Etiology


Pathophysiology

  • Type I (common; typical or isthmus-dependent flutter): caused by a counterclockwise (more common) or clockwise (less common) macroreentrant activation of cardiac muscle fibers in the right atrium that travels along the tricuspid annulus and passes through the cavotricuspid isthmus
    • Different from AFib, which originates from pulmonary vein ostia

Clinical features


Diagnostics

Atrial flutter vs atrial fibrillation

FeatureAtrial FlutterAtrial Fibrillation
Site of OriginRight Atrium (re-entrant circuit involving the cavotricuspid isthmus).Left Atrium (ectopic foci, most commonly near the pulmonary vein ostia).
PathophysiologyOrganized macro-reentrant circuit.Chaotic multiple atrial foci.
ECG RhythmRegular or regularly irregular.Irregularly irregular.
Atrial Waves (ECG)“Sawtooth” flutter waves (~300 bpm).Fibrillatory waves (no P waves).
Management PearlCatheter ablation is highly curative.Lifelong anticoagulation (CHA₂DS₂-VASc score) is key to prevent stroke.

ECG

  • Narrow complex tachycardia
  • Regular atrial activity at ~300 bpm
  • Loss of the isoelectric baseline
  • “Saw-tooth” pattern of inverted flutter waves in leads II, III, aVF
    • Anticlockwise Reentry: Commonest form of atrial flutter (90% of cases). Retrograde atrial conduction produces
      • Inverted flutter waves in leads II,III, aVF
      • Positive flutter waves in V1 — may resemble upright P waves
  • Upright flutter waves in V1 that may resemble P waves
  • Ventricular rate depends on AV conduction ratio (see below)

Handy Tips For Spotting Flutter

Rapid Recognition

  • Narrow complex tachycardia at 150 bpm (range 130-170)? Yes -> Suspect flutter!
  • Turn the ECG upside down and closely examine the inferior leads (II, III + aVF) for flutter waves

Vagal Maneuvers +/- Adenosine

RR intervals

  • In atrial flutter with variable block the R-R intervals will be multiples of the P-P interval — e.g. assuming an atrial rate of 300bpm (P-P interval of 200 ms), the R-R interval would be 400 ms with 2:1 block, 600 ms with 3:1 block, and 800 ms with 4:1 block
  • Look for identical R-R intervals occurring sporadically along the rhythm strip; then look to see whether there is a mathematical relationship between the various R-R intervals on the ECG
  • In contrast, atrial fibrillation will be completely irregular, with no patterns to be discerned within the R-R intervals

Treatment

  1. Hemodynamically Unstable (Hypotension, shock, AMS, severe angina):
    • Urgent synchronized DC cardioversion.
  2. Hemodynamically Stable - Rate Control (Initial):
    • AV nodal blocking agents: Beta-blockers (e.g., Metoprolol) or Non-DHP CCBs (e.g., Diltiazem, Verapamil). Note: Atrial flutter is notoriously harder to rate-control than AFib.
  3. Hemodynamically Stable - Rhythm Control:
    • Elective synchronized cardioversion (requires prior TEE to r/o LAA thrombus OR 3 weeks of therapeutic anticoagulation prior to attempt).
    • Pharmacologic cardioversion (e.g., Ibutilide, Amiodarone, Dofetilide).
    • Rhythm Control Caveat (The “1:1 Conduction” Trap)
      • If using Class IC or IA antiarrhythmics (e.g., Flecainide, Propafenone) for rhythm control in AFlutter, the atrial rate slows down (e.g., from 300 bpm to 200 bpm).
      • This slower rate allows the AV node to recover, potentially leading to 1:1 AV conduction (ventricular rate suddenly jumps to 200 bpm), causing hemodynamic collapse.
      • Rule: Always ensure adequate AV nodal blockade (BB or CCB) is on board before starting these antiarrhythmics in AFlutter. c
  4. Stroke Prevention (Anticoagulation):
    • Risk is equivalent to AFib. Assess using CHA2DS2-VASc score.
    • DOACs (Apixaban, Rivaroxaban) or Warfarin indicated based on score (≥2 in men, ≥3 in women) and valve status.
  5. Definitive/Long-term Management:
    • Catheter Ablation: Radiofrequency ablation of the CTI. Considered first-line definitive therapy due to high success rate (>90%) and low complication risk.