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ESSENTIALS OF DIAGNOSIS
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ESSENTIALS OF DIAGNOSIS
Rapid, regular tachycardia presenting classically with 2 to 1 block in the AV node and ventricular heart rate of 150 beats/min.
ECG shows “sawtooth” pattern of atrial activity (rate 300 beats/min).
Stroke risk should be considered equivalent to that with atrial fibrillation.
Catheter ablation is highly successful and is considered the definitive treatment for typical atrial flutter.
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GENERAL CONSIDERATIONS
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Atrial flutter is less common than fibrillation. It may occur in patients with structurally normal hearts but is more commonly seen in patients with COPD, valvular or structural heart disease, ASD, or surgically repaired congenital heart disease.
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Patients typically present with reports of palpitations, fatigue, or mild dizziness. In situations where the arrhythmia is unrecognized for a prolonged period of time, symptoms and signs of HF (dyspnea, exertional intolerance, edema) due to tachycardia-induced cardiomyopathy may develop. The ECG typically demonstrates a “sawtooth” pattern of atrial activity in the inferior leads (II, III, and AVF). The reentrant circuit generates atrial rates of 250–350 beats/min, usually with transmission of every second, third, or fourth impulse through the AV node to the ventricles (eFigures 12–10, 12–11, 12–12).
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Ventricular rate control is accomplished using the same agents used in atrial fibrillation, but it is generally more difficult. Conversion of atrial flutter to sinus rhythm with class I antiarrhythmic agents is also difficult to achieve, and administration of these medications has been associated with slowing of the atrial flutter rate to the point at which 1:1 AV conduction can occur at rates in excess of 200 beats/min, with subsequent hemodynamic collapse. The intravenous class III antiarrhythmic agent ibutilide has been significantly more successful in converting atrial flutter (see Table 12–1). About 50–70% of patients return to sinus rhythm within 60–90 minutes following the infusion of this agent. Electrical cardioversion is also very effective for atrial flutter, with approximately 90% of patients converting following synchronized shocks of 100–200 J.
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Although the organization of atrial contractile function in this arrhythmia may provide some protection against thrombus formation, the risk of thromboembolism should be considered equivalent to that with atrial fibrillation due to the common coexistence of these arrhythmias. As with atrial fibrillation, anticoagulation should be established for at least 3 weeks or thrombus excluded with TEE pre-cardioversion for atrial flutter of greater than 48 hours or of unknown duration. Anticoagulation should be continued for at least 4 weeks after electrical or chemical cardioversion and chronically in patients with risk factors for thromboembolism.
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Catheter ablation is the treatment of choice for long-term management of atrial flutter owing to the high success rate and safety of the procedure. The anatomy of the typical circuit is well defined and catheter ablation within the right atrium results in immediate and ...