AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

Atrial flutter is a relatively common atrial tachyarrhythmia. After atrial fibrillation, atrial flutter is the most significant of the atrial tachyarrhythmias.

Atrial flutter has traditionally been characterized as a macroreentrant arrhythmia with atrial rates between 240-400 beats per minute.

Atrial flutter is defined by the presence of stable, uniform atrial activation (flutter waves).

Atrial flutter, depending on the ventricular rate, can impede cardiac output and lead to atrial thrombus formation, with risk of systemic embolization.

Atrial flutter commonly includes some form of A-V block. Most commonly atrial depolarization is conducted at a 2:1 ratio, though it can also be conducted at a 4:1 ratio, and less commonly at a 3:1 or 5:1 ratio.

Pathophysiology

Multiple re-entrant or primarily generated (ectopic) atrial waveforms bombard the atrioventricular (AV) node.

The two forms of atrial flutter are known as type I and type II. Type I is the most common form.

Atrial flutter, type I, is also referred to as typical, common, or counter-clockwise isthmus-dependent atrial flutter and involves a re-entrant circuit that encircles the tricuspid annulus of the right atrium, with a depolarizing stimulus traveling up the atrial septum, experiencing epicardial break-through superiorly, and traveling back down the atrial free wall. (A clockwise variant of this circuit also exists.)

Type II atrial flutter, also known as atypical aflutter, is still poorly characterized, but may result from an intraatrial reentrant circuit operating at a faster rate.

Type I has traditionally been distinguished by a rate of 240-340 beats, and the ability to be entrained by atrial pacing. Type II has a rate greater than 340 beats.

Atrial flutter is associated in patients with heart failure, valvular disease, chronic obstructive pulmonary disease, hyperthyroidism, pericarditis, pulmonary embolism, and a history of open heart surgery.

Frequency

United States

Atrial flutter affects approximately 88 out of 100,000 new patients each year. In the United States, this represents approximately 200,000 patients presenting with atrial flutter annually.

Mortality/Morbidity

For the most part, morbidity and mortality are due to complications of rate (ie, syncope, congestive heart failure [CHF]). In patients who suffer from atrial flutter, the risk of embolic occurrences approaches that of atrial fibrillation.

Sex

Men are affected more often than women, with a 2:1 male-to-female ratio.

Age

The prevalence of atrial fibrillation increases with age and varies from 1 case out of 200 persons for people younger than 60 years, to almost 9 cases out of 100 persons for people over 80 years.

• Aged 25-35 years: 2-3/1000 people
• Aged 55-64 years: 30-90/1000 people
• Aged 65-90 years: 50-90/1000 people

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

Symptomatic atrial flutter is typically a manifestation of the rapid ventricular rate that decreases cardiac output.

• Palpitations
• Fatigue or poor exercise tolerance
• Mild dyspnea
• Presyncope
• Less common symptoms include angina, profound dyspnea, or syncope. Symptomatic embolic events are rare, but must be considered.

Physical

Pertinent physical findings are limited to cardiovascular system. If embolization has occurred from intermittent AF, findings are related to brain and/or peripheral vascular involvement.

• Tachycardia may or may not be present, depending on the degree of AV block associated with the atrial flutter activity.
• • Cardiac rate, often approximately 150 beats per minute because of a 2:1 AV block (This is dependent on the atrial firing rate, which may be influenced by medications as well as intrinsic cardiac factors.)
  • Regular or slightly irregular heartbeat
• Hypotension is possible, but normal blood pressure is observed more commonly.
• Peripheral embolization may occur, if associated with AF.
• CHF may be found, usually caused by left ventricle dysfunction.

Causes

• Patients at highest risk include those with long-standing hypertension, valvular heart disease (rheumatic), left ventricular hypertrophy, coronary artery disease with or without depressed left ventricular function, pericarditis, pulmonary embolism, hyperthyroidism, and diabetes. Additionally, CHF for any reason is a noted contributor to this disorder.
• Additional causes include the following:
• • Postoperative revascularization
  • Digitalis toxicity
  • Rare causes
    • Myotonic dystrophy in childhood (case report by Suda K, Matsumura M, Hayashi Y)

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Narrow complex tachyarrhythmias

Wide complex tachyarrhythmias

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Imaging Studies

• Chest radiographic findings are usually normal. Look for radiographic evidence of pulmonary edema in subacute cases.
• Obtain thyroid function studies.
• Obtain serum electrolyte and digoxin levels if appropriate.
• Obtain CBCs if anemia is suspected or a history of recent or current blood loss is associated with presenting symptoms.
• Consider obtaining blood gases in patients with hypoxia, or carbon monoxide intoxication. Also, seek a history of stimulant drug usage (eg, ginseng, cocaine, ephedra, methamphetamine).

Other Tests

• Electrocardiography (ECG)
• • Atrial rate during typical (ie, type I) atrial flutter is usually 250-350 beats per minute, although class IA and IC antiarrhythmic drugs and amiodarone can reduce the rate to approximately 200 beats per minute. If this occurs, the ventricles can respond in a 1:1 fashion to the slower atrial rate.
  • Atrial rate ordinarily is about 300 beats per minute. In untreated patients, the ventricular rate is half the atrial rate (ie, 150 beats per minute). A significantly slower ventricular rate in the absence of drugs suggests abnormal AV conduction.
  • Atrial flutter can conduct to the ventricle in a 1:1 fashion, producing a ventricular rate of 300 beats per minute in children, in patients with the pre-excitation syndrome, in those whose AV nodes conduct rapidly, and occasionally in patients with hyperthyroidism.
  • Rate in atypical (ie, type II) flutter is 350-450 beats per minute. Re-entry within the right atrial (tricuspid annulus) is responsible for most cases of atrial flutter.
  • In cases of typical atrial flutter, ECG reveals identically recurring regular sawtooth flutter waves (see Image 1) and evidence of continual electrical activity.
  • Flutter waves are often visualized best in leads II, III, aVF, or V1. The flutter waves for typical (type I) atrial flutter are inverted (negative) in these leads because of a counterclockwise re-entrant pathway. Sometimes they are upright (positive) when the re-entrant loop is clockwise. Flutter waves (particularly 2:1) can deform the ST complex in such a manner as to mimic an ischemic injury pattern on the 12-lead ECG.
  • Flutter and fibrillation often coexist with alternating patterns (ie, fib-flutter, flitter) in the same tracing.
• Transthoracic Echocardiogram
• • A transthoracic echocardiogram can be performed to evaluate right and left atrial size, as well as the size and function of the right and left ventricles, which assists in diagnosing valvular heart disease, LVH, and pericardial disease.

    Transthoracic echocardiogram has low sensitivity for intra-atrial thrombi, and is the preferred modality for testing atrial flutter.

• Exercise Testing
• • Exercise testing can be utilized to identify exercise-induced atrial fibrillation and to evaluate ischemic heart disease.
• Holter Monitoring
• • A Holter monitor can be used to help identify arrhythmias in patients with non-specific symptoms, identify triggers, and detect associated atrial arrhythmias.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Prehospital Care

In general, avoiding class I and III agents (eg, procainamide) in the prehospital setting is safest because of possible induction of 1:1 conduction. Generally, the rate can be slowed safely with calcium channel blockers or beta-adrenergic blockers.

Emergency Department Care

• Assess airway, breathing, and circulation. Hemodynamic concerns will dictate initial treatment.
• Blood pressure can be supported and rate controlled with medication.
• Look for underlying causes. At times, treatment of the underlying disorder (eg, thyroid disease, valvular heart disease) is necessary to effect conversion to sinus rhythm.

Consultations

• Most cases will require internal medicine or cardiology consultation.
• A cardiologist may become involved, primarily if the patient presents with complicating factors or an obvious ongoing cardiac ischemia (or infarction) not treatable with rate reduction measures and standard chest pain protocols.

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

If the patient is unstable (eg, hypotension, poor perfusion), synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice. Cardioversion often requires low energies (<50 J). If the electrical shock results in AF, a second shock at a higher energy level is used to restore normal sinus rhythm (NSR).

To slow the ventricular response, verapamil or diltiazem may be the appropriate initial treatment. Adenosine produces transient AV block and can be used to reveal flutter waves (see Image 1). These drugs generally do not convert atrial flutter to NSR.

If the flutter cannot be cardioverted, terminated by pacing, or slowed by the drugs mentioned above, digoxin can be administered alone or with either a calcium antagonist or beta-blocker. IV amiodarone has been shown to slow the ventricular rate and is considered as effective as digoxin.

Digoxin toxicity is very rarely a cause of flutter; however, ascertaining that flutter is not caused by digoxin toxicity is important. Another caveat is to beware of the vagolytic action of quinidine, procainamide, and disopyramide if used to slow the flutter rate. These drugs can effect AV conduction, resulting in a 1:1 ventricular response to the atrial flutter. Before administration of these drugs, be sure to slow the conduction rate with digoxin or calcium channel blockers.

Rate control is the goal of medication in atrial flutter or AF (see Atrial Fibrillation).

Beta-adrenergic blockers are especially effective in the presence of thyrotoxicosis and increased sympathetic tone.

Other antiarrhythmic drugs that can terminate atrial flutter/fibrillation include procainamide, disopyramide, propafenone, sotalol, flecainide, amiodarone, and ibutilide.

A newer agent is dofetilide, a recently approved class III antiarrhythmic. Another drug, azimilide, has been studied in the recent Azimilide Postinfarct Survival Evaluation (ALIVE) trial, a post-heart attack survival study. Additional data from ALIVE further support the ongoing development of azimilide as a treatment for supraventricular arrhythmias. Fewer patients in sinus rhythm at baseline developed atrial fibrillation/flutter during the trial on azimilide compared to placebo.

Another drug on the horizon is dronedarone, a deiodinated derivative of amiodarone that has no organ toxicity. Its use will extend to both atrial and ventricular arrhythmias. At present, dronedarone is an experimental agent that has multiple actions (all 4 Von Williams class effects). Unlike amiodarone, it does not have the iodine moiety. The lack of iodination may offer a better side-effect profile. Dronedarone has been shown to (1) have antiadrenergic effects, (2) prolong atrial and ventricular refractory periods, and (3) prolong atrioventricular node conduction as well as the paced QRS complex. In animal models, dronedarone has been shown to decrease ischemia-induced ventricular arrhythmias. The clinical effects of dronedarone are currently being examined in patients with atrial fibrillation and in patients with ICDs.

Antiarrhythmic drugs alone control atrial flutter in only 50-60% of patients. Since the early 1990s, radiofrequency catheter ablation has been used to interrupt the re-entrant circuit in the right atrium and prevent recurrences of atrial flutter. Radiofrequency ablation is immediately successful in more than 90% of cases and avoids the long-term toxicity observed with antiarrhythmic drugs.

When considering drug therapy for atrial flutter/fibrillation, remember the treatment caveat "electrical cardioversion is the preferred modality in the patient whose condition is unstable."

Drug Category: Calcium channel blockers

Reduce the rate of AV nodal conduction and control ventricular response. Formulations administered IV are discussed only as they relate to the control of severe symptoms (eg, rapid ventricular rate in emergent situations).

Drug Category: Beta-blockers

Slow the sinus rate and decrease AV nodal conduction. Now have more of a secondary role in rate control in atrial flutter/fibrillation. Be sure to monitor blood pressure carefully.

Drug Category: Class I antiarrhythmics

Used for chemical conversion into sinus rhythm. Alter the electrophysiologic mechanisms responsible for arrhythmia.

Drug Category: Class III antiarrhythmics

Establish a chemical conversion to sinus rhythm.

Drug Category: Cardiac glycosides

Decrease AV nodal conduction primarily by increasing vagal tone. Used mainly in the context of AF and atrial flutter with CHF.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Further Inpatient Care

• The issue of stroke risk and anticoagulation in patients with atrial flutter is controversial; however, Seidl et al recently studied 191 consecutive patients admitted to the hospital with atrial flutter and found that the risk of thromboembolism may be higher than previously thought.
• Since atrial contractility should remain intact in patients with flutter, suggestions have been made that thrombus formation is unlikely. However, patterns were noted in this study, including the following:
• • Eleven patients (6%) had a history of an embolic event at presentation.
  • Within the first 48 hours after cardioversion, 2% experienced a cerebral embolism.
  • One additional patient in the study had a transient ischemic event despite anticoagulation.
  • Whether these embolic events were due to atrial flutter per se or if they were caused by intermittent AF, which is known to occur in patients with atrial flutter, is unknown.
  • Preliminary results from this study support anticoagulation for patients with atrial flutter.
  • Vidaillet et al (2002) studied the overall mortality rate in a group of patients with atrial flutter and AF and compared it to the mortality rate in a control group. They found that the mortality rates were similar for patients in all arrhythmia subgroups - 41% in atrial flutter, 45% in AF, and 47% in patients with both conditions. The mortality rate in population matched control subjects was found to be 22%. The mortality rate among patients with AF was determined to be somewhat higher than that among patients with atrial flutter alone.
• Catheter Ablation Treatment
• • Given the recognized difficulty in achieving permanent suppression of atrial flutter with chemical treatment, catheter ablation is increasingly the treatment of choice in clinically significant atrial flutter.

    Advances in electrophysiologic mapping and catheter ablation techniques have improved the efficacy of this treatment modality to greater than 90%.

Transfer

• Transfer to a referral center may be indicated for patients who present to the emergency department (ED) with complications of atrial flutter, including the following:
• • Bradycardia (eg, from sick sinus syndrome) requiring pacemaker therapy
  • Unresponsive rate despite adequate medical therapy; after electrical cardioversion, referral for electrophysiologic ablation may be appropriate. These patients generally are transferred from one inpatient facility to another.
  • Embolic complications requiring surgical therapy (ie, arterial embolization), cerebrovascular accident (CVA), AF, or atrial flutter requiring neurointensive care

Complications

• Stroke
• Embolization (arterial)
• CHF
• Severe bradycardia
• Myocardial rate-related ischemia

Prognosis

• With AF and atrial flutter, the relative risk for development of stroke is 4.1% compared with control subjects.

Patient Education

• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education articles Atrial Flutter and Palpitations.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• Watch for development of severe bradycardia during treatment. This may cause severe hypotension and death if not carefully monitored.
• Rarely, AF or atrial flutter may be due to pericardial disease or effusion or carbon monoxide intoxication. Keep these rare events in mind when dealing with the unusual case of a patient who does not respond to standard therapy.
• While radiofrequency (RF) ablation is beyond the domain of the ED physician, complications of this procedure are reported in the literature. The physician must be knowledgeable of these complications when treatment options are proposed to the patient and family members. Of interest is a report by Sassone et al of thermal-related right coronary artery damage secondary to RF therapy in a patient with resultant myocardial infarction.

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Alan D Clark, MD† , to the development and writing of this article.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  Type I atrial flutter unmasked by adenosine (Adenocard).
	View Full Size Image
Media type:  Rhythm Strip

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

• Braunwald E. Heart disease: A Textbook of Cardiovascular Medicine. 5th ed. Philadelphia: WB Saunders Co;1997:641-656.
• Galve E, Rius T, Ballester R, et al. Intravenous amiodarone in treatment of recent-onset atrial fibrillation: results of a randomized, controlled study. J Am Coll Cardiol. Apr 1996;27(5):1079-82. [Medline].
• Goodacre S, Irons R. ABC of clinical electrocardiography: Atrial arrhythmias. BMJ. Apr 27 2002;324(7337):594-597. [Medline].
• Niebauer MJ, Chung MK. Management of atrial flutter. Cardiol Rev. Sep-Oct 2001;9(5):253-8. [Medline].
• Perry JC, Fenrich AL, Hulse JE, et al. Pediatric use of intravenous amiodarone: efficacy and safety in critically ill patients from a multicenter protocol. J Am Coll Cardiol. Apr 1996;27(5):1246-50. [Medline].
• Pritchett EL. Management of atrial fibrillation. N Engl J Med. May 7 1992;326(19):1264-71. [Medline].
• Prystowsky EN, Benson DW Jr, Fuster V, et al. Management of patients with atrial fibrillation. A Statement for Healthcare Professionals. From the Subcommittee on Electrocardiography and Electrophysiology, American Heart Association. Circulation. Mar 15 1996;93(6):1262-77. [Medline]. [Full Text].
• Sassone B, Leone O, Martinelli GN, Di Pasquale G. Acute myocardial infarction after radiofrequency catheter ablation of typical atrial flutter: histopathological findings and etiopathogenetic hypothesis. Ital Heart J. May 2004;5(5):403-7. [Medline].
• Seidl K, Rameken M, Siemon G. Atrial flutter and thromboembolism risk. Cardiol Rev. 1999;16(12):25-28.
• Suda K, Matsumura M, Hayashi Y. Myotonic dystrophy presenting as atrial flutter in childhood. Cardiol Young. Feb 2004;14(1):89-92. [Medline].
• Vidailett H, Granada J, Massen K. A population-based study of mortality among patients with atrial fibrillation or flutter. Am J Med. Oct 1 2002;113(5):365-70. [Medline].
• Waldo A. Treatment of atrial flutter. Heart. Aug 2000;84(2):227-32. [Medline].

Article Last Updated: Oct 11, 2006