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Figure 13-12

Atrial paroxysmal tachycardia—onset in middle of record (lead I)

re-entrant circus movement feedback pathways that set up local repeated self-re-excitation. Because of the rapid rhythm in the irritable focus, this focus becomes the pacemaker of the heart.

The term "paroxysmal" means that the heart rate becomes rapid in paroxysms, with the paroxysm beginning suddenly and lasting for a few seconds, a few minutes, a few hours, or much longer. Then the paroxysm usually ends as suddenly as it began, with the pacemaker of the heart instantly shifting back to the sinus node.

Paroxysmal tachycardia often can be stopped by eliciting a vagal reflex. A type of vagal reflex sometimes elicited for this purpose is to press on the neck in the regions of the carotid sinuses, which may cause enough of a vagal reflex to stop the paroxysm. Various drugs may also be used. Two drugs frequently used are quini-dine and lidocaine, either of which depresses the normal increase in sodium permeability of the cardiac muscle membrane during generation of the action potential, thereby often blocking the rhythmical discharge of the focal point that is causing the paroxysmal attack.

Atrial Paroxysmal Tachycardia

Figure 13-12 demonstrates in the middle of the record a sudden increase in the heart rate from about 95 to about 150 beats per minute. On close study of the electrocardiogram during the rapid heartbeat, an inverted P wave is seen before each QRS-T complex, and this P wave is partially superimposed onto the normal T wave of the preceding beat. This indicates that the origin of this paroxysmal tachycardia is in the atrium, but because the P wave is abnormal in shape, the origin is not near the sinus node.

A-V Nodal Paroxysmal Tachycardia. Paroxysmal tachycardia often results from an aberrant rhythm that involves the A-V node. This usually causes almost normal QRS-T complexes but totally missing or obscured P waves.

Atrial or A-V nodal paroxysmal tachycardia, both of which are called supraventricular tachycardias, usually occurs in young, otherwise healthy people, and they generally grow out of the predisposition to tachycardia after adolescence. In general, supraventricular tachycardia frightens a person tremendously and may cause weakness during the paroxysm, but only seldom does permanent harm come from the attack.

Ventricular Paroxysmal Tachycardia

Figure 13-13 shows a typical short paroxysm of ventricular tachycardia. The electrocardiogram of ventricu

Figure 13-13

Ventricular paroxysmal tachycardia (lead III).

lar paroxysmal tachycardia has the appearance of a series of ventricular premature beats occurring one after another without any normal beats interspersed.

Ventricular paroxysmal tachycardia is usually a serious condition for two reasons. First, this type of tachycardia usually does not occur unless considerable ischemic damage is present in the ventricles. Second, ventricular tachycardia frequently initiates the lethal condition of ventricular fibrillation because of rapid repeated stimulation of the ventricular muscle, as we discuss in the next section.

Sometimes intoxication from the heart treatment drug digitalis causes irritable foci that lead to ventricular tachycardia. Conversely, quinidine, which increases the refractory period and threshold for excitation of cardiac muscle, may be used to block irritable foci causing ventricular tachycardia.

Ventricular Fibrillation

The most serious of all cardiac arrhythmias is ventricular fibrillation, which, if not stopped within 1 to 3 minutes, is almost invariably fatal. Ventricular fibrillation results from cardiac impulses that have gone berserk within the ventricular muscle mass, stimulating first one portion of the ventricular muscle, then another portion, then another, and eventually feeding back onto itself to re-excite the same ventricular muscle over and over—never stopping. When this happens, many small portions of the ventricular muscle will be contracting at the same time, while equally as many other portions will be relaxing. Thus, there is never a coordinate contraction of all the ventricular muscle at once, which is required for a pumping cycle of the heart. Despite massive movement of stimulatory signals throughout the ventricles, the ventricular chambers neither enlarge nor contract but remain in an indeterminate stage of partial contraction, pumping either no blood or negligible amounts. Therefore, after fibrillation begins, unconsciousness occurs within 4 to 5 seconds for lack of blood flow to the brain, and irretrievable death of tissues begins to occur throughout the body within a few minutes.

Multiple factors can spark the beginning of ventricular fibrillation—a person may have a normal heartbeat one moment, but 1 second later, the ventricles are in fibrillation. Especially likely to initiate fibrillation are (1) sudden electrical shock of the heart, or (2) ischemia of the heart muscle, of its specialized conducting system, or both.

Phenomenon of Re-entry—"Circus Movements" as the Basis for Ventricular Fibrillation

When the normal cardiac impulse in the normal heart has traveled through the extent of the ventricles, it has no place to go because all the ventricular muscle is refractory and cannot conduct the impulse farther. Therefore, that impulse dies, and the heart awaits a new action potential to begin in the atrial sinus node.

Under some circumstances, however, this normal sequence of events does not occur. Therefore, let us explain more fully the background conditions that can initiate re-entry and lead to "circus movements," which in turn cause ventricular fibrillation.

Figure 13-14 shows several small cardiac muscle strips cut in the form of circles. If such a strip is stimulated at the 12 o'clock position so that the impulse travels in only one direction, the impulse spreads progressively around the circle until it returns to the 12 o'clock position. If the originally stimulated muscle fibers are still in a refractory state, the impulse then dies out because refractory muscle cannot transmit a second impulse. But there are three different conditions that can cause this impulse to continue to travel around the circle, that is, to cause "re-entry" of the impulse into muscle that has already been excited. This is called a "circus movement."

First, if the pathway around the circle is too long, by the time the impulse returns to the 12 o'clock position, the originally stimulated muscle will no longer be refractory and the impulse will continue around the circle again and again.

Second, if the length of the pathway remains constant but the velocity of conduction becomes decreased enough, an increased interval of time will elapse before the impulse returns to the 12 o'clock position. By this time, the originally stimulated muscle might be out of

Figure 13-14

the refractory state, and the impulse can continue around the circle again and again.

Third, the refractory period of the muscle might become greatly shortened. In this case, the impulse could also continue around and around the circle.

All these conditions occur in different pathological states of the human heart, as follows: (1) A long pathway typically occurs in dilated hearts. (2) Decreased rate of conduction frequently results from (a) blockage of the Purkinje system, (b) ischemia of the muscle, (c) high blood potassium levels, or (d) many other factors. (3) A shortened refractory period commonly occurs in response to various drugs, such as epinephrine, or after repetitive electrical stimulation. Thus, in many cardiac disturbances, re-entry can cause abnormal patterns of cardiac contraction or abnormal cardiac rhythms that ignore the pace-setting effects of the sinus node.

Chain Reaction Mechanism of Fibrillation

In ventricular fibrillation, one sees many separate and small contractile waves spreading at the same time in different directions over the cardiac muscle. The reentrant impulses in fibrillation are not simply a single impulse moving in a circle, as shown in Figure 13-14. Instead, they have degenerated into a series of multiple wave fronts that have the appearance of a "chain reaction." One of the best ways to explain this process in fibrillation is to describe the initiation of fibrillation by electric shock caused by 60-cycle alternating electric current.

Fibrillation Caused by 60-Cycle Alternating Current. At a central point in the ventricles of heart A in Figure 13-15, a 60-cycle electrical stimulus is applied through a stimulating electrode. The first cycle of the electrical stimulus causes a depolarization wave to spread in all directions, leaving all the muscle beneath the electrode in a refractory state.After about 0.25 second, part of this muscle begins to come out of the refractory state. Some portions come out of refractoriness before other

Stimulus point Dividing impulses

Blocked impulse

Figure 13-15

Blocked impulse

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