Tachyarrhythmias

Published on 07/02/2015 by admin

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Last modified 07/02/2015

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Tachyarrhythmias

Srikanth Hosur, MD and Adebola Adesanya, MD, MPH

Tachyarrhythmias are classified as either narrow complex tachycardias (NCT) or wide complex tachycardias (WCT), based on the width of the QRS complexes. NCTs are further classified as atrioventricular (AV) node-passive or AV node-active tachycardias, based on whether the AV node is involved in the propagation and maintenance of the arrhythmia. AV node-passive tachycardias have a regular rhythm, as in atrial tachycardia or atrial flutter, or an irregular rhythm, as in multifocal atrial tachycardia, atrial flutter with varying conduction, or atrial fibrillation. (AV node reentry tachycardia [AVNRT]) or accessory pathway-dependent tachycardia. The accessory pathway conduction can be orthodromic (using the AV node as forward conduction) and, hence, have a narrow complex, or antidromic (using the accessory pathway as forward conduction and the AV node itself for retrograde conduction) and, hence, have a wide complex.

It is important to understand the mechanisms of these arrythmias because AV node-active tachycardias can usually be terminated by maneuvers that prolong AV node conduction, such as vagal maneuvers, or the administration of drugs, such as adenosine (Figure 36-1).

Narrow complex tachycardias

Treatment

NCTs can be treated medically or by cardioversion. The administration of adenosine and vagal maneuvers are helpful only in the termination of AV node-active tachycardias. Although all NCTs can be terminated using synchronized cardioversion, the use of cardioversion should be reserved for patients in whom the arrhythmia is accompanied by hemodynamic instability.

In patients with hemodynamically stable NCTs, diltiazem, 0.25 mg/kg, is preferred over β-adrenergic receptor blocking agents or verapamil because dilitiazem has less negative inotropy. Patients with a low ejection fraction are candidates for amiodarone administered intravenously as a bolus of 150 mg that can be repeated. Procainamide is useful as a second-line agent in this situation.

Adenosine should be given in a central or antecubital vein at a dose of 6 to 12 mg. It is short acting, has a half-life of 12 to 18 sec, and can cause flushing, bronchospasm, and chest pain. Adenosine is antagonized by the administration of methylxanthines, such as aminophylline.