Figure 13-7

Complete A-V block (lead II).

from the atria into the ventricles occurs. In this instance, the ventricles spontaneously establish their own signal, usually originating in the A-V node or A-V bundle. Therefore, the P waves become dissociated from the QRS-T complexes, as shown in Figure 13-7. Note that the rate of rhythm of the atria in this electrocardiogram is about 100 beats per minute, whereas the rate of ventricular beat is less than 40 per minute. Furthermore, there is no relation between the rhythm of the P waves and that of the QRS-T complexes because the ventricles have "escaped" from control by the atria, and they are beating at their own natural rate, controlled most often by rhythmical signals generated in the A-V node or A-V bundle.

Stokes-Adams Syndrome—Ventricular Escape. In some patients with A-V block, the total block comes and goes; that is, impulses are conducted from the atria into the ventricles for a period of time and then suddenly impulses are not conducted. The duration of block may be a few seconds, a few minutes, a few hours, or even weeks or longer before conduction returns. This condition occurs in hearts with borderline ischemia of the conductive system.

Each time A-V conduction ceases, the ventricles often do not start their own beating until after a delay of 5 to 30 seconds. This results from the phenomenon called overdrive suppression. This means that ventricular excitability is at first in a suppressed state because the ventricles have been driven by the atria at a rate greater than their natural rate of rhythm. However, after a few seconds, some part of the Purkinje system beyond the block, usually in the distal part of the A-V node beyond the blocked point in the node, or in the A-V bundle, begins discharging rhythmically at a rate of 15 to 40 times per minute and acting as the pacemaker of the ventricles. This is called ventricular escape.

Because the brain cannot remain active for more than 4 to 7 seconds without blood supply, most patients faint a few seconds after complete block occurs because the heart does not pump any blood for 5 to 30 seconds, until the ventricles "escape." After escape, however, the slowly beating ventricles usually pump enough blood to allow rapid recovery from the faint and then to sustain the person. These periodic fainting spells are known as the Stokes-Adams syndrome.

Occasionally the interval of ventricular standstill at the onset of complete block is so long that it becomes detrimental to the patient's health or even causes death. Consequently, most of these patients are provided with an artificial pacemaker, a small battery-operated electrical stimulator planted beneath the skin, with electrodes usually connected to the right ventricle. The pacemaker provides continued rhythmical impulses that take control of the ventricles.

Incomplete Intraventricular Block— Electrical Alternans

Most of the same factors that can cause A-V block can also block impulse conduction in the peripheral ventricular Purkinje system. Figure 13-8 shows the condition known as electrical alternans, which results from partial intraventricular block every other heartbeat. This electrocardiogram also shows tachycardia (rapid heart rate), which is probably the reason the block has occurred, because when the rate of the heart is rapid, it may be impossible for some portions of the Purkinje system to recover from the previous refractory period quickly enough to respond during every succeeding heartbeat. Also, many conditions that depress the heart, such as ischemia, myocarditis, or digitalis toxicity, can cause incomplete intraventricular block, resulting in electrical alternans.

Premature Contractions

A premature contraction is a contraction of the heart before the time that normal contraction would have been expected. This condition is also called extrasystole, premature beat, or ectopic beat.

Causes of Premature Contractions. Most premature contractions result from ectopic foci in the heart, which emit abnormal impulses at odd times during the cardiac rhythm. Possible causes of ectopic foci are (1) local areas of ischemia; (2) small calcified plaques at different points in the heart, which press against the adjacent cardiac muscle so that some of the fibers are irritated; and (3) toxic irritation of the A-V node, Purkinje system, or myocardium caused by drugs, nicotine, or caffeine. Mechanical initiation of premature contractions is also frequent during cardiac catheterization; large numbers of premature contractions often occur when the catheter enters the right ventricle and presses against the endocardium.

Premature Atrial Contractions

Figure 13-9 shows a single premature atrial contraction. The P wave of this beat occurred too soon in the heart cycle; the P-R interval is shortened, indicating that the ectopic origin of the beat is in the atria near the A-V node. Also, the interval between the premature contraction and the next succeeding contraction is slightly prolonged, which is called a compensatory pause. One of the reasons for this is that the premature contraction originated in the atrium some distance from the sinus node, and the impulse had to travel through a considerable amount of atrial muscle before it discharged the sinus node. Consequently, the sinus node discharged late in the premature cycle, and this made the succeeding sinus node discharge also late in appearing.

Premature atrial contractions occur frequently in otherwise healthy people. Indeed, they often occur in athletes whose hearts are in very healthy condition. Mild toxic conditions resulting from such factors as smoking, lack of sleep, ingestion of too much coffee, alcoholism, and use of various drugs can also initiate such contractions.

Pulse Deficit. When the heart contracts ahead of schedule, the ventricles will not have filled with blood normally, and the stroke volume output during that contraction is depressed or almost absent. Therefore, the pulse wave passing to the peripheral arteries after a premature contraction may be so weak that it cannot be felt in the radial artery. Thus, a deficit in the number of radial pulses occurs when compared with the actual number of contractions of the heart.

A-V Nodal or A-V Bundle Premature Contractions

Figure 13-10 shows a premature contraction that originated in the A-V node or in the A-V bundle. The P wave is missing from the electrocardiographic record

Figure 13-10 shows a premature contraction that originated in the A-V node or in the A-V bundle. The P wave is missing from the electrocardiographic record

Partial intraventricular block—"electrical alternans" (lead III)

Atrial premature beat (lead I)

Partial intraventricular block—"electrical alternans" (lead III)

Atrial premature beat (lead I)

Premature beat

Premature beat

Figure 13-10

A-V nodal premature contraction (lead III).

Figure 13-11

ing with normal contractions. PVCs cause specific effects in the electrocardiogram, as follows:

1. The QRS complex is usually considerably prolonged. The reason is that the impulse is conducted mainly through slowly conducting muscle of the ventricles rather than through the Purkinje system.

2. The QRS complex has a high voltage for the following reasons: when the normal impulse passes through the heart, it passes through both ventricles nearly simultaneously; consequently, in the normal heart, the depolarization waves of the two sides of the heart—mainly of opposite polarity to each other—partially neutralize each other in the electrocardiogram. When a PVC occurs, the impulse almost always travels in only one direction, so that there is no such neutralization effect, and one entire side or end of the ventricles is depolarized ahead of the other; this causes large electrical potentials, as shown for the PVCs in Figure 13-11.

3. After almost all PVCs, the T wave has an electrical potential polarity exactly opposite to that of the QRS complex, because the slow conduction of the impulse through the cardiac muscle causes the muscle fibers that depolarize first also to repolarize first.

Some PVCs are relatively benign in their effects on overall pumping by the heart; they can result from such factors as cigarettes, coffee, lack of sleep, various mild toxic states, and even emotional irritability. Conversely, many other PVCs result from stray impulses or reentrant signals that originate around the borders of infarcted or ischemic areas of the heart. The presence of such PVCs is not to be taken lightly. Statistics show that people with significant numbers of PVCs have a much higher than normal chance of developing spontaneous lethal ventricular fibrillation, presumably initiated by one of the PVCs. This is especially true when the PVCs occur during the vulnerable period for causing fibrillation, just at the end of the T wave when the ventricles are coming out of refractoriness, as explained later in the chapter.

Figure 13-11

Premature ventricular contractions (PVCs) demonstrated by the large abnormal QRS-T complexes (leads II and III). Axis of the premature contractions is plotted in accordance with the principles of vectorial analysis explained in Chapter 12; this shows the origin of the PVC to be near the base of the ventricles.

of the premature contraction. Instead, the P wave is superimposed onto the QRS-T complex because the cardiac impulse traveled backward into the atria at the same time that it traveled forward into the ventricles; this P wave slightly distorts the QRS-T complex, but the P wave itself cannot be discerned as such. In general, A-V nodal premature contractions have the same significance and causes as atrial premature contractions.

Premature Ventricular Contractions

The electrocardiogram of Figure 13-11 shows a series of premature ventricular contractions (PVCs) alternat

Vector Analysis of the Origin of an Ectopic Premature Ventricular Contraction. In Chapter 12, the principles of vectorial analysis are explained. Applying these principles, one can determine from the electrocardiogram in Figure 13-11 the point of origin of the PVC as follows: Note that the potentials of the premature contractions in leads II and III are both strongly positive. Plotting these potentials on the axes of leads II and III and solving by vectorial analysis for the mean QRS vector in the heart, one finds that the vector of this premature contraction has its negative end (origin) at the base of the heart and its positive end toward the apex. Thus, the first portion of the heart to become depolarized during this premature contraction is near the base of the ventricles, which therefore is the locus of the ectopic focus.

Paroxysmal Tachycardia

Some abnormalities in different portions of the heart, including the atria, the Purkinje system, or the ventricles, can occasionally cause rapid rhythmical discharge of impulses that spread in all directions throughout the heart. This is believed to be caused most frequently by

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