Atrial Flutter Workup

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

Approach Considerations

Electrocardiography (ECG) is essential in making the diagnosis. Transthoracic echocardiography is the preferred modality for evaluating atrial flutter.

The history and physical examination findings guide laboratory studies. Although hyperthyroidism is a rare cause of atrial flutter, asymptomatic hyperthyroidism, especially in elderly patients, can manifest as atrial fibrillation or flutter and should be excluded with thyroid function studies.

Obtain a complete blood count if anemia is suspected or the patient has a history of recent or current blood loss associated with presenting symptoms. Serum electrolytes and pulmonary function tests may be indicated based on the history. Obtain serum electrolyte and digoxin levels if appropriate.

Consider obtaining blood gas measurements in patients with hypoxia or carbon monoxide intoxication. Also, seek a history of stimulant drug usage (eg, ginseng, cocaine, ephedra, methamphetamine).

Chest radiography may be useful in evaluation of lung disease and the pulmonary vasculature. Chest radiographic findings are usually normal in patients with atrial flutter, but radiographic evidence of pulmonary edema may be present in subacute cases.

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Electrocardiography

In the common form of type I atrial flutter, the ECG shows sawtooth flutter (F) waves. Flutter waves are often visualized best in leads II, III, aVF, or V1 (see the image below). 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.

Twelve-lead ECG of type I atrial flutter. Note negTwelve-lead ECG of type I atrial flutter. Note negative sawtooth pattern of flutter waves in leads II, III, and aVF.

In typical (ie, type I) atrial flutter, the atrial rate is usually 250-350 beats per minute. The ventricular response may be regular or irregular. In patients with typical (ie, type I) atrial flutter, 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. The rate in atypical (ie, type II) flutter is 350-450 beats per minute.

The ventricular rate is a fixed mathematical relationship of flutter waves and the resulting QRS complexes. Variable AV conduction can also be seen (commonly present with 2:1 or 3:1 AV conduction). With 1:1 AV conduction, hemodynamic collapse may occur.

Deterioration to 1:1 conduction is a particular risk in patients with a preexcitation syndrome (Wolff-Parkinson-White). An ECG clue to a preexcitation syndrome is a very short PR interval (< .115s) and no delta wave.

Morphology of the flutter wave can predict findings in the electrophysiology laboratory. A negative flutter wave in the inferior limb leads and a positive flutter wave in V1 are highly predictive of a counterclockwise circuit; however, with positive flutter waves in the inferior limb leads and negative flutter waves in V1, differentiating between clockwise type I atrial flutter and atypical forms of non–isthmus-dependent intra-atrial reentry is difficult.

Flutter and fibrillation often coexist with alternating patterns (ie, fib-flutter, flitter) in the same tracing.

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Diagnostic Aids

Vagal maneuvers can be helpful in determining the underlying atrial rhythm if flutter waves are not seen well.

Adenosine, administered in an intravenous push followed with an intravenous bolus with flush, can also be helpful in making the diagnosis of atrial flutter by transiently blocking the AV node (see the image below).

Type I atrial flutter unmasked by adenosine (AdenoType I atrial flutter unmasked by adenosine (Adenocard).

Exercise testing can be utilized to identify exercise-induced atrial fibrillation and to evaluate ischemic heart disease.

A Holter monitor can be used to help identify arrhythmias in patients with nonspecific symptoms, identify triggers, and detect associated atrial arrhythmias.

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Echocardiography

Transthoracic echocardiography is the preferred modality for evaluating atrial flutter. It can 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, left ventricular hypertrophy (LVH), and pericardial disease.

Transthoracic echocardiography has low sensitivity for intra-atrial thrombi. Transesophageal echocardiography is the preferred technique to detect thrombus in the left atrium.

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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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  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].

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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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