EDAITUTOR
ED Briefs · Cardiology v1.0 Educational use only

Atrial
Fibrillation

Stability first. Pre-excitation second. Cause-or-consequence always. — how to think when AF walks in with a red flag, not another AF explainer.

Stable?Irregular + broad?Cause or consequence?
Adult retrieval — ARV (VIC)

Call early for unstable AF, refractory shock, or when cardioversion / critical-care support exceeds local capability. Confirm destination and pathway with local protocols and retrieval services.

A number is not stability

“BP over 90” does not mean stable. Ongoing ischaemia, pulmonary oedema, syncope, or HR >150 with symptoms are adverse features that call for cardioversion — even with a “normal” blood pressure. And newly-detected AF is not proven new-onset: treat duration as uncertain until an abrupt onset from a known sinus baseline is established.

Start here — pick the presentation, or read the three gates
AF + shock / syncopeCase 4 · cardiovert now AF + heart failureCase 6 · adverse features AF + borderline BPCase 6 · “100” ≠ stable AF + WPW / broad & irregularCase 5 · do-not-give list AF + PE / post-opCase 3 · treat the driver New AF + chest painCase 1 · ACS until proven New AF + uncertain onsetCase 2 · the 48h line AF + valve / structural diseasemech valve · mitral stenosis

Three gates, in order

  • 1. Adverse features? — if yes, and due to AF, synchronised cardioversion comes before any drug trial.
  • 2. Irregular and broad? — suspect pre-excited AF; the whole drug logic inverts.
  • 3. Cause or consequence? — is AF driving the illness, or is sepsis / PE / ACS / bleeding driving the AF?

Two rules that recur

  • Newly-detected ≠ new-onset — onset is uncertain until proven.
  • Anticoagulation is a separate decision from rhythm — and there are three of them (see below).
Gate 1 · Adverse features? shock · ongoing ischaemia · pulmonary oedema · syncope · HR >150 with symptoms → YES = cardiovert now
Gate 2 · Irregular AND broad? beat-to-beat QRS change, very short RR → treat as pre-excited AF / VT — AV-nodal blockers OFF
Gate 3 · Cause or consequence? hunt the driver sepsis · PE · ACS · bleeding · thyroid · electrolytes
Stable, primary AF → rate vs rhythm + duration & anticoagulation
◯ the spineStable → pre-excitation → cause-or-consequence. Most clinicians can rate-control AF; the value is knowing which patient is not a rate-control problem, and why.
Unstable AF — adverse features due to the rhythm

Adverse features (any one)

  • Shock / hypotension / poor perfusion
  • Ongoing myocardial ischaemia
  • Acute pulmonary oedema
  • Syncope or altered consciousness
  • HR >150 with symptoms

ANZCOR: SBP <90, HR >150, chest pain or heart failure each warrant immediate treatment — not only a BP threshold.

Synchronised cardioversion

  • 200 J biphasic, synchronised (2025 AHA: start high, don't ladder up)
  • Confirm SYNC before every shock — many defibrillators revert after each one
  • Sedate when feasible — dose-reduced · never delay the shock in a deteriorating patient
  • Failed? check sync / pad contact / change vector to AP / escalate energy
  • Refractory: amiodarone 300 mg → re-shock → 900 mg/24h (crit-care + cardiology)
🔴 overridesUnknown AF duration does NOT delay emergency cardioversion. Instability wins over the timing rule every time.
Anticoagulate around the shock, not instead of it: give parenteral anticoagulation (IV unfractionated heparin bolus ± infusion, or LMWH) before cardioversion if it can be given without delaying it — a bolus takes seconds while pads and sedation are being prepared — and immediately afterwards if it cannot. Then continue for ≥4 weeks. Weigh first against active bleeding, major trauma or head strike from the syncope.

Cardioversion fixes the rhythm, not the cause

  • If sinus rhythm returns but BP, chest pain or dyspnoea don't improve — another shock cause is still active (OMI, PE, sepsis, haemorrhage, severe AS, tamponade).
  • In the elderly, cardioversion can unmask sinus-node disease, pauses or high-grade block — keep pads on, pacing available.
  • Persistent hypotension after conversion → titrated vasopressor (e.g. noradrenaline) while you treat the driver — it never substitutes for it.
Pre-excited AF (WPW) — a rhythm-control emergency, not rate control

Recognise it

  • Irregularly irregular + broad, with beat-to-beat QRS change
  • Very short RR in parts of the strip — shortest pre-excited RR <250 ms = high-risk pathway
  • Rate 140 is not benign — the average hides the fast, pre-excited beats
  • If irregular + broad and uncertain, treat as pre-excited AF / VT until senior review

☍ See worked ECGs — LITFL pre-excitation

Terminate, don't rate-control

  • Unstable → synchronised DCCV 200 J now
  • Stable → synchronised DCCV, or IV procainamide, or IV ibutilide (doses below)
  • Don't cycle antiarrhythmics — first drug fails or QRS/QT worsens → cardiovert
  • Definitive care = accessory-pathway ablation → disposition always involves EP

Do NOT give any AV-nodal blocker

  • Adenosine
  • Beta-blockers (metoprolol, esmolol)
  • Diltiazem / verapamil
  • Digoxin
  • IV amiodarone — now contraindicated here too

Blocking the AV node removes the “brake,” favours accessory-pathway conduction and can precipitate VF. The amiodarone point is a reversal of older algorithms — 2023 ACC/AHA and 2024 ESC advise against it in pre-excited AF. Reconcile any conflicting local protocol with cardiology urgently.

Stable AF — cause-or-consequence, then rate vs rhythm

First ask why now? — is AF the primary problem, or a response to something dangerous?

ACS / occlusion MI Pulmonary embolism Sepsis / infection Haemorrhage / anaemia Thyrotoxicosis Electrolytes (K⁺, Mg) Alcohol / stimulants Hypovolaemia / pain

☍ Confirm the rhythm — LITFL AF ECG library (AF vs flutter, aberrancy)

🔴 the trapDon't suppress a compensatory tachycardia. If the rate is holding up perfusion against PE, sepsis or bleeding (esp. with RV strain), reflex rate control can tip the patient into hypotension. Treat the driver first.

RRate control

usual first line
  • Metoprolol IV — if no acute HF, shock, bronchospasm or conduction disease
  • Diltiazem IV — only if LVEF >40%, no oedema/hypotension
  • Don't stack IV beta-blocker + CCB (bradycardia, AV block)
endpoint: symptoms + rate ≈ <110, not 60

RhRhythm control

selected patients
  • Attractive if young, first episode, reversible causes excluded
  • Only if onset proven <24h, no structural disease, low stroke risk
  • Otherwise anticoagulate / TOE first (see Cardioversion)
definite <24h + low risk → ED pathway

WWait & see

RACE 7 ACWAS
  • Rate control + delayed cardioversion was non-inferior at 4 weeks
  • ~69% converted spontaneously within 48h
  • Less attractive if presyncope, structural disease or an unresolved driver
safe follow-up essential
AF + structural / valvular disease — what actually changes

Why they decompensate faster

  • Loss of the atrial kick (~20–30% of cardiac output) matters far more in severe MS, severe AS, HOCM, LVH / diastolic dysfunction
  • Tachycardia shortens diastole — in MS the transmitral gradient rises (→ pulmonary oedema); in AS coronary perfusion falls
  • In severe MS, new AF is often the trigger for acute pulmonary oedema

Practical effect: rate control is more urgent, they tolerate rapid AF poorly, and the threshold to cardiovert is lower.

Drug choices that change

  • Flecainide / propafenone (class Ic) — first-line for pharmacological cardioversion only in a structurally normal heart. Contraindicated in CAD, LV dysfunction or significant structural disease (CAST).
  • Structural disease → amiodarone is the antiarrhythmic option.
  • Flecainide in flutter → risk of 1:1 conduction with paradoxical ventricular acceleration — pair with an AV-nodal blocker.
  • Diltiazem / verapamil — avoid if LVEF <40% or decompensated HF (as elsewhere on this page).

DOACs are contraindicated in only two situations — but absolutely

  • Mechanical prosthetic valve
  • Moderate–severe mitral stenosis (rheumatic)

Both require a vitamin K antagonist (warfarin). RE-ALIGN (dabigatran in mechanical valves) was stopped early for excess thromboembolic and bleeding events; INVICTUS found VKA superior to rivaroxaban in rheumatic heart disease. These patients are anticoagulated regardless of CHA₂DS₂-VA score — untreated risk is very high.

“Valvular AF” is an obsolete label

  • Don’t ask “is this valvular AF?” — ask “mechanical valve, or moderate–severe mitral stenosis?” If neither, a DOAC is appropriate.
  • Bioprosthetic valves (beyond ~3 months), valve repair, MR, AS and TAVI → treat as ordinary AF — DOAC is fine.
  • Cardioversion: LA thrombus risk is higher in mitral stenosis, so a short reported duration is less reassuring — lower your threshold for TOE. Sinus maintenance is also less likely with a dilated left atrium.
  • Emerging only: FLECA-ED is reappraising flecainide in stable CAD with preserved EF — investigational, not current practice.
Cardioversion timing — the duration & anticoagulation rule
ScenarioThresholdBefore elective cardioversion
UnstableAny durationCardiovert now. Anticoagulate as soon as feasible afterwards.
Aus (NHFA/CSANZ)>48h or uncertain3 weeks therapeutic anticoagulation or TOE to exclude LA thrombus.
ESC 2024>24hDelay unless ≥3 weeks anticoagulation or TOE-excluded thrombus.
Definite <24hLow stroke risk, no structural diseaseED cardioversion reasonable via local pathway (electrical or pharmacological, RAFF2).
After cardioversionAll patientsAnticoagulate ≥4 weeks; long-term is decided by stroke risk, not by rhythm outcome.

What's changed — and what hasn't

  • ESC moved the line from 48h to 24h — when onset is uncertain, both Australian and ESC guidance converge on “no unprotected elective cardioversion.”
  • RACE 7 ACWAS — delayed cardioversion is non-inferior, so “wait & see” with rate control is a legitimate strategy in the right patient.
  • Instability overrides all timing. The duration rule is for elective cardioversion of a stable patient.
POCUS in ED AF — what each view changes
Look forWhat it changes
LV systolic functionPoor EF → avoid diltiazem/verapamil; favour cautious beta-blockade or amiodarone. Preserved EF widens your options.
RV dilatation / strainSeptal flattening + dilated RV → PE as the driver (Cases 3 & 4). Don't slow a compensatory rate.
B-lines / effusionPulmonary oedema (Case 6) → loop diuretic + cautious rate control; low threshold to cardiovert.
Pericardial effusionTamponade as a shock cause — cardioversion won't fix it.
Valves / severe ASSevere AS or acute MR → careful with afterload & rate; a distinct cause of decompensation.
IVC (in context)Supports volume & RV assessment — interpret alongside the clinical picture, not alone.
◯ caveatPOCUS supports decisions; it does not exclude. A normal scan does not rule out ACS, PE or significant valve disease — correlate with ECG, troponin and trajectory.
Drug doses — teaching values, verify against local protocol / AMH / current PI
AgentTeaching doseCautions
Metoprolol2.5–5 mg IV over ~2 min; repeat ~5-minutely, up to 3 doses / 15 mg. Reassess after each.Avoid: decompensated HF, hypotension, bronchospasm, conduction disease.
Diltiazem0.25 mg/kg IV over 2 min; infusion 5–10 mg/h per local protocol.LVEF >40% only. Avoid oedema/hypotension. Don't stack with IV beta-blocker.
Digoxin0.25 mg IV; repeat to max ~1.5 mg/24h. Slow onset — adjunct, not monotherapy.Dose for age/renal/weight/K⁺; the “max” is not a target, esp. in the elderly.
Amiodarone (rate)300 mg IV over ~1h, then 10–50 mg/h over 24h.Hypotension, bradycardia, may chemically cardiovert. Usable in structural HD.
Amiodarone (rescue)Unstable, DCCV failed: 300 mg IV over 10–20 min → re-shock → 900 mg/24h.Contraindicated in pre-excited AF (see below).
Procainamide20–50 mg/min IV (or ~1 g over 30 min); maint. 1–4 mg/min.Stop if AF ends, hypotension, QRS ↑>50%, or 17 mg/kg reached. Monitored area only.
Ibutilide≥60 kg: 1 mg IV over 10 min; <60 kg: 0.01 mg/kg. May repeat once.QT prolongation / torsades. Correct K⁺/Mg first; prolonged telemetry after.
● Amiodarone — when it's rescue
  • Unstable AF after failed cardioversion (Case 4)
  • Rate control when beta-blockers & CCBs unsuitable, esp. structural heart disease (Case 6)
● Amiodarone — when it's forbidden
  • Pre-excited AF / WPW (Case 5) — may worsen accessory-pathway conduction → VF
  • Contemporary ACC/AHA & ESC now class it contraindicated in this rhythm
Anticoagulation — three separate decisions

1Peri-cardioversion

the procedure
  • Duration uncertain / >48h → 3 weeks anticoag or TOE before elective
  • Anticoagulate at cardioversion and ≥4 weeks after
  • Independent of the long-term decision

2Long-term (stroke)

CHA₂DS₂-VA
  • Age ≥75 = 2 points; female sex no longer scored
  • Score 0 (Cases 2,3,5) → usually no lifelong anticoag
  • Score ≥2 (Cases 1,4,6) → anticoag unless contraindicated
  • DOAC preferred — except mechanical valve or mod–severe MS

3Treating a driver

e.g. PE
  • Confirmed PE (Case 3) → therapeutic anticoagulation in its own right
  • Recent surgery / bleeding → consider IV UFH (stoppable/reversible)
  • Coordinate with the ACS antiplatelet plan — don't accumulate independently
◯ noteDon't dose-reduce a DOAC simply because the patient is elderly — each agent has specific renal, weight and age criteria. Restoring sinus rhythm does not remove long-term embolic risk.
See the ECGs — external FOAMed libraries (opens in a new tab)
LITFL · ECG Library

Atrial fibrillation

Core morphology — irregularly irregular, absent P waves, fine vs coarse fibrillatory waves, and when the QRS is broad.

litfl.com → LITFL · ECG Library

AF / flutter in pre-excitation

Four worked ECGs of AF with WPW — rates to 300 bpm, beat-to-beat QRS variation, intermittent pre-excitation with delta waves.

litfl.com → LITFL · ECG Library

Irregular broad-complex — the differential

AF with aberrancy vs AF with WPW vs polymorphic VT — the list to run when Gate 2 fires.

litfl.com → Dr Smith’s ECG Blog

Expert ECG interpretation

Case-based emergency cardiology from Stephen Smith & associate editors — searchable archive of AF, WPW and wide-complex cases.

drsmithsecgblog.com → Dr Smith’s ECG Blog · case

A young man with palpitations

Pre-excited AF in a young patient — shortest pre-excited RR <250 ms, no AV-nodal blockers, electrical cardioversion, then ablation. Maps onto Case 5.

blog archive → LITFL · Top 100

100 ECG quiz cases

Self-assessment ECGs for exam practice — several are AF with pre-excitation presented as undifferentiated broad-complex tachycardias.

litfl.com →
◯ noteExternal FOAMed resources, linked for the ECG images in their original context. Not affiliated with ED AI Tutor — content and availability are controlled by those sites.
Six worked cases — tap to expand the reasoning
Case 1 · 85M, chest pain + palpitations, AF 150, “stable”ACS until proven
Impression: first-detected rapid AF in a high-risk elder with chest pain. Not low-risk because the BP is normal. Red flagsPersistent ischaemic pain is instability even at normal BP → ongoing pain + dynamic ECG changes or oedema shift toward urgent cardioversion. Key decisions
  • Is AF causing the pain, or is ACS/PE/dissection causing AF? Treat suspected ACS in parallel (aspirin 300 mg, local pathway).
  • Stable + uncertain duration → cautious rate control (metoprolol) over reflex cardioversion.
  • Repeat the ECG after rate reduction — the single most useful consultant move.
Anticoagulation & dispoAge alone gives CHA₂DS₂-VA ≥2 → long-term anticoagulation likely. Monitored admission + cardiology, not discharge after one dose of metoprolol.
Case 2 · 45F, palpitations + presyncope 2 days, rapid AF, stablethe 48h line
Impression: first symptomatic AF with presyncope, sitting on the cardioversion timing boundary. Red flagsPresyncope reopens the differential — PE, tachy-brady, pauses, VT, bleeding, pregnancy. Key decisions
  • “2 days” ≈ 48h and onset unproven → treat duration as uncertain: no unprotected cardioversion.
  • Pathways: TOE-guided early cardioversion, or rate control + 3 weeks anticoag then elective.
  • Hunt reversible causes harder in the young (thyroid, stimulants, PE, pregnancy).
Anticoagulation & dispoLikely CHA₂DS₂-VA 0 → no lifelong anticoag — but peri-cardioversion anticoag is a separate yes. Recurrent presyncope → monitored admission.
Case 3 · 45F, presyncope 5h, recent knee replacementtreat the driver
Impression: new rapid AF after major orthopaedic surgery — PE until assessed, not uncomplicated AF. Red flagsRecent surgery + immobility + presyncope. Absence of chest pain does not exclude PE; prophylaxis reduces but doesn't eliminate risk. Key decisions
  • PERC can't be used; post-op D-dimer lacks specificity → go to CTPA if moderate/high suspicion.
  • Don't aggressively slow a compensatory rate if PE/haemorrhage is possible.
  • Two pathways: trigger suspected → treat cause; triggers excluded + onset definitely 5h → ED cardioversion reasonable.
Anticoagulation & dispoAF stroke score likely 0; but a confirmed PE needs therapeutic anticoagulation — agent shaped by fresh surgery/bleeding (consider UFH). Monitored assessment.
Case 4 · 78M, syncope, AF 180, BP 80/50, GCS 14cardiovert now
Impression: unstable, peri-arrest AF — three ANZCOR adverse features at once. ImmediateSynchronised cardioversion, not a metoprolol trial. 200 J biphasic; confirm sync every shock; sedate if feasible but don't delay. Key decisions
  • Failed shock → check sync/pads, change vector (AP), escalate energy → refractory: amiodarone 300 mg → re-shock → 900 mg/24h.
  • Is AF the cause of shock or secondary (sepsis, PE, ACS, bleeding, tamponade)?
  • Persistent shock after sinus rhythm → another cause active. Elderly → watch for unmasked brady/pauses (pacing ready).
Anticoagulation & dispoUnknown duration doesn't delay the shock. Syncope + head strike → coordinate anticoag with CT brain. ICU/CCU + cardiology.
Case 5 · 50F, AF with WPW, HR 140, stabledo-not-give list
Impression: pre-excited AF until proven otherwise — a rhythm-control emergency; a rate of 140 doesn't make it benign. Do NOT giveAdenosine, beta-blockers, diltiazem/verapamil, digoxin, IV amiodarone — AV-nodal block favours the accessory pathway → VF. Key decisions
  • Stable options: synchronised DCCV 200 J, or procainamide, or ibutilide — don't cycle antiarrhythmics.
  • Any instability → immediate synchronised cardioversion.
  • Definitive care = accessory-pathway ablation.
Anticoagulation & dispoWPW changes the electrical danger, not the thromboembolic rules. Monitored obs + cardiology/EP; discharge only with a clear recurrence plan (avoid AV-nodal blockers).
Case 6 · 88M, known AF + CCF, chest pain + SOB, HR 180, BP 100/70“100” ≠ stable
Impression: rapid AF with acute decompensation — three adverse features (HR >150, chest pain, heart failure) despite BP 100/70. ImmediateLow threshold for synchronised cardioversion (200 J) if ischaemia/oedema/poor perfusion is due to the rhythm. Key decisions
  • Avoid diltiazem/verapamil and reflex beta-blockers in decompensated CCF. Amiodarone if agents unsuitable — but don't let it delay cardioversion.
  • Treat ACS and acute heart failure in parallel (loop diuretic, NIV if appropriate; nitrates cautious at BP 100/70).
  • No haemodynamic improvement after conversion → another shock cause is active.
Anticoagulation & dispoCHA₂DS₂-VA ≥4 (HF + HT + age) → long-term anticoagulation. ICU/CCU-level monitoring + cardiology.

ED AI Tutor · ED Reference Series · v1.0 · for clinicians and trainees. Always follow local protocols and senior clinician oversight.