7. Atrial Flutter
Atrial flutter is less common than fibrillation. It occurs most often in patients with COPD but may be seen also in those with rheumatic or coronary heart disease, congestive heart failure, atrial septal defect, or surgically repaired congenital heart disease. Ectopic impulse formation occurs at atrial rates of 250-350/min, with transmission of every second, third, or fourth impulse through the atrioventricular node to the ventricles. Ventricular rate control is accomplished using the same agents utilized in atrial fibrillation, but it is much more difficult with atrial flutter than with atrial fibrillation.
Conversion of atrial flutter to sinus rhythm with class I antiarrhythmic agents is also difficult to achieve, and administration of these drugs has been associated with slowing of the atrial flutter rate to the point where 1:1 atrioventricular conduction can occur at rates in excess of 200/min, with subsequent hemodynamic collapse. The intravenous class III antiarrhythmic agent ibutilide has been significantly more successful in converting atrial flutter. About 50-70% of patients return to sinus rhythm within 60-90 minutes following the infusion of 1-2 mg of this agent. Electrical cardioversion is also very effective for atrial flutter, with approximately 90% of patients converting following shocks of as little as 25-50 J.
The persistence of atrial contractile function in this arrhythmia provides some protection against thrombus formation, though the risk of systemic embolization remains slightly increased. Precardioversion anticoagulation is not necessary for atrial flutter of less than 48 hours’ duration except in the setting of mitral valve disease. However, anticoagulation is prudent in chronic atrial flutter, particularly since transient periods of atrial fibrillation are common in these patients.
Chronic atrial flutter is often a difficult management problem, since rate control is difficult. Amiodarone is probably the pharmacologic agent of choice, since it has the potential of both maintaining sinus rhythm and helping with rate control when flutter recurs.
Atrial flutter can follow a typical or atypical reentry circuit around the atrium. The anatomy of the typical circuit has been well defined and allows for radiofrequency ablation within the atrium to interrupt the circuit and eliminate atrial flutter. This technique should be considered in patients refractory to drug therapy.
Niebauer MJ et al: Management of atrial flutter. Cardiol Rev 2001;9:253.
Wu RC et al: Catheter ablation of atrial flutter and macroreentrant atrial tachycardia. Curr Opin Cardiol 2002;17:58.
8. Multifocal (Chaotic) Atrial Tachycardia
This is a rhythm characterized by varying P-wave morphology (by definition, three or more foci) and markedly irregular PP intervals. The rate is usually between 100 and 140/min, and atrioventricular block is unusual. Most patients have severe associated COPD. Treatment of the underlying condition is the most effective approach; verapamil, 240-480 mg daily in divided doses, is also of value in some patients.
McCord J et al: Multifocal atrial tachycardia. Chest 1998;113: 203.
9. Atrioventricular Junctional Rhythm
The atrial-nodal junction or the nodal-His bundle junctions may assume pacemaker activity for the heart, usually at a rate of 40-60/min. This may occur in patients with myocarditis, coronary artery disease, and digitalis toxicity as well as in individuals with normal hearts. The rate responds normally to exercise, and the diagnosis is often an incidental finding on electrocardiographic monitoring, but it can be suspected if the jugular venous pulse shows cannon a waves. Junctional rhythm is often an escape rhythm because of depressed sinus node function with sinoatrial block or delayed conduction in the atrioventricular node. Nonparoxysmal junctional tachycardia results from increased automaticity of the junctional tissues in digitalis toxicity or ischemia and is associated with a narrow QRS complex and a rate usually less than 120-130/min. It is usually considered benign when it occurs in acute myocardial infarction, but the ischemia that induces it may also cause ventricular tachycardia and ventricular fibrillation.
Revision date: July 6, 2011
Last revised: by Andrew G. Epstein, M.D.