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Atrial fibrillation

SNOMED: 49436004881 words•Updated 03/03/2026
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Exam Tips

  • AF is an ECG diagnosis: absent P waves plus irregularly irregular R-R intervals; pulse check alone is screening, not confirmation.
  • In OSCEs, always pair diagnosis with two risk frameworks: stroke risk (CHA2DS2-VASc) and bleeding risk (e. g, ORBIT/HAS-BLED).
  • Do not withhold anticoagulation solely because AF is paroxysmal; stroke risk can be comparable to persistent forms when risk factors are present.
  • Red flag viva point: avoid AV nodal blockers in pre-excited AF (WPW pattern) due to risk of ventricular fibrillation.
  • When discussing management, explicitly mention contraindications (DOACs in mechanical valves/mitral stenosis, verapamil plus beta-blocker, flecainide in structural heart disease).
  • Image cue for revision: review a standard ECG strip demonstrating AF (absent P waves, fibrillatory baseline, irregular QRS timing) in your cardiology ECG atlas.

Definition

Atrial fibrillation (AF) is a sustained supraventricular tachyarrhythmia caused by disorganized atrial electrical activity, producing ineffective atrial contraction and an irregularly irregular ventricular rhythm. It may be paroxysmal, persistent, long-standing persistent, or permanent, and can be symptomatic or entirely asymptomatic while still carrying significant thromboembolic risk.

Pathophysiology

AF usually begins with ectopic firing (classically near the pulmonary vein ostia) and multiple re-entry wavelets within atrial tissue. Electrical remodelling (shortened atrial refractory periods) and structural remodelling (fibrosis, dilatation, inflammation) help perpetuate AF ('AF begets AF'). Loss of coordinated atrial systole reduces ventricular filling and can lower cardiac output; a rapid/irregular ventricular response may cause tachycardia-induced cardiomyopathy. Blood stasis, especially in the left atrial appendage, promotes thrombus formation and embolic stroke.

Risk Factors

  • Increasing age (prevalence rises progressively with age)
  • Hypertension (major modifiable driver)
  • Heart failure (especially HFrEF)
  • Ischaemic heart disease
  • Valvular heart disease (including mitral valve pathology)
  • Cardiomyopathy with atrial or ventricular dilatation/hypertrophy
  • Congenital heart disease
  • Wolff-Parkinson-White syndrome and other pre-excitation disorders
  • Sick sinus syndrome
  • Recent cardiothoracic surgery
  • Acute illness (e. g, pneumonia, pulmonary embolism, sepsis)
  • COPD
  • Chronic kidney disease
  • Electrolyte disturbance (especially hypokalaemia)
  • Thyrotoxicosis
  • Diabetes mellitus
  • Obstructive sleep apnoea
  • Alcohol excess
  • Obesity
  • Smoking
  • High-endurance athletic training
  • Medication-related triggers (e. g, excess thyroxine, lithium, beta-2 agonists)

Clinical Features

Symptoms

  • Palpitations
  • Breathlessness
  • Reduced exercise tolerance
  • Fatigue and poor sleep
  • Chest discomfort or chest pain
  • Dizziness or presyncope/syncope
  • May present with stroke/TIA symptoms as first manifestation
  • Can be asymptomatic and detected incidentally

Signs

  • Irregularly irregular pulse
  • Variable first heart sound intensity
  • Tachycardia (often around 90-170 bpm if untreated)
  • Pulse deficit (apical rate greater than radial rate)
  • Signs of heart failure (raised JVP, crackles, peripheral oedema) in decompensation
  • Haemodynamic instability in severe rapid AF (hypotension, shock, pulmonary oedema)

Investigations

12-lead ECG:No discrete P waves, fibrillatory baseline, irregularly irregular R-R intervals; confirms AF when rhythm strip shows AF pattern for at least 30 seconds.
Ambulatory ECG monitoring (24-hour Holter or longer event monitoring):Intermittent AF episodes in suspected paroxysmal AF when office ECG is non-diagnostic.
Transthoracic echocardiography:Assesses left atrial size, LV function, valvular disease, and structural heart disease; helps stratify recurrence and management strategy.
Blood tests: FBC, U&Es, creatinine/eGFR, LFTs, TFTs, glucose/HbA1c:Identifies precipitating or contributory causes (e. g, thyrotoxicosis, infection, renal dysfunction, electrolyte disturbance) and supports safe drug dosing.
Stroke and bleeding risk assessment (CHA2DS2-VASc and ORBIT/HAS-BLED):Guides anticoagulation decisions and risk-factor modification rather than diagnosing AF itself.
Chest X-ray (if clinically indicated):May show cardiomegaly, pulmonary oedema, or alternative pulmonary pathology precipitating AF.

Management

Lifestyle Modifications

  • Treat reversible triggers (infection, thyrotoxicosis, electrolyte disturbance, hypoxia).
  • Reduce alcohol intake and stop smoking.
  • Weight reduction in overweight/obesity and optimize blood pressure/diabetes control.
  • Screen and treat obstructive sleep apnoea when suspected.
  • Promote regular moderate exercise and cardiovascular risk reduction.

Pharmacological Treatment

Rate control (first-line in many patients)

  • Bisoprolol 2.5-10 mg once daily
  • Diltiazem MR 120-360 mg once daily
  • Verapamil 40-120 mg three times daily (or MR preparation)
  • Digoxin 62.5-250 micrograms once daily (especially if sedentary or with heart failure)

Use a beta-blocker or rate-limiting calcium-channel blocker first; consider digoxin add-on if rate remains uncontrolled. Avoid verapamil with beta-blockers (heart block/bradycardia risk). Non-dihydropyridine calcium-channel blockers are generally avoided in HFrEF.

Rhythm control / cardioversion support

  • Flecainide 50-100 mg twice daily
  • Amiodarone oral loading then maintenance (e. g, 200 mg three times daily for 1 week, then 200 mg twice daily for 1 week, then 200 mg daily)
  • Sotalol 80-160 mg twice daily (specialist use)

Used when rhythm-control strategy is chosen (symptomatic AF, younger patients, tachycardia cardiomyopathy, or failed rate control). Flecainide is contraindicated in structural/ischaemic heart disease. Amiodarone requires monitoring (thyroid, liver, pulmonary, ocular) and has major interaction/toxicity burden.

Stroke prevention (anticoagulation)

  • Apixaban 5 mg twice daily (reduce to 2.5 mg twice daily in selected high-risk patients)
  • Rivaroxaban 20 mg once daily with food (dose reduction in renal impairment)
  • Edoxaban 60 mg once daily (reduce to 30 mg once daily when indicated)
  • Dabigatran 150 mg twice daily (110 mg twice daily in selected patients)
  • Warfarin dose-adjusted to INR 2.0-3.0 if DOAC unsuitable

Offer according to CHA2DS2-VASc risk and bleeding profile. DOACs are generally preferred for non-valvular AF. Do not use DOACs in mechanical heart valves or moderate-to-severe mitral stenosis; use warfarin instead. Check renal function before and during treatment, review interactions, and counsel on bleeding red flags.

Surgical / Interventional

  • Catheter ablation (typically pulmonary vein isolation) for symptomatic AF, often after drug failure or earlier in selected patients.
  • Electrical cardioversion for persistent AF when restoring sinus rhythm is appropriate.
  • AV node ablation with permanent pacing for refractory rate control when medications and rhythm strategies fail.
  • Left atrial appendage occlusion in selected patients with contraindication to long-term anticoagulation.

Complications

  • Ischaemic stroke and systemic thromboembolism
  • Heart failure or acute pulmonary oedema
  • Tachycardia-induced cardiomyopathy and LV dysfunction
  • Worsening myocardial ischaemia/angina with poor rate control
  • Recurrent hospital admission and reduced quality of life
  • Cognitive decline and vascular dementia
  • Increased all-cause and cardiovascular mortality

Prognosis

Prognosis depends on comorbidity burden, ventricular rate control, and thromboembolic prevention. Paroxysmal AF still carries meaningful stroke risk, and progression to persistent/permanent AF is common over time (often several percent per year, higher with age, obesity, heart failure, CKD, COPD, diabetes, and left atrial enlargement). AF recurrence after cardioversion is frequent, so long-term follow-up and risk-factor management are central.

Sources & References

💊BNF Drug References(22)

✅NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 466, 467)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1033, 1034)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 238)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 469, 470)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 523)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 214, 215)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 426)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1021, 1022)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 536, 537)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1209)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 244, 245)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 463)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 176)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 293)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 175)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 175)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 175)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 203, 204, 205)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 377, 378)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 499)[context]

Sources

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