(See also Overview of Arrhythmias.)
Atrial flutter is much less common than atrial fibrillation, but its causes and hemodynamic consequences are similar. Many patients with atrial flutter also have periods of atrial fibrillation.
Typical atrial flutter is due to a large reentrant circuit involving most of the right atrium. The atria depolarize at a rate of 250 to 350 beats/minute (typically 300 beats/minute). Because the atrioventricular (AV) node cannot usually conduct at this rate, typically half of the impulses get through (2:1 block), resulting in a regular ventricular rate of 150 beats/minute. Sometimes the block varies from moment to moment, causing an irregular ventricular rhythm. Less commonly, a fixed 3:1, 4:1, or 5:1 block may be present.
The probability of a thromboembolic event is thought to be about half of that in atrial fibrillation (unless atrial fibrillation is also occurring).
Symptoms of atrial flutter depend primarily on ventricular rate and the nature of any underlying heart disorder. If ventricular rate is < 120 beats/minute and regular, there are likely to be few or no symptoms. Faster rates and variable AV conduction usually cause palpitations, and decreased cardiac output may cause symptoms of hemodynamic compromise (eg, chest discomfort, dyspnea, weakness, syncope). Close inspection of the jugular venous pulse reveals flutter a waves.
The diagnosis of atrial flutter is by electrocardiography (ECG). In typical flutter, ECG shows continuous and regular atrial activation with a sawtooth pattern, most obvious in leads II, III, and aVF (see figure Atrial flutter).
Carotid sinus massage can increase AV block and better expose the typical flutter waves. A similar response may follow pharmacologic AV nodal blockade (eg, with adenosine), but such therapy does not terminate atrial flutter.
Treatment of atrial flutter focuses on ventricular rate control, rhythm control, and prevention of thromboembolism.
Pharmacologic rate control is more difficult to achieve in atrial flutter than in atrial fibrillation. Thus, for most patients, electrical conversion (using synchronized cardioversion or overdrive pacing) is the treatment of choice for an initial episode and is mandatory with 1:1 AV conduction or hemodynamic compromise. Typically, low-energy (50 joules) conversion is effective. Anticoagulation, as in atrial fibrillation, is necessary before cardioversion.
If drugs are used to restore sinus rhythm, rate must first be controlled with beta-blockers or nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem). Many of the antiarrhythmic drugs that can restore sinus rhythm (especially class Ia and Ic) can slow atrial flutter, shorten AV nodal refractoriness (by their vagolytic effects), or do both enough to allow 1:1 conduction with paradoxical increase in ventricular rate and hemodynamic compromise. These drugs may be used for long-term maintenance as required to prevent recurrence.
An antitachycardia pacing system is an alternative to long-term use of antiarrhythmics in selected patients. Also, ablation procedures designed to interrupt the atrial reentrant circuit may effectively prevent atrial flutter, particularly typical atrial flutter.
Patients with chronic or recurrent atrial flutter require an oral anticoagulant (warfarin titrated to an INR of 2 to 3, a direct thrombin inhibitor, or a factor Xa inhibitor). The choice among the therapies is based on the same considerations as for atrial fibrillation.
Atrial flutter is a rapid, regular atrial rhythm that rarely may cause an irregular or nontachycardic QRS response, depending on the degree and type of block present.
After initial rate control with drugs such as beta-blockers and nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem), most patients should have synchronized cardioversion.
Anticoagulation is necessary before cardioversion.
Long-term oral anticoagulation to prevent stroke is required for patients with chronic or recurrent atrial flutter.
Drugs Mentioned In This Article
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|CARDIZEM, CARTIA XT, DILACOR XR|