Zainul Abedin

The Ventricular Arrhythmias

Ventricular rhythms originate from sites distal to the penetrating bundle of His. In the majority of cases, the resulting QRS complexes are abnormally wide, exhibit axis deviation, and have a range of bizarre morphologies. In some cases, however, ventricular ectopic impulses arise in the distal conduction structures themselves and therefore exhibit narrow QRS complexes. Three basic mechanisms are thought to account for the majority of ventricular rhythms: enhanced automaticity, reentry, and early and late afterdepolarizations. In the case of enhanced automaticity, single or multiple excitable foci spontaneously discharge impulses. In the case of reentry, the sinus impulse traverses a circuit within the distal conduction system or ventricular myocardium, forming a single ectopic ventricular beat if conduction through the circuit is an isolated event, or producing ventricular tachycardia if conduction through the circuit is repetitive. A reentry circuit may consist of anatomically separate pathways with differing conduction properties, or disparate conduction properties (anisotropy) in contiguous myocardium may provide a functional basis for reentry. If the circuit is very small, the mechanism is called micro-reentry. If the circuit consists of larger structures, such as a bundle branch and the contiguous myocardium, the resulting mechanism is called macro-reentry. (The reentry mechanism is described in detail in Chapters 11 and 13.) Early after-depolarization, an early depolarization that occurs before repolarization is complete, is now widely believed to be the physiologic substrate of polymorphic ventricular tachycardia.

The Echo Phenomenon and Dual Pathways

Under certain conditions, the presence of two anatomically or functionally separate pathways can be detected from evidence provided by the surface (scalar) electrocardiogram. Dual pathways with differing physiologic characteristics result in asynchronous conduction. Such asynchrony may present electrocardiographically as (1) atrioventricular nodal reentry, (2) echo beats, (3) the appearance of two different PR or RP intervals, and (4) dual ventricular response. Dual pathways manifesting as echo beats, two different PR/RP intervals, or dual ventricular response are discussed in this chapter. Atrioventricular nodal reentry is discussed at length in Chapter 13.

The Atrial Arrhythmias

The supraventricular tachycardias can be divided into those arrhythmias originating within the atria per se and those in which the atrioventricular node or accessory atrioventricular connections play a role. The latter arrhythmias are discussed in Chapter 13. Four important tachyarrhythmias, namely, atrial fibrillation, atrial flutter, atrial tachycardia, and multifocal atrial tachycardia, are considered in this chapter, as are premature atrial complexes and ectopic atrial rhythm.

Escape and Capture

The sinus node functions as the primary cardiac pacemaker because it has the fastest inherent rate of impulse formation. During each cardiac cycle, the sinoatrial node retains control of the cardiac rhythm because all the slower, subsidiary, pacemackers are passively depolarized and reset as the sinus impulse spreads throughout the conduction system. However, if sinus node impulse generation fails or if conduction of the sinus impulse blocks, the conduction system contains many other potential, latent pacemaking sites that are capable of assuming control.

The Sinus Rhythms

The driving impulse of the heart ordinarily arises in the P cells of the sinoatrial node. Pace-making foci are not, however, limited to the sinus node; others exist outside of it in the atrial myocardium. This observation has lead some electrocardiographers to speak of the atrial pace-making complex, a term that includes foci both within and outside of the sinus node.

Sick Sinus Syndrome

The commonly used term sick sinus syndrome refers to a constellation of disorders of sinus rhythm that includes (1) inappropriate sinus bradycardia, (2) barious forms of sinoatrial block, (3) sinus arrest, (4) tachycardia-bradycardia syndrome, (5) sinoatrial nodal suppression by ectopic beats, and (6) sinoatrial reentry. This group of arrhythmias is very often associated with other manifestations of conduction system disease, such as aytrioventricular, fascicular, and bundle branch block, and suppression of escape rhythms from subsidiary pacemakers.

The Junctional Rhythms

The atrioventricular junction is generally considered to include the lower atrial walls and septum adjacent to the annuli of the atrioventricular valves (sometimes called “the atrial floor”), the atrioventricular node, and the penetrating portion of the bundle of His. The myocardium of the atrial floor and the fibers of the bundle of His contain latent pacemaking sites with inherenet automaticity, capable of generating extrasystolic beats and rhythms.

Supraventricular Reentry Tachycardia

Reentry, or reciprocation, occurs when an impulse travels away from its point of origin using one pathway, then reverses direction and returns to the point of origin by means of a second pathway. In order to initiate or sustain a tachycardia that utilizes the mechanism of reentry, the following three preconditions are necessary: n n1 n ntwo functionally or anatomically separate pathways that form a circuit must exist n n n n n2 n nconduction in one of the pathways must initially exhibit unidirectional block, and n n n n n3 n nprolonged conduction in the second pathway must be of sufficient duration to allow repolarization (recovery) of the first pathway.

Multilevel Atrioventricular Block

In most cases of atrioventricular block, a single level of conduction delay is sufficient to explain the electrocardiographic findings. Consequently, the AV node and distal conduction structures are represented in laddergrams as a one-tiered structure. However, in the case of rapid atrial arrhythmias, as many as three consecutive levels of conduction delay, each with its own conduction characteristics, may be postulated to explain the observed atrioventricular conduction ratios.

The Wolff-Parkinson-White Syndrome

In early fetal life, the atrial and ventricular myocardia are continuous. After approximately the first month of gestation, the formation of the annulus fibrosus begins the anatomical and electrical separation of the atria and ventricles, leaving the atrioventricular node and bundle of His as the only electrical connection between the upper and lower chambers. In approximately 0.3% of the population (3 of every 1000 individuals), however, this process of electrical isolation is incomplete. In these subjects, unobliterated myocardial strands persist, making one, or at times more, direct electrical connections between the atrial and ventricular myocardium. These congenitally anomalous fibers are known as accessory pathways or bypass tracts.