Atrial fibrillation

Etiology

• Atrial remodeling due to:
  • Age-related myocardial changes
  • HTN (most common c ), CAD, HF, OSA, Obesity, DM2.
• Foci of rapid electrical activity:
  • Commonly originate in pulmonary veins
  • Alcohol intake & ↑ sympathetic drive may contribute
• Pre-Excited AF: Occurs in pts with Wolff-Parkinson-White (WPW) syndrome (accessory pathway/Bundle of Kent). c

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Pathophysiology

• The new onset of Afib triggers a vicious circle that can ultimately lead to long-standing Afib with atrial remodeling:
  1. Afib is triggered by one or both of the following
     • Bursts of electrical activity from automatic foci near the pulmonary vein ostia (left atrium) or in diseased, fibrotic atrial tissue
     • Pre-excitation of the atria as a result of aberrant pathways (e.g., WPW syndrome)
  2. Afib is sustained by re-entry rhythms and/or rapid focal ectopic firing
     • Re-entry rhythms are more likely to occur with enlarged atria, diseased heart tissue, and/or aberrant pathways (e.g., WPW syndrome).
  3. Atrial remodeling
     • Electrophysiological changes in the atria occur within a few hours of Afib onset (electrical modeling).
     • If Afib persists, atrial fibrosis and dilatation (structural remodeling) occur within a few months.
     • Electrical and structural remodeling increase susceptibility to Afib, resulting in a vicious circle.
• Effects of Afib
  • The atria contract rapidly but ineffectively and in an uncoordinated fashion → stasis of blood within the atria, especially in atrial appendage → risk of thromboembolism and stroke
  • Irregular activation of the ventricles by conduction through the AV node → tachycardia

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Clinical features

• Often asymptomatic (incidental finding).
• Sx: Palpitations, fatigue, dyspnea, lightheadedness.

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Diagnostics

Atrial flutter vs atrial fibrillation

Feature	Atrial Flutter	Atrial Fibrillation
Site of Origin	Right Atrium (re-entrant circuit involving the cavotricuspid isthmus).	Left Atrium (ectopic foci, most commonly near the pulmonary vein ostia).
Pathophysiology	Organized macro-reentrant circuit.	Chaotic multiple atrial foci.
ECG Rhythm	Regular or regularly irregular.	Irregularly irregular.
Atrial Waves (ECG)	“Sawtooth” flutter waves (~300 bpm).	Fibrillatory waves (no P waves).
Management Pearl	Catheter ablation is highly curative.	Lifelong anticoagulation (CHA₂DS₂-VASc score) is key to prevent stroke.

Link to original

ECG

QRS complex

• Typically narrow QRS complex (< 0.12 seconds)
• Wide QRS complex may be seen in some situations:
  • Aberrant conduction, e.g., bundle branch block or preexcitation (as seen in Afib with WPW)
  • Complete AV block with a ventricular escape rhythm
  • Ashman phenomenon: intermittent aberrant ventricular conduction results in isolated or short runs of wide QRS complexes

Warning

Wide QRS complex may indicate preexcited Afib or aberrant conduction.

Workup

• Transthoracic Echocardiogram (TTE): Assess LA size, LV function, valvular dz, intracardiac thrombus.
  • Expected: LA enlargement (remodeling) c , Mitral Stenosis or Mechanical Valve, HFrEF (EF < 40%),
• Labs: TSH (r/o hyperthyroidism), CMP (K+, Mg2+, renal function), CBC.
• Troponins: Only if ACS suspected (ischemia can be cause or result).

CHA2DS2-VASc score

• Purpose: Estimates thromboembolic (stroke) risk in patients with non-valvular Atrial Fibrillation (AFib) to guide the initiation of systemic anticoagulation.

Scoring system

• C - CHF or LVEF $\le$ 40% (+1)
• H - Hypertension (+1)
• A - Age $\ge$ 75 years (+2)
• D - Diabetes Mellitus (+1)
• S - Stroke, TIA, or prior thromboembolism (+2)
• V - Vascular disease (prior MI, PAD, or aortic plaque) (+1)
• A - Age 65–74 years (+1)
• Sc - Sex category (Female) (+1)

Treatment Thresholds

• 0 (M) or 1 (F): No therapy.
• 1 (M) or 2 (F): Consider oral anticoagulation based on shared decision-making (consider patient preference, bleeding risk).
• $\ge$ 2 (M) or $\ge$ 3 (F): Oral anticoagulation is recommended.

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Treatment

• Hemodynamically Unstable (Hypotension, AMS, pulmonary edema, active ischemia):
  • Immediate Synchronized Cardioversion.
• Hemodynamically Stable:
  1. Rate Control (Preferred initial strategy for most): Target HR < 110 bpm.
     • Beta-blockers (e.g., Metoprolol).
     • Non-dihydropyridine CCBs (Diltiazem, Verapamil) - Avoid in HFrEF.
     • Digoxin (used if pt has borderline BP or concurrent HFrEF).
  2. Rhythm Control (Indicated if symptomatic despite rate control, younger pts, or HF exacerbated by AFib):
     • Antiarrhythmics (Amiodarone, Flecainide, Sotalol).
     • Elective synchronized cardioversion (Must r/o LA thrombus via TEE or ensure 3 weeks of therapeutic anticoagulation prior).
     • Catheter ablation (if refractory).

Pre-Excited AF

• Tx of Choice: Procainamide or Ibutilide (Chemical cardioversion). c
• CONTRAINDICATED (“ABCD”): Adenosine, Beta-blockers, Calcium channel blockers, Digoxin.
• Why? Blocking the AV node removes the refractory “braking” mechanism, forcing all 300+ atrial impulses down the accessory pathway, rapidly degenerating into Ventricular Fibrillation (VF).

• Anticoagulation (Stroke Prevention):
  • Assess stroke risk using CHA2DS2-VASc score (CHF, HTN, Age $\ge$ 75 [2 pts], DM, Stroke/TIA/TE [2 pts], Vascular dz, Age 65-74, Sex category [Female]).
  • Score $\ge$ 2 (Men) or $\ge$ 3 (Women): Oral anticoagulation indicated.
  • DOACs (Apixaban, Rivaroxaban, Dabigatran): First-line for non-valvular AFib. c
  • Warfarin: ONLY indicated for “Valvular AFib” (moderate-to-severe mitral stenosis or mechanical heart valve).

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