Mechanisms of Arrhythmias

Two main mechanisms for the initiation and perpetuation of arrhythmias have been proposed. Putative mechanisms include disorders of impulse formation and disorders of impulse conduction. These may occur alone or in combination and result in isolated electrical events and sustained arrhythmias. Alterations in automaticity or triggered activity are two main areas of disordered impulse formation. Clinical examples of abnormal automaticity include inappropriate sinus tachycardia, multifocal atrial tachycardia, sinus pauses, idioventricular rhythm post-MI, and ectopy in heart failure. Triggered activity, or spontaneous depolarization dependent on prior stimulation, is characterized as early or late after depolarizations. This mechanism may be responsible for arrhythmic events during hypoxia, use of sotalol or the metabolite of procainamide, or in patients with idiopathic and acquired long QT syndrome and digitalis toxicity.

Changes in impulse conduction can be clinically divided into block with or without reentry. Simple block occurs when the propagation of the impulse results in an inadequate depolarization stimulus to the adjacent tissue and the impulse terminates. Clinical examples include SA or AV block or simple bundle branch block. In SA block, normal depolarization of the SA node is inadequate to excite adjacent tissue, resulting in absence of a P wave. In AV block, block may occur within the AV node or as it attempts to depolarize His tissue, resulting in a P wave followed by a delayed or absent QRS complex. On the surface ECG, differentiation between block in the AV node or His bundle is only a guess. Bundle branch block or hemiblock is a result of block in a specific branch of the specialized conduction tissue. Activation of tissue beyond the bundle branches must then occur through slower myocyte-to-myocyte activation.

In block with reentry, unidirectional block within a tissue results in activation of adjacent tissue (Fig. 27-33). Tissue not initially activated then becomes excited by the conducting tissue. Tissue that has had time to recover excitability may then be activated again in a single or perpetual event. Clinical examples may occur within the SA node, AV node, within the atrium such as atrial flutter, and in Purkinje and myocardial tissue as ventricular tachycardia. Additional macroreentrant rhythms include atrial reentry and preex-citation with orthodromic and antidromic reciprocating tachycardias.

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