MECHANISMS OF ARRHYTHMOGENESIS



The anatomy of the cardiac conduction system and basic electrophysiological principles are dis­cussed in Chapter 1. The genesis of cardiac ar­rhythmias is divided into disorders of impulse formation, disorders of impulse conduction, and combinations of the two (Table 8-1). One cannot unequivocally determine the mechanism for most clinical arrhythmias, but each arrhythmia may be most consistent with or best explained by a par­ticular electrophysiological mechanism. Disor­ders of impulse formation are defined as an inappropriate discharge rate of the normal pacemaker (the sinus node) or abnormal discharge from an ectopic pacemaker that usurps control of the atrial or ventricular rhythm. An appropriate discharge rate of a subsidiary pacemaker that takes control of the cardiac rhythm upon sinus slowing is termed an escape beat. or rhythm, whereas an inappropriately rapid discharge rate of an ectopic pacemaker (abnormally increased automaticity) that usurps control of the cardiac rhythm from the normal sinus mechanism is termed a premature complex or, when they occur in a series, an ectopic tachycardia.

Parasystole may be due to abnormal automat­icity and refers to an ectopic atrial or ventricular pacemaker that discharges regularly and appears to be protected from the dominate cardiac rhythm by entrance block into the area of abnormal au­tomaticity. Therefore, it may depolarize the myo­cardium intermittently whenever the myocar­dium is excitable, but it is not discharged by the dominant rhythm. In addition, the abnormal focus may demonstrate variable degrees of exit block, and thus it may intermittently fail to depolarize the myocardium at a time when it would be ex­pected. Characteristic features of ventricular par­asystole are (1) premature ventricular parasystolic complexes that are a multiple of a common in­teger, (2) coupling of premature ventricular com­plexes to preceding normally conducted com­plexes that is not fixed, as it often is in patients with nonparasystolic premature ventricular com­plexes, and (3) periodic fusion complexes be­tween the parasystolic and the normally con­ducted beat.

Disorders of impulse conduction include con­duction delay and block that can result in brady-arrhythmias and provide the basis for re-entry, the most common mechanism responsible for ar­rhythmia development. Re-entry can occur at any level of the cardiac electrical system, including the sinus node, the atria, the AV node, the His-Purkinje system, and the ventricular myocardium. Normal cardiac tissue has relative homogeneity of conduction and refractoriness so that an impulse starts at the sinus node, travels through the atrium, the AV node, and the His-Purkinje system. and terminates with organized depolarization of ventricular muscle. Once all tissues are depolar­ized, the impulse is extinguished because there is no further tissue to activate. However, a re-entrant or reciprocating rhythm can occur within various tissues if certain criteria are met, giving rise to a continuous reactivation of tissue and generating a tachycardia. For re-entry to occur (Fig. 8-1) there must be two functionally dissociated path­ways, permitting the impulse to travel in one di­rection down one pathway but blocking it in the other pathway. Thus, the pathway with longer re­fractoriness may block a premature impulse trav­eling antegradely. The first pathway, having shorter refractoriness but slower conduction, con­ducts the impulse to the distal common pathway with a delay that permits it to travel retrogradely up the second pathway and find the proximal tis­sue re-excitable. If this circus movement contin­ues, a tachycardia occurs.