Atrial Flutter 

Atrial flutter is a cardiac arrhythmia characterized by atrial rates of between 240 and 400 beats per minute and some degree of atrioventricular node conduction block. In the common form of atrial flutter (type I atrial flutter), the electrocardiogram (ECG) demonstrates a negative sawtooth pattern in leads II, III, and aVF. (See the image below.)

Atrial flutter has many clinical aspects that are similar to atrial fibrillation (ie, underlying disease, predisposing factors, complications, medical management). However, the underlying mechanism of atrial flutter makes this arrhythmia amenable to cure with percutaneous catheter-based techniques.

Some patients have both atrial flutter and atrial fibrillation. 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.

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 Clinical.) Electrocardiography (ECG) is essential in making the diagnosis. Transthoracic echocardiography 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 be done when the patient is in atrial flutter as well. (See Treatment.)

In humans, the most common form of atrial flutter (type I, or classic) 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 3D electroanatomic map of type I atrial flutter is shown in the video below:

Animal models have been used to demonstrate that an anatomical block (surgically created) or a functional block of conduction between the superior vena cava and 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). 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, counterclockwise around the tricuspid valve annulus when viewed in the left antero-oblique fluoroscopic view) of the atrial septum (see 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 ablation procedures and may result in faster ventricular rates than seen during atrial fibrillation. Thus, tricuspid isthmus dependency is not a prerequisite for atrial flutter. Often, the atrial rate is faster (340-350 bpm) in atypical flutter and the arrhythmia cannot be entrained.

Atrial flutter is associated with a variety of cardiac disorders. In most studies, approximately 30% of patients with atrial flutter have coronary artery heart disease, 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 has been associated with atrial flutter.

In addition, the following conditions are also associated with atrial flutter:

• Hypoxia
• Chronic obstructive pulmonary disease
• Pulmonary embolism
• Hyperthyroidism
• Pheochromocytoma
• Diabetes
• Electrolyte imbalance
• Alcohol consumption
• Obesity
• Digitalis toxicity
• Myotonic dystrophy in childhood (rare)^[1]

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.

United States statistics

Atrial flutter is much less common than atrial fibrillation. From 1985-1990, of patients admitted to US hospitals with a diagnosis of supraventricular tachycardia, 77% had atrial fibrillation and 10% had atrial flutter. Based on a study of patients referred for tertiary care centers, the incidence of atrial flutter in the United States is estimated at 200,000 new cases per year.^[2]

Sex- and age-related demographics

Atrial flutter is associated with a male predominance. 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 people
• 55-64 years: 30-90 cases per 1000 people
• 65-90 years: 50-90 cases per 1000 people

Prognosis depends on the patient's underlying medical condition. Any 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 in the left atrium has been described in patients with atrial flutter (0-21%). Thromboembolic complications have also been described.^[3]

Due to conduction properties of the atrioventricular node, many people with atrial flutter will have a faster ventricular response than those with atrial fibrillation. Heart rate is often more difficult to control with atrial flutter than with atrial fibrillation.

For the most part, morbidity and mortality are due to complications of rate (ie, syncope, congestive heart failure). In patients with atrial flutter, the risk of embolic occurrences approaches that of atrial fibrillation. Patients with Wolff-Parkinson-White syndrome can develop life-threatening ventricular responses, and so should be considered for catheter ablation of their accessory bypass tract.

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 between 0.8% (supraventricular tachycardia) and 6% (ventricular tachycardia associated with structural heart disease), depending on the ablation procedure performed. They reported renal insufficiency was the only independent predictor of a major complication.^[4]

Data from the Framingham study suggest that patients with atrial fibrillation do not live as long as patients without atrial fibrillation (ie, controls). 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, while others have not. Atrial fibrillation is thought to possibly be more responsive to antiarrhythmic agents after atrial flutter has been eliminated.

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 (flecainide) should also receive an AV nodal 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% compared with control subjects.^[5]

Patient education regarding medications and diet is important. Patients taking warfarin should avoid major changes in their diet unless they consulting 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.

For patient education information, see the Heart Center and Stroke Center, as well as Atrial Flutter, Heart Rhythm Disorders, Stroke, Supraventricular Tachycardia, and Palpitations.