Ecg quiz

1. Right bundle branch block + LPHP
2. Right axis deviation
3. 3rd degree AV block

1. Sinus tachycardia
2. First degree AV block
3. Left bundle branch block
4. Hyperkalemia

1. Atrial fibrillation with a slow ventricular response
2. Digoxin ECG changes
3. Premature supraventricular beat (1st complex on ECG)

1. Non-sustained monomorphic ventricular tachycardia

1.Prolonged QT interval
2. T wave abnormality consistent with acute intracranial pathology

2. Cabrera's sign - possible myocardial
infarction Cabrera’s sign is used to diagnose
an acute myocardial infarction in the
setting of a left bundle branch block and
consists of notching at 40 milliseconds in
the upslope of the S wave in lead V3 and
V4. This has a poor sensitivity of 27% for
myocardial infarction

Left Bundle Branch Block (LBBB)

1. Atrial tachycardia 150/MIN.

1. Atrial flutter with a slow ventricular response

Accelerated idioventricular rhythm( 60-100)

2. Pulmonary embolism (S1Q3T3)

1. Multifocal atrial tachycardia
2. Old inferior myocardial infarction
3. Premature supraventricular beat with aberrancy

1. Accelerated idioventricular rhythm
2. AV disocciation

1. Atrial fibrillation with a slow ventricular response
2. Right bundle branch block
3. Prolonged QT interval (with normal QTc interval)

1. AV Nodal Reentry Tachycardia (AVNRT)

2. Posterior myocardial infarction
the causes of a R wave being larger than the S wave in lead V1 include
 a posterior myocardial infarction,
 right bundle branch block,
 WPW Type A,
 right ventricular hypertrophy,
 ventricular tachycardia with a right bundle branch block pattern
 isolated posterior wall hypertrophy (can occur with Duchenne's muscular dystrophy).

1.Premature ventricular contractions
2. Non-specific ST-T wave abnormalities, consider digoxin effect

Hypertrophic obstructive cardiomyopathy (HOCM)
Hypertrophic obstructive cardiomyopathy (HOCM) is a pathologic cardiac condition in which the interventricular septum is
abnormally thickened. The classic finding in HOCM is large dagger-like “septal Q waves” in the lateral leads due to the
abnormally hypertrophied interventricular septum. The apical variant of hypertrophic cardiomyopathy does not result in septal
Q waves as the septum is normal in thickness in this condition. The cardiac apex is thickened resulting in diffuse T wave changes
throughout the precordial leads.

1. Atrial fibrillation with an uncontrolled ventricular response
2. ST changes consistent with ischemia or digoxin effect
3. Left axis deviation
4. Left ventricular hypertrophy

ST changes consistent with ischemia - specifically, occlusion of the left main coronary artery
This ECG shows dramatic ST depression that is downsloping consistent with ischemia. The changes are
quite pronounced. One classic teaching helps to diagnose a left main coronary artery occlusion. This is
ST segment elevation in lead aVR greater than the ST elevation in lead V1 along with ST depression in
the precordial leads.

2. Anterior myocardial infarction
3. Left anterior fascicular block

3. Premature ventricular contractions

•Absence of typical RBBB or LBBB morphology
•Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and
negative in I + aVF.
•Very broad complexes (>160ms)
•AV dissociation (P and QRS complexes at different rates)
•Capture beats — occur when the sinoatrial node transiently ‘captures’
the ventricles, in the midst of AV dissociation, to produce a QRS complex
of normal duration.
•Fusion beats — occur when a sinus and ventricular beat coincides to
produce a hybrid complex.
•Positive or negative concordance throughout the chest leads, i.e. leads
V1-6 show entirely positive (R) or entirely negative (QS) complexes, with
no RS complexes seen.
•Brugada’s sign – The distance from the onset of the QRS complex to the
nadir of the S-wave is > 100ms
•Josephson’s sign – Notching near the nadir of the S-wave
•RSR’ complexes with a taller left rabbit ear. This is the most specific
finding in favour of VT. This is in contrast to RBBB,
where the right rabbit ear is taller.

1. Ventricular tachycardia
2. Indeterminate axis

1. Normal sinus rhythm
2. T wave abnormality consistent with intracranial process or ischemia (Wellen's phenomenon)
3. Prolonged QT interval

Ventricular paced rhythm

Sinus bradycardia
2. Wolff-Parkinson-White (WPW) Syndrome - Type A

Incomplete right bundle branch block
3. Prolonged QT interval
4. Polymorphic ventricular tachycardia (Torsades de Pointes)

2. Two to one AV block (2:1 AV block)

1. Sinus bradycardia
3. Digoxin effect

2. T wave abnormality consistent with Wellen's phenomenon
3. Left atrial enlargement
4. Poor R wave progression

4. Premature ventricular contractions - ventricular couplet
5. Premature atrial contraction

2. Left posterior fascicular block

2. 1st degree AV block

2. Premature atrial contractions - atrial bigeminy
3. Old lateral myocardial infarction
4. Non-specific ST-T wave abnormality

1. Normal sinus rhythm
3. Hyperkalemia

2. Intermittent right bundle branch block - rate dependent

2. Second degree type I AV block
5. Left atrial enlargement - P-mitrale pattern

2. S1-Q3-T3 pattern of acute right heart strain (McGinn-White
sign) from pulmonary embolism

2. Low voltage
3. Electrical alternans

2. Arrhythmogenic right ventricular dysplasia (ARVD) with
epsilon waves

2. ST depression consistent with ischemia

3. Hyperacute T wave abnormality

2. Wolff-Parkinson-White Type B

2. Premature ventricular contractions in a pattern of
ventricular bigeminy

1. Atrial fibrillation with a rapid ventricular response

. Anterior myocardial infarction versus left ventricular
aneurysm

1. Accelerated junctional rhythm

2. Inferior myocardial infarction

1. Junctional rhythm
2. Hyperkalemia

2. Right ventricular hypertrophy with strain
3. Right atrial enlargement

2. Hyperacute T waves consistent with myocardial infarction
This patient had acute chest pains and a normal potassium
level. Subsequently, anterior ST elevation developed.
Hyperacute T waves are the very first sign of a myocardial
infarction,

Anterior myocardial infarction
This ECG shows an anteiroseptal myocardial infarction with
hyperacute T waves and "tombstoning" of the ST segment

1. Bidirectional ventricular tachycardia
2. Digoxin toxicity
Bidirectional ventricular tachycardia is a rare, but
pathognomonic rhythm for digoxin toxicity. There are two
distinct QRS morphologies alternating every other beat

3. Chapman's sign indicating possible acute myocardial infarction
Chapman's sign is used to diagnose an acute myocardial infarction in the setting of a left
bundle branch block and consists of a notch in the upslope of the R wave in lead I, aVL or V6.
This has a low sensitivity, but a specificity of about 90%.

4. Early repolarization

2. Premature atrial contractions
3. Dextrocardia

2. 2nd degree type I AV block (Wenckebach)

. Atrial fibrillation with a slow ventricular response
2. Digoxin effect

1. Ventricular pacing
2. Atrial fibrillation

. Non-conducted premature atrial contractions (blocked PACs)

2. Old inferior myocardial infarction

3. Non-specific T wave abnormality
4. Baseline wobble artifact

3. SVT with aberrancy - rate dependent left
bundle branch block
Using the Brugada criteria, we see that there is no concordance (QRS complex down in V1 and up in V6), the R to S
interval is not greater than 100 ms and there is no AV dissociation that is obvious. We then examine the
morphology criteria when the pattern is that of a left bundle. There is no identifiable Q wave or QS in lead V6
which would have favored VT. The is no wide R wave that is 40 ms or greater in V1 or V2 which would have favored
VT. There is no slur or notch in the downstroke of the S wave in lead V1 or V2. Lastly, the duration of the onset of
the QRS complex to the peak of the S wave is not > 60 ms.

1. Sinus tacycardia
2. Wolff-Parkinson-White with alternans

2. SVT with aberrancy and a rate-dependent left bundle
branch block

1. Ectopic atrial rhythm

Wolff-Parkinson-White Type B with inferior pseudoinfarction pattern

Ventricular couplets
3. T wave alternans

4. Two to one AV block (2:1 AV block)

2. Inferior MI
3. Premature ventricular contractions

1. Ventricular tachycardia
This ECG meets the Brugada criteria for ventricular tachycardia based on the
presence of AV dissociation. Look at the rhythm strip in lead V1 and you will
intermittently see P waves prior the QRS complexes. March them out to see
even more that are consistent. Also, the R-S is about exactly 100 ms in lead V1
and V2 which would meet criteria as well.

2. Non-specific interventricular conduction delay
4. Fusion beats

2. Isolated posterior wall hypertrophy
Without the clinical history this diagnosis is impossible to make based on the
ECG alone. This ECG was from a patient with Duchenne's Muscular Dystrophy
who had posterior wall hypertrophy confirmed on an echocardiogram. This is
one of the causes of an R:S ratio > 1 in lead V1. Other causes of a large R wave
in lead V1 include a right bundle branch block, WPW Type A, right ventricular
hypertrophy and a posterior wall myocardial infarction.

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