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


Answers to Self-Assessment Problems

Case 1

Severe hyperkalemia. Note the markedly prolonged PR interval peaked T waves and widened QRS complex.


Case 2

Hyperacute phase of anterior wall ST elevation myocardial infarction. Note the marked ST elevations in leads V1 through V6, I, and aVL, with reciprocal ST depressions in leads III and aVF. Q waves are present in leads V3 through V6. Also note left axis deviation with possible prior inferior wall infarction.


Case 3

Sustained monomorphic ventricular tachycardia. Note the wide-complex tachycardia (QRS duration up to 0.20 sec) with a wide R wave in lead V1, a QS wave in lead V6, and extreme axis deviation.


Case 4

Sinus rhythm with complete (third-degree) heart block. Note the idioventricular (or very slow junctional) rhythm at about 33 beats/min.


Case 5

Sinus tachycardia with electrical alternans. This combination is highly specific for pericardial effusion with tamponade. (See Chapter 11 .)


Case 6

Acute pericarditis. Note the diffuse ST elevations (leads I, II, III, aVF, and V3 through V6) with PR segment deviations (up in lead aVR, down in leads V4, V5, and V6). This patient gets the taxi.


Case 7

Acute ST elevation anterior myocardial infarction. ST elevations are localized to leads V1, V2, V3, I, and aVL, with poor R wave progression in leads V1, V2, and V3. In addition, note the reciprocal ST depressions in leads II, III, and aVF. This patient needs an ambulance immediately.


Case 8

Wolff-Parkinson-White (WPW) pattern. Note the triad of short PR intervals, wide QRS complexes, and delta waves (i.e., slurring of the early part of the QRS complexes in leads I, aVL, V1, V2, and so forth).


Case 9

Sinus rhythm with isorhythmic AV dissociation.


Case 10

Atrial flutter with 2:1 AV block.


Case 11

Left-right arm lead reversal, which accounts for the negative P waves and negative QRS complexes in lead I.


Case 12

Sinus rhythm with Wenckebach-type AV block.


Case 13

Atrial tachycardia at 150 beats/min with variable AV block.


Case 14

Right bundle branch block with acute anterior Q wave myocardial infarction. Note the Q waves in leads V1, V2, and V3, with ST elevations in leads V1 through V5 and aVL.


Case 15

Right bundle branch block with anterior subendocardial ischemia. Note the ST depressions in leads V2, V3, and V4.


Case 16

Wandering atrial pacemaker.


Case 17

Normal (and hungry) neonate. Note the very narrow QRS complex (about 0.06 sec) with a rightward axis, tall R wave in lead V1, and fast sinus rate (125 beats/min). All of these findings are appropriate for the patient's age (see Chapter 23 ).


Case 18

Dextrocardia with situs inversus. Note the apparently reversed limb and chest leads. This patient has a normal heart (right side of chest) and an inflamed appendix (left side of lower abdomen!).


Case 19

Sinus rhythm with prolonged PR interval. The ECG shows left atrial abnormality, left ventricular hypertrophy, and right bundle branch block. Q waves and ST elevations are seen in leads V1 through V5, I, and aVL. The findings are consistent with left ventricular aneurysm, which was confirmed with echocardiography.


Case 20

Atrial fibrillation with a slow and at times regularized ventricular response should make you suspect digitalis toxicity. ST-T changes are consistent with digitalis toxicity or ischemia, in particular.


Case 21

Atrial tachycardia with 2:1 AV block. (A very subtle “extra” P wave in the ST segment is best seen in leads V1 and V2.) An important cause of this arrhythmia is digitalis toxicity. The ECG shows low voltage in the extremity (limb) leads. Because of the poor R wave progression, this patient may have had a previous anterior myocardial infarction. Based on precordial voltage, left ventricular hypertrophy is present. ST-T changes are consistent with digitalis toxicity, ischemia, left ventricular hypertrophy, and so on.

The theme common to Cases 20 and 21, therefore, is digitalis toxicity.


Case 22

c. Amiodarone. Note the markedly prolonged QT(U) interval.


Case 23

Mitral stenosis. The ECG shows signs of right ventricular hypertrophy (i.e., relatively tall R waves in lead V1 with right axis deviation) and left atrial abnormality.


Case 24

Pulmonic stenosis. The ECG shows signs of right ventricular hypertrophy (relatively tall R waves in lead V1 with right axis deviation) and right atrial abnormality.


Case 25

2:1 sinoatrial (SA) block causes an entire P-QRS-T cycle to be “dropped.” This patient has symptomatic sick sinus syndrome and requires a permanent pacemaker.


Case 26

Atrioventricular nodal reentrant tachycardia (AVNRT). In some of the beats, small retrograde P waves (negative in lead II, positive in lead aVR) are visible immediately after the QRS complex, at the very beginning of the ST segment.


Case 27

Atrial flutter with 2:1 AV conduction. Note the flutter waves at a rate of 300 beats/min (e.g., leads aVR and aVL).


Case 28

Inferoposterolateral myocardial infarction. Note the Q waves in leads II, III, aVF, V5, and V6, and the tall R waves in leads V1 and V2.


Case 29

Sinus rhythm with a markedly prolonged QT(U) interval (about 0.6 sec). This patient has a hereditary type of long QT syndrome. Syncope was caused by recurrent episodes of a torsades de pointes –type of ventricular tachycardia.


Case 30

Atrial fibrillation with Wolff-Parkinson-White (WPW) syndrome. The clue to the diagnosis is the extremely rapid wide-complex tachycardia (about 300 beats/min at times) with a very irregular rate.


Case 31

Sinus rhythm at 100 beats/min with advanced second-degree atrioventricular block (3:1 conduction pattern). The QRS complexes show a bifascicular block pattern (right bundle branch block and left anterior fascicular block). Evidence of left atrial abnormality and left ventricular hypertrophy is also present. Note that one of the P waves is partly hidden in the T waves (see V1). The patient required a permanent pacemaker.


Case 32

Sinus rhythm at 95 beats/min with a 4:3 Wenckebach AV block. Note the group beating pattern. This arrhythmia was due to an acute/evolving Q wave inferior myocardial infarction.


Case 33

Junctional rhythm at 60 beats/min. Note the negative P waves “hidden” at the end of the ST segments.


Case 34

Atrial tachycardia with 2:1 AV block. Note the “hidden” P wave in the ST segments. The atrial rate is 160 beats/min with a ventricular rate of 80 beats/min.


Case 35

Acute cor pulmonale, in this case due to massive pulmonary embolism. Note the sinus tachycardia, S1QIII pattern, poor R wave progression, and prominent anterior T wave inversions, caused here by right ventricular overload (formerly called “strain”).


Case 36

Multifocal atrial tachycardia (MAT).


Case 37

Atrial fibrillation (AF).


Case 38

Sinus rhythm with intermittent left bundle branch block. First, three sinus beats are conducted with a left bundle branch block pattern; the next three beats occur with a normal QRS complex. Note the rate slowing, which is associated with normalization of the QRS complex. Therefore the left bundle branch block here is related to increase in the rate (acceleration- or tachycardia-dependent bundle branch block).


Case 39

Sinus rhythm with transient accelerated idioventricular rhythm.


Case 40

Sinus rhythm with atrial bigeminy and blocked atrial premature beats. The arrow points to a subtle P wave from an atrial premature beat. This beat came so early that it cannot conduct through the AV node, which is still refractory after the previous sinus beat.


Case 41

Hypercalcemia. Note the short QT interval with very abbreviated ST segment; thus the T wave appears to take off right from the end of the QRS complex.


Case 42

Hypothermia. Note the characteristic J (Osborn) waves, best seen in leads V3, V4, and V5.


Case 43

Acute inferolateral myocardial infarction superimposed on a ventricular pacemaker pattern. Note the ST elevations in leads II, III, aVF, V5, and V6, and the reciprocal ST depressions in leads V1, V2, and V3.


Case 44

B. Diffuse ST depressions (except in lead aVR), most marked in the anterior leads. These findings are consistent with non–Q wave myocardial infarction.


Case 45

A. Q waves and ST-T changes consistent with evolving inferoposterolateral myocardial infarction.


Case 46

C. Q waves and persistent ST elevations consistent with anterior wall myocardial infarction and ventricular aneurysm.


Case 47

D. Diffuse ST elevations and characteristic PR segment deviations, diagnostic of acute pericarditis.


Case 48

Hypocalcemia. Calculate the QTC, with QT = 0.48 sec and RR = 0.85 sec. Hence QTc = 0.48/√0.85 = 0.52 The prolonged QTC here is due to a long ST segment. The T wave is normal. Thus the most likely diagnosis is hypocalcemia. In contrast, hypokalemia generally flattens the T wave and prolongs the QT(U) interval.


Case 49

Note the combination of the tall peaked T waves from hyperkalemia with the voltage criteria for left ventricular hypertrophy (LVH). (Left atrial abnormality is also present.) This combination strongly suggests chronic renal failure, the most common cause of hyperkalemia. Patients with hyperkalemia typically have hypertension as well, leading to LVH. QT prolongation may also be present in patients with chronic renal failure from concomitant hypocalcemia. The QT interval here is prolonged for the rate (QTc =.50), which may be due to hypocalcemia, another common finding with chronic renal failure.


Case 50

Cardiac arrest. The rhythm strip shows sinus rhythm with ST segment depressions that are consistent with ischemia, followed by the abrupt onset of ventricular flutter degenerating quickly into ventricular fibrillation. The treatment is defibrillation/resuscitation as described in Chapter 19 .