Ekg Cel Mai Bun

ECG Self-Study Module
for the Internal Medicine Clerkship
Revised 2/2012
Girish L. Kalra, MD
ECG self-study module
Page |3
Introduction
No matter your eventual specialty, ECG interpretation is an important skill to possess as a practicing
physician. Many learned this skill as students during their internal medicine clerkship experience.
While numerous texts and web resources cover the essentials of ECG interpretation, published sources
for medical student ECG practice are more limited. As a third-year medical student, you will gain the
most practice by reading your patients electrocardiograms and getting immediate feedback on your
interpretation from residents and attendings.
This module was designed to give you an additional source for practice. We recommend you start with
the first ECG and practice reading each tracing using a specific step-by-step method from memory. You
may use the proposed method or your own. After you have interpreted the tracing, you will be given a
clinical case description and a multiple-choice question. Immediate feedback is given with an
explanation of the correct answer.
Each tracing was chosen for a specific learning objective tailored to the third-year medical student. Most
tracings and cases were taken from ECG Wave-Maven (http://ecg.bidmc.harvard.edu) an excellent
web-based tool for practicing ECG interpretation. If, after completing this module, you desire extra
practice or exposure to more challenging cases and "zebras," we recommend you give ECG Wave-Maven
a try.
Regarding the clerkship's ECG quiz

You will be presented with 3 ECGs and asked to interpret each on paper and draw the QRS axis. Don't
worry -- there will be no cases, questions, or answer choices. The quiz ECGs will be randomly taken,
verbatim, from the first 20 abnormal ECGs in this module (Cases #1-20). No tracing after #20 will be on
the exam (see top-right of each ECG for numbering).
Cases 21 and onwards complete the review of basic topics. They are presented purely for your added
learning and practice.
Page |4
Essential topics covered
Normal ECG
Conduction system abnormalities
o Atrioventricular blocks (1st, 2nd, 3rd)
o Bundle branch blocks
Secondary repolarization abnormality
Chamber enlargement
o Left and right atrial abnormality
o Left and right ventricular hypertrophy
Secondary repolarization abnormality or "strain" pattern
Ischemia / Infarction
o Acute ST-segment myocardial infarction (anterior, lateral, inferior, septal) and reciprocal
ST depressions
o T-wave inversions (ischemia)
o Primary ST segment depression (subendocardial ischemia or infarction)
o Prior infarction
Arrhythmias
o Atrial (atrial fibrillation, atrial flutter, multifocal atrial tachycardia)
o Supraventricular tachycardia
o Ventricular (torsades, ventricular tachycardia, ventricular fibrillation)
Pericardial disease (pericarditis, pericardial effusion, cardiac tamponade)
Miscellaneous
o Cardiomyopathy
o Hyperkalemia and hypokalemia
o Pulmonary embolism
o Pre-excitation / Wolff-Parkinson-White syndrome (WPW)
Further reading / practice

1. ECG Wave-Maven: http://ecg.bidmc.harvard.edu
2. ECG Learning Center: http://library.med.utah.edu/kw/ecg
3. Rapid Interpretation of EKG's by Dale Dubin - Paperback
4. The Only EKG Book You'll Ever Need by Malcolm S. Thaler - Paperback
5. ECG Rhythm Simulator: http://www.skillstat.com/learn.htm (<-- very quick practice for identifying
heart rhythms. Use game mode.)
Page |5
A proposed method of ECG interpretation with examples of simplified criteria
Subheading
Rate
Rhythm
+
Intervals
Axis
Hypertrophy
Step
Is the rate regular?

Rate
Rhythm
PR interval (>0.20s = AVB)
QRS duration (>0.10s = IVCD or incomplete BBB; 0.12s = BBB width)
QT interval (normal is < R-R; QTc > 0.44s = prolonged)
QRS axis (draw it; normal is not enough. Prerequisite is memorizing lead orientation fig 2)
3 steps: 1) Find the isolelectric lead 2) Choose the correct perpendicular 3) Fine-tune it
QRS transition / R wave progression (normal transition V3V4)

(Optional) T wave vector
LVH? (SV1 + RV5 > 35mm; or RaVL > 11mm [ > 13mm if left axis deviation])
RVH? (in V1, R > S)
LAA? (in V1, biphasic or predominantly negative P wave. Should be sufficiently wide)
RAA? (in II, peaked P wave taller than 2.5 mm. [avoid V1 criteria -- less sensitive])
Low voltage? (don't take too long on this) (formal criteria: low voltage by limb lead criteria = no QRS
complex in any limb leads is greater than 5 mm total amp, from top to bottom. Low voltage by precordial lead criteria = no QRS
complex > 10 mm total amp in any precordial leads)
Infarction
(Alphabetical
order)
Q waves? (pathologic Q > 0.04 s width OR deeper than 1/4 R wave height; many other criteria)
S wave in lead I? (looking for S1Q3 +/- T3 pattern)
ST segment elevation / depression?
T wave inversions? Peaking?
Figure 1. ECG waves and intervals.

From ECG Learning Center.
http://library.med.utah.edu/kw/ecg/ecg_outline/Lesson1/ind
ex.html
Figure 2. Orientation of frontal plane leads.

From BMJ. 2002 Feb 16;324(7334):415-8.
Page |6
Before we start, look over the following rhythm strips and try to identify the abnormality (discussions
will follow later in text):
All From ECG A Pictorial Primer. http://www.medicine-on-line.com/html/ecg/e0001en_files/08.htm
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Page |7
Page |8
Answers:
1. Torsades de pointes. A potentially fatal multifocal ventricular tachycardia that can be
triggered in patients with prolonged QT intervals. Treat with IV magnesium.
2. Ventricular fibrillation.
3. Monomorphic ventricular tachycardia.
4. Atrial fibrillation. More to follow.
5. Supraventricular tachycardia. More to follow.
6. Atrial flutter with variable conduction. More to follow.
7. PAC (premature atrial contraction), or PAB (premature atrial beat). More to follow.
8. PJC (premature ventricular contraction), or PJB. More to follow.
9. PVC (premature ventricular contraction), or PVC. More to follow.
10. Junctional escape rhythm. More to follow.
Module Case i
Case #233
ECG Wave-Maven
Copyright 2003
Beth Israel Deaconess Medical Center
http://ecg.bidmc.harvard.edu
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
ECG Wave-Maven / Beth Israel Deaconess Medical Center
25 mm/sec, 10 mm/mV
P a g e | 10
Case i (Wave-Maven # 233)

Which of the following statements about this ECG from a 23-yr-old woman with chest pain is correct?
a)
The ECG is within normal limits
b)
The ECG shows right ventricular hypertrophy
c)
The ECG shows left ventricular hypertrophy
d)
The ECG is consistent with severe hypokalemia
e)
The ECG is consistent with severe hypocalcemia
Answer:
a) The ECG shows sinus rhythm at a rate of about 60/min and is completely within normal limits. The electrical axis
(about +50 degrees) and basic intervals (PR, QRS and QT) are all normal. The P waves are normal. The QRS
complexes have a normal morphology. The precordial leads show normal R wave progression (transition zone
between V2 and V3). The ventricular repolarization (ST-T complex) is physiologic (with a normal QT interval)
making severe hypokalemia or hypocalcemia unlikely.
Severe hypokalemia generally causes repolarization (QT-U) prolongation (usually with flat T waves and sometimes
ST sagging). Severe hypocalcemia prolongs the plateau phase of the ventricular action potential, associated QT
prolongation due to a stretched out ST segment.
Additional comments:
As noted, this normal ECG reveals normal sinus rhythm at 60 bpm. The PR interval is less than 0.20 s, making it
normal. Remember that the PR interval is measured from the beginning of the P wave to the beginning of the QRS
complex (rather than to the R wave itself). Sinus rhythm is indicated by regular sinus P waves, the presence of a
QRS complex following every P wave, and a P wave preceding every QRS complex. A normal transition occurs
between V3 and V4. While the P wave is slightly negative in V1, it is not sufficiently deep or wide to suggest any
left atrial abnormality. T wave inversions in lead V1 can often be normal, particularly in young patients.
Additionally, as most ventricular myocardium is oriented away from lead aVR, inverted T waves in aVR are normal
and expected. Normal Q waves are also commonly seen in lead aVR.
Module Case #1
Case #371
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 12
Case #1 (Wave-Maven # 371)

Elderly woman with known coronary artery disease, status post bypass surgery, is admitted for chest pain. What is
the major diagnosis?
a) Acute pulmonary embolism
b) Acute pericarditis
c)
Brugada syndrome
d) Acute lateral ST elevation MI

e)
Acute inferior ST depression MI
Answer:
The ECG shows sinus rhythm with a single isolated VPB (4th beat on the rhythm strip). There are ST segment elevations in leads
I and aVL, and less apparent changes in V5 and V6, accompanied by reciprocal ST segment depressions in leads III and aVF.
Two days prior to this ECG, the patient had had stents placed in the saphenous vein graft (SVG) to the obtuse marginal and
diagonal vessels for treatment of an acute coronary syndrome. One day post procedure she re-developed substernal chest pain
and was found to have in-stent thrombosis of the SVG graft. To the diagonal vessel. She underwent a successful percutaneous
intervention. Creatine kinase peaked at 2,181 IU.
As noted, this ECG shows an acute lateral ST elevation MI. To help localize the infarction, remember that the
lateral leads, which represent the lateral portion of the left ventricle, are I, aVL, V5, and V6. They are usually
supplied by the circumflex artery. The inferior leads are II, III, and aVF; they are supplied by the right coronary
artery. The septal leads are V1 and V2; they are typically supplied by the septal branches of the proximal left
anterior descending artery. The anterior leads are V3 and V4; they represent the anterior portion of the left
ventricle and are supplied by the left anterior descending artery, usually in the region of the diagonal branches.
Notice the ST depressions in the inferior leads. These represent reciprocal ST depressions, which are commonly
seen with STEMI's in opposing leads. Lateral MI's usually have reciprocal changes in the inferior leads, while
inferior MI's usually have reciprocal changes in the lateral leads. While ST depressions can represent
subendocardial ischemia, in this case, they are an inverted reflection of the primary process (acute STEMI).
Remember that ST elevations are never reciprocal changes in the setting of acute ischemia.
Also seen are small, barely diagnostic Q waves in the lateral leads; these represent necrosis and can be seen in
contiguous leads with prior MI and current MI. Lateral T waves inversions are also present, consistent with
ischemia.
As noted, a PVC (premature ventricular contraction; or VPB, ventricular premature beat) is present. Because this
premature QRS complex is wide and different in morphology than the native QRS, we know the origin of this
ectopic beat is ventricular. The next sinus P wave does not cause depolarization because the ventricle is still
refractory from the PVC; thus there is a complete compensatory pause until the next P wave. A PAC (premature
atrial contraction; or PAB, premature atrial beat) is a premature native-looking QRS complex that immediately
follows a non-sinus-appearing P wave, which represents an ectopic atrial beat. A PJC (premature junctional
contractuion; or PJB, premature junctional beat) is an early native-appearing QRS complex that is precipitated by
a premature ectopic impulse in the AV junction; typically, a preceding P wave is not seen.
Module Case #2
Case #200
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 14

This ECG (with some baseline artifact) from an elderly man shows which of the following?
a) Sinus tachycardia with Mobitz type I second degree AV block
b) Sinus tachycardia with Mobitz type II second degree AV block
c)
Sinus tachycardia with blocked premature atrial complexes
d) Sinus rhythm with sinus exit block

e)
Ectopic atrial rhythm with AV Wenckebach
Answer:
b) Sinus tachycardia is present with intermittent non-conducted P waves. The three P waves that fail to conduct on
this tracing all come "on time," so they are not blocked premature atrial complexes (PACs). Furthermore, they are
not preceded by PR prolongation, nor is the PR interval following these nonconducted P waves shorter than the
preceding ones. Hence, Mobitz I (AV Wenckebach) is excluded. Rather, the pattern here is that of Mobitz II AV
block, strongly suggesting block below the AV node (infranodal block). That the QRS complex is not wide suggests
that the block is within the His bundle itself (intra-Hisian). The occurrence of AV block here at a somewhat fast
sinus rate is also consistent with infranodal block since factors that increase heart rate (decreased vagal tone;
increased sympathetic tone) facilitate AV nodal conduction. The pattern of Mobitz II AV block can be simulated by
concealed junctional or His extrasystoles. (Reference: S Barold, DL Hayes. Mayo Clin Proc 2002;76:44-57.)
This ECG represents Mobitz II AV block, which is characterized by normal sinus P waves, consistent PR intervals,
and intermittently non-conducted beats (intermittent P wave with no following QRS complex). It is suggestive of
advanced conduction system disease.
Remember that 1st degree AV block is characterized by a consistently prolonged PR interval.
2nd degree AV block is broken into different types: Mobitz type I AV block (or Wenckebach) is characterized by
progressive PR prolongation followed by a dropped beat. Mobitz type II AV block is described above. Unspecified
fixed (eg, 2:1, 3:2 AV block) or variable conduction blocks are classified as 2nd degree AV blocks, though they are
not technically Mobitz type I or II.
3rd degree AV block indicates complete AV dissociation. Atrial activity is seen independent of ventricular activity,
which relies on various "backup" foci of electrical activity to generate a QRS rhythm. A narrow QRS rhythm
suggests a backup electrical focus within the AV junction is pacing the ventricle; we call this a junctional escape
rhythm. It is typically slower than sinus rhythm. A wide QRS rhythm suggests a backup focus within the ventricle is
pacing the ventricles; this is a ventricular escape rhythm or idioventricular rhythm. Ventricular escape rhythms
are typically much slower.
Module Case #3
Case #13
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 16

A middle-aged woman with a history of a "heart murmur" since childhood presents with worsening dyspnea. The
ECG is most consistent with which ONE of the following major diagnoses?
a) Mitral regurgitation
b) Mitral stenosis
c)
Aortic regurgitation
d) Aortic stenosis
e)
Pulmonic stenosis
Answer:
The ECG reveals sinus rhythm with the following abnormalities: left atrial abnormality (LAA) with a relatively tall R
wave in lead V1 and an inverted T wave in that lead, along with right axis deviation (RAD). The combination of a
predominant R wave (even with overall low amplitude QRS voltage) and rightward axis deviation with a normal
QRS duration suggests right ventricular hypertrophy. This pattern along with left atrial abnormality should make
one strongly consider mitral stenosis. An important finding on this ECG is the relatively tall R wave in V1. The
differential diagnosis of this finding includes: normal, childhood ECG, posterior myocardial infarction (usually with
Q's inferiorly), RVH (usually with right axis and T wave inversions in V1-V2), rightward displacement of the heart
(e.g. left pneumothorax), Wolf-Parkinson-White with posterior or lateral wall pre-excitation, hypertrophic
cardiomyopathy with large septal forces (usually see large lateral Q waves as well), RBBB. In this case, the presence
of RAD and anterior T wave strain suggests RVH as the cause for the tall R in V1, and the concomitant presence of
LAA strongly suggests the diagnosis of mitral stenosis. The patient in fact had severe mitral stenosis, which was
treated surgically.
Note: The S1Q3T3 pattern ( rS complex in lead I, qR and T wave inversion in lead III) noted here is sometimes
attributable to RV overload due to pulmonary embolism (see Case 146). However, this pattern is non-specific and
may be seen with a variety of causes of RV overload, acute and chronic, as well as in other settings. The presence
of marked left atrial abnormality and the absence of sinus tachycardia are both against a unifying diagnosis of
acute pulmonary embolism in this case. Also of note is the absence of the anticipated right precordial T inversions
often associated with RV overload syndromes (formerly called an RV "strain" pattern).
Note that evidence for LAA here is best seen at higher gain. The P waves are broad (>120ms in duration) in
multiple leads and there is a biphasic P wave in lead V1 with a broad (>40ms) terminal portion. The late P wave
forces also go toward lead aVL.
Mitral stenosis. The LAA (left atrial abnormality; or LAE, left atrial enlargement) is quite noticeable in V1 (biphasic
P wave, broad in many leads, predominantly negative terminal component). Also consistent with LAA is the
notching of the P wave in lead II. RVH is noted by the predominantly positive QRS complex in V1, and it supported
by a vertical (generally downward-facing) QRS axis, or frank right axis deviation. The above-noted differential for
tall R waves in V1 is complete; the most common causes, however, are RBBB, RVH, and posterior MI (the R is a
180-degree reflection of a Q wave that would appear on a hypothetical posterior / back lead.). As noted, the
S1Q3T3 pattern (S in I, Q in III (can be tiny), and inverted T in III) that is present here is seen with many acute or
chronic right heart processes. It is occasionally seen with pulmonary embolism.
Module Case #4
Case #16
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 18

60-yr-old female with a history of anti-phospholipid syndrome who presented with chest pain. What is the
diagnosis?
Answer:
Sinus rhythm with AV Wenckebach with 4:3 conduction in the setting of an acute inferior wall infarction. The ECG
demonstrates Q waves and ST elevation in leads 2, 3, and aVF. There are also reciprocal ST segment depressions in
leads 1, aVL and V2-3. The rhythm is Wenckebach showing progressive prolongation of the PR intervals, shortening
of the R-R intervals and block of every fourth P wave. The presence of "group" beating is easily recognized and
characteristic of Wenckebach and is often associated with high vagal tone or nodal ischemia in the setting of an
inferior wall myocardial infraction (MI). The block is at the level of the AV node.
Inferior ST elevation MI, sinus rhythm with Mobitz type I (Wenckebach ) 2nd degree AV block.
If you look closely at the rhythm strip, you will notice that several P waves are missing -- looking closer, you should
notice that they are "buried" within ST segments. If you "march out" the P waves by making successive tick marks
that are slightly more than 3 large boxes apart, you should be able to find them.
Module Case #5
Case #363
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 20

A young adult man with chest discomfort and dyspnea presents to the emergency ward. The ECG is diagnostic of
which ONE of the following?
a) Acute pericarditis
b) Acute anterior ST elevation myocardial infarction
c)
Acute pulmonary embolism
d) Early repolarization (normal) variant

e)
Brugada pattern
Answer:
Borderline sinus tachycardia is present at rate of about 95/min. Precordial voltage is prominent. The ECG shows
classic findings for acute pericarditis with diffuse (leads I, II, III, aVL, aVF, V2-V6) upsloping ST segment elevations
and concomitant PR segment deviations (up in aVR and down in other leads that show ST depressions).
Clinically, the patient had recurrent pericarditis, with an acute exacerbation or recurrence. He also had pericardial
effusion, without tamponade physiology on the day of this ECG but with right ventricular collapse noted on the
following day. Echocardiogram also showed a moderate pericardial effusion. He underwent pericardiocentesis and
subsequently a subtotal pericardiectomy (pericardial stripping) procedure for his idiopathic pericardial
inflammatory syndrome.
The prominent precordial voltage here is non-diagnostic in a young adult male. The patient did have hypertension
and concentric left ventricular hypertrophy. The only ECG evidence for hemodynamic compromise is the
borderline resting tachycardia. Low voltage and electrical alternans are absent. Some useful references include:
NEJM 2004: 351:21 and Circulation 2005;112:1921
Acute pericarditis. As noted, the diffuse ST segment elevation is suggestive of pericarditis rather than STEMI,
which is characterized by regional ST elevations in a particular anatomic distribution and reciprocal changes.
Additionally, in acute pericarditis, the ST segment elevation is typically concave (or "smiling") in shape. Compare
this to STEMI, in which the ST segment is typically flat or convex ("frowning" or "tombstone") in morphology (see
module cases #1 and #4).
In pericarditis, down-sloping PR depressions are typically seen in leads with the greatest ST elevations, while upsloping PR elevation is seen in aVR, where ST depression is present. Diffuse low voltage can often be seen,
suggesting pericardial effusion. Electrical alternans represents beat-to-beat variation in the voltage of the ECG
elements (QRS, and often P, ST, and T); this is seen with tamponade.
Also, of note, the miniscule q's in II, III, aVF, V4, V5, V6 are non-diagnostic.
Module Case #6
Case #26
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 22

This ECG "speaks" major clues about the underlying major medical condition in this 77-year-old woman. What does
it say?
Answer:
ECG shows sinus rhythm with left ventricular hypertrophy (LVH), left atrial abnormality and tall peaked T waves
best seen in the precordial leads (with non-specific infero-lateral ST depressions). Also present are left axis
deviation consistent with left anterior fascicular block and a borderline long QT. Putting it all together, the peaked
T waves indicate increased K+ (6.3 mEq/L) with LVH suggesting renal failure associated with hypertension, which
was the case here. The long QT with stretchout ST segment phase goes with decreased calcium seen with renal
failure as well. ST depressions could be from LVH or primary ischemia, in addition to multiple other causes. So
when you see the triad of "tented" T waves (hyperkalemia) with long QT (ST segment prolongation consistent with
hypocalcemia) and LVH (hypertension) the patient virtually always has renal failure.
Hyperkalemia suggesting renal failure. LVH and LAA suggesting HTN.
Easily noticed in patients with hyperkalemia are tall, symmetrically peaked T waves. As hyperkalemia progresses,
progressive QRS widening and P wave flattening is seen. P waves disappear and progressively widening QRS
complexes eventually degenerate into a "sine-wave" pattern in late hyperkalemia.
Of note, the q waves in I and aVL are likely "septal q waves," which are commonly seen in the lateral leads
(especially aVL) in patients with advanced hypertension. While the q of septal depolarization is usually barely
noticeable, in LVH it is commonly more prominent due to hypertrophy of the septum.
The patient also has a slightly wide QRS complex (>0.120 s), consistent with intraventricular conduction delay.
Module Case #7
Case #11
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 24

51-year-old male with bicuspid aortic valve, aortic insufficiency and hypertension who had an episode of chest pain
2 days prior to this tracing.
Answer:
This ECG shows sinus rhythm at about 65 beats/min with diffuse, prominent anterior T wave inversions consistent
with probable ischemia/non-Q wave myocardial infarction (MI). Sometimes this pattern is referred to as Wellens
T waves (de Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with unstable
angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J.
1989;117:657 665 or "LAD-T wave" pattern. The ECG also shows findings consistent with left atrial abnormality
and left ventricular hypertrophy, along with non-specific mild PR prolongation (220 msec), QT prolongation for rate
(480 msec), and borderline left axis deviation. Ischemia/infarction should be on the top of your differential
diagnosis list in this patient with a recent history of chest pain. A tracing during the episode of chest pain revealed
1-2 mm ST elevation in leads I, aVL, V3-V6. Cardiac catheterization revealed noncritical coronary artery disease and
global left ventricular dysfunction. A subsequent echocardiogram taken on the day of this tracing revealed normal
left ventricular function. Most likely the patient had a transient thrombus or spasm in the proximal LAD, with
severe myocardial "stunning." Enzymes were only slightly elevated. Other specific diagnoses to consider in a
patient with diffuse deeply inverted T waves include 1) CNS disease (intracranial hemorrhage, head injury, tumor);
2) apical hypertrophic cardiomyopathy (usually most marked in the mid-lateral precordial leads; 3) intermittent
right ventricular pacing or intermittent LBBB ("memory T waves"; usually with upright T waves in I and
aVL;[Shvilkin A, Ho KKL, Rosen MR, Josephson ME. T vector direction differentiates post-pacing from ischemic T
wave inversion in the precordial leads. Circulation 2005; 111:969-974]); 4) takotsubo (stress) cardiomyopathy (left
ventricular apical "ballooning" pattern on angiogram), and 5) idiopathic global T wave inversions (a diagnosis of
exclusion).
In this patient, these diffuse, deep anterolateral T wave inversions are consistent with ischemia.
Module Case #8
Case #136
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 26

What is the mechanism of the bradycardia in this 61-year-old man.
a) Sinus bradycardia with left bundle branch block (LBBB)
b) Sinus rhythm with 2:1 AV block and LBBB
c)
Sinus rhythm with complete (third degree) AV heart block
d) Atrial tachycardia with block

e)
Idioventricular escape rhythm
Answer:
Sinus rhythm is present at about 72/min with 2:1 AV block and complete left bundle branch block (LBBB).
Prominent left atrial abnormality (LAA) is also noted.
The patient had a history of prior silent inferior myocardial infarction (MI), hypertension, and mitral regurgitation (the latter
two factors accounting for the prominent LAA). He underwent dual chamber pacemaker implantation for his new 2:1 seconddegree AV block, with marked bradycardia. The location of the AV block was likely infranodal, given the presence of the left
bundle branch block (LBBB). The PR of the conducted beats is only slightly prolonged (220ms), and therefore not, by itelf,
indicative of the location of the AV block (nodal vs. infranodal); see Case #5.
Sinus rhythm with 2:1 AV block and LBBB, LAA.
The wide (>0.120 s) QRS that follows the P waves represents a bundle branch block. We can identify whether it is a
left or right bundle branch block by conceptualizing lead V1. Anatomically, V1 sits on the right-center of the chest,
directly over the right ventricle. Thus, out of all of our 12 leads, lead V1 is best suited to record the electrical
depolarization of the right ventricle. In V1, depolarization of the RV is characterized by a positive R wave (that is, a
deflection above the horizontal); this is why a patient with RVH has a positive QRS complex in V1.
In bundle branch block, one ventricle's His-Purkinje system is not functioning. In a RBBB, for example, the fast
conducting fibers of the right bundle branch cannot transmit the initial impulse required to initiate RV
depolarization. The impulse is instead conducted slowly from the LV and septum through myocytes until it brings
about complete ventricular depolarization. Because complete depolarization takes longer, the QRS is wide.
Because depolarization due to an intact His-Purkinje system is fast (typically 0.080 s, or two boxes), we can easily
identify the location of the block by determining which ventricle is still depolarizing at the very end of the wide
QRS complex. Because it lacks fast-conducting innervation from the AV node, in a bundle branch block, the
"blocked" ventricle depolarizes last. Because V1 sits over the right ventricle, in a RBBB, the terminal
portion of the QRS complex is always positive in V1 -- indicating that the right ventricle is depolarizing last. In LBBB,
the terminal QRS (and most of the QRS, for that matter) is always negative in lead V1. In this patient, the entire
QRS complex is negative in V1. This is typical of a LBBB.
Another finding here is a secondary repolarization abnormality, which is always seen in patients with
BBBs or ventricular-origin QRS complexes, and is characterized by ST depressions and T wave inversions in leads
where the QRS complex (particularly the terminal portion) is positive. Leads with negative QRS complexes (esp.
terminal QRS) tend to have ST elevations and upright T waves. These repolarization changes are due to an
abnormal initial depolarization process; they are typically normal and expected. Look carefully at the QRS in each
lead to ensure you understand this concept. With the exception of V4, this ECG generally follows this rule.
Module Case #9
Case #86
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 28

34-year-old male. What's going on here?
Answer:
ECG shows classic findings of acute/hyperacute anterior wall Q wave myocardial infarction (MI), with reciprocal
inferior ST depressions. The distribution of changes is consistent with a proximal left anterior descending (LAD)
occlusion which was confirmed at cardiac catheterization and treated with angioplasty/stent. Premature
atherosclerosis here was associated with multiple risk factors for coronary artery disease:hypertension,
hyperlipidemia, family history and tobacco.
Acute anterior ST-elevation MI with hyperacute T waves. The nonexistent R wave progression in V1-V4 with late
precordial QRS transition is due to the anterior MI.
The sequence of ECG changes in a transmural Q-wave or ST-elevation MI is traditionally taught as follows.
Initially, hyperacute T wave changes occur (increased amplitude and width), followed by ST-segment elevation.
Pathologic Q waves appear, ST elevation decreases, and hyperacute T waves gradually become T wave inversions.
Eventually, ST elevations resolve and T wave inversions normalize. Finally, the patient is left with Q waves
representing myocardial scar or fibrosis ("old MI").
Module Case #10

Case #317
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 30

This ECG from an 85 year woman shows all of the following abnormalities EXCEPT which one?
a) Atrial flutter with 4:1 conduction
b) Right bundle branch block
c)
Left axis deviation consistent with left anterior fascicular block
d) Left ventricular hypertrophy

e)
Mobitz II AV block
Answer:
The ECG shows atrial flutter with a 4:1 conduction pattern (the flutter rate is about 240 cycles/min and the
ventricular response about 60/min) with right bundle branch block, and left axis deviation consistent with left
anterior fascicular block. The R wave of about 15 mm (1.5 mV) in aVL is consistent with underlying left ventricular
hypertrophy, as is the sum of the R wave in aVL plus the S wave in V3 (> 20mm in women by Cornell criteria). There
are also nonspecific ST-T changes in lead aVL and non-diagnostically slow R wave progression in V1-V4. Mobitz II
AV block is not present.
The patient had a history of sick sinus syndrome with the brady-tachy variant (atrial fibrillation and flutter) and had
previously undergone dual chamber pacemaker implantation (no pacing activity evident here at these
atrial/ventricular rates).
Atrial flutter with 4:1 conduction, RBBB, left axis deviation (QRS ~ -45 degrees), LVH.
At initial glance, determining the rhythm is challenging on this tracing. After lead II, the next best lead for
identifying atrial activity is V1 -- try to make a habit of looking there. V1 clearly shows atrial flutter waves
depolarizing at a rate of slightly less than 300/min (slightly longer than one large box). Only 1 out of every four
waves are conducted to the ventricles, consistent with 4:1 block. Usually, atrial flutter conducts at a 2:1 rate,
producing a ventricular heart rate of 150 bpm, though it often conducts at a "variable" rate instead (more later). In
most patients, atrial flutter's characteristic "saw-tooth" pattern is typically best seen in lead II.
While it is difficult (incorrect) to use voltage criteria to diagnose LVH when LBBB is present or RVH when RBBB is
present, you can diagnose LVH in patients with RBBB and vice-versa.
Module Case #11

Case #195
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 32

The following ECG from a middle-aged man with congestive heart failure is most consistent with which
diagnosis?
a) Recurrent pulmonary emboli
b) Malignant hypertension
c)
Mitral stenosis
d) Chronic obstructive pulmonary disease

e)
Inferolateral myocardial infarction
Answer:
b) The ECG shows evidence of severe left ventricular hypertrophy (LVH) with prominent precordial voltage, left
atrial abnormality, lateral ST-T abnormalities and a somewhat leftward QRS axis (-15 degrees). The patient had
malignant hypertension with congestive heart failure (CHF), accounting also for the sinus tachycardia (blood
pressure initially 280/180 mmHg). Recurrent pulmonary emboli may lead to pulmonary hypertension and right
ventricular hypertrophy (RVH). Mitral stenosis leads to left atrial abnormality (or atrial fibrillation) with signs of
RVH. Severe chronic obstructive pulmonary disease (COPD) is often associated with low voltage QRS complexes,
slow R wave progression and a vertical or rightward QRS axis, as well as right atrial overload. The ST-T changes
here are nonspecific and could be due to LVH alone, coronary disease, etc. However, the ECG is not consistent with
extensive inferolateral myocardial infarction (MI) per se.
Severe LVH, LAA, ST-T changes suggestive of secondary repolarization abnormality.
Note the ST depressions in T wave inversions in I, aVL, and V6. Similar to patients with BBB, those with severe
longstanding LVH or RVH can sometimes have secondary repolarization abnormalities on their ECGs. In general,
the ST-T changes are less impressive, and they tend to mirror the mean (entire) QRS complex, rather than just
the terminal portion of the QRS, as is seen in BBB. Inspect each of the leads to ensure you understand this
concept. It is important to note that secondary repolarization abnormalities are only sometimes seen in severe
longstanding LVH/RVH. Do not overlook ischemia as the diagnosis without additional clinical information and a
prior ECG.
Note, this patient meets LVH by several criteria. Using Sokolow-Lyon Index, you may add SV1 to RV6 (instead of
RV5) to meet the 35mm cutoff. The aVL criteria is met (> 11mm in aVL without overt LAD), as well as the Cornell
voltage criteria (SV3 + RaVL > 20 (female) or > 28 (male)). The QRS complexes are also touching in the left
precordial leads (V4-V6), an informal way to suggest LVH.
Also note, an isolated QS complex in V1 does not necessary indicate prior or current MI, particularly when the
initial r wave is subsequently noticeable in V2.
Module Case #12

Case #263
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 34

Elderly man seen in emergency department in transfer with chest pain. All of the following findings are present
EXCEPT?
a) Marked ST depressions consistent with severe global ischemia
b) Left atrial abnormality
c)
QT prolongation
d) Prior inferior and probable lateral Q wave myocardial infarction

e)
Baseline artifact
Answer:
The ECG shows sinus rhythm at about 65 bpm with profound ischemic ST segment depression, most marked in the
precordial leads, consistent with severe subendocardial ischemia and probable acute non-Q wave myocardial
infarction. The QT interval, however, is not prolonged (0.41 second at rate of 65 bpm) and the PR interval is at the
upper limits of normal (0.20 second). Broad P waves are present (biphasic in lead V1 with 60-80 ms low, amplitude
component--esp. on magnified gain) consistent with left atrial abnormality. Q waves (40-50ms) in the inferiorlateral leads are consistent with prior myocardial infarction(s). Baseline artifact is most evident in limb leads.
Profound ST depressions of this type usually indicate severe multivessel disease, and sometimes left main coronary
disease. The fact that the ST depressions are most marked in the antero-lateral leads, and seen in the inferior
leads, is against these ST depressions being reciprocal from an acute posterior ST elevation MI. In the latter, case
ST depressions are usually most marked in V1-V3. The use of postero-lateral lateral leads (V7-V9) may be useful in
selected cases in looking for "hidden" evidence of acute ST elevation MI.
The patient experienced severe chest pain and was transferred from an outside facility in cardiogenic shock. En
route to the cardiac catheterization laboratory, he developed refractory pulseless electrical activity and ventricular
fibrillation.
Severe ST segment depression, consistent with subendocardial ischemia and probable MI. Pathologic Q's in the
inferior leads consistent with prior MI. Borderline Q's in the lateral chest leads, which could represent prior lateral
MI. LAA is a very borderline call, likely based on the broadness of the P wave in II.
Module Case #13

Case #194
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 36

A middle-aged woman with recent onset palpitations. This arrhythmia is most consistent with which endocrine
disorder?
a) Hyperthyroidism
b) Hypothyroidism
c)
Hyperparathyroidism
d) Addison's disease
e)
Cushing's disease
Answer:
a) The rhythm is atrial fibrillation with a rapid ventricular response. Left ventricular hypertrophy (LVH) by voltage is
noted. The patient was markedly hyperthyroid. An estimated 5-15% of patients with hyperthyroidism (especially
older ones) will develop atrial fibrillation. Conversely, a low TSH level was reported in about 5% of patients with
recent onset atrial fibrillation (or flutter) (Krahn AD, et al. Arch Intern Med 1996:156:2221-2224). Hypothyroidism
as well as Addison's disease may be associated with low QRS voltage, non-specific ST-T changes, and sinus
bradycardia.
Hyperparathyroidism may produce signs of hypercalcemia (short QT interval; see Case 67). Cushing's disease may
be associated with LVH (hypertension) and a long Q-T(U) (hypokalemia).
Rapid atrial fibrillation due to hyperthyroidism.
Note the QRS irregularity and no discretely identifiable atrial waves. This is sometimes called "fine" atrial
fibrillation. "Coarse" atrial fibrillation is also irregular, but poorly-defined waves of atrial depolarization are
noticeable (more to come). In contrast, atrial flutter is regular and is characterized by atrial flutter waves
depolarizing at a rate of approximately 240-350 bpm; typically half the waves are conducted to the ventricles,
resulting in a ventricular rate of 150 bpm. Atrial flutter's "saw-tooth" pattern is most easily identified in lead II.
Module Case #14

Case #326
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 38

Very elderly woman brought to the emergency department by her family for evaluation of a recent fall with
complaints of fatigue and weakness. She was noted to have a very slow pulse. What is the rhythm?
a) Sinus rhythm with Mobitz II AV block
b) Sinus rhythm with isorhythmic AV dissociation
c)
Sinus rhythm with third degree (complete) AV block
d)
Sinus bradycardia with right bundle branch block (RBBB) and blocked atrial premature beats in a bigeminal
pattern
e)
Atrial tachycardia with complete heart block
Answer:
This ECG shows sinus rhythm at rate about 75 bpm with complete heart block and a wide (QRS 160 milliseconds)
complex escape mechanism at rate of about 36 bpm with a right bundle branch block/left axis deviation
morphology. There is no relationship between the sinus P waves and the much slower QRS complexes. Prominent
biphasic P waves in lead V1 are consistent with left atrial abnormality. Left ventricular hypertrophy (very
prominent R in aVL) and slow initial R wave progression are also present, with non-diagnostic T wave inversions.
Marked QT interval prolongation (QTc 600 milliseconds) is present.
The patient was admitted and a permanent dual-chamber pacemaker was implanted. Patients with complete heart
block may have syncope (Stokes-Adams syndrome) from marked bradycardia alone or from transient episodes of
torsade de pointes ventricular tachycardia in the setting of long QT syndrome that is sometimes associated with
the bradycardia.
Sinus rhythm with 3rd degree AV block and ventricular escape rhythm at 36 bpm, LAA, possible LVH, probable
secondary repolarization abnormality.
See discussion for module case #2 (AV blocks).
Regarding calculating the heart rate, while the 300-150-100 75-60-50 rule is helpful for regular normal rates, an
alternate strategy is needed for estimating the excessively slow rates and irregular rhythms. Remember that each
12-lead ECG is 10 seconds in duration. To estimate the rate, simply count the number of QRS complexes on the
rhythm strip and multiply by 6 to determine the ventricular rate per minute. You can do the same to estimate
atrial rates.
Module Case #15

Case #304
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 40

ECG from a 34 year old woman with human immunodeficiency virus (HIV) infection. No cardiac murmur was noted.
What is the most likely cause of the right axis deviation?
a) WPW preexcitation
b) Left posterior fascicular block
c)
Posterior myocardial infarction
d) Lead reversal (left-right arm)

e)
Pulmonary hypertension
Answer:
The ECG shows sinus tachycardia with evidence of severe right ventricular hypertrophy (RVH) due to a pressure load. The
diagnostic findings include: right axis deviation with a tall R wave in lead V1 (in this case as part of a qR complex), T wave
inversions in the right-mid precordial leads, and peaked P waves due to associated right atrial abnormality. The S1Q3T3 pattern
morphology here, while nonspecific, may also be seen with RV overload syndromes, acute or chronic.
There are two major general classes of abnormalities causing pressure-load related RVH: pulmonary hypertension (with
multiple possible etiologies) and pulmonic valve stenosis or other abnormalities of pulmonary outflow obstruction. The patient
had severe pulmonary hypertension, which has been reported in association with HIV infection. (For general review of
pulmonary hypertension, see, for example, Ann Internal Med 2005; 143:282.)
Left/right arm lead reversal causes right axis deviation but with a negative P wave in lead I and does not affect the precordial
leads. The normal PR interval and absence of a delta wave preclude a WPW pattern. True posterior MI does not cause an
initial Q in lead V1 and is almost invariably associated with evidence of lateral and or inferior Q wave MI. (The inferior Q waves
here are relatively narrow.) Left posterior fascicular block is a diagnosis of exclusion that can only be made when other causes
of marked right axis deviation have been ruled out, including right ventricular overload syndromes, lateral MI, right ventricular
conduction abnormalities, hypertrophic cardiomyopathy, etc.
Advanced RVH due to severe pulmonary HTN, right axis deviation (QRS + 120 degrees), RAA, S1Q3T3 pattern,
probable secondary repolarization abnormality, inferior Q's likely due to advanced RVH.
Note the right atrial abnormality, which is characterized by a tall, peaked P wave taller than 2.5 mm in lead II. An
deep, inverted P in lead V1 can sometimes be seen in patients with particularly severe RAA due to progressive,
posteriorly-directed right atrial enlargement directly beneath lead V1. The P wave is generally narrow and should
not be mistaken for a LAA.
Also present is a probable secondary repolarization abnormality (or "strain" pattern) due to severe, longstanding
RVH. Inspecting each lead, you should notice T wave inversions and ST depressions in leads with mostly positive
QRS complexes, while upright ST-T waves are seen in leads that are mostly negative. Contrast this to BBB, where
secondary repolarization abnormalities tend to more closely oppose the terminal portion of the QRS complex.
Remember again that secondary repolarization abnormalities are only sometimes seen in severe, long-standing,
LVH/RVH; their presence cannot rule out ischemia.
Module Case #16

Case #180
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 42

Which abnormality is not present in the following ECG?
a) Left ventricular hypertrophy
b) Evolving anterior wall myocardial infarction pattern
c)
Left axis deviation
d) Left posterior fascicular block

e)
QT prolongation
Answer:
d) This ECG shows a classic evolving anterior infarct pattern with loss of precordial R wave progression (V1-V4) and
ischemic ST-T changes. There is also left axis deviation (consistent with left anterior fascicular block), QT
prolongation (QTc is about 0.49sec) and voltage criteria for left ventricular hypertrophy:sum of the R in aVL plus S
in V3 are greater than 28mm (2.8mV) in men or greater than 20mm (2.0mV) in women. The QT prolongation in this
context is likely due to the evolving myocardial infarction pattern with prominent T wave inversions reflecting
prolonged ventricular repolarization. (Other factors such as drug effects or hypokalemia are not excluded.) Left
posterior fascicular block (LPFB) causes marked right axis deviation (i.e., 120 degrees or more positive), just the
opposite of what is seen here, and is a diagnosis of exclusion. This diagnosis requires ruling out other and usually
more common causes of rightward QRS axis, including physiologic variant (especially in infants and children), right
ventricular overload states, including right ventricular hypertrophy, severe chronic obstructive lung disease, etc
and lateral myocardial infarction (with Q waves in I and aVL and a rightward axis shift by "default"). LPFB is
uncommon as an isolated abnormality and is typically seen in conjunction with right bundle branch block as a form
of bifascicular block.
Ischemic anterior T wave inversions and primary ST-T changes consistent with evolving MI. LVH by aVL criteria. Left
axis deviation (~ - 35 degrees).
Note the T wave inversions in V2-V6, which are consistent with anterior ischemia. What makes this
morphologically even more suggestive with ischemia is that the ST segments and T waves are directed in opposite
directions in these leads. This is sometimes called a primary ST-T abnormality. Compare this to the previous case
(module case #15), which demonstrated a likely benign secondary repolarization abnormality with mostly
congruent ST segments and T waves.
Module Case #17

Case #35
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 44

Tachycardia and a touch of cyanosis (rhythm and blues). What is major finding in this patient with congestive heart
failure (CHF)?
a) Sinus tachycardia
b) Atrial flutter
c)
Atrial fibrillation
d) Multifocal atrial tachycardia

e)
Av nodal reentrant tachycardia (AVNRT)
Answer:
The major finding is narrow complex tachycardia with atrial rate of about 300 indicating atrial flutter with a slightly
variable ventricular response (2:1 conduction, some 3:1 and probably some AV Wenckebach). Atrial flutter is
sometimes mistaken (by housestaff at institutions other than your own) for sinus tachycardia. Look, for instance, at
V1 where the flutter waves are hard to see vs. lead II where they are more apparent. If only a V1 type lead were
available, the mechanism could be readliy mistaken.
Atrial flutter with (mostly) 2:1 conduction. The flutter waves are easy to discern in lead II. Whenever you see a
ventricular rate of 150 bpm, look closely for flutter waves.
The Q wave in III is not seen in contiguous leads (eg, aVF). It does not necessarily indicate prior MI.
Module Case #18
Case #146
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 46

42-year-old woman with recent "charlie horse" in left leg, dyspnea, and syncope. What is the leading diagnosis?
Answer:
Acute cor pulmonale secondary to pulmonary embolism (PE). This diagnosis is strongly suggested by the
combination of sinus tachycardia, S1 Q3 T3 pattern (S wave in lead I with QR waves in III and aVF, along with T
wave inversions), incomplete right bundle branch block, and right precordial T wave inversions. The patient had
bilateral pulmonary emboli secondary to deep venous thrombosis (DVT).
Sinus tachycardia, borderline LAD (-30) with early precordial transition. S1Q3T3 pattern
As noted , the S1Q3T3 pattern can be seen in many acute or chronic RV overload states. It is only sometimes seen
in acute pulmonary embolism. Notice that the patient's T wave inversions are in a more right-sided distribution (III
> aVF; and V1 > V2 > V3), consistent with a right ventricular process.
Module Case #19

Case #149
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 48

What is this rhythm?
a) Atrial flutter with variable block
b) Atrial fibrillation
c)
Wandering atrial pacemaker (WAP)
d) Atrio-ventricular reentrant tachycardia (AVRT)

e)
Multifocal atrial tachycardia (MAT)
Answer:
e) Three or more consecutive ectopic (non-sinus) P waves are present at a rapid rate. The patient had an
exacerbation of severe chronic obstructive pulmonary disease (COPD), a common substrate in patients with
multifocal atrial tachycardia (MAT). In contrast, wandering atrial pacemaker (WAP) is a slower rhythm, usually with
more gradual change in P waves.
(Note that some of the ectopic P waves are non-conducted.)
Multifocal atrial tachycardia (MAT) is an irregularly irregular rhythm that is most commonly confused with atrial
fibrillation. It is characterized by 3 or more discrete, multifocal P' waves, typically with variable P'R intervals. It
sometimes alternates with periods of sinus rhythm.The rate is typically 100-250 bpm, though if the rate is normal,
it is called multifocal atrial rhythm. MAT is most commonly seen in elderly patients with pulmonary disease.
The primary differential for an irregular narrow complex (normal QRS width) rhythm is atrial fibrillation, MAT, and
AV blocks (eg, variable blocks and other 2nd degree AVBs). AV blocks are usually evident.
Respiratory sinus arrhythmia, which is normal, can also produce some irregularity on the ECG due to vagallymediated respiratory variations in heart rate. It is most commonly seen with low-normal heart rates, particularly in
younger patients.
Module Case #20

Case #207
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 50

The following ECG, from a 62-year-old patient with increasing dyspnea, is most consistent with which diagnosis?
a) Pericardial tamponade
b) Chronic obstructive pulmonary disease
c)
Massive acute pulmonary embolism
d) Acute anterior myocardial infarction

e)
Myxedema
Answer:
A) This ECG shows the classic triad of findings for pericardial effusion with cardiac tamponade. These findings
include: 1) sinus tachycardia; 2) low QRS voltages; and 3) electrical alternans (best seen in leads V3 and V4 in this
case). This triad is highly specific for cardiac tamponade, but of limited sensitivity.
Electrical alternans in cardiac tamponade is marked by beat-to-beat alternation of the QRS complex (and other
waveform components) usually with sinus tachycardia. This so-called 2:1 alternans is due to mechanical effects of
the heart swinging to-and-fro in the pericardial effusion. With tamponade, the heart systematically shifts in
position on a beat-to-beat basis, accounting for the alternating QRS vector and amplitude in multiple leads.
Chronic obstructive pulmonary disease may be associated with low voltage complexes and sinus tachycardia as
seen here, but not with electrical alternans.
Massive pulmonary embolism would also not account for the combination of low voltage and electrical alternans,
nor would acute anterior myocardial infarction. (The poor R wave progression in leads V1-V2 here is non-specific.)
Myxedema may cause low voltage due to pericardial effusion. However, this syndrome generally does not lead to
tamponade physiology and is most likely to be associated with sinus bradycardia.
This patient had known non-small cell metastatic lung cancer. Transthoracic echocardiogram confirmed a large
pericardial effusion, with right ventricular diastolic collapse, consistent with tamponade physiology. The patient
underwent pericardiocentesis with drainage of about 1L of serosanguinous fluid.
A follow-up ECG (several weeks after the pericardiocentesis) was notable for increased QRS voltage and
disappearance of the electrical alternans. However, the resting sinus tachycardia persisted in association with
widespread metastatic disease and related problems.
Module Case #21

Case #12
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 52

The patient is an elderly female with a known history of left bundle branch block who presented to the emergency
ward with shortness of breath. What is the diagnosis?
Answer:
Sinus bradycardia, left bundle branch block (LBBB ) with primary ST-T wave changes. The ECG demonstrates a
bundle (LBBB) morphology with primary biphasic and inverted T waves in leads 2, 3 and F. Uncomplicated bundle
branch blocks should have "secondary" T wave changes. That is the ST-T waves should be opposite in direction to
the major vector of the QRS. For example, if this ECG with LBBB was uncomplicated, the ST-T waves in the inferior
leads would be upright. This patient has inverted T waves suggesting that a "primary" or ischemic process is
evolving in the inferior distribution. She did in fact rule in for a myocardial infarction with a CK of 700 and 21% MB
fraction. This example illustrates that ischemic ECG changes can sometimes be read despite the presence of a
bundle branch block.
This is an excellent example of active ischemia in a patient with a LBBB. When inspecting each lead to verify
whether the ST and T changes appear to be an expected secondary repolarization abnormality, leads III and aVF
stand out for having unexpected T wave inversions in leads where one would expect very positive T waves. This is
consistent with a primary T wave abnormality, consistent with ischemia. The opposing lateral leads are similarly
incongruent.
See module case #8 for more discussion regarding secondary repolarization abnormalities seen with BBB.
Module Case #22

Case #25
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 54

A 38-yr-old woman with weakness. Previous ECG was normal and she was on no medications. What is the most
likely diagnosis?
a) Hypercalcemia
b) Hypernatremia
c)
Hypokalemia
d) Hypocalcemia
e)
Hyponatremia
Answer:
The ECG shows sinus bradycardia with diffuse T wave flattening or inversions, and markedly prominent U waves.
These are best seen in leads V2 and V3, but are essentially invisible in lead aVL. The two most common causes of
this finding are 1) Hypokalemia (K+ here was 2.4 mEq/L) and 2) Drugs, especially the class 1A antiarrhythmics (like
quinidine, procainamide, disopyramide) and related agents (like the phenothiazines and tricyclics), etc. Patients
with hereditary (congenital) long QT syndromes due to "channelopathies" may show a similar finding (see Case 1).
This ventricular repolarization prolongation pattern is of great importance because it identifies patients at high risk
of torsade de pointes type of polymorphic ventricular tachycardia.
As noted, hypokalemia causes T wave flattening or inversions, and U waves, which are deflections immediately
following T waves. Also seen is QT(U) prolongation. U waves are typically best seen in the precordial leads,
especially V1-V3. If you wish, you can consider adding a step to your ECG reading algorithm to keep from missing
these.
Module Case #23

Case #288
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 56

51 year old woman with a dilated cardiomyopathy and atrial arrhythmias after chemotherapy for breast cancer.
What is the rhythm?
a) Atrial fibrillation (AF)
b) Atrial tachycardia with block
c)
Atrial flutter with variable block
d) Sinus rhythm with atrial bigeminy

e)
AV nodal reentrant tachycardia (AVNRT)
Answer:
This ECG shows classic flutter waves. The grouped beating (bigeminal) pattern here represents a repetitive
variable block mechanism (2:1 and 4:1 conduction). For comparison see also Case #188.
The ECG also shows nonspecific findings consistent with her cardiomyopathy (biventricular dilation and a markedly
reduced ejection fraction): slow R wave progression V1-V3, borderline low limb lead voltage and diffuse precordial
T wave inversions.
Though atrial flutter with 2:1 block is most common, atrial flutter with variable conduction is seen very frequently.
The flutter waves are easy to recognize in lead II.
Module Case #24

Case #299
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 58

24 year old woman with a history of asthma, palpitations and dizziness. The ECG shows which of one of the
following findings?
a) Left bundle branch block
b) Anteroseptal myocardial infarction
c)
Wolff-Parkinson-White (WPW) pre-excitation
d) Right bundle branch block

e)
Left posterior fascicular block
Answer:
The ECG shows sinus rhythm with the classic WPW triad of a short PR interval (60 msec), delta waves, and a wide
QRS duration (130 msec). The delta waves (slurring or notching) of the initial QRS are positive in leads I, II, III, aVL,
aVF, and V3-6. They are negative in aVR and markedly negative in V1-V2. These findings suggest an anteroseptal
(versus right sided) bypass tract. The QRS axis more vertical than +30 degrees (+35 degrees in this case) favors an
anteroseptal location.
Cardiac electrophysiologic (EP) study confirmed a right anteroseptal bypass tract with inducible narrow complex
atrio-ventricular reentrant tachycardia (AVRT) using the bypass tract to conduct in a retrograde direction. The
bypass tract was successfully ablated using a catheter ablation technique. Anteroseptal bypass tracts of this type
are relatively uncommon, occurring in only about 5% of cases of WPW.
Short PR interval and delta waves consistent with pre-excitation through an accessory pathyway (eg, WPW
syndrome).
Localizing the accessory pathway is neither a medical student nor a medical resident competency.
Module Case #25

Case #226
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 60

60-yr-old woman complains of the sudden onset of palpitations. This resting ECG is most consistent with which of
the following diagnoses? (Note that there is some artifactual distortion of the waveforms in the last beats in leads
aVR, aVL and aVF.)
a) Sinus tachycardia
b) Paroxysmal supraventricular tachycardia, most likely AV nodal reentrant tachycardia
c)
Atrial flutter with 2:1 block
d) Multifocal atrial tachycardia

e)
Atrial fibrillation with a regularized ventricular response
Answer:
The ECG shows a very fast and very regular narrow complex tachycardia at a rate of 200/min. The rate is much too fast for
resting (or exertional) sinus tachycardia in this older age group and no sinus P waves are seen. The regularity and absence of
multiple different P wave excludes multifocal atrial tachycardia (MAT.) Regularization of the ventricular response with atrial
fibrillation (AF) is rare and usually only seen at much slower rates (i.e., under 110-120/min). No flutter waves are seen and
usually the ventricular response with atrial flutter and 2:1 conduction is 120-160/min. Atrial flutter at a flutter rate of 400/min
(to give a regular ventricular response at 200/min) or at 200/min with 1:1 conduction would be highly unusual.
The narrow complex tachycardia here is most likely a specific type of paroxysmal supraventricular tachycardia (PSVT.) The
pathophysiology involves a small reentrant circuit in the AV node area, and therefore is termed AV nodal reentrant tachycardia
(AVNRT). With typical AVNRT, the P waves are often not apparent due to simultaneous stimulation of atria and ventricles.
Alternatively, retrograde (negative in lead II, positive in aVR) P waves may appear just before the QRS or, more commonly, just
after the QRS (at the J point, just after the QRS). In the present ECG, no definite P waves are seen, although retrograde P waves
just after the QRS are not excluded.
For an excellent introductory discussion of the electrophysiology of PSVTs due to AVNRT and related arrhythmias, see
http://www.blaufuss.org/.
Acute therapy of sustained AVNRT usually involves vagal maneuvers (Valsalva or carotid sinus massage, if not contraindicated),
and then intravenous drugs, especially adenosine, calcium channel blockers (diltiazem or verapamil), or sometimes betablockers, depending on the clinical context. For patients with hemodynamic collapse (shock), pulmonary edema or severe
ischemia who do not respond promptly to initial therapy, synchronized DC cardioversion may be required.Therapeutic options
to prevent recurrences of AVNRT include radiofrequency (RF) catheter ablation and drugs. The ECG in this case also shows nonspecific ST-T changes during the tachycardia.
SVT, likely AVNRT. Supraventricular tachycardia (SVT) is likely the most common cause of a fast, regular, narrow
complex rhythm that lacks obvious P waves. AVNRT, which is the most common cause of SVT, is characterized by a
re-entrant loop that causes rapid depolarization of the ventricles, immediately followed by retrograde (backwards)
depolarization of the atria as an impulse leaves the re-entrant circuit at the top of the AV node.
The normal sinus P wave is positive in lead II because it moves inferiorly and leftward toward the AV node.
Because retrograde atrial activation from the AV node occurs from the bottom-up immediately following
ventricular depolarization, the P wave is inverted (retrograde P) and typically buried within the QRS complex.
Occasionally, the retrograde P is noticeable immediately following or within the terminal portion of the QRS
complex, producing a pseudo-S wave in lead II, pseudo-R wave in avR, and pseudo-R wave in V1.
Module Case #26

Case #289
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 62

88 year old woman in the emergency department with complaints of diffuse abdominal pain, intermittent
ventricular tachycardia and hypotension. What life threatening problems are present?
a) Sinus tachycardia and findings consistent with pulmonary emboli
b) Sinus tachycardia and findings consistent with hyperkalemia
c)
Sinus tachycardia and findings of tricyclic overdose
d) Sinus tachycardia and findings of Brugada syndrome

e)
Sinus tachycardia with complete heart block and ST elevations consistent with acute anterior myocardial
infarction.
Answer:
The ECG shows sinus tachycardia (P wave rate about 100 bpm) with complete heart block (junctional escape rate
about 50 bpm) and a massive current injury due to anterior ST elevation myocardial infarction (MI).
This monophasic current of injury is sometimes referred to as tombstone pattern, less formally, (for comparison,
see also Cases #37,273). Q waves are present in both inferior and anterior leads from the current (and/or prior) MI.
The patient underwent cardiac catheterization that revealed diffuse LAD disease with distal occlusion treated with
a stent and also had intraortic balloon pump and pacemaker placement. She died of intractable cardiogenic shock
the same day.
Anterior STEMI, Q waves, 3rd degree AVB with junctional escape rhythm. Left atrial abnormality, left axis
deviation.
Module Case #27

Case #61
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 64

84-year-old woman with congestive heart failure, not on digitalis. What's the major finding?
Answer:
The main abnormality is the rhythm: it's NOT sinus-- there is a hidden P wave so that atrial rate is 150 and the
ventricular rate is 75. Therefore, this is atrial tachycardia with 2:1 block. The "extra" P waves just after QRS are
best seen in lead V1. In addition there is underlying incomplete right bundle branch block and borderline QT
prolongation. Always look for hidden atrial activity!
Atrial tachycardia (or ectopic atrial tachycardia) with 2:1 conduction. Again, whenever the rhythm isn't entirely
clear, remember to inspect lead V1 for hidden atrial activity.
Atrial tachycardia is a rhythm generated by an ectopic focus within the atria. It is characterized by an aberrantappearing non-sinus P wave.
Module Case #28

Case #353
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 66

40 year-old female with chronic (permanent) atrial fibrillation. This ECG is most consistent with which ONE of the
following major diagnoses?
a) Severe aortic stenosis (AS)
b) Severe mitral regurgitation (MR)
c)
Acute anterior myocardial infarction
d) Chronic pulmonary disease (cor pulmonale syndrome)

e)
Tetralogy of Fallot
Answer:
This ECG shows atrial fibrillation with an average ventricular response rate of about 55 bpm. Slow R wave
progression waves in V1-V4, with right precordial T wave inversions, diffuse low voltage and right axis deviation
are most consistent with right ventricular overload secondary to severe pulmonary disease.
The clinical diagnoses included morbid obesity, pulmonary hypertension and severe pulmonary disease with
respiratory failure. In contrast, right ventricular hypertrophy with tetralogy of Fallot (pulmonic stenosis) is
associated with tall R waves in the right precordial leads.
Low voltage and coarse atrial fibrillation.
This is an example of "coarse" atrial fibrillation, which is sometimes confused with atrial flutter. Remember that
atrial fibrillation is generally disorganized and irregularly irregular, distinguishing it from atrial flutter.
Compare to fine atrial fibrillation (module case #13).
Module Case #29
Case #92
ECG Wave-Maven
Copyright 2003
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 68

62-year-old female. Can you relate the arrhythmia to the other findings? Note: right-sided chest leads!
Answer:
The rhythm is sinus with long, atypical AV Wenckebach cycles (e.g., probable 6:5 block). The reason for the type 1
second degree AV block is apparent from the rest of the tracing which shows classic findings of an acute
inferior/right ventricular myocardial infarction, consistent with proximal to mid-occlusion of the right coronary
artery (RCA). The finding of ST elevation in lead III>II, as present here, is also consistent with this finding (see
Zimetbaum et al. Am J Cardiol 1998;81:918).
Right-sided chest leads (V1R-V6R) are occasionally employed to help facilitate the diagnosis of right ventricular MI.
They are oriented on the right anterior chest wall, directly opposite to where V1-V6.
While changes seen in posterior myocardial infarction can be deduced by conceptualizing inverted images of
findings seen on the anterior chest leads, leads V7-V9 are infrequently utilized to aid in the diagnosis. See images
below for positioning.
Figure 3. Orientation of right-sided chest leads (V1R-V6R) and posterior leads (V7-V9). From BMJ. 2002 Apr
6;324(7341):831-4.
Module Case #30

Case #295
ECG Wave-Maven
Copyright 2000-2007
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
II
25 mm/sec, 10 mm/mV
P a g e | 70

What is the etiology of the wide QRS?
a) Sinus rhythm with complete left bundle branch block
b) Accelerated idioventricular rhythm
c)
A-V sequential pacing
d) Atrial sensed and ventricular paced pattern

e)
Sinus rhythm with Wolff-Parkinson-White pre-excitation
Answer:
This ECG shows both atrial and ventricular pacing. The atrial and ventricular spikes are clearly seen, i.e., in lead II
before each P wave there is an atrial spike and before each QRS there is a ventricular spike at a rate of 60 bpm. All
of the ventricular beats are of the left bundle branch block pattern (QRS duration of 0.18 second), with a
prolonged QT interval of 0.50 second, possibly secondary to amiodarone therapy. (See Case # 158 for comparison.)
This patient had a history of atrial fibrillation and ventricular tachycardia for which he was started on amiodarone
therapy and subsequentially developed a profound bradycardia for which a dual chamber pacemaker was
implanted.
A-V sequential pacing is characterized by an atrial spike preceding every P wave and a ventricular spike preceding
every QRS complex. The wide QRS indicates that ventricular depolarization is initiated by an impulse originating in
the ventricle; this is initiated by the ventricular lead.
An atrial pacemaker demonstrates an atrial spike preceding every P wave, but AV conduction is normal and a
native (typically narrow) QRS follows.
Ventricular pacing is notable for pacing spikes preceding wide QRS complexes.

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ECG Self-Study Module

for the Internal Medicine Clerkship

ECG self-study module

Regarding the clerkship's ECG quiz

ECG self-study module

Essential topics covered

Further reading / practice

ECG self-study module

A proposed method of ECG interpretation with examples of simplified criteria

Is the rate regular?

QRS transition / R wave progression (normal transition V3V4)

Figure 1. ECG waves and intervals.

Figure 2. Orientation of frontal plane leads.

ECG self-study module

ECG self-study module

ECG self-study module

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case i (Wave-Maven # 233)

The ECG is within normal limits

The ECG shows right ventricular hypertrophy

The ECG shows left ventricular hypertrophy

The ECG is consistent with severe hypokalemia

The ECG is consistent with severe hypocalcemia

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #1 (Wave-Maven # 371)

d) Acute lateral ST elevation MI

Acute inferior ST depression MI

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #2 (Wave-Maven # 200)

Sinus tachycardia with blocked premature atrial complexes

d) Sinus rhythm with sinus exit block

Ectopic atrial rhythm with AV Wenckebach

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #3 (Wave-Maven # 13)

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #4 (Wave-Maven # 16)

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #5 (Wave-Maven # 363)

Acute pulmonary embolism

d) Early repolarization (normal) variant

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #6 (Wave-Maven # 26)

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #7 (Wave-Maven # 11)

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #8 (Wave-Maven # 136)

Sinus rhythm with complete (third degree) AV heart block

d) Atrial tachycardia with block

Idioventricular escape rhythm

ECG Wave-Maven / Beth Israel Deaconess Medical Center

ECG self-study module

Case #9 (Wave-Maven # 86)

Module Case #10

ECG Wave-Maven / Beth Israel Deaconess Medical Center