Atrial flutter

Introduction

Atrial flutter is a type of supraventricular tachycardia which originates from a macro-re-entrant circuit in the atria. The atrial rate is typically around 300 beats/min with 2:1 conduction ratio the ventricular rate is 150 beats/min.

Conduction to ventricles:

  • AV node cannot conduct at rates greater than 200 bpm > ventricular rate is a fraction of atrial rate
  • 2:1 conduction – most often in atrial flutter, ventricular rate around 150 bpm
  • 3:1 conduction – ventricular rate around 100 bpm

Atrial flutter usually starts with trigger beats that initiate the arrhythmia.

Classification

Types of atrial flutter depend on anatomical position and direction of the macro-re-entrant circuit.

1) Typical atrial flutter - common (counter-clockwise) and reverse (clockwise)

Typical atrial flutter involves counterclockwise, or less commonly clockwise, conduction in the right atrium in a circuit around the cavotricuspid isthmus (tissue that lies between the tricuspid valve annulus and the inferior vena cava). 

Common typical flutter (counter-clockwise)

  • most common type, 90% of typical atrial flutters
  • F waves – typical sawtooth pattern
  • negative flutter waves in inferior leads (II, III, aVF)
  • positive F waves in lead V1 (these may resemble broad P waves)

Reverse typical flutter (clockwise)

  • the ECG image is reversed
  • positive flutter waves in inferior leads (II, III, aVF) 
  • inverted flutter waves in lead V1 (often broad, resembling P waves)
  • this type is hard to distinguish from atypical flutter

ECG findings

  • Narrow complex tachycardia at a rate around 150 bpm
  • Rate does not change over time
  • Typical sawtooth pattern = flutter waves best seen in the inferior leads II, III, aVF
  • Absence of isoelectric baseline 
  • in rates >150 bpm it can be difficult to identify flutter waves. To slow ventricular response, use vagal maneuvers or medication to slow AV node conduction (adenosine, verapamil)

Picture 1 Mechanism and electrocardiographic pattern of typical atrial flutter (left) and reverse typical atrial flutter (right)

García Cosío F, Pastor A, Núñez A, Magalhaes AP, Awamleh P. Flúter auricular: perspectiva clínica actual [Atrial flutter: an update]. Rev Esp Cardiol. 2006 Aug;59(8):816-31. Spanish. PMID: 16938231.



2) Atypical atrial flutter

Introduction

Atypical atrial flutter is a type of supraventricular tachycardia which originates from a macro-re-entrant circuit in the atria that does not involve the CTI (cavotricuspid isthmus) with ECG patterns differing from the typical and reverse typical flutter.

 Classification and ECG findings

  1. Atypical right atrial flutters - lesion macroreentrant tachycardia (an atriotomy scar or suture line can act as an obstacle to conduction and create reentry – most common) or nonatriotomy-related right atrial flutter (areas of low voltage in the right atrium)

  1. Atypical left atrial flutters – post-ablation AF (incomplete ablation lines from either a transvenous catheter ablation or a surgical Maze procedure) or left atrial macroreentry (anatomic obstacle like the mitral annulus)

ECG findings

- P waves are absent
- F waves are regular, but there may be an isoelectric appearance between F waves 
- No clear F wave morphology - atrial scar can alter conduction velocity and direction

Right atrial flutters
 
– negative F wave in V1

Left atrial flutters
   - variable morphology
  - positive or isoelectric F waves in V1
   - often positive F waves in the inferior leads II, III, aVF

Lower loop re-entry (around the inferior vena cava) - negative F waves in the inferior leads 

Upper loop re-entry (right atrium) - positive F waves in the inferior leads and negative, flat, or barely positive F waves in lead I.

Causes

- Right atrial atypical flutter is associated with atrial sutures and patches used for complex congenital heart disease surgery or following surgical atriotomy. Rate control is often difficult due to the regularity and usually slow rate of the tachycardia

- Left atrial atypical flutters have circuits around electrically silent areas of abnormal tissue, following medical interventions or progressive atrial degeneration/fibrosis (AF ablation, surgery for different conditions with incisions or cannulation)

- In some cases, electrophysiological study is the only way to find the mechanism causing atypical flutter and plan an ablation, when needed.

ECG 1

Typical atrial flutter with variable AV-block

  • narrow complex typical flutter with ventricular rate at 85 bpm
  • variable AV block raging from 1:1 to 4:1
  • negative flutter waves in II, III, aVF
  • positive flutter waves in V1

ECG 2

Typical atrial flutter with variable AV block

  • narrow complex atrial flutter with ventricular rate at 80 bpm
  • negative flutter waves in inferior leads II, III, aVF
  • positive flutter waves in lead V1
  • absence of isoelectric baseline

ECG no. 3

Typical atrial flutter with 4:1 conduction

  • atrial rate 250 bpm with 4:1 conduction to ventricles at rate 63 bpm
  • typical negative flutter waves in inferior leads II, III, aVF
  • positive flutter waves in lead V1

ECG 4

Adenosine demasking typical atrial flutter

  • typical atrial flutter with conduction 1:1 and ventricular rate at 250 bpm
  • adenosine completely blocks the AV node for 10 – 30 s and slow-downs the ventricular rate while revealing classical flutter waves.


ECG 5

Atypical atrial flutter with variable block

  • narrow complex atypical flutter
  • atrial rate 375 bpm
  • ventricular rate 115 bpm
  • positive flutter waves in V1 – suggesting left atrium re-entrant circuit
  • positive to almost isoelectric flutter waves in the inferior leads II, III, aVF


ECG 6 

Atypical atrial flutter with 2:1 block

  • narrow complex atypical flutter
  • positive flutter waves in V1 – suggesting left atrium re-entrant circuit

Management

- Decreasing atrioventricular (AV) nodal conduction physiologically with a vagotonic maneuver (such as the Valsalva maneuver or carotid sinus massage) or with a rapidly acting drug (such as adenosine, verapamil, or esmolol) will increase the AV nodal block and reveal the atrial F waves.

Acute therapy

  1. Hemodynamically unstable patient – urgent synchronized cardioversion
  2. Hemodynamically stable – diagnostic use of adenosine and pharmacological termination or cardioversion

Adenosine

- is useful for diagnostic purposes, - by decreasing atrioventricular (AV) nodal conduction with a vagotonic maneuver or with adenosine the atrial F waves are revealed

- AV node is not involved in the flutter circuit > adenosine does not terminate the rhythm

Pharmacological termination

- i.v. ibutilide or i.v. or oral dofetilide (in-hospital) are recommended for conversion to sinus rhythm

Synchronized cardioversion

- Low-energy

High-rate atrial pacing

- might be considered for termination of atrial flutter in the presence of an implanted pacemaker or defibrillator

Rate control therapy (not often successful)

- Beta blockers - i.v. esmolol, i. v. metoprolol

- Calcium channel blockers (verapamil/diltiazem i.v.)


Chronic therapy

- Catheter ablation – recommended for all symptomatic or recurrent atrial flutters

- Beta-blockers or non-dihydropyridine calcium channel blockers (verapamil or diltiazem) should be considered if ablation is not desirable or feasible


Anticoagulation

  • patients with atrial fibrillation, atrial flutter or any supraventricular tachycardia with fast atrial action are at risk of thrombus formation and thromboembolism 
  • effective anticoagulation is recommended in acute settings pre-cardioversion as well as chronic oral anticoagulation in persistent arrhythmias
  • to estimate embolic risk use CHA2DS2-VASc scoring system
  • to estimate bleeding risk use HAS-BLED risk score
  • oral anticoagulants – warfarin, NOAC (dabigatran, apixaban,..)
  • parenteral anticoagulants – unfractionated heparin or low molecular weight heparin

Picture 2 Treatment of atrial flutter as per ESC guidelines


References

  1. CAMM, A. J., LÜSCHER, T. F., & SERRUYS, P. W. (2009). The ESC textbook of cardiovascular medicine. Oxford, Oxford University Press
  2. HARRIGAN, Richard A., William J. BRADY a Theodore C. CHAN. The ECG in Emergency Medicine. Emergency Medicine Clinics of North America [online]. 2006, 24(1) [cit. 2021-01-29]. ISSN 07338627. Dostupné z: doi:10.1016/j.emc.2005.08.001
  3. Strauss, David G., et al. Marriott's Practical Electrocardiography. Wolters Kluwer, 2021
  4. Bibas, Lior et al. “Diagnosis and management of supraventricular tachycardias.” CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne vol. 188,17-18 (2016): E466-E473. doi:10.1503/cmaj.160079
  5. https://litfl.com/atrial-flutter-ecg-library/
  6. Brugada J, Katritsis DG, Arbelo E, Arribas F, Bax JJ, Blomström-Lundqvist C, Calkins H, Corrado D, Deftereos SG, Diller GP, Gomez-Doblas JJ, Gorenek B, Grace A, Ho SY, Kaski JC, Kuck KH, Lambiase PD, Sacher F, Sarquella-Brugada G, Suwalski P, Zaza A; ESC Scientific Document Group. 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2020 Feb 1;41(5):655-720. doi: 10.1093/eurheartj/ehz467. PMID: 31504425.
  7. García Cosío F, Pastor A, Núñez A, Magalhaes AP, Awamleh P. Flúter auricular: perspectiva clínica actual [Atrial flutter: an update]. Rev Esp Cardiol. 2006 Aug;59(8):816-31. Spanish. PMID: 16938231.