Pathophysiology | Etiology | Diagnosis | Symptoms | Treatment | Special Situations
Atrial flutter is similar to atrial fibrillation in that the rhythm originates in the atrium and causes a narrow complex tachycardia, which carries thromboembolic risk. Typical atrial flutter results from a reentrant circuit around the tricuspid valve and through the cavo-tricuspid isthmus. This anatomically makes ablation much easier than in atrial fibrillation, which occurs in the pulmonary veins. The atrial rates during atrial flutter vary from 250 to 350 beats per minutes, slower than the 400 to 600 bpm seen in atrial fibrillation. Frequently, a 2:1 conduction ratio occurs, resulting in a ventricular rate of 150 bpm.
Pathophysiology – Atrial Flutter
Atrial flutter can described as “typical” (a.k.a. type I) or “atypical” (a.k.a. type II) based on the anatomic location that it originates. Also, atrial flutter can be described as “clockwise” or “counterclockwise” depending on the direction of the circuit.
Typical atrial flutter is counterclockwise in direction and originates from a reentrant circuit around the tricuspid valve annulus and through the cavo-tricuspid isthmus. This results in negatively-directed flutter waves in the inferior leads. At times, the direction of the circuit can reverse, causing clockwise atrial flutter from the same anatomical location. This appears as positively-directed flutter waves in the inferior leads.
Atypical atrial flutter originates from the left atrium or areas in the right atrium (such as surgical scars) and has a variable appearance on ECG in regards to the flutter waves.
Etiology – Atrial Flutter
The etiology of atrial flutter is similar to that of atrial fibrillation. Identifying the etiology of cannot be under-emphasized, as treating the cause is frequently necessary to eliminate recurrences of atrial flutter.
The classic mnemonic “PIRATES” encompases a vast majority of the causes:
Pulmonary embolus, pulmonary disease, post-operative, pericarditis
Ischemic heart disease, idiopathic (“lone AF”), intravenous central line (in right atrium)
Rheumatic valvular disease (specifically mitral stenosis or mitral regurgitation)
Anemia, alcohol (“holiday heart”), advanced age, autonomic tone (vagally-mediated atrial fibrillation)
Thyroid disease (hyperthyroidism)
Elevated blood pressure (hypertension), electrocution
Sleep apnea, sepsis, surgery
Historically, hypertension was thought to be the most common cause of atrial flutter; however, obstructive sleep apnea is present in about 40% of patients, and it is well known that OSA causes hypertension. The exact proportion of atrial flutter caused directly by OSA remains unclear.
Diagnosis – Atrial Flutter
Diagnosing atrial flutter is done predominantly on the surface ECG. Sinus P waves are absent. The classic “sawtooth” pattern occurs, as the reentrant circuit around the tricuspid valve is large, resulting in high-amplitude P waves.
Distinguishing between clockwise and counterclockwise atrial flutter was described previously.
The ventricular rate is frequently elevated and regular ― the latter of which is an important factor that allows for differentiation between atrial flutter and atrial fibrillation. However, if “variable conduction” of the atrial flutter waves to the ventricles is present, the QRS complexes can be irregularly irregular. Also, multifocal atrial tachycardia, or MAT, can be irregularly irregular.
When the heart rate is significantly elevated ― that is, greater than 150 bpm ― it is frequently difficult to differentiate atrial flutter from atrial fibrillation, atrial tachycardia or atrioventricular nodal reentrant tachycardia, or AVNRT. In this situation, giving adenosine will transiently slow the ventricular rate, unmasking the atrial flutter waves and allowing a more definitive diagnosis to be made.
On physical examination, the heart rhythm will be frequently tachycardic and usually regular but, as above, may be irregularly irregular if variable conduction is present. Findings of congestive heart failure may be present depending on the ventricular rate, duration of atrial flutter and other factors. There will never be a S4 heart sound present during atrial flutter, as this heart sound is produced when atrial contraction forces blood into a noncompliant left ventricle. Normal atrial contraction is lost during atrial flutter.
Diagnosing a left atrial appendage thrombus ― which can result in thromboembolism, frequently causing stroke ― must be done using transesophageal echocardiography or cardiac CT (less commonly used). It is important to note that transthoracic echocardiography does not detect left atrial appendage thrombi in the vast majority of patients. TEE findings of a LAA thrombus include direct visualization of a mobile echodensity within the appendage. The echodensity should move independent of the walls of the atrium; this helps to distinguish artifact from thrombus. Pulse wave Doppler can be used in the LAA to determine the flow velocity. A velocity of less than 0.4 meters/second indicates a higher risk in general for thromboembolism.
Symptoms – Atrial Flutter
The symptoms of atrial flutter relate to tachycardic heart rate either causing palpitations or decreased overall cardiac output (from loss of atrial contraction and fast ventricular rates) resulting in congestive heart failure. If hypotension is present from a significantly reduced cardiac output, dizziness and even syncope (loss of consciousness) can occur.
Treatment – Atrial Flutter
The approach to the management of patients with atrial flutter requires the consideration of two distinct areas ― alleviating symptoms of atrial flutter and preventing thromboembolism.
There are two main approaches which can be utilized to alleviate symptoms of atrial fibrillation — a “rate control” strategy or a “rhythm control” strategy.
The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial evaluated using a rate control strategy vs. a rhythm control strategy and included a number of patients with atrial flutter in addition to atrial fibrillation. There was no difference in mortality between these approaches; thus, an individualized approach is recommended based on the degree of symptoms and the patient’s personal preference. In practice, atrial flutter ablation is commonly utilized in typical atrial flutter, as the procedure is much easier than atrial fibrillation ablation with a high success rate and low complication risk.
Commonly, controlling the ventricular rate in atrial flutter can completely resolve symptoms, and no further therapy is needed. This is done using AV blocking medications, either intravenously in the acute setting or orally for long-term therapy. Atrial flutter tends to be more difficult to control with AV blocking medications than atrial fibrillation.
Selecting the appropriate AV blocking agent requires knowledge of other indications and contraindications for these drugs ― specifically, knowledge of the left ventricular systolic function is important. AV blocking agents used in atrial flutter include beta-blockers, nondihydropyridine calcium channel blockers and digoxin.
Beta-blockers (atenolol, metoprolol, carvedilol and others) antagonize beta-receptors (see review of beta-adrenergic blockers), resulting in decreased conduction through the AV node, which reduces the heart rate in patients with atrial fibrillation. Caution is advised in patients with asthma, as antagonizing beta-2 receptors can cause bronchospasm. In severe left ventricular systolic dysfunction (reduced ejection fraction), beta-blockers can acutely decrease cardiac output leading to severe hypotension, acute heart failure and even cardiogenic shock. Despite this, beta-blockers are considered safe when used cautiously in this setting.
Nondihydropyridine calcium channel blockers (diltiazem, verapamil) decrease AV conduction by antagonizing voltage gated calcium channels, decreasing intracellular calcium. Because these drugs reduce left ventricular inotropy (contractility) via the same mechanism, they are generally not recommended for use in the setting of left ventricular systolic dysfunction (reduced ejection fraction).
Digoxin blocks the sodium/potassium ATPase pump. The mechanism by which this decreases AV conduction is not clear, but is perhaps due to increased vagal tone. Intracellular calcium within the cardiac myocytes is increased by digoxin, resulting in increased inotropy (contractility); thus, digoxin is frequently used when atrial fibrillation and left ventricular systolic dysfunction coexist. Digoxin is effective to reduce ventricular rates at rest but not effective during physical activity. Therefore, it is recommended to use digoxin in combination with a beta-blocker or nondihydropyridine calcium channel blocker.
Rarely, the above medications are not able to adequately reduce the ventricular rate, and AV nodal ablation with permanent pacemaker implantation is needed.
A rhythm control strategy is employed when rate control is not successful in completely eliminating symptoms from atrial flutter or if the ventricular rate is refractory to the above mentioned AV blocking medications. This can be done using cardioversion, antiarrhythmic drug therapy or ablation.
The term “cardioversion” is used to describe an action taken to restore sinus rhythm. This can be done either electrically by delivering a shock (direct current cardioversion, or DCCV) or chemically with certain drugs (class IA, class IC or class III antiarrhythmic drugs).
Once sinus rhythm is restored, antiarrhythmic drug therapy can be utilized to maintain sinus rhythm, especially if the risk of recurrence is high such as in severe left atrial enlargement, severe valvular heart disease or uncontrolled sleep apnea.
Antiarrhythmic drugs used to treat atrial fibrillation or flutter include the following:
Class IA (quinidine, procainamide, disopyramide): Although class IA drugs are effective to treat atrial flutter, they are not commonly utilized for this purpose due to side-effects and significant proarrhythmia, except in special situations (atrial flutter with Wolff-Parkinson-White). These agents block cardiac sodium channels and depress phase 0 of the action potential. Procainamide can cause drug-induced lupus erythematosus, detected by measuring anti-histone antibodies. Quinidine can cause cinchonism.
Class IB (lidocaine, mexiletine): These agents are not effective to treat atrial fibrillation or atrial flutter and are used for ventricular arrhythmias.
Class IC (flecainide, propafenone, moricizine): These drugs are commonly used to maintain sinus rhythm in patients with atrial flutter. Significant coronary artery disease is a contraindication to their use, as this increases the risk for proarrhythmia and sudden cardiac death. These agents must be used in combination with an AV blocking agent in order to prevent rapid atrial flutter conduction (1:1 conduction) through the AV node resulting in very fast ventricular rates if a breakthrough episode occurs because they also act to increase AV nodal conduction. These drugs may be proarrhythmic in the setting of left ventricular hypertrophy (wall thickness > 1.4 cm). Flecainide can be used with a “pill-in-the-pocket” approach. If documented to be successful and safe while hospitalized, flecainide can be used on an as-needed basis in the outpatient setting. Note that propafenone is hepatically cleared (not recommended with liver disease), whereas flecainide is renally cleared.
Class III (amiodarone, sotalol, bretylium, dofetilide, dronedarone, ibutilide): These drugs are also commonly used in atrial flutter and act by blocking potassium channels. Amiodarone is very effective but toxicity is a concern. The half-life of amiodarone is 42 days. Sotalol is proarrhythmic in the setting of LVH. Amiodarone and dofetilide are preferred in patients with left ventricular systolic dysfunction (reduced ejection fraction). Dronedarone is not safe with systolic heart failure or in the setting of permanent atrial flutter. Bretylium is rarely used.
Atrial flutter ablation can be utilized as an initial rhythm control strategy instead of antiarrhythmic drugs, as this procedure is low risk with a high success rate ― unlike that of atrial fibrillation, for which success rates vary, and there is higher risk for complication. See the comparison chart below:
Atrial Fibrillation Ablation
Atrial Flutter Ablation
Originates from pulmonary veins*
Transseptal puncture required
Higher complication risk
Variable success rates**
Antiarrhythmic drugs used first
Originates from tricuspid annulus*
No transseptal puncture required
Lower complication risk
Consistently high success rate
Ablation commonly used first
*Less commonly, atrial fibrillation originates from the right atrium including the superior vena cava or coronary sinus. Atypical atrial flutter may originate from left atrium on occasion but is less common.
**Duration of atrial fibrillation and left atrial volume is main determinant of success rates
Special Situations – Atrial Flutter
1:1 Conduction of Atrial Flutter
When a class IC antiarrhythmic drug is used for atrial flutter, an AV blocking agent must be used simultaneously to avoid a paradoxical increase in ventricular rates. The atrial rate during atrial flutter is between 250 and 350 bpm. At this rate, the AV node is usually refractory long enough to block at least every other beat from conducting to the ventricles. The class IC antiarrhythmic drugs can slow the atrial rate and increase AV nodal conduction as well.
If the atrial rate is slowed ― for example, from 300 to 200 bpm ― the AV node may not be refractory long enough to block any of these atrial impulses. Originally, if 2:1 conduction was occurring with the atrial rate of 300 bpm, the ventricular rate would be 150 bpm. If the atrial rate is slowed to 200 bpm, and 1:1 conduction occurs, the ventricular rate would be faster at 200 bpm despite a lower atrial rate.