Atrial Flutter Clinical Presentation

  • Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Nov 15, 2011
 

History

Symptoms in patients with atrial flutter typically reflect decreased cardiac output as a result of the rapid ventricular rate. Typical symptoms include the following:

  • Palpitations
  • Fatigue or poor exercise tolerance
  • Mild dyspnea
  • Presyncope

Less common symptoms include angina, profound dyspnea, or syncope. Thromboembolic events are possible with this arrhythmia. In addition, patients may have symptoms of the conditions that are causing the atrial flutter. These may be noncardiac (eg, hyperthyroidism, pulmonary disease) or cardiac. The clinician should attempt to elicit information about factors that may have precipitated the episode of atrial flutter (eg, alcohol, caffeine).

Determining when the onset of symptoms occurred is critical, as the duration of the episode affects management. Atrial flutter for longer than 48 hours requires anticoagulation with warfarin or transesophageal echo to rule out thrombus in the left atrium prior to cardioversion to sinus rhythm. In patients with a past history of atrial flutter, the history should include precipitating causes and modes of termination of the arrhythmia.

Atrial flutter can cause hypotension, angina, congestive heart failure, and rarely syncope due to rapid ventricular response in the setting of compromised left ventricular function. A history of pre-excitation syndrome (Wolff-Parkinson-White) indicates a need for caution, as these patients are at risk for 1:1 conduction of the flutter waves, which can cause ventricular fibrillation (VF).

Atrial flutter rhythm itself is unstable and usually reverts either to atrial fibrillation or sinus rhythm. It would be unusual for a patient to remain in stable chronic atrial flutter.

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Physical Examination

The patient’s general appearance and vital signs are important for determining the urgency with which to restore sinus rhythm. Thus, the initial cardiopulmonary evaluation and monitoring for signs of cardiac or pulmonary failure help guide initial management.

Pay careful attention to heart rate, blood pressure, and oxygen saturation. Tachycardia may or may not be present, depending on the degree of atrioventricular (AV) block associated with the atrial flutter activity.

The heart rate is often approximately 150 beats per minute because of a 2:1 AV block (this depends on the atrial firing rate, which may be influenced by medications as well as intrinsic cardiac factors.) The pulse may be regular or slightly irregular, as the AV block may be variable. Hypotension is possible, but normal blood pressure is observed more commonly.

Other points in the physical examination are as follows:

  • Palpate the neck/thyroid gland for goiter
  • Evaluate the neck for jugular venous distention
  • Auscultate the lungs for rales or crackles
  • Auscultate the heart for extra heart sounds and murmurs
  • Palpate the point of maximum impulse on the chest wall
  • Assess the lower extremities for edema or impaired perfusion

If embolization has occurred from intermittent atrial flutter, findings are related to brain and/or peripheral vascular involvement. In addition to neurologic insult, other complications of atrial flutter may include the following:

  • Embolization (arterial)
  • Congestive heart failure (CHF)
  • Severe bradycardia
  • Myocardial rate–related ischemia
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Contributor Information and Disclosures
Author

Lawrence Rosenthal, MD, PhD, FACC, FHRS  Associate Professor of Medicine, Director, Section of Cardiac Pacing and Electrophysiology, Director of EP Fellowship Program, Division of Cardiovascular Disease, University of Massachusetts Memorial Medical Center

Lawrence Rosenthal, MD, PhD, FACC, FHRS is a member of the following medical societies: American College of Cardiology, American Heart Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Cynthia Anne Ennis, DO  Electrophysiology Fellow, University of Massachusetts Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Brian Olshansky, MD  Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

References

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  2. Granada J, Uribe W, Chyou PH, Maassen K, Vierkant R, Smith PN, et al. Incidence and predictors of atrial flutter in the general population. J Am Coll Cardiol. Dec 2000;36(7):2242-6. [Medline].

  3. Ghali WA, Wasil BI, Brant R, Exner DV, Cornuz J. Atrial flutter and the risk of thromboembolism: a systematic review and meta-analysis. Am J Med. Feb 2005;118(2):101-7. [Medline].

  4. Bohnen M, Stevenson WG, Tedrow UB, et al. Incidence and predictors of major complications from contemporary catheter ablation to treat cardiac arrhythmias. Heart Rhythm. Nov 2011;8(11):1661-6. [Medline].

  5. Biblo LA, Yuan Z, Quan KJ, Mackall JA, Rimm AA. Risk of stroke in patients with atrial flutter. Am J Cardiol. Feb 1 2001;87(3):346-9, A9. [Medline].

  6. Melsen WG, Rovers MM, Bonten MJ. Ventilator-associated pneumonia and mortality: a systematic review of observational studies. Crit Care Med. Oct 2009;37(10):2709-18. [Medline].

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  8. Falk RH, Pollak A, Singh SN, Friedrich T. Intravenous dofetilide, a class III antiarrhythmic agent, for the termination of sustained atrial fibrillation or flutter. Intravenous Dofetilide Investigators. J Am Coll Cardiol. Feb 1997;29(2):385-90. [Medline].

  9. Abi-Mansour P, Carberry PA, McCowan RJ, Henthorn RW, Dunn GH, Perry KT. Conversion efficacy and safety of repeated doses of ibutilide in patients with atrial flutter and atrial fibrillation. Study Investigators. Am Heart J. Oct 1998;136(4 Pt 1):632-42. [Medline].

  10. Stambler BS, Wood MA, Ellenbogen KA, Perry KT, Wakefield LK, VanderLugt JT. Efficacy and safety of repeated intravenous doses of ibutilide for rapid conversion of atrial flutter or fibrillation. Ibutilide Repeat Dose Study Investigators. Circulation. Oct 1 1996;94(7):1613-21. [Medline].

  11. Stambler BS, Wood MA, Ellenbogen KA. Antiarrhythmic actions of intravenous ibutilide compared with procainamide during human atrial flutter and fibrillation: electrophysiological determinants of enhanced conversion efficacy. Circulation. Dec 16 1997;96(12):4298-306. [Medline].

  12. Vos MA, Golitsyn SR, Stangl K, Ruda MY, Van Wijk LV, Harry JD, et al. Superiority of ibutilide (a new class III agent) over DL-sotalol in converting atrial flutter and atrial fibrillation. The Ibutilide/Sotalol Comparator Study Group. Heart. Jun 1998;79(6):568-75. [Medline]. [Full Text].

  13. Vos MA, Golitsyn SR, Stangl K, Ruda MY, Van Wijk LV, Harry JD, et al. Superiority of ibutilide (a new class III agent) over DL-sotalol in converting atrial flutter and atrial fibrillation. The Ibutilide/Sotalol Comparator Study Group. Heart. Jun 1998;79(6):568-75. [Medline]. [Full Text].

  14. Berger M, Schweitzer P. Timing of thromboembolic events after electrical cardioversion of atrial fibrillation or flutter: a retrospective analysis. Am J Cardiol. Dec 15 1998;82(12):1545-7, A8. [Medline].

  15. Grimm RA, Stewart WJ, Arheart K, Thomas JD, Klein AL. Left atrial appendage "stunning" after electrical cardioversion of atrial flutter: an attenuated response compared with atrial fibrillation as the mechanism for lower susceptibility to thromboembolic events. J Am Coll Cardiol. Mar 1 1997;29(3):582-9. [Medline].

 
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The anatomy of classic counterclockwise atrial flutter. This demonstrates an oblique view of the right atrium and shows some of the crucial structures. The isthmus of tissue responsible for atrial flutter is seen anterior to the orifice of the coronary sinus. The Eustachian ridge is part of the crista terminalis that separates the roughened part of the right atrium from the smooth septal part of the right atrium.
Type I counterclockwise atrial flutter. This 3-dimensional electroanatomic map of the tricuspid value and right atrial show the activation pattern displayed in color format. Red is early and blue is late relative to a fixed point in time. Activation travels in a counterclockwise direction.
Twelve-lead ECG of type I atrial flutter. Note negative sawtooth pattern of flutter waves in leads II, III, and aVF.
Atypical LA flutter.
The 3-dimensional electroanatomic map of type I atrial flutter. The colors progress from blue to red to white and represent relative conduction time in the right atrium (early to late). An ablation line (red dots) has been created on the tricuspid ridge extending to the inferior vena cava. This interrupts the flutter circuit.RAA: right atrial appendage; CSO: coronary sinus os; IVC: inferior vena cava; TV: tricuspid valve annulus.
Type I atrial flutter unmasked by adenosine (Adenocard).
 
 
 
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