Atrial Fibrillation (AFib)

• Atrial fibrillation (AF) involves disorganized electrical activity in the atria, leading to ineffective contraction and irregular ventricular rhythm.
• AF is the most common heart arrhythmia among adults, increasing in prevalence with age, affecting 10% of those over 85.

Types of AF

• Paroxysmal: Episodes lasting >30 seconds, resolving spontaneously or with intervention within 7 days, often within 48 hours.
• Persistent: Episodes lasting longer than 7 days, including those requiring cardioversion.
• Permanent: AF accepted by both patient and clinician, with no attempts planned to restore sinus rhythm.

Cardiac Conduction System

• Electrical impulses start in the sinoatrial node (SAN) in the right atrium, with the rate influenced by the autonomic nervous system.
• Sympathetic nervous system increases SAN impulse rate, while the parasympathetic decreases it.
• Impulses travel through the atria to the atrioventricular node (AVN), causing atrial contraction
• The AVN delays the impulse before it travels through the Bundle of His, bundle branches, Purkinje fibers, resulting in ventricular contraction.

Pathophysiology of Atrial Fibrillation

• AF is a supraventricular arrhythmia originating above the ventricles.
• Often starts in left atrial myocytes near the pulmonary veins.
• Atrial ectopics from pulmonary veins cause micro re-entry circuits, leading to chaotic electrical activity and sustained AF.
• This chaotic activity passes through the AVN irregularly, causing an irregularly irregular ventricular rate.
• Ventricular rate variability depends on AVN conduction speed; faster AVN conduction can cause tachycardia.
• Ineffective atrial contraction from chaotic activity leads to blood stasis, increasing risk of thrombosis, TIA, stroke, and systemic embolization.

Causes of Atrial Fibrillation

• Conditions stretching the atria and altering electrical properties increase AF risk.
• Addressing underlying conditions improves prognosis and sinus rhythm maintenance.
• Causes are split into cardiac and non-cardiac.

Cardiac Causes

• Hypertension: Most common risk factor.
• Ischaemic heart disease
• Heart failure with reduced ejection fraction
• Structural pathology: Valve stenosis or regurgitation.
• Congenital heart disease
• Atrial or ventricular dilation/hypertrophy
• Pre-excitation syndromes: Wolff-Parkinson-White syndrome.
• Sick sinus syndrome
• Inflammatory conditions: Pericarditis or myocarditis.
• Infiltrative conditions: Amyloidosis.

Non-Cardiac Causes

• Acute infection
• Electrolyte imbalances: Hypokalemia or hyponatremia.
• Pulmonary embolism
• Thyrotoxicosis or hypothyroidism
• Diabetes mellitus

Risk factors for AF

• Male sex
• Caucasian ethnicity
• Increasing age
• Alcohol
• Cigarette smoking
• Obesity
• Co-morbidities: Chronic kidney disease and obstructive sleep apnoea.
• Caffeine intake is not typically a risk factor

Clinical Features - History

• AF may be asymptomatic, found incidentally, or via patient-initiated monitoring.
• Typical symptoms include breathlessness, chest discomfort, palpitations, light-headedness, reduced exercise tolerance.
• Syncope can occur due to bradycardia, especially with paroxysmal AF when sinus rhythm returns.
• TIA or stroke can be the presenting sign.

Important history points

• Presence of pre-existing cardiac disease
• Past medical history of cardiac and non-cardiac conditions
• Medications
• Social history: Alcohol, smoking, obesity.

Clinical Examination

• Thorough cardiovascular examination is necessary.
• Clinical findings: Irregularly irregular pulse, radial-apical deficit.
• Possible heart failure signs: Raised JVP, added heart sounds, crackles, ankle swelling.

Differential Diagnoses

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

Investigations - Bedside

• Basic observations: Vital signs, to assess haemodynamic instability.
• 12-lead ECG: Diagnostic; shows tachycardia, irregularly irregular rhythm, absent P-waves, fibrillation waves, chaotic baseline.
• Ambulatory ECG: To capture symptomatic episodes of suspected paroxysmal AF

Investigations - Laboratory

• Full blood count: To assess for acute infection.
• Urea & electrolytes: To assess for electrolyte imbalances.
• Liver function tests: Baseline before anticoagulants.
• Thyroid function tests: T4 and TSH levels for hyperthyroidism.
• CRP: To assess for acute infection
• Clotting screen: Baseline before anticoagulants.
• NT-proBNP: To assess for underlying heart failure

Investigations - Imaging

• Echocardiogram: Assesses structural or valvular disease and LV systolic dysfunction.
• Chest X-ray: To assess for changes associated with heart failure

Diagnosis of AF criteria

• ECG recording of ≥30 seconds showing no discernible repeating P-waves.
• Irregular RR intervals.

Management - Immediate

• ABCDE assessment to identify adverse features (shock, syncope, myocardial ischaemia, heart failure).
• Synchronized direct current cardioversion if adverse features are present.

Management - Ongoing

• Anticoagulation is primary.
• Management includes rhythm and rate control.
• Choice depends on symptoms and maintaining sinus rhythm.
• No clear prognostic benefit to restoring sinus rhythm.
• Managing modifiable risk factors is essential.
• Refer to a specialist if symptoms are uncontrolled in primary care.

Rhythm Control

• Can be electrical or chemical cardioversion.
• Appropriate for new-onset AF.