Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)

Part IV. SELF-ASSESSMENT PROBLEMS

Answers to Chapter Questions

Part 1 Basic Principles and Patterns

Chapter 1

 

1.   

See Fig. 1-1 .

 

2.   

An electrocardiogram (ECG) is a graph that records cardiac electrical activity by means of electrodes placed on the surface of the body.

 

3.   

True

 

Chapter 2

 

1.   

 

a.   

50 beats/min

 

b.   

150 beats/min

 

c.   

Approximately 170 beats/min. Seventeen QRS cycles occur in 6 seconds. Notice the irregularity of the QRS complexes and the absence of P waves. This rhythm is atrial fibrillation (see Chapter 15 ).

 

2.   

 

a.   

Abnormally wide QRS complex (0.16 sec)

 

b.   

Abnormally long PR interval (approximately 0.3 sec)

 

c.   

Abnormally long QT interval (0.4 sec) for rate. The RR interval measures 0.6 sec; therefore the heart rate is 100 beats/min (see Table 2-1 ). The rate-corrected (QTc = QT/√RR) is also prolonged, at 0.52 sec (0.4/√0.6). Normal is 0.44 sec or less.

 

3.   

 

a.   

Prolong the PR interval.

 

4.   

 

b.   

Prolong the QRS interval.

 

5.   

 

a.   

R wave

 

b.   

qRS complex

 

c.   

QS complex

 

d.   

RSR′ complex

 

e.   

QR complex

 

6.   

Drugs (amiodarone, disopyramide, ibutilide, procainamide, quinidine, sotalol), electrolyte abnormalities (hypocalcemia, hypokalemia), systemic hypothermia, and myocardial infarction. SeeChapter 24 for more extensive list.

 

7.   

 

c.   

Depolarization of the His bundle is not seen on the ECG. This physiologic event occurs during the isolectric part of the PR interval. His bundle activation, however, can be recorded using a special electrode system inside the heart during cardiac electrophysiologic (EP) procedures.

 

Chapter 3

 

1.   

Lead II = lead I + lead III; therefore, according to Einthoven's equation, lead III = lead II - lead I, as shown below:

 


Notice that the voltages of the P wave, QRS complex, and T wave in lead II are equal to the sum of the P, QRS, and T voltages in leads I and III.

 

2.   

The voltages in lead II do not equal those in leads I and III. The reason is that leads II and III were mislabeled. When you reverse the labels, the voltage in lead II equals the voltages in leads I and III.

 

3.   

See Fig. 3-7C .

 

4.   

The positive poles of leads aVR and II point in opposite directions (see Fig. 3-7 ).

 

Chapter 4

 

1.   

 

a.   

Yes. The P waves are positive (upright) in lead II and negative in lead aVR, with a rate of about 75 beats/min.

 

b.   

Electrically vertical. The R waves are most prominent in leads II, III, and aVF.

 

c.   

The transition zone is in lead V3. Notice that the RS complexes have the R wave approximately equal to the S wave.

 

d.   

The PR interval is about 0.16 sec. This is within normal range (0.12 to 0.2 sec).

 

e.   

The QRS width is 0.08 sec. This is normal (less than or equal to 0.1 sec).

 

f.    

Yes

 

2.   

No. Although a P wave appears before each QRS complex, it is negative in lead II. With sinus rhythm, the P should be positive (upright) in lead II. Thus, in this patient, the pacemaker must be outside the sinus node (ectopic), probably in a low atrial focus near the atrioventricular junction. Inverted P waves such as these are called retrograde because the atria are depolarized in the opposite direction from normal (i.e., from the bottom to the top rather than from the top [sinus node] to the bottom [atrioventricular junction]; see also Chapters 13 and 14 ).

 

Chapter 5

 

1.   

The QRS axis is roughly +60°. Notice that the QRS complex in lead aVL is biphasic. Therefore the mean QRS axis must point at a right angle to -30°. In this case, the axis is obviously about +60° because leads II, III, and aVF are positive. Note that the R wave in lead III is slightly taller than the R wave in lead I. If the axis were exactly +60°, these waves would be equally tall. Thus the axis must be somewhat more positive than +60°, probably around +70°. Estimating the QRS axis to within 10° or 20° is usually quite adequate for clinical diagnosis.

 

2.   

A, lead II; B, lead I; C, lead III. Explanation: If the mean QRS axis is -30°, the QRS axis is pointed toward lead I (which is at 0°) and away from lead III (which is at +120°). Obviously lead I must be B and lead III must be C. Lead II is A, which is biphasic. The positive pole of lead II is at +60° on the hexaxial diagram. If the mean QRS axis is -30°, lead II must show a biphasic complex because the mean QRS axis is at right angles to that lead.

 

3.   

 

e.   

Left anterior fascicular block (hemiblock)

 

Chapter 6

 

1.   

 

a.   

About 75 beats/min

 

b.   

The PR interval is prolonged (about 0.22 sec) indicating mild “first-degree AV block” (see Chapter 17 ). The P wave in lead II is also abnormally wide and notched (notice the two humps) as a result of left atrial abnormality (enlargement).

 

2.   

True

 

Chapter 7

 

1.   

See Fig. 7-6 .

 

2.   

 

a.   

0.12 sec

 

b.   

Right bundle branch block

 

c.   

Secondary T wave inversions can be seen in the right chest leads with right bundle branch block (see text and answer to Question 4).

 

3.   

Left bundle branch block. The PR interval is also somewhat long (0.24 sec) due to prolonged AV conduction (“first-degree AV block”).

 

4.   

Primary T wave abnormalities are due to actual changes in ventricular repolarization caused, for example, by drugs, ischemia, or electrolyte abnormalities. These abnormalities are independent of changes in the QRS complex. Secondary T wave changes, by contrast, are related entirely to alterations in the timing of ventricular depolarization and are seen in conditions in which the QRS complex is wide. For example, with bundle branch block, a change in the sequence of depolarization also alters the sequence of repolarization, causing the T wave to point in a direction opposite the last deflection of the QRS complex. Thus, with right bundle branch block, the T waves are secondarily inverted in leads with an rSR′ configuration (e.g., V1, V2, and sometimes V3) due to a delay in right ventricular repolarization. With left bundle branch block, the secondary T wave inversions are seen in leads with tall wide R waves (V5 and V6) due to a delay in left ventricular repolarization. Secondary T wave inversions are also seen with ventricular paced beats (see Fig. 7-8 ) and the Wolff-Parkinson-White preexcitation pattern ( Chapter 12 ). Sometimes, primary and secondary T wave changes are seen on the same ECG, as when ischemia develops in a patient with a bundle branch block (see Fig. 8-21 ).

 

5.   

True

 

6.   

True

 

7.   

True

 

8.   

False. It will produce a right bundle branch block pattern since the left ventricle will be stimulated before the right.

 

Chapters 8 and 9

 

1.   

 

a.   

100 beats/min

 

b.   

Yes. In leads II, III, and aVF, with reciprocal ST depressions in leads V2 to V4, I, and aVL

 

c.   

Yes. Best seen in leads III and aVf

 

d.   

Acute inferior wall infarction

 

2.   

 

a.   

About +90°. Between 80° and 90° is acceptable.

 

b.   

No

 

c.   

No. Notice the inverted T waves in leads V2 to V6, I, and aVl.

 

d.   

Anterior wall infarction, possibly recent or evolving

 

3.   

Reciprocally depressed

 

4.   

Ventricular aneurysm

 

5.   

 

b.   

Non–Q wave infarction

 

6.   

Marked ST segment depressions. This patient had severe ischemic chest pain with a non–Q wave infarct.

 

7.   

The ECG shows a right bundle branch block pattern with an evolving anterior Q wave infarct. With uncomplicated right bundle branch block, the right chest leads show an rSR′ pattern. Note that leads V1, V2, and V3 show wide QR waves (0.12 sec) because of the anterior Q wave myocardial infarction and right bundle branch block. The ST elevations in leads V1, V2, and V3 and the T wave inversions across the chest leads are consistent with recent or evolving myocardial infarction.

 

8.   

False. Thrombolytic therapy only has demonstrated benefit in acute ST segment elevation MI (STEMI), not with non–ST segment elevation MI.

 

Chapter 10

 

1.   

 

b.   

Early repolarization pattern

 

d.   

Ventricular aneurysm

 

g.   

Pericarditis

 

2.   

 

a.   

Digitalis effect, B

 

b.   

Hyperkalemia, A

 

c.   

Hypokalemia, C

 

3.   

 

b.   

Hypokalemia

 

Chapter 11

 

1.   

 

a.   

Pericardial effusion with cardiac tamponade

 

2.   

False

 

Chapter 12

 

1.   

 

d.   

Wolff-Parkinson-White (WPW) pattern. Notice the diagnostic triad of a wide QRS complex, a short PR interval, and a delta wave (slurred initial portion of the QRS complex). Compare this with Figs. 12-3 and 12-4 , which also show the WPW pattern. These patterns are sometimes mistaken for hypertrophy (tall R waves) or infarction (pseudoinfarction Q waves). The negative delta waves in lead aVL and positive waves in lead V1 are consistent with a left lateral bypass tract in this case.

 

Part 2 Cardiac Rhythm Disturbances

Chapter 13

 

1.   

Yes. The P waves are negative in lead aVR and positive in lead II. Do not be confused by the unusual QRS complexes (positive in lead aVR and negative in lead II) produced by the abnormal axis deviation. The diagnosis of normal sinus rhythm depends only on the P waves.

 

2.   

No. Each QRS complex is preceded by a P wave. Notice, however, that the P waves are negative in lead II. These retrograde P waves indicate an ectopic pacemaker, probably located in a low atrial site near the AV junction.

 

3.   

 

d.   

Isoproterenol

 

4.   

True

 

Chapter 14

 

1.   

The palpitations could be due to occasional atrial premature beats. Notice that the fifth complex is an atrial premature beat (or possibly a junctional premature beat because the P wave is not seen).

 

2.   

Junctional escape beat. Notice that it comes after a pause in the normal rhythm and is not preceded by a P wave.

 

3.   

 

a.   

Approximately 210 beats/min. Count the number of QRS complexes in 6 sec and multiply by 10.

 

b.   

(2) Paroxysmal supraventricular tachycardia (PSVT). A retrograde P wave may be seen just after the QRS complex, making atrioventricular nodal reentrant tachycardia (AVNRT) the most likely mechanism for the arrhythmia. A concealed bypass tract, however, cannot be excluded here.

 

4.   

False. PSVT is not a sinus rhythm variant, but is due to an ectopic rhythm originating in the atria (atrial tachycardia) or the AV node area (AV nodal reentrant tachycardia) or involving an atrioventricular bypass tract (AV reentrant tachycardia).

 

Chapter 15

 

1.   

 

a.   

About 300 beats/min

 

b.   

About 75 beats/min

 

c.   

Atrial flutter with 4:1 atrioventricular (AV) conduction

 

2.   

 

a.   

About 70 beats/min. Count the number of QRS complexes in 6 sec and multiply by 10.

 

b.   

Atrial fibrillation. This is a subtle example because the fibrillatory waves are of very low amplitude. The diagnosis of atrial fibrillation is suspected when an irregular ventricular response is found along with fine wavering of the baseline between QRS complexes.

 

3.   

Slower

 

4.   

Faster

 

5.   

False

 

6.   

False

 

Chapter 16

 

1.   

Ventricular tachycardia (monomorphic)

 

2.   

Torsades de pointes. Notice the changing orientation and amplitude of the QRS complexes with this type of polymorphic ventricular tachycardia. Contrast this type of polymorphic ventricular tachycardia with the monomorphic ventricular tachycardia in Question 1, where all QRS complexes are the same.

 

3.   

Hypoxemia, digitalis or other drug toxicity, hypokalemia, hypomagnesemia (see text)

 

4.   

Sinus rhythm with ventricular bigeminy

 

Chapter 17

 

1.   

 

a.   

Sinus rhythm with AV Wenckebach block. Notice the succession of P waves, with increasing PR intervals followed by a nonconducted (dropped) P wave. This pattern leads to “group beating.” Blocked premature atrial complexes can also cause group beating, but the nonconducted P wave comes early (before the next sinus P wave is due). The P waves in this example come on time.

 

2.   

 

a.   

100 beats/min

 

b.   

42 beats/min

 

c.   

No

 

d.   

Sinus rhythm with complete heart block. Notice that some of the P waves are hidden in QRS complexes or T waves.

 

3.   

True.

 

Chapter 18

 

1.   

Hypokalemia, hypomagnesemia, hypoxemia, acute myocardial infarction, renal failure (Other answers can be found in the text of Chapter 18 .)

 

2.   

True

 

3.   

False

 

4.   

False

 

5.   

True

 

6.   

False

 

7.   

True

 

Chapter 19

 

1.   

No. By definition, patients with electromechanical dissociation have relatively normal electrical activity. The problem is that this electrical activity is not associated with adequate mechanical (pumping) action, due, for example, to diffuse myocardial injury, pericardial tamponade, or severe loss of intravascular volume. A pacemaker would not help in this situation because the patient's heart already has appropriate electrical stimulation.

 

2.   

 

a.   

Idioventricular escape rhythm

 

b.   

External cardiac compression artifacts

 

3.   

Digitalis (digoxin), epinephrine, cocaine, flecainide (also quinidine, procainamide, disopyramide, ibutilide, dofetilide, and most other antiarrhythmic agents)

 

Chapter 20

 

1.   

 

a.   

Irregular

 

b.   

No. The baseline shows an irregular fibrillatory pattern.

 

c.   

Atrial fibrillation

 

2.   

Ventricular tachycardia

 

3.   

Paroxysmal supraventricular tachycardia (probably atrioventricular nodal reentrant tachycardia; see Chapter 14 )

 

4.   

Sinus rhythm with 2:1 AV block, indicated by a sinus rate of about 74 beats/min and a ventricular rate of about 37 beats/min

 

5.   

Digitalis toxicity, excess beta blocker, excess calcium channel blocker (e.g., verapamil or diltiazem), amiodarone, lithium carbonate, hyperkalemia, hypothyroidism

 

Chapter 21

 

1.   

 

b.   

Symptomatic bradyarrhythmia

 

2.   

 

b.   

Failure to pace. In this example of intermittent failure to pace, the fourth pacemaker spike is not followed by a QRS complex. The two most common causes of failure to pace (with a pacemaker spike that does not capture) are dislodgment of the electrode wire and fibrosis around the pacing wire tip. In some cases of pacemaker failure, no pacing spikes are seen (see Fig. 21-9 ).

 

3.   

Atrial pacing. Notice the sharp pacemaker spike before each P wave, which is followed by a normal QRS complex (see Fig. 21-3 ).

 

4.   

b.

 

5.   

False.

 

Chapter 23

 

1.   

Syncope can be caused by a variety of bradyarrhythmias or tachyarrhythmias, including marked sinus bradycardia, sinus arrest, atrioventricular (AV) junctional escape rhythms, second- or third-degree AV block, atrial fibrillation with an excessively slow ventricular response, sustained ventricular tachycardia, paroxysmal supraventricular tachycardias (PSVTs), and atrial fibrillation or flutter with a rapid ventricular response.

 

2.   

False

 

3.   

False. The sensitivity of a test is a measure of how well the test can detect a given abnormality. False-positive results (abnormal results in normal subjects) lower a test's specificity, not its sensitivity.