Atrial flutter is a cardiac arrhythmia characterized by atrial rates of 240-400 beats/min and some degree of atrioventricular (AV) node conduction block. For the most part, morbidity and mortality are due to complications of rate (eg, syncope and congestive heart failure [CHF]). See the image below.
Signs and symptoms
Signs and symptoms in patients with atrial flutter typically reflect decreased cardiac output as a result of the rapid ventricular rate. Typical symptoms include the following:
Fatigue or poor exercise tolerance
Less common symptoms include angina, profound dyspnea, or syncope. Tachycardia may or may not be present, depending on the degree of AV block associated with the atrial flutter activity.
Physical findings include the following:
The heart rate is often approximately 150 beats/min because of a 2:1 AV block
The pulse may be regular or slightly irregular
Hypotension is possible, but normal blood pressure is more commonly observed
Other points in the physical examination are as follows:
Palpate the neck and 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 or peripheral vascular involvement. Other complications of atrial flutter may include the following:
Myocardial rate–related ischemia
See Presentation for more detail.
The following techniques aid in the diagnosis of atrial flutter:
ECG – This is an essential diagnostic modality for this condition
Vagal maneuvers – These can be helpful in determining the underlying atrial rhythm if flutter waves are not seen well
Adenosine – This can be helpful in the diagnosis of atrial flutter by transiently blocking the AV node
Exercise testing – This can be utilized to identify exercise-induced atrial fibrillation and to evaluate ischemic heart disease
Holter monitor – This can be used to help identify arrhythmias in patients with nonspecific symptoms, to identify triggers, and to detect associated atrial arrhythmias
Transthoracic echocardiography (TTE) 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, and this information facilitates diagnosis of valvular heart disease, left ventricular hypertrophy (LVH), and pericardial disease.
See Workup for more detail.
General treatment goals for symptomatic atrial flutter are similar to those for atrial fibrillation. They include the following:
Control of ventricular rate – This can be achieved with drugs that block the AV node; intravenous (IV) calcium channel blockers (eg, verapamil and diltiazem) or beta blockers can be used, followed by initiation of oral agents
Restoration of sinus rhythm – This can be done by means of electrical or pharmacologic cardioversion or RFA; successful ablation reduces or eliminates the need for long-term anticoagulation and antiarrhythmic medications
Prevention of recurrent episodes or decrease in their frequency or duration – In general, the use of antiarrhythmic drugs in atrial flutter is similar to that in atrial fibrillation
Prevention of thromboembolic complications – Adequate anticoagulation, as recommended by the American College of Chest Physicians, has been shown to decrease thromboembolic complications in patients with chronic atrial flutter and in patients undergoing cardioversion
Minimization of adverse effects from therapy – Because atrial flutter is a nonfatal arrhythmia, carefully assess the risks and benefits of drug therapy, especially with antiarrhythmic agents
Atrial flutter is a cardiac arrhythmia characterized by atrial rates of 240-400 beats/min, usually with some degree of atrioventricular (AV) node conduction block. In the most common form of atrial flutter (type I atrial flutter), electrocardiography (ECG) demonstrates a negative sawtooth pattern in leads II, III, and aVF.
Type I (typical or classic) atrial flutter involves a single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus. The circuit most often travels in a counterclockwise direction. Type II (atypical) atrial flutter follows a different circuit; it may involve the right or the left atrium. (See Pathophysiology.)
Atrial flutter is associated with a variety of cardiac disorders. In most studies, approximately 60% of patients with atrial flutter have coronary artery disease (CAD) or hypertensive heart disease; 30% have no underlying cardiac disease. Uncommon forms of atrial flutter have been noted during long-term follow-up in as many as 26% of patients with surgical correction of congenital cardiac anomalies. (See Etiology.)
Symptoms in patients with atrial flutter typically reflect decreased cardiac output as a result of the rapid ventricular rate. The most common symptom is palpitations. Other symptoms include fatigue, dyspnea, and chest pain. (See Presentation.) ECG is essential in making the diagnosis. Transthoracic echocardiography (TTE) is the preferred modality for evaluating atrial flutter. (See Workup.)
Intervening to control the ventricular response rate or to return the patient to sinus rhythm is important. Consider immediate electrical cardioversion for patients who are hemodynamically unstable. Consider catheter-based ablation as first-line therapy in patients with type I typical atrial flutter if they are reasonable candidates. Ablation is usually done as an elective procedure; however, it can also be done when the patient is in atrial flutter. (See Treatment.)
Atrial flutter is similar to atrial fibrillation in many respects (eg, underlying disease, predisposing factors, complications, and medical management), and some patients have both atrial flutter and atrial fibrillation. However, the underlying mechanism of atrial flutter makes this arrhythmia amenable to cure with percutaneous catheter-based techniques.
In humans, the most common form of atrial flutter (type I) involves a single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus (most often in a counterclockwise direction), with an area of slow conduction located between the tricuspid valve annulus and the coronary sinus ostium (subeustachian isthmus). A 3-dimensional electroanatomic map of type I atrial flutter is shown in the video below.
Animal models have been used to demonstrate that an anatomic block (surgically created) or a functional block of conduction between the superior vena cava and the inferior vena cava, similar to the crista terminalis in the human right atrium, is key to initiating and maintaining the arrhythmia.
The crista terminalis acts as another anatomic conduction barrier, similar to the line of conduction block between the 2 venae cavae required in the animal model. The orifices of both venae cavae, the eustachian ridge, the coronary sinus orifice, and the tricuspid annulus complete the barrier for the reentry circuit (see the image below). Type I atrial flutter is often referred to as isthmus-dependent flutter. Usually, the rhythm is due to reentry, there is an excitable gap, and the rhythm can be entrained.
Type I counterclockwise atrial flutter has caudocranial activation (ie, activation counterclockwise around the tricuspid valve annulus when viewed in the left antero-oblique fluoroscopic view) of the atrial septum (see the image below).
Type I atrial flutter can also have the opposite activation sequence (ie, clockwise activation around the tricuspid valve annulus). Clockwise atrial flutter is much less common. When the electric activity moves in a clockwise direction, the ECG will show positive flutter waves in leads II, III, and aVF and may appear somewhat sinusoidal. This arrhythmia is still considered type I, isthmus-dependent flutter; it is usually called reverse typical atrial flutter.
Type II (atypical) atrial flutters are less extensively studied and electroanatomically characterized. Atypical atrial flutters may originate from the right atrium, as a result of surgical scars (ie, incisional reentry), or from the left atrium, specifically the pulmonary veins (ie, focal reentry) or mitral annulus (see the image below). Left atrial flutter is common after incomplete left atrial linear ablation procedures (for atrial fibrillation). Thus, tricuspid isthmus dependency is not a prerequisite for type II atrial flutter.
Atrial flutter is associated with a variety of cardiac disorders. In most studies, approximately 30% of patients with atrial flutter have CAD, 30% have hypertensive heart disease, and 30% have no underlying cardiac disease. Rheumatic heart disease, congenital heart disease, pericarditis, and cardiomyopathy may also lead to atrial flutter. Rarely, mitral valve prolapse or acute myocardial infarction (MI) has been associated with atrial flutter.
In addition, the following conditions are also associated with atrial flutter:
Chronic obstructive pulmonary disease (COPD)
Myotonic dystrophy in childhood (rare) 
Atrial flutter may be a sequela of open heart surgery. After cardiac surgery, atrial flutter may be reentrant as a result of natural barriers, atrial incisions, and scar. Some patients develop atypical left atrial flutter after pulmonary vein isolation for atrial fibrillation.
Although there are no clearly defined genetic conditions that cause atrial flutter, in many cases there is likely an underlying genetic susceptibility to acquiring it. Genome-wide association studies (GWAS) have identified genes associated with atrial flutter. 
The PITX2 (paired-like homeodomain 2) gene on chromosome locus 4q25 is known to play a major role in left-right asymmetry of the heart and has been found to have a strong association with atrial fibrillation  and an even stronger association with typical atrial flutter.  There are not yet any clinically available genetic tests that can identify persons at increased risk for atrial flutter.
United States statistics
Atrial flutter is much less common than atrial fibrillation. Of the patients admitted to US hospitals with a diagnosis of supraventricular tachycardia between 1985 and 1990, 77% had atrial fibrillation and 10% had atrial flutter. On the basis of a study of patients referred to tertiary care centers, the incidence of atrial flutter in the United States is estimated to be approximately 200,000 new cases per year. 
Sex- and age-related demographics
In a study of 100 patients with atrial flutter, 75% were men. In another study performed at a tertiary care study, atrial flutter was 2.5 times more common in men.
Patients with atrial flutter, as with atrial fibrillation, tend to be older adults. In one study, the average age was 64 years. The prevalence of atrial fibrillation increases with age, as follows:
25-35 years: 2-3 cases per 1000 population
55-64 years: 30-90 cases per 1000 population
65-90 years: 50-90 cases per 1000 population
The prognosis for atrial flutter depends on the patient’s underlying medical condition. Any prolonged atrial arrhythmia can cause a tachycardia-induced cardiomyopathy. Intervening to control the ventricular response rate or to return the patient to sinus rhythm is important. Thrombus formation in the left atrium has been described in patients with atrial flutter (0-21%). Thromboembolic complications have also been described. 
Because of the conduction properties of the AV node, many people with atrial flutter will have a faster ventricular response than those with atrial fibrillation. The heart rate is often more difficult to control with atrial flutter than with atrial fibrillation, because of increased concealed conduction in those with atrial fibrillation.
For the most part, morbidity and mortality result from complications of rate (eg, syncope and congestive heart failure [CHF]). In patients with atrial flutter, the risk of embolic occurrences approaches that seen in atrial fibrillation. Patients with Wolff-Parkinson-White syndrome who develop atrial flutter can develop life-threatening ventricular responses and therefore should be considered for catheter ablation of their accessory bypass tract.
Data from the Framingham study suggest that patients with atrial fibrillation do not live as long as patients without atrial fibrillation (ie, control subjects). No data are available on atrial flutter.
The prognosis for patients with type I atrial flutter who undergo catheter ablation is excellent, with a very low recurrence rate. The picture is not as clear for patients with both atrial flutter and atrial fibrillation. Some reports have documented fewer episodes of atrial fibrillation after successful flutter ablation; others have not. It is possible that atrial fibrillation may be more responsive to antiarrhythmic agents after atrial flutter has been eliminated.
Bohnen et al performed a prospective study to assess the incidence and predictors of major complications from contemporary catheter ablation procedures.  Major complication rates ranged from 0.8% (supraventricular tachycardia) to 6% (ventricular tachycardia associated with structural heart disease), depending on the ablation procedure performed. Renal insufficiency was the only independent predictor of a major complication.
Numerous reports indicate that patients with atrial fibrillation who are given class IC antiarrhythmic agents may convert to atrial flutter with faster ventricular rates. Thus, patients receiving type IC agents (eg, flecainide) should also receive an AV node−blocking drug such as a beta blocker or calcium channel blocker. In patients with both atrial fibrillation and atrial flutter, the relative risk for development of stroke is 4.1% in comparison with control subjects. 
Patient education regarding medications and diet is important. Patients taking warfarin should avoid making major changes in their diet until they have consulted with their healthcare providers. Specifically, a sudden change in the consumption of green leafy vegetables, which are sources of vitamin K, can affect coagulation in patients taking warfarin, which inhibits vitamin K synthesis. This education is not needed with newer drugs that avoid these drug-drug or drug-food interactions.
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