Atrial Flutter

Introduction
Background

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 it amenable to cure this arrhythmia with percutaneous catheter-based techniques.

Some patients have both atrial flutter and atrial fibrillation. The elimination of atrial flutter has been noted to reduce or eliminate episodes of atrial fibrillation. Left untreated, persistent atrial flutter can degenerate into chronic 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.

Pathophysiology

In most studies, approximately 30% of patients have no underlying cardiac disease, 30% have coronary artery heart disease, and 30% have hypertensive heart disease. Other conditions are also associated with atrial flutter, including cardiomyopathy, hypoxia, chronic obstructive pulmonary disease, thyrotoxicosis, pheochromocytoma, electrolyte imbalance, and alcohol consumption.

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.

In humans, the most common form of atrial flutter (type I [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).

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. 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.

Classic 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.

Classic atrial flutter can also have the opposite activation sequence (ie, clockwise activation around the tricuspid valve annulus). Clockwise atrial flutter is much less common. This arrhythmia is still considered type I, isthmus-dependent, clockwise flutter.

Type II (atypical) atrial flutters are less extensively studied and electroanatomically characterized. Atypical atrial flutters may originate from the right atrium (surgical scars [ie, incisional reentry]) or from the left atrium (pulmonary veins [ie, focal reentry] or mitral annulus).

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 can not be entrained.


Frequency
United States

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.1

Mortality/Morbidity

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.

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.

Sex

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.
Age

Patients with atrial flutter, as with atrial fibrillation, tend to be older adults. In one study, the average age was 64 years (range 27-86 y).
Clinical
History

The severity of symptoms and the patient's underlying cardiac condition dictate the initial management approach.


The most common symptom is palpitations. Other symptoms include fatigue, dyspnea, and chest pain.
Address symptoms of other noncardiac conditions (eg, hyperthyroidism, pulmonary disease) or cardiac conditions associated with atrial flutter that may be reversible.
The most common symptom is palpitations. Other symptoms include fatigue, dyspnea, and chest pain.
Assessing the onset of symptoms/palpitations is critical. Atrial flutter (of a duration >48 h) requires anticoagulation with warfarin or transesophageal echo to rule out thrombus in the left atrium prior to cardioversion to sinus rhythm. Thus, the duration of the episode and the onset of atrial fibrillation or flutter may affect the timing of cardioversion and the need to address anticoagulation.
Precipitating causes and modes of termination of the arrhythmia.
Previous response to pharmacologic therapy.
Often, atrial flutter is not as well tolerated as atrial fibrillation. This may be due to the rapid and difficult-to-control ventricular response, especially with minimal exertion.
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.
Physical
The general appearance and vital signs of the patient are important when 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.
Evaluate the vitals with a close eye on heart rate, blood pressure, and oxygen saturation.
Palpate the neck/thyroid gland for goiter.
Evaluate the neck for jugular venous distention.
Auscultate the lungs for rales/crackles.
Auscultate/palpate the heart for extra heart sounds and murmurs, and palpate the point of maximum impulse.
Examine the extremities to access for lower extremity edema/perfusion.
Causes
Atrial flutter is most often associated with left ventricular dysfunction, rheumatic heart disease, congenital heart disease, and postcardiac surgery.
Thyroid disease, obesity, pericarditis, pulmonary disease, and pulmonary embolism have been associated with atrial fibrillation and atrial flutter. Rarely, mitral valve prolapse has been associated with atrial flutter.
Rarely, atrial flutter can be associated with an acute myocardial infarction.
Postcardiac 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.

http://emedicine.medscape.com/article/151210-overview