Cardiac arrhythmias occur because of abnormalities of impulse formation, impulse propagation, or a combination of the two disorders. Abnormal impulse formation may involve the following: (1) accelerated or decelerated normal phase four depolarization in the SA and AV nodes and in the His-Purkinje system; (2) abnormal automatic mechanisms, such as slow response automaticity in depolarized Purkinje fibers and atrial and ventricular myocardium; and (3) triggered sustained rhythmic activity consequent to early or delayed afterdepolarizations. Clinically, altered normal automaticity can be responsible for sinus bradycardia or tachycardia and slow junctional and ventricular escape rhythms. Altered normal automaticity in Purkinje fibers that survive myocardial infarction or abnormal automaticity in diseased Purkinje fibers and atrial or ventricular myocardium may generate idioventricular rhythms, parasystole, and atrial or ventricular tachyarrhythmias. Potentially triggered activity could cause atrial and ventricular tachyaarhythmias, but the significance and incidence of triggered arrhythmias remain to be determined. Abnormal impulse propagation results from depressed active or passive membrane properties. Reduced action potential amplitude, upstroke velocity, excitability, and cell-to-cell coupling can produce slow conduction, block, and reentrant excitation. Reentry involves unidirectional block and slow conduction around a fixed anatomic or electrophysiologic obstacle, a vortex of conduction around a central area of unexcited myocardium ('leading circle' concept), or electrotonic current flow to and fro across an inexcitable gap (reflection). Slow conduction and block can permit latent pacemaker escape and precipitate various reentrant tachyarrhythmias. There is good evidence to suggest that dual AV nodal pathways and accessory in patients having the Wolff-Parkinson-White syndrome sustain reentrant excitation and that reentry can occur within the atrium and ventricle. Bundle branch and sinus node reentry appear to be less common clinically. Abnormal impulse formation and propagation interact with one another to alter the degree of entrance and exit block surrounding a spontaneously depolarizing region of myocardium, and to accelerate, decelerate, entrain, and completely suppress spontaneous discharges of an ectopic focus. The clinical consequences of subthreshold stimuli delivered to a parasystolic focus include a wide spectrum of arrhythmias, depending on the relative discharge rates of the pacemaker sites, and the degree of entrance and exit block. Modulation of parasystolic rhythms by changes in the sinus rate have been demonstrated recently and there have been reports of termination of arrhythmia following a single subthreshold stimulus (annihilation). As new mechanisms for the development of cardiac arrhythmias are identified, the tests used to identify previously described mechanisms may need to be revised. For example, initiation and termination of a presumed reentrant tachycardia by a single premature stimulus does not exclude triggered activity or initiation and annihilation of pacemaker activity as possible mechanisms. Therefore, it is still possible, given present discriminating techniques, to be unequivocably certain about the mechanisms responsible for most clinically occurring cardiac arrhythmias.
ASJC Scopus subject areas