01OverviewDefinition, clinical context and the essential points that orientate the chapter.
AF is disorganised atrial electrical activity producing ineffective atrial contraction and irregular AV conduction. It may be paroxysmal, persistent or permanent; symptom burden and ventricular rate do not reliably predict thromboembolic risk.
A practical UK assessment has four simultaneous questions: is the patient unstable; is the diagnosis secure; is rate or rhythm control appropriate now; and is anticoagulation indicated?
NICE NG196 is the principal UK source. RCUK 2025/2026 governs peri-arrest treatment. ESC or current UK SmPC doses below are explicitly labelled where NICE names a medicine but does not give a regimen.
Key points
- Suspect AF with an irregular pulse in a patient with palpitations, breathlessness, dizziness/syncope, chest discomfort, stroke or TIA; confirm with a 12-lead ECG.
- Typical ECG: no consistent sinus P waves and an irregularly irregular ventricular response; AF may be slow, controlled or rapid.
- If a 12-lead ECG misses suspected paroxysmal AF, NICE uses a 24-hour monitor when episodes are asymptomatic or less than 24 hours apart, and longer event/ECG monitoring when symptoms are more than 24 hours apart.
- Treat the patient, not the rate: haemodynamic instability caused by AF requires immediate synchronised cardioversion.
- For stable acute AF, NICE allows rate or rhythm control when onset is under 48 hours, but favours rate control when onset is over 48 hours or uncertain.
- Use CHA2DS2-VASc for stroke risk and ORBIT for bleeding risk; a high bleeding score should prompt modification and closer review, not automatic denial of anticoagulation.
- NICE offers a DOAC at CHA2DS2-VASc 2 or more and says to consider one for a man scoring 1; do not use aspirin alone for AF stroke prevention.
- Long-term rate control is usually a standard beta-blocker or rate-limiting calcium-channel blocker; digoxin is conditional, especially for non-paroxysmal AF in a sedentary person or when other options are unsuitable.
- Never stop anticoagulation solely because sinus rhythm has returned or AF is no longer detected; reassess stroke and bleeding risks and the person's preferences.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Ageing and hypertensive atrial disease
Ageing and hypertension promote atrial stretch, fibrosis and conduction heterogeneity. Vascular disease commonly coexists and contributes to the overall thromboembolic-risk profile, while AF prevalence rises markedly in older adults.
Structural heart disease
Heart failure, ischaemic heart disease, cardiomyopathy and especially significant valve disease are associated with atrial pressure loading, dilatation or fibrosis, making AF more likely and influencing rate, rhythm and anticoagulation decisions.
Systemic and reversible triggers
Sepsis, hypoxia, pulmonary embolism, thyrotoxicosis, electrolyte disturbance, acute bleeding and drug toxicity can precipitate AF. Treating the trigger is essential, but does not by itself eliminate future recurrence or thromboembolic risk.
Lifestyle, sleep and inherited susceptibility
Obesity, obstructive sleep apnoea and alcohol excess promote atrial remodelling and recurrence. Familial susceptibility is more relevant in younger patients without obvious structural disease.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Atrial triggers arise
Rapid ectopic activity, often near the pulmonary veins, initiates disorganised atrial activation. Acute illness or autonomic change can lower the threshold in a susceptible atrium.
- 2An abnormal substrate sustains AF
Atrial dilatation, fibrosis and non-uniform refractoriness can support interacting wavefronts, local drivers and re-entry instead of organised sinus propagation. Longer episodes can promote further electrical and structural remodelling.
- 3Atrial contraction is lost
Chaotic atrial activation abolishes effective atrial systole. Irregular impulses reaching the AV node create an irregular ventricular response, reducing filling and output in vulnerable patients.
- 4Thrombus can form
Poor left-atrial-appendage emptying, endothelial dysfunction and a prothrombotic milieu permit thrombus formation. Embolisation can occlude cerebral or systemic arteries regardless of symptom burden.
- 5Persistent rate drives remodelling
Sustained rapid ventricular activation can impair LV function and produce tachycardia-mediated cardiomyopathy, which may improve when durable rate or rhythm control is achieved.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Irregularly irregular R-R intervals with absent consistent sinus P waves and fibrillatory atrial activity. A regular ventricular response should trigger a search for flutter with fixed block, junctional rhythm, pacing or complete AV block rather than reflexively labelling AF.
Shock (often SBP below 90 mmHg with hypoperfusion), syncope with severe or ongoing hypotension, myocardial ischaemia, severe heart failure with pulmonary oedema, or immediately post-ROSC.
Very rapid, irregular broad-complex tachycardia with varying QRS morphology in a patient with an accessory pathway. It can deteriorate to VF: avoid AV-nodal blockers such as adenosine, verapamil/diltiazem, beta-blockers and digoxin; seek expert help for procainamide or cardioversion.
Look for ACS, stroke/TIA, acute heart failure, sepsis, thyrotoxicosis, pulmonary embolism, hypoxia, electrolyte disturbance, bleeding or drug toxicity; AF may be a marker rather than the primary problem.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
ABCDE assessment, observations, continuous ECG/BP/SpO2 monitoring and 12-lead ECGFirst step - Why
- Confirm AF, document rate/QRS/QT and identify instability, ischaemia, pre-excitation or another rhythm.
- Interpretation and limitations
- Attribute adverse features to the arrhythmia only after treating immediately reversible causes; an irregular broad rhythm is not routine AF with bundle-branch block until pre-excitation and polymorphic VT have been considered.
- 02
Focused history and record review - Why
- Establish exact onset or last known sinus rhythm, symptoms, previous AF/cardioversion, stroke/TIA, bleeding, heart failure, valve disease, drugs/alcohol and anticoagulant adherence.
- Interpretation and limitations
- Uncertain onset is managed like prolonged AF for cardioversion safety; missing DOAC doses may invalidate assumed pre-cardioversion anticoagulation.
- 03
FBC, U&E/creatinine, magnesium, LFTs, TFTs and glucose; troponin only when clinically indicated - Why
- Find anaemia, infection, renal/hepatic impairment, electrolyte or thyroid triggers and establish safe prescribing baselines.
- Interpretation and limitations
- For DOAC dosing calculate creatinine clearance with Cockcroft-Gault rather than relying on eGFR; recheck renal function when acutely unwell or when it may have changed.
- 04
Ambulatory ECG when paroxysmal AF is suspected but not captured - Why
- Obtain symptom-rhythm correlation and diagnostic ECG evidence.
- Interpretation and limitations
- NICE: 24 hours if asymptomatic episodes are suspected or symptoms are under 24 hours apart; otherwise use an event recorder or ECG technology for a duration matched to symptom frequency.
- 05
Transthoracic echocardiography - Why
- Assess LV function, valves, chamber size and structural disease when this affects long-term management, rhythm control/cardioversion, or antiarrhythmic choice.
- Interpretation and limitations
- NICE says not to perform TTE solely to refine stroke risk when anticoagulation has already been agreed on clinical criteria.
- 06
CHA2DS2-VASc and ORBIT - Why
- Quantify stroke and bleeding risk for shared anticoagulation decisions.
- Interpretation and limitations
- Offer a DOAC at CHA2DS2-VASc 2 or more; consider one for a man scoring 1. Use ORBIT to identify reversible bleeding risks and monitoring needs.
- 07
TOE when an early cardioversion strategy is being considered after prolonged or uncertain-duration AF - Why
- Look for left atrial/appendage thrombus when a TOE-guided strategy could avoid waiting three weeks.
- Interpretation and limitations
- A TOE-guided and conventional three-week anticoagulation strategy are both acceptable in NICE when expertise and facilities exist; absence of thrombus does not remove the need for peri/post-cardioversion anticoagulation.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Atrial flutter with variable block
Flutter may also be irregular, but careful ECG inspection reveals organised repetitive atrial waves, commonly around 300 per minute in untreated typical flutter, rather than absent consistent P waves.
Sinus rhythm with frequent ectopy
Premature atrial or ventricular beats create an irregular pulse, but underlying sinus P waves recur predictably and each irregularity can be related to a premature complex, often followed by a pause.
Multifocal atrial tachycardia
MAT is irregular but retains discrete P waves with at least three morphologies and varying PR intervals, commonly during severe pulmonary illness; an isoelectric baseline remains visible.
Focal atrial tachycardia with variable block
A regular abnormal atrial P-wave sequence continues despite variable AV conduction. Identifying the organised atrial rate distinguishes it from fibrillatory activity.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01ImmediateAF causing life-threatening instabilityFirst stepShock, syncope with severe/ongoing hypotension, myocardial ischaemia, pulmonary oedema/severe heart failure, or immediately post-ROSC.+
- 1Call for expert/resuscitation help, perform ABCDE, attach monitor/defibrillator pads, obtain IV access and treat reversible causes.
- 2EscalationUse synchronised cardioversion. RCUK considers an initial shock at the defibrillator's maximum output reasonable for AF; make up to three synchronised attempts with escalation/local device settings.
- 3Provide careful sedation or anaesthesia if conscious and feasible, but do not let it create a dangerous delay.
- 4If shocks fail and instability persists, RCUK permits amiodarone 300 mg IV over 10-20 minutes OR procainamide 10-15 mg/kg IV (maximum 1 g) over 20 minutes according to availability/contraindications, then repeat synchronised cardioversion.
- 5Do not delay emergency cardioversion to anticoagulate. Start anticoagulation as soon as safe and complete stroke/bleeding assessment.
02Acute stableChoose rate or rhythm control by duration and contextConfirmed AF without life-threatening instability.+
- 1Treat triggers and confirm onset. NICE: if onset is under 48 hours, offer either rate or rhythm control; if over 48 hours or uncertain, offer rate control and do not perform routine immediate cardioversion.
- 2Select a rate-control class conditionally. With EF above 40%, RCUK lists a beta-blocker, verapamil, diltiazem or digoxin. With EF below 40%, it suggests a beta-blocker or digoxin and a resting target below 110/min; seek senior input in acute decompensated heart failure and do not use verapamil/diltiazem.
- 3If pharmacological cardioversion is chosen, NICE offers flecainide or amiodarone when there is no structural/ischaemic heart disease, and amiodarone when structural disease is present. This is a specialist choice, not a universal sequence.
- 4NICE says offer heparin at presentation in new-onset AF when anticoagulation is absent/subtherapeutic and no contraindication exists, continuing until full assessment and appropriate antithrombotic therapy; it does not specify one fixed dose, so use the local weight/renal protocol.
- 5Threshold nuance: the March 2026 RCUK peri-arrest algorithm says anticoagulate when AF duration exceeds 24 hours, whereas NICE NG196 uses 48 hours for its acute rhythm-control branch. Treat this as a governance/senior decision, not permission to cardiovert between 24 and 48 hours without considering embolic risk.
03Elective cardioversionProlonged or uncertain-duration AFRhythm control is appropriate but AF has lasted more than 48 hours or duration is uncertain.+
- 1NICE: maintain therapeutic anticoagulation for at least three weeks before cardioversion while controlling rate, or consider an experienced-service TOE-guided strategy when a shorter pre-cardioversion interval is appropriate.
- 2For AF persisting over 48 hours, NICE prefers electrical rather than pharmacological cardioversion.
- 3Non-NICE ESC typical: continue therapeutic anticoagulation for at least four weeks after cardioversion, then continue long term according to thromboembolic risk rather than apparent sinus rhythm alone.
- 4Document adherence, renal function and dose appropriateness before calling a patient therapeutically anticoagulated.
04Long termSymptoms, stroke prevention and specialist rhythm controlAfter acute stabilisation or for incidentally detected/chronic AF.+
- 1Offer rate control first in most people, except when AF has a reversible cause, is new-onset, is causing heart failure, atrial flutter is suitable for ablation, or clinical judgement favours rhythm control.
- 2Use a standard beta-blocker or diltiazem/verapamil monotherapy according to symptoms, rate, comorbidity and preference. Consider digoxin monotherapy only for non-paroxysmal AF in a sedentary person or when other options are unsuitable.
- 3If monotherapy fails and symptoms are due to poor rate control, NICE permits two of beta-blocker, diltiazem and digoxin; it does not recommend combining beta-blocker with verapamil.
- 4Consider rhythm control when symptoms persist despite adequate rate control or rate control fails. Refer promptly, within four weeks of failed treatment or recurrence after cardioversion, when specialist management is needed.
- 5Consider catheter ablation after discussion when antiarrhythmic treatment fails or is not tolerated; continue anticoagulation decisions according to CHA2DS2-VASc/ORBIT.
Key medicines and prescribing safety10 treatments · regimens, roles and cautions+
Atenolol IV/PO (licensed SmPC example of beta-blockade; not a mandatory NICE preference)
Acute arrhythmia: 2.5 mg IV over 2.5 minutes; repeat at 5-minute intervals to response, maximum 10 mg. Alternative infusion: 0.15 mg/kg over 20 minutes. After control, 50-100 mg PO once daily is the cited maintenance regimen.Avoid or reduce in bradycardia, hypotension, high-grade block, acute decompensated heart failure and severe bronchospasm; adjust for renal impairment. Do not combine IV beta-blockade with IV verapamil.
Verapamil IV
5-10 mg by slow IV injection over at least 2 minutes with continuous ECG/BP observation; if necessary, a further 5 mg after 5-10 minutes.Do not use in hypotension, HFrEF/pulmonary oedema, high-grade AV block without pacing, broad-complex tachycardia, or pre-excited AF. IV verapamil with beta-blockers can cause profound hypotension or AV block.
Digoxin IV
If no cardiac glycoside was taken in the previous 2 weeks: total load 500-1000 micrograms IV, with about half first and remaining fractions at 4-8-hour intervals after reassessment; give each fraction by infusion over 10-20 minutes. Maintenance must be individualised to age, lean body weight and renal function.Check renal function, potassium, interactions and previous digoxin exposure; monitor ECG and toxicity. Avoid in pre-excited AF. A serum level is interpretable only when sampled at an appropriate post-dose interval.
Flecainide (specialist rhythm control; non-NICE dose detail)
Current UK oral SmPC maintenance example: 50 mg PO twice daily initially for supraventricular arrhythmias, titrated if required to maximum 300 mg/day. Non-NICE ESC 'pill-in-the-pocket' typical single dose: 200-300 mg PO only after safety/efficacy has been established in a monitored setting and with a clinician-prescribed AV-nodal blocker where appropriate.NICE says do not use class Ic drugs in known ischaemic or structural heart disease. Avoid in LV dysfunction, significant valve disease, cardiogenic shock, important conduction disease or Brugada pattern; check QRS/PR, renal function and interactions. Proarrhythmia and 1:1 flutter are recognised risks.
Amiodarone IV
SmPC usual infusion: 5 mg/kg IV over 20 minutes to 2 hours in 250 mL 5% glucose, with repeat infusion according to response up to 1200 mg/24 h. RCUK rescue after failed cardioversion in an unstable tachyarrhythmia: 300 mg IV over 10-20 minutes, then reattempt cardioversion; a 900 mg/24 h infusion may follow.Hospital/specialist use with ECG/BP and defibrillation/pacing available. IV bolus is problematic in severe hypotension/circulatory collapse. Avoid as long-term rate control; monitor thyroid, liver, lung, eyes, QT/bradycardia and major interactions, including warfarin and digoxin.
Apixaban for non-valvular AF
5 mg orally twice daily. Reduce to 2.5 mg twice daily when at least 2 apply: age 80 years or older, body weight 60 kg or less, or serum creatinine 133 micromol/L or more. The cited SmPC also uses 2.5 mg twice daily for NVAF with CrCl 15–29 mL/min.Calculate Cockcroft–Gault CrCl and check FBC, liver function, bleeding and interactions. Avoid active significant bleeding, another therapeutic anticoagulant and mechanical valves; use a VKA for mechanical valves or moderate-to-severe rheumatic mitral stenosis.
Dabigatran for non-valvular AF
150 mg orally twice daily. Use 110 mg twice daily at age 80 years or older or with verapamil; consider 110 mg twice daily at age 75–80, CrCl 30–50 mL/min or when bleeding/gastrointestinal risk is increased.Contraindicated if CrCl is below 30 mL/min. Calculate Cockcroft–Gault CrCl and review FBC, liver function, bleeding and P-gp interactions; avoid another therapeutic anticoagulant, mechanical valves and high-risk antiphospholipid syndrome.
Edoxaban for non-valvular AF
60 mg orally once daily. Reduce to 30 mg once daily when CrCl is 15–50 mL/min, body weight is 60 kg or less, or with ciclosporin, dronedarone, erythromycin or ketoconazole.Not recommended below CrCl 15 mL/min. Calculate Cockcroft–Gault CrCl and review FBC, liver function, bleeding and interactions; avoid another therapeutic anticoagulant, mechanical valves and high-risk antiphospholipid syndrome.
Rivaroxaban for non-valvular AF
20 mg orally once daily with food; reduce to 15 mg once daily with food when CrCl is 15–49 mL/min.Not recommended below CrCl 15 mL/min. Calculate Cockcroft–Gault CrCl and review FBC, liver function, bleeding and interactions; avoid another therapeutic anticoagulant, mechanical valves and high-risk antiphospholipid syndrome.
Warfarin/VKA
Individualised oral dosing to INR 2.0-3.0 for AF; there is no safe universal loading dose. NICE defines poor control as, among other criteria, TTR below 65% and recommends reassessment.Frequent INR during initiation/interaction/illness, then stable-interval monitoring; review diet, alcohol, adherence and interacting medicines.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Ischaemic stroke and systemic embolism
Left-atrial-appendage thrombus can embolise to the brain, limbs or viscera. Risk depends more on clinical factors than AF symptoms, ventricular rate or apparent return to sinus rhythm.
Heart failure and tachycardiomyopathy
Loss of atrial contraction and an uncontrolled ventricular rate impair filling and output. Persistent tachycardia can cause reversible LV dysfunction, while AF also destabilises established heart failure.
Haemodynamic collapse or ischaemia
Very rapid AF can shorten filling and coronary perfusion enough to cause hypotension, pulmonary oedema or myocardial ischaemia, particularly with severe structural heart disease.
Bleeding during anticoagulant treatment
Stroke prevention exposes patients to gastrointestinal, intracranial and other bleeding. Bleeding assessment should identify modifiable risks and monitoring needs rather than automatically deny anticoagulation.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- During acute treatment: continuous ECG, BP, SpO2, mental state and perfusion; record a post-conversion 12-lead ECG and watch for bradycardia, QT/QRS change or recurrence.
- For DOACs: baseline and periodic FBC, Cockcroft-Gault CrCl and LFTs; review sooner with dehydration, acute illness, weight change, bleeding or interacting medicines.
- For warfarin: INR and TTR; address INR above 5/8, repeated INR below 1.5 or TTR below 65% as defined by NICE.
- For digoxin: renal function, potassium/magnesium, rate and toxicity; consider a correctly timed serum digoxin level when toxicity, non-adherence, renal change or interaction is suspected.
- For amiodarone: ECG, thyroid and liver tests; pulmonary symptoms/imaging and eye/neurological review according to duration and local monitoring protocol.
- Review symptoms, rate, anticoagulation indication and modifiable risks at least annually and after any major clinical change; do not equate successful ablation/cardioversion with removal of stroke risk.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
A high bleeding score is not a veto
ORBIT is for risk communication, correction of anaemia/uncontrolled BP/alcohol or interacting drugs, and planning review. NICE explicitly warns against withholding anticoagulation solely because of age or falls risk.
Time thresholds are not perfectly aligned
NICE's acute cardioversion split remains 48 hours; RCUK's March 2026 peri-arrest algorithm flags anticoagulation when AF exceeds 24 hours. State which authority you are following and escalate uncertain cases.
Rate control is not automatically 'first' for everyone
New-onset AF, a reversible trigger, AF-mediated heart failure, ablatable flutter or persistent symptoms may favour rhythm control. NICE asks for clinical judgement rather than a rigid ladder.
Do not cardiovert pre-excited AF with AV-nodal drugs
Blocking the AV node can favour conduction down the accessory pathway and accelerate the ventricles. Cardioversion or expert-guided procainamide is the RCUK branch.
A normal snapshot does not erase AF
Paroxysmal AF can be absent on clinic ECG. NICE says anticoagulation should not be stopped solely because AF is no longer detectable.
11Common pitfallsFrequent interpretation and management errors.
- 01
Calling any irregular rhythm AF without confirming it on a 12-lead ECG.
- 02
Delaying cardioversion in AF-caused life-threatening instability while waiting for anticoagulation or a perfect history.
- 03
Using verapamil/diltiazem in acute decompensated HFrEF or any AV-nodal blocker in pre-excited AF.
- 04
Reducing a DOAC 'because the patient is old' without meeting the product-specific criteria; underdosing can leave stroke risk untreated.
- 05
Using eGFR rather than Cockcroft-Gault CrCl to choose a DOAC dose.
- 06
Using aspirin alone for AF stroke prevention or stopping anticoagulation after apparent rhythm cure without reassessment.