Atrial Fibrillation

Atrial Fibrillation is the most common sustained cardiac arrhythmia, affecting ~2% of the UK population. It is classified as Paroxysmal (terminates spontaneously <7 days), Persistent (lasts >7 days), or Permanent (accepted by patient/physician). The primary clinical concern in AF is the five-fold increased risk of embolic stroke due to thrombus formation in the left atrial appendage. AF also contributes to tachycardia-induced cardiomyopathy and heart failure. NICE guidelines emphasize the use of the CHA2DS2-VASc score to assess stroke risk and the ORBIT (or HAS-BLED) score to assess bleeding risk before starting anticoagulation. Rate control (aiming for a resting heart rate <90-110 bpm) is the standard first-line approach for most, particularly those >65 or with minimal symptoms. Rhythm control (Restoration of sinus rhythm via DCCV or antiarrhythmics) is preferred in younger patients, those with symptomatic AF despite rate control, or if AF is causing heart failure. Anticoagulation (DOACs preferred over Warfarin) is indicated if the CHA2DS2-VASc score is ≥2 (consider if 1 in men).

The pathophysiology of AF involves both initiation (triggers) and maintenance (substrate). Ectopic electrical firing, often originating from the sleeves of pulmonary vein musculature, triggers rapid atrial activation. For AF to persist, the atrium must undergo electrical and structural 'remodelling'. Chronic rapid rates lead to a shortening of the atrial refractory period (electrical remodelling) and atrial dilatation/fibrosis (structural remodelling). This creates a 're-entry' circuit where multiple wavelet of depolarization can propagate. The chaotic atrial electrical activity leads to a loss of the 'atrial kick' (responsible for 20% of ventricular filling), which can reduce cardiac output. The AV node acts as a filter, but at high rates, the ventricular response remains rapid and irregular. Thrombus formation occurs due to Virchow’s Triad: stasis (as the atria are not contracting), endothelial damage/dysfunction, and a systemic pro-thrombotic state associated with AF.

AF may be asymptomatic (silent AF) or present with palpitations, dyspnoea, fatigue, light-headedness, or syncope. In acute cases (e.g., sepsis or thyrotoxicosis), it can present with acute heart failure or angina. Examination reveals the classic irregularly irregular pulse and a deficit between the apical and radial pulse rates. Risk factors include aging, hypertension, valvular heart disease (especially Mitral Stenosis), obesity, alcohol excess ('holiday heart syndrome'), sleep apnoea, and hyperthyroidism. The most dreaded complication is ischaemic stroke, which tends to be more severe and disabling when caused by AF. In the long term, AF can lead to heart failure through 'tachycardiomyopathy'.

1. Bedside: 12-lead ECG (Diagnostic), Pulse check, Blood pressure.
2. Bloods: TFTs (rule out hyperthyroidism), Electrolytes (K+ and Mg2+ can trigger AF), FBC (anaemia/infection), Coagulation screen, Renal function (for DOAC dosing).
3. Imaging: Transthoracic Echocardiogram (TTE) to check for structural heart disease or LA enlargement; Transoesophageal Echo (TOE) if planning DCCV to rule out LA thrombus.
4. Special: 24-hour Holter monitor if paroxysmal AF is suspected but not seen on initial ECG.

1. Stroke Prevention: Assess CHA2DS2-VASc. If score ≥2 (or 1 in men), offer DOAC (e.g., Apixaban 5mg BD). Use ORBIT score to assess bleeding risk.
2. Rate Control: First-line: Beta-blocker (e.g., Bisoprolol) or rate-limiting Calcium Channel Blocker (e.g., Diltiazem). Digoxin is added if sedentary or co-existent Heart Failure.
3. Rhythm Control: Indicated if symptomatic, young, or new-onset (<48h). Options: Pharmacological (Flecainide if no structural heart disease, Amiodarone if heart failure present) or DC Cardioversion (DCCV).
4. Acute Management (<48h): If haemodynamically unstable, immediate DCCV. If stable, rate control or DCCV (if anticoagulated or thrombus excluded by TOE).
5. Advanced: Catheter ablation (Pulmonary Vein Isolation) for symptomatic paroxysmal AF.