The Mechanism of Arrhythmias
The heart contains other pacemakers than the S-A node, and they serve as emergency backup. These are the secondary pacemaker located in the A-V node and the tertiary pacemaker located in the cells of the Purkinje system (see chap. 2). Under certain conditions cells of other parts of the conducting system connecting the A-V node with both ventricles are able to initiate electrical stimulation of the heart; furthermore, most ordinary muscle cells, the role of which is contraction and relaxation, may under abnormal conditions take on the role of pacemaker. Ordinarily the secondary and tertiary pacemakers kick in only if an impulse from above fails to arrive; such single heartbeats or series of beats are said to be activated by default; they are referred to as escape beats , and a series of them represent an escape rhythm . However, these reserve pacemakers may assume an active role and discharge an electrical impulse out of turn, before the expected stimulation from above arrives. Such premature single impulses are called ectopic beats , and groups of them are called ectopic rhythms; they represent abnormal stimulation of the heart by usurpation (figs. 24–25).
Ectopic beats or rhythms may originate at any point of the conducting
Figure 24. Atrial arrhythmias exemplified by strips of single electrocardiographic leads.
(a) Premature (ectopic) atrial beat (no. 4). (b) A short run (paroxysm) of atrial tachycardia
(seven beats). (c) Atrial fibrillation: there are no P waves, only rapid and irregular atrial
deflections; the response of the ventricular complexes is totally irregular.
system or even in abnormally stimulated heart muscle cells. Impulses originating in the upper part of the conducting system, including the A-V node, are termed supraventricular; their appearance in the electrocardiogram is identical with that of normal beats, as their impulses are transmitted along normal pathways to the ventricle, causing its depolarization and initiating its contraction. Ectopic impulses originating in the lower portion of the conducting system are called ventricular beats or rhythms. These impulses stimulate the ventricle in an abnormal sequence, which expresses itself in the electrocardiogram by wider, abnormal QRS complexes and T waves (fig. 25a).
Sequential ectopic beats are almost always at a faster than normal rate, that is, are ectopic tachycardias (supraventricular or ventricular). Supraventricular tachycardia can usually, though not always, be identified by electrocardiography as either atrial or junctional (A-V nodal) in origin. Occasionally it is associated with impulses traveling to the ventricle along abnormal pathways, shown in the electrocardiogram as wide complexes similar to those present in ventricular tachycardia.
Figure 25. Ventricular arrhythmias exemplified by strips of single
electrocardiographic leads. (a) Premature ventricular beat. (b) A
short run (paroxysm) of ventricular tachycardia (seven beats).
(c) Ventricular fibrillation: chaotic, small, rapid complexes incapable of
maintaining coordinated heartbeat produce cardiac arrest. Note that
ventricular complexes in a and b are broader than, and
differ in shape from, normal complexes.
Abnormal activity of designated pacemaker cells or stimulated myocardial fibers is not the only mechanism for the origin of ectopic beats or ectopic rhythms. The alternative mode of production of arrhythmias is reentry , a phenomenon to which an important arrhythmogenic role has been attributed. To explain the concept of reentry, it is necessary to recapitulate some facts of normal electrophysiology. The cardiac conducting system transmits electrical impulses sequentially from the S-A node through the atrium to the A-V node, then along the bundle of His and its branches to the ventricles. This basically unidirectional conducting system is capable of conducting impulses in the reverse direction as well, though this does not take place under normal conditions. However, in the presence of arrhythmias impulses activating the ventricles may first send signals back to the atria, so that atrial contraction follows ventricular contraction. All cardiac cells (contractile myocardial cells as well as conducting fibers) have a refractory period: immediately
after a cell's designated function (contraction or conduction) is completed, there is a short time in which they do not respond to stimulation. The refractory period accounts for the fact that once the impulse reaches its final destination, it cannot travel backward. However, if there is an abnormal slowing within any portion of the conducting system (including its final pathway inside the ventricular muscle), the impulse may be reactivated when conduction is already responsive after the refractory period is over. The reactivated impulse may stimulate the ventricle into an additional (premature) contraction, an echo beat , and may travel forward or backward to any part of the heart, producing various arrhythmias.
An echo beat represents the simplest kind of reentry. More complex situations arise when the relationship between velocity of conduction forward and backward permits impulses to travel back and forth at regular, rapid rates (most frequently between 180 and 250 beats a minute), producing reentry tachycardia. Both supraventricular tachycardia (featuring narrow QRS complexes in the electrocardiogram) and ventricular tachycardia (featuring broad complexes) can be caused by reentry.
The electrocardiographic appearance of arrhythmias produced by abnormal impulse formation and that caused by reentry are almost identical and cannot always be differentiated. Yet such a differentiation can be of some practical importance because certain drugs may control one mechanism but not the other. Furthermore, certain varieties of reentry arrhythmias have been successfully treated by surgery.
More-advanced disturbances of the cardiac rhythm are flutter and fibrillation of the atria or the ventricles. The mechanism of these arrhythmias is somewhat similar to reentry: the electrical impulse is never extinguished but travels continuously through the affected portion of the heart. Atrial flutter produces a rapid, regular response, usually at a rate of 300 beats a minute, initiating a weak contraction of the atrial muscle. Because of their refractory period the ventricles are unable to respond to each atrial contraction, only to every other impulse (hence the ventricular rate is usually about 150 beats a minute, and the rhythm is regular). Atrial fibrillation occurs when the impulse travels through the atria at still-faster rates, leading to a chaotic twitching of the atrial muscle, which no longer can contract. The ventricles respond only to some
of the more powerful impulses and in an irregular fashion. The ventricular rate in atrial fibrillation (not influenced by drugs) is usually between 150 and 180 beats a minute, and its rhythm is totally irregular (fig. 24c). Flutter and fibrillation also affect the ventricles. But whereas the cardiac function can be maintained despite a weak or absent atrial contraction, ventricular fibrillation or flutter is tantamount to cessation of the circulatory function of the heart—cardiac arrest.