Advanced Concepts in Arrhythmias

by Nicholas G. Tullo, MD, FACC, FHRS

Puzzle Pieces

Classification of Arrhythmias

Arrhythmias are classified in various ways.  The electrophysiologic mechanism of the arrhythmia serves as one classification scheme, and the anatomic location of the arrhythmia serves to further distinguish various rhythm disturbances. Electrophysiologic mechanisms are divided into disorders of impulse conduction and disorders of impulse generation.  Disorders of impulse conduction include bradyarrhythmias due to conduction block, such as AV block and sinoatrial exit block.  This category also includes tachycardias due to reentry.  Reentry describes a mechanism of tachycardia that involves a wavefront of depolarization circulating around a pathway of normal and/or abnormal cardiac tissues (referred to as a circus movement).  In order to have reentry, several conditions are required. The first is that a discrete pathway or pathways must be present.  These pathways should have heterogeneous conduction properties that may allow for intermittent slowing or block in only part of the circuit.  Conduction delay is necessary in order to prevent the leading edge of the wavefront from running into its own tail and thus allow a sustained circus movement to occur.  The delay in conduction may be in a small part of the circuit, but this allows the rest of the circuit to recover from refractoriness and accept the next wavefront.  These pathways serve as the “substrate” of the tachycardia.  The initiation of a reentry tachycardia requires a “trigger.”  A premature beat usually serves as the trigger to initiate a circus movement.

The other electrophysiologic mechanism, disorders of impulse generation, includes abnormal automaticity and triggered activity.  Examples of abnormal automaticity include sinus node dysfunction resulting in bradycardia, as well as “automatic” tachycardias such as accelerated idioventricular rhythm (AIVR) and automatic atrial tachycardias.  Triggered activity includes early afterdepolarizations and delayed afterdepolarizations.  These are cellular phenomena that appear to cause certain arrhythmias in man.  Torsades de pointes is a type of polymorphic ventricular tachycardia most likely caused by early afterdepolarizations. Multifocal atrial tachycardia (MAT) and arrhythmias that occur in the setting of digoxin toxicity appear to be due to delayed afterdepolarizations.  Arrhythmias due to delayed afterdepolarizations most often respond to calcium channel blockers such as verapamil because this cellular disturbance is probably caused by a problem with intracellular calcium overload or abnormalities in calcium channels.