DESCRIPTION

• Atrial flutter (Afl) is a reentrant tachycardia utilizing a circuit defined by the tricuspid annulus, with the anterior free wall of the right atrium activated in the craniocaudal direction and the septum in the caudocranial direction.
• An isthmus between the inferior vena cava and the tricuspid annulus is the lower turnaround point; because it is narrow, it can be targeted for interruption by radiofrequency energy with subsequent cure of the arrhythmia.
• The Afl circuit around the tricuspid annulus can support reentry in either the clockwise or counterclockwise direction:
  • Counterclockwise reentry around the tricuspid annulus is called typical, usual, or common Afl and is characterized by negative (sawtooth) flutter waves in EKG leads II, III, and aVF. The flutter wave is positive in V1 and negative in V6.
  • Clockwise reentry around the tricuspid annulus is called unusual or uncommon atrial flutter and is characterized by positive flutter waves in EKG leads II, III, and aVF. These flutter waves often have a notch in the upstroke. The flutter wave is negative in V1 and positive in V6.
• Prior left atrial surgery (MAZE) or extensive left atrial catheter ablation can significantly alter the EKG appearance of right atrial flutter
• The term atypical Afl has been used for not only isthmus-dependent clockwise Afl, but also atrial tachycardias not dependent on isthmus conduction.

Pregnancy Considerations

• May exacerbate arrhythmias in young women
• If there is significant underlying heart disease, pregnancy may be either dangerous or contraindicated.
• Warfarin is associated with congenital birth defects such that risk–benefit ratio weighted against its use for Afl in this situation.

EPIDEMIOLOGY

Incidence

• Increases as the population ages
• Incidence may be up to 30% following open-heart surgery.
• Common after surgery for congenital heart disease

Prevalence

Dependent on age and presence of underlying heart disease

RISK FACTORS

• Prior cardiac surgery
• HTN
• Treatment with IC antiarrhythmic drugs or amiodarone for atrial fibrillation—20% of patients will have Afl as their recurrent arrhythmia

ETIOLOGY

• Idiopathic
• Structural heart disease (including coronary and valvular heart disease and cardiomyopathy)
• Following open-heart surgery:
  • In children/young adults, atypical Afls may use atrial incisions or prosthetic material (atrial septal defect patch) as an anatomic barrier around which reentry occurs.
• Usual, counterclockwise Afl may occur for the 1st time in patients treated with class IC antiarrhythmic drugs (ie, flecainide, propafenone).
• Class IC antiarrhythmic often slow the atrial flutter rate such that 1:1 atrioventricular (AV) conduction can occur, leading to a faster ventricular response than at baseline when the Afl rate was faster but degree of AV block greater.

Outline

• Description
  • Pregnancy Considerations
• Epidemiology
  • Incidence
  • Prevalence
• Risk Factors
• Etiology

Signs and symptoms:

• None
• Palpitations
• Dyspnea
• Fatigue
• CHF
• Angina

DIAGNOSTIC TESTS & INTERPRETATION

• EKG is essential to establish diagnosis and determine if arrhythmia is amenable to ablative therapy (eg, dependent on the isthmus discussed previously).
• Ambulatory monitor (especially useful if paroxysmal) and evaluate heart rate (HR) during Afl
• Echo to evaluate structural heart disease (myocardial and valvular)

Lab

Check for hyperthyroidism

Imaging

• Cardiac catheterization and angiography if coronary artery disease suspected
• Echo if hypertensive or valvular heart disease is suspected

DIFFERENTIAL DIAGNOSIS

• Atrial fibrillation (irregularly irregular, no flutter waves on EKG)
• Atrial tachycardia (regular)
• AV reentrant and AV nodal reentrant tachycardias (regular)
• Junctional tachycardia (rare, regular)
• Multifocal atrial tachycardia (irregular)

Outline

• Information
• Diagnostic Tests & Interpretation
  • Lab
  • Imaging
• Differential Diagnosis

• Rate control:
  • Acutely: IV -blocker (metoprolol, atenolol, esmolol) or calcium channel blocker (diltiazem, verapamil)
  • Chronically: -Blocker (metoprolol, atenolol) or calcium channel blocker (diltiazem, verapamil)
• Rhythm control:
  • Acutely: Ibutilide, procainamide, oral flecainide, or propafenone
  • Chronically: Propafenone, flecainide, sotalol, or amiodarone (less common: Quinidine, procainamide, disopyramide—due to concerns of extracardiac side effects)
  • QT-prolonging drugs are contraindicated if history of torsade de pointes ventricular tachycardia

ADDITIONAL TREATMENT

General Measures

• The standard of therapy is slowing of the ventricular rate with drugs that block the AV node, followed by the administration of an antiarrhythmic drug (class I or III) to restore and maintain sinus rhythm.
• Conversion to sinus rhythm can be accomplished by drug therapy, electrical cardioversion, rapid atrial pacing (transvenous pacing electrode, or rarely via the esophagus), and most with RF ablation.
• The magnitude of risk for stroke attributable to Afl cardioversion is believed to be similar to atrial fibrillation (AF), thus considerations for anticoagulation are the same as for AF.
• After cardiac surgery, the epicardial atrial pacing wire can be used to overdrive pace terminate Afl in the ICU.

Additional Therapies

• Catheter ablation of Afl isthmus is curative in nearly 100% of patients if done by electrophysiologists skilled in the technique.
• For young patients and those who wish to avoid long-term drug dependency, it is the management of choice.

IN-PATIENT CONSIDERATIONS

Admission Criteria

• Often patients can be treated for Afl on a completely outpatient basis.
• Criteria for admission include complications of Afl such as an uncontrolled ventricular response, heart failure, or angina as a consequence of Afl, and for the initiation of antiarrhythmic drug therapy, especially drugs that are associated with proarrhythmia.
• Controversy exists as to who needs to be admitted for drug initiation, with considerations being:
  • Age (and hence altered drug metabolism)
  • Underlying heart disease (proarrhythmia potential)

Outline

• Additional Treatment
  • General Measures
  • Additional Therapies
• In-Patient Considerations
  • Admission Criteria

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

• If anticoagulation chosen:
  • Follow INR, which should be 2–3 for optimal protection against embolization and minimization of risk for bleeding.
  • Start warfarin carefully.
• Follow EKG and response to antiarrhythmic drugs:
  • Watch for ventricular proarrhythmia related to antiarrhythmic drug therapy.
• Assess ventricular control in Afl with Holter or ambulatory monitoring.
• Bleeding as consequence of anticoagulation

DIET

Appropriate for underlying disease or syndrome such as diabetes, coronary artery disease, heart failure, and HTN.

PATIENT EDUCATION

• Importance of anticoagulation and control of INR to prevent stroke if anticoagulated
• Be vigilant for bleeding as a consequence of anticoagulation, and for proarrhythmia from antiarrhythmic drugs.

PROGNOSIS

• Depends on age and population in question
• Patients with Afl in the absence of other diseases have a normal prognosis, and probably a very low risk for stroke.
• In contrast, patients with structural heart disease will have prognosis determined by their underlying disease.

Outline

• Follow-Up Recommendations
  • Patient Monitoring
• Diet
• Patient Education
• Prognosis

CODES

ICD9

427.32 Atrial flutter

SNOMED

5370000 atrial flutter (disorder)

ADDITIONAL READING

• Cosio FG, Arribas F, López-Gil M, et al. Radiofrequency ablation of atrial flutter. J Cardiovasc Electrophysiol. 1996;7:60–70.
• Olshansky B, Wilber DJ, Hariman RJ. Atrial flutter—update on the mechanism and treatment. PACE. 1992;15:2308–2335.
• Windecker S, Kay GN, Epstein AE, et al. Atrial flutter. Cardiac Electrophysiol Rev. 1997;1/2:52–60.
• Wood KA, Eisenberg SJ, Kalman JM, et al. Risk of thromboembolism in chronic atrial flutter. Am J Cardiol. 1997;79:1043–1047.

Peter Ott