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i!1GUBH|Hi|H% Mean QRS electrical axis. This axis can be ^HllllHIHlFestimated by using Einthoven's triangle and the net voltage of the QRS complex in any two of the bipolar limb leads. It can also be estimated by inspection of the six limb leads (see text for details). ECG tracings are from Figure 13.14.

Figure 13.17A shows respiratory sinus arrhythmia, an increase in the heart rate with inspiration and a decrease with expiration. The presence of a P wave before each QRS complex indicates that these beats originate in the SA node. Intervals between successive R waves of 1.08, 0.88, 0.88, 0.80, 0.66, and 0.66 seconds correspond to heart rates of 56, 68, 68, 75, 91, and 91 beats/min. The interval between the beginning of the P wave and the end of the T wave is uniform, and the change in the interval between beats is primarily accounted for by the variation in time between the end of the T wave and the beginning of the P wave. Although the heart rate changes, the interval during which electrical activation of the atria and ventricles occurs does not change nearly as much as the interval between beats. Respiratory sinus arrhythmia is caused by cyclic changes in sympathetic and parasympathetic neural activity to the SA node that accompany respiration. It is observed in individuals with healthy hearts.

Figure 13.17B shows an ECG during excessive stimulation of the parasympathetic nerves. The stimulation releases ACh from nerve endings in the SA and AV nodes; ACh suppresses the pacemaker activity, slows the heart

Heart Pacemaker And NevesNode Suppresses

rate, and increases the distance between P waves. The fourth and fifth QRS complexes are not preceded by P waves. When a QRS complex is recorded without a preceding P wave, it reflects the fact that ventricular excitation has occurred without a preceding atrial contraction, which means that the ventricles were excited by an impulse that originated below the atria. The normal configuration of the QRS complex suggests that the new pacemaker was in the AV node or bundle of His and that ventricular excitation proceeded normally from that point. This is called junctional escape.

The ECG in Figure 13.17C is from a patient with atrial fibrillation. In this condition, atrial systole does not occur because the atria are excited by many chaotic waves of depolarization. The AV node conducts excitation whenever it is not refractory and a wave of atrial excitation reaches it. Unless there are other abnormalities, conduction through the AV node and ventricles is normal and the resulting QRS complex is normal. The ECG shows QRS complexes that are not preceded by P waves. The ventricular rate is usually rapid and irregular. Atrial fibrillation is associated with nu merous disease states, such as cardiomyopathy, pericarditis, hypertension, and hyperthyroidism, but it sometimes occurs in otherwise normal individuals.

The ECG in Figure 13.17D shows a premature ventricular complex (PVC). The first three QRS complexes are preceded by P waves,- then after the T wave of the third QRS complex, a QRS complex of increased voltage and longer duration occurs. This premature complex is not preceded by a P wave and is followed by a pause before the next normal P wave and QRS complex. The premature ventricular excitation is initiated by an ectopic focus, an area of pacemaker activity in other than the SA node. In panel D, the focus is probably in the Purkinje system or ventricular muscle, where an aberrant pacemaker reaches threshold before being depolarized by the normal wave of excitation. Once the ectopic focus triggers an action potential, the excitation is propagated over the ventricles. The abnormal pattern of excitation accounts for the greater voltage, change of mean electrical axis, and longer duration (inefficient conduction) of the QRS complex. Although the abnormal wave of excitation reached the AV node, retrograde conduction usually dies out in the AV node. The next normal atrial excitation (P wave) occurs but is hidden by the inverted T wave associated with the abnormal QRS complex. This normal wave of atrial excitation does not result in ventricular excitation. Ventricular excitation does not occur because, when the impulse arrives, a portion of the AV node is still refractory following excitation by the premature complex. As a consequence, the next "scheduled" ventricular beat is missed. A prolonged interval following a premature ventricular beat is the compensatory pause.

Premature beats can also arise in the atria. In this case, the P wave is abnormal but the QRS complex is normal. Premature beats are often called extrasystoles, frequently a misnomer because there is no "extra" beat. However, in some cases, the premature beat is interpolated between two normal beats, and the premature beat is indeed "extra."

In Figure 13.17E, both P waves and QRS complexes are present, but their timing is independent of each other. This is complete atrioventricular block in which the AV node fails to conduct impulses from the atria to the ventricles. Because the AV node is the only electrical connection between these areas, the pacemaker activities of the two become entirely independent. In this example, the distance between P waves is about 0.8 sec, giving an atrial rate of 75 beats/min. The distance between R waves averages 1.2 sec, giving a ventricular rate of 50 beats/min. The atrial pacemaker is probably in the SA node, and the ventricular pacemaker is probably in a lower portion of the AV node or bundle of His.

AV block is not always complete. Sometimes the PR interval is lengthened, but all atrial excitations are eventually conducted to the ventricles. This is first-degree atrioventricular block. When some, but not all, of the atrial excita tions are conducted by the AV node, it is second-degree atrioventricular block. If atrial excitation never reaches the ventricles, as in the example in Figure 13.17E, it is third-degree (complete) atrioventricular block.

The ECG Provides Three Types of Information About the Ventricular Myocardium

The ECG provides information about the pattern of excitation of the ventricles, changes in the mass of electrically active ventricular myocardium, and abnormal dipoles resulting from injury to the ventricular myocardium. It provides no direct information about the mechanical effectiveness of the heart; other tests are used to study the efficiency of the heart as a pump (see Chapter 14).

The Pattern of Ventricular Excitation. Disease or injury can affect the pattern of ventricular depolarization and produce an abnormality in the QRS complex. Figure 13.18 shows a normal QRS complex (Fig. 13.18A) and two examples of complexes that have been altered by impaired conduction. In Figure 13.18B, the AV bundle branch to the right side of the heart is not conducting (i.e., there is right bundle-branch block), and depolarization of right-sided myocardium, therefore, depends on delayed electrical activity coming from the normally depolarized left side of the heart. The resulting QRS complex has an abnormal shape because of aberrant electrical conduction and is prolonged because of the increased time necessary to fully depolarize the heart. In Figure 13.18C, the AV bundle branch to the left side of the heart is not conducting (i.e., there is left bundle-branch block), also resulting in a wide, deformed QRS complex.

Deformed Skeleton

QRS complex. B, patient with right bundle-branch block. C, patient with left bundle-branch block

Rv ECGs (leads V2 and V6) of patients with various conditions. A, patient with normal

QRS complex. B, patient with right bundle-branch block. C, patient with left bundle-branch block

Skeletal Muscle Hypertrophy

»Right ventricular hypertrophy. Leads I, aVF, and V! of a patient are shown.

Skeletal Muscle Hypertrophy

Effects of A, Large P waves (lead III) caused by atrial hypertrophy. B, Altered QRS complex (leads V! and V5) produced by left ventricular hypertrophy.

tricular hypertrophy (see Fig. 13.20B). Left ventricular hypertrophy rotates the direction of the major dipole associated with ventricular depolarization to the left, causing large S waves in V1 and large R waves in V5.

Changes in the Mass of Electrically Active Ventricular Myocardium. The recording in Figure 13.19 shows the effect of right ventricular enlargement on the ECG. The increased mass of right ventricular muscle changes the direction of the major dipole during ventricular depolarization, resulting in large R waves in lead V1. The large S waves in lead I and the large R waves in lead aVF are also characteristic of a shift in the dipole of ventricular depolarization to the right. This illustrates how a change in the mass of excited tissue can affect the amplitude and direction of the QRS complex.

Figure 13.20 shows the effects of atrial hypertrophy on the P waves of lead III (see Fig. 13.20A) and the altered QRS complexes in leads V1 and V5 associated with left ven-

Abnormal Dipoles Resulting From Ventricular Myocardial Injury. Myocardial ischemia is present when a portion of the ventricular myocardium fails to receive sufficient blood flow to meet its metabolic needs. In this case, the supply of ATP may decrease below the level required to maintain the active transport of ions across the cell membrane. The resulting alterations in the membrane potential in the ischemic region can affect the ECG. Normally, the ECG is at baseline (zero voltage) during

• The interval between the completion of the T wave and the onset of the P wave (the TP interval), during which all cardiac cells are at their resting membrane potential

• The ST segment, during which depolarization is complete and all ventricular cells are at the plateau (phase 2) of the action potential

Skeletal Muscle Action Potential

tential plateau), all areas are depolarized and true zero is recorded. Because zero baseline is set arbitrarily (on the ECG recorder), a depressed diastolic baseline (TP segment) and an elevated ST segment cannot be distinguished. Regardless of the mechanism, this is referred to as an elevated ST segment. B, The ECG (lead V1) of a patient with acute myocardial infarction.

Electrocardiogram changes in myocardial injury. A, Dark shading depicts depolarized ventricular tissue. ST segment elevation can occur with myocar-dial injury. The apparent zero baseline of the ECG before depolarization is below zero because of partial depolarization of the injured area (shading). After depolarization (during the action po-

tential plateau), all areas are depolarized and true zero is recorded. Because zero baseline is set arbitrarily (on the ECG recorder), a depressed diastolic baseline (TP segment) and an elevated ST segment cannot be distinguished. Regardless of the mechanism, this is referred to as an elevated ST segment. B, The ECG (lead V1) of a patient with acute myocardial infarction.

With myocardial ischemia, the cells in the ischemic region partially depolarize to a lower resting membrane potential because of a lowering of the potassium ion concentration gradient, although they are still capable of action potentials. As a consequence, a dipole is present during the TP interval in injured hearts because of the voltage difference between normal (polarized) and abnormal (partially polarized) tissue. However, no dipole is present during the

ST interval because depolarization is uniform and complete in both injured and normal tissue (this is the plateau period of ventricular action potentials). Because the ECG is designed so that the TP interval is recorded as zero voltage, the true zero during the ST interval is recorded as a positive or negative deflection (Fig. 13.21). These deflections during the ST interval are of major clinical utility in the diagnosis of cardiac injury.

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