease)

Electrical cardioversion involves delivering controlled shocks using a defibrillator to restore sinus rhythm, typically under sedation or general anaesthesia.

Delayed cardioversion

Used when AF has been present for > 48 hours and the patient is stable.

• Electrical cardioversion is recommended.
• Transoesophageal echocardiography-guided cardioversion may be used where available.
• Amiodarone can be considered before and after electrical cardioversion to reduce recurrence.

Patients must receive anticoagulation for at least 3 weeks before delayed cardioversion because AF lasting beyond 48 hours increases the likelihood of atrial thrombus formation, and restoring sinus rhythm may dislodge a clot and cause stroke. Patients remain rate controlled while awaiting cardioversion.

Long-Term Rhythm Control Medications

• Beta blockers first-line
• Dronedarone second-line for maintaining sinus rhythm after successful cardioversion
• Amiodarone is useful in patients with heart failure or left ventricular dysfunction

Management of Paroxysmal AF

Some patients with paroxysmal AF may be candidates for a “pill-in-the-pocket” strategy, where they take medication only when an episode begins.

To be suitable, patients must:

• Have infrequent episodes
• Have no structural heart disease
• Be able to recognise AF symptoms and understand when to take treatment

Flecainide is typically used. A key concern is that flecainide may convert AF into atrial flutter with 1:1 AV conduction, producing a very rapid ventricular rate.

Even in paroxysmal AF, anticoagulation decisions are still made using CHA₂DS₂-VASc, just like permanent AF.

Ablation

If medication for rate or rhythm control is ineffective or not tolerated, two ablation strategies are available:

• Left atrial ablation
• AV node ablation with permanent pacemaker

Left atrial ablation

Performed in a catheter laboratory (cath lab) under sedation or general anaesthesia. A catheter is introduced via a femoral vein and advanced under X-ray guidance to the heart. The interatrial septum is punctured to access the left atrium. Electrical mapping is performed to locate abnormal conduction pathways. Radiofrequency energy (heat) is then applied to ablate the target area, leaving non-conductive scar tissue. The intention is to eliminate the arrhythmia source and restore sinus rhythm.

AV node ablation + pacemaker

This catheter procedure destroys the AV node, disconnecting atrial electrical activity from the ventricles. After ablation, atrial impulses cannot reach the ventricles. A permanent pacemaker is required to control ventricular rhythm (and is inserted before ablation). Stroke prevention still requires anticoagulation.

Anticoagulation

Chaotic atrial activity promotes blood stasis in the left atrium, particularly within the left atrial appendage, enabling thrombus formation. A clot can embolise from the left atrium → left ventricle → aorta → carotid arteries → cerebral circulation, where it can obstruct a cerebral artery and cause an ischaemic stroke.

Anticoagulants reduce clot formation by interfering with the clotting cascade.

• Without anticoagulation, AF carries an annual stroke risk of around 5% (depending on individual factors).
• With anticoagulation, stroke risk falls to around 1–2% per year (depending on individual factors).
• Anticoagulation reduces stroke risk by roughly two-thirds.

However, anticoagulation also carries a risk of major bleeding of approximately 2.5–8% per year, depending on the patient.

NICE (2021) recommends:

• DOACs first-line
• Warfarin second-line if DOACs are contraindicated

TOP TIP: NICE head injury guidance (updated 2019) states that any patient who sustains a head injury while on anticoagulation should have a CT head to exclude intracranial bleeding. Falls are common in practice—remember that head injury + anticoagulation automatically meets criteria for CT. Patients starting anticoagulation should be advised that a head injury warrants urgent medical assessment (A&E) for this reason.

Direct-Acting Oral Anticoagulants (DOACs)

DOACs are oral anticoagulants that do not require INR monitoring, unlike warfarin. They are appropriate for most patients, including those with cancer, and have a half-life of about 6–14 hours.

Mechanisms:

• Apixaban, edoxaban, rivaroxaban: direct factor Xa inhibitors
• Dabigatran: direct thrombin inhibitor

Dosing frequency:

• Apixaban and dabigatran: twice daily
• Edoxaban and rivaroxaban: once daily

Reversal agents (for uncontrolled or life-threatening bleeding):

• Andexanet alfa (reverses apixaban and rivaroxaban)
• Idarucizumab (monoclonal antibody against dabigatran)

Advantages over warfarin:

• No routine monitoring
• No issues with time in therapeutic range (if adherence is good)
• No major interaction problems
• Similar or slightly better stroke prevention in AF
• Similar or slightly lower bleeding risk compared with warfarin

Common indications:

• Stroke prevention in AF
• Treatment of DVT and PE
• Post-op VTE prophylaxis after hip or knee replacement

Warfarin

Warfarin is a vitamin K antagonist. Vitamin K is required for several clotting factors; warfarin blocks vitamin K action and prolongs the prothrombin time.

The INR (international normalised ratio) measures anticoagulation effect by comparing the patient’s prothrombin time to that of an average healthy adult.

• INR 1 = normal clotting time
• INR 2 = prothrombin time is twice normal (clot forms twice as slowly)

Warfarin requires frequent INR monitoring and dose adjustments. It is taken once daily, commonly around 6 pm in hospital so the INR is available before dose decisions. The AF target INR is 2–3.

Time in therapeutic range (TTR) is the proportion of time INR remains within target:

• INR too low → higher stroke risk
• INR too high → higher bleeding risk

Warfarin metabolism depends on cytochrome P450 in the liver, so INR changes with medications that alter P450 activity, including many antibiotics. INR must be checked closely when starting new drugs, and doses adjusted.

INR is also affected by diet, particularly:

• Vitamin K-rich foods (e.g. leafy greens)
• Substances affecting P450 (e.g. cranberry juice, alcohol)

Therefore, INR monitoring should increase when diet changes.

Vitamin K reverses warfarin in cases of very high INR or significant bleeding. Warfarin has a half-life of 1–3 days.

CHA₂DS₂-VASc

CHA₂DS₂-VASc estimates stroke risk in AF to guide anticoagulation decisions. The higher the score, the greater the risk of stroke/TIA.

It includes:

• C – Congestive heart failure
• H – Hypertension
• A₂ – Age >75 (2 points)
• D – Diabetes
• S₂ – Prior stroke/TIA (2 points)
• V – Vascular disease
• A – Age 65–74
• S – Sex (female)

NICE (2021) recommendations:

• Score 0 → no anticoagulation
• Score 1 → consider anticoagulation in men (women score 1 automatically)
• Score ≥2 → offer anticoagulation

Aspirin alone is not used to prevent stroke in AF (it used to be an option historically).

Bleeding Risk (ORBIT)

NICE recommends the ORBIT score to estimate major bleeding risk in AF patients on anticoagulation. The simplest method is an online calculator. ORBIT factors can be remembered with:

• O – Older age (≥75)
• R – Renal impairment (GFR <60)
• B – Prior bleeding (GI or intracranial)
• I – Iron: low haemoglobin or haematocrit
• T – Treatment with antiplatelet medication

For most AF patients, the untreated stroke risk is greater than the bleeding risk associated with anticoagulation.

Left Atrial Appendage Occlusion

For patients who have a high stroke risk but cannot take anticoagulants, left atrial appendage occlusion is an alternative.

The left atrial appendage is a small pouch in the left atrial wall and is the commonest location for thrombus formation. The procedure involves inserting a catheter via the femoral vein, advancing it to the right atrium, puncturing the interatrial septum to enter the left atrium, and deploying a plug within the left atrial appendage to prevent blood entry.

Last updated Dec 2025