Atrial fibrillation is a supraventricular tachyarrhythmia characterized by disorganized, rapid atrial electrical activity resulting in irregular ventricular response and loss of effective atrial contraction.

Exam domain	One-glance essentials
Definition / diagnosis	Atrial fibrillation = uncoordinated atrial activation with ineffective atrial contraction; the most common sustained arrhythmia ^[2] ECG shows absent P waves, fibrillatory baseline and irregularly irregular RR intervals ^[2]
Epidemiology / risks	Common substrates: age, hypertension, IHD, heart failure and mitral valve disease ^[2] Reversible triggers include thyrotoxicosis, sepsis, hypoxia/PE, alcohol and K/Mg disturbance ^[2]
Core mechanism	Pulmonary-vein ectopy triggers multiple atrial re-entry wavelets in dilated/fibrotic atria ^[2] Loss of atrial kick + rapid ventricular rate lowers output; LAA stasis creates thromboembolism ^[2]
Clinical picture	*Sudden irregular palpitations with breathlessness, polyuria or variable symptoms; some patients are asymptomatic* ^[1] Pulse is irregularly irregular with variable volume; JVP has no coordinated a wave ^[2]
Investigations	Confirm on 12-lead ECG; use Holter/event/loop monitoring if paroxysmal AF is not captured ^[2] Check CBC, renal/liver function, TFT, K and Mg; TTE assesses valves, LA size and LVEF ^[2] TOE excludes LAA thrombus before cardioversion when duration > 48 hours/unknown without prior anticoagulation ^[2]
Management	*Three pillars: rate control + rhythm control + anticoagulation* ^[1] *Haemodynamic instability → immediate synchronised DC cardioversion* ^[1] Stable: treat cause; rate-control by LVEF, consider rhythm control, and anticoagulate according to stroke risk ^[2]
Complications	Cardioembolic stroke/systemic embolism from LAA thrombus ^[2] Rapid AF may cause acute HF or reversible tachycardia-induced cardiomyopathy ^[2] AF promotes further electrical/structural remodelling: AF begets AF ^[2]
Prevention / follow-up	*CHA₂DS₂-VASc ≥ 2 in men or ≥ 3 in women → oral anticoagulation* ^[1] Control BP, obesity, OSA, alcohol and other triggers; anticoagulation after ablation remains risk-score based ^[2]
Exam traps	Rheumatic mitral stenosis/mechanical valve AF → warfarin, not a DOAC ^[2] AF > 48 hours/unknown: anticoagulate ≥ 3 weeks or perform TOE before elective cardioversion; continue ≥ 4 weeks after ^[2] AF with WPW: avoid AV-nodal blockers; use procainamide or cardioversion ^[2]

References

^[1] Lecture slides: GC 089. Syncope and irregular heart beat.pdf ^[2] Senior notes: Maksim Medicine Notes.pdf

Atrial Fibrillation (AF)

Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterised by uncoordinated atrial activation with consequently ineffective atrial contraction ^[1]^[2]. The name itself tells you the pathology:

"Atrial" = of the atria
"Fibrillation" = quivering, disordered electrical activity (from Latin fibrilla = small fibre)

So instead of the atria contracting in a single coordinated squeeze (driven by sinus node → atrial depolarisation wave), you get hundreds of chaotic micro-re-entrant wavefronts meandering through the atrial myocardium simultaneously. The result:

Atrial rate so fast (350–600 bpm) that distinct P waves are not discernible on ECG ^[3]
Variable conduction at the AV node → irregularly irregular ventricular rhythm ^[2]^[3]
Loss of the "atrial kick" (the final 15–25% of ventricular filling that depends on coordinated atrial contraction) → ↓ cardiac output, especially in patients with stiff ventricles (e.g. HFpEF, hypertrophic cardiomyopathy)

High Yield – Why 'Irregularly Irregular'?

The AV node is bombarded by 350–600 impulses per minute from the chaotic atria. It cannot conduct all of them (its refractory period saves the ventricles). But because the arriving impulses are themselves random, the AV node conducts them at variable intervals → the R-R intervals on ECG are completely unpredictable. This is the hallmark: irregularly irregular RR intervals ^[2]^[3].

AF is the MOST common sustained cardiac arrhythmia ^[1]^[2]^[3] — this is consistently the #1 exam fact.

2. Epidemiology

Male predominance ^[1]
More common with increasing age ^[1]^[3]:
- ~1% at age 60–64 years
- ~9% at age > 80 years ^[3]
Global lifetime risk ~25% (i.e. 1 in 4 adults will develop AF)
Prevalence in Hong Kong is rising due to population ageing and increasing burden of hypertension, obesity, and diabetes ^[4]

With ageing:

Atrial fibrosis accumulates → disrupts normal conduction pathways → creates substrates for re-entry
Diastolic dysfunction worsens → ↑ left atrial pressure → atrial dilatation
Co-morbidities (HTN, IHD, valvular disease) become more prevalent
Sick sinus syndrome (degenerative disease of SA node) becomes more common → tachy-brady syndrome where AF is the "tachy" component

3. Anatomy and Physiology Relevant to AF

To understand AF, you must first understand normal sinus rhythm:

SA node (right atrium, near SVC-RA junction) fires at 60–100 bpm → dominant pacemaker
Depolarisation wave spreads through atrial myocardium → coordinated atrial contraction → P wave on ECG
Impulse reaches AV node (at the crux of the heart, in the interatrial septum near the coronary sinus os) → conduction slows (PR interval) → allows atrial systole to complete before ventricular systole begins
Impulse travels down His bundle → bundle branches → Purkinje fibres → coordinated ventricular contraction → QRS complex

Critical Concept – Pulmonary Vein Sleeves

Sleeves of atrial muscle extend into the pulmonary veins (PVs) ^[3]. These myocardial sleeves are the most common source of ectopic triggers that initiate AF. They have shorter refractory periods, higher automaticity, and are prone to generating rapid bursts of electrical activity. To coordinate sinus rhythm, there are normally micro-electric circuits in the pulmonary veins draining into the LA ^[5]. When the LA dilates (e.g. from mitral stenosis or hypertension), these pulmonary veins are dilated and their structure is distorted, creating abnormal micro-electric circuits that increase the risk for AF ^[5].

This is exactly why pulmonary vein isolation (PVI) is the cornerstone of catheter ablation for AF — you electrically disconnect these sleeves from the rest of the left atrium ^[5].

The LAA is a blind-ended pouch arising from the left atrium
In AF, the LAA has very sluggish blood flow (no coordinated contraction, just quivering)
> 90% of left atrial thrombi in non-valvular AF form in the LAA
This is why LAA occlusion devices (e.g. Watchman device) are an alternative to anticoagulation in selected patients
Clot usually occurs in the left atrial appendage during MS, due to the dilated left atrium ^[6]

The AV node has a long refractory period and decremental conduction (the faster it is stimulated, the more it slows down). This property is what saves ventricular rate in AF — without the AV node's filtering, 350–600 impulses per minute would reach the ventricles, causing ventricular fibrillation and death.

Danger – AF with Accessory Pathway (WPW)

In Wolff-Parkinson-White (WPW) syndrome, an accessory pathway bypasses the AV node. If AF develops, atrial impulses can conduct directly to the ventricles via the accessory pathway without AV nodal filtering → extremely rapid, irregular wide-complex tachycardia (AF with anterograde accessory pathway conduction ^[7]) → can degenerate into VF → cardiac arrest. NEVER give AV nodal blocking agents (digoxin, verapamil, diltiazem) in this setting — they enhance conduction down the accessory pathway by removing the "competing" AV nodal pathway. Use IV procainamide or DC cardioversion.

4. Aetiology (with Hong Kong Focus)

The causes of AF can be remembered by thinking: what dilates the atria, what irritates the atria, and what drives the sympathetic nervous system?

Cause	Mechanism	HK Relevance
Hypertension (common) ^[1]	Chronic pressure overload → LVH → diastolic dysfunction → ↑ LA pressure → LA dilatation	Most common cause in HK. Very high prevalence of HTN in the ageing population
Ischaemic heart disease (IHD) (common) ^[1]	Atrial ischaemia (right coronary artery supplies SA node) + LV dysfunction → ↑ LA pressure → LA dilatation	Major burden; IHD is a leading killer in HK
Valvular heart disease (esp. mitral valve) ^[1]	MS → mechanical obstruction → ↑ LA pressure → LA dilatation. MR → volume overload → LA dilatation. 50–75% of patients with mitral stenosis have concomitant AF ^[5]	Rheumatic heart disease still seen in older HK Chinese patients; degenerative MR increasingly common with ageing
Congenital heart disease (e.g. ASD) ^[1]	ASD → LA/RA volume overload → atrial dilatation	Detected more in adult congenital heart disease clinics
Rheumatic heart disease ^[1]	Post-streptococcal immune-mediated valvulitis → chronic valvular scarring and atrial remodelling	Historical burden in HK; less common now but still seen
Hypertrophic cardiomyopathy (HCM) ^[1]	LV outflow obstruction + diastolic dysfunction → ↑ LA pressure → LA dilatation	Important cause in younger patients; AF in HCM is a red flag for stroke
Myocarditis / Pericarditis ^[1]	Inflammation of atrial myocardium → electrical instability	Viral myocarditis (e.g. Coxsackie, COVID-19) can trigger AF
Post-cardiac surgery ^[2]	Direct atrial handling/inflammation + pericardial irritation + sympathetic activation	Very common post-CABG or valve surgery (up to 30–40%)

Cause	Mechanism
Hypoxia (pneumonia, acute exacerbation of COPD) ^[1]	Hypoxia → pulmonary vasoconstriction → pulmonary HTN → right atrial dilatation. Also, ↑ sympathetic drive from hypoxaemia
Obstructive sleep apnoea (OSA) ^[1]	Intermittent hypoxia + intrathoracic pressure swings + autonomic dysfunction → atrial remodelling. Very relevant in HK given rising obesity
Pulmonary embolism ^[1]	Acute ↑ right heart pressures → right atrial dilatation → atrial arrhythmias

Cause	Mechanism
Thyrotoxicosis ^[1]^[8]	Excess T3/T4 → ↑ cardiac β-adrenergic receptor sensitivity + direct effect on ion channels → ↑ atrial automaticity and shortened refractory period. AF is a complication of Graves' disease ^[8]
Electrolyte disorders (hypokalaemia, hypomagnesaemia) ^[1]^[2]	Alter resting membrane potential and repolarisation → ↑ susceptibility to arrhythmias
High catecholamine states (stress, infection, pheochromocytoma) ^[2]	Sympathetic activation → ↑ automaticity of ectopic foci (especially PV sleeves)

Cause	Mechanism
Alcohol ^[1]^[9]	"Holiday Heart Syndrome": binge drinking → direct toxic effect on atrial myocardium + dehydration + ↑ sympathetic tone + electrolyte disturbance (hypoK, hypoMg). Alcohol is associated with AF (cardiac arrhythmias) ^[9]
Cocaine / Theophylline / Amphetamines ^[1]	Sympathomimetic → ↑ catecholamines → ↑ atrial automaticity
Caffeine ^[2]	Mild sympathomimetic; controversial whether moderate intake truly causes AF, but can exacerbate pre-existing AF
Smoking ^[2]	Nicotine → sympathetic activation; also promotes atrial fibrosis
Ivabradine (I_f inhibitor) ^[2]	Blocks funny current in SA node but may paradoxically facilitate AF by altering atrial electrophysiology

Cause	Mechanism
Sepsis ^[1]	Systemic inflammation + catecholamine surge + electrolyte imbalance + direct myocardial dysfunction
Surgery (non-cardiac) ^[1]	Stress response + pain + fluid shifts + electrolyte changes
Lone AF	AF in patients < 60 years with no identifiable cardiac, pulmonary, or metabolic cause. Diagnosis of exclusion. Likely genetic predisposition or subclinical atrial pathology
Old age (associated with sick sinus syndrome) ^[2]	Degenerative fibrosis of SA node and atrial tissue → both bradycardia and AF (tachy-brady syndrome)

Hong Kong-Specific Points

In HK, hypertension and IHD are overwhelmingly the most common causes. Rheumatic heart disease (→ mitral stenosis → AF) is declining but still encountered in older patients. Thyrotoxicosis (Graves' disease) is common in young-to-middle-aged women. Alcohol-related AF ("Holiday Heart") is seen in social/binge drinkers. OSA is increasingly recognised as a contributor given the rising obesity prevalence.

5. Pathophysiology

5.1 The "Trigger and Substrate" Model

AF requires two things:

A trigger — an ectopic focus that fires rapidly and initiates the arrhythmia
A substrate — abnormal atrial tissue that can sustain the arrhythmia once triggered

Most commonly in sleeves of atrial muscles extending into pulmonary veins ^[3]
These PV sleeves have unique electrophysiological properties:
- Shorter action potential duration
- Higher resting membrane potential (closer to threshold → easier to fire)
- Heterogeneous conduction properties
Other triggers: ↑ sympathetic tone (e.g. hyperthyroidism, sepsis, post-operative state) ^[3], vagal tone (lone AF in young patients, often nocturnal)

Atrial dilatation: stretches myocytes → alters ion channel function → shortens refractory period → allows more simultaneous re-entrant wavefronts → minimum number of re-entrant circuits required to sustain AF is facilitated by atrial dilatation ^[3]
Atrial fibrosis: disrupts normal cell-to-cell coupling → creates areas of slow conduction and conduction block → allows re-entry
The result: multiple wandering re-entrant circuits within the atria ^[3]

Critical Concept – AF Begets AF

Atrial fibrillation begets atrial fibrillation: structural and electrical remodelling occurs at each episode → higher risk of further AF ^[2]^[3]. This is a self-perpetuating cycle:

AF → rapid atrial rate → shortens atrial refractory period (electrical remodelling, within hours-days)
AF → atrial dilatation + fibrosis (structural remodelling, over weeks-months)
Both → more substrate for AF → harder to restore and maintain sinus rhythm
This is why early intervention (rhythm control) may be better than waiting — the longer AF persists, the harder it is to treat.

Loss of atrial kick → ↓ ventricular filling by ~15–25% → ↓ cardiac output
- Particularly symptomatic in patients with stiff ventricles (HCM, HFpEF, aortic stenosis) who rely heavily on atrial contribution
Rapid ventricular rate → ↓ diastolic filling time → further ↓ CO
- If sustained, can cause tachycardia-induced cardiomyopathy (reversible dilated cardiomyopathy)
Stasis of blood in the atria (especially LAA) → thromboembolism risk → stroke, systemic embolisation

Virchow's triad is perfectly illustrated in AF:

Component	How AF contributes
Stasis	Loss of coordinated atrial contraction → blood pools in LAA
Endothelial injury	Atrial endocardial damage from rapid electrical activity and structural remodelling
Hypercoagulability	AF activates the coagulation cascade; ↑ tissue factor, ↑ fibrinogen, ↑ D-dimer, platelet activation

→ This is why anticoagulation is a cornerstone of AF management. The stroke risk in non-valvular AF is ~5%/year without anticoagulation (varies by CHA₂DS₂-VASc score).

6. Classification

Classification	Description ^[1]
Paroxysmal	AF that terminates spontaneously or with intervention within < 7 days of onset. Self-terminating or intermittent, often triggered in pulmonary veins. Episodes may recur with variable frequency ^[1]
Persistent	Continuous AF sustained > 7 days ^[1]
Long-standing persistent	Continuous AF sustained > 12 months (1 year) ^[1]
Permanent	Joint decision by patient and clinician to cease further attempts to restore or maintain sinus rhythm (SR) ^[1]. This is a management decision, not a pathophysiological state — the patient has AF, and everyone agrees to accept it

Exam Trap – Paroxysmal AF

A common error is defining paroxysmal AF as "< 48 hours." The correct definition per AHA/ESC guidelines is < 7 days (either self-terminating or cardioverted within 7 days). The 48-hour mark is clinically important for a different reason: it determines whether you need to rule out LA thrombus before cardioversion (if AF has lasted > 48h or duration unknown → need TOE or ≥ 3 weeks of therapeutic anticoagulation before cardioversion). Some older notes ^[2] quote "< 48h" for paroxysmal — be aware this is the older or simplified definition.

Classification	Definition ^[1]
Non-valvular AF	AF in the absence of rheumatic mitral stenosis (MS), a mechanical or bioprosthetic heart valve, or mitral valve repair ^[1]
Valvular AF	AF with moderate-to-severe rheumatic MS, or prosthetic heart valve

Why does this matter? Patients with valvular AF require warfarin — NOACs/DOACs are NOT indicated. This is the only native valvular disease that requires warfarin; for other valvular disease, NOAC is good enough ^[6]. The reason is that trials proving NOAC efficacy (RE-LY, ROCKET-AF, ARISTOTLE, ENGAGE AF-TIMI 48) specifically excluded patients with significant mitral stenosis and mechanical valves.

Any AF episode diagnosed for the first time, regardless of duration or symptoms
Important to classify because it determines further workup and management strategy

7. Clinical Features

Symptom	Mechanism
Irregular palpitations ^[2]^[10]	Patient perceives the irregularly irregular heartbeat. Unlike AVNRT (sudden onset, regular, terminated by vagal manoeuvres), AF palpitations are usually at rest; trivial movements (e.g. bending) may trigger; vagal manoeuvres may relieve ^[10]. Onset is sudden; character is irregular, usually fast; slower in elderly ^[10]
Shortness of breath (SOB) / exertional dyspnoea ^[2]	↓ CO from loss of atrial kick + rapid ventricular rate → inadequate cardiac output during exercise. In severe cases → pulmonary congestion from ↑ LA pressure
Fatigue / exercise intolerance	↓ CO → inadequate tissue oxygen delivery, especially during exertion
Syncope / presyncope / dizziness ^[2]	Rapid ventricular rate → ↓ diastolic filling → ↓ CO → cerebral hypoperfusion. Also possible with very slow AF (if concomitant AV block)
Polyuria ^[10]	Atrial distension → ↑ atrial natriuretic peptide (ANP) release → diuresis. This is why patients may notice frequent urination during palpitation episodes
Breathlessness (dyspnoea) ^[10]	Especially if concomitant heart failure or rapid ventricular response → pulmonary congestion
Chest pain / tightness	Rapid ventricular rate → ↑ myocardial oxygen demand + ↓ diastolic filling time (→ ↓ coronary perfusion) → supply-demand mismatch → angina. This can occur even without underlying coronary artery disease
Embolic symptoms	Stroke (sudden hemiplegia, aphasia), acute limb ischaemia (6Ps), mesenteric ischaemia (acute abdominal pain), renal infarction (flank pain + haematuria) — these may be the presenting features of previously undiagnosed AF
Asymptomatic	Many patients (up to 30%) have "silent AF" detected incidentally on ECG or pulse check. This is dangerous because they still carry stroke risk

High Yield – SOCRATES for AF Palpitations (from CFB Slides)

From the CFB cardiovascular history-taking lecture ^[10]:

Site: –
Onset: Sudden
Character: Irregular, usually fast; slower in elderly
Radiation: –
Associated features: Polyuria, breathlessness
Timing: Variable
Exacerbating/relieving factors: Usually at rest, trivial movements (e.g. bending) may trigger. Vagal manoeuvres may relieve
Severity: Very variable, may be asymptomatic

Sign	Mechanism
Irregularly irregular pulse with variable volume ^[2]	Variable R-R intervals → variable diastolic filling time → variable stroke volume → variable pulse volume. This is THE defining sign — if you feel an irregularly irregular pulse, AF is the #1 diagnosis until proven otherwise
Pulse deficit	Apical heart rate > radial pulse rate. Some heartbeats are too weak (from very short diastolic filling times) to generate a palpable radial pulse. Count both simultaneously — the difference is the "pulse deficit"
Absent "a" wave in JVP ^[2]^[5]	The "a" wave represents atrial contraction. In AF, there is no coordinated atrial contraction → the "a" wave disappears. You may see irregular "v" waves or fibrillatory flickering
Varying intensity of S1	S1 intensity depends on the position of the mitral valve leaflets at the onset of ventricular systole, which depends on the preceding diastolic filling time. Variable R-R intervals → variable leaflet positions → variable S1 loudness
Mitral valve lesion signs (if valvular AF) ^[2]	Mid-diastolic rumbling murmur (MS), pansystolic murmur at apex (MR)
Signs of heart failure (if decompensated)	Raised JVP, bilateral basal crepitations, peripheral oedema, displaced apex beat (dilated LV), S3 gallop
Signs of the underlying cause	Thyroid signs (tremor, exophthalmos, goitre with bruit in Graves'), signs of chronic lung disease (barrel chest, pursed lip breathing), malar flush (MS), signs of alcohol use

Sign	Underlying Complication
Acute hemiplegia / dysphasia	Cardioembolic stroke
Cold, pale, pulseless limb (6Ps)	Acute limb ischaemia from embolism. Cardiac origin emboli (80%) → AF is the most common cause ^[11]^[12]
Acute abdomen with pain out of proportion to findings	Mesenteric ischaemia from embolism. Embolism to mesenteric arteries is most frequently due to dislodged thrombus from LA... AF may predispose to arterial embolism ^[13]

8. ECG Features of AF

This is extremely high yield for data interpretation stations.

Feature	Description
Absent P waves ^[2]^[7]	No organised atrial depolarisation → no discrete P waves
Irregular baseline / fibrillatory waves (f waves) ^[2]^[7]	The chaotic atrial electrical activity produces low-amplitude, irregular undulations of the baseline. These are the fibrillary waves ^[7]
Irregularly irregular RR intervals ^[2]^[7]	Due to variable AV conduction of the chaotic atrial impulses
Usually fast (rapid ventricular response) ^[2]	Untreated AF typically has a ventricular rate of 100–160 bpm
If slow, suspect AV block ^[2]	If AF has a slow and regular ventricular rate, suspect complete heart block with a junctional or ventricular escape rhythm ("regularised AF")
Narrow QRS (usually)	Because ventricular depolarisation still occurs via the normal His-Purkinje system (unless there is a pre-existing bundle branch block or accessory pathway conduction)

Variant	Key Feature	Clinical Significance
AF with rapid ventricular response (RVR)	HR > 100 bpm, irregularly irregular	Most common presentation; needs rate control
AF with slow ventricular response	HR < 60 bpm, irregularly irregular	Consider: concomitant AV block, digoxin toxicity, sick sinus syndrome, excessive beta-blocker/CCB
AF with wide QRS	Irregular wide complexes	DDx: AF with bundle branch block, AF with accessory pathway conduction (WPW — irregular wide complex tachycardia ^[7]), AF with rate-related aberrant conduction
AF with LVH	Tall QRS voltages + ST-T changes	Machine may automatically change calibration — always check the voltage calibration! Have to ask patient to get another ECG with the correct calibration ^[7]

ECG Pitfall – AF with LVH

The ECG machine may automatically change the calibration (voltage) when it detects large QRS complexes from LVH. This means ST-depression cannot be appreciated properly. Always check the calibration mark (should be 10mm/mV). If it says "half standard" or shows a 5mm calibration mark, the voltages are halved and you may miss LVH criteria or ST changes ^[7].

9. Investigations

12-lead ECG: confirms diagnosis (absent P waves, irregular baseline, irregularly irregular R-R intervals)
Continuous cardiac monitoring: in acute settings for rate assessment and rhythm surveillance

Investigation	Purpose
CBC ^[2]	Anaemia (high-output state can trigger AF), infection (WCC)
LRFT (Liver and Renal Function Tests) ^[2]	Baseline before starting anticoagulation and antiarrhythmics; renal function determines NOAC dosing
Bone profile (Calcium) ^[2]	Hypercalcaemia can cause arrhythmias
TFT (Thyroid Function Tests) ^[2]	Essential — must exclude thyrotoxicosis as a reversible cause. In HK, always check TSH in new-onset AF
Magnesium ^[2]	Hypomagnesaemia predisposes to AF and makes it harder to treat
Coagulation profile	Baseline before anticoagulation
Troponin	If suspecting ACS as the trigger
BNP / NT-proBNP	If heart failure is suspected

Investigation	Purpose
Echocardiogram ^[2]	For structural heart disease and LA thrombus ^[2]. Assess LA size, LV function (EF), valvular disease, wall motion abnormalities (IHD), LVH, pericardial effusion
Transoesophageal echocardiogram (TOE)	Gold standard for detecting LAA thrombus; required before cardioversion if AF duration > 48h and patient not adequately anticoagulated
Chest X-ray	Cardiomegaly, pulmonary congestion, underlying lung disease

Investigation	Indication
24h Holter monitor ^[2]	For slow AF / long pauses ^[2]; to detect paroxysmal AF if ECG is normal at time of consultation; to assess rate control adequacy
Event recorder / implantable loop recorder	For infrequent paroxysmal AF not captured on Holter
Exercise stress test	If IHD is suspected as the underlying cause
CT pulmonary angiogram	If PE is suspected as the trigger

10. CHA₂DS₂-VASc Score

This is the key risk stratification tool for stroke risk in non-valvular AF, used to guide anticoagulation decisions.

From the GC lecture slides ^[14]:

Letter	Risk Factor	Points
C	Congestive heart failure	1
H	Hypertension	1
A₂	Age ≥ 75	2
D	Diabetes mellitus	1
S₂	Stroke / systemic thromboembolism	2
V	Vascular disease (prior MI, PAD, aortic plaque)	1
A	Age 65–74	1
Sc	Sex category (female)	1

Maximum score = 9

From the GC lecture slides ^[14]:

Anticoagulation is indicated if score ≥ 2 for males / ≥ 3 for females ^[14]

Score	Recommendation
0 (male) or 1 (female — the 1 point is from female sex alone)	No anticoagulation needed
1 (male) or 2 (female)	Consider anticoagulation (weigh benefits vs bleeding risk)
≥ 2 (male) or ≥ 3 (female)	Anticoagulation recommended ^[14]

Why Is Female Sex a Risk Factor but Scored Differently?

Female sex alone does not independently warrant anticoagulation — it is a "risk modifier" rather than an independent driver. A woman with a CHA₂DS₂-VASc of 1 (from female sex alone) has a very low stroke risk. Hence, the threshold is ≥ 3 for women (i.e. ≥ 2 points from risk factors other than sex).

11. Anticoagulation in AF – CHA₂DS₂-VASc Guided

	Valvular AF (Rheumatic MS, Mechanical Valve)	Non-Valvular AF
Anticoagulant of choice	Warfarin (target INR 2.0–3.0 for MS; 2.5–3.5 for mechanical valve)	NOAC (preferred) or Warfarin
NOAC use	Contraindicated ^[6]	First-line

NOAC	Mechanism	Key Points
Dabigatran (Pradaxa)	Direct thrombin (factor IIa) inhibitor	Reversible with idarucizumab; renal excretion (dose-adjust in CKD); BID dosing
Rivaroxaban (Xarelto)	Direct factor Xa inhibitor	OD dosing (with food); partial renal excretion
Apixaban (Eliquis)	Direct factor Xa inhibitor	BID dosing; least renal excretion among NOACs; preferred in elderly/CKD
Edoxaban (Lixiana)	Direct factor Xa inhibitor	OD dosing; dose-reduce if CrCl 15–50 or body weight ≤ 60kg

Advantages of NOACs over Warfarin: predictable pharmacokinetics, no routine INR monitoring, fewer drug/food interactions, rapid onset, lower risk of intracranial haemorrhage.

Contraindications to NOACs: valvular AF (mechanical valve, moderate-severe rheumatic MS), severe CKD (CrCl < 15–30 depending on agent), pregnancy/breastfeeding, antiphospholipid syndrome.

12. Management Overview (Rate, Rhythm, Anticoagulation)

The core management framework for AF has three pillars: Rate control + Rhythm control + Anticoagulation ^[2]

12.1 Acute Management

From the GC lecture slides and Maksim notes ^[2]^[14]:

DC cardioversion (120–200J biphasic) ^[2]
This takes priority over everything — if the patient is hypotensive, in cardiogenic shock, or acutely decompensated, cardiovert immediately regardless of anticoagulation status

Treat underlying cause if possible: e.g. hyperthyroidism, PE, sepsis / pneumonia, hypokalaemia/hypomagnesaemia ^[2]
Rate control: First-line in most patients

Must check whether there are features of acute pulmonary oedema (APO) → avoid BB / CCB if APO present ^[2]

EF	First-line Rate Control
EF ≥ 40%	Beta-blockers (e.g. IV metoprolol 2–5 mg bolus over 2 min) or CCB (e.g. IV diltiazem 0.25 mg/kg bolus over 2 min or IV verapamil) ^[2]
EF < 40%	Beta-blockers (e.g. IV metoprolol 2–5 mg bolus over 2 min) or IV digoxin 0.25 mg ^[2]

Why Avoid CCB in HFrEF?

Non-dihydropyridine CCBs (verapamil, diltiazem) have negative inotropic effects — they reduce myocardial contractility. In a patient with EF < 40%, this can precipitate acute decompensated heart failure or cardiogenic shock. Beta-blockers also have negative inotropic effects but have proven mortality benefit in HFrEF when used carefully. Digoxin has no negative inotropic effect (in fact, it is a positive inotrope) and slows AV conduction → safe in HFrEF.

Target resting heart rate: < 110 bpm (lenient) is acceptable in most patients (RACE II trial); < 80 bpm (strict) if still symptomatic
Oral agents:
- Beta-blockers: bisoprolol, metoprolol, atenolol
- Non-dihydropyridine CCBs: diltiazem, verapamil (only if EF preserved)
- Digoxin: add-on if above insufficient; useful in sedentary patients (controls resting but not exercise HR)
- Amiodarone: last resort for rate control (significant toxicity profile)

Rhythm control aims to restore and maintain sinus rhythm. Indications:

Symptomatic despite adequate rate control
Young patients
First-detected AF
Heart failure driven by AF (tachycardia-induced cardiomyopathy)
Patient preference

Methods:

Pharmacological cardioversion: flecainide (no structural heart disease), amiodarone (structural heart disease or HF)
Electrical cardioversion (DC cardioversion): synchronised shock
Catheter ablation (pulmonary vein isolation): AF ablation electrically isolates the PV ^[6] — increasingly first-line for paroxysmal AF refractory to drugs (EARLY-AF, STOP-AF trials)
Maintenance antiarrhythmics: flecainide, propafenone (Class IC — only if no structural heart disease), sotalol, dronedarone, amiodarone

Acute	Long-term
IV amiodarone	Class I AAD
IV lignocaine	Sotalol
IV procainamide	Amiodarone
Overdrive pacing	Catheter ablation, surgery
Cardioversion/Defibrillation	ICD implantation in high-risk patients
	Correct reversible factors if present

13. Special Scenarios

AF is the most common cardiac source of embolic stroke. Arrhythmias — Atrial fibrillation is listed as a major cause of cardioembolic stroke ^[15]
Cardioembolic strokes tend to be large (major vessel occlusion), haemorrhagic transformation risk is higher
Secondary prevention: lifelong anticoagulation (NOAC or warfarin depending on valvular status)

50–75% of patients with MS have AF ^[5]
Mechanism: LA dilatation → distortion of PV structures → abnormal micro-electric circuits ^[5]
Anticoagulation: MUST use warfarin (not NOAC) ^[6]
Left atrium enlarged → stasis of blood → systemic embolisation ^[5]

AF is a complication of Graves' disease ^[8]
Heart failure → high output HF may also develop ^[8]
Treatment: control thyrotoxicosis first (anti-thyroid drugs), then rate control with beta-blockers (propranolol also treats thyrotoxic symptoms)
AF often reverts to sinus rhythm once euthyroid

Cardiac origin emboli (80%): AF is the most common source ^[11]^[12]
Emboli lodge at bifurcation points (femoral bifurcation most common) ^[12]
Clinical features: 6Ps (Pain, Pallor, Pulseless, Perishingly cold, Paraesthesia, Paralysis)

AF may predispose to arterial embolism to mesenteric vessels ^[13]
Classical presentation: acute severe periumbilical pain in an old patient with AF with pain out of proportion to physical findings ^[16]

Single-chamber ventricular pacing (VVI) → indicated in AF ^[17] — because there is no point pacing the atrium if it is fibrillating; you only need to ensure adequate ventricular rate
This is in contrast to sinus node dysfunction where dual-chamber (DDD) pacing is preferred

Familial AF: mutations in genes encoding potassium channels (KCNQ1, KCNE2), sodium channels (SCN5A), connexins → altered atrial electrophysiology
Brugada syndrome and Long QT syndrome can occasionally present with AF as well as their more classical ventricular arrhythmias
Not as high-yield as the acquired causes for HKUMed exams, but worth knowing

High Yield Summary

Definition: AF = supraventricular tachyarrhythmia with uncoordinated atrial activation → ineffective atrial contraction → irregularly irregular ventricular rhythm. Most common sustained cardiac arrhythmia.
Classification: Paroxysmal (< 7 days), Persistent (> 7 days), Long-standing persistent (> 1 year), Permanent (accepted). Valvular AF (rheumatic MS, mechanical valve → warfarin only) vs Non-valvular AF (NOAC or warfarin).
Aetiology: Cardiac (HTN, IHD, mitral valve disease, HCM, post-surgery), Respiratory (COPD, PE, OSA), Metabolic (thyrotoxicosis, hypoK, hypoMg), Drugs (alcohol "Holiday Heart", cocaine), Sepsis, Old age.
Pathophysiology: Trigger (PV sleeve ectopic foci) + Substrate (atrial dilatation/fibrosis → multiple re-entrant circuits). AF begets AF (electrical + structural remodelling).
Clinical Features: Irregular palpitations, SOB, fatigue, syncope, polyuria, embolic events. Signs: irregularly irregular pulse with variable volume, pulse deficit, absent a-wave JVP, variable S1.
ECG: Absent P waves, fibrillatory baseline, irregularly irregular R-R, usually narrow QRS.
Investigations: ECG, CBC, LRFT, TFT, Mg, bone profile, echo, ± Holter.
CHA₂DS₂-VASc: ≥ 2 (male) or ≥ 3 (female) → anticoagulate.
Management: Rate control (BB, CCB if EF ≥ 40%; BB, digoxin if EF < 40%) + Rhythm control (cardioversion, antiarrhythmics, ablation) + Anticoagulation (NOAC for non-valvular; warfarin for valvular).
Valvular AF (rheumatic MS) = warfarin ONLY. NOACs are contraindicated.
AF with WPW → NEVER give AV nodal blockers → DC cardioversion or IV procainamide.

Active Recall - Atrial Fibrillation

^[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – Atrial Fibrillation section (p.499–501) ^[2] Senior notes: Maksim Medicine Notes.pdf – Cardiology, Atrial Fibrillation (p.23) ^[3] Senior notes: Ryan Ho Cardiology.pdf – Atrial Fibrillation section (p.93) ^[4] General epidemiological data for HK AF prevalence ^[5] Senior notes: Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf (p.7) ^[6] Senior notes: Block A - Three Cases of Dyspnea.pdf (p.3) ^[7] Senior notes: Block A - Cardiology Data Interpretation.pdf (p.8, p.11) ^[8] Senior notes: Block A - I am losing weight and sweating all the time.pdf (p.11) ^[9] Senior notes: Block A - WCS32 Chest pain on exertion_ ischaemic heart disease; angina pectoris.pdf (p.11) ^[10] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf (p.36) ^[11] Senior notes: Maksim Surgery Notes.pdf – Acute limb ischaemia (p.168) ^[12] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf – Acute arterial ischaemia (p.920) ^[13] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf – Ischaemic bowel disease (p.718) ^[14] Lecture slides: GC 089. Syncope and irregular heart beat.pdf (p.26) ^[15] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf – Stroke aetiology (p.1140) ^[16] Senior notes: Maksim Surgery Notes.pdf – Ischaemic bowel disease (p.92) ^[17] Senior notes: Block A - Syncope and irregular heartbeat_ Cardiac arrhythmia; Heart blocks, Bradycardia.pdf (p.30)

Differential Diagnosis of Atrial Fibrillation

The differential diagnosis of AF really splits into two clinical scenarios that you will face:

You see the ECG and need to decide: "Is this really AF, or something that mimics it?" — the ECG differential.
The patient presents with symptoms (palpitations, SOB, syncope, embolic event) and you need to think broadly — the clinical-presentation differential.

Let's work through both systematically.

The hallmark of AF on ECG is irregular narrow complex tachycardia, no P waves ^[7]. But several other rhythms can look similar. The classic exam question is:

A patient presents with an irregularly irregular pulse. What are the 6 main differential diagnoses? ^[1]

Differential	Key ECG Features	How to Distinguish from AF
Atrial fibrillation ^[1]	Absent P waves, irregular baseline (fibrillatory waves), irregularly irregular RR ^[7]^[3]	The diagnosis itself — chaotic baseline, no discernible P waves
Atrial flutter with variable AV block ^[1]^[7]	Saw-tooth appearance of flutter waves (F waves) at ~300 bpm, but with varying conduction ratio (2:1, 3:1, 4:1 alternating) → irregular ventricular response	Saw-tooth P waves if you cover the QRS without isoelectric segment ^[7]. Use vagal manoeuvres or ATP to unmask flutter waves — ATP blocks the AV node, not the atrial tachycardia ^[7], so you'll reveal the underlying flutter waves while temporarily slowing ventricular rate
Atrial tachycardia with variable AV block ^[1]^[7]	Discrete, identifiable P waves of abnormal morphology (not sinus); atrial rate 110–250 bpm ^[3]; variable block means irregular RR intervals	P waves are present and discrete (unlike fibrillatory baseline). Atrium driving QRS, so either 1:1 ratio or greater than 1 ^[7]. Isoelectric baseline is preserved between P waves (cf. AF where it is not)
Multifocal atrial tachycardia (MAT) ^[1]^[3]	Irregularly irregular rate with average atrial rate > 100 bpm; ≥ 3 P-wave morphologies in the same lead; flat isoelectric line preserved (cf AF) ^[3]	The key distinguisher is that discrete P waves ARE visible and there are ≥ 3 different P-wave shapes (reflecting ≥ 3 ectopic foci). The isoelectric baseline is preserved ^[3] — in AF it is replaced by chaotic fibrillatory waves. MAT is associated with pulmonary disease (~60%), congestive HF, hypoK, hypoMg ^[3]
Multifocal atrial rhythm (MAR) ^[1]	Same as MAT but atrial rate ≤ 100 bpm ^[1]. ≥ 3 P-wave morphologies, absence of one dominant pacemaker	Distinguished from MAT purely by rate. Often an incidental finding in elderly patients with chronic lung disease
Very frequent ectopic beats (atrial or ventricular premature beats) ^[1]	Underlying sinus rhythm is present but heavily interrupted by frequent ectopics. The ectopics have different morphology from sinus beats	On careful inspection you can identify underlying sinus P waves between the ectopics. The "irregularity" is due to the premature beats interrupting regular sinus rhythm, not due to a continuously chaotic atrial mechanism. A longer rhythm strip helps — you'll see the regular sinus "scaffold" with premature interruptions

High Yield – The 6 DDx of Irregularly Irregular Pulse

From Felix Lai's notes and direct past paper question ^[1]: AF, atrial flutter with variable block, atrial tachycardia with variable block, MAT, MAR, and very frequent ectopic beats. This is a commonly tested list. The key differentiator is whether P waves (or flutter waves) are visible and whether an isoelectric baseline is preserved.

When the ECG shows an irregular wide-complex tachycardia, the differential changes and becomes more dangerous ^[7]:

Differential	Key Features	Clinical Significance
AF with pre-existing bundle branch block	Irregularly irregular, wide QRS with typical BBB morphology (e.g. RBBB: rsR′ in V1; LBBB: broad notched R in I, V5-6)	Relatively benign — the QRS is wide because of the conduction delay in the His-Purkinje system, not because of a ventricular focus. Treat as standard AF
AF with anterograde accessory pathway conduction (WPW) ^[7]	Irregularly irregular, wide QRS, axis doesn't change every beat ^[7], very rapid rate (can be > 200 bpm), varying QRS morphology. Either RBBB or accessory pathway ^[7]	Life-threatening! Unfiltered conduction to ventricles → can degenerate into VF. NEVER give AV nodal blockers (verapamil, diltiazem, digoxin). Treat with DC cardioversion or IV procainamide
Polymorphic VT (PVT) ^[7]	Everything irregular — not just rate, but also morphology, amplitude and axis ^[7]	Distinguished from AF with accessory pathway because in PVT the QRS axis and morphology change beat-to-beat. Torsades de pointes is a type of PVT → when there is a prolonged QTc ^[7]. Life-threatening — needs immediate defibrillation

Exam Pearl – Irregular Wide Complex Tachycardia

From the cardiology data interpretation session ^[7]: When you see an irregular wide complex tachycardia, there are 3 different differentials: AF with BBB, AF with accessory pathway conduction, and polymorphic VT. The axis behaviour is your friend: axis doesn't change every beat → more likely AF (with BBB or accessory pathway); axis changes every beat → PVT ^[7].

Sometimes AF is confused with other narrow-complex tachycardias. The distinguishing feature is regularity:

Differential	Rate	Regularity	P Waves	Key Distinguisher
Sinus tachycardia	100–160 bpm	Regular	Normal, upright P before each QRS	Onset is gradual ^[10]; normal P-wave morphology; rate responds to vagal manoeuvres with gradual slowing
Atrial flutter with fixed block (e.g. 2:1) ^[7]	Ventricular rate ~150 bpm (classic "150 bpm tachycardia")	Regular	Regular P wave, saw-tooth appearance → atrial flutter with 2:1 AV block ^[7]	Very regular rate at ~150 should always make you suspect flutter. Saw-tooth flutter waves become apparent when you slow AV conduction with vagal manoeuvres or adenosine
AV nodal re-entrant tachycardia (AVNRT) ^[7]	140–250 bpm	Regular	Sometimes can't even identify P wave; pseudo-R in V1 and pseudo-S in inferior leads ^[7]	Regular, sudden onset and offset, terminated by vagal manoeuvres (Valsalva, carotid sinus massage) or adenosine
Orthodromic AVRT ^[7]	140–250 bpm	Regular	Retrograde P waves visible after QRS	Requires an accessory pathway; terminates with adenosine
AF	Variable	Irregularly irregular	Absent	The irregularity is the key — if it's truly regular, it's not AF

The GC lecture slide emphasises that syncope/palpitation are not diagnoses — AF, complete heart block are. The aim of all Hx/PE/Ix is to arrive at the diagnosis, assess severity, identify the underlying cause, and guide management ^[18].

When a patient complains of palpitations and you haven't yet obtained an ECG, think systematically. The GC lecture on syncope and irregular heartbeat ^[18] and the Block A arrhythmia lecture ^[17] provide a framework:

Differential diagnosis of palpitation — classify into 4 categories ^[17]:

Cardiac causes ^[17]
- Primary cardiac causes: arrhythmia, valvular heart disease (e.g. pressure overload in AS — need to pump harder to overcome increased afterload), cardiomyopathy, low-output state (need to pump harder/faster), pacing ^[17]
- High-output states / systemic causes: pregnancy, anaemia, fever, Paget's disease ^[17]
Drug-related causes ^[17]
- Medications: sympathomimetics, anticholinergics, vasodilators, beta-blocker withdrawal ^[17]
- Other substances: amphetamine, cocaine, caffeine, nicotine, alcohol ^[17]
Metabolic causes ^[17]
- Thyrotoxicosis, pheochromocytoma, hypoglycaemia, electrolyte disturbances (potassium, magnesium) ^[17]
Psychiatric causes ^[17]
- Panic attack, anxiety, stress, depression, somatisation ^[17]

The point here is that palpitations ≠ AF. You must consider all these categories before anchoring on AF.

If a patient presents with an acute stroke and is found to have AF, you must also consider other embolic sources and non-embolic stroke mechanisms:

Category	Examples
Cardioembolic (AF being one)	AF, atrial flutter, sick sinus syndrome, MI with mural thrombus, valvular disease, IE, prosthetic valves, atrial myxoma, NBTE ^[15]
Large vessel atherosclerosis	Carotid artery stenosis, intracranial atherosclerosis
Small vessel disease	Lacunar infarct from hypertensive lipohyalinosis
Other	Arterial dissection, vasculitis, hypercoagulable states, paradoxical embolism (PFO + DVT)

AF may be an incidental finding in a patient whose stroke is actually due to carotid stenosis. Equally, AF may be the cause of the stroke. Clinical context (stroke territory, echocardiographic findings, carotid imaging) determines which mechanism is dominant.

Once you confirm AF, you must find the cause. This was covered in detail in the aetiology section, but the differential for the cause of AF is itself a structured list:

Category	Conditions to Exclude
Cardiac structural	HTN (most common overall), IHD, mitral valve disease (50–75% of MS patients have AF ^[5]), cardiomyopathy (DCM — ECG in DCM is usually abnormal with AF, AV block, LBBB ^[19]), congenital HD (ASD)
Respiratory	COPD exacerbation, pneumonia, PE, OSA
Endocrine/Metabolic	Thyrotoxicosis ^[18]^[8] — always check TFT; hypoK, hypoMg
Drug/Substance	Alcohol ("Holiday Heart") ^[9], cocaine, excess caffeine
Sepsis/Infection	Any systemic infection → ↑ catecholamines → AF trigger
Post-surgical	Post-cardiac surgery (up to 30–40%), post-thoracic surgery
Lone AF	No structural heart disease; occurs in ~50% of paroxysmal AF, ~20% of persistent/permanent AF ^[3]. Diagnosis of exclusion

The GC lecture slide explicitly states: the aim is to determine severity (too fast? too slow? haemodynamic compromise?) and the underlying cause (thyrotoxicosis? medications?) ^[18].

The following flowchart summarises the clinical approach when you encounter an irregular pulse or suspect AF:

8. Key Differentiating Manoeuvres

These transiently block or slow AV nodal conduction. The response helps you differentiate:

Rhythm	Response to Vagal Manoeuvre / Adenosine
Sinus tachycardia	Gradual slowing, then gradual return when effect wears off
Atrial flutter	Unmasking of flutter waves (F waves become obvious as ventricular rate drops); ATP blocks the node, not the tachycardia ^[7]
Atrial tachycardia	ATP is a sinus blocker → does not affect atrial arrhythmias ^[7] — the atrial tachycardia continues, but you see it more clearly as the ventricular response slows
AVNRT / AVRT	Terminates the tachycardia (because the AV node is an essential part of the re-entry circuit)
AF	Transient slowing of ventricular rate reveals fibrillatory baseline; rhythm does not terminate

Why Does Adenosine Terminate AVNRT but Not AF?

In AVNRT and AVRT, the AV node is part of the re-entrant loop. Blocking the AV node with adenosine breaks the loop → the tachycardia terminates. In AF and atrial flutter/tachycardia, the re-entry circuits are entirely within the atrial tissue — the AV node is merely a bystander conducting whatever reaches it. Blocking the AV node slows the ventricular response but the atrial chaos continues.

When the QRS is wide, you need to decide between VT and SVT with aberrancy. Key criteria from the data interpretation session ^[7]:

AV dissociation → favours VT (P waves march independently of QRS) ^[7]
Capture beats and fusion beats → pathognomonic for VT ^[7]
Negative concordance (all precordial leads show negative QRS) → useful in diagnosing VT ^[7]
QRS complex in aVR with large initial R wave → favours VT ^[7]
Northwest axis → favours VT ^[7]

If none of these are present and the rhythm is irregular → think AF with BBB or accessory pathway conduction.

Feature	AF	Atrial Flutter (variable block)	MAT	Frequent Ectopics
P waves	Absent	Flutter waves (saw-tooth)	≥ 3 morphologies, discrete	Sinus P + ectopic P
Baseline	Fibrillatory	Saw-tooth, no isoelectric line	Isoelectric line preserved ^[3]	Isoelectric between sinus beats
Regularity	Irregularly irregular	Irregular if variable block	Irregularly irregular	Irregular
Rate	Usually 100–160 bpm	Atrial 300 bpm; ventricular depends on block ratio	> 100 bpm	Normal sinus rate + premature beats
Vagal response	Slows VR, reveals f waves	Unmasks F waves	No change in atrial rate	Ectopics may suppress transiently
Association	HTN, IHD, valvular, thyroid, alcohol	Similar to AF; also post-cardiac surgery	Pulmonary disease (~60%), HF, hypoK/Mg ^[3]	Stress, caffeine, alcohol

High Yield Summary – Differential Diagnosis of AF

6 DDx of irregularly irregular pulse: AF, atrial flutter with variable block, AT with variable block, MAT, MAR, frequent ectopics ^[1].
Key ECG distinguisher: Is there a fibrillatory baseline with NO P waves (= AF) or are discrete P waves / flutter waves visible (= something else)?
Isoelectric baseline preserved → MAT or AT, NOT AF ^[3].
Irregular wide-complex tachycardia has 3 DDx: AF with BBB, AF with accessory pathway (WPW), polymorphic VT ^[7]. Axis changes every beat → PVT; axis stable → AF-related.
Vagal manoeuvres/adenosine help: terminate AVNRT/AVRT; slow VR and unmask flutter/AT waves; slow VR in AF but don't terminate it.
Once AF is confirmed, always look for the cause: TFT (thyrotoxicosis), echo (structural heart disease), electrolytes (K, Mg), history (alcohol, drugs, surgery).
Don't forget: AF may be an incidental finding in a patient presenting with stroke — but you still need to determine if it is the CAUSE of the stroke or a bystander.

Active Recall - Differential Diagnosis of AF

References

^[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – Case study: 6 DDx of irregularly irregular pulse (p.498–500) ^[3] Senior notes: Ryan Ho Cardiology.pdf – MAT, Atrial Flutter and Fibrillation sections (p.92–94) ^[5] Senior notes: Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf (p.6–7) ^[7] Senior notes: Block A - Cardiology Data Interpretation.pdf (p.8, p.10–11) ^[8] Senior notes: Block A - I am losing weight and sweating all the time.pdf (p.14) ^[9] Senior notes: Block A - WCS32 Chest pain on exertion_ ischaemic heart disease; angina pectoris.pdf (p.11) ^[10] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf (p.36) ^[15] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf – Stroke aetiology (p.1140) ^[17] Senior notes: Block A - Syncope and irregular heartbeat_ Cardiac arrhythmia; Heart blocks, Bradycardia.pdf (p.7) ^[18] Lecture slides: GC 089. Syncope and irregular heart beat.pdf (p.7) ^[19] Senior notes: Block A - Inherited Cardiac conditions.pdf (p.7)

Diagnostic Criteria, Algorithm, and Investigations for Atrial Fibrillation

1. Diagnostic Criteria — How Do You Actually "Diagnose" AF?

Unlike many conditions in medicine that rely on clinical criteria scores (e.g. Framingham for HF, Duke for IE), the diagnosis of AF is fundamentally an electrocardiographic diagnosis. There are no "clinical criteria" to fulfil — you need to see it on an ECG (or equivalent rhythm recording).

All three of the following must be present:

ECG Criterion	Description	Why This Feature Exists (First-Principles)
1. Absence of distinct repeating P waves ^[1]	No organised atrial depolarisation is discernible. Instead, the baseline shows chaotic, low-amplitude undulations (fibrillatory waves / f waves) ^[7]	In AF, there are 350–600 simultaneous micro-re-entrant wavefronts in the atria. No single wavefront is large enough to generate a discrete P wave on surface ECG. The summation of hundreds of tiny wavefronts produces the chaotic baseline — the fibrillary wave ^[7]
2. Irregular RR intervals (when AV conduction is present) ^[1]	R-R intervals are completely unpredictable — irregularly irregular ^[2]^[3]	The AV node is bombarded by chaotic, random impulses at 350–600/min. It conducts whichever impulses arrive after its refractory period has ended, but since the arriving impulses are themselves random, the conducted beats are at random intervals
3. Irregular atrial activity ^[1]	The atrial electrical activity on the baseline is disorganised — no repeating pattern, no isoelectric segment between "P waves"	Distinguishes AF from other rhythms where atrial activity IS organised (e.g. flutter = saw-tooth, AT = discrete abnormal P waves, MAT = ≥ 3 discrete P morphologies with isoelectric baseline preserved ^[3])

Key Point – AF is an ECG Diagnosis

You cannot diagnose AF on clinical grounds alone. An irregularly irregular pulse is highly suggestive, but the differential includes atrial flutter with variable block, MAT, and frequent ectopics ^[1]. You need the ECG to confirm. Conversely, some patients have AF that is only captured on ambulatory monitoring — a single resting ECG may be normal if the AF is paroxysmal.

Per the 2020 ESC guidelines (and reaffirmed in 2024 EHRA consensus), a minimum of 30 seconds of continuous AF on a single-lead or 12-lead ECG recording is required to make a definitive diagnosis. This threshold exists to avoid overcalling brief, non-sustained atrial arrhythmias.

Once AF is confirmed on ECG, you classify it by temporal pattern and valvular status (covered in the prior section). This is not part of "diagnostic criteria" per se, but is an essential next step:

Paroxysmal (< 7 days, self-terminating)
Persistent (> 7 days)
Long-standing persistent (> 12 months)
Permanent (accepted; no further rhythm control pursued)
Valvular (rheumatic MS, mechanical/bioprosthetic valve) vs Non-valvular

The algorithm below integrates the clinical pathway from initial suspicion through to definitive diagnosis, classification, aetiology workup, and risk stratification.

The GC lecture slide states: The aim of all Hx/PE/Ix is to arrive at: (1) Diagnosis — syncope/palpitation are not diagnoses, AF/complete heart block are; (2) Severity — too fast? too slow? haemodynamic compromise?; (3) Underlying cause — thyrotoxicosis? medications? ^[18]

3. Investigation Modalities — Systematic Approach

Think of investigations in AF as answering four questions:

Is it AF? → ECG / ambulatory monitoring
What is it doing to the heart? → Echo, BNP
Why does this patient have AF? → Bloods (TFT, electrolytes), Echo (structural), CXR (pulmonary)
What is the thromboembolic risk? → CHA₂DS₂-VASc, TOE (if considering cardioversion)

The single most important investigation. ECG: chamber enlargement, AF ^[20].

Finding	Interpretation	Why It Matters
Absent P waves + irregular baseline (fibrillatory waves) ^[7]	Confirms AF	Diagnostic criterion #1 and #3
Irregularly irregular RR intervals ^[7]	Confirms AF; assess ventricular rate	Guides rate control targets
Rapid ventricular response (> 100 bpm) ^[2]	Acute AF or inadequately controlled AF	Needs rate control; risk of tachycardia-induced cardiomyopathy
Slow ventricular response (< 60 bpm) ^[2]	If slow, suspect heart block ^[2]; also consider digoxin toxicity, excessive BB/CCB	May need Holter to assess for pauses → pacemaker
LVH (tall QRS voltages ± ST-T changes)	Suggests hypertensive heart disease as the cause	Machine may automatically change calibration due to LVH → ST-depression can't be appreciated → have to ask patient to get another ECG with correct calibration ^[7]
P mitrale (broad, bifid P wave in lead II or V3) ^[20]^[21]	LA dilatation ^[21] — suggests chronicity, possible mitral valve disease	Helps determine cause and severity
P pulmonale (tall, peaked P wave in II) ^[21]	RA dilatation ^[21] — suggests pulmonary hypertension or right heart disease	Seen if there is an underlying respiratory cause or longstanding MS with secondary PAH
RVH pattern (R > S in V1, right axis deviation)	Right ventricular hypertrophy — chronic pulmonary HTN	Suggests pulmonary cause (COPD, PE, PAH) or longstanding mitral stenosis
Delta waves (if in sinus rhythm at another time)	WPW / accessory pathway	Critical to identify because management of AF differs dramatically (no AV nodal blockers!)
Poor R wave progression / low voltage ^[6]	Underlying cardiomyopathy (DCM)	Suggests myocardial disease as the cause
ST depression / T wave inversion	May indicate ischaemia, LV strain, digoxin effect	Helps assess for IHD as a cause or demand ischaemia from rapid rate

ECG Calibration Trap

The ECG machine automatically changed the calibration... automatically adjusted the voltage... since the left ventricular hypertrophy... ST-depression, can't appreciate... have to ask patient to get another ECG with the correct calibration ^[7]. Always check the calibration marker on every ECG you read! Standard calibration = 10 mm/mV (1 mV = 2 large squares). If the machine has halved the standard, all voltages are artificially reduced and you will miss LVH criteria and ST changes.

Choice is dependent on how often patient gets symptoms → you want to catch those events ^[22]. Some indications are for diagnosis → you need the cardiac monitoring data as part of the diagnostic criteria ^[22].

Modality	Duration	When to Use	Key Findings
24-hour Holter monitor ^[2]	24–72 hours	For slow AF / long pauses ^[2]; frequent (daily) paroxysmal symptoms; assess rate control adequacy	Captures AF episodes, measures average/minimum/maximum ventricular rate, identifies significant pauses (> 3 seconds → pacemaker consideration)
Event recorder (external loop recorder)	2–4 weeks	Symptoms occurring weekly but not daily	Patient-activated recording when symptoms occur; can capture paroxysmal AF episodes
Implantable loop recorder (ILR)	Up to 3 years	Infrequent symptoms (e.g. monthly); cryptogenic stroke (to detect occult AF)	Continuously monitors; auto-detects AF episodes; increasingly used post-cryptogenic stroke to identify "subclinical" AF requiring anticoagulation
Smartwatch / wearable ECG	Continuous	Screening in high-risk populations; patient self-monitoring	Can detect irregular pulse; single-lead ECG confirmation. Emerging role but requires confirmation with medical-grade ECG

Investigation	Rationale	Key Findings and Interpretation
CBC ^[2]	Anaemia → high-output state → can trigger or worsen AF. WCC → infection/sepsis as trigger	Hb < 70 g/L may be a contributing factor; leucocytosis suggests infectious trigger
LRFT (Liver and Renal Function Tests) ^[2]	Baseline before starting anticoagulation (NOAC dosing requires CrCl). Liver disease → coagulopathy affecting anticoagulation choice	CrCl determines NOAC dose (e.g. dabigatran contraindicated if CrCl < 30; apixaban can be used down to CrCl 15). Elevated ALT/AST → consider alcohol-related cause or hepatic congestion from HF
Bone profile (Calcium) ^[2]	Hypercalcaemia can precipitate arrhythmias	Corrected calcium > 2.6 mmol/L warrants investigation for hyperparathyroidism, malignancy
TFT (Thyroid Function Tests) ^[2]^[8]^[18]	Essential — must exclude thyrotoxicosis as a reversible cause. Underlying cause — thyrotoxicosis? ^[18]. AF is a complication of Graves' disease ^[8]	Suppressed TSH with elevated fT4/fT3 → thyrotoxicosis. If confirmed, AF often reverts to sinus rhythm once euthyroid. Subclinical hyperthyroidism (low TSH, normal fT4) also needs monitoring for AF and osteoporosis ^[8]
Magnesium ^[2]	Hypomagnesaemia predisposes to AF and reduces efficacy of rate/rhythm control agents	Mg < 0.7 mmol/L → replace before attempting cardioversion; improves success of rhythm control
Potassium ^[2]	Hypokalaemia → ECG changes (U waves, flat T, prolonged QT), increased arrhythmia risk	Cardiac arrhythmia, particularly when K < 2.0 mmol/L ^[23]. Target K > 4.0 mmol/L in patients with arrhythmias
Coagulation profile (PT/INR, APTT)	Baseline before anticoagulation. Also relevant if liver disease suspected	Prolonged INR without warfarin → liver disease → affects anticoagulation strategy
Troponin	Rule out ACS as the trigger for new-onset AF, or detect demand ischaemia from rapid ventricular rate	Mildly elevated troponin from rate-related demand ischaemia is common and doesn't automatically mean ACS. Markedly elevated + ischaemic symptoms → consider ACS as the primary problem
BNP / NT-proBNP	Assess for heart failure — both as a cause and consequence of AF	Elevated BNP/NT-proBNP in AF may reflect HF or can be mildly raised from AF alone (atrial stretch → ANP/BNP release). Very high levels suggest significant HF requiring echocardiography

3.4 Echocardiography

Echocardiogram for structural heart disease and LA thrombus ^[2]. This is the key imaging investigation in AF because it answers several questions simultaneously.

Parameter	What to Look For	Clinical Significance
LA size / volume	LA dilatation (normal LA anteroposterior diameter < 4.0 cm; normal indexed volume < 34 mL/m²)	Dilated LA → substrate for AF; predicts lower success of cardioversion and higher recurrence. Causes: HTN, mitral valve disease, cardiomyopathy
LV function (LVEF)	Systolic function (normal ≥ 50%)	LVEF determines rate control strategy ^[2]: EF ≥ 40% → BB or CCB; EF < 40% → BB or digoxin (avoid non-DHP CCB). Also detects tachycardia-induced cardiomyopathy (reversible ↓ EF from prolonged rapid AF)
LV diastolic function	E/A ratio, E/e′, deceleration time	Diastolic dysfunction → ↑ LA pressure → LA dilatation → AF. Also means the patient is heavily dependent on atrial kick — loss of this in AF causes disproportionate symptoms
Valvular heart disease ^[1]^[20]	Mitral stenosis (significant if < 1.5 cm² ^[21]), mitral regurgitation, aortic stenosis/regurgitation	Determines valvular vs non-valvular AF → dictates anticoagulation choice (warfarin vs NOAC). Echocardiogram allows direct visualisation of valvular architecture, chamber size, chamber function ^[20]
Regional wall motion abnormalities ^[24]	Hypokinesis, akinesis, dyskinesis	Suggests underlying IHD (prior MI) as cause of AF
RV function / RVSP	Tricuspid regurgitant jet velocity → estimated PASP. RV systolic pressure = PAH ^[22]	Elevated RVSP suggests pulmonary hypertension — either from chronic left heart disease or primary pulmonary cause
Pericardial effusion	Effusion around the heart	May suggest pericarditis/myocarditis as the trigger
4-chamber dilatation + ↓ LV systolic function ^[24]	Dilated cardiomyopathy pattern	DCM as the cause of AF; ECG in DCM: AF, AV block, LBBB ^[19]

Transoesophageal for those heart chambers located posteriorly → left atrial appendage, or for patients with thick chest wall (e.g. obese patients) ^[22]. Better visualisation of vegetations ^[22].

Indication in AF	Rationale
Pre-cardioversion if AF duration > 48 hours (or unknown) and patient not on ≥ 3 weeks therapeutic anticoagulation	Most sensitive and specific to detect LA thrombus as a source of systemic embolism ^[1]. If thrombus is present → cardioversion is contraindicated (risk of dislodging clot → stroke). Must anticoagulate for ≥ 3 weeks, then repeat TOE before cardioversion
Suspected infective endocarditis	TOE is superior to TTE for detecting vegetations, especially on mitral valve (posterior structure best seen by TOE)
Poor TTE windows	Obese patients, those on mechanical ventilation, post-surgical patients

When Is TOE Required Before Cardioversion?

If AF has been present for > 48 hours or duration is unknown, and the patient has NOT been on therapeutic anticoagulation for ≥ 3 weeks, you must perform TOE to rule out LA/LAA thrombus before cardioversion. If the patient HAS been on ≥ 3 weeks of therapeutic anticoagulation, you can proceed with cardioversion without TOE (the anticoagulation should have prevented new thrombus formation and allowed existing thrombus to organise/resolve). If AF is < 48 hours, thrombus formation is unlikely and cardioversion can proceed directly (though some guidelines still recommend anticoagulation peri-cardioversion).

Finding	Interpretation
Cardiomegaly (CTR > 50%)	Suggests underlying structural heart disease (DCM, valvular disease)
LA enlargement	Straightening or convexity of the left heart border (left atrial appendage enlargement); double density sign behind the right heart border; splaying of the carina (LA pushes up the left main bronchus) ^[21]
Pulmonary congestion	Upper lobe diversion, Kerley B lines, alveolar oedema → suggests HF as cause/consequence of AF
Kerley A and B lines ^[21]	Interstitial oedema from elevated LA pressure → suggests mitral stenosis or LV failure
Pleural effusion	May indicate HF (bilateral, R > L)
Hyperinflated lungs	COPD → hypoxia-driven AF

Investigation	Indication	Key Findings
Exercise testing ^[20]	Objective assessment of functional capacity ^[20]; assess rate control during exercise; evaluate for exercise-induced AF; detect underlying IHD	Inadequate rate control if HR remains disproportionately elevated; ischaemic changes suggest CAD
Cardiac MRI	Suspected cardiomyopathy (DCM, HCM, ARVC); cardiac amyloidosis; myocarditis	Late gadolinium enhancement pattern → indicating fibrosis ^[19]; atrial fibrosis mapping is an emerging tool for AF ablation planning
Cardiac catheterisation ^[20]	Assess any associated coronary artery disease; visualise pressure gradient; preoperative planning ^[20]	Required before cardiac surgery (e.g. mitral valve replacement + CABG)
CT pulmonary angiogram	Suspected pulmonary embolism as trigger for AF	PE can cause atrial arrhythmias (e.g. AF) — identified as ECG finding in PE ^[25]
Sleep study (polysomnography)	Suspected obstructive sleep apnoea	OSA is an independent risk factor for AF and AF recurrence post-cardioversion; treating OSA improves AF control
Electrophysiology study (EPS)	Pre-ablation mapping; suspected accessory pathway (WPW)	Identifies trigger foci (PV sleeves), maps re-entrant circuits; determines if accessory pathway is high-risk (shortest pre-excited RR < 250 ms → conduction too fast, patient requires ablation ^[22])

These are the high-yield patterns from the cardiology data interpretation session ^[7]:

ECG Pattern	Interpretation	Clinical Action
Irregular narrow complex tachycardia, no P wave → AF ^[7]	Standard AF with rapid ventricular response	Rate control ± rhythm control
AF with fibrillary wave ^[7]	Same as above — the fibrillary wave is the hallmark of AF	Distinguish from flutter (saw-tooth) and MAT (discrete P waves)
Irregular wide complex tachycardia, axis doesn't change every beat → AF with accessory pathway conduction ^[7]	Either RBBB or accessory pathway ^[7] — requires careful distinction	If accessory pathway → avoid AV nodal blockers; DC cardioversion or procainamide
AF with LVH → machine changed calibration → ST-depression can't be appreciated ^[7]	Left ventricular hypertrophy with ST-T abnormalities ^[7]	Request repeat ECG with standard calibration (10 mm/mV)
Saw-tooth appearance → atrial flutter with 2:1 AV block, NOT AF ^[7]	Regular narrow complex ~150 bpm	Don't confuse with AF — flutter has organised atrial activity

Once AF is confirmed, the next step is risk stratification for thromboembolism. This was covered in detail in the prior section, but it is integral to the diagnostic algorithm:

CHA₂DS₂-VASc: Anticoagulation if ≥ 2 for males / ≥ 3 for females ^[14]

Component	Points
C — Congestive heart failure	1
H — Hypertension	1
A₂ — Age ≥ 75	2
D — Diabetes mellitus	1
S₂ — Stroke / systemic thromboembolism	2
V — Vascular disease	1
A — Age 65–74	1
Sc — Sex category (female)	1

Bleeding risk is assessed with the HAS-BLED score (Hypertension, Abnormal renal/liver function, Stroke, Bleeding history, Labile INR, Elderly > 65, Drugs/alcohol). A high HAS-BLED score does NOT mean "don't anticoagulate" — it means "monitor closely and modify reversible bleeding risk factors."

Category	Investigations	Key Question Answered
Confirm diagnosis	12-lead ECG (± ambulatory monitoring)	Is it AF?
Assess cause	TFT ^[2]^[18], K, Mg ^[2], CBC, LRFT, Echo ^[2]	Why does this patient have AF?
Assess impact	Echo (LVEF, LA size), BNP, CXR	What is AF doing to the heart?
Assess risk	CHA₂DS₂-VASc, HAS-BLED	Should we anticoagulate?
Pre-cardioversion	TOE (if AF > 48h and not anticoagulated ≥ 3 weeks)	Is there a clot in the LAA?
Selected cases	Holter (pauses), sleep study (OSA), EPS (ablation planning), cardiac MRI (cardiomyopathy)	Specific clinical questions

High Yield Summary — Diagnosis and Investigations of AF

AF is an ECG diagnosis: absent P waves + fibrillatory baseline + irregularly irregular RR. Minimum 30 seconds of continuous recording.
If suspected but not captured on resting ECG: use ambulatory monitoring — Holter (daily symptoms), event recorder (weekly), ILR (infrequent or cryptogenic stroke).
Mandatory bloods in ALL new AF: CBC, LRFT, TFT, K, Mg, bone profile.
Echo is essential: determines cause (valvular, structural), LVEF (guides rate control strategy), LA size (predicts cardioversion success).
TOE before cardioversion if AF > 48 hours and not on ≥ 3 weeks anticoagulation → rule out LA/LAA thrombus.
Always check TFT — thyrotoxicosis is a reversible cause. Always check K and Mg — easily correctable factors that improve treatment response.
ECG calibration pitfall: LVH may cause machine to auto-adjust voltage → miss ST changes. Always verify calibration mark.
CHA₂DS₂-VASc is part of the diagnostic workup, not just management — it determines anticoagulation from day one.

Active Recall - Diagnosis and Investigations of AF

References

^[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – AF: Diagnosis, DDx (p.498–502) ^[2] Senior notes: Maksim Medicine Notes.pdf – Cardiology, Atrial Fibrillation (p.23) ^[3] Senior notes: Ryan Ho Cardiology.pdf – MAT, AF sections (p.92–94) ^[6] Senior notes: Block A - Three Cases of Dyspnea.pdf (p.1) ^[7] Senior notes: Block A - Cardiology Data Interpretation.pdf (p.8, p.11) ^[8] Senior notes: Block A - I am losing weight and sweating all the time.pdf (p.11, p.43) ^[14] Lecture slides: GC 089. Syncope and irregular heart beat.pdf (p.26) ^[18] Lecture slides: GC 089. Syncope and irregular heart beat.pdf (p.7) ^[19] Senior notes: Block A - Inherited Cardiac conditions.pdf (p.7–8) ^[20] Senior notes: Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf (p.3) ^[21] Senior notes: Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf (p.8–9) ^[22] Senior notes: Block A - Introduction to CVS investigations (including ECG).pdf (p.11) ^[23] Senior notes: Block A - Electrolyte and Acid-Base Disorders.pdf (p.27) ^[24] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – HF: Investigations (p.366) ^[25] Lecture slides: Respiratory Two cases of acute shortness of breath - case 1.pdf (p.6)

Management of Atrial Fibrillation

Management: Rate control + Rhythm control + Anticoagulation (SAQ!!) ^[2]

This triad should be your reflex whenever you encounter AF — in any exam question, in any clinical scenario, in any OSCE station. Think of it as:

Rate control — protect the heart from the rapid ventricular response (the acute danger)
Rhythm control — restore and maintain sinus rhythm where appropriate (the long-term goal in some patients)
Anticoagulation — protect the brain from embolic stroke (the silent killer)

Every single management decision in AF maps onto one of these three pillars.

3. Acute Management

High Yield – Unstable AF = DC Cardioversion

If the patient is haemodynamically unstable (hypotension, cardiogenic shock, acute pulmonary oedema, ongoing myocardial ischaemia, altered consciousness), DC cardioversion (120–200J biphasic) ^[2] takes priority over everything else. Do not waste time with pharmacological rate control. Do not worry about anticoagulation status — the risk of stroke from cardioverting is far less than the risk of death from haemodynamic collapse.

Synchronized cardioversion — the shock is synchronised with the R wave to avoid delivering energy during the vulnerable period of ventricular repolarisation (the T wave), which would risk inducing VF ^[26].

Energy levels (from the ACLS/critical care framework) ^[26]:

For AF (irregular narrow complex): give 120–200J biphasic and increase stepwise ^[26]
Requires consent with sedation (midazolam) + analgesics (morphine) as it is quite painful ^[26]
Absolute contraindication: sinus tachycardia (only absolute contraindication) ^[26]

3.2 Haemodynamically Stable AF

Treat underlying cause if possible: e.g. hyperthyroidism, PE, sepsis/pneumonia, hypoK/Mg ^[2]

This is crucial — if you don't address the trigger, rate/rhythm control will be a losing battle. For example:

Thyrotoxicosis → antithyroid drugs + beta-blockers
Sepsis → antibiotics + source control
Hypokalaemia → IV/oral potassium replacement (target K > 4.0)
Hypomagnesaemia → IV MgSO₄
Alcohol → cessation, hydration, electrolyte correction

Must check whether there are features of APO → avoid BB / CCB ^[2]

This is because both beta-blockers and non-dihydropyridine CCBs have negative inotropic effects — in a patient with acute pulmonary oedema (APO), these drugs can worsen cardiac output and precipitate cardiogenic shock.

Clinical Scenario	First-Line Agents	Mechanism	Practical Details
EF ≥ 40% (preserved systolic function) ^[2]	Beta-blockers: e.g. IV metoprolol 2–5 mg bolus over 2 min ^[2]	β₁-blockade → ↓ AV nodal conduction velocity + ↑ AV nodal refractory period → fewer impulses reach ventricles	Can repeat every 5 min up to 15 mg total. Convert to oral once stable (e.g. bisoprolol 2.5–10 mg OD)
EF ≥ 40% (alternative) ^[2]	Non-DHP CCB: e.g. IV diltiazem 0.25 mg/kg bolus over 2 min or IV verapamil ^[2]	Block L-type calcium channels in AV node → ↓ conduction velocity → ↓ ventricular rate	Contraindicated in HFrEF — negative inotropy can precipitate shock ^[2]^[27]
EF < 40% (reduced systolic function) ^[2]	Beta-blockers: e.g. IV metoprolol 2–5 mg bolus over 2 min ^[2]	Same mechanism as above. Beta-blockers have proven mortality benefit in HFrEF (when used carefully at low starting doses)	Start low, go slow. Avoid if acute decompensation with cardiogenic shock
EF < 40% (alternative/add-on) ^[2]	IV digoxin 0.25 mg ^[2]	Digoxin ("digit-" from Digitalis purpurea, foxglove) increases vagal tone → ↑ AV nodal refractory period → ↓ ventricular rate. Also a mild positive inotrope (inhibits Na⁺/K⁺-ATPase → ↑ intracellular Ca²⁺ → ↑ contractility)	Safe in HFrEF because it does NOT reduce contractility. Onset is slow (hours) compared to BB/CCB (minutes). Useful as an add-on or when BB/CCB are contraindicated
APO / acute decompensated HF	IV digoxin (preferred) or IV amiodarone	Digoxin: as above. Amiodarone: multi-channel blocker with rate-slowing and some rhythm-controlling properties	Amiodarone has some negative inotropic effect but less than BB/CCB; used when other agents fail or are contraindicated

From the HKU Handbook of Internal Medicine 2024 ^[28]:

Atrial flutter/fibrillation post-MI:

Digoxin 0.25 mg IV/PO stat, then 0.25 mg PO q8h for 2 more doses as loading, maintenance 0.0625–0.25 mg daily ^[28]

Diltiazem 5–15 mg IV over 5–10 mins, then 5–15 μg/kg/min ^[28]

Amiodarone 5 mg/kg IV infusion over 60 mins as loading, maintenance 600–900 mg infusion/24h ^[28]

Why Is Digoxin Often First-Line Post-MI?

Post-MI patients frequently have reduced LVEF. Non-DHP CCBs (verapamil, diltiazem) are contraindicated if BP low or on beta-blocker or reduced LVEF ^[3]. Digoxin provides rate control without negative inotropy, making it safer in this context.

4.1 Comparing the Two Strategies

Comparing rate control vs rhythm control: similar mortality and thromboembolic events ^[2]. The landmark AFFIRM and RACE trials showed no mortality difference. However, the more recent EAST-AFNET 4 trial (2020) suggested that early, systematic rhythm control (within 1 year of diagnosis) may reduce cardiovascular outcomes — so the pendulum is shifting.

	Rate Control	Rhythm Control
Goal	Accept AF, control ventricular rate to prevent symptoms and tachycardia-induced cardiomyopathy	Restore and maintain sinus rhythm
Advantages	More simplified regimens, cheaper, fewer side effects ^[2]	Better symptom relief, may prevent atrial remodelling, avoids long-term haemodynamic compromise of AF
Preferred if	Asymptomatic/mildly symptomatic, older ^[2]	Symptomatic (e.g. HF), younger, shorter disease duration (may prevent ventricular remodelling) ^[2]
Anticoagulation	Still required based on CHA₂DS₂-VASc	Still required — catheter ablation provides symptomatic relief only, not lower risk of stroke → anticoagulation may still be required ^[2]

High Yield – AFFIRM Trial Conclusion

Rate control if asymptomatic/mildly symptomatic, older. Rhythm control if symptomatic (e.g. HF), younger, shorter disease duration ^[2]. However, with EAST-AFNET 4 data, the trend is now towards earlier rhythm control in many patients. The in-house exam will likely still test the classic AFFIRM framework.

5. Chronic Rate Control — Details

Target HR < 80 if symptomatic, < 110 if asymptomatic ^[2]

The RACE II trial showed that lenient control (< 110) was non-inferior to strict control (< 80) for composite cardiovascular outcomes
But if patients remain symptomatic despite lenient control, aim for stricter targets

Agent	Class	Mechanism	Indication	Contraindication
Beta-blockers (e.g. bisoprolol, metoprolol, atenolol) ^[2]^[27]	Class II	β₁-blockade → ↓ AV conduction + ↑ AV refractory period	First-line, most effective and common ^[2]. Ventricular rate control in AF ^[27]. Safe in HFrEF (proven mortality benefit)	AV block, sinus node dysfunction, bradycardia; bronchial asthma; vasospasm angina, PAD, Raynaud; depression ^[27]
Non-DHP CCB (verapamil, diltiazem) ^[2]^[27]	Class IV	Block L-type Ca²⁺ channels in AV node → ↓ conduction	Ventricular rate control in AF ^[27]. Good for patients where BB contraindicated (e.g. asthma)	Contraindicated in HF (EF < 40%) ^[2]^[27]; AV block; concurrent BB (risk of profound bradycardia)
Digoxin ^[2]	—	↑ Vagal tone → ↑ AV refractory period. Also mild positive inotrope	Preferred if HFrEF ^[2]; useful as add-on. Controls resting HR well but poor exercise HR control (vagal tone ↓ during exercise)	Renal impairment (renally excreted → accumulation → toxicity); hypokalaemia (↑ digoxin toxicity); WPW (paradoxical ↑ ventricular rate)
Amiodarone ^[2]	Class III (multi-channel)	K⁺, Na⁺, Ca²⁺ channel blocker + anti-adrenergic. Slows AV conduction	Last resort ^[2] for rate control. Used when other agents fail, or in acute setting with HFrEF	Long-term toxicity: thyroid, pulmonary fibrosis, hepatotoxicity, corneal deposits, photosensitivity. Avoid in younger patients if possible

Surgical: when drugs fail ^[2]:

Method	Description	Indication
Block and pace ^[2]	AV node blockade drugs + pacemaker (usually VVI(R) / DDD(R)) ^[2]	Drugs partially slow AV conduction; pacemaker provides backup if excessive slowing
Ablate and pace ^[2]	AV node RFA + pacemaker (usually VVI(R) / DDD(R)) ^[2]	Complete AV node ablation creates intentional complete heart block; pacemaker provides reliable ventricular pacing. Definitive rate control. Single-chamber ventricular pacing → indicated in AF ^[17]

Why VVI pacing in AF? Because the atria are fibrillating — there is no point sensing or pacing the atrium. You only need to ensure adequate ventricular rate. "VVI" = Ventricle paced, Ventricle sensed, Inhibited (i.e. the pacemaker only fires if the ventricle doesn't depolarise on its own within a set interval).

6. Rhythm Control — Details

Symptomatic AF despite adequate rate control
Young patients (< 65) with new-onset AF
Heart failure caused or worsened by AF (tachycardia-induced cardiomyopathy)
First episode of AF
Patient preference
Symptomatic (e.g. HF), younger, shorter disease duration ^[2]

Aspect	Detail
Mechanism	Delivery of a current over a very short interval → depolarise heart → abolish all prevailing abnormal rhythm → hope that SAN will take the lead again as pacemaker ^[26]
Energy	120–200J biphasic for AF ^[26] (start at 120J, increase stepwise if unsuccessful)
Synchronisation	Synchronized shock with QRS complex → avoid R-on-T phenomenon (torsades then VF) ^[26]
Sedation	Requires consent with sedation (midazolam) + analgesics (morphine) ^[26]
Timing	If AF < 48h → can cardiovert directly (low thrombus risk). If AF > 48h or duration unknown → either TOE to exclude thrombus OR ≥ 3 weeks therapeutic anticoagulation first
Post-cardioversion	Anticoagulate for ≥ 4 weeks post-cardioversion (even if successful), because atrial "stunning" persists → thrombus can still form. Then reassess long-term anticoagulation need with CHA₂DS₂-VASc

6.3 Pharmacological Cardioversion (Antiarrhythmic Drugs)

This is where the Vaughan Williams classification becomes clinically relevant. The choice depends on whether the patient has structural heart disease or not.

From Felix Lai's comprehensive table ^[1]:

Feature	Detail
Mechanism	Na⁺ channel blockers ^[1]
Use	Cardioversion = ✓; Maintenance = ✓ ^[1]
Preferred in	Patients with no or minimal structural heart disease (CAD/MI/HF/HT/LVH) ^[1]
"Pill-in-the-pocket" strategy	Selected patients can self-administer to terminate AF outside the hospital shortly after onset of symptomatic AF ^[1]
Contraindications	CAD (drug-induced ventricular proarrhythmia; increases mortality in post-MI patients) ^[1]; HF (ventricular proarrhythmia) ^[1]; LV dysfunction (negatively inotropic) ^[1]; Atrial flutter (slowing of atrial rate → 1:1 AV conduction with paradoxically increased ventricular rate → concomitant AV nodal blocking agents required) ^[1]^[2]

Why Are Class IC Agents Dangerous in Structural Heart Disease?

Class IC agents block Na⁺ channels, which slows conduction velocity throughout the heart. In patients with scarred myocardium (post-MI) or impaired ventricular function, this creates new conduction inhomogeneities → sets up the substrate for re-entrant ventricular arrhythmias (VT/VF). This was demonstrated in the CAST trial, which showed increased mortality in post-MI patients on flecainide/encainide ^[1]. Hence the absolute rule: no Class IC agents if structural heart disease.

The flutter risk: by slowing the atrial flutter rate (e.g. from 300 to 200 bpm), the AV node may suddenly be able to conduct 1:1 (it could block 300 bpm but not 200 bpm) → ventricular rate jumps to 200 bpm → haemodynamic collapse. This is why concomitant AV nodal blocking agents (BB/CCB) are required whenever Class IC agents are used ^[1]^[2].

From Felix Lai's table and Maksim notes ^[1]^[2]:

Agent	Use	Preferred In	Key Issues
Amiodarone ^[1]	Cardioversion = ✓; Maintenance = ✓	MOST effective antiarrhythmic for maintenance of sinus rhythm. Drug of choice in post-MI/CAD, HF, HTN with LVH ^[1]	Prolonged QT → TdP; ILD (irreversible!); thyroid dysfunction; bradycardia; phlebitis (IV); inhibits CYP3A4 and CYP2C9 → dose adjustment for warfarin (↑INR) and digoxin ^[1]. Avoid in younger patients ^[1] due to cumulative toxicity. Contraindicated: prolonged QT, sinus/AV node dysfunction, lung disease ^[1]
Dronedarone ^[1]	Cardioversion = ✗; Maintenance = ✓	Post-MI/CAD. Structural analogue of amiodarone ^[1] without iodine moiety (less thyroid/pulmonary toxicity)	Less effective than amiodarone. Contraindicated in NYHA III–IV HF (ANDROMEDA trial showed increased mortality) and permanent AF (PALLAS trial showed increased cardiovascular events)
Sotalol ^[2]	Cardioversion = limited; Maintenance = ✓	Patients with IHD	Non-selective beta-blocker + Class III (K⁺ channel blocker). S/E: QT prolongation → TdP ^[2]. Contraindicated in HFrEF (negative inotropy) and asthma
Dofetilide ^[2]	Cardioversion = ✓; Maintenance = ✓	HF patients (DIAMOND trial showed no increase in mortality)	Pure IKr blocker. QT prolongation → TdP — requires in-hospital initiation with QT monitoring

Feature	Detail
Mechanism	Na⁺ channel blocker (intermediate kinetics) + some K⁺ channel blocking
Use	Acute pharmacological cardioversion; also used for AF with WPW (slows conduction in accessory pathway)
Key role in AF	IV procainamide is one of the safest options for acute wide-complex irregular tachycardia when WPW is suspected
Side effects	Hypotension, QT prolongation, lupus-like syndrome (chronic use)

Catheter ablation (RFA/cryoablation): electrically isolate areas around pulmonary veins ^[2]^[6]

Aspect	Detail
Principle	AF ablation as a treatment → electrically isolate the PV ^[6]. Since the pulmonary vein sleeves are the main trigger source, creating circumferential ablation lesions around the PV ostia electrically disconnects them from the left atrium
Techniques	Radiofrequency ablation (RFA) — uses heat; Cryoablation (cryoballoon) — uses cold. Pulsed field ablation (PFA) — emerging technique using non-thermal electric fields
Efficacy	75%, much lower if persistent AF ^[2]. Paroxysmal AF responds better because the substrate is less advanced
Indications	Symptomatic paroxysmal AF refractory to ≥ 1 antiarrhythmic drug (Class I recommendation); increasingly used as first-line in paroxysmal AF (EARLY-AF, STOP-AF, CABANA trials). Also for persistent AF in selected patients
Critical point	Symptomatic relief only, not lower risk of stroke → anticoagulation may still be required ^[2]
Complications	PV stenosis (~1%), cardiac tamponade (~1%), stroke (~0.5%), phrenic nerve palsy (cryoablation), oesophageal fistula (rare but fatal)

Surgery: MAZE ablation ^[2]

Creates a "maze" of surgical incisions (or ablation lines) in both atria to interrupt re-entrant circuits and channel electrical impulses along a defined pathway from SA node to AV node
Usually performed concomitantly with other cardiac surgery (e.g. mitral valve surgery + MAZE)
Rarely done as a standalone procedure

7. Anticoagulation — The Third Pillar

Indications (must know!!) ^[2]:

All valvular AF (high stroke risk) ^[2] — warfarin only
Non-valvular AF with CHA₂DS₂-VASc score ≥ 2 for male, ≥ 3 for female ^[2]^[14]

Anticoagulation if ≥ 2 for M / ≥ 3 for F ^[14] — from the GC lecture slide on syncope and irregular heartbeat.

CHA₂DS₂-VASc Score	Recommendation
0 (male) or 1 (female, where 1 = female sex alone)	No anticoagulation
1 (male) or 2 (female)	Consider anticoagulation — weigh benefits vs bleeding risk
≥ 2 (male) or ≥ 3 (female)	Oral anticoagulation recommended ^[2]^[14]

Scenario	Agent	Target / Details
Valvular AF (rheumatic MS, mechanical valve)	Warfarin	INR 2.0–3.0 (native valve); 2.5–3.5 (mechanical valve). This is the only native valvular disease that requires warfarin, cannot use NOAC or DOAC ^[6]. Valvular AF, prosthetic valves → contraindicated for DOAC ^[29]
Non-valvular AF	NOAC preferred over warfarin	See table below

NOAC Comparison

NOAC	Target	Dosing	Renal Threshold	Reversal Agent	Key Points
Dabigatran (Pradaxa)	Direct thrombin (IIa) inhibitor	150 mg BID (110 mg BID if ≥ 80y or high bleeding risk)	Contraindicated if CrCl < 30	Idarucizumab ^[29]	Only NOAC with a fully validated reversal agent. BID dosing less convenient. GI side effects (dyspepsia) common
Rivaroxaban (Xarelto)	Direct factor Xa inhibitor	20 mg OD with food (15 mg OD if CrCl 15–49)	Caution if CrCl < 15	Andexanet alfa (limited)	OD dosing (convenient). Must take with food (improves absorption by ~40%)
Apixaban (Eliquis)	Direct factor Xa inhibitor	5 mg BID (2.5 mg BID if ≥ 2 of: age ≥ 80, weight ≤ 60 kg, Cr ≥ 133 μmol/L)	Can be used down to CrCl ~15	Andexanet alfa (limited)	Least renal excretion (~27%) → safest in CKD. Lowest bleeding risk in ARISTOTLE trial. Often first choice in elderly
Edoxaban (Lixiana)	Direct factor Xa inhibitor	60 mg OD (30 mg OD if CrCl 15–50, weight ≤ 60 kg, or concomitant P-gp inhibitor)	Not recommended if CrCl > 95 (paradoxically less effective)	Andexanet alfa (limited)	OD dosing. Unique upper CrCl limit

NOAC Reversal and Bleeding Management

Idarucizumab ("I dare you sizumab") ^[29] — the monoclonal antibody fragment that binds and neutralises dabigatran. Instant and complete reversal. Andexanet alfa — recombinant modified factor Xa that acts as a decoy to bind factor Xa inhibitors. At the moment not fully registered as an antidote; clinical benefit not well established from big clinical studies; case by case, specific use, grey area ^[29].

For all NOACs: if active bleeding → stop NOAC, activate massive transfusion protocol, give tranexamic acid, consider PCC (prothrombin complex concentrate 4-factor) as a non-specific reversal measure.

7.3 Special Anticoagulation Scenarios

Medical treatment for MS: anticoagulation (valvular AF) — Warfarin, for those with history of embolisation, or paroxysmal/sustained AF ^[20]. Warfarin with target INR = 2.5 ^[30]. NOAC not powerful enough; in mitral stenosis the blood is basically stagnant in the left atrium, massive chance of developing clots ^[20].

This is a common clinical dilemma: the patient needs anticoagulation for AF AND dual antiplatelet therapy (DAPT) for their stent.

"Triple therapy" (OAC + aspirin + P2Y12 inhibitor) carries very high bleeding risk
Current approach: short-duration triple therapy (1–4 weeks) → then dual therapy (OAC + single antiplatelet, usually clopidogrel) for up to 12 months → then OAC alone
In general, patients with CAD who undergo PCI need to be on double antiplatelet therapy for 1 year ^[29] — but in AF patients, the duration is shortened to reduce bleeding

Warfarin is teratogenic (especially in first trimester — nasal hypoplasia, stippled epiphyses = "warfarin embryopathy"). NOACs are also contraindicated in pregnancy (insufficient safety data).

First trimester: LMWH (enoxaparin)
Second and third trimester: LMWH or warfarin (warfarin relatively safer after organogenesis)
Peripartum: switch back to LMWH (shorter half-life, reversible with protamine)

From Felix Lai's comprehensive hypertension management table ^[31]:

Atrial fibrillation (prevention): ACEI/ARB and BB are recommended ^[31] Atrial fibrillation (ventricular rate control): BB and CCB ^[31]

This highlights that treating hypertension with ACEI/ARB may prevent AF development by reducing LA pressure overload and subsequent remodelling.

8. Management in Special Contexts

Beta-blockers (propranolol) are first-line for rate control — they also control adrenergic symptoms of thyrotoxicosis (tremor, sweating, tachycardia)
Graves' disease complicated by AF → requires more aggressive treatment → can go directly for definitive therapy (radioactive ablation, thyroidectomy) ^[8]
AF often reverts to sinus rhythm once patient becomes euthyroid → avoid antiarrhythmics if possible until thyroid status normalised

HFpEF management — Treat precipitating factors, e.g. AF ^[32]:

Rate control: Beta-blocker, verapamil, diltiazem ^[32] — slowing HR increases diastolic filling time, which is particularly important in HFpEF where the stiff ventricle needs longer to fill
Rhythm control is often more beneficial in HFpEF than HFrEF because these patients are heavily dependent on atrial kick

What to do	What to NEVER do
DC cardioversion (if unstable)	AV nodal blockers: digoxin, verapamil, diltiazem (paradoxically enhance accessory pathway conduction)
IV procainamide or IV amiodarone (if stable) — slow accessory pathway conduction
Definitive: catheter ablation of accessory pathway

WPW and sudden cardiac death → if shortest pre-excited RR < 250 ms, conduction too fast, patient requires ablation ^[22]

Very common (30–40% post-CABG, up to 60% post-valve surgery)
Often self-limiting within 6–8 weeks
Acute: rate control with BB (first-line) or amiodarone
Prophylaxis: perioperative amiodarone or BB reduces incidence
Anticoagulation: if AF persists > 48h, follow standard CHA₂DS₂-VASc guidelines

For patients who cannot tolerate long-term anticoagulation (e.g. recurrent life-threatening bleeding, intracranial haemorrhage):

Watchman device — a plug inserted percutaneously into the LAA via transseptal puncture → seals the LAA → prevents thrombus from embolising
Evidence: PROTECT-AF and PREVAIL trials showed non-inferiority to warfarin
Not yet a first-line alternative to NOACs, but an important option in selected patients

High Yield Summary – Management of AF

Three pillars: Rate control + Rhythm control + Anticoagulation — mention all three in EVERY exam answer.
Acute unstable AF: DC cardioversion 120–200J biphasic, synchronised. No delay.
Acute stable AF: Treat cause first. Rate control: BB or CCB if EF ≥ 40%; BB or digoxin if EF < 40%. Avoid BB/CCB if APO.
Rate vs rhythm: AFFIRM showed similar mortality. Rate control = simpler, cheaper, fewer side effects (preferred if older, asymptomatic). Rhythm control = if young, symptomatic, HF, short disease duration.
Rate control targets: HR < 110 if asymptomatic (lenient), < 80 if symptomatic (strict).
Rhythm control drugs: No structural heart disease → Class IC (flecainide). Structural HD/HF → Class III (amiodarone). Class IC is CONTRAINDICATED in structural heart disease (proarrhythmic).
Catheter ablation: PV isolation. 75% success (paroxysmal). Symptomatic relief only — does NOT eliminate stroke risk → continue anticoagulation.
Anticoagulation: All valvular AF → warfarin. Non-valvular AF → CHA₂DS₂-VASc ≥ 2M/≥ 3F → NOAC preferred.
Valvular AF (rheumatic MS, mechanical valve): Warfarin ONLY. NOACs contraindicated.
AF with WPW: NEVER AV nodal blockers. Use DC cardioversion or IV procainamide.

Active Recall - Management of AF

References

^[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – AF Treatment: Antiarrhythmic drugs table (p.504) ^[2] Senior notes: Maksim Medicine Notes.pdf – Cardiology, AF chronic management (p.24) ^[3] Senior notes: Ryan Ho Cardiology.pdf – AF treatment, post-MI arrhythmias (p.93, p.139) ^[6] Senior notes: Block A - Three Cases of Dyspnea.pdf (p.3) ^[8] Senior notes: Block A - I am losing weight and sweating all the time.pdf (p.11) ^[14] Lecture slides: GC 089. Syncope and irregular heart beat.pdf (p.26) ^[17] Senior notes: Block A - Syncope and irregular heartbeat_ Cardiac arrhythmia; Heart blocks, Bradycardia.pdf (p.30) ^[20] Senior notes: Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf (p.12) ^[22] Senior notes: Block A - Introduction to CVS investigations (including ECG).pdf (p.11) ^[26] Senior notes: Ryan Ho Critical Care.pdf – Tachyarrhythmia management (p.39–40) ^[27] Senior notes: Block A - WCS32 Chest pain on exertion_ IHD; angina pectoris.pdf (p.41) ^[28] Lecture slides: Handbook of Internal Medicine 2024.pdf – Arrhythmia management post-MI (p.29) ^[29] Senior notes: Block A - Clinical pharmacology of antiplatelets and anticoagulation.pdf (p.5) ^[30] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – MS medical treatment (p.456) ^[31] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – Hypertension drug recommendations (p.332) ^[32] Senior notes: Block A - Shortness of breath on exertion_ heart failure.pdf (p.40)

Complications of Atrial Fibrillation

AF is not just "an irregular heartbeat." It is a condition that, left unchecked, drives a cascade of serious downstream complications. Each complication can be understood from first principles by tracing back to the three fundamental haemodynamic and prothrombotic consequences of AF:

Stasis of blood → thromboembolism
Loss of atrial kick + rapid ventricular rate → reduced cardiac output → heart failure
Chronic rapid rate → structural myocardial damage (remodelling)

1. Thromboembolic Complications

This is the single most feared complication of AF and the primary reason anticoagulation exists.

Pathophysiology (from first principles):

In AF, the atria quiver rather than contract → blood pools, especially in the left atrial appendage (LAA), a blind-ended pouch where flow velocity is extremely low
Formation of atrial thrombi usually in the left atrial appendage (LAA) ^[33]
Clot usually occurs in the left atrial appendage during MS, due to the dilated left atrium ^[6]
Virchow's triad is perfectly fulfilled: stasis (no atrial contraction), endothelial injury (rapid electrical activity damages endocardium), hypercoagulability (AF activates coagulation cascade)
Thrombus fragments → enters left ventricle → aorta → cerebral arteries → ischaemic stroke

Clinical significance:

AF increases stroke risk 5-fold compared to patients in sinus rhythm
AF-related strokes tend to be larger and more disabling than non-AF strokes because cardioembolic clots occlude major proximal vessels (MCA, ICA) rather than small perforating arteries
Up to 25–30% of all ischaemic strokes are attributable to AF — and many patients have undiagnosed AF at the time of their stroke
Anticoagulants for cardioembolic ischaemic stroke: e.g. warfarin, NOAC (if non-valvular AF) ^[34]

Clue to cardioembolic stroke (from neurology notes) ^[35]:

Sudden onset, large focal (or multifocal) deficit, maximal at onset with subsequent improvement
Risk factors: AF, VHD, HF, IHD, DCMP
Signs: irregular pulse, heart murmur

The same LA/LAA thrombus can embolise to any organ in the systemic arterial circulation:

Target Organ	Clinical Presentation	Notes
Brain	Ischaemic stroke (see above)	Most common site (~80% of emboli)
Limbs	Acute limb ischaemia (6Ps: Pain, Pallor, Pulseless, Perishingly cold, Paraesthesia, Paralysis)	Cardiac origin emboli (80%): AF is the most common cause ^[11]^[12]
Mesenteric arteries	Acute mesenteric ischaemia — severe periumbilical pain out of proportion to findings	Embolism to mesenteric arteries most frequently due to dislodged thrombus from LA ^[13]
Splenic artery	Splenic infarction — LUQ pain, fever	Most commonly cerebral thromboembolism but other organs such as coronary arteries (MI), spleen and kidneys may also be involved ^[36]
Renal arteries	Renal infarction — flank pain, haematuria, elevated LDH	Same mechanism as above
Coronary arteries	Acute MI from coronary embolism	Rare but described ^[36]

High Yield – GC Lecture: Complications of Valvular Heart Disease

The GC lecture on "Fever and a murmur" lists the following symptoms of valvular heart disease ^[37]:

Palpitations — commonly atrial fibrillation ^[37]
Complications: (a) thromboembolism, (b) infective endocarditis, (c) problems during pregnancy ^[37]

This reinforces that AF is both a consequence of valvular disease AND a driver of further complications (thromboembolism).

A unique and important complication scenario:

The risk of cardioembolism is much higher in those with long-standing AF. Two main sources of cardioembolism include: (1) pre-existing LA thrombus getting dislodged during cardioversion; (2) post-cardioversion atrial stunning leading to formation of thrombus (much more common in long-standing AF as the recovery of atrial function is typically much slower in these patients) ^[3]

Pre-existing thrombus dislodgement: cardioversion restores coordinated contraction → the newly contracting atrium squeezes out any thrombus that had formed during AF → embolism
Post-cardioversion stunning: even after successful cardioversion, the atria are "stunned" (mechanically inactive despite electrical sinus rhythm) for days to weeks → blood still pools → NEW thrombus can form → embolism

This is precisely why:

TOE to exclude thrombus is required if AF > 48h and not anticoagulated
Anticoagulation must continue for at least 4 weeks post-cardioversion regardless of success

2. Heart Failure

AF and heart failure have a bidirectional, mutually destructive relationship: AF causes HF, and HF causes AF. Understanding this vicious cycle is critical.

Pathophysiology:

Sustained rapid ventricular rate (typically > 100 bpm for weeks to months) → chronic myocardial energy depletion → contractile dysfunction → dilated cardiomyopathy with reduced LVEF
The name tells you: "tachycardia-induced" = caused by fast rate; "cardiomyopathy" = disease of the heart muscle
Key point: this is REVERSIBLE — if the ventricular rate is controlled (rate or rhythm control), LVEF can normalise over weeks to months
This is one of the strongest arguments for adequate rate control in AF

Loss of atrial kick (15–25% of ventricular filling) → acutely reduces cardiac output
This is especially devastating in patients with stiff ventricles (HFpEF, HCM, aortic stenosis) who rely heavily on the atrial contribution to ventricular filling
The rapid ventricular rate further shortens diastolic filling time → even less filling → even lower output
Onset of AF often precipitates heart failure or exacerbates symptoms such as dyspnoea or haemoptysis in patients with MS ^[36]
Leads to cardiac decompensation since there is loss of atrial contraction which is important in generation of adequate LA pressure to maintain blood flow across the stenotic valve ^[36]

The reverse is also true:

HF → elevated filling pressures → LA dilatation → substrate for AF
Heart rhythm disorders (tachycardia, loss of AV synchronicity) are listed as causes of HF ^[38]
The combination of AF + HF confers a worse prognosis than either alone

AF ↔ HF: The Vicious Cycle

HF → ↑ LA pressure → LA dilatation → substrate for AF → loss of atrial kick + rapid rate → worsens HF → further LA dilatation → more AF... This self-perpetuating loop is why early and aggressive management of both conditions is essential.

Complications of Graves' disease: Atrial fibrillation; Heart failure → high output HF ^[8]

In thyrotoxicosis, the excess thyroid hormones cause:

↑ Metabolic rate → ↑ tissue oxygen demand → ↑ cardiac output
Direct effect on cardiac β-adrenergic receptors → ↑ heart rate and contractility
Combined with AF (rapid, uncontrolled ventricular rate) → the heart cannot sustain the high output → decompensation

Atrial fibrillation begets atrial fibrillation: structural and electrical remodelling occurs at each episode → higher risk of AF ^[2]

Type of Remodelling	Time Course	Mechanism	Consequence
Electrical remodelling	Hours to days	Rapid atrial rates → shortening of atrial action potential duration and effective refractory period (downregulation of L-type Ca²⁺ channels)	Makes AF easier to sustain and harder to cardiovert
Structural remodelling	Weeks to months	Atrial fibrosis, myocyte hypertrophy, inflammation, apoptosis	Creates permanent substrate for re-entry; explains progression from paroxysmal → persistent → permanent

This is why early intervention (rhythm control, ablation) before extensive remodelling occurs is increasingly favoured, particularly in younger patients with shorter AF duration.

Progressive LA dilatation from AF itself creates a pathological positive feedback loop:

Larger LA → more re-entrant circuits can be sustained → AF is harder to terminate
Larger LA → more blood stasis → higher thromboembolic risk
Larger LA → worse prognosis for cardioversion success and ablation outcomes

4. Complications of AF Occurring in the Context of Specific Diseases

Complications of MS: ^[36]

Atrial fibrillation — occurs in 45% of patients due to elevation of LA pressure and subsequent LA enlargement ^[36]
Systemic thromboembolism — occurs in patients with AF or infective endocarditis ^[36]
Right-sided heart failure — chronic pulmonary hypertension leads to increased RV and RA pressures, RV enlargement and functional TR ^[36]

AF itself is a major driver of decompensation in MS: onset of AF often precipitates heart failure ^[36]. The loss of coordinated atrial contraction is particularly harmful because in MS, the stenotic valve already limits LV filling — without the atrial "push," blood cannot cross the stenotic orifice adequately → acute ↓ CO → pulmonary congestion.

AF is one of the three causes of acute decompensation of mitral stenosis (along with chest infection and pregnancy) ^[20].

Complications of MR: atrial fibrillation, pulmonary hypertension, heart failure ^[39]. Complications of mitral valve prolapse: progressive severe MR, emboli, atrial fibrillation ^[40].

In MR, the regurgitant volume overloads the LA → progressive dilatation → substrate for AF.

AF occurs in 10–16% of AMI patients ^[41]. It can be:

Transient — due to atrial ischaemia (RCA supplies SA node and atrial tissue), sympathetic surge, electrolyte disturbance
Persistent — suggests more extensive infarction, LV dysfunction with elevated filling pressures

Common and frequently transient, can be a sign of impending or overt LVF ^[3]

Management in the post-MI setting: Digoxin 0.25 mg IV/PO stat; Diltiazem IV; or Amiodarone IV ^[28]

ECG in DCM is usually abnormal with: atrial fibrillation, AV block, LBBB ^[19]

DCM → biventricular dilatation → all four chambers enlarged → substrate for both AF and ventricular arrhythmias.

5. Complications of AF Treatment

It is important to recognise that the treatments for AF can themselves cause complications:

Complication	Mechanism	Management
Bleeding (most common)	Anticoagulation shifts haemostatic balance → increased bleeding tendency	Minor: local measures, hold dose. Major: stop anticoagulant, reverse if available (idarucizumab for dabigatran ^[29]; PCC for factor Xa inhibitors or warfarin), transfuse as needed
Intracranial haemorrhage	The most feared complication — can be fatal or devastating	NOACs have ~50% lower ICH rate compared to warfarin (major advantage)
GI bleeding	Particularly with dabigatran (direct mucosal effect) and rivaroxaban	Dose adjustment; consider apixaban (lower GI bleeding risk)

STOPP Criteria: Antiplatelet agents in combination with vitamin K antagonist, direct thrombin inhibitor or factor Xa inhibitors in patients with chronic atrial fibrillation (no added benefit), unless concurrent coronary artery stent(s) ^[42]. This highlights the increased bleeding risk from unnecessary combination therapy.

STOPP Criteria: Antiplatelet agents as alternatives to vitamin K antagonists, direct thrombin inhibitors or factor Xa inhibitors for stroke prevention in patients with chronic atrial fibrillation (no evidence of efficacy) ^[42]. Antiplatelets are NOT a substitute for anticoagulation in AF.

Drug	Complication	Why It Happens
Flecainide / Propafenone (Class IC)	Proarrhythmia (VT/VF), paradoxical 1:1 flutter conduction	Na⁺ channel blockade in scarred myocardium creates re-entry substrate; slows atrial flutter rate allowing 1:1 AV conduction
Amiodarone (Class III)	Interstitial lung disease (ILD, irreversible!); thyroid dysfunction (hypo or hyperthyroidism); prolonged QT → Torsades de pointes; hepatotoxicity; corneal microdeposits; photosensitivity; bradycardia ^[1]	Amiodarone contains iodine → directly toxic to thyroid and lungs. Blocks multiple ion channels → prolongs repolarisation
Sotalol	QT prolongation → TdP; bradycardia; bronchospasm	Non-selective β-blocker + K⁺ channel blocker
Digoxin	Toxicity (nausea, yellow vision, bradycardia, bigeminy, VT)	Narrow therapeutic window; toxicity exacerbated by hypokalaemia (K⁺ and digoxin compete for Na⁺/K⁺-ATPase binding site)

Complications of catheter ablation ^[3]:

Cardiac tamponade (~1%) due to perforation ^[3]
PV stenosis (1–3%): SOBOE, cough, chest pain, haemoptysis ^[3]
Embolic events: stroke, TIA ^[3]
Entry site complications: e.g. pseudoaneurysm, infection ^[3]
Oesophageal fistula (rare but potentially fatal — the LA is directly anterior to the oesophagus)
Phrenic nerve palsy (cryoablation — the right phrenic nerve runs close to the right superior PV)

Thromboembolism — as discussed above (pre-existing thrombus dislodgement + post-cardioversion stunning)
Skin burns — from paddle placement
Proarrhythmia — rarely, cardioversion can trigger other arrhythmias (VT/VF), especially if patient is hypokalaemic or has digitalis toxicity

An increasingly recognised complication:

AF is associated with a 1.4–1.6× increased risk of dementia, independent of clinical stroke
Mechanisms: subclinical cerebral microemboli, cerebral hypoperfusion from reduced CO, chronic cerebral microbleeds from anticoagulation
Anticoagulation appears to reduce (but not eliminate) this risk

Often underappreciated but clinically significant:

Chronic fatigue, exercise intolerance, anxiety about palpitations, fear of stroke
Frequent hospital visits for rate/rhythm management, blood tests (INR monitoring for warfarin)
Restriction on activities (alcohol avoidance, lifestyle modification)
Psychological impact: depression, anxiety disorders

Category	Complications	Key Mechanism
Thromboembolic	Ischaemic stroke, systemic embolism (limb, mesenteric, renal, splenic, coronary), post-cardioversion embolism	Blood stasis in LAA → thrombus formation → embolisation
Cardiac	Heart failure (tachycardia-induced cardiomyopathy, acute decompensation), acute MI (coronary embolism)	Loss of atrial kick + rapid rate → ↓ CO; chronic rapid rate → myocardial damage
Remodelling	"AF begets AF" (electrical + structural), progressive LA enlargement	Self-perpetuating cycle of atrial remodelling
Neurological	Cognitive decline, dementia	Subclinical cerebral microemboli + chronic hypoperfusion
Treatment-related	Bleeding (anticoagulation), proarrhythmia (antiarrhythmics), tamponade/PV stenosis (ablation), post-cardioversion embolism	Iatrogenic: shifting haemostatic balance, drug toxicity, procedural complications
QoL	Fatigue, exercise intolerance, anxiety, depression	Chronic symptoms + burden of treatment

High Yield Summary – Complications of AF

Stroke is the most devastating complication. AF increases stroke risk 5-fold. Cardioembolic strokes are large-territory, high-morbidity events. > 90% of thrombi form in the LAA.
Heart failure: bidirectional relationship. Tachycardia-induced cardiomyopathy is reversible with rate control. Loss of atrial kick is especially harmful in MS, HCM, HFpEF.
AF begets AF: electrical remodelling (hours-days) + structural remodelling (weeks-months) → progressive, self-perpetuating disease.
Systemic embolism beyond stroke: acute limb ischaemia, mesenteric ischaemia, renal/splenic infarction.
AF decompensates mitral stenosis → pulmonary oedema. AF + MS = warfarin obligatory.
Treatment complications: bleeding from anticoagulants (ICH most feared); proarrhythmia from Class IC drugs (in structural HD) and amiodarone (QT prolongation → TdP, thyroid, lung, liver toxicity); ablation complications (tamponade, PV stenosis, stroke).
Cognitive decline/dementia: increasingly recognised, partially mitigated by anticoagulation.
Post-cardioversion embolism: due to pre-existing thrombus dislodgement OR post-cardioversion atrial stunning → anticoagulate ≥ 4 weeks post-cardioversion.

Active Recall - Complications of AF

References

^[1] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – AF Treatment: Antiarrhythmic drugs table (p.504) ^[2] Senior notes: Maksim Medicine Notes.pdf – Cardiology, AF (p.23–24) ^[3] Senior notes: Ryan Ho Cardiology.pdf – AF ablation complications, post-MI AF (p.96, p.139) ^[6] Senior notes: Block A - Three Cases of Dyspnea.pdf (p.3) ^[8] Senior notes: Block A - I am losing weight and sweating all the time.pdf (p.11) ^[11] Senior notes: Maksim Surgery Notes.pdf – Acute limb ischaemia (p.168) ^[12] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf – Acute arterial ischaemia (p.920) ^[13] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf – Ischaemic bowel disease (p.718) ^[19] Senior notes: Block A - Inherited Cardiac conditions.pdf (p.7) ^[20] Senior notes: Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf (p.12) ^[28] Lecture slides: Handbook of Internal Medicine 2024.pdf – Arrhythmia management post-MI (p.29) ^[29] Senior notes: Block A - Clinical pharmacology of antiplatelets and anticoagulation.pdf (p.5) ^[33] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – AF Complications (p.511–513) ^[34] Senior notes: Ryan Ho Neurology.pdf – Secondary prevention of ischaemic stroke (p.83) ^[35] Senior notes: Ryan Ho Neurology.pdf – Clues to stroke subtype (p.79) ^[36] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – Complications of MS (p.457) ^[37] Lecture slides: GC 050. Fever and a murmur.pdf (p.5) ^[38] Senior notes: Block A - Shortness of breath on exertion_ heart failure.pdf (p.38) ^[39] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – Complications of MR (p.463) ^[40] Senior notes: Block A - Fever and a murmur_ Valvular heart diseases; Infective endocarditis.pdf (p.15) ^[41] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf – Complications of AMI (p.421) ^[42] Lecture slides: GC 079 (supp-2) STOPP-START-V3.pdf (p.3)

High Yield Summary

Definition: AF = supraventricular tachyarrhythmia with uncoordinated atrial activation → ineffective atrial contraction → irregularly irregular ventricular rhythm. Most common sustained cardiac arrhythmia.
Classification: Paroxysmal (< 7 days), Persistent (> 7 days), Long-standing persistent (> 1 year), Permanent (accepted). Valvular AF (rheumatic MS, mechanical valve → warfarin only) vs Non-valvular AF (NOAC or warfarin).
Aetiology: Cardiac (HTN, IHD, mitral valve disease, HCM, post-surgery), Respiratory (COPD, PE, OSA), Metabolic (thyrotoxicosis, hypoK, hypoMg), Drugs (alcohol "Holiday Heart", cocaine), Sepsis, Old age.
Pathophysiology: Trigger (PV sleeve ectopic foci) + Substrate (atrial dilatation/fibrosis → multiple re-entrant circuits). AF begets AF (electrical + structural remodelling).
Clinical Features: Irregular palpitations, SOB, fatigue, syncope, polyuria, embolic events. Signs: irregularly irregular pulse with variable volume, pulse deficit, absent a-wave JVP, variable S1.
ECG: Absent P waves, fibrillatory baseline, irregularly irregular R-R, usually narrow QRS.
Investigations: ECG, CBC, LRFT, TFT, Mg, bone profile, echo, ± Holter.
CHA₂DS₂-VASc: ≥ 2 (male) or ≥ 3 (female) → anticoagulate.
Management: Rate control (BB, CCB if EF ≥ 40%; BB, digoxin if EF < 40%) + Rhythm control (cardioversion, antiarrhythmics, ablation) + Anticoagulation (NOAC for non-valvular; warfarin for valvular).
Valvular AF (rheumatic MS) = warfarin ONLY. NOACs are contraindicated.
AF with WPW → NEVER give AV nodal blockers → DC cardioversion or IV procainamide.

High Yield Summary – Differential Diagnosis of AF

6 DDx of irregularly irregular pulse: AF, atrial flutter with variable block, AT with variable block, MAT, MAR, frequent ectopics ^[1].
Key ECG distinguisher: Is there a fibrillatory baseline with NO P waves (= AF) or are discrete P waves / flutter waves visible (= something else)?
Isoelectric baseline preserved → MAT or AT, NOT AF ^[3].
Irregular wide-complex tachycardia has 3 DDx: AF with BBB, AF with accessory pathway (WPW), polymorphic VT ^[7]. Axis changes every beat → PVT; axis stable → AF-related.
Vagal manoeuvres/adenosine help: terminate AVNRT/AVRT; slow VR and unmask flutter/AT waves; slow VR in AF but don't terminate it.
Once AF is confirmed, always look for the cause: TFT (thyrotoxicosis), echo (structural heart disease), electrolytes (K, Mg), history (alcohol, drugs, surgery).
Don't forget: AF may be an incidental finding in a patient presenting with stroke — but you still need to determine if it is the CAUSE of the stroke or a bystander.

High Yield Summary — Diagnosis and Investigations of AF

AF is an ECG diagnosis: absent P waves + fibrillatory baseline + irregularly irregular RR. Minimum 30 seconds of continuous recording.
If suspected but not captured on resting ECG: use ambulatory monitoring — Holter (daily symptoms), event recorder (weekly), ILR (infrequent or cryptogenic stroke).
Mandatory bloods in ALL new AF: CBC, LRFT, TFT, K, Mg, bone profile.
Echo is essential: determines cause (valvular, structural), LVEF (guides rate control strategy), LA size (predicts cardioversion success).
TOE before cardioversion if AF > 48 hours and not on ≥ 3 weeks anticoagulation → rule out LA/LAA thrombus.
Always check TFT — thyrotoxicosis is a reversible cause. Always check K and Mg — easily correctable factors that improve treatment response.
ECG calibration pitfall: LVH may cause machine to auto-adjust voltage → miss ST changes. Always verify calibration mark.
CHA₂DS₂-VASc is part of the diagnostic workup, not just management — it determines anticoagulation from day one.

High Yield Summary – Management of AF

Three pillars: Rate control + Rhythm control + Anticoagulation — mention all three in EVERY exam answer.
Acute unstable AF: DC cardioversion 120–200J biphasic, synchronised. No delay.
Acute stable AF: Treat cause first. Rate control: BB or CCB if EF ≥ 40%; BB or digoxin if EF < 40%. Avoid BB/CCB if APO.
Rate vs rhythm: AFFIRM showed similar mortality. Rate control = simpler, cheaper, fewer side effects (preferred if older, asymptomatic). Rhythm control = if young, symptomatic, HF, short disease duration.
Rate control targets: HR < 110 if asymptomatic (lenient), < 80 if symptomatic (strict).
Rhythm control drugs: No structural heart disease → Class IC (flecainide). Structural HD/HF → Class III (amiodarone). Class IC is CONTRAINDICATED in structural heart disease (proarrhythmic).
Catheter ablation: PV isolation. 75% success (paroxysmal). Symptomatic relief only — does NOT eliminate stroke risk → continue anticoagulation.
Anticoagulation: All valvular AF → warfarin. Non-valvular AF → CHA₂DS₂-VASc ≥ 2M/≥ 3F → NOAC preferred.
Valvular AF (rheumatic MS, mechanical valve): Warfarin ONLY. NOACs contraindicated.
AF with WPW: NEVER AV nodal blockers. Use DC cardioversion or IV procainamide.

High Yield Summary – Complications of AF

Stroke is the most devastating complication. AF increases stroke risk 5-fold. Cardioembolic strokes are large-territory, high-morbidity events. > 90% of thrombi form in the LAA.
Heart failure: bidirectional relationship. Tachycardia-induced cardiomyopathy is reversible with rate control. Loss of atrial kick is especially harmful in MS, HCM, HFpEF.
AF begets AF: electrical remodelling (hours-days) + structural remodelling (weeks-months) → progressive, self-perpetuating disease.
Systemic embolism beyond stroke: acute limb ischaemia, mesenteric ischaemia, renal/splenic infarction.
AF decompensates mitral stenosis → pulmonary oedema. AF + MS = warfarin obligatory.
Treatment complications: bleeding from anticoagulants (ICH most feared); proarrhythmia from Class IC drugs (in structural HD) and amiodarone (QT prolongation → TdP, thyroid, lung, liver toxicity); ablation complications (tamponade, PV stenosis, stroke).
Cognitive decline/dementia: increasingly recognised, partially mitigated by anticoagulation.
Post-cardioversion embolism: due to pre-existing thrombus dislodgement OR post-cardioversion atrial stunning → anticoagulate ≥ 4 weeks post-cardioversion.

Atrial Fibrillation

1. Definition

2. Epidemiology

2.1 Prevalence and Incidence

2.2 Why Does Age Matter?

3. Anatomy and Physiology Relevant to AF

3.1 Normal Cardiac Conduction

3.2 The Pulmonary Veins – The "Trigger Zone"

3.3 The Left Atrial Appendage (LAA) – The "Clot Factory"

3.4 The AV Node – The "Gatekeeper"

4. Aetiology (with Hong Kong Focus)

4.1 Cardiac Causes

4.2 Respiratory Causes

4.3 Endocrine / Metabolic Causes

4.4 Drug / Substance-Induced

4.5 Other Causes

5. Pathophysiology

5.1 The "Trigger and Substrate" Model

5.1.1 Triggers

5.1.2 Substrate

5.1.3 "AF Begets AF"

5.2 Haemodynamic Consequences

5.3 Thromboembolic Risk – Virchow's Triad in AF

6. Classification

6.1 By Temporal Pattern (2020 ESC / AHA Guidelines)

6.2 By Valvular Status

6.3 First Detected AF

7. Clinical Features

7.1 Symptoms (with Pathophysiological Basis)

7.2 Signs (with Pathophysiological Basis)

7.3 Complications Presenting as Signs

8. ECG Features of AF

8.1 Classic ECG Findings

8.2 AF Variants on ECG

9. Investigations

9.1 Bedside

9.2 Blood Tests

9.3 Imaging

9.4 Additional Investigations

10. CHA₂DS₂-VASc Score

10.1 Score Components

10.2 Anticoagulation Decision

11. Anticoagulation in AF – CHA₂DS₂-VASc Guided

11.1 Valvular vs Non-Valvular AF

11.2 NOACs (Non-Vitamin K Oral Anticoagulants) / DOACs

12. Management Overview (Rate, Rhythm, Anticoagulation)

12.1 Acute Management

Haemodynamically Unstable

Haemodynamically Stable

12.2 Long-Term Rate Control

12.3 Rhythm Control

12.4 Management of VT/VF (for comparison, from the same lecture) [14]

13. Special Scenarios

13.1 AF and Stroke

13.2 AF and Mitral Stenosis

13.3 AF and Thyrotoxicosis

13.4 AF and Acute Limb Ischaemia

13.5 AF and Mesenteric Ischaemia

13.6 Pacemaker Considerations in AF

14. Inherited/Genetic Considerations

Active Recall - Atrial Fibrillation

References

1. ECG Differential — "Irregularly Irregular Rhythm: Is It Truly AF?"

2. ECG Differential — "Wide Complex Irregular Tachycardia: AF or Something Worse?"

3. ECG Differential — "Narrow Complex Regular Tachycardia: Is It AF or Something Else?"

4. Clinical Presentation Differential — Presenting with Palpitations

5. Clinical Presentation Differential — Presenting with Stroke/Embolic Event

6. Differential by Underlying Cause — "Why Does This Patient Have AF?"

7. Diagnostic Approach Algorithm

8. Key Differentiating Manoeuvres

8.1 Vagal Manoeuvres and Adenosine (ATP)

8.2 Differentiation Criteria for Wide Complex Tachycardia

9. Summary Table – AF vs Its Closest Mimics

Active Recall - Differential Diagnosis of AF

1. Diagnostic Criteria — How Do You Actually "Diagnose" AF?

1.1 ECG Diagnostic Criteria for AF

1.2 Minimum Duration for Diagnosis

1.3 Classification After Diagnosis

2. The Diagnostic Algorithm — A Step-by-Step Clinical Approach

3. Investigation Modalities — Systematic Approach