ECG Problems

Problem 1
Questions
1 What does this ECG show?
2 What is the mechanism of this?
Problem 2
Questions
1 What does this ECG show?
2 What other type of ECG recording should be performed? Why should this be done?
3 Should this ECG be repeated? When it should it be repeated and why?
Problem 3
Questions
1 What does this ECG show?
Problem 4
Questions
1 What rhythm does this ECG show?
2 What is the mechanism of this arrhythmia?
3 How can the atrial rhythm be demonstrated more clearly?
Problem 5
Questions
1 What does this ECG show?
Problem 6
Questions
1 What does this ECG show?
2 What immediate action should be taken?
Problem 7
Questions
1 What does this ECG show?
Problem 8
Problem 9
Problem 10
Questions
1 What does this ECG show?
2 What is the cause?
MCQ 2
 MCQ 3
• The answer is E. (Chap. 269e) Mr. Wilson is suffering an acute inferolateral
myocardial infarction (MI).
• Note the ST elevations in the inferior leads (II, III, aVF) and in V6 (lateral
precordial lead). Also, the striking ST depressions in the anterior precordial
leads (V1–V4) are indicative of posterior ischemia.
• Here, the presence of ST depressions in an anterior lead represents the
“mirror” of ST elevations in a posterior location. One can visualize the
ECG pattern in the anterior leads upside down to see thereciprocal nature of
the ST depressions. Although on initial glance, the QRS pattern appears
wide in the anterior leads suggesting ventricular tachycardia, on further
examination, there are P waves present that are associated with each QRS
(seen most clearly in leads II and V1); thus, the rhythm is sinus tachycardia.
The wide appearance of the QRS is due to the striking ST deviation.
MCQ 4
MCQ 5
MCQ 6
MCQ 7
The answer is D. (Chap. 235) The electrocardiogram (ECG) (see Figure IV-17) is a classic
triad indicating pericardial effusion, often with tamponade. Low voltage, sinus tachycardia,
and electrical alternans are best seen in leads V and V . This triad is highly specific
3 4

for pericardial effusion, usually with tamponade physiology, but it is of limited sensitivity.
Although chronic obstructive pulmonary disease exacerbation and myocardial amyloidosis
can cause low ECG voltage, they are not associated with electrical alternans, and the
former is usually not associated with hypotension unless acidosis or hypoxia is severe.
Anterior myocardial infarction is hallmarked by ST elevation in V –V and often I and aVL.
1 3

The ECG in pulmonary embolism may demonstrate the McGinn-White sign, of

S1Q3T3 (prominent S wave in lead I, with Q waves and T wave inversion in lead III).
However, these ECG findings in acute pulmonary embolism are neither sensitive nor
specific.
 MCQ 18
IV-56. Ms. Handrew presents with complaints of occasional
palpitations. Her rhythm strip (Figure IV-56) is most
consistent with which of the following rhythms?
A. Atrial flutter with variable conduction
B. Multifocal premature ventricular contractions
C. Nonsustained ventricular tachycardia
D. Normal rhythm
E. Sustained ventricular tachycardia
• The answer is B. (Chap. 247) The rhythm strip in
Figure IV-56 demonstrates multifocal premature
ventricular contractions (PVCs). The two PVCs
shown have different morphologies.
• Atrial flutter would have the stereotypical sawtooth P
waves which are not present. Ventricular tachycardia
(VT) would have repeated wide complex tachycardia
— nonsustained VT is defined as VT that lasts <30
seconds, whereas VT lasting >30 seconds or requiring
intervention for termination is deemed sustained VT.
 MCQ 9

IV-66. You are called to the room of an unresponsive 78-year-old. Rhythm strip is shown in
Figure below. He is pulseless.
The most correct first action is which of the following?
A. Administer 100% oxygen by nonrebreather face mask
B. Administer 5 mg IV metoprolol
C. Administer procainamide IV
D. Administer 1 g calcium gluconate IV
E. Unsynchronized defibrillation with 200 J
 MCQ 9
• The answer is E. (Chap. 250) This patient is in
ventricular fibrillation. Immediate
defibrillation is required and treatment should
proceed along advanced cardiac life support
protocol. Defibrillation in this case should
precede administration of oxygen. Medications
will not be effective in the absence of
circulation.
A 55-year-old woman seeks medical attention because of progressive exertional
dyspnea and rapid heart action. At age 12 she suffered from rheumatic fever, and
a heart murmur has been subsequently noted. She has had intermittent episodes
of atrial fibrillation over the past 2 years with good rate control on metoprolol
succinate. Her vital signs include a heart rate of 80 beats/min, blood pressure
130/80 mm Hg, and respirations 16 breaths/min. She has inspiratory rales at the
lung bases. Her cardiac impulse is displaced laterally. There is a loud S1, a
single S2, an apical opening snap, a holodiastolic rumbling murmur at the apex,
and a soft diastolic blowing murmur along the left sternal border. Isometric
handgrip augments the diastolic murmurs. She has mild peripheral edema. Her
ECG is shown in Fig. 4.27. The most likely valve lesions are
A. Mitral regurgitation and tricuspid stenosis
B. Mitral stenosis and mitral regurgitation
C. Mitral stenosis and aortic regurgitation
D. Mitral stenosis and pulmonic regurgitation
E. Tricuspid stenosis and pulmonic regurgitation
• This woman has rheumatic heart disease. She has mitral stenosis (MS) based on the loud S1 and
apical opening snap. Many patients with advanced MS have an early blowing diastolic murmur
along the left sternal border and a normal systemic pulse pressure. In the majority of such
patients, the murmur is due to mild aortic regurgitation (AR) and it is usually of little clinical
importance. However, approximately 10% of patients with MS have severe rheumatic AR. This
can usually be recognized by peripheral signs of AR, such as a widened pulse pressure and signs
of left ventricular (LV) enlargement by ECG and chest radiograph, with confirmation by
echocardiography. In patients with multivalvular disease, a proximal valve lesion may mask the
presence of a more distal abnormality.
• Thus, significant AR may not be easily auscultated in patients with severe MS. The widened
pulse pressure, in particular, may be absent in the presence of severe MS. Furthermore, the
apical diastolic Austin Flint murmur associated with AR may be mistaken for the rumbling
murmur of MS. These two murmurs may be distinguished during auscultation by means of
bedside maneuvers. Isometric handgrip and squatting augment the diastolic murmur of AR (and
the associated
• Austin Flint murmur), but have little effect on the murmur of MS. In this patient, the response to
handgrip is consistent with the presence of an Austin Flint murmur.
• The fact that the ECG of this patient shows LV hypertrophy in addition to left atrial enlargement
is inconsistent with simple MS and suggests that the degree of superimposed AR is significant.
There is no evidence on examination of tricuspid stenosis or mitral regurgitation. Pulmonic
regurgitation due to pulmonary hypertension in patients with MS can also cause an early
diastolic murmur along the left sternal border. However, such a murmur would be associated
with a loud pulmonic component of S2 and would not intensify with handgrip.
That’s all folks !!