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Control of ventricular rate in atrial flutter

Leonard I Ganz, MD, FHRS, FACC
Jordan M Prutkin, MD, MHS, FHRS
Section Editor
Bradley P Knight, MD, FACC
Deputy Editor
Gordon M Saperia, MD, FACC


Atrial flutter is a relatively common supraventricular arrhythmia characterized by rapid, regular atrial depolarizations at a characteristic rate around 300 beats/min and a regular ventricular rate corresponding to one-half or one-quarter of the atrial rate (150 or 75 beats/minute). It is an electrically unstable rhythm, meaning that it frequently degenerates into atrial fibrillation or reverts to sinus rhythm within hours or days. In patients who present with or who have recurrent episodes associated with a rapid ventricular rate, slowing of the rate may be necessary to either reduce symptoms or prevent tachycardia-mediated cardiomyopathy.

For the purpose of this topic, rate control means lowering the heart rate, which in the case of atrial flutter is usually difficult to achieve. Thus, for many patients, radiofrequency ablation (and permanent restoration of sinus rhythm) is the preferred long-term approach to patients with atrial flutter. (See "Atrial flutter: Maintenance of sinus rhythm", section on 'RF catheter ablation'.)

The physiologic and clinical rationales for ventricular rate control in atrial flutter and the modalities used to achieve this goal will be reviewed here. Other issues such as the causes of atrial flutter, the embolic risk associated with this arrhythmia, and the restoration and maintenance of sinus rhythm are discussed separately. (See "Overview of atrial flutter" and "Restoration of sinus rhythm in atrial flutter" and "Embolic risk and the role of anticoagulation in atrial flutter" and "Atrial flutter: Maintenance of sinus rhythm".)


The ventricular rate in atrial flutter is principally determined by the rate at which impulses exit the atrioventricular (AV) node. With a regular atrial rate of 300 beats/min, the ventricular rate is usually about 150 beats/min. This ventricular rate is determined by the refractory period of a healthy AV node, such that every other impulse (2:1) traverses the AV node and travels to the ventricles. In the absence of drugs that slow AV nodal conduction, a higher degree of AV block (eg, 3:1 or 4:1) suggests AV nodal disease; in these settings, the ventricular rates would be roughly 100 and 75 beats/min, respectively.  

Even input/output ratios (eg, 2:1 or 4:1 conduction) are more common than odd ratios (eg, 3:1 or 5:1). Odd ratios probably reflect bilevel block in the AV node. Sometimes, variable conduction may occur with alternating or seemingly random patterns of 2:1, 3:1, 4:1, or other conduction patterns, again due to varying levels of block in the AV node. On the other hand, a 1:1 response with typical atrial flutter usually suggests possible hyperthyroidism, catecholamine excess, parasympathetic withdrawal, or the existence of an accessory bypass tract in the pre-excitation syndrome. (See "Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome".)

An important exception can occur in patients taking antiarrhythmic drugs, which can slow the atrial flutter rate so that 1:1 conduction occurs in circumstances such as the absence of a bypass tract or catecholamine excess. This occurs most commonly with the class IC drugs, particularly when used in the absence of concomitant AV nodal blocking agents, but can also occur with dronedarone or even amiodarone. Also, 1:1 conduction of "slow" atrial flutter can occur in patients with marked right atrial enlargement.

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Literature review current through: Dec 2017. | This topic last updated: Sep 08, 2016.
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