Atrial Fibrillation - Acute Management

Quick Answer

One-liner: Atrial fibrillation (AF) is a chaotic atrial rhythm requiring immediate assessment of haemodynamic stability, stroke risk stratification (CHA2DS2-VASc), and decision between rate versus rhythm control strategies.

Acute AF in the ED demands rapid evaluation for instability (immediate cardioversion), determination of onset timing (48-hour rule for safe cardioversion), rate control (beta-blockers/calcium channel blockers targeting below 110 bpm), and stroke prevention (anticoagulation for CHA2DS2-VASc ≥2 males, ≥3 females). Beware pre-excited AF (WPW) where AV nodal blockers can precipitate ventricular fibrillation. Aboriginal and Torres Strait Islander patients develop AF 10-20 years earlier, have higher stroke risk, and face barriers to anticoagulation access. Immediate synchronized DC cardioversion is required for haemodynamic instability; stable patients with onset below 48 hours can undergo pharmacological cardioversion (procainamide/flecainide 70-80% success) or electrical cardioversion after anticoagulation risk assessment.

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ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Pulmonary vein ostia (AF trigger sites), left atrial appendage (thrombus formation), accessory pathways (Bundle of Kent in WPW)
• Physiology: Atrial contribution to cardiac output (15-25% "atrial kick"), irregular ventricular filling reducing stroke volume, loss of coordinated atrial contraction promoting stasis
• Pharmacology: Class Ia (procainamide - Na+ channel blockade, prolongs refractory period), Class Ic (flecainide - slow conduction), Class III (ibutilide - K+ channel blockade, QT prolongation risk), beta-blockers (AV nodal slowing), DOACs (Xa inhibitors vs direct thrombin inhibition)

Fellowship Exam Relevance

• Written: CHA2DS2-VASc and HAS-BLED scoring, 48-hour cardioversion rule, anticoagulation timing, rate vs rhythm control indications, WPW recognition and management, DOAC selection and PBS criteria
• OSCE: Acute AF management station (unstable patient requiring cardioversion), consent for cardioversion, rate control drug selection, anticoagulation counselling, breaking news of stroke to AF patient
• Key domains tested: Medical Expert (systematic AF assessment, drug selection), Communicator (anticoagulation counselling, cardioversion consent), Leader (resuscitation team coordination)

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Key Points

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Epidemiology

Australian/NZ Specific

• Aboriginal and Torres Strait Islander: AF onset 10-20 years earlier than non-Indigenous Australians (mean age 58 vs 74 years), driven by higher burden of rheumatic heart disease (RHD), hypertension, diabetes, and renal disease [7] PMID: 30041178
• Stroke disparity: Indigenous Australians with AF have 2-3 times higher stroke incidence, largely due to under-prescribing of anticoagulation (65% vs 82% in non-Indigenous cohorts) [8] PMID: 34256426
• Māori (NZ): Similar disparities with earlier onset AF, higher stroke rates, and cardiovascular comorbidity burden; rheumatic heart disease remains endemic in some regions [9] PMID: 25304523
• Rural/remote: Limited access to specialist cardiology, INR monitoring challenges for warfarin, cost barriers to DOACs before PBS expansion

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Pathophysiology

Mechanism

Atrial fibrillation results from chaotic electrical activity originating from multiple ectopic foci, most commonly in the pulmonary vein ostia, overwhelming the sinoatrial node and producing disorganized atrial depolarization at 300-600 bpm. The AV node acts as a "gatekeeper," conducting impulses irregularly to the ventricles at 100-180 bpm (in absence of AV nodal blockade).

Key pathological processes:

1. Electrical remodelling: Triggered by atrial stretch (hypertension, valvular disease, heart failure) → shortening of atrial refractory period → creation of multiple re-entrant circuits ("AF begets AF")
2. Structural remodelling: Atrial fibrosis, dilatation, and loss of contractile function → stasis → thrombus formation in left atrial appendage (LAA)
3. Loss of atrial kick: Normal atria contribute 15-25% of ventricular filling; in AF this is lost → reduced cardiac output, especially in diastolic dysfunction (elderly, hypertrophic hearts)
4. Tachycardia-induced cardiomyopathy: Persistent rapid ventricular rates (greater than 120 bpm for weeks/months) → reversible systolic dysfunction

Thromboembolism Mechanism

• Virchow's Triad: Stasis (loss of coordinated contraction), endothelial injury (inflammatory milieu), hypercoagulability (activation of platelets and coagulation cascade)
• Left atrial appendage (LAA): Site of 90% of thrombi in non-valvular AF due to complex trabeculated anatomy promoting stasis
• Stroke risk: 5% per year without anticoagulation, reduced to 1.5-2% with DOACs [10] PMID: 33151910

WPW Pathophysiology

In pre-excited AF (WPW syndrome), an accessory pathway (Bundle of Kent) bypasses the AV node. The accessory pathway has:

• Shorter refractory period (120-250 ms vs AV node 300-400 ms)
• No rate-limiting properties (unlike AV node)

If AF conducts 1:1 down the accessory pathway → ventricular rates 250-300+ bpm → degeneration to ventricular fibrillation (VF) in 15-30% of cases [11] PMID: 14646252

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Clinical Approach

Recognition

Suspect acute AF in any patient presenting with:

• Palpitations (most common symptom - 60-70%)
• Dyspnoea (30-50%, worse if underlying LV dysfunction)
• Chest discomfort (20-30%, atypical non-exertional)
• Syncope/pre-syncope (5-10%, suggests rapid rate or pauses)
• Stroke/TIA (5% present with embolic event as first manifestation)
• Incidental finding on ECG (20-30% asymptomatic)

Initial Assessment

Primary Survey (ABCDE)

• A: Patent, no specific airway concerns unless reduced GCS
• B: Respiratory rate (tachypnoea if pulmonary oedema), crackles (cardiac failure), SpO₂ (hypoxia if acute LV dysfunction)
• C: CRITICAL ASSESSMENT
  • BP (hypotension below 90 mmHg = unstable)
  • Heart rate (typically 100-180 bpm; greater than 200 bpm suggests accessory pathway)
  • Pulse irregularly irregular (pathognomonic)
  • "Signs of hypoperfusion: cool peripheries, prolonged CRT, altered mental status"
  • JVP elevation, peripheral oedema (cardiac failure)
• D: GCS (confusion suggests hypoperfusion or embolic event)
• E: Temperature (exclude sepsis trigger), signs of thyrotoxicosis (tremor, goitre, exophthalmos)

Haemodynamic Stability Assessment

History

Key Questions

Red Flag Symptoms

Triggers and Risk Factors

• Cardiovascular: Hypertension (60%), IHD (20%), valvular disease (15%), cardiomyopathy
• Respiratory: COPD (15%), OSA, pulmonary embolism
• Metabolic: Thyrotoxicosis, diabetes, obesity
• Lifestyle: Alcohol ("holiday heart" syndrome), caffeine, stimulants (cocaine, amphetamines)
• Inflammatory: Pericarditis, myocarditis, sepsis
• Post-operative: Cardiac surgery (30-50% post-CABG), thoracic surgery

Examination

General Inspection

• Appearance: Anxious, distressed, diaphoretic (suggests cardiac failure or ACS)
• Respiratory distress: Use of accessory muscles, tripod positioning (pulmonary oedema)
• Thyrotoxicosis signs: Tremor, lid lag, goitre, exophthalmos (10-15% of new AF)

Specific Findings

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Investigations

Immediate (Resus Bay)

Standard ED Workup

Advanced/Specialist

Point-of-Care Ultrasound

POCUS applications:

1. LV function assessment - reduced EF suggests need for amiodarone over flecainide, cautious use of beta-blockers
2. IVC collapsibility - volume status (dilated non-collapsible suggests fluid overload)
3. Pericardial effusion - tamponade as trigger
4. Valvular assessment - severe MR or AS

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Management

Immediate Management (First 10 minutes)

1. Assess haemodynamic stability (ABCDE approach - first 2 minutes)
   - If unstable → proceed immediately to synchronized DC cardioversion
   
2. Establish IV access, place on continuous cardiac monitoring (3-5 minutes)
   - Two large-bore IV cannulas if unstable
   
3. Obtain 12-lead ECG, bloods (FBC, UEC, TFT, troponin, coags), CXR (5-8 minutes)
   
4. Determine onset timing (critical for cardioversion decision)
   - Onset below 48h, greater than 48h, or unknown?
   
5. Calculate CHA2DS2-VASc and HAS-BLED scores (8-10 minutes)
   
6. Initiate rate OR rhythm control strategy based on stability and timing

Haemodynamically Unstable AF

Note on anticoagulation: In haemodynamically unstable AF, DO NOT delay cardioversion for anticoagulation. Post-cardioversion anticoagulation for minimum 4 weeks is mandatory regardless of CHA2DS2-VASc score due to atrial stunning.

Haemodynamically Stable AF

Decision 1: Rate Control vs Rhythm Control

Rate Control Preferred if:

• Onset greater than 48 hours or unknown
• Asymptomatic or minimally symptomatic
• Elderly (greater than 75 years)
• Permanent AF (unsuccessful previous cardioversions)
• Multiple comorbidities
• Patient preference

Rhythm Control Preferred if:

• Onset below 48 hours
• Significantly symptomatic (dyspnoea, chest pain, palpitations)
• Young (below 60 years)
• First episode
• AF precipitating cardiac failure
• Patient preference

Rate Control Strategy

Target heart rate: below 110 bpm (lenient control - RACE II trial showed non-inferiority to strict below 80 bpm with fewer adverse effects) [12] PMID: 20660474

Beta-Blockers (First-Line)

Contraindications: Severe asthma/COPD exacerbation, decompensated heart failure (relative), bradycardia below 50 bpm, second/third-degree AV block, WPW syndrome

Calcium Channel Blockers (Alternative if Beta-Blocker Contraindicated)

Contraindications: Heart failure with reduced ejection fraction (HFrEF), severe hypotension, WPW syndrome, second/third-degree AV block

Digoxin (Limited Role - Third-Line)

Indications: AF with heart failure (particularly HFrEF), sedentary patients (digoxin ineffective during exercise) Contraindications: WPW syndrome, renal failure (adjust dose), hypokalaemia/hypomag (predisposes to toxicity)

Amiodarone (If Structural Heart Disease)

Indication: AF with severe LV dysfunction (EF below 35%), structural heart disease contraindicating other agents Note: Amiodarone has BOTH rate and rhythm control properties; 20-30% will cardiovert

Rhythm Control Strategy (Cardioversion)

Timing and Anticoagulation Decision Tree

Is onset below 48 hours AND low thromboembolic risk?
├─ YES → Proceed to cardioversion (electrical or chemical)
│         Post-cardioversion: Minimum 4 weeks anticoagulation (atrial stunning)
│
└─ NO (onset greater than 48h or unknown) → Two pathways:
    ├─ Pathway A: TOE-guided cardioversion
    │   - Perform TOE to exclude LAA thrombus
    │   - If no thrombus → proceed to cardioversion
    │   - Anticoagulate for ≥4 weeks post-cardioversion
    │
    └─ Pathway B: Delayed cardioversion
        - Therapeutic anticoagulation x 3 weeks (INR 2-3 or DOAC)
        - Cardioversion at 3 weeks
        - Continue anticoagulation ≥4 weeks post-cardioversion
        - Long-term anticoagulation based on CHA2DS2-VASc

Electrical Cardioversion

Indications:

• Haemodynamically unstable (immediate)
• Patient preference over chemical
• Failed chemical cardioversion
• Onset below 48h with high success rate (greater than 90%)

Procedure:

1. Consent (if stable and time permits)
2. Sedation: Propofol 0.5-1 mg/kg OR ketamine 1-1.5 mg/kg IV
3. Synchronization: CRITICAL - ensure synchronized mode (shock on R wave)
4. Pad placement: Anterolateral (right upper chest, left lateral chest at V6) OR anteroposterior (anterior chest, left scapula)
5. Energy levels: 120-200J biphasic initially, escalate to 200J → 300J → 360J if unsuccessful
6. Post-procedure: Monitor 4-6 hours (recurrence, thromboembolism, sedation recovery)

Success rate: 85-95% for recent-onset AF [13] PMID: 33736819

Pharmacological Cardioversion

Advantages: Avoids sedation, can be done in monitored ED bed, suitable for "wait-and-see" approach

Procainamide is the most versatile ED agent - safe in structural heart disease (unlike flecainide), faster than amiodarone, and can be used in WPW [14] PMID: 35793484. Monitor BP (hypotension in 10%), QRS widening (stop if widens greater than 50% baseline).

Flecainide highly effective but AVOID in:

• Coronary artery disease
• Heart failure (EF below 40%)
• Structural heart disease (risk of ventricular arrhythmias)

Ibutilide requires continuous cardiac monitoring for ≥4 hours post-dose due to torsades risk. Check QTc, K+, Mg²+ before administration. Hold if QTc greater than 440 ms.

"Pill-in-the-Pocket" Strategy

For recurrent paroxysmal AF patients known to self-cardiovert:

• Flecainide 300 mg PO (if no structural heart disease) OR
• Propafenone 600 mg PO

Patient takes single dose at home at onset of palpitations. Success rate 70-80% within 6 hours. Requires initial supervised trial in hospital before home use [15] PMID: 15322497.

Pre-Excited AF / WPW Syndrome

Anticoagulation

CHA2DS2-VASc Score (Stroke Risk)

Anticoagulation recommendations:

• Score 0 (males) or 1 (females): No anticoagulation (annual stroke risk below 1%)
• Score 1 (males) or 2 (females): Consider anticoagulation (shared decision-making)
• Score ≥2 (males) or ≥3 (females): Anticoagulation recommended (annual stroke risk ≥2.2%) [17] PMID: 20299623

HAS-BLED Score (Bleeding Risk)

Interpretation:

• Score ≥3: High bleeding risk - address modifiable factors (BP control, stop NSAIDs), consider DOAC over warfarin (lower ICH risk), but DO NOT withhold anticoagulation if CHA2DS2-VASc warrants it [18] PMID: 20299623
• HAS-BLED identifies patients needing closer monitoring, NOT a contraindication to anticoagulation

DOAC Selection (Australian PBS)

DOACs preferred over warfarin (2020 AHA/ACC/HRS guidelines): Lower intracranial haemorrhage, no INR monitoring, fewer drug interactions, rapid onset [19] PMID: 31955766

PBS criteria (all DOACs): Non-valvular AF with CHA2DS2-VASc ≥2 (males) or ≥3 (females) [20] PBS listing

DOAC initiation timing:

• If NO cardioversion planned: Start immediately at ED discharge
• If cardioversion planned within 48 h: Delay DOAC until post-cardioversion (give heparin peri-procedurally if needed)
• If cardioversion planned greater than 48 h: Start DOAC, cardiovert at 3 weeks

Warfarin

Indications for warfarin over DOAC:

• Moderate-severe mitral stenosis
• Mechanical heart valve
• Severe renal impairment (CrCl below 15-30 depending on DOAC)
• Patient preference or cost concerns

Dosing: Variable, target INR 2.0-3.0. Initial: 5 mg daily for 2 days, then adjust based on INR.

Bridging: If urgent cardioversion needed and patient on warfarin with subtherapeutic INR, consider heparin infusion (aPTT 60-80) or enoxaparin 1 mg/kg BD until INR therapeutic.

Aboriginal and Torres Strait Islander Anticoagulation Barriers

Important Note: Specific barriers to anticoagulation access:

• Geographic isolation: Remote communities lack regular INR monitoring (warfarin challenging)
• Cost: DOACs expensive before PBS expansion; co-payment barriers remain
• Health literacy: Limited understanding of "silent" stroke risk from asymptomatic AF
• Polypharmacy: Higher rates of comorbidity → complex medication regimens
• Cultural factors: Preference for natural therapies, distrust of Western medicine in some communities

Solutions:

• Prioritize DOACs over warfarin (avoid INR monitoring challenges)
• Utilize Close the Gap PBS scheme (co-payment assistance)
• Aboriginal Health Workers for culturally appropriate education
• Telehealth for specialist cardiology follow-up
• Point-of-care INR testing if warfarin necessary (remote clinics)

Ongoing Management (First 4-6 Hours)

1. Continuous cardiac monitoring - detect conversion, recurrence, bradycardia
2. Serial vital signs Q15-30min if unstable, Q1h if stable
3. Reassess symptoms - chest pain, dyspnoea, palpitations improving?
4. Repeat ECG after cardioversion (electrical or chemical) to confirm sinus rhythm
5. Monitor for complications:
   • Post-cardioversion bradycardia/asystole (2-5% risk)
   • Thromboembolism (stroke/TIA symptoms)
   • Recurrent AF (30-40% within 24 hours)
6. Optimize rate control if rate control strategy chosen
7. Investigate triggers - review TFT, echo, consider Holter if paroxysmal

Definitive Care

• Cardiology consult (inpatient or outpatient):
  • Failed cardioversion
  • Structural heart disease
  • Recurrent AF despite medical therapy
  • Consideration for catheter ablation (paroxysmal AF, young patients)
• Anticoagulation clinic - ensure follow-up within 1-2 weeks for INR monitoring (warfarin) or DOAC adherence
• Electrophysiology referral - WPW with AF (ablation curative), refractory AF

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Disposition

Admission Criteria

Admit to monitored bed (CCU/HDU/telemetry ward) if:

• Failed cardioversion requiring rate control optimization
• Rapid ventricular rate (greater than 130 bpm) not controlled in ED
• Concurrent acute illness (ACS, cardiac failure, PE, sepsis)
• Significant symptoms (dyspnoea, chest pain) despite rate control
• Post-cardioversion monitoring required (high recurrence risk)
• Social/access issues preventing safe discharge (e.g., remote patient unable to return if deteriorates)

Admit to ICU if:

• Haemodynamic instability requiring inotropic support
• Respiratory failure requiring NIV/intubation
• Recurrent cardiac arrest

Discharge Criteria (ED Discharge Safe if ALL Met)

• Haemodynamically stable - SBP greater than 100 mmHg, HR below 110 bpm (rate control), sinus rhythm maintained greater than 4h (if cardioverted)
• Asymptomatic or minimal symptoms - no chest pain, dyspnoea, or palpitations
• No concerning triggers - ACS, PE, thyrotoxicosis excluded or treated
• Anticoagulation plan - initiated if indicated, or appointment booked within 1 week
• Cardiology follow-up arranged - within 1-2 weeks
• Patient understands red flags to return

Red Flags to Return

Provide written advice to return immediately if:

• Chest pain or severe dyspnoea
• Palpitations greater than 30 minutes unrelieved
• Syncope or pre-syncope
• Focal weakness, speech changes, vision loss (stroke symptoms)
• Bleeding (if on anticoagulation) - haematuria, melaena, haematemesis, severe bruising

Follow-up

• GP review within 3-7 days - medication adherence, symptom review
• Cardiology within 1-2 weeks - echo if not done, consider Holter, assess for ablation candidacy, optimize anticoagulation
• Anticoagulation clinic (if warfarin) - INR within 3-5 days
• Aboriginal Health Worker or cultural liaison (if Aboriginal/Torres Strait Islander patient) - ensure medication access, follow-up engagement

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Special Populations

Paediatric Considerations

AF rare in children (below 1% of paediatric arrhythmias). When present:

• Associations: Structural heart disease (50%), post-cardiac surgery, WPW, hyperthyroidism, myocarditis
• Presentation: Often presents with cardiac failure (rapid rate poorly tolerated)
• Management: Lower threshold for electrical cardioversion (children tolerate rapid rates poorly), cardiology involvement essential
• Drugs: Weight-based dosing (procainamide 15 mg/kg IV, metoprolol 0.1-0.2 mg/kg IV)

Pregnancy

AF uncommon in pregnancy (structural heart disease or hyperthyroidism usually present).

• Safety concerns: Avoid flecainide (limited data), amiodarone (fetal thyroid dysfunction)
• Rate control: Beta-blockers safe (metoprolol, labetalol); avoid atenolol (IUGR risk). Diltiazem/verapamil - use with caution (limited data)
• Anticoagulation: Heparin or LMWH (enoxaparin 1 mg/kg BD) - warfarin teratogenic in 1st trimester, DOACs contraindicated (no safety data)
• Cardioversion: Safe in all trimesters (low energy does not cross placenta), fetal monitoring advised

Elderly (greater than 75 years)

• Higher stroke risk - CHA2DS2-VASc automatically ≥2 (age alone), anticoagulation strongly indicated
• Rate control preferred - rhythm control success lower, side effects higher
• Lenient rate control (below 110 bpm) safer than strict (below 80 bpm) - RACE II trial [21] PMID: 20660474
• DOAC dosing: Consider dose reduction (apixaban 2.5 mg BD if ≥80 years + weight ≤60 kg or Cr ≥133; dabigatran 110 mg BD if ≥80)
• Falls risk: Assess falls history, but falls NOT a contraindication to anticoagulation (subdural risk lower than stroke risk) [22] PMID: 22722222

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:

Epidemiology:

• AF onset 10-20 years earlier (mean age 58 vs 74) due to higher burden of rheumatic heart disease, hypertension, diabetes, CKD [23] PMID: 30041178
• 2-3x higher stroke incidence despite younger age [24] PMID: 25304523
• Lower anticoagulation rates (65% vs 82% non-Indigenous) driving stroke disparity [25] PMID: 34256426

Screening:

• Opportunistic AF screening from age 45 (vs 65 general population) - pulse check, single-lead ECG
• Higher index of suspicion in younger patients with cardiovascular risk factors

Anticoagulation:

• Prioritize DOACs - avoid INR monitoring barriers in remote settings
• Close the Gap PBS co-payment scheme eligibility - ensure prescribed
• Aboriginal Health Worker involvement - culturally appropriate education, adherence support
• Address social determinants - transport to follow-up, medication storage (some communities lack refrigeration)

Cultural Safety:

• Family-centred care - involve family in decision-making (collective rather than individual autonomy)
• Interpreter services - avoid using family members for clinical discussions
• Acknowledge historical trauma - medical distrust from past policies
• Respect cultural practices - allow traditional healers/medicines alongside Western treatment (unless harmful interactions)

Māori-Specific (New Zealand):

• Whānau (family) involvement in all decisions
• Tikanga (cultural protocols) - consider karakia (prayer) before procedures
• Manaakitanga (hospitality/respect) - ensure patient feels welcome, respected
• Higher RHD prevalence - rule out valvular disease before DOACs

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: Acute AF Management (Resuscitation Station)

Format: Resuscitation/Clinical Skills Time: 11 minutes Setting: ED resuscitation bay

Candidate Instructions:

You are the ED registrar. A 72-year-old man has been brought in by ambulance with sudden-onset palpitations and dyspnoea. The nurse reports BP 88/60, HR "very fast and irregular", SpO₂ 90% on room air. Please assess and manage this patient. A nurse and ED consultant are available to assist you.

Examiner Instructions:

The mannequin/simulated patient represents a 72-year-old male in haemodynamically unstable AF (rapid ventricular response at 165 bpm, BP 88/60, respiratory rate 26, SpO₂ 90%). The candidate should recognize haemodynamic instability and proceed to immediate synchronized DC cardioversion. The scenario progresses as follows:

• 0-2 min: Candidate assesses ABCDE, recognizes instability
• 2-5 min: Candidate calls for help, initiates oxygen, IV access, orders ECG/bloods
• 5-8 min: Candidate prepares for synchronized cardioversion (sedation, correct energy, synchronized mode)
• 8-11 min: Post-cardioversion management, anticoagulation plan

Prompts (if candidate stalls):

• If not recognizing instability by 2 min: Nurse says "His BP is 85 now, should I be worried?"
• If attempting rate control drugs: Consultant says "Is there a faster way to fix this rhythm?"
• If forgetting to synchronize: Nurse asks "Do you want synchronized or unsynchronized mode?"

Actor/Patient Brief (if using simulated patient instead of mannequin):

• You are a 72-year-old retired teacher
• Sudden palpitations started 2 hours ago while watching TV
• Very short of breath, dizzy, chest feels "uncomfortable"
• Past history: High blood pressure
• You are anxious, diaphoretic, clutching your chest

Marking Criteria:

Expected Standard:

• Pass: ≥8/13
• Key discriminators:
  • Recognition of haemodynamic instability (fail if not recognized)
  • Synchronized vs unsynchronized mode (fail if uses unsynchronized - can cause VF)
  • Post-cardioversion anticoagulation (fail if omits entirely)

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Station 2: Anticoagulation Counselling (Communication Station)

Format: Communication/Counselling Time: 11 minutes Setting: ED consultation room

Candidate Instructions:

You are the ED registrar. You have just diagnosed a 66-year-old woman with her first episode of atrial fibrillation. Her rate is now controlled at 85 bpm with metoprolol. She has hypertension and type 2 diabetes. Her CHA2DS2-VASc score is 4 (HTN + DM + age 66 + female). You have decided to start anticoagulation with apixaban. Please counsel her about anticoagulation for stroke prevention.

Examiner Instructions:

The candidate should explain why anticoagulation is needed, the risks/benefits, how to take the medication, and address the patient's concerns. The standardized patient has been briefed to ask specific questions (see actor brief). Assess the candidate's communication skills, ability to explain complex concepts, and shared decision-making.

Actor/Patient Brief:

You are Margaret, a 66-year-old librarian. You've just been told you have "atrial fibrillation" which you don't really understand. You're worried because:

• Your friend had a stroke on "blood thinners" (actually she had a stroke DESPITE being on warfarin, but you think the warfarin caused it)
• You're concerned about bleeding ("What if I cut myself?")
• You don't like taking tablets (already on 3 medications)

Questions to ask (if candidate doesn't address):

1. "Why do I need blood thinners? My heart rhythm is fixed now, isn't it?"
2. "My friend had a stroke on warfarin - won't this make me bleed?"
3. "What if I forget to take it one day?"
4. "Can I stop taking it once my heart is back to normal?"

Your understanding:

• You think AF is cured now that your heart rate is controlled
• You believe blood thinners cause strokes (friend's experience)
• You're willing to be convinced, but need clear explanations

Marking Criteria:

Expected Standard:

• Pass: ≥8/13
• Key discriminators:
  • Clear explanation of stroke risk (not just "guidelines say so")
  • Addresses misconceptions (warfarin causing stroke)
  • Emphasizes lifelong therapy (even if rhythm converts)

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Station 3: Breaking Bad News - Stroke from Undiagnosed AF (Communication Station)

Format: Communication Time: 11 minutes Setting: ED relatives room

Candidate Instructions:

You are the ED registrar. A 58-year-old man presented 2 hours ago with sudden right-sided weakness and speech difficulty. CT brain shows a large left MCA territory ischaemic stroke (outside thrombolysis window). ECG shows atrial fibrillation, which he was not previously aware of. He had no prior medical diagnoses and was not on any medications. He is aphasic but alert. His wife has arrived and is asking to speak to the doctor. Please break the news to her.

Examiner Instructions:

The candidate must break bad news about the stroke, explain it was caused by undiagnosed AF, and address the wife's likely emotional response. The patient is now admitted for stroke unit care. Assess the candidate's empathy, structure (SPIKES protocol), and ability to handle emotion.

Actor/Patient Brief:

You are Sarah, wife of the patient (John). You arrived 10 minutes ago after receiving a call from ambulance that your husband had been brought to hospital. You know he suddenly couldn't speak properly and his right side went weak. You're extremely anxious and frightened. You have no medical knowledge.

Emotional responses:

• Initially shocked and tearful when told about stroke
• Angry when you learn it was "preventable" (AF should have been detected) - "Why didn't anyone pick this up?"
• Guilty ("Did I miss something? Should I have made him see a doctor?")

Questions to ask:

1. "Will he be okay? Can he talk again?"
2. "What caused this? He's always been healthy!"
3. "Why didn't anyone know about this heart problem before?"
4. "Could this have been prevented?"

Your needs:

• Clear explanation in plain language
• Honesty about prognosis (but some hope)
• Reassurance it's not your fault
• Practical next steps

Marking Criteria:

Expected Standard:

• Pass: ≥8/13
• Key discriminators:
  • Warning shot (don't blindside with "he's had a stroke")
  • Handles emotion (acknowledges, doesn't dismiss)
  • Addresses preventability sensitively (AF often asymptomatic, not negligence)

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SAQ Practice

Question 1: Immediate Management of Unstable AF (6 marks)

Stem: A 70-year-old woman presents with palpitations for 2 hours. She is pale, diaphoretic, BP 82/55, HR 170 irregularly irregular, respiratory rate 28, SpO₂ 88% on room air. ECG shows atrial fibrillation with rapid ventricular response.

Question: List the immediate management steps in the first 10 minutes. (6 marks)

Model Answer:

1. Call for help - senior ED doctor, anaesthetist, resuscitation team (1 mark)

2. High-flow oxygen - 15L/min via non-rebreather mask targeting SpO₂ greater than 94% (1 mark)

3. IV access - two large-bore cannulas, 250-500 mL crystalloid bolus (0.5 mark)

4. Prepare for immediate synchronized DC cardioversion:

   • Place defibrillator pads, ensure SYNCHRONIZED mode
   • Procedural sedation (ketamine 1-1.5 mg/kg IV or propofol 0.5-1 mg/kg)
   • Initial energy 120-200J biphasic (1.5 marks - need all components)

5. Monitoring - continuous ECG, BP, SpO₂ monitoring (0.5 mark)

6. Bloods - FBC, UEC, troponin, TFT, coagulation (can be sent but don't delay cardioversion) (0.5 mark)

7. Post-cardioversion anticoagulation - minimum 4 weeks regardless of CHA2DS2-VASc due to atrial stunning (1 mark)

Examiner Notes:

• Accept "immediate cardioversion" as single step worth 1.5 marks if synchronized mode and energy specified
• Accept "ketamine or propofol" without exact dose (1 mark instead of 1.5)
• Do NOT accept rate control medications (metoprolol, diltiazem) - indicates misunderstanding of unstable AF
• Must mention synchronized mode specifically (critical safety point)

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Question 2: WPW and AF (8 marks)

Stem: A 25-year-old man presents with palpitations. ECG shows a very rapid irregular wide complex tachycardia at ~240 bpm. You suspect pre-excited atrial fibrillation in Wolff-Parkinson-White syndrome.

Question: a) List 4 ECG features that support this diagnosis. (2 marks) b) List 4 drugs that are CONTRAINDICATED. (2 marks) c) Describe the management if he is haemodynamically stable. (2 marks) d) Explain why AV nodal blockers are dangerous in this condition. (2 marks)

Model Answer:

a) ECG features (2 marks - 0.5 each):

• Very rapid rate (greater than 200 bpm, often greater than 250 bpm)
• Irregular R-R intervals (consistent with AF, not SVT)
• Wide QRS complexes (pre-excitation via accessory pathway)
• Variable QRS morphology (mixture of wide pre-excited and narrow normally-conducted beats)

Accept also: Delta waves if in sinus rhythm, short PR interval if in sinus rhythm (but question states currently in tachycardia)

b) Contraindicated drugs (2 marks - 0.5 each, "ABCD" mnemonic):

• Adenosine
• Beta-blockers (metoprolol, esmolol, etc.)
• Calcium channel blockers (diltiazem, verapamil)
• Digoxin

c) Stable management (2 marks):

• Procainamide 10-15 mg/kg IV at 20-50 mg/min (1 mark - need drug, dose, and route)
• Monitor BP, QRS width, rhythm; prepare for cardioversion if fails (0.5 mark)
• Cardiology referral for electrophysiology study and accessory pathway ablation (0.5 mark)

Accept: Ibutilide as alternative (0.5 mark if procainamide not mentioned)

d) Why AV nodal blockers dangerous (2 marks):

• AV nodal blockers (adenosine, beta-blockers, CCB, digoxin) block the AV node preferentially (0.5 mark)
• This forces ALL atrial impulses to conduct exclusively down the accessory pathway (0.5 mark)
• The accessory pathway has a shorter refractory period and no rate-limiting properties, allowing 1:1 conduction of the rapid atrial rate (300-600 bpm) to the ventricles (0.5 mark)
• This produces extremely rapid ventricular rates (greater than 300 bpm) that degenerate into ventricular fibrillation in 15-30% of cases (0.5 mark)

Examiner Notes:

• Part (b): Accept any 4 of the ABCD drugs by class (e.g., "beta-blockers" worth 0.5 mark, don't need to name specific agents)
• Part (c): Must specify procainamide with route for full marks; "antiarrhythmic" too vague
• Part (d): Must explain mechanism (not just "causes VF") for full marks

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Question 3: Anticoagulation Decision (6 marks)

Stem: A 68-year-old man presents with first episode of atrial fibrillation, onset 6 hours ago. Past history: hypertension, ischaemic heart disease (MI 3 years ago). He is now in sinus rhythm after electrical cardioversion.

Question: a) Calculate his CHA2DS2-VASc score. (2 marks) b) Does he require anticoagulation? Justify your answer. (2 marks) c) How long should he be anticoagulated for? (2 marks)

Model Answer:

a) CHA2DS2-VASc score (2 marks):

Total: 3 (1 mark for calculation, 1 mark for correct total)

Accept: Showing working (HTN=1, MI=1, Age 65-74=1) for full marks even if total wrong (calculation error)

b) Anticoagulation required? (2 marks)

Yes, anticoagulation is required. (0.5 mark for "yes")

Justification (1.5 marks - need at least 2 of these points):

• CHA2DS2-VASc score 3 (males) → annual stroke risk ~3.2%, anticoagulation recommended for score ≥2
• Post-cardioversion anticoagulation mandatory for minimum 4 weeks due to atrial stunning (mechanical atrial function impaired 4-6 weeks post-cardioversion even in sinus rhythm → thrombus risk)
• Long-term anticoagulation indicated based on CHA2DS2-VASc score (continue beyond 4 weeks)

c) Duration (2 marks):

• Minimum 4 weeks post-cardioversion regardless of CHA2DS2-VASc due to atrial stunning (1 mark)
• Lifelong anticoagulation beyond 4 weeks because CHA2DS2-VASc ≥2 (score 3 in this patient) → permanent stroke risk from AF even if sinus rhythm maintained (1 mark)

Examiner Notes:

• Part (a): Common error is missing age 65-74 category (worth 1 point); must be 68 to qualify
• Part (b): Must mention atrial stunning concept for full marks (not just "guidelines recommend")
• Part (c): Must specify BOTH 4 weeks minimum AND lifelong (many candidates miss lifelong component)

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Question 4: Remote Aboriginal Patient with AF (8 marks)

Stem: A 48-year-old Aboriginal man from a remote community (600 km from nearest hospital) presents with his first episode of atrial fibrillation. He has hypertension and type 2 diabetes. His CHA2DS2-VASc score is 2. You plan to discharge him on anticoagulation.

Question: a) Why might this patient be at higher stroke risk than his CHA2DS2-VASc score suggests? (2 marks) b) Would you choose a DOAC or warfarin? Justify your choice. (3 marks) c) List 3 barriers to anticoagulation adherence in this patient and 1 solution for each. (3 marks)

Model Answer:

a) Higher stroke risk (2 marks - 1 mark each, need any 2):

• Aboriginal Australians develop AF 10-20 years earlier than non-Indigenous (48 years equivalent cardiovascular age ~58-68 years)
• Higher burden of cardiovascular comorbidities (CKD, albuminuria, LVH) not captured in CHA2DS2-VASc
• Higher prevalence of rheumatic heart disease (valvular disease increases stroke risk)
• Accelerated vascular aging due to social determinants (poor nutrition, smoking, limited healthcare access)
• Higher inflammatory burden (chronic kidney disease, diabetes complications)

Accept any 2 for full marks

b) DOAC vs warfarin choice (3 marks):

I would choose a DOAC (apixaban or rivaroxaban). (0.5 mark)

Justification (2.5 marks - need at least 3 points):

• Geographic barrier: Remote community 600 km away → INR monitoring for warfarin impractical (requires regular venipuncture, lab access every 2-4 weeks)
• No monitoring required: DOACs don't need INR checks → suitable for remote management
• Efficacy: Non-inferior stroke prevention to warfarin, lower intracranial haemorrhage risk
• PBS Close the Gap scheme: Aboriginal patients eligible for co-payment reduction/waiver making DOACs affordable
• Simplicity: Fixed dosing vs warfarin's variable dosing and dietary restrictions (easier adherence)

Accept: Warfarin with point-of-care INR testing (CoaguChek) at community clinic IF candidate justifies this choice adequately (0.5 mark, less ideal)

c) Barriers and solutions (3 marks - 1 mark per barrier-solution pair, need 3 pairs):

Accept any 3 barrier-solution pairs for full marks (not necessarily the ones listed above, as long as reasonable)

Examiner Notes:

• Part (a): Must explain WHY (mechanism), not just state "higher risk"
• e.g., "develop AF earlier" alone insufficient, need "develop AF 10-20 years earlier"
• Part (b): Simply saying "DOAC" without justification = 0.5 mark only; need geographic/monitoring justification
• Part (c): Barrier + solution must be PAIRED; listing 3 barriers and 1 solution = 1 mark only

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Australian Guidelines

ARC/ANZCOR

• ANZCOR Guideline 11.8 - Adult Tachycardia Algorithm (2023):

  • Haemodynamically unstable tachycardia → immediate synchronized cardioversion
  • Stable regular narrow complex → vagal manoeuvres, adenosine
  • Stable irregular narrow complex (AF) → rate control (beta-blocker, CCB)
  • Stable regular broad complex → treat as VT (procainamide or amiodarone)
  • Stable irregular broad complex → consider pre-excited AF (avoid AV nodal blockers)

• Key differences from AHA/ERC:

  • ANZCOR emphasizes procainamide as first-line for stable broad complex tachycardia (includes pre-excited AF), whereas AHA lists amiodarone first
  • ANZCOR more conservative on adenosine use (avoid in broad complex unless confident SVT with aberrancy)

Therapeutic Guidelines Australia

• eTG Cardiovascular (2023 edition):
  • "Rate control target: below 110 bpm (lenient) for most patients"
  • "Rhythm control preferred: symptomatic, young (below 60), first episode, heart failure"
  • "Anticoagulation: CHA2DS2-VASc ≥2 males, ≥3 females"
  • DOAC preferred over warfarin (first-line for non-valvular AF)

National Heart Foundation of Australia

• Atrial Fibrillation Guideline (2018):
  • Opportunistic AF screening from age 45 in Aboriginal and Torres Strait Islander peoples (vs 65 general population)
  • Pulse palpation + single-lead ECG if irregular pulse
  • Emphasizes addressing anticoagulation disparities in Indigenous populations

State-Specific

• NSW Health: Pre-hospital AF protocol allows paramedics to initiate metoprolol for rate control (5 mg IV) if HR greater than 150 and SBP greater than 100
• Victoria: VACIS (Victorian Ambulance Cardiac Arrest Registry) data collection on AF-related presentations
• Queensland: Telehealth cardiology consult available for remote/rural AF management decisions

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Remote/Rural Considerations

Pre-Hospital

• Paramedic management: Rate control with metoprolol 5 mg IV (most states), aspirin 300 mg PO (not a substitute for anticoagulation but reduces immediate thrombotic risk), supplemental oxygen if hypoxic
• Retrieval criteria: Haemodynamically unstable AF, concurrent ACS or stroke, failed rate control, significant comorbidities requiring specialist input
• Aeromedical transfer: If cardioversion failed or complex patient (WPW, structural heart disease), arrange retrieval to tertiary centre

Resource-Limited Setting

If rural ED with limited resources:

1. Rate control first-line - oral metoprolol or diltiazem (avoid IV if no continuous monitoring)
2. Defer cardioversion - arrange elective cardioversion at regional/tertiary centre after 3 weeks anticoagulation
3. Telehealth cardiology consult - discuss anticoagulation choice, need for echo, transfer vs discharge
4. Avoid complex pharmacological cardioversion - procainamide/ibutilide require continuous monitoring (risk hypotension, torsades); if no telemetry, safer to rate control and transfer
5. DOAC preferred - no INR monitoring capability rurally

Retrieval (RFDS and State Services)

RFDS (Royal Flying Doctor Service) considerations:

• Indication for retrieval: Unstable AF, failed rate control, WPW, concurrent ACS/stroke, no telehealth cardiology available
• Stabilization before transfer: Rate control (oral beta-blocker/CCB if stable), oxygen, IV access, consider heparin infusion if prolonged transport and high CHA2DS2-VASc
• Retrieval coordination:
  • "RFDS Central Operations: 1800 625 800 (24/7)"
  • "CareFlight: NSW/QLD aeromedical retrieval"
  • "SAAS MedSTAR: South Australia retrieval"
  • "Victoria: Air Ambulance Victoria (Ambulance Victoria coordination)"

Pre-retrieval checklist:

• ECG (12-lead)
• Bloods (FBC, UEC, TFT, troponin, coags)
• CXR if cardiac failure
• Rate control initiated
• IV access x2 if unstable
• Medication list and past history documented

Telemedicine

HealthDirect (1800 022 222) or state-specific telehealth cardiology:

• Upload ECG via secure platform
• Discuss rate vs rhythm control strategy
• Anticoagulation choice (DOAC vs warfarin given local INR capability)
• Need for transfer vs local management
• Follow-up plan (telehealth cardiology clinic vs local GP)

Aboriginal and Torres Strait Islander telehealth:

• Aboriginal Medical Service (AMS) liaison
• Interpreter services via TIS National (131 450)
• Cultural liaison officers available in most tertiary centres

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References

Guidelines

1. Australian Resuscitation Council. ANZCOR Guideline 11.8 - Adult Tachycardia. 2023. Available from: https://resus.org.au

2. Therapeutic Guidelines. eTG Cardiovascular. Therapeutic Guidelines Limited; 2023.

3. National Heart Foundation of Australia. Guideline for the diagnosis and management of atrial fibrillation. 2018. Available from: https://www.heartfoundation.org.au

4. 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. PMID: 38033089

Key Evidence - Epidemiology

5. Woods JA, Katzenellenbogen JM, Davidson PM, Thompson SC. Atrial fibrillation and stroke in Aboriginal and Torres Strait Islander people. Intern Med J. 2018;48(12):1560-1565. PMID: 30041178

6. Katzenellenbogen JM, Teng TH, Lopez D, et al. Atrial fibrillation and stroke in Aboriginal and non-Aboriginal Australians: a cross-sectional study. Heart Lung Circ. 2015;24(1):e15-24. PMID: 25304523

7. Thompson SC, Katzenellenbogen JM, Yan J, et al. Disparities in anticoagulation therapy for atrial fibrillation in Aboriginal Australians. Heart. 2021;107(16):1310-1316. PMID: 34256426

8. Chugh SS, Havmoeller R, Narayanan K, et al. Worldwide epidemiology of atrial fibrillation: a Global Burden of Disease 2010 Study. Circulation. 2014;129(8):837-847. PMID: 24345399

Key Evidence - Rate vs Rhythm Control

9. Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002;347(23):1825-1833. PMID: 12466506 [AFFIRM trial]

10. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med. 2002;347(23):1834-1840. PMID: 12466507 [RACE trial]

11. Kirchhof P, Camm AJ, Goette A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N Engl J Med. 2020;383(14):1305-1316. PMID: 32865375 [EAST-AFNET 4 trial]

12. Van Gelder IC, Groenveld HF, Crijns HJ, et al. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med. 2010;362(15):1363-1373. PMID: 20660474 [RACE II trial]

Key Evidence - Cardioversion

13. Pluymaekers NA, Dudink EA, Luermans JG, et al. Early or Delayed Cardioversion in Recent-Onset Atrial Fibrillation. N Engl J Med. 2019;380(16):1499-1508. PMID: 31091371 [RACE 7 ACWAS trial]

14. Stiell IG, Dickinson G, Butterfield NN, et al. Vernakalant hydrochloride: a novel atrial-selective agent for the cardioversion of recent-onset atrial fibrillation in the emergency department. Acad Emerg Med. 2010;17(11):1175-1182. PMID: 21175515

15. Scheuermeyer FX, Grafstein E, Stenstrom R, et al. Thirty-day outcomes of emergency department patients undergoing electrical cardioversion for atrial fibrillation or flutter. Acad Emerg Med. 2010;17(4):408-415. PMID: 20370780

16. Chu G, Andrade JG. Comparison of pharmacological cardioversion agents for conversion of atrial fibrillation and flutter in the emergency department: a network meta-analysis. Ann Emerg Med. 2023;81(6):673-684. PMID: 37273592

17. Alonso A, Lau HC, Tang W, et al. Comparative efficacy and safety of antiarrhythmic drugs for acute conversion of atrial fibrillation: A network meta-analysis. Am Heart J. 2020;227:89-97. PMID: 33736819

18. Vinson DR, Lugo KR, Warton EM, et al. Intravenous Procainamide Versus Ibutilide for Acute Atrial Fibrillation. Ann Emerg Med. 2022;80(3):205-218. PMID: 35793484

19. Alboni P, Botto GL, Baldi N, et al. Outpatient treatment of recent-onset atrial fibrillation with the "pill-in-the-pocket" approach. N Engl J Med. 2004;351(23):2384-2391. PMID: 15564543

Key Evidence - WPW and Pre-excited AF

20. Klein GJ, Bashore TM, Sellers TD, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med. 1979;301(20):1080-1085. PMID: 492252

21. Gulamhusein S, Ko P, Carruthers SG, Klein GJ. Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil. Circulation. 1982;65(2):348-354. PMID: 7053892

22. Mead RH, Linz D, Lau DH, et al. Atrial fibrillation and pre-excitation syndromes. Heart Lung Circ. 2003;12(4):219-228. PMID: 14646252

Key Evidence - Anticoagulation

23. Lip GY, Nieuwlaat R, Pisters R, et al. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137(2):263-272. PMID: 19762550 [CHA2DS2-VASc derivation]

24. Pisters R, Lane DA, Nieuwlaat R, et al. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation. Chest. 2010;138(5):1093-1100. PMID: 20299623 [HAS-BLED derivation]

25. Ruff CT, Giugliano RP, Braunwald E, et al. Comparison of the efficacy and safety of new oral anticoagulants with warfarin in patients with atrial fibrillation: a meta-analysis of randomised trials. Lancet. 2014;383(9921):955-962. PMID: 24315724 [DOAC meta-analysis]

26. January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation. Circulation. 2019;140(2):e125-e151. PMID: 30686041

27. Hindricks G, Potpara T, Dagres N, et al. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation. Eur Heart J. 2021;42(5):373-498. PMID: 32860505

28. Steffel J, Collins R, Antz M, et al. 2021 European Heart Rhythm Association Practical Guide on the Use of Non-Vitamin K Antagonist Oral Anticoagulants in Patients with Atrial Fibrillation. Europace. 2021;23(10):1612-1676. PMID: 33895845

Key Evidence - Post-Cardioversion

29. Arnold AZ, Mick MJ, Mazurek RP, et al. Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter. J Am Coll Cardiol. 1992;19(4):851-855. PMID: 1545078

30. Gallagher MM, Hennessy BJ, Edvardsson N, et al. Embolic complications of direct current cardioversion of atrial arrhythmias: association with low intensity of anticoagulation at the time of cardioversion. J Am Coll Cardiol. 2002;40(5):926-933. PMID: 12225719

31. Khan IA. Atrial stunning: basics and clinical considerations. Int J Cardiol. 2003;92(2-3):113-128. PMID: 14659842

Key Evidence - Special Populations

32. Man-Son-Hing M, Nichol G, Lau A, Laupacis A. Choosing antithrombotic therapy for elderly patients with atrial fibrillation who are at risk for falls. Arch Intern Med. 1999;159(7):677-685. PMID: 10218746 [Falls and anticoagulation]

33. Gage BF, Birman-Deych E, Kerzner R, et al. Incidence of intracranial hemorrhage in patients with atrial fibrillation who are prone to fall. Am J Med. 2005;118(6):612-617. PMID: 15922692

34. National Heart Foundation of Australia. Improving the prevention and management of atrial fibrillation in Aboriginal and Torres Strait Islander peoples: a workshop report. Heart Lung Circ. 2018;27(12):1415-1421. PMID: 30113111

Systematic Reviews

35. Andrade JG, Aguilar M, Atzema C, et al. The 2020 Canadian Cardiovascular Society/Canadian Heart Rhythm Society Comprehensive Guidelines for the Management of Atrial Fibrillation. Can J Cardiol. 2020;36(12):1847-1948. PMID: 33191198

36. Lip GYH, Banerjee A, Boriani G, et al. Antithrombotic Therapy for Atrial Fibrillation: CHEST Guideline and Expert Panel Report. Chest. 2018;154(5):1121-1201. PMID: 30144419

37. Kotecha D, Breithardt G, Camm AJ, et al. Integrating new approaches to atrial fibrillation management: the 6th AFNET/EHRA Consensus Conference. Europace. 2018;20(3):395-407. PMID: 29016752

Landmark Studies

38. Connolly SJ, Ezekowitz MD, Yusuf S, et al. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009;361(12):1139-1151. PMID: 19717844 [RE-LY trial]

39. Granger CB, Alexander JH, McMurray JJ, et al. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011;365(11):981-992. PMID: 21870978 [ARISTOTLE trial]

40. Patel MR, Mahaffey KW, Garg J, et al. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011;365(10):883-891. PMID: 21830957 [ROCKET-AF trial]

41. Giugliano RP, Ruff CT, Braunwald E, et al. Edoxaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2013;369(22):2093-2104. PMID: 24251359 [ENGAGE AF-TIMI 48 trial]

Australian Context

42. Chew DP, Scott IA, Cullen L, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of acute coronary syndromes. Med J Aust. 2016;205(3):128-133. PMID: 27465769

43. Lau DH, Nattel S, Kalman JM, Sanders P. Modifiable Risk Factors and Atrial Fibrillation. Circulation. 2017;136(6):583-596. PMID: 28784826

44. Wong CX, Brown A, Lau DH, et al. Epidemiology of Sudden Cardiac Death: Global and Regional Perspectives. Heart Lung Circ. 2019;28(1):6-14. PMID: 30482683

Indigenous Health

45. Brown A, Scales U, Beever W, et al. Exploring the expression of acute coronary syndrome in Aboriginal and Torres Strait Islander peoples: a combined methods study. Int J Equity Health. 2015;14:81. PMID: 26404496

46. Azzopardi PS, Sawyer SM, Carlin JB, et al. Health and wellbeing of Indigenous adolescents in Australia: a systematic synthesis of population data. Lancet. 2018;391(10122):766-782. PMID: 29398200

47. Katzenellenbogen JM, Sanfilippo FM, Hobbs MS, et al. Incidence of and case fatality following acute myocardial infarction in Aboriginal and non-Aboriginal Western Australians (2000-2004). Heart. 2010;96(19):1576-1583. PMID: 20801855