1. Low-energy cardioversion (25 to 50 J) is very successful in converting more than 90 percent of cases of atrial flutter into sinus rhythm. Energies less than 10 J should be avoided, as they are more likely to convert atrial flutter into atrial fibrillation than into sinus rhythm.

2. If cardioversion is contraindicated, control of ventricular rate can be achieved with digoxin, verapamil, diltiazem, esmolol, or propranolol. If there is 1:1 conduction and the rate is 300 and above, preexcitation should be considered and procainamide may be the drug of first choice.

3. Quinidine or procainamide can be used for 1:2 conduction after ventricular rate control is achieved to chemically slow or convert atrial flutter or prevent recurrence of the dysrhythmia.

4. Intravenous esmolol will convert up to 60 percent of patients with new-onset atrial flutter to sinus rhythm.

5. Intravenous verapamil will occasionally convert atrial flutter into sinus rhythm (up to 30 percent) or atrial fibrillation (up to 20 percent).

6. Some of the newer antiarrhythmics may also have a role in the chemical conversion of atrial flutter. Ibutilide (Corvert), mentioned earlier, can convert both atrial flutter and fibrillation to normal sinus rhythm. This drug should be used in new-onset atrial flutter (AF) because of the chance of emboli if used in long-term AF. Ibutilide is very effective in the conversion of atrial flutter or atrial fibrillation; however, there is a significant chance of torsades de pointes (TdP). To reduce the chance of TdP, it is suggested that the K+ and the corrected QT (QTc) interval be checked prior to administration of the agent. This agent should not be given in the presence of hypokalemia, prolonged QTc, or history of congestive heart failure (CHF). The chance of TdP can extend 4 to 6 h after the drug is given.

ATRIAL FIBRILLATION Atrial fibrillation occurs when there are multiple small areas of atrial myocardium continuously discharging and contracting. There is no uniform atrial depolarization and contraction—instead, only a quivering of the atrial wall. While the atrial rate is usually above 400, the ventricular rate is limited by the refractory period of the AV node or an accessory pathway. The ECG characteristics of atrial fibrillation are (1) fibrillatory waves of atrial activity, best seen in leads V 1, V2, V3, and aVF; and (2) irregular ventricular response, usually around 170 to 180 in patients with a healthy AV node ( Fig.,,,..24-10). Disease or drugs (especially digoxin) may reduce AV node conduction and markedly slow ventricular response. A more rapid ventricular response may be seen in patients with bypass tracts, and the rate in these patients has been suggested as a way of estimating the refractory period of the accessory path. Rates above 300 are possible and dangerous. In this case, since ventricular activation occurs by way of the bypass tract, the QRS complex is usually wide. The configuration of the aberrancy may vary with the site of the one or more accessory pathways.

FIG. 24-10. Atrial fibrillation.

Clinical Significance Atrial fibrillation can occur in a paroxysmal or in a sustained manner. Predisposing factors for atrial fibrillation are increased atrial size and mass, increased vagal tone, and variation in refractory periods between different parts of atrial myocardium. Atrial fibrillation is usually found in association with four disorders: rheumatic heart disease, hypertension, ischemic heart disease, and thyrotoxicosis. Less common causes are chronic lung disease, pericarditis, acute alcoholic intoxication, or atrial septal defect.

In patients with left ventricular failure, left atrial contraction contributes significantly to cardiac output. The loss of effective atrial contraction, as in atrial fibrillation, may produce heart failure in these patients. Atrial fibrillation also predisposes to peripheral venous and atrial emboli, with the risk of pulmonary and systemic arterial embolism. Up to 15 percent of patients per year in chronic atrial fibrillation have at least one embolic episode. Conversion from chronic atrial fibrillation to sinus rhythm also carries up to a 1 to 2 percent risk of arterial embolism. Patients with chronic atrial fibrillation are frequently anticoagulated.

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