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Atrial fibrillation (AF) is the most common irregular heart rhythm, where the upper chambers of the heart quiver instead of beating steadily. It can cause palpitations, breathlessness and tiredness, and because blood can pool and clot, it raises the risk of stroke. Management has three parts: reducing stroke risk (often with blood thinners), controlling the heart rate or rhythm, and treating underlying causes. Staying active, a healthy weight and limiting alcohol all help. This page explains AF and how it is managed.
Atrial fibrillation is the most common sustained arrhythmia and a major driver of stroke, heart failure, and hospital presentation in Australia. Management has shifted decisively toward integrated, structured care emphasising rhythm control in symptomatic patients, comprehensive risk-factor modification, and shared decision-making about anticoagulation.
Definition
Atrial fibrillation (AF) is an irregular and often rapid supraventricular arrhythmia characterised on ECG by absent P waves, irregular RR intervals, and fibrillatory atrial activity. It is classified as first-detected, paroxysmal (terminates within seven days), persistent (lasting > 7 days), long-standing persistent (> 1 year), or permanent (accepted as ongoing without rhythm control).
Pathophysiology
AF arises from a combination of triggers (most commonly ectopic foci in the pulmonary veins) acting on a vulnerable atrial substrate (fibrosis, stretch, ion channel remodelling). The arrhythmia itself promotes further atrial remodelling — "AF begets AF" — making earlier intervention increasingly favoured.
Loss of atrial contraction reduces cardiac output (particularly in HFpEF and during exercise), promotes intra-atrial stasis (raising thromboembolic risk), and tachycardia-induced cardiomyopathy may develop with poorly controlled ventricular rates.
Co-morbidities
Hypertension, heart failure, valvular heart disease, ischaemic heart disease, obstructive sleep apnoea, obesity, diabetes, hyperthyroidism, chronic kidney disease, and chronic lung disease. The AF-OSA association is particularly strong and bidirectional.
Prevalence
AF affects approximately 2% of Australian adults overall, rising sharply with age to > 10% in those over 80. Substantial undiagnosed AF is identified through opportunistic screening, particularly using single-lead ECG devices and consumer wearables.
Causes and risk factors
Modifiable: hypertension, obesity, OSA, alcohol (clear dose-response), endurance exercise (paradoxically increased risk at extremes), poor glycaemic control, and physical inactivity.
Non-modifiable: age, male sex, family history, prior cardiac surgery, and inherited cardiomyopathies.
Symptoms
Palpitations, breathlessness, fatigue, reduced exercise tolerance, lightheadedness, chest discomfort, and (in poorly rate-controlled AF) heart failure symptoms. A substantial minority of AF is asymptomatic and detected incidentally or following a complication such as stroke.
Diagnosis
Why diagnosis matters
Untreated AF carries a five-fold risk of stroke, with strokes typically larger and more disabling than non-AF strokes. Diagnosis enables stroke prevention, symptom-directed rhythm and rate control, and management of contributing risk factors.1,2
How the diagnosis is made
A 12-lead ECG demonstrating AF for ≥ 30 seconds (or for the duration of the recording) confirms diagnosis. Holter monitoring, event recorders, implantable loop recorders, and patch-based extended monitoring are used to detect paroxysmal AF. Single-lead consumer devices and wearables are increasingly accepted as a source of presumptive diagnosis pending confirmation.
Baseline assessment
Echocardiography (LV function, atrial size, valvular assessment), TSH, electrolytes, renal function, FBC, fasting glucose or HbA1c, lipid profile, and (where indicated) screening for OSA. Symptom severity is graded using the EHRA scale.
Risk stratification
Stroke risk: CHA₂DS₂-VASc score guides anticoagulation. Bleeding risk: HAS-BLED, ORBIT, or ABC-bleeding scores identify modifiable bleeding factors rather than withholding therapy. The 2023 ACC/AHA and 2024 ESC AF guidelines emphasise that elevated bleeding risk should prompt risk-factor modification, not omission of anticoagulation.
Management
The AF-CARE framework
Modern AF management is organised around the AF-CARE pathway (or analogous frameworks): Comorbidity and risk factor management, Avoid stroke and thromboembolism, Reduce symptoms with rate and rhythm control, and Evaluation and dynamic reassessment.3
Anticoagulation
Oral anticoagulation is recommended for most patients with CHA₂DS₂-VASc ≥ 2 (men) or ≥ 3 (women), and considered for CHA₂DS₂-VASc 1 (men) or 2 (women). DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) are first-line for most non-valvular AF; warfarin remains the standard for AF with mechanical valves or moderate-to-severe mitral stenosis.
Aspirin is not effective for stroke prevention in AF and should not be used as a substitute for anticoagulation.
Rate control
Beta-blockers (bisoprolol, metoprolol) and non-dihydropyridine CCBs (diltiazem, verapamil) are first-line for rate control. Digoxin is an adjunct, particularly in heart failure or limited mobility. Resting heart rate target is typically < 110 bpm for asymptomatic patients (lenient control) and < 80 bpm for symptomatic patients (strict control).4
Rhythm control
Rhythm control is increasingly favoured for symptomatic patients, those with recent-onset AF, heart failure with reduced EF, and where AF is contributing to tachycardia-mediated cardiomyopathy. Options include antiarrhythmic drug therapy (flecainide, sotalol, amiodarone), electrical cardioversion, and catheter ablation (pulmonary vein isolation).5,6,7
Early rhythm control (within one year of diagnosis) reduces cardiovascular events in selected populations per the EAST-AFNET 4 trial. Catheter ablation is now a first-line option for symptomatic paroxysmal AF in patients suitable for the procedure.
Comprehensive risk factor management
Weight loss (≥ 10% sustained), blood pressure control, alcohol reduction (ideally abstinence or ≤ 3 drinks/week), treatment of OSA, glycaemic control, and structured aerobic exercise. The Adelaide LEGACY and CARDIO-FIT studies established that aggressive risk factor modification substantially reduces AF burden.8,9,10,11
Identifying an acute event
Sustained palpitations with haemodynamic compromise, syncope, chest pain, or symptoms of heart failure or stroke warrant emergency presentation. Patients should have a clear action plan and access to formal cardiology review.
Medications
Anticoagulants
DOACs: apixaban (5 mg bd, reduced dose 2.5 mg bd if two of: age ≥ 80, weight ≤ 60 kg, creatinine ≥ 133 µmol/L), rivaroxaban (20 mg daily, 15 mg if CrCl 15–49), dabigatran (150 mg bd, 110 mg bd if age ≥ 80 or bleeding risk), edoxaban (60 mg daily, 30 mg if CrCl 15–50 or weight ≤ 60 kg). Specific reversal agents (idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors) are available in Australian centres.
Rate-control agents
Beta-blockers (bisoprolol, metoprolol, atenolol, carvedilol where coexisting heart failure), non-dihydropyridine CCBs (diltiazem, verapamil — avoid in HFrEF), digoxin (target trough 0.5–0.9 ng/mL).
Rhythm-control agents
Flecainide (avoid in structural heart disease, often used with rate-controlling agent), sotalol (monitor QTc), amiodarone (broad efficacy, multi-system toxicity profile: thyroid, hepatic, pulmonary, ocular, dermatologic — requires structured monitoring).
Left atrial appendage occlusion
A non-pharmacological alternative for stroke prevention in selected patients with contraindications to long-term anticoagulation, delivered through specialist electrophysiology services.
Multi-system manifestations
Stroke and systemic embolism
Ischaemic stroke is the principal complication of untreated AF. Patients with stroke or TIA on adequate anticoagulation warrant assessment for alternative or contributing causes and consideration of LAA occlusion.
Heart failure
AF and heart failure are bidirectionally linked. Tachycardia-induced cardiomyopathy may improve substantially with rate or rhythm control. Catheter ablation in HFrEF has shown mortality and hospitalisation benefit in selected populations (CASTLE-AF and successor trials).
Cognitive decline
AF is associated with accelerated cognitive decline and dementia, even in patients without clinical stroke. The extent to which anticoagulation modifies this is an area of active investigation.
Sleep-disordered breathing
OSA is present in over half of patients with AF and is associated with reduced success of rhythm control (cardioversion, ablation). Active screening and treatment of OSA is now considered core AF care.12
Living with atrial fibrillation
Exercise prescription
Regular moderate-intensity aerobic exercise reduces AF burden and improves symptoms. Patients with paroxysmal AF should be reassured that exercise is safe and beneficial, while extreme endurance training (very prolonged high-intensity activity) carries a paradoxical increased AF risk and is generally not recommended once AF is established.13,14
Alcohol and caffeine
Alcohol is a clear AF trigger with dose-response evidence; the AF-LIFE trial confirmed substantial reductions in AF burden with abstinence. Caffeine in moderate amounts does not appear to trigger AF in most patients despite common assumptions, but individual triggers vary and patients should be supported in identifying their own.15
Travel and anticoagulation
Anticoagulation should not be interrupted for travel. Patients should carry medication, a current medication list, and (for warfarin) ensure INR monitoring is arranged at the destination. Long-haul travel does not require additional measures beyond usual VTE prevention.
Prognosis
With contemporary integrated care including anticoagulation, risk-factor modification, and timely rhythm control where indicated, long-term outcomes have improved substantially. Untreated AF carries excess stroke, heart failure, and all-cause mortality risk.
Psychological dimension
Anxiety, hypervigilance to palpitations, and quality-of-life impairment are common. Education, reassurance about prognosis with appropriate treatment, and psychological referral where needed are integral to care.
Role of the physiotherapist
The physiotherapist delivers and supervises exercise and cardiac rehabilitation, using rate rather than a single target where the rhythm is irregular, supports risk-factor and weight management (both reduce AF burden), and educates on safe, confident activity and recognising symptoms that need review.
Warning signs
Part 1 · References
- Van Gelder IC, Rienstra M, Bunting KV, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the EACTS. Eur Heart J 2024;45(36):3314–3414.
- Brieger D, Amerena J, Attia J, et al. National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the diagnosis and management of atrial fibrillation 2018. Heart Lung Circ 2018;27(10):1209–1266.
- Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation. Circulation 2024;149(1):e1–e156.
- Van Gelder IC, Groenveld HF, Crijns HJGM, et al. Lenient versus strict rate control in patients with atrial fibrillation (RACE II). N Engl J Med 2010;362(15):1363–1373.
- Kirchhof P, Camm AJ, Goette A, et al. Early rhythm-control therapy in patients with atrial fibrillation (EAST-AFNET 4). N Engl J Med 2020;383(14):1305–1316.
- Marrouche NF, Brachmann J, Andresen D, et al. Catheter ablation for atrial fibrillation with heart failure (CASTLE-AF). N Engl J Med 2018;378(5):417–427.
- Packer DL, Mark DB, Robb RA, et al. Effect of catheter ablation vs antiarrhythmic drug therapy on mortality, stroke, bleeding, and cardiac arrest among patients with atrial fibrillation: the CABANA randomized clinical trial. JAMA 2019;321(13):1261–1274.
- Pathak RK, Middeldorp ME, Meredith M, et al. Long-term effect of goal-directed weight management in an atrial fibrillation cohort: a long-term follow-up study (LEGACY). J Am Coll Cardiol 2015;65(20):2159–2169.
- Pathak RK, Elliott A, Middeldorp ME, et al. Impact of CARDIOrespiratory FITness on arrhythmia recurrence in obese individuals with atrial fibrillation: the CARDIO-FIT study. J Am Coll Cardiol 2015;66(9):985–996.
- Lau DH, Nattel S, Kalman JM, Sanders P. Modifiable risk factors and atrial fibrillation. Circulation 2017;136(6):583–596.
- Chung MK, Eckhardt LL, Chen LY, et al. Lifestyle and risk factor modification for reduction of atrial fibrillation: a scientific statement from the American Heart Association. Circulation 2020;141(16):e750–e772.
- Traaen GM, Aakerøy L, Hunt TE, et al. Effect of continuous positive airway pressure on arrhythmia in atrial fibrillation and sleep apnea: a randomized controlled trial. Am J Respir Crit Care Med 2021;204(5):573–582.
- Elliott AD, Verdicchio CV, Mahajan R, et al. An exercise and physical activity program in patients with atrial fibrillation: the ACTIVE-AF randomized controlled trial. JACC Clin Electrophysiol 2023;9(4):455–465.
- Andersen K, Farahmand B, Ahlbom A, et al. Risk of arrhythmias in 52 755 long-distance cross-country skiers: a cohort study. Eur Heart J 2013;34(47):3624–3631.
- Voskoboinik A, Kalman JM, De Silva A, et al. Alcohol abstinence in drinkers with atrial fibrillation. N Engl J Med 2020;382(1):20–28.
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
Supervised exercise, breathing technique and self-management education are the mainstay of cardiorespiratory physiotherapy for this condition.
Clinical evidence
Part 1 covers the same condition without the technical detail. What follows is the evidence base behind it, written for clinicians — the literature, the reasoning and the gaps.
For clinicians: this summary supports clinical reasoning and is not a protocol. Check current guidelines and local policy before applying it, and read it alongside the key references and guidelines directory.
Framing. Contemporary AF care is no longer a choice between rate and rhythm control but an integrated pathway — the ESC AF-CARE framework (comorbidity and risk-factor management, avoiding stroke, reducing symptoms, evaluation and dynamic reassessment) and the Australian guideline both place risk-factor modification alongside anticoagulation as disease-modifying therapy rather than adjunct advice.1,2 That is what brings AF into physiotherapy scope: weight, fitness, alcohol, blood pressure and sleep apnoea are all treatment targets with arrhythmia outcomes attached.
Rhythm, rate and intervention
- Early rhythm control within 12 months of diagnosis reduced a composite of cardiovascular death, stroke and hospitalisation in EAST-AFNET 4 (HR 0.79), shifting practice away from watchful rate control in newly diagnosed patients.3
- Lenient rate control (resting HR < 110 bpm) was non-inferior to strict control in RACE II — relevant because rehabilitation is often deferred while clinicians chase a number that the evidence does not require.4
- Catheter ablation reduced mortality and heart-failure hospitalisation in AF with reduced ejection fraction (CASTLE-AF); in the broader CABANA population it did not significantly reduce the primary composite but improved symptom burden and quality of life.5,6
Risk-factor modification and exercise
- Weight loss is dose-dependent. In LEGACY, sustained loss of ≥ 10% body weight produced roughly six-fold greater arrhythmia-free survival than < 3%, with weight fluctuation > 5% partly reversing the benefit.7
- Fitness independently predicts freedom from AF. CARDIO-FIT showed a gain of ≥ 2 METs conferred substantially higher arrhythmia-free survival, additive to weight loss.8
- Supervised exercise is now RCT-supported therapy. ACTIVE-AF (six-month aerobic programme plus incidental activity) reduced AF recurrence and symptom severity at 12 months — the strongest direct evidence for physiotherapy-delivered care in this population.9
- Alcohol abstinence lengthened time to recurrence and reduced AF burden in a randomised trial of regular drinkers; CPAP for coexisting OSA improves burden in observational and some randomised data, though the RCT signal is weaker than the epidemiology suggests.10,11
- The dose curve is U-shaped. Long-term high-volume endurance training raises AF incidence in the same population in which moderate activity lowers it — worth naming when advising a masters athlete.12
Physiotherapy implications
- Heart rate is an unreliable prescription variable in AF. Beat-to-beat variability, pulse deficit and rate-control medication all decouple HR from workload; prescribe by RPE (Borg 11–14), the talk test or a workload target, and treat wrist-worn optical HR readings as approximate at best.
- Screen for the modifiable set at intake — BMI and waist, alcohol intake, snoring/witnessed apnoeas (STOP-Bang), blood pressure control — and route them back to the GP or cardiologist rather than treating exercise as the sole intervention.13,14,15
- Anticoagulation changes the risk calculus, not the prescription: avoid contact and high-fall-risk activities, review falls risk in older patients, and document any unexplained bruising or bleeding.
- Respect procedural windows: after ablation limit heavy lifting and groin-loading for the interval the electrophysiology service specifies (commonly around two weeks), expect symptomatic recurrences during the three-month blanking period, and do not interpret them as programme failure.
- New irregular pulse with haemodynamic symptoms — syncope, chest pain, rapid uncontrolled rate, acute breathlessness — stops the session and is escalated the same day.
Clinical reasoning
- Ask what limits the patient: rate-related exertional breathlessness responds to medical optimisation, whereas deconditioning responds to training. Treating the wrong one wastes a programme.
- Permanent AF is not a contraindication to intensity — it is a contraindication to HR-based prescription.
- Frame weight and alcohol change as antiarrhythmic treatment with a numbers-attached rationale; the LEGACY/CARDIO-FIT data are far more persuasive to patients than generic lifestyle advice.7,8
- Coordinate timing with cardiology: rehabilitation started immediately post-cardioversion or post-ablation needs the treating team's parameters, not assumptions.
Evidence gaps
- Optimal exercise modality, intensity and duration in AF remain undefined; ACTIVE-AF tested one aerobic prescription, and high-intensity interval and resistance protocols are under-studied.
- Almost all risk-factor trials come from specialist AF clinics in selected, largely obese cohorts — generalisability to frail, older, multimorbid community patients is unestablished.
- The threshold at which endurance training turns from protective to arrhythmogenic is unknown, as is whether it is reversible with de-training.
- Wearable-detected subclinical AF has outpaced the evidence on what, if anything, should change in exercise prescription when it is found.
References for the clinical evidence summary
- Van Gelder IC, Rienstra M, Bunting KV, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the EACTS. Eur Heart J 2024;45(36):3314–3414.
- Brieger D, Amerena J, Attia J, et al. National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the diagnosis and management of atrial fibrillation 2018. Heart Lung Circ 2018;27(10):1209–1266.
- Kirchhof P, Camm AJ, Goette A, et al. Early rhythm-control therapy in patients with atrial fibrillation (EAST-AFNET 4). N Engl J Med 2020;383(14):1305–1316.
- Van Gelder IC, Groenveld HF, Crijns HJGM, et al. Lenient versus strict rate control in patients with atrial fibrillation (RACE II). N Engl J Med 2010;362(15):1363–1373.
- Marrouche NF, Brachmann J, Andresen D, et al. Catheter ablation for atrial fibrillation with heart failure (CASTLE-AF). N Engl J Med 2018;378(5):417–427.
- Packer DL, Mark DB, Robb RA, et al. Effect of catheter ablation vs antiarrhythmic drug therapy on mortality, stroke, bleeding, and cardiac arrest among patients with atrial fibrillation: the CABANA randomized clinical trial. JAMA 2019;321(13):1261–1274.
- Pathak RK, Middeldorp ME, Meredith M, et al. Long-term effect of goal-directed weight management in an atrial fibrillation cohort: a long-term follow-up study (LEGACY). J Am Coll Cardiol 2015;65(20):2159–2169.
- Pathak RK, Elliott A, Middeldorp ME, et al. Impact of CARDIOrespiratory FITness on arrhythmia recurrence in obese individuals with atrial fibrillation: the CARDIO-FIT study. J Am Coll Cardiol 2015;66(9):985–996.
- Elliott AD, Verdicchio CV, Mahajan R, et al. An exercise and physical activity program in patients with atrial fibrillation: the ACTIVE-AF randomized controlled trial. JACC Clin Electrophysiol 2023;9(4):455–465.
- Voskoboinik A, Kalman JM, De Silva A, et al. Alcohol abstinence in drinkers with atrial fibrillation. N Engl J Med 2020;382(1):20–28.
- Traaen GM, Aakerøy L, Hunt TE, et al. Effect of continuous positive airway pressure on arrhythmia in atrial fibrillation and sleep apnea: a randomized controlled trial. Am J Respir Crit Care Med 2021;204(5):573–582.
- Andersen K, Farahmand B, Ahlbom A, et al. Risk of arrhythmias in 52 755 long-distance cross-country skiers: a cohort study. Eur Heart J 2013;34(47):3624–3631.
- Chung MK, Eckhardt LL, Chen LY, et al. Lifestyle and risk factor modification for reduction of atrial fibrillation: a scientific statement from the American Heart Association. Circulation 2020;141(16):e750–e772.
- Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation. Circulation 2024;149(1):e1–e156.
- Lau DH, Nattel S, Kalman JM, Sanders P. Modifiable risk factors and atrial fibrillation. Circulation 2017;136(6):583–596.
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