Arrhythmias Detected by the Electrocardiograph

Arrhythmias, or abnormal heart rhythms, can be detected and described by the abnormal ECG tracings they produce. Although proper clinical interpretation of electrocardiograms requires information not covered in this chapter, some knowledge of abnormal rhythms is interesting in itself and is useful in gaining an understanding of normal physiology.

Since a heartbeat occurs whenever a normal QRS complex is seen, and since the ECG chart paper moves at a known speed so that its x-axis indicates time, the cardiac rate (beats per minute) can be easily obtained from an ECG recording. A cardiac rate slower than 60 beats per minute indicates bradycardia; a rate faster than 100 beats per minute is described as tachycardia (fig. 13.32).

Both bradycardia and tachycardia can occur normally. Endurance-trained athletes, for example, often have heart rates ranging from 40 to 60 beats per minute. This athlete's bradycar-dia occurs as a result of higher levels of parasympathetic inhibition of the SA node and is a beneficial adaptation. Activation of

398 Chapter Thirteen

398 Chapter Thirteen

Sinus bradycardia Ventricular tachycardia

Sinus bradycardia Ventricular tachycardia

(a) Sinus tachycardia (b) Ventricular fibrillation

■ Figure 13.32 Some arrhythmias detected by the ECG. In (a) the heartbeat is paced by the normal pacemaker—the SA node (hence the name sinus rhythm). This can be abnormally slow (bradycardia—42 beats per minute in this example) or fast (tachycardia—125 beats per minute in this example). Compare the pattern of tachycardia in (a) with the tachycardia in (b). Ventricular tachycardia is produced by an ectopic pacemaker in the ventricles. This dangerous condition can quickly lead to ventricular fibrillation, also shown in (b).

(a) Sinus tachycardia (b) Ventricular fibrillation

■ Figure 13.32 Some arrhythmias detected by the ECG. In (a) the heartbeat is paced by the normal pacemaker—the SA node (hence the name sinus rhythm). This can be abnormally slow (bradycardia—42 beats per minute in this example) or fast (tachycardia—125 beats per minute in this example). Compare the pattern of tachycardia in (a) with the tachycardia in (b). Ventricular tachycardia is produced by an ectopic pacemaker in the ventricles. This dangerous condition can quickly lead to ventricular fibrillation, also shown in (b).

the sympathetic division of the ANS during exercise or emergencies ("fight or flight"), causes a normal tachycardia.

Abnormal tachycardia occurs if the heart rate increases when the person is at rest. This may be due to abnormally fast pacing by the atria (caused, for example, by drugs), or to the development of abnormally fast ectopic pacemakers—cells located outside the SA node that assume a pacemaker function. This abnormal atrial tachycardia thus differs from normal, or sinus, (SA node) tachycardia. Ventricular tachycardia results when abnormally fast ectopic pacemakers in the ventricles cause them to beat rapidly and independently of the atria. This is very dangerous because it can quickly degenerate into a lethal condition known as ventricular fibrillation.

Flutter and Fibrillation

Extremely rapid rates of electrical excitation and contraction of either the atria or the ventricles may produce flutter or fibrillation. In flutter, the contractions are very rapid (200 to 300 per minute) but are coordinated. In fibrillation, contractions of different groups of myocardial fibers occur at different times, so that a coordinated pumping action of the chambers is impossible.

Atrial flutter usually degenerates quickly into atrial fibrillation. This causes the pumping action of the atria to stop. Since the ventricles fill to about 80% of their end-diastolic volume before atrial contraction normally occurs, however, the heart is still able to eject a sufficient quantity of blood into the circulation. People who have atrial fibrillation can thus live for many years. People who have ventricular fibrillation (fig. 13.32), by contrast, can live for only a few minutes before the brain and heart—which are very dependent upon oxygen for their metabolism—cease to function.

Fibrillation is caused by a continuous recycling of electrical waves, known as circus rhythms, through the myocardium. This recycling is normally prevented by the fact that the entire myocardium enters a refractory period (due to the long duration of action potentials, as previously discussed). If some cells emerge from their refractory period before others, however, electrical waves can be continuously regenerated and conducted. Recycling of electrical waves along continuously changing pathways produces uncoordinated contraction and an impotent pumping action.

Circus rhythms are thus produced whenever impulses can be conducted without interruption by nonrefractory tissue. This may occur when the conduction pathway is longer than normal, as in a dilated heart. It can also be produced by an electric shock delivered at the middle of the T wave, when different myocar-dial cells are in different stages of recovery from their refractory period. Finally, circus rhythms and fibrillation may be produced by damage to the myocardium, which slows the normal rate of impulse conduction.

Fibrillation can sometimes be stopped by a strong electric shock delivered to the chest. This procedure is called electrical defibrillation. The electric shock depolarizes all of the myocardial cells at the same time, causing them all to enter a refractory state. Conduction of circus rhythms thus stops, and the SA node can begin to stimulate contraction in a normal fashion. This does not correct the initial problem that caused circus rhythms and fibrillation, but it does keep the person alive long enough to take other corrective measures.

AV Node Block

The time interval between the beginning of atrial depolarization— indicated by the P wave—and the beginning of ventricular depolarization (as shown by the Q part of the QRS complex) is called the P-R interval (see fig. 13.21). In the normal heart, this time

Clinical Investigation Clues

Remember that Jason's ECG showed sinus tachycardia.

■ What might produce this condition?

■ How would this ECG finding be related to the doctor's observations of Jason's radial pulse?

Heart and Circulation 399

Third-degree AV block

Figure 13.33 Atrioventricular (AV) node block. In first-degree block, the P-R interval is greater than 0.20 second (in the example here, the P-R interval is 0.26-0.28 second). In second-degree block, P waves are seen that are not accompanied by QRS waves. In this example, the atria are beating 90 times per minute (as represented by the P waves), while the ventricles are beating 50 times per minute (as represented by the QRS waves). In third-degree block, the ventricles are paced independently of the atria by an ectopic pacemaker. Ventricular depolarization (QRS) and repolarization (T) therefore have a variable position in the electrocardiogram relative to the P waves (atrial depolarization).

Third-degree AV block

Figure 13.33 Atrioventricular (AV) node block. In first-degree block, the P-R interval is greater than 0.20 second (in the example here, the P-R interval is 0.26-0.28 second). In second-degree block, P waves are seen that are not accompanied by QRS waves. In this example, the atria are beating 90 times per minute (as represented by the P waves), while the ventricles are beating 50 times per minute (as represented by the QRS waves). In third-degree block, the ventricles are paced independently of the atria by an ectopic pacemaker. Ventricular depolarization (QRS) and repolarization (T) therefore have a variable position in the electrocardiogram relative to the P waves (atrial depolarization).

interval is 0.12 to 0.20 second in duration. Damage to the AV node causes slowing of impulse conduction and is reflected by changes in the P-R interval. This condition is known as AV node block (fig. 13.33).

First-degree AV node block occurs when the rate of impulse conduction through the AV node (as reflected by the P-R interval) exceeds 0.20 second. Second-degree AV node block occurs when the AV node is damaged so severely that only one out of every two, three, or four atrial electrical waves can pass through to the ventricles. This is indicated in an ECG by the presence of P waves without associated QRS waves.

In third-degree, or complete, AV node block, none of the atrial waves can pass through the AV node to the ventricles. The atria are paced by the SA node (follow a normal "sinus rhythm"), but the ventricles are paced by an ectopic pacemaker (usually located in the bundle of His or Purkinje fibers). Since the SA node is the normal pacemaker by virtue of the fact that it has the fastest cycle of electrical activity, the ectopic pacemaker in the ventricles causes them to beat at an abnormally slow rate. The bradycardia that results is usually corrected by insertion of an artificial pacemaker.

A number of abnormal conditions, including a blockage in conduction of the impulse along the bundle of His, require the insertion of an artificial pacemaker.

This is a battery-powered device, about the size of a locket, which may be placed in permanent position under the skin. The electrodes from the pacemaker are guided through a vein to the right atrium, through the tricuspid valve, and into the right ventricle. The electrodes are fixed to the trabeculae carnae and are in contact with the wall of the ventricle. When these electrodes deliver shocks—either at a continuous pace or on demand (when the heart's own impulse doesn't arrive on time)—both ventricles are depolarized and contract, and then repolarize and relax, just as they do in response to endogenous stimulation.

Test Yourself Before You Continue

1. Explain how cholesterol is carried in the plasma and how the concentrations of cholesterol carriers are related to the risk for developing atherosclerosis.

2. Explain how angina pectoris is produced and discuss the significance of this symptom.

3. Define bradycardia and tachycardia, and give normal and pathological examples of each condition. Also, describe how flutter and fibrillation are produced.

4. Explain the effects of first-, second-, and third-degree AV node block on the electrocardiogram.

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