1. Treatment is directed toward the underlying disorder. With decompensated lung disease, oxygen and bronchodilators improve pulmonary function and arterial oxygenation and decrease atrial ectopy. Theophylline agents have been associated with the production or exacerbation of this dysrhythmia.

2. Specific antiarrhythmic treatment is rarely indicated. Standard antiarrhythmics appear to be ineffective in suppressing these multiple sites of atrial ectopy, and toxic side effects from these agents have been reported. Likewise, attempts to slow the ventricular rate by depressing AV nodal conduction with digoxin is also difficult without producing toxic side effects. Recently, three modes of therapy have been described that may be helpful in some patients. Magnesium sulfate 2 g IV over 60 s followed by a constant infusion of 1 to 2 g/h has been shown to reduce atrial ectopy in these patients and is sometimes associated with conversion to sinus rhythm. The full antiarrhythmic effect of magnesium requires supplemental potassium to maintain serum potassium levels above 4 meq/L. Intravenous verapamil (5 to 10 mg) slows the ventricular response in most patients, decreases atrial ectopy in some patients, and is associated with conversion to sinus rhythm in many patients. The b-adrenergic antagonists esmolol, acebutolol, and metoprolol all decrease the ventricular rate in MFAT, and metoprolol is associated with conversion to sinus rhythm in a majority of patients. However, theoretically, b-adrenergic therapy may worsen bronchospasm. The value of such specific antiarrhythmic treatment in MFAT is unproven.

3. Cardioversion has no effect on these multiple sites of atrial ectopy.

ATRIAL FLUTTER Atrial flutter usually originates from a localized area within the atria. The exact mechanism—whether reentry, automatic focus, or triggered dysrhythmia—is not yet known. Intracardiac studies demonstrate electrical activity usually originating in the inferior right atrium and propagating upward and to the left. ECG characteristics of atrial flutter are (1) regular atrial rate between 250 and 350 (most commonly 280 and 320); (2) sawtooth flutter waves directed superiorly and most visible in leads II, III, aVF; and (3) AV block, usually 2:1, but occasionally greater, causing an irregular ventricular response ( Fig 24:9). One-to-one AV

conduction may occur in the presence of bypass tracts or if drugs are used to slow the atrial rate to the level that the junction will be able to conduct one-to-one. If the ventricular rate is greater than 300, this should definitely be investigated with EP studies. Carotid sinus massage is a useful technique to slow the ventricular response, increase the AV block, and unmask flutter waves.

FIG. 24-9. Atrial flutter.

Clinical Significance Atrial flutter is usually associated with heart disease. It is most commonly found in patients with ischemic heart disease or acute myocardial infarction. Less common causes include congestive cardiomyopathy, pulmonary embolus, myocarditis, blunt chest trauma, and, rarely, digoxin toxicity. Atrial flutter may be a transitional dysrhythmia between sinus rhythm and atrial fibrillation.

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