Lucan · Conditions

Atrial fibrillation

Australian guidance: NHFA / CSANZ Australian AF Guidelines 2018+

1. Definition and epidemiology

Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterised by disorganised atrial electrical activity and an irregularly irregular ventricular response. AF occurs in 2 to 4% of the population in developed nations including Australia, making it the most common sustained cardiac arrhythmia. AF related stroke accounts for at least 25% of ischaemic stroke in Australia and is associated with significant mortality and disability, with 10% of all ischaemic strokes linked to previously undetected AF.

2. Pathophysiology

AF arises from two interacting mechanisms per Robbins (Ch 12): ectopic focal firing, often from the pulmonary vein ostia, and multiple reentrant wavelets propagating through structurally altered atrial tissue. Atrial fibrosis, dilatation, and inflammation disrupt normal conduction by creating heterogeneous refractory periods that sustain chaotic re-entry. The resulting loss of coordinated atrial contraction reduces cardiac output by approximately 15 to 20% and causes blood stasis in the left atrial appendage, a major site of thrombus formation. The left atrial appendage thrombus is the principal source of cardioembolic stroke in AF. Structural heart disease, hypertension, ageing, and sympathetic activation all promote the atrial remodelling that perpetuates AF. Once established, AF begets AF: ongoing electrical and mechanical remodelling makes spontaneous cardioversion progressively less likely as AF duration extends.

3. Clinical presentation and diagnostic criteria

Patients present with palpitations, dyspnoea, fatigue, reduced exercise tolerance, pre-syncope, or chest discomfort. A substantial minority are entirely asymptomatic, and stroke risk is equivalent regardless of symptom burden. Examination reveals an irregularly irregular pulse and may show a pulse deficit between apical and radial rates. AF is classified as paroxysmal (self-terminating within 7 days), persistent (lasting more than 7 days), long-standing persistent (more than 12 months), or permanent (where cardioversion is no longer pursued). Diagnosis requires confirmation by a 12-lead electrocardiogram (ECG): absent P waves replaced by fibrillatory baseline and an irregularly irregular ventricular response. Treatment should not be commenced on clinical grounds alone without ECG confirmation.

4. Investigations and AU-specific cutoffs

Initial diagnostic workup recommended by the NHFA/CSANZ guidelines includes the following, performed at new diagnosis:

• Full blood count
• Electrolytes (correct hypokalaemia and hypomagnesaemia, which are precipitants)
• Renal function (baseline creatinine, creatinine clearance for NOAC dosing)
• Thyroid stimulating hormone (TSH): must be checked in all newly diagnosed AF; delay in acutely unwell patients
• Transthoracic echocardiography: quantifies left ventricular function, atrial size, and identifies valvular disease
• Transoesophageal echocardiography: indicated when findings may affect management, particularly before electrical or pharmacological cardioversion to exclude left atrial appendage thrombus

Opportunistic screening is recommended for all patients aged 65 years or over: pulse palpation followed by a 12-lead ECG if an irregular rhythm is detected. This can be performed by practice nurses during chronic care consultations or immunisations.

5. Management

Management follows four pillars: rate or rhythm control, anticoagulation for stroke prevention, risk factor management, and shared decision-making with the patient.

Acute haemodynamic instability: Immediate synchronised electrical cardioversion is required when AF causes haemodynamic compromise (acutely altered mental state, ongoing chest pain, acute left ventricular failure, hypotension, or signs of shock). Procedural sedation is required; seek experienced clinician input. Clinical instability is rarely present when the ventricular rate is below 150 beats per minute; other causes of instability should be considered in that context.

Rate control: Beta-blockers and non-dihydropyridine calcium channel blockers (diltiazem, verapamil) are first-line rate control agents. Digoxin may be added in patients with heart failure with reduced ejection fraction. Target resting heart rate is generally below 100 beats per minute.

Rhythm control: Electrical cardioversion or pharmacological cardioversion with flecainide or amiodarone may be appropriate for selected patients. Catheter ablation is an alternative for paroxysmal AF not controlled by drug therapy.

Stroke prevention: Stroke risk is stratified using the CHA2DS2-VA score. Oral anticoagulation is recommended when the score is 2 or more, and should be considered when the score is 1. Antiplatelet therapy is not recommended for stroke prevention regardless of stroke risk level.

Risk factor modification targets per NHFA guidelines: - Blood pressure at or below 130/80 mmHg - BMI below 27 kg/m2 with at least 10% weight loss in overweight patients - HbA1c at or below 6.5% in patients with diabetes - Alcohol limited to 3 or fewer standard drinks per week - Sleep apnoea management with CPAP if the apnoea-hypopnoea index is 15 or more per hour

6. Pharmacology and AU PBS notes

NOACs are preferred over warfarin for non-valvular AF. They are at least as effective as warfarin in preventing stroke and systemic embolism, carry a lower intracranial haemorrhage risk, and are easier to use clinically. Warfarin remains the anticoagulant of choice when creatinine clearance (CrCl) is below 30 mL/min, as NOACs are not approved or evidence-based at this level of renal impairment.

AU-specific NOAC dosing adjustments:

PBS notes: NOACs are PBS subsidised for non-valvular AF with a CHA2DS2-VA score of 1 or more. When a patient on warfarin is stable and willing, switching to a NOAC is reasonable and consistent with Australian guideline recommendations. Antiplatelet agents should not be used as a substitute for anticoagulation in patients with AF. If dual antiplatelet therapy is required (e.g. within 12 months of acute coronary syndrome or stent), minimise the duration of triple therapy, use aspirin and clopidogrel if dual antiplatelet therapy is required, and discontinue all antiplatelet therapy after 12 months.

Female sex is not included in the Australian CHA2DS2-VA scoring system, as female sex alone or with one additional risk factor does not confer a consistent or sufficient increased stroke risk in Australian data.

7. Complications and monitoring

Stroke and systemic embolism are the principal complications, driven by left atrial appendage thrombus formation. AF related stroke tends to be more severe and disabling than stroke from other causes.

Heart failure can result from rapid uncontrolled ventricular rates causing tachycardia-mediated cardiomyopathy, which may be partially reversible with rate control.

Other complications: pericardial or haemodynamic deterioration following cardioversion without adequate anticoagulation; proarrhythmia from antiarrhythmic agents including QT prolongation and torsades de pointes with sotalol.

Monitoring schedule: - Renal function for all patients on NOACs: at least annually; more frequently in patients with chronic kidney disease or intercurrent illness - CHA2DS2-VA score reassessed annually, as stroke risk factors accumulate with age and new comorbidities - Thyroid function monitored in patients on amiodarone (risk of hypothyroidism and hyperthyroidism) - Treatment adherence assessed regularly using patient-centred strategies; approximately one-third to half of patients discontinue NOAC therapy within 2.5 years of initiation - Blood pressure and metabolic risk factor targets reviewed at each chronic disease review

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.