ECG SHORT NOTE

Chula EP team
 Chula EP Team

Table of contents
I. Technique 1
II. Steps in Rapid Interpretation of ECG 2
Normal variants of ECG waveforms 2
III. Important ECG diagnostic 4
Normal sinus rhythm 4
Sinus bradycardia 4
Sinus arrhythmia 4
Wandering atrial pacemaker 4
Coronary sinus rhythm 4
SA exit block 5
Sinus pause and Sinus arrest 5
Sinus tachycardia 5
Sinus node reentrant tachycardia (SNRT) 5
Interatrial block 6
Premature Atrial Contractions (PACs) 7
Atrial Tachycardia (AT) 7
Multifocal Atrial Tachycardia (MAT) 8
Atrial Flutter (AFL) 8
Atrial Fibrillation (AF) 8
Junctional Rhythms 9
Premature Junctional Contractions (PJCs) 9
Accelerated Junctional Rhythm 9
Junctional Ectopic Tachycardia (JET) 10
Atrioventricular (AV) block 10
Premature ventricular contractions (PVCs) 11
Ventricular Parasystole 13
Ventricular Tachycardia 14
Accelerated Idioventricular Rhythm (AIVR) 14
Idiopathic fascicular VT (Interfascicular VT) 14
Right Ventricular Outflow Tract (RVOT) Tachycardia 14
Ventricular Flutter 14
Polymorphic Ventricular Tachycardia (PMVT, PVT) 15
Bidirectional VT 15
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Bundle branch reentry Ventricular Tachycardia (BBRVT) 15

Electrical storm definition 16
Right atrial enlargement 16
Left atrial enlargement 16
Biatrial enlargement 16
Right ventricular enlargement 16
Left ventricular enlargement 17
Biventricular enlargement 18
Complete right bundle branch block 18
Left Anterior Fascicular Block (LAFB) 18
Left Posterior Fascicular Block (LPFB) 18
Left Septal Fascicular Block (LSFB) 19
Complete left bundle branch block 19
Bifascicular Block 19
Trifascicular block 19
Masquerading bundle branch block 20
Nonspecific intraventricular conduction delay (IVCD) 20
Ashman phenomenon 20
STEMI 20
Sgarbossa 22
Modified Sgarbossa 22
Reperfusion therapy of STEMI 23
Ischemic ST depression 23
Reciprocal Change ST depression 24
Ischemic T wave inversion 24
Non-specific ST-T changes 24
Pathological Q wave 24
Fragmented QRS (fQRS) 24
Ventricular preexcitation (WPW syndrome) 25
The Lown-Ganong-Levine syndrome (LGL) 27
Arrhythmia in ventricular preexcitation 27
Special tachyarrhythmia related to ventricular preexcitation 28
Low voltage 29
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IV. ECG findings and clues in some cardiac disease and medical conditions 30
Myocarditis 30
Pericarditis 30
Pericardial effusion 31
Hypertrophic cardiomyopathy 31
Dilated cardiomyopathy 31
ARVC 32
Atrial septal defect (ASD) 32
Ebstein’s anomaly 32
Acute pulmonary embolism 33
COPD 33
Hypothyroidism 34
Raised intracranial pressure 34
Hypothermia 34
Digitalis effects and intoxication 35
Tricyclic antidepressants(TCA) toxicity 36
Hyperkalemia 36
Hypokalemia 37
Hypercalcemia 37
Hypocalcemia 37
Hypomagnesemia 37
Hypermagnesemia 37
V. Differential causes of abnormal ECG patterns 38
ECG Artifact 38
Poor R wave progression (PRWP) 38
Dominant R wave in V1 (Prominent Anterior Force, PAF) 38
RSr' or rSR’ in V1-V2 38
Left Axis Deviation (LAD) 39
Right Axis Deviation (RAD) 39
PR depression 39
Short PR interval 39
Variable PR interval 40
Regular bradycardia 40
AV dissociation (AVD) 40
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Group beating rhythm 40

Regular narrow complex tachycardias 40
Short RP regular narrow complex tachycardias 41
Long RP regular narrow complex tachycardias 41
Irregular narrow complex tachycardias 41
Regular wide complex tachycardias 41
Clues for DDx cauese of wide complex tachycardias 41
The Brugada Criteria for diagnose VT 42
Ultra-simple Brugada criteria: RWPT (R Wave Peak Time) 42
Vereckei criteria 42
The aVR ‘Vereckei’ 43
Sasaki criteria for VT 43
Irregular wide complex tachycardias 44
ST depression 44
ST elevation 44
Understanding J wave syndrome 44
ECG diagnostic criteria of Brugada pattern (BrP) 45
ST elevation in lead aVR 46
Prominent R wave in aVR 47
Tall upright T Waves 47
Global T wave Inversion 48
Deep T Wave Inversion 48
Typical inverted T waves changes in LVH (systolic overload pattern) 49
Biphasic T waves 49
‘Camel Hump’ T waves 49
Flattened T waves 49
Pseudo MI pattern from pseudo Q wave or loss of R wave amplitude 50
Long QT 50
Short QT 51
Prominent U waves 51
Inverted U waves 52
Low voltage 52
VI. Interesting Eponymous ECG and ECG signs 53
V. References 57
 ECG Short Note
I. Technique

: Keep standardization and avoid lead misplacement

: The best F/U ECG should be made from

- Same equipment
- Same lead positions
- Same body position

N.B. - Some important points

1. Accidental misplacement of the lead electrodes is a common cause of ECG abnormality and make
wrong diagnosis e.g. ectopic atrial rhythm, chamber enlargement or myocardial ischemia and
infarction e.g. pseudo-lateral or inferior wall MI from limb leads misplacement and anteroseptal
wall MI from precordial leads misplacement.
2. When the limb leads (LA, RA, LL) are exchanged without disturbing the neutral electrode (RL/N),
Einthoven’s triangle is “flipped” 180 degrees or rotated, resulting in leads that switch positions,
become inverted or remain unchanged (depending on their initial position and vector).
3. Exchanging one of the limb leads with the neutral electrode (RL/N) disrupts Einthoven’s triangle
and distorts the zero-signal received from Wilson’s central terminal, altering the appearance of
both limb and precordial leads. Limb leads may be grossly affected, taking on the appearance of
other leads or being reduced to an isoelectric baseline (falsely interpreted as lead
dislodgement as seen in chest leads, which is impossible occurred in limb leads). However,
with reversal between Rt and Lt leg electrode, the Einthoven’s triangle is preserved as the
electrical signals from each leg are virtually identical. The ECG is therefore unchanged!!!!!
4. After complete making 12 lead ECG, the first useful ECG waveform is P wave in lead aVR
because the Positive P wave in aVR have only three possible causes
- Rt and Lt arm lead reversal (most common cause of positive P wave in aVR in clinical practice)
- Dextrocardia
- Non-sinus P wave
5. If the sinus P wave is unexpectedly larger in lead I than lead II (it is usually the other way
around). The LA/LL reversal should be considered.
6. Negative sinus P wave in V2 is rare and biphasic sinus P wave in V2 is also uncommon, and
their presence should alert one to the probability of high placement of V1 and V2, which can
produce ECG that mimic LAE, RBBB, anteroseptal wall MI, and ventricular repolarization
abnormality.
7. Placement of the limb leads onto the torso distorts the ECG waveforms causing a rightward shift of
the mean QRS axis, a significant reduction in R-wave amplitude in leads I and aVL, and a
significant increase in R-wave amplitude in leads II, III and aVF, which may produce a loss of
inferior Q waves and the development of new Q waves in aVL.
8. Always thinking about leads misplacement when the F/U ECG shows significantly unexplained
changes of axis and ECG morphologies.
9. The good F/U ECG technique is very essential for detection of dynamic ST and/or T wave
changes.

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II. Steps in Rapid Interpretation of ECG

1. Standardization (sensitivity, speed, lead placement and filtering)
2. Rate
3. Rhythm
4. Axis
5. Hypertrophy or chamber enlargement
6. Ischemia or MI
7. Others (IVCD, WPW, BrS, LQTS, etc.)

Normal ECG parameters and axis

1. P wave duration ≤ 0.11 sec

2. PR interval 0.12 to 0.20 sec
3. QRS duration < 0.10 sec
4. QTc: Men 0.36-0.44 sec, Women 0.37-0.45 sec

N.B. - The normal time to intrinsicoid deflection (the time from onset of the QRS complex to the peak
of the R wave on the ECG, which is used interchangeable with ventricular activation time (VAT) or R
wave peak time (RWPT), in V1 is < 0.035 sec and in V5 and V6 is < 0.045 sec.

Mean P wave axis: 0 to + 75 degrees

Mean QRS axis: -30 to + 90 degrees

Mean T wave axis: 0 to + 90 degrees

QRS-T angle in frontal plane < 50 degrees

Normal variants of ECG waveforms

1. P wave may be positive, biphasic or negative in III, aVL and V1

2. Small q wave is commonly seen in lead I, II, aVF and V4-V6. Q waves of varying size are normal
in lead aVR. A larger Q wave (≥ 0.04 sec or ≥ 25% of R wave) may be seen in lead III alone.
3. There is useful maneuver of recording lead II, III and aVF during a deep breath. When there is
no true inferior infarct, this deep breath will cause the Q (which is of positional origin) to become
smaller or disappear altogether.
4. Benign Q waves in the inferior leads, in contrast to the pathologic Q waves of infarction, reflect
the orientation of initial forces horizontally and to the left rather than superiorly and to the right.
Consequently, when positional Q waves are present in the inferior leads, lead aVR will usually
not show an rS type of complex, but show a QS, QR or Qr type.
5. T wave may be upright, biphasic or inverted in III, aVL, aVF and V1 and always inverted in aVR.
- In young adult may have inverted T wave in V1-V3, with decrement T wave depth from
V1 to V3 (Persistent Juvenile T wave pattern).
- In some patients there are features of Benign T wave Inversion (sometimes associated
with Benign Early Repolarization, BER) which have ECG changes of:
1. There is a relatively short QT interval (QTc ≤ 0.42 sec).
2. The T-wave inversion does not evolve and is generally stable over time.
3. The leads with T-wave inversion (left precordial) usually have some ST elevation.
4. Right precordial leads often have ST elevation typical of early repolarization.
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5. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves.

6. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude.
7. Lead II, III, and aVF also frequently have T-wave inversion.

N.B. - The benign T wave inversions with ST changes are common in young male, athletes or
African-Americans than in Asians.

6. The ST-T changes in Benign Early Repolarization (BER) has a characteristic appearance:
- There is elevation of the J point.
- The ST segment and the ascending limb of the T wave form an upward concavity.
- The T wave is usually upright tall and slightly asymmetrical.
- The descending limb of the T wave is straighter and slightly steeper than the ascending
limb.
- ST segment/T wave ratio is ≤ 0.25.
- Characteristic “fish-hook” appearance in V4-V6.
- Absence of PR depression.
- ECG changes usually stable over time.

7. The J point is the junction between the termination of the QRS complex and the beginning of the
ST segment. Analyze the J point for position (elevated or depressed) and shape (notched or
slurred)
8. The normal ST vector is towards lead II and V5 (anterior and leftward).
9. Isoelectric baseline is the TP segment which is the portion of the ECG from the end of the T wave
to the beginning of the P wave. This segment should always be at baseline and is used as a
reference to determine whether the ST segment is elevated or depressed
10. Normal T wave height is 1/8 to 2/3 of preceding QRS complex height.
11. Normal U wave height is ≤ 25% of preceding T wave height, usually best seen in lead V2-V4.
12. Left axis deviation which has positive QRS in lead I and negative QRS in lead aVF also need
Negative QRS in lead II for diagnosis.

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III. Important ECG diagnostic

Normal sinus rhythm criteria

- Regular rhythm at a rate of 60-100 bpm (or age-appropriate rate in children).

- Each QRS complex is preceded by a normal P wave.
- Normal P wave axis: P waves should be upright in leads I and II, inverted in aVR.

Sinus bradycardia criteria

- Sinus rhythm with rate of < 60 bpm (severe sinus bradycardia if rate ≤ 40 bpm)
- DDx causes of Pseudo Sinus bradycardia
1. Bigeminy non-conducted PACs (clue…try to find PACs)
2. Second degree SA exit block type II (may be indistinguishable from sinus bradycardia, if no
intermittent block pattern seen during 12-lead ECG)
3. Second degree 2:1 AV block (one sinus P wave is hidden in T wave; clue… try to find it !!!!)

Sinus arrhythmia criteria

- All P waves are come from SA node and have the same P wave morphology but the PP interval
varies by ≥ 0.16 sec or (Maximal sinus cycle length - Minimal sinus cycle length)/Minimal sinus
cycle length ≥ 10%
- There are three types of sinus arrhythmia:

1. Respiratory-related sinus arrhythmia: Sinus rate Increases with Inspiration

2. Non-respiratory-related sinus arrhythmia: Not related to respiratory cycle but related to vagal
tone
3. Ventriculophasic sinus arrhythmia: Seen in patients with second or complete AV block. The PP
interval containing the QRS complex is shorter than the PP interval not containing the QRS
complex.

Wandering atrial pacemaker criteria

- There are at least 3 distinctly different P wave morphologies.

- Slightly irregular of PP interval with relatively constant PR interval.
- Ventricular rate ≤ 100 bpm

Coronary sinus rhythm criteria

- Negative P wave in II, III, aVF and positive in I, aVR

- PR interval 0.12-0.20 sec
- Constant PR interval
- Ventricular rate ≤ 100 bpm
N.B. Commonly interpretation as Low atrial rhythm

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SA exit block criteria

1. First degree SA exit block

- Delayed impulse transmission to the RA, all sinus impulses reach the RA.
- It could not detectable on the surface ECG
2. Second degree SA exit block
- Type I (Wenckebach): Progressive lengthening of the impulse transmission, culminating in
failure of transmission; The P-P interval progressively shortens prior to the dropped P
wave.
Clues….All P waves must have same morphology with gradual shortening of PP interval
then abrupt lengthening of PP interval.
- Type II: Intermittent dropped P waves with a constant transmission interval (constant P-P
intervals). The pause surrounding the dropped P wave is an exact multiple of the
preceding P-P interval.
3. Third degree SA exit block
- None of the sinus impulses are conducted to the RA.
- Indistinguishable from sinus arrest (which came from abnormal sinus node
automaticity; stop firing of the impulse) on the surface ECG.

Sinus pause and Sinus arrest criteria

Sinus pause: No sinus impulse at least 2 second-pause with recovery of sinus P wave.

N.B. - The non-conducted PACs can mimic sinus pause (clue…find the PACs before pause)

Sinus arrest: No sinus impulse usually ≥ 3 seconds without recovery of sinus P wave.

Sinus tachycardia criteria

- Sinus rhythm with rate of > 100 bpm

- With very fast heart rates, the P waves may be hidden in the preceding T wave, producing
a ‘camel hump’ appearance.

Sinus node reentrant tachycardia (SNRT) criteria

- Abrupt onset/termination of sinus rate

- Rate may vary from 100-150 bpm
- Similar P wave morphology compared to regular sinus beats (upright in lead II, III and aVF)
- Unable to distinguish from sinus tachycardia on ECG unless abrupt onset/termination
seen.

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DDx of SNRT

1. Inappropriate sinus tachycardia (IST)

IST is originated from enhanced sinus node automaticity without appropriate causes. It has non-
paroxysmal pattern. The monitoring ECG shows warm up and cool down phenomenon without
abrupt onset/termination pattern of reentry.

2. Intra-atrial reentrant tachycardia (IART) near the sinus node

- Type of intra-atrial reentrant tachycardia which has the reentry circuit near SA node
- It has abrupt onset/termination, triggered by PACs same as SNRT.
- For confirm the diagnosis……needed EP study.

Interatrial block criteria

1. Partial Interatrial Block (First degree)

- The electrical impulse is conducted from the right atrium to left atrium through the normal
propagation route but with a delay at the Bachmann's bundle region.
• P wave duration ≥ 0.12 sec
• Usually bimodal (“notched”) in lead II, III and aVF, and sometimes in lead V4-V6.
• The P wave electrical axis is normal.

N.B. - The interatrial blocks (IAB) criteria is mimic LAE criteria and is frequently associated with
true LAE (confirmed by other cardiac investigations). If the P wave in V1 has biphasic P wave
with a negative component ≥ 0.04 sec may indicate associated LAE.

2. Second degree Interatrial Block

- Similar to the AV block or SA block, interatrial block may occur transiently on a beat-to-
beat basis. The P wave show transient morphology changes in the same recording from
partial interatrial block to advanced interatrial block pattern or vice versa.

3. Advanced Interatrial Block (Third degree)

- The electrical impulse is blocked in the upper and middle part of the interatrial septum esp.
in the Bachmann’s bundle so the left atrial activation occurs mainly via muscular
connections in the vicinity of coronary sinus which it will transmit the impulse from the
lower part up to the upper part of the left atrium.

- The ECG shows

• P wave duration ≥ 0.12 sec
• P wave are usually bimodal in lead I
• P wave are biphasic or “positive-negative” in lead II, III and VF and also
often in V1 to V3–V5 because of caudocranial activation of the LA.

N.B. - Sometimes the initial positive component of the P wave on inferior leads may be
very small mimicking a completely negative P wave, suggesting a low atrium or coronary
sinus rhythm. However, the P wave is truly sinus because the positive polarity in the
other leads especially V5-V6, confirms the sinus in origin.

………Moreover, advanced interatrial block is commonly present in the setting of left

atrial enlargement.

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………It was demonstrated that this type of block is very frequently accompanied by
paroxysmal atrial arrhythmia esp. atypical Atrial flutter, AF in patients with VHD and
cardiomyopathies (Bayes syndrome).

Premature Atrial Contractions (PACs) criteria

- P wave which has a different morphology and axis to the sinus P waves, happened prematurely.
- The abnormal P wave may be hidden in the preceding T wave, producing a “peaked” or “camel
hump” appearance — if this is not appreciated the PACs may be mistaken for a PJCs.
- PACs that reach the SA node may depolarize it, causing the SA node to “reset”; this results in a
longer-than-normal interval before the next sinus beat arrives (“post-extrasystolic pause”).
Unlike with PVCs, this pause is not equal to double the preceding RR interval (not a “full
compensatory pause”).
- PACs arriving early in the cycle may be conducted aberrantly, usually with a RBBB morphology
(Ashman phenomenon) as the RBB has a longer refractory period than the left. They can be
differentiated from PVCs by the presence of a preceding non-sinus P wave.
- PACs arriving very early in the cycle may not be conducted to the ventricles and create the ECG
of non-conducted PACs.

Classification of Premature Atrial Contractions (PACs)

PACs may be either:

- Unifocal: arising from a single ectopic focus; each PACs is identical.

- Multifocal: arising from two or more ectopic foci; multiple P-wave morphologies.

PACs often occur in repeating patterns:

- Bigeminy: every other beat is a PACs

- Trigeminy: every third beat is a PACs
- Quadrigeminy: every fourth beat is a PACs
- Couplet: two consecutive PACs
- Triplet: three consecutive PACs

Atrial Tachycardia (AT) criteria

- Non-sinus P waves foci

- At least three consecutive identical non-sinus P waves with rate > 100 bpm
- QRS complexes usually have normal morphology unless pre-existing bundle branch block,
bypass tract or rate related aberrant conduction etc.

N.B. - Classification of AT depends on tachyarrhythmia mechanisms

• From abnormal automaticity will cause…..Automatic AT (AAT)

• From reentry will cause…..Intra-atrial reentrant tachycardia (IART)
• From triggered activity (Delayed After Depolarizations, DADs) will cause…..Adenosine-
sensitive AT (also called verapamil-sensitive AT or cAMP-mediated AT)

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Multifocal Atrial Tachycardia (MAT) criteria

- Atrial rate > 100 bpm

- At least 3 distinct P-wave morphologies in the same lead
- Irregularly irregular rhythm with varying PP, PR and RR intervals
- Isoelectric baseline between P-waves (the important key to differentiate from AF)

N.B. - It must have no single dominant atrial pacemaker (i.e. not just sinus rhythm with frequent
PACs). Some P waves may be non-conducted; others may be aberrantly conducted to the ventricles.

Atrial Flutter (AFL) criteria

- Regular atrial activity, commonly has the atrial rate of 300 bpm.
- Flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF.
- Flutter waves in V1 may mimic sinus P waves.
- Loss of the isoelectric baseline.

Simple Classification of AFL

This is based on the anatomical location and direction of the re-entry circuit.

1. Typical Atrial Flutter (Common or Type I Atrial Flutter)

Involves the IVC & tricuspid isthmus in the reentry circuit. Can be further classified based on
the direction of the circuit:

1.1 Counterclockwise AFL: This is the commonest form of atrial flutter (90% of cases).
- Inverted flutter waves in leads II, III, aVF
- Positive flutter waves in V1 – may resemble upright P waves

1.2 Clockwise AFL: This uncommon variant produces the opposite pattern:
- Positive flutter waves in leads II, III, aVF
- Broad, inverted flutter waves in V1

2. Atypical Atrial flutter (Uncommon or Type II Atrial Flutter)

- Does not fulfil criteria for typical atrial flutter.
- Often associated with higher atrial rates and rhythm instability.
- Less amenable to treatment with ablation and more likely to degenerate to AF.

N.B. - The typical AFL 2:1 AV conduction with ventricular rate of 150 bpm is common and can
mimic sinus tachycardia so “A ventricular Rate of Exactly 150 bpm is 2:1 Atrial Flutter until
proven otherwise”

Atrial Fibrillation (AF) criteria

- Irregularly irregular rhythm
- No P waves
- Absence of an isoelectric baseline
- Variable ventricular rate
- QRS complexes usually < 0.12 sec unless pre-existing bundle branch block, bypass tract, or rate
related aberrant conduction etc.

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- Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse
(amplitude >0.5mm)

N.B. - In very fine AF with CHB with junctional escape rhythm. The ECG can mimic sinus arrest with
junctional escape rhythm because the fibrillation P wave could not be seen clearly

Classification is dependent on the presentation and duration of atrial fibrillation as below:

- First episode or first-detected AF regardless of symptoms or duration

- Recurrent AF – More than 2 episodes of AF
- Paroxysmal AF – Self terminating episode ≤ 7 days
- Persistent AF – Not self-terminating, duration > 7 days
- Long-standing persistent AF ≥ 1 year
- Permanent (Accepted) AF – Duration > 1 year in which rhythm control interventions are not
pursued or are unsuccessful.

Junctional Rhythms Criteria

- Junctional (escape) rhythms originate at or around the AV node and the Bundle of His.
- The impulse travels up the atria and down to the ventricles resulting in inverted P waves (in II, III,
aVF) that can occur prior to, during or after the QRS.
• If inverted P before QRS the PR interval usually < 0.12 sec
• If inverted P after QRS the RP interval usually < 0.12 sec except there is dual AV node
physiology
- The QRSd < 0.12 sec unless pre-existing bundle branch block, bypass tract or rate related
aberrant conduction etc.

N.B. - During junctional rhythms, in some cases there are truly no retrograde P waves if the
impulse does not travel up into the atrium (retrograde VA block); in this setting the AV
dissociation is commonly seen

Junctional rhythms are arbitrarily classified by their rate:

1. Junctional Escape Rhythm: 40-60 bpm (AVJ subsidiary pacemaker rate)

2. Junctional Bradycardia: < 40 bpm (rate below AVJ subsidiary pacemaker rate)
3. Junctional Tachycardia: > 100 bpm (whenever rate above 100 bpm = Tachycardia!!!!!)
4. Accelerated Junctional Rhythm: 60-120 bpm (rate above AVJ subsidiary pacemaker rate

Premature Junctional Contractions (PJCs) criteria

- Premature Junctional Contractions (PJCs) is a premature beat that occurs from AV junction prior
to the next sinus beat

N.B. - Concealed PJCs can mimic second degree AV block.

Accelerated Junctional Rhythm criteria

- Junctional rate 60-120 bpm (because the maximal enhanced automaticity rate of AVJ usually not
faster than 120 bpm).
- The mechanisms of arrhythmia came from enhanced automaticity or triggered activity at AV
junction.
- Lacks the sudden onset and termination.

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- Common after cardiac surgery, digitalis intoxication, AMI, myocarditis, COPD, catecholamine
excess.

N.B. - Nonparoxysmal junctional tachycardia (NPJT) is now called Accelerated Junctional Rhythm
and Paroxysmal junctional tachycardia is now called PSVT.

Junctional Ectopic Tachycardia (JET) criteria

- Junctional ectopic tachycardia (JET) is the most common arrhythmia in children following cardiac
surgery.
- Abnormal automaticity of AV junction, rate 100-220 bpm.
- Retrograde P waves may be present and appear before, during or after the QRS complex.
- In some cases there are no retrograde P waves….JET with AV dissociation.
- Incessant nature can cause tachycardia-induced cardiomyopathy.
- Occasionally there are present with irregular NCT and misdiagnosed as AF or MAT

Atrioventricular (AV) block criteria

1. First degree AV block
- Sinus rhythm, PR interval > 0.20 sec.
2. Second degree AV block
2.1 Typical or classical Wenckebach or Mobitz type I
- Gradually progressive PR interval prolongation occurs before the blocked sinus impulse
(ratio of P to conducted beats = n: n-1).
- The greatest PR increment typically occurs between the first and second beats of a cycle,
gradually decreasing in subsequent beat.
- Shortening of the PR interval occurs after the blocked sinus impulse, provided that the P
wave is conducted to the ventricle.
- Junctional escape beats may occur along with non-conducted P waves.
- The pause containing the dropped beat is less than twice the shortest R-R interval.
- Regularly irregular (group beats pattern) of the RR cycle when the A-V ratio is fixed.
- Post-block PR-interval shortening remains the cornerstone of the diagnosis of
Mobitz I block, regardless of whether the periodicity has typical or atypical features.
- In typical AV Wenckebach phenomenon, The PR intervals increase with decreasing
increments making the RR intervals shorten before block.

N.B. - In Atypical AV Wenckebach pattern is characterized by

- Block of a single P wave preceded by gradual but irregular P-R prolongation from
disproportionate increments or decrements of the P-R intervals with unpredictable
changes anywhere within a conducted sequence.
- Again…….In both typical and atypical of type I block, the P-R interval after the
blocked impulse always shortens if the P wave is conducted to the ventricle.
2.2 Mobitz type II
- Constant PR interval in all conducted beat (ratio of P to conducted beats = n: n-1)
- The QRS of conducted beats usually show fascicular block, bundle branch block or
bifascicular block.
- The RR interval including the blocked P wave is the multiple of the PP interval.

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Some important points of second degree AV block

The 2:1 Second Degree Atrioventricular (AV) Block Diagnostic criteria

- There are only one of every other two P waves can be conducted to the ventricles.
- 2:1 AV block can be either Mobitz Type I (Wenckebach) or Mobitz Type II.

The followings may help to differentiate the two types:

- Response to carotid sinus massage:

- AV block worsens if the block is Wenckebach (block level is intranodal).
- AV block improves if the block is Mobitz Type II (block level is infranodal).
- Response to atropine:
- AV block improves if the block is Wenckebach.
- AV block worsens if the block is Mobitz Type II.
- Response to exercise:
- AV block improves if the block is Wenckebach.
- AV block worsens if the block is Mobitz Type II.
- QRS width: A QRS complex with a normal width suggests that the block is Wenckebach. If
the QRS complex is wider than normal, the block is thought to be Mobitz Type II.
N.B. – In approximately 25% of cases of Mobitz Type II, the block is located in the Bundle of
His (intraHisian type of infranodal AV block), producing a narrow QRS complex.
-- In Mobitz Type I may occur in the presence of a pre-existing bundle branch block or
IVCD, producing a wide QRS complex.
- The PR interval of the conducted P wave:
- generally prolonged if the block is Wenckebach (PR > 0.30 sec, ≥ 95% associated
with a pathologic condition in the AV node).
- PR interval is normal (< 0.16 secm) if the block is Mobitz Type II (infranodal).

N.B. - Condition which can mimic 2:1 second degree AV block

1. Bigeminy non-conducted PACs

2. Concealed PJCs

…High-grade AV block occurs if there are ≥ 3 consecutive blocked P waves (conduction ratio ≥ 3:1)

…Paroxysmal High-grade AV block (PAVB) has two types

1. Tachycardia-dependent PAVB (phase 3 block): more common findings

2. Bradycardia-dependent PAVB (phase 4 block)

3. Third degree AV block or complete heart block

- Independent atrial and ventricular activities producing AV dissociation (AVD).
- Atrial mechanism may be sinus or ectopic.
- Ventricular mechanism may be AV junction or ventricular escape rhythm.
- Ventriculophasic sinus arrhythmia in 30% of cases.

Premature ventricular contractions (PVCs) criteria

- Ventricular premature which occurs earlier than would be expected for the next sinus impulse.
- QRSd ≥ 0.12 sec with abnormal morphology (not so wide or not so bizarre if the PVCs originated
from ventricular fascicle).
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- Discordant ST segment and T wave changes

• “Discordance” describes a pattern of repolarization abnormality (seen in LBBB,
ventricular paced rhythms, PVCs, VT in which the ST segment and T wave are directed
opposite to the main vector of the QRS complex.
• ST depression and T wave inversion in leads with a dominant R wave.
• ST elevation with upright T waves in leads with a dominant S wave.
- Retrograde capture of the atria may or may not occur

N.B. - Retrograde capture describes the process whereby the ectopic impulse is conducted
retrogradely through the AV node, producing atrial depolarization. This is visible on the ECG as an
inverted P wave esp.in leads II, III, aVF (“retrograde P wave”), usually occurring after the QRS
complex.

- The most unusual post-PVC event is when retrograde activation of the AV junction re-enters the
ventricles as a ventricular echo (pseudo interpolated PVCs).
- Usually followed by a full compensatory pause because the sinus node timing is not
interrupted; one sinus P wave isn't able to reach the ventricles because they are still refractory
from the PVCs; the following sinus impulse occurs on time based on the sinus rate. In contrast,
PACs are usually followed by an incomplete pause because the PACs usually enters the sinus
node and resets its timing

N.B. - Not all PVCs are followed by a full compensatory pause. There are other two patterns of
pauses:

• Incomplete pause (as found in PACs): This PVCs has retrograde impulse which capture
the atrium and reset the sinus node and be followed by an incomplete pause.
• No pause at all: if a PVC occurs early enough (especially if the heart rate is slow), it may
appear sandwiched in between two normal beats. This is called an interpolated PVC.
- The sinus impulse following the PVCs may be conducted with a longer PR interval because of
retrograde concealed conduction by the PVCs into the AV junction slowing subsequent
conduction of the sinus impulse.

ECG clues for differential diagnosis of PVCs vs PACs with aberration

1. Preceding ectopic P wave favors PACs with aberration

- Carefully look at T wave because the ectopic P wave may be hidden in the ST-T wave of the
previous beat producing a “peaked” or “camel hump” T wave.

N.B.-- In late-coupled PVCs (end diastolic PVCs) may have sinus P wave preceding the
PVCs beat.

2. Analyze the compensatory pause: A full compensatory pause favors PVCs

- Be aware of exceptions to this simple rule because PVCs can activate the atria retrogradely
and reset the sinus node (incomplete pause) and PACs can rarely fail to reset the sinus
node (in this setting this rare PACs can show full compensatory pause).
3. Long-Short Rule (Ashman Phenomenon): favors PACS with aberration
4. Analyze the QRS morphology of the funny-looking beat. This is one of the most rewarding of
the clinical clues, especially in lead V1. Since aberrancy is almost always in the form of a bundle
branch block morphology. More typical of RBBB or LBBB morphology in V1 favors aberrant
ventricular conduction, more atypical of RBBB or LBBB morphology in V1 favors PVCs.

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Classification of PVCs

PVCs may be either:

- Unifocal: Arising from a single ectopic focus; each PVC is identical and usually has fixed
coupling interval.
- Multifocal: Arising from two or more ectopic foci; multiple QRS morphologies, different
coupling interval.

The origin of each PVCs can be discerned from the QRS morphology:

- PVCs arising from the RV have a LBBB-like morphology (V1 negative QRS complex).
- PVCs arising from the LV have a RBBB-like morphology (V1 positive QRS complex).
- PVCs arising from RVOT or LVOT have positive QRS complex in lead II,III,aVF
- PVCs arising from RV apex or LV apex have negative QRS complex in lead II,III,aVF

PVCs often occur in repeating patterns:

- Bigeminy — every other beat is a PVC.

- Trigeminy — every third beat is a PVC.
- Quadrigeminy — every fourth beat is a PVC.
- Couplet — two consecutive PVCs.
- Triplet — three consecutive PVCs.

Lown's grading of PVCs

- Grade 0 No PVCs
- Grade I Unifocal and infrequent PVCs; <30 PVCs per hour
- Grade II Unifocal and frequent PVCs; ≥30 PVCs per hour
- Grade III Multifocal
- Grade IVA 2 consecutive beats (couplets)
- Grade IVB ≥3 consecutive beats (salvos)
- Grade V "R on T" phenomena

Ventricular Parasystole criteria

- QRSd ≥ 0.12 sec
- Varying coupling intervals
- The inter-ectopic intervals (i.e., timing between PVCs) are some multiple (i.e., 1x, 2x, 3x, . . . etc.)
of the basic rate of the parasystolic focus.
- PVCs have uniform morphology unless fusion beats occur (frequent appearance of fusion beats).

N.B. - Usually entrance block is present around the ectopic focus, which means that the primary
rhythm (e.g., sinus rhythm) is unable to enter the ectopic site and reset its timing.

- May also see exit block; i.e., the output from the ectopic site may occasionally be blocked (i.e.,
no PVC when one is expected).

- Parasystolic rhythms may also be seen in the atria and AV junction.

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Ventricular Tachycardia criteria

- Three or more beats in a row on an ECG that originate from the ventricle at a rate >100 bpm
• Non-sustained: ≥ 3 consecutive ventricular complexes terminating spontaneously in < 30
sec
• Sustained: Duration ≥ 30 sec or requiring intervention due to hemodynamically unstable
N.B. - Hemodynamically unstable: e.g. hypotension, chest pain, cardiac failure, decreased
conscious level.
- Monomorphic VT (MVT): VT originated from a single focus within the ventricles. Produces
uniform QRS complexes within each lead, each QRS is identical (except for fusion/capture
beats).
- Polymorphic VT (PMVT): VT in which there are multiple ventricular foci with the resultant QRS
complexes varying in amplitude, axis and duration.

Accelerated Idioventricular Rhythm (AIVR) criteria

- QRSd ≥ 0.12 sec
- Regular rhythm with the rate of 60-120 bpm (because the maximal enhanced automaticity rate of
Purkinje system usually not faster than 120 bpm) …Slow VT
- Often seen fusion and capture beats

Idiopathic fascicular VT (Interfascicular VT) criteria

- Monomorphic ventricular tachycardia with RBBB pattern
- QRS duration 0.10 – 0.14 sec (this is narrower than other forms of VT, because of fascicular in
origin)
- Short RS interval (onset of R to nadir of S wave) of 60-80 ms – the RS interval is usually ≥ 100
ms in other types of VT
- Fascicular tachycardia can be classified based on ECG morphology corresponding to the
anatomical location of the re-entry circuit: Axis deviation depending on anatomical site of re-entry
circuit
1. Posterior fascicular VT (90-95% of cases): RBBB morphology + LAD; arises close to the LPF
2. Anterior fascicular VT (5-10% of cases): RBBB morphology + RAD; arises close to the LAF
3. Upper septal fascicular VT (rare): atypical morphology – usually RBBB but may resemble
LBBB; arises from the region of the upper septum

Right Ventricular Outflow Tract (RVOT) Tachycardia criteria

- QRS duration ≥ 0.12 sec
- LBBB Morphology (Negative QRS in V1)
- Inferior axis (positive QRS in II, III, aVF)
- Precordial transition (R/S = 1 by V3 or V4)
- Atrioventricular dissociation (in slower VT rate)
- Ventricular rate > 100 bpm

Ventricular Flutter criteria

- Very fast VT rate of 250-350 bpm seen as large continuous sine Wave
- No identifiable P waves; QRS complexes or T waves fused together
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Polymorphic Ventricular Tachycardia (PMVT, PVT) criteria

- PMVT is VT which there are QRS complexes with frequent and rapid changes in morphology,
axis, or both; classification broadly based on the Q-T interval.
1. PMVT with QT prolongation commonly known as Torsades de Pointes (TdP).
- Torsades de Pointes (twisting of the points) was used to describe cycles of
ventricular tachycardia with alternating electric polarity and amplitude, such that
the peaks of the QRS complexes appeared to be twisting around the isoelectric
line of the recording.
2. PMVT without QT prolongation: induced by a variety of clinical scenarios
- Acute myocardial ischemia (the most common cause)
- Acute myocarditis
- Structural heart disease: severe HF, ICM, DCM, HCM, ARVC, severe AS etc.
- Genetic arrhythmic syndromes: BrS, ERS, CPVT, SQTS
- Idiopathic VF

N.B. - Idiopathic VF is a clinical entity in which no cardiac anatomic or functional

abnormality can be identified despite extensive clinical evaluation for the cause of VF.

- The short-coupled TdP is a rare variant of a PMVT which often results in VF

(some cases are also reported as idiopathic VF). The ECG monitoring showed
TdP-like pattern but with normal QT intervals, initiated by PVCs with short
coupling interval (200-300 msec). The morphology of isolated PVCs that initiated
the TdP commonly has LBBB-like morphology and LAD.

Bidirectional VT criteria
- VT with a two QRS morphologies with alternating QRS axis of opposite polarities (Ping-Pong
effect). It commonly has CRBBB in precordial leads with alternating between LAFB and LPFB
pattern in limb leads, occasionally alternating between RBBB and LBBB.

Causes of Bidirectional VT

1. Digitalis toxicity
2. Catecholaminergic polymorphic VT (CPVT)
3. Anderson-Tawil syndrome (Congenital LQTS 7)
4. Myocarditis
5. Acute coronary syndrome
6. Hypokalemia
7. Metastatic cardiac tumor
8. Herbal aconitine poisoning

Bundle branch reentry Ventricular Tachycardia (BBRVT) criteria

- BBRVT is usually seen in patients with an acquired structural heart disease esp. DCM and
significant conduction system impairment.
- ECG during sinus rhythm shows IVCD, most common has LBBB with or without PR interval
prolongation.
- VT with fast rates, frequently > 200 bpm, is usually present with near-syncope, syncope or SCD.
- VT is a typical bundle branch block pattern (most common LBBB pattern) and may have identical
QRS morphology during sinus rhythm ( wrongly diagnosed SVT with preexisting LBBB).
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- BBRVT with a LBBB pattern characteristically shows rapid intrinsicoid deflection in the right
precordial leads indicating that initial ventricular activation occurs through the His Purkinje
system.
- During BBRVT with a LBBB pattern the activation propagates in the antegrade direction down the
right bundle (RB) and in the retrograde direction up the left bundle (LB).
- During BBRVT with RBBB pattern the direction of activation is reversed.

Electrical storm definition

- Occurrence of ≥ 2 VT/VF episodes or ≥ 3 appropriate ICD therapies for VT/VF in a 24-h period

Right atrial enlargement criteria

- P wave in inferior leads (especially in lead II) ≥ 2.5 mm (P pulmonale)
- Positive part of P wave V1 or V2 ≥ 1.5 mm
- Increase area under the initial positive portion of the P wave in lead V1 ≥ 0.06 mm-sec
- Rightward shift of mean P wave axis to above 75 degree

Left atrial enlargement criteria

- P wave duration in inferior leads (especially in lead II) ≥ 0.12 sec
- Prominent notching of P wave, usually in lead II, with interval between notches of ≥ 0.04 sec (P
mitrale)
- Ratio between the duration of P wave in lead II and duration of the PR segment ≥ 1.6
- Increased duration and depth of terminal-negative portion of P wave in lead V1 (P terminal force)
so that area subtended by ≥ 0.04 mm-sec.
- Leftward shift of mean P wave axis to between -30 degrees and -45 degrees

Biatrial enlargement criteria

- The P wave in inferior leads (especially in lead II) is taller (≥ 2.5 mm) and wider (≥ 0.12 sec).
- The first part of P wave is positive and peaked in V1–V2 (positive ≥ 1.5 mm) with a slow P
terminal force (duration ≥ 1 mm).
- Signs of left atrial enlargement with right P wave axis (The opposite case is not valid because the
P wave axis can be on the left side in isolated RAE of patients with congenital heart diseases).

Right ventricular enlargement criteria

- Dominant R wave in V1 (≥ 7mm tall and R/S ratio > 1)
- Dominant S wave in V5 or V6 (≥ 7mm deep and R/S ratio < 1)
- qR in V1
- Intrinsicoid deflection time in V1 ≥ 0.035 sec (QRSd ≤ 0.10 sec)
- Right axis deviation of ≥ 110°

Supporting criteria

- Right atrial enlargement (P pulmonale)

- Right ventricular strain pattern; ST depression/T wave inversion in the right precordial (V1-3) and
inferior (II, III, aVF) leads
- S1 S2 S3 pattern; far right axis deviation with dominant S waves in lead I, II and III
- Deep S waves in the lateral leads (I, aVL, V5-V6)

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N.B. - There are no universally accepted criteria for diagnosing RVH in the presence of RBBB;
the standard voltage criteria could not apply accurately. However, the presence of
incomplete/complete RBBB with a tall R’ wave (≥10-15 mm) in V1, right axis deviation of ≥ +110°
and supporting criteria (such as RV strain pattern or P pulmonale) would be suggestive of RVH.

Left ventricular enlargement criteria

Limb Leads:

- R wave in lead I + S wave in lead III ≥ 25 mm

- R wave in aVL ≥ 11 mm
- R wave in lead I ≥ 15 mm
- R wave in aVF ≥ 20 mm

Precordial Leads:

- R wave in V5 or V6 ≥ 26 mm
- R wave in V5 or V6 plus S wave in V1 ≥ 35 mm
- Largest R wave plus largest S wave in precordial leads ≥ 45 mm

N.B. - Common used criteria:

- Sokolow-Lyon voltages: SV1 + RV5 or RV6 ≥ 35 mm or RaVL ≥ 11 mm

- Cornell voltage criteria: SV3 + RaVL ≥ 28 mm for men and ≥ 20 mm for women
- New criteria: Deepest S wave in any lead plus the S wave in lead V4 ≥ 28 mm for men and ≥ 23
mm for women

Supporting criteria

- Intrinsicoid deflection time in leads V5 or V6 ≥ 0.045 sec (QRSd ≤ 0.10 sec)

- ST segment depression and T wave inversion in the left-sided leads
- Left atrial enlargement
- Left axis deviation
- ST elevation in the right precordial leads V1-3 (“discordant” to the deep S waves)
- Prominent U waves (proportional to increased QRS amplitude)

N.B. - Although not universally accepted, the following criteria are proposed for the diagnosis of LVH
in the presence of LBBB

- Left atrial abnormality

- QRS width ≥ 0.16 sec
- The sum of the amplitudes of S wave in V2 and R wave in V5 or V6 ≥ 45 mm
- The amplitude of S wave in V3 ≥ 25 mm

N.B. - The criteria that are suggested for the diagnosis of LVH in the presence of RBBB are

- The amplitude of S wave in V1 ≥ 2 mm

- The R wave amplitude in V5 or V6 ≥ 15 mm
- Left axis deviation
- R wave in lead I ≥ 11 mm

N.B. - The criteria that are suggested for the diagnosis of LVH in the presence of LAFB are

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- S in III + the maximal precordial R + the maximal precordial S ≥ 30 mm

- R in aVL ≥ 13 mm

Biventricular enlargement criteria

1. In the presence of LVH with additional signs indicating RVH:
- Right atrial enlargement
- Right axis deviation
- Deep S waves in V5-6
2. In the presence of RVH with additional signs indicating LVH:
- Left axis deviation
- Tall R waves and deep S waves in V2-5
3. Katz-Wachtel phenomenon of large biphasic QRS complexes
- tall R waves + deep S waves ≥ 50 mm in any lead of V2-4
4. P pulmonale in limb leads and LVH in precordial leads

Complete right bundle branch block criteria

- QRSd ≥ 0.12 sec (CRBBB), 0.10-0.12 sec (ICRBBB)
- Wide, notched secondary R wave (rsr’, rsR’ or rSR’ patterns) in V1-2 (usually has right tall rabbit
ear pattern)
- Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
- ST depression and T wave inversion in V1-V2(V3) without ST-T changes in lateral leads

N.B. - Remember that in RBBB the initial force (0.06 sec) are unaffected by the conduction
abnormality so the standard diagnostic criteria for MI still apply.

Left Anterior Fascicular Block (LAFB) criteria

- Left axis deviation (usually between -45 and -90 degrees)
- QRS duration normal or slightly prolonged (0.08-0.11 sec)
- qR pattern in lead I and aVL
- rS pattern in lead II, III, aVF (S in lead III is deeper than lead II) r in II > r in aVF > r in III
- Intrinsicoid deflection time in aVL ≥ 0.045 sec

N.B. - In LAFB the terminal conduction delay in aVR occurs after that of aVL (counterclockwise
loop)

- In LAFB can diminish or mask the diagnostic pathological Q wave of inferior infarction
because the initial force (via posterior fascicle) are directed inferiorly.
- When there are Q wave in lead II or there are notching (fragmented) of the QRS in the
inferior leads in the presence of LAFB suggest that an inferior wall MI coexists.

Left Posterior Fascicular Block (LPFB) criteria

- Right axis deviation (≥ +100 degrees)
- QRS duration normal or slightly prolonged (0.08-0.11 sec)
- rS pattern in lead I and aVL
- qR pattern in lead II, III and aVF
- Intrinsicoid deflection time in aVF ≥ 0.045 sec
- No evidence of any other causes of right axis deviation

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Left Septal Fascicular Block (LSFB) criteria

- QRS duration normal or slightly prolonged (0.08-0.11 sec)
- R wave of V1 ≥ 5 mm or R wave of V2 ≥ 15 mm
- R/S ratio in V1 ≥ 2; or R/S ratio in V2 ≥ 2
- S wave depth in V1 or V2 ≤ 5 mm
- Possible small q wave in V2 or V1 and V2
- RS or Rs in V2 and V3 (frequent rS in V1) with R wave "in crescendo" from V1 to V3 and
decreasing from V5 to V6
- Absence of q wave in V5, V6 and lead I (absence of the initial trans-septal force)
- Intrinsicoid deflection time in V1and V2 ≥ 0.035 sec

N.B. - For confirm the diagnosis, the other causes of dominant R in V1, V2 (Prominent Anterior
Force) should be excluded.

Complete left bundle branch block criteria

- QRSd ≥ 0.12 sec
- Wide, notched monophasic R wave in V5 and V6 and also in I and aVL
- Small or absent initial R wave in V1 and V2, followed by deep S waves (rS or QS patterns)
- Absent septal q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL) if
pathological Q wave seen in V5-V6 the old anteroseptal wall MI is suggested.
- Intrinsicoid deflection time in V5 and V6 ≥ 0.06 sec

Associated Features

- Appropriate discordance: the ST segments and T waves always go in the opposite direction to
the main vector of the QRS complex
- Poor R wave progression in the chest leads
- Left axis deviation

Bifascicular Block: has 3 possible causes

1. The combination of RBBB with LAFB

2. The combination of RBBB with LPFB
3. CLBBB (LAFB+LPFB)

Trifascicular block: has 2 types

1. Incomplete trifascicular block: Which has three different patterns:
1.1. Bifascicular block with first or second-degree AV block (AV block should be caused by
infranodal block)
1.2. CRBBB with alternating LAFB and LPFB
1.3. Alternate RBBB and LBBB
2. Complete trifascicular block:
- The ECG show evidence of complete AV block with ventricular escape rhythm (the QRS
morphology of bifascicular block pattern!!!)

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Masquerading bundle branch block: There are 2 types

1. The standard type

- The standard type of ‘Masquerading’ bundle branch block, the precordial leads from V1 to V6
are suggestive of RBBB, whereas the limb leads resemble LBBB.
2. The precordial type
- The precordial type of ‘Masquerading’ bundle branch blocks the left precordial leads from V4
to V6 resemble LBBB pattern and RBBB in right precordial leads from V1 to V3

Nonspecific intraventricular conduction delay (IVCD) criteria

- QRSd ≥ 0.11 sec without meeting the criteria of RBBB or LBBB

Ashman phenomenon criteria

- A relatively long cycle immediately preceding the cycle terminated by the aberrant QRS complex.
A short-long-short interval is even more likely to initiate aberration. Aberration can be RBBB
(common) or LBBB (less common) or both pattern in the same patient.
- The RBBB aberrancy beat should have normal orientation of the initial QRS vector. The
concealed perpetuation of aberration is possible, such that a series of wide QRS supraventricular
beats is possible.
- Irregular coupling interval of aberrant and preceding QRS complexes.
- Lack of a fully compensatory pause (which is never seen in atrial fibrillation).

ECG in STEMI
STEMI criteria
- New ST elevation at the J point in two contiguous leads of ≥ 1 mm in all leads other than V2-V3.
- For V2-V3 the following cut points apply: ≥ 2 mm in men ≥40 years, ≥ 2.5 mm in men <40 years
or ≥ 1.5 mm in women.

Localization of Infarction:

- Septal: V1 and V2
- Anterior: V3 and V4 (V2-V5)
- Lateral: V5 and V6
- Anteroseptal: V1-V4
- Anterolateral: V3-V6
- Extensive anterior: V1-V6, I and aVL
- Inferior: II, III, aVF
- High Lateral: I, aVL
- Posterior: tall R wave and ST depression in V1-V2

Some important points about STEMI

1. How to recognize an inferior STEMI?

- ST elevation in lead II, III and aVF
- Progressive development of Q waves in II, III and aVF
- Reciprocal ST depression in aVL (± lead I)

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RCA occlusion is suggested by:

- ST elevation in lead III > lead II
- Presence of reciprocal ST depression in lead I
- Signs of right ventricular infarction: STE in V4R (sometimes also had STE in V1)

Circumflex occlusion is suggested by:

- ST elevation in lead II ≥ lead III

- Absence of reciprocal ST depression in lead I
- Signs of lateral infarction: ST elevation in the lateral lead I and aVL or V5-6

2. Posterior MI is suggested by the following changes in V1-3:

- Horizontal ST depression
- Tall, broad R waves (≥ 0.03 sec)
- Upright T waves
- Dominant R wave (R/S ratio > 1) in V2

N.B. - Record posterior leads whenever suspicious of ACS and it is not showing on the 12-lead,
because It can manifest in posterior leads only

…..In ACS, considering ST depression in V2 and V3 due to posterior STEMI until proven
otherwise.

…..In CRBBB normally has up to 1 mm of ST depression in V1-V3, but ONLY when there is an R'
wave!! (except….when the R'-wave is very large, such as in RVH)

3. The first step to spotting RV infarction is to suspect it… in all patients with inferior STEMI…In
patients presenting with inferior STEMI, right ventricular infarction is suggested by the
presence of:
- ST elevation in lead III > lead II: because lead III is more “rightward facing” than lead II and
hence more sensitive to the injury current produced by the right ventricle.
- ST elevation in V1: the only standard ECG lead that looks directly at the right ventricle.
- ST elevation in V1 > V2
- ST elevation in V1 but ST depression in V2 (highly specific for RV MI)
- Isoelectric ST segment in V1 with marked ST depression in V2

N.B. - Right ventricular infarction is confirmed by the presence of ST elevation in the right-sided
leads (V3R-V6R)

4. Occlusion of the LAD proximal to the first septal perforator

- STE in aVR of at least 0.5 mm but < STE in V1 in anterior STEMI predicts septal AMI
(occlusion of the LAD proximal to the first septal perforator) and was negatively correlated
with a long wraparound, LAD that affected the inferior wall. This is intuitive, as a proximal
occlusion would lead to basal wall STEMI and distal occlusion of a wraparound LAD would
lead to inferior STE which would reciprocally attenuate the STE in aVR or lead to STD in
aVR.
- In this setting of anterior STEMI the associated STE in aVR is not reciprocal to any ST
depression, but directly indicative of basal septum injury.

N.B. - In NonSTE-ACS, STE in aVR is reciprocal to diffuse ST depression and is a result of global
subendocardial ischemia.
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5. Occlusion of Left main

- STE in aVR > STE in V1

N.B. - In both STEMI and Non-STEMI, the degree of STE in aVR correlates with worse disease
and worse outcomes, independent of the clinical presentation; these patients must be treated
aggressively with early angiography and revascularization.

6. Lead aVL is incredibly useful.

- New ST-depression (without LBBB or LVH) in aVL in the clinical setting of an ACS, is
almost certainly due to ischemia. In patients with acute chest pain who have any ST
elevation, aVL is also a very useful lead to differentiate between pericarditis and MI. Because
in pericarditis has no reciprocal ST depression in aVL.

N.B. - When STE in several location of anterior, inferior, and lateral leads appeared in ACS
Settings but patient has hemodynamically stable, the apical wall MI should be considered.

- Acute anterior wall MI with new CRBBB (not tachycardia dependent) has higher mortality
rate because CRBBB is related to ischemia of RBB in the right septal area, indicate proximal
LAD occlusion.

Sgarbossa Criteria
The original three criteria used to diagnose infarction in patients with LBBB are:

1. Concordant ST elevation ≥ 1mm in leads with a positive QRS complex (score 5)

2. Concordant ST depression ≥ 1 mm in V1-V3 (score 3)
3. Excessively discordant ST elevation ≥ 5 mm in leads with a negative QRS complex (score 2)

These criteria are specific, but not sensitive for myocardial infarction. A total score of ≥ 3 is reported to
have a specificity of 90% for diagnosing myocardial infarction.

Modified Sgarbossa Criteria

- ≥ 1 lead with ≥1 mm of concordant ST elevation
- ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression
- ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined
by ST height ≥ 25% of the depth of the preceding S-wave

The new formula for DDx Anterior STEMI vs Early repolarization is

= 0.052 x QTc-B - 0.151 x QRSV2 - 0.268 x RV4 + 1.062 x STE60V3

The cutpoint with the highest accuracy (92.0%) was at a cutoff value of 18.2 (higher indicative of LAD
occlusion)

Definitions

- QTc-B is the computerized Bazett-corrected QT interval

- QRSV2 is the entire QRS in millimeters in lead V2
- RV4 is the R-wave amplitude in millimeters in lead V4
- STE60V3 is ST elevation, relative to the PQ junction, at 60 msec after the J-point, in millimeters

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This formula cannot be used if the patient has ECG clues of STE > Early repolarization as the followings

1. Greater than 5 mm ST elevation in at least one lead

2. Just a single lead of V2-V6 with a straight or convex ST segment elevation
3. Any ST depression (inferior or anterior)
4. There is terminal QRS distortion (absence of both S wave and J wave) in V2 and V3
5. Any pathologic Q-waves in V2-V4
6. T-wave inversion in any of V2-V6

N.B. - In anterior STE: If there is one lead of V1-V4 in which the T/QRS ratio is greater than 0.36, then
acute STEMI is the likely diagnosis

ECG of Reperfusion therapy of STEMI

- With a reperfused infarct related artery (IRA) and intact microcirculation, ST segments usually fall
rapidly within 3 hours of reperfusion.
- Approximately 80% of cases with IRA reperfusion manifest 50% ST recovery within 60 - 90
minutes.
- Non-reperfused IRA, in which ST segments fall gradually and plateau, with or without persistent
elevation. Plateauing occurs as early as 6 to 12 hours, due to myocardial cell death.
- ST resolution is an accurate predictor of reperfusion, especially in patients whose ECG’s show
ST elevation ≥ 4 mm.
- If leads with ST elevation develop terminal T-wave inversion within 60 - 90 minutes of
thrombolysis, reperfusion is highly likely.
- In non-reperfused AMI, 90% show gradual T-wave inversion (over 48 hrs ), with a depth < 3 mm.
- Early T-wave inversion (< 24 hours) is associated with greater IRA patency than later inversion
(However because T-wave inversion usually indicates some myocardial injury, rapid ST
resolution without any T-wave inversion may be evidence that reperfusion occurred before
myocardial cell death).
- Terminal T-wave inversion undergoes further development into symmetric T-wave inversion.
- T-waves inversion of reperfusion late in the course of AMI or non-reperfused AMI are usually < 3
mm, in contrast with inverted T-waves of reperfused AMI, which are ≥ 3 mm.
- With posterior AMI, if the T-wave is upright before reperfusion and there is ST recovery,
reperfusion usually results in precordial T-waves (especially V2) becoming fully upright and taller
and wider than before AMI onset.
- Occurrence of early accelerated idioventricular rhythm (AIVR) indicates reperfusion with 97%
specificity but only 45% sensitivity.
- Q-wave and R-wave changes are not accurate markers of AMI reperfusion.
- The ECG is the most accurate measure of occlusion and reperfusion, even better than
angiogram, laboratory values, or patient symptoms.

Ischemic ST depression criteria

- New horizontal or downsloping ST depression ≥ 0.5 mm in ≥ 2 anatomical contiguous leads
N.B -The J point is the junction between the end of the QRS complex and the beginning of the ST
segment.
- The ST segment should depress at J80 at least 0.5 mm below the isoelectric segment
- J80 means at the 80 msec after the J point (J0 or J zero)
- If ST depression at J0 = J80 …called horizontal ST depression
- If ST depression at J0 < J80 …called downsloping ST depression
- If ST depression at J0 > J80 ...called upsloping ST depression
- ST depression ≥ 1 mm is more specific and conveys a worse prognosis.
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- ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of NSTEMI and predicts

significant mortality.
- Upsloping ST depression is non-specific for myocardial ischemia except for a pattern of up-
sloping ST depression with symmetrically peaked T waves (de Winter’s T Waves).

Reciprocal Change ST depression criteria

ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically
opposite leads:

- Inferior STEMI produces reciprocal ST depression in aVL (± lead I)

- Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II)
- Reciprocal ST depression in V1-3 occurs with posterior infarction

Ischemic T wave inversion criteria

- At least 1 mm depth of T wave inversion
- Present in ≥ 2 continuous leads that have dominant R waves (R/S ratio > 1)
- Dynamic T wave changes

N.B. - T wave inversion is a normal variant in leads III, aVR and V1

Non-specific ST-T changes criteria

- ST depression < 0.5 mm

- ST elevation < 1 mm
- T wave inversion < 1 mm
- T wave flattening
- Upsloping ST depression

ECG criteria of pathological Q wave

1.“Classic” criteria : Q-wave with a duration≥ 0.04 sec and/or a depth ≥ 25% of the R-wave
N.B. - Width is more important than depth
2.Consensus 2007 criteria
: Any Q-wave in leads V2–V3 ≥ 0.02 sec or QS complex in leads V2 and V3
: Q-wave ≥ 0.03 sec and ≥ 0.1 mV deep or QS complex in leads I, II, aVL, aVF or V4–V6 in any 2 leads
of a contiguous lead grouping (I, aVL, V6; V4–V6; II, III, and aVF)
: R-wave ≥ 0.04 sec in V1–V2 and R/S ≥ 1 with a concordant positive T-wave in the absence of a
conduction defect

ECG criteria of Fragmented QRS (fQRS)

1. In the setting of QRSd < 0.12 sec
- The QRS complexes with the presence of an additional R wave (R') or notching in the nadir
of the S wave, or the presence of more than one R' (fragmentation) in two contiguous leads,
corresponding to a major coronary territory. It is necessary that the QRS morphology must
not fit into any classical BBB.
2. In the setting of QRSd ≥ 0.12 sec
- The QRS complex with >2 R’ waves or notches in the R or S wave in a wide QRS complex of
BBB, ventricular pace, or PVCs in 2 contiguous leads corresponding to a major coronary

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territory. If the QRS complex of PVCs only has 2 notches in the R waves, they considered the
QRS complex to be fQRS-positive when the notches were >0.04 sec apart and present in two
contiguous leads.
- The other purposed criteria of fQRS in RBBB as
• ≥4 spikes in one or
• ≥8 spikes (summation) in all of the leads V1, V2 and V3

N.B. - ECG recording that is used to detect fQRS is not a specific setting and is the same as
routine 12-lead ECG recording: high-pass filter: 0.05-20 Hz (usually 0.15 Hz), low-pass filter: 100-
150 Hz, AC filter: 50 or 60 Hz, paper speed: 25-50 mm/sec (usually 25mm/sec) and voltage:
1mm/mV.

- Contiguous leads mean anterior leads (V1–V5), lateral leads (I, aVL, and V6), or inferior
leads (II, III, and aVF).

Ventricular preexcitation (WPW syndrome) criteria

- PR interval <0.12 sec
- Delta wave: slurring slow rise of initial portion of the QRS
- QRSd ≥ 0.11 sec
- ST Segment and T wave discordant changes i.e. in the opposite direction to the major component
of the QRS complex

N.B. - Pseudo-infarction pattern can be seen in up to 70% of WPW – due to negatively deflected delta
waves in the inferior/anterior leads (“pseudo-Q waves”), or as a prominent R wave in V1-3 (mimicking
posterior infarction).

- WPW may be described easily as type A or B.

• Left sided bypass tract or Type A has a positive delta wave in all precordial leads with
R/S > 1 in V1.
• Right sided bypass tract or Type B has a negative delta wave in leads V1 and V2

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………For more accurate location of bypass tract there are 4 steps

Step 1:

- If there is negative or isoelectric delta wave in lead I or the height of R > S in V1, a left free wall
BT is present then go to lead aVF if….
- Positive delta wave in aVF then… left lateral (LL) or left anterolateral (LAL) BT
- Isoelectric or negative delta wave in aVF then… left posterior (LP)/left posterolateral(LPL) BT
- If the criteria in lead I and V1 are not fulfilled, go to step 2

Step 2: Lead II is examined.

- A negative delta wave in lead II identifies the…. subepicardial posteroseptal (PS) BT.
- If the delta wave in lead II is isoelectric or positive, proceed to step 3.

Step 3: Lead V1 is examined

- A negative or isoelectric delta wave in lead V1 then go to aVF

• Negative delta wave in lead aVF then posteroseptal (PS) or at the coronary sinus ostium BT
• Isoelectric delta wave in lead aVF then PS tricuspid annulus (PSTA) or the PS mitral annulus
(PSMA) BT
• Positive delta wave in aVF then anteroseptal/right anterior paraseptal (AS/RAPS) or MSTA
BT. These two regions are differentiated by examining the R/S ratio in lead III
o R ≥ S identifies …anteroseptal/right anterior paraseptal (AS/RAPS) BT
o R < S identifies …mid-septal tricuspid annulus (MSTA) BT
- A positive delta wave in V1 then go to step 4

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Step 4: Positive delta in V1 then go to aVF

- Positive delta wave in aVF then ….RA or RAL BT

- Isoelectric or negative delta wave in aVF….go to lead II
- Positive delta wave in lead II then…. RL BT
- Isoelectric delta wave in lead II then…. RP/RPL BT

N.B. - The polarity of the delta wave was measured within the initial 20 msec of the preexcitation and
was classified as positive (+), negative (-), or isoelectric (±)

Bypass tract behavior

- The bypass tract (accessory pathway or Kent bundles) is usually a strand of atrial myocardium
joining the atrium to the ventricle at the level of the tricuspid or mitral annulus. It has different
property and behavior
1. Has both antegrade and retrograde conduction property
2. Has only retrograde conduction property (concealed bypass tract)
3. Has only antegrade conduction property (Mahaim fiber)
- If there is antegrade conduction property, the ECG shows ventricular preexcitation pattern (delta
wave) during sinus or during preexcited tachycardia. The degree of preexcitation depends on BT
location, refractory period of the bypass tract and AV node. The intermittent ventricular
preexcitation (intermittent WPW) can be found in patient who has BT with long refractory period.
- In concealed BT, there is no delta wave during sinus rhythm at all.
- In concealed BT which has only retrograde property, can cause orthodromic AVRT but cannot
create antidromic AVRT or preexcited tachycardia. The EP study is essential for definite
diagnosis of orthodromic AVRT using the concealed bypass tract.
- Usually the BT has fast conduction velocity property but in some patients the BT has slowly
conduction velocity property making the long RP during orthodromic AVRT and making the larger
excitable gaps in reentry circuit causing the more sustained and more incessant tachycardia as
seen in PJRT.

The Lown-Ganong-Levine syndrome (LGL)

Clinical syndrome consisting of paroxysms of tachycardia and ECG findings of

1. PR interval < 0.12 sec

2. Normal QRS duration and no delta wave

N.B. - The BT in LGL syndrome connects distally to the bundle of His (James bundle, Atrio-Hisian
bypass tract) not to the ventricular myocardium as in WPW (Kent bundle, Atrio-ventricular
bypass tract). Therefore in LGL syndrome there will not have a delta wave.

Arrhythmia in ventricular preexcitation

1. Most common is orthodromic atrioventricular reentrant tachycardia (AVRT)
N.B. - In some cases after prolonged orthodromic AVRT, it can degenerate to AF (tachycardia
beget tachycardia; the more rapid rate the more easy to degenerate). In such cases the ECG will
demonstrate…
- AF with ventricular preexcitation (AF with WPW or Pre-excited AF): if that bypass tract
has antegrade conduction.

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- AF without ventricular preexcitation: if that bypass tract has only retrograde conduction
(concealed BT).
2. Less common are pre-excited tachycardias (almost always has WCT, never has NCT)
- Antidromic AVRT
- AT/AFL with preexcitation
- AVNRT with preexcitation
- AF with WPW (degenerate from orthodromic AVRT and could be life threatening due to
rapid VR)

N.B. - The pre-excited tachycardias always have wide QRS complexes because of the impulses
are conducted via bypass tract to ventricular muscle not ventricular fascicle, making the
propagation of the impulses delayed.

3. Polymorphic VT (degenerate from AF with WPW; the more rapid VR, the more easy to
degenerate)

N.B. - The typical clinical scenarios before WPW patients develop SCD are Sinus rhythm with
ventricular preexcitation ➛ Orthodromic AVRT ➛ AF with WPW ➛ PMVT ➛ VF ➛ SCD

ECG features of Atrial Fibrillation with WPW are:

- varying ventricular rate depend on AV node and BT refractory period, usually has ventricular rate
> 180 bpm (if the shortest RR interval ≤ 250 msec, predicts higher risk for SCD).
- Irregular Wide QRS complexes due to abnormal ventricular depolarization via bypass tract.
- QRS complexes change in morphology from variable degree of ventricular preexcitation.
- Axis remains stable (except if there are ≥ 2 bypass tracts).

Special tachyarrhythmia related to ventricular preexcitation

1. Permanent Junctional Reciprocating Tachycardia (PJRT)
- PJRT is caused by an AVRT using the AV node as the antegrade limb and a slowly
conducting bypass tract (BT) as the retrograde limb.
- The location of the BT is commonly right posteroseptal with an atrial insertion close to the
ostium of the coronary sinus, but other locations have been reported.
- Chronic uncontrolled tachycardia has been reported to result in tachycardia-induced
cardiomyopathy.
- ECG manifestation of PJRT include
• Incessant regular NCT (if no aberration conduction) interrupted by short periods of sinus
rhythm
• Initiation of the tachycardia by changes in sinus rate
• Increase in tachycardia rate in response to exercise
• Slowing of the rate in response to increased vagal tone
• Inverted P waves in II, III, aVF leads
• Long RP interval
• Absent of preexcitation during sinus rhythm (concealed bypass tract)

2. Mahaim Fiber Tachycardia

- Mahaim tachycardia is an unusual form of antidromic AVRT using a decremental bypass tract
(special BT which has decremental property like AV node) that conducts only in anterograde
direction.

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- Mahaim fiber can be atriofascicular, nodofascicular, nodoventricular, and fasciculoventricular

BT.
- During sinus rhythm has minimal or no preexcitation, no septal q waves in left precordial
leads and usually has typical rS pattern in lead III.
- A high degree of day-to-day variability of manifested delta wave and the "concertina" effect is
observed in many patients.
N.B. – Concertina effect of preexcitation:
• Varying QRS width due to varying degrees of preexcitation
• More preexcitation – shorter PR interval and wider QRS duration
• Predictor of relatively long refractory period of bypass tract
• Marker of low risk of sudden death
- Anterograde conduction over atriofascicular fibers yields a typical LBBB pattern with variable
axis, however superior axis being the most common.
- QRS complex is usually larger with anterograde conduction over an atrioventricular pathway,
with a slurred QRS onset due to distal muscular insertion, which can be better appreciated in
the r wave of V2 to V4 (>0.04 sec in atrioventricular pathways).
- During tachycardia commonly has regular wide complex tachycardia (WCT) with LBBB
morphology and left axis deviation.

Low voltage criteria

- The amplitudes of all the QRS complexes in the limb leads are ≤ 5 mm; or
- The amplitudes of all the QRS complexes in the precordial leads are ≤ 10 mm.

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IV. ECG findings and clues in some cardiac disease and medical
conditions
ECG findings in Myocarditis
- Sinus tachycardia
- QRS/QT prolongation
- Diffuse T wave inversion
- Ventricular arrhythmias
- AV conduction defects

N.B. - With inflammation of the adjacent pericardium, ECG features of pericarditis can also been seen
(myopericarditis).

- The most common abnormality seen in myocarditis is sinus tachycardia with non-specific ST
segment and T wave changes.

ECG findings in pericarditis

Pericarditis is classically associated with ECG changes that evolve through four stages.
Stage 1 – widespread STE and PR depression with reciprocal changes in aVR (during first two weeks)
Stage 2 – normalization of ST changes; generalized T wave flattening (1 to 3 weeks)
Stage 3 – flattened T waves become inverted (3 to several weeks)
Stage 4 – ECG returns to normal (several weeks onwards)

N.B. - Less than 50% of patients progress through all four classical stages and evolution of changes may
not follow this typical pattern.

ECG clues in pericarditis

- Generalized upwardly concave ST elevation (STE in II > III).

- There is never STE in aVR.
- PR depression (more specific if greater than 0.8 mm and present in both limb and chest leads)
most prominent in inferior leads.
- Inverted T wave occurs only after ST normalized.
- ST segment height/T wave height ratio in V6 ≥ 0.25
- Spodick’s sign (downsloping of TP segment)
- No QT prolongation
- Absence of “fish hook” appearance in V4 (V4-V6)

Important points about the steps to distinguish pericarditis from STEMI:

1. Is there ST depression in a lead other than aVR or V1? This is a STEMI.

2. Is there convex up or horizontal ST elevation? This is a STEMI.
3. Is there ST elevation greater in III than II? This is a STEMI.

Now look for PR depression in multiple leads… this suggests pericarditis (especially if there is a
friction rub!)

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Features suggesting Benign early repolarization (BER)

- Absence of PR depression
- The T wave is peaked and slightly asymmetrical and the descending limb of the T wave is
straighter and slightly steeper than the ascending limb.
- ST segment/T wave ratio < 0.25.
- Characteristic “fish-hook” appearance in V4 (V4-V6).
- ECG changes usually stable over time.

ECG findings in pericardial effusion

Massive pericardial effusion produces a triad of:

1. Low QRS voltage

2. Tachycardia
3. Electrical alternans

N.B. – If we found bradycardia instead of tachycardia, hypothyroidism should be considered.

The pathophysiologic mechanisms that cause electrical alternans are

- Repolarization alternans (ST, T, U alternans):

• T wave alternans during Long QTS
• ST or U alternans during Acute Coronary Syndrome (ACS)
- Conduction and refractoriness alternans (P, PR, QRS alternans): QRS alternans during
orthodromic AVRT, intermittent LAFB during tachycardia.
- Alternans due to cardiac motion: Massive pericardial effusion

ECG findings in Hypertrophic cardiomyopathy

- LVH with secondary ST-T changes (systolic overload pattern)
- Asymmetrical septal hypertrophy produces deep, narrow (“dagger-like”) Q waves in the lateral
(V5-6, I, aVL) and inferior (II, III, aVF) leads. These may mimic prior myocardial infarction,
although the Q-wave morphology is different: infarction Q waves are typically ≥ 0.04 sec duration
while septal Q waves in HCM are < 0.04 sec. Lateral Q waves are more common than inferior Q
waves in HCM.
- LA enlargement
- There is an association between HCM and Wolff-Parkinson-White (WPW) syndrome.
- Atrial fibrillation and supraventricular tachycardias are common.
- Ventricular dysrhythmias (e.g. VT) also occur and may be a cause of sudden death.

N.B. - In Apical HCM seen most frequently in Japanese patients, there is localized hypertrophy of LV
apex, causing a “spade-shaped” configuration of the LV cavity on ventriculography. The classic ECG
finding in apical HCM is giant T-wave inversion in the precordial leads (Yamaguchi syndrome).

ECG findings in Dilated cardiomyopathy

- Left atrial enlargement -> may progress to atrial fibrillation
- Biatrial enlargement
- Left ventricular hypertrophy or biventricular enlargement
- Left bundle branch block (RBBB can also occur)
- Left axis deviation
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- Poor R-wave progression with QS complexes in V1-4 (“pseudo-infarction” pattern)

- Frequent ventricular ectopics and ventricular bigeminy
- Ventricular dysrhythmias (VT/VF, bundle branch reentry VT)

N.B. - Likewise, with or without LBBB, large QRS voltage in the precordial leads with relatively small
QRS voltage in the limb leads often indicates dilatation of both ventricles

ECG findings in ARVC

- Epsilon wave (most specific finding, seen in 30% of patients)
- T wave inversions in V1-3 (85% of patients)
- Prolonged S-wave upstroke of 0.055 sec in V1-3 (95% of patients)
- Localized QRS widening of 0.11 sec in V1-3
- Paroxysmal episodes of ventricular tachycardia with LBBB morphology (e.g. right ventricular VT)

N.B. - Fontaine leads are useful in increasing the sensitivity of detection of Epsilon waves in ARVC.
The Fontaine bipolar precordial leads are placed at the manubrium of sternum, xiphoid, and V4
positions using the right arm connection, left arm connection, and left foot connection, respectively.

ECG findings in atrial septal defect (ASD)

- First degree AV block
- ASD primum have a left axis deviation of the QRS complex
- ASD secundum have a right axis deviation of the QRS complex
- Sinus venosus ASD exhibit a left axis deviation of the P wave (not the QRS complex)
- ICRBBB or CRBBB
- RAE
- RVH
- Atrial tachyarrhythmia esp. AF
- Particularities: "Crochetage" pattern in II, III, aVF
N.B.
- QRS morphologic changes in V1 may correlates to RV pressure in ASD with significant Lt to
Rt shunt
- if it has CRBBB pattern…. RV has lower pressure than LV
- If it has dominant monophasic R wave pattern….. RV has equal pressure to LV
- If it has qR pattern …….RV has higher pressure than LV

ECG findings in Ebstein’s anomaly

- The amplitude of P wave is very high (Himalayan P waves).
N.B. - it may be even higher than the following QRS complex.
- The R waves in leads V1 and V2 are small with low-amplitude multiphasic atypical RBBB may be
QR or Qr complexes in leads V1 to V3.
- Bizarre morphologies of the terminal QRS pattern result from infra-Hisian conduction disturbance
and abnormal activation of the atrialized right ventricle.
- Wolff-Parkinson-White (WPW) syndrome: right sided bypass tract about 25%.
- Prolongation of PR interval (first degree AV block) if no WPW.
- Deep Q waves in lead II and III.
- Nonspecific T wave changes in precordial leads.
- Atrial flutter or atrial fibrillation
- Ventricular arrhythmias

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ECG findings in acute pulmonary embolism

- Sinus tachycardia: the most common abnormality; seen in 44% of patients
- Complete or incomplete RBBB: associated with increased mortality
- Right ventricular strain pattern: T wave inversions in the right precordial leads (V1-4) ± the inferior
leads (II, III, aVF). This pattern is seen in up to 34% of patients and is associated with high
pulmonary artery pressures.
- Right axis deviation: seen in 16% of patients.
- Dominant R wave in V1: a manifestation of acute right ventricular dilatation.
- Prominent R in aVR
- Right atrial enlargement (P pulmonale): peaked P wave in lead II ≥ 2.5 mm in height (9%).
- SI QIII TIII pattern (McGinn-White sign) – deep S wave in lead I, Q wave in III, inverted T wave in
III. This “classic” finding is neither sensitive nor specific for pulmonary embolism; found in only
20% of patients with PE.
- Clockwise rotation – shift of the R/S transition point towards V6 with a persistent S wave in V6
(“pulmonary disease pattern”), implying rotation of the heart due to right ventricular dilatation.
- Atrial tachyarrhythmias – AF, flutter, atrial tachycardia. Seen in 8% of patients.
- Non-specific ST segment and T wave changes, including ST elevation and depression. Reported
in up to 50% of patients with PE.
NB. - Simultaneous T wave inversions in the inferior leads (esp. lead III) and right precordial
leads (V1-4) is the most specific finding in favour of PE, with reported specificities of up to 99% in
one study.

ECG findings in COPD

The most typical ECG findings in emphysema are:

- Rightward shift of the P wave axis with prominent P waves in the inferior leads and flattened or
inverted P waves in leads I and aVL.
- Rightward shift of the QRS axis towards +90 degrees (vertical axis) or beyond (right axis
deviation).
- Exaggerated atrial depolarization causing PR and ST segments that “sag” below the TP baseline.
- Low voltage QRS complexes, especially in the left precordial leads (V4-6).
- Clockwise rotation of the heart with delayed R/S transition point in the precordial leads +/-
persistent S wave in V6. There may be complete absence of R waves in leads V1-3 (the “SV1-
SV2-SV3” pattern).

With development of Cor pulmonale, the following additional changes are seen:

- Right atrial enlargement (P pulmonale)

- Right ventricular hypertrophy

Other ECG changes that may be seen include:

- Right bundle branch block (usually due to RVH)

- Multifocal atrial tachycardia (M.A.T.)

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ECG findings in Hypothyroidism

Severe hypothyroidism (myxedema) causes a triad of:

1. Bradycardia
2. Low QRS voltage
3. Widespread T-wave inversions (usually without ST deviation)

Other ECG changes that may be seen include:

- QT prolongation
- First degree AV block
- Intraventricular conduction delay

ECG findings in raised intracranial pressure

- Widespread giant T-wave inversions (“cerebral T waves”)
- QT prolongation
- Bradycardia (the Cushing reflex – indicates imminent brainstem herniation)

Other possible ECG changes that may be seen:

- ST segment elevation/depression — this may mimic myocardial ischemia or pericarditis.

- Increased U wave amplitude
- Other rhythm disturbances: sinus tachycardia, junctional rhythms, PVCs, PACs, AF

NB. - In some cases, these ECG abnormalities may be associated with echocardiographic evidence
of regional ventricular wall motion abnormality (so-called “neurogenic stunned myocardium”)

ECG changes due to raised ICP are most commonly seen with massive intracranial hemorrhage:

- Subarachnoid hemorrhage
- Intraparenchymal hemorrhage (hemorrhagic stroke)

They may also be seen with

- Massive ischemic stroke causing cerebral edema (e.g. MCA occlusion)

- Traumatic brain injury
- Cerebral metastases (rarely)

ECG findings in Hypothermia

Hypothermia may produce the following ECG abnormalities:

- Bradyarrhythmias
- Osborne Waves
- U wave
- Prolonged PR, QRS and QT intervals
- PACs, AF
- PVCs
- Cardiac arrest due to VT, VF or asystole
- Shivering artefact

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ECG finding in digitalis effects and intoxication

Digoxin effect:

- Downsloping ST depression with a characteristic “Salvador Dali sagging” appearance.

- Flattened, inverted, or biphasic T waves
- Shortened QT interval
- Mild PR prolongation of up to 0.24 sec (due to increased vagal tone)
- Prominent U waves
- Peaking of the terminal portion of the T waves

N.B. - The morphology of the QRS complex/ST segment is variously described as either “slurred”,
“sagging” or “scooped” and resembling either a “reverse tick”, “hockey stick” or “Salvador
Dali’s moustache”.

- The most common T-wave abnormality is a biphasic T wave with an initial negative
deflection and terminal positive deflection. This is usually seen in leads with a dominant R wave
(e.g. V4-6). The first part of the T wave is typically continuous with the depressed ST segment.
The terminal positive deflection may be peaked, or have a prominent U wave superimposed upon
it.

Digoxin Toxicity:

Digoxin can cause a multitude of dysrhythmias. Dysrhythmias are usually due to:

- Delay After Depolarization (DAD) type of Triggered activity from increased intracellular calcium.
- Decreased AV conduction from increased vagal effects at the AV node.

Digitalis Toxicity: Major Arrhythmias

1. Bradycardias
- Sinus bradycardia, SA block or sinus arrest
- Junctional bradycardia
- Intra-nodal AVB ….Wenckebach AV block or CHB
2. Tachycardias from DAD mechanism
- Atrial tachycardia …common ECG is PAT with AV block
- Accelerated junctional rhythms (Nonparoxysmal junctional tachycardia)
- Ventricular arrhythmias of …frequent PVCs, monomorphic VT (fascicular VT), Bidirectional
ventricular tachycardia, Polymorphic VT or Ventricular fibrillation

Digitalis toxicity is least likely or could not induce all of these arrhythmias

- Sinus tachycardia
- PSVT (previously called Paroxysmal junctional tachycardia)
- AIVR (or called Nonparoxysmal VT)
- Parasystole or parasystolic tachycardia
- Mobitz type II AV block
- Fascicular block, BBB, Bifascicular block
- Infranodal CHB

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 Chula EP Team

ECG findings in Tricyclic antidepressants(TCA) toxicity

- Sinus tachycardia
- Wide QRS (usually also has CRBBB- like morphology), Brugada pattern
- Tall R wave in aVR (usually ≥ 3mm)
- R/S ration in aVR ≥ 0.7
- RAD
- QT prolongation

The degree of QRS broadening on the ECG is correlated with adverse events:

- QRS ≥ 100 ms is predictive of seizures

- QRS ≥ 160 ms is predictive of ventricular arrhythmias (e.g. VT)

ECG findings in Hyperkalemia

Serum potassium 5.5 - 6.5mEq/L is associated with repolarization abnormalities:

- Tall and Peaked (Tented) T waves (usually the earliest sign of hyperkalemia)

Serum potassium 6.5 - 7.5 mEq/L is associated with progressive paralysis of the atria:

- ST elevation and slightly widening of QRS complex, Brugada pattern, fascicular block
- P wave widens and flattens
- PR segment lengthens
- P waves eventually disappear

Serum potassium 7.5 - 8.5 mEq/L is associated with conduction abnormalities and bradycardia:

- Prolonged QRS interval with bizarre QRS morphology

- Any kind of conduction block (bundle branch blocks, fascicular blocks)
- Failure of cardiac capture by pacemaker
- Sinus bradycardia or AF with slow VR
- Development of a sine wave appearance (a pre-terminal rhythm)

Serum potassium level of > 8.5 mEq/L causes cardiac arrest due to:

- Asystole
- Ventricular fibrillation
- PEA with bizarre, wide complex rhythm

N.B. - The only ECG sign of severe and life-threatening hyperkalemia may simply be bradycardia.
There may be no QRS widening or peaking of T-waves.

- In individual patients, the serum potassium level may not correlate closely with the ECG
changes. Patients with relatively normal ECGs may still experience sudden hyperkalemic cardiac
high-grade AV block with slow junctional and ventricular escape rhythms.

- Tall and Peaked T wave when associated with QT prolongation is suggestive of

hyperkalemia with hypocalcemia (in isolated hyperkalemia there is normal or slightly short QT
interval) : This condition is commonly found in CKD

- In the presence of IVCD caused by hyperkalemia, the duration of the QRS complex is
shortened by hypernatremia and prolonged by hyponatremia.
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ECG findings in Hypokalemia

ECG changes when serum potassium < 3.0 mEq/L

- Increased P wave amplitude (pseudo P pulmonale)

- Prolongation of the PR interval
- T wave flattening and inversion
- Biphasic T wave of down-up pattern (roller-coaster sign)
- ST depression
- Prominent U waves (best seen in the precordial leads)
- Apparent long QT interval due to fusion of the T and U waves (= long QU interval)

With worsening hypokalemia…

- Frequent PACs and PVCs

- Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia
- Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and TdP

ECG findings in Hypercalcemia

- Prolongation of QRS complexes
- Shortening of the QT interval caused by shortening or absence of the ST segment
- PR prolongation or AV block
- Osborn waves (J waves) may be seen
- Ventricular irritability and VF arrest has been reported with extreme hypercalcemia

ECG findings in Hypocalcemia

- Hypocalcemia causes QTc prolongation primarily by prolonging the ST segment.
- The T wave is typically left unchanged.
- Dysrhythmias are uncommon, although atrial fibrillation has been reported.
- TdP rarely occurs, less common than with hypokalemia or hypomagnesemia.

ECG findings in Hypomagnesemia

- Slight prolongation of PR interval
- Slight prolongation of QRS complexes
- ST depression
- Broad, flattened T-waves
- Prominent U waves
- QT prolongation, TdP

ECG findings in Hypermagnesemia

- Increase PR
- Prolongation QRS complexes
- Peaked T waves and flattened p waves
- Complete AV block and asystole

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V. Differential causes of abnormal ECG patterns

Causes of ECG Artifact
1. Loose lead artifact
2. Wandering baseline artifact breathing loose or dry electrodes
3. Muscle tremor artifact
4. Electromagnetic interference (EMI)
5. CPR compression artifact
6. Arterial pulse tapping artifact

Causes of poor R wave progression (PRWP)

PRWP is defined by R wave height ≤ 3 mm in V3 and R in V1 < R in V2 < R in V3

1. Prior anteroseptal MI
2. Left Ventricular Hypertrophy
3. Right Ventricular Hypertrophy (usually seen in COPD)
4. LBBB
5. LAFB
6. Ventricular preexcitation (WPW type B)
7. Dilated cardiomyopathy
8. Inaccurate lead placement (misplace to higher position)
9. More vertical heart position or low diaphragm position
10. Clockwise cardiac rotation

Causes of dominant R wave in V1 (Prominent Anterior Force, PAF)

1. RVH
2. Posterior wall (and/or lateral) MI
3. Hypertrophic CM
4. Duchenne muscular dystrophy
5. CRBBB
6. Ventricular preexcitation (WPW Type A)
7. Left septal fascicular block
8. Misplacement of chest leads
9. Displacement of heart toward right side of chest
10. Abnormality of the thorax or intrathoracic tissues which might cause counterclockwise rotation.
11. Normal variants

Causes of rSr' or rSR’ in V1-V2

A. Benign Patterns: narrow -r' of fast inscription, unlike in CRBBB or BrS, both of which have a wider
R'.
1. Higher placement of leads V1, V2
2. Normal variant, with late activation of the posterobasal LV
3. Incomplete RBBB
4. Athletes: 35-50% due to physiologic RV enlargement
5. Pectus Excavatum, due to change of heart location in chest
B. Pathological Patterns: wider-R' often taller then -r, with slower ascent/descent.
1. Type 2 Brugada pattern

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2. RV enlargement, hypertrophy from a variety of pathologies

3. Arrhythmogenic RV cardiomyopathy (ARVC)
4. WPW syndrome
5. Hyperkalemia
6. Na+ channel blockers (class I AADs, TCAs)

Causes of Left Axis Deviation (LAD)

1. LVH
2. LAFB
3. CLBBB
4. Old inferior wall MI
5. Ventricular preexcitation (posteroseptal bypass tract)
6. COPD (found in less than 10%)
7. Some types of congenital heart disease (Ostium primum ASD, Endocardial cushion defect,
Tricuspid atresia, Single ventricle, Corrected TGA, DORV with infracristal VSD.
8. Obesity, pregnancy or markedly ascites produce higher diaphragm.
9. Ventricular rhythm or cardiac pacing from apex.
10. Hyperkalemia
11. Normal variants

Causes of Right Axis Deviation (RAD)

1. RVH
2. Old lateral wall MI
3. LPFB
4. COPD
5. Acute pulmonary embolism
6. Dextrocardia
7. Ventricular preexcitation
8. Ventricular rhythm
9. Sodium channel blocker toxicity
10. Hyperkalemia
11. Right and left arm reversal
12. Normal findings in tall slim adults

Causes of PR depression
1. Pericarditis
2. Atrial infarction
3. Normal variant (atrial repolarization)

N.B. - PR has significantly depressed if more than 0.8 mm.

Causes of Short PR interval

1. Enhanced AV nodal conduction (EAVNC): association with increase sympathetic tone
2. Ventricular preexcitation
3. Subsidiary pacemaker rhythm (fixed PR interval)
- Atrial ectopic rhythm, if atrial foci close to AV node (negative P wave in inferior leads)
- Junctional escape rhythm (if retrograde P wave seen before QRS complex)
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4. Isorhythmic AV dissociation (varying PR interval)

- Isorhythmic between sinus and Junctional rhythm
- Isorhythmic between sinus and Ventricular rhythm
5. Congenitally hypoplastic AV node or anatomically small AV node
6. Normal variants

Causes of variable PR interval

1. Intermittent conduction over slow pathway
2. Intermittent conduction over accessory pathway
3. Type I (Wenckebach) AV block
4. Concealed conduction from premature beats into AV junction
5. Intermittent junction rhythm and AV dissociation
6. Fluctuation of sympathovagal balance
7. Paced rhythm with dynamic AV delay

Causes of regular bradycardia

1. Sinus bradycardia
2. Sinus arrest with escape rhythms
3. 2:1 Second degree SA exit block
4. 2:1 Second degree AV block
5. Third degree AV block with escape rhythms
6. Bigeminy non-conducted PACs
7. Bigeminy PJCs/PVCs

Causes of AV dissociation (AVD)

1. Complete AV Block (commonly has atrial rate > ventricular rate)
2. Isorhythmic AV Dissociation (commonly has atrial rate = ventricular rate)
3. Interference AV Dissociation (commonly has atrial rate < ventricular rate)

Causes of group beating rhythm

1. Wenckebach SA block
2. Second degree AV block (with 3:2, 4:3, 5:4 AV conduction pattern)
3. Geminy pattern of PACs or PVCs
4. Junctional rhythm with retrograde VA induce echo beat
5. PVCs with retrograde VA induce echo beat
6. Escape-Capture Bigeminy

Causes of regular narrow complex tachycardia (NCT)

1. AV node dependent NCT
- AV nodal reentrant tachycardia (AVNRT)
- Atrioventricular reentrant tachycardia (AVRT)
2. AV node independent NCT
- Sinus tachycardia
- Atrial tachycardia
- Atrial flutter
- Junctional ectopic tachycardia
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Causes of short RP regular narrow complex tachycardias (NCT)

1. Typical AVNRT
2. Orthodromic AVRT
3. Sinus tachycardia with first degree AV block
4. SNRT with first degree AV block
5. AT with first degree AV block
6. Junctional ectopic tachycardia

Causes of long RP regular narrow complex tachycardias (NCT)

1. Atypical AVNRT
2. Sinus tachycardia
3. Sinus node reentrant tachycardia (SNRT)
4. AT
5. Orthodromic AVRT using slowly conducting bypass tract (Commonly found in PJRT)

Causes of Irregular NCT

1. Atrial fibrillation
2. Atrial flutter with variable block
3. Multifocal atrial tachycardia
4. Others

Causes of regular wide complex tachycardia (WCT)

1. Ventricular tachycardia (about 75-80% of cases)
2. SVT with abnormal intraventricular conduction (15-30%)
- SVT with BBB aberration (fixed or functional)
- Pre-excited SVT (SVT with ventricular activation occurring over a bypass tract); (1-5 % of all)
- SVT with wide QRS (nonspecific IVCD) due to abnormal muscle-muscle spread of impulse
(Congenital HD, cardiomyopathy)
- SVT with wide complex due to drug or electrolyte-induced changes (hyperkalemia, Class Ia,
Ic drugs or Amiodarone)
3. Ventricular paced rhythms
4. Pseudo WCT
5. Artifact

Clues for DDx causes of WCT

A: AV dissociation (suggestive of VT)
Axis (extreme axis suggestive of VT)
B: Beat (capture beats, fusion beats; suggestive of VT)
C: Concordance (suggestive of VT)
D: Duration of QRS complex (if ≥ 0.14 sec in V1 positive or ≥ 0.16 sec in V1 negative;
suggestive of VT)
E: Experience from practice and using special criteria
N.B. - Use modified Lewis lead to identify P wave more clearly
• Place the Right Arm electrode on the patient’s manubrium
• Place the Left Arm electrode on the 5th intercostal space of right sternal border
• Place the Left Leg electrode on the right lower costal margin
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The Brugada Criteria for diagnose VT

Step 1: Absence of an RS complex in all precordial leads

- The same as having positive or negative concordance

- Any RS complexes present in V1-6 –> move on to the next step of the algorithm

Step 2: RS interval ≥ 100ms in one precordial lead

- Time from the onset of the R wave to the nadir of the S wave
- If the RS interval is ≥ 100 ms –> VT is diagnosed
- If the RS interval is < 100 ms –> move on to step 3

Step 3: AV dissociation

Step 4: Morphological Criteria for VT

WCT with RBBB-like morphology (V1 positive WCT)

V1 morphological criteria: three patterns are indicative of VT.

1. Smooth monophasic R wave or a wide (> 30 msec) R wave

2. Notched downslope to the R wave — the taller left rabbit ear (= Marriott’s sign)
3. qR complex (small Q wave, tall R wave) in V1

V6 morphological criteria: the following patterns are indicative of VT.

1. QS complex — a completely negative complex with no R wave (= strongly suggestive of VT).

2. R/S ratio < 1 — small R wave, deep S wave (indicates VT only if LAD is also present).

WCT with LBBB-like morphology (V1 negative WCT)

V1 morphological criteria: three patterns are indicative of VT.

1. Initial R wave > 30-40 msec duration

2. Notching or slurring of the S wave (Josephson’s sign)
3. RS interval (time from R wave onset to S wave nadir) > 60-70 msec

V6 morphological criteria: the presence of Q waves in V6 is indicative of VT.

1. QS waves in V6 (as with RBBB-like patterns, this finding is very specific for VT)
2. qR pattern = small q wave, large R wave

Ultra-simple Brugada criteria: RWPT (R Wave Peak Time)

- If there is RWPT ≥ 50 msec in lead II indicative of VT
- RWPT = Duration from the QRS depolarization onset until the first change of polarity
(independent of whether the QRS deflection is positive or negative) as measured in lead II.

Vereckei criteria: following criteria were suggestive of VT

Step 1: The presence of AV dissociation

Step 2: The presence of an initial R-wave in lead aVR

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Step 3: QRS morphology unlike BBB or FB

Step 4: Measuring the voltage during the initial 40 ms (Vi), the terminal 40 ms (Vt), their ratio
(Vi/Vt) Vi/Vt ≤ 1 was suggestive of VT.

The aVR ‘Vereckei’ Criteria for VT in lead aVR were

Step 1: The presence of an initial R-wave

Step 2: Width of an initial r or q wave > 40 ms

Step 3: Notching on the initial downstroke of a predominantly negative QRS complex

Step 4: Vi/Vt ≤ 1

Sasaki criteria for VT

Step 1: Initial R in aVR?

Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100
msec

Step 3: Initial r or q ≥ 40 msec in any leads?

Other suggestive clues

1. Combination of LBBB and RAD is almost always due to VT.

2. RBBB with a normal axis is very uncommon in VT.
3. Concordant pattern in precordial leads is uncommon in SVT, with the exception of pre-excited
tachycardia.
4. Negative concordance in limb leads is another way of describing extreme axis and suggests VT.

If old ECG available

1. WCT with QRS narrower than NSR is strongly in favor of VT.

2. Different BBB morphology during baseline vs during WCT strongly suggests VT. Because if
RBBB is present in SR and LBBB develops with SVT, then CHB must happen (except in rare
cases).
3. Presence of multiple WCT configurations is in favor of VT.
4. Same QRS morphology during baseline rhythm and WCT suseggest SVT (exception: BBRVT).

N.B. – Pre-excited SVTs (ventricular activation entirely or primarily over an anomalous AV

connection) has an ECG pattern consistent with VT…

- In Inter-fascicular VT and BBRVT, the ECG morphological criteria suggest SVT with
aberration, but it is VT!!!! (clue…try to find AV dissociation)

The very important concepts

- All of the criteria (for DDx VT and SVT with aberration) are useful only for SVT which has
intraventricular conduction delay in bundle branch.

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- If the causes of IVCD come from delay in Purkinje system, from abnormal muscle-muscle spread,
due to drugs or electrolyte-induced, we cannot DDx from VT by above special or morphological
criteria.
- if the ECG doesn’t look like typical aberration, it is most likely VT.

Causes of Irregular WCT

1. Polymorphic ventricular tachycardia/ Torsades de Pointes
2. Atrial fibrillation with aberrant conduction
3. Atrial fibrillation with WPW (Pre-excited AF)
4. Atrial flutter with variable block and aberrant conduction
5. Multifocal atrial tachycardia with aberrant conduction
6. Others

Causes of ST depression
1. Myocardial ischemia or infarction
- Acute subendocardial ischemia or non–ST elevation myocardial infarction
- Reciprocal change with acute transmural ischemia
2. Non-myocardial ischemia
- Left or right ventricular hypertrophy (“strain” pattern)
- Secondary ST-T changes (ST depression move discordant to QRS): LBBB, RBBB,
nonspecific IVCD, WPW, ventricular pacing
- Drugs (e.g., digitalis)
- Metabolic conditions (e.g., hypokalemia)
- Miscellaneous conditions (e.g., cardiomyopathy)
3. Physiologic and normal variants

Causes of ST elevation
1. Acute STEMI (transmural myocardial ischemia including Takotsubo CM and Prinzmetal’s angina)
2. LV aneurysm
3. Acute pericarditis/ myopericarditis
4. Hyperkalemia
5. Benign early repolarization (BER)
6. Complete LBBB, RV pacing
7. LVH
8. J wave syndrome (Early repolarization syndrome, Brugada syndrome)
9. Others: Post cardioversion, Acute pulmonary embolism, Hypercalcemia, SAH, Cocaine use,
Hypothermia, tumor invading the ventricle etc.

Understanding J wave syndrome:

- J wave syndrome has emerged from a benign ECG abnormality to a proarrhythmic state and
a significant cause of VF responsible for SCD.
- J wave names after junction point of QRS with ST segment on ECG and reflects junction
point (J Point) of end of depolarization with initiation of repolarization.
- The J-wave syndromes (JWSs) consist of two syndromes
1. Early repolarization syndrome (ERS) is called when ECG of Early Repolarization pattern
(seen in lateral, inferior, inferolateral or right precordial leads), associated with VT/VF in
the absence of structural HD.
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- ER was defined as J point elevation of ≥ 1 mm in ≥ 2 leads in inferior, lateral or right

precordial leads.
- Types of Early Repolarization pattern (ERP)
• Type 1: ER pattern predominantly in the lateral precordial leads (V4, V5, V6)
• Type 2: ER pattern predominantly in the inferior or infero-lateral leads (II, III, aVF,
V4-V6)
• Type 3: ER pattern globally in the inferior, lateral, and right precordial leads.
- Morphological Classification of ER pattern are physiological (benign) or pathological
(malignant).
• J point with rapidly ascending ST segment, considered a benign form.
• J point with horizontal or descending ST segment, considered a malignant form.

2. Brugada syndrome (BrS) is called when ECG of Brugada pattern (seen in right precordial
leads, V1-V3) associated with VT/VF in the absence of structural HD.
- Morphological Classification of Brugada pattern (BrP)
• Type 1 Coved pattern: initial ST elevation ≥ 2 mm, slowly down sloping with
negative symmetric T wave in V1 or V2 (V3).
• Type 2 Saddle back pattern: The high take-off (r`) is ≥2 mm and followed by ST
elevation with elevation ≥ 0.5 mm with positive T wave in V2 and T wave variable
in V1.

N.B. - If there is some doubt, it is necessary to record the ECG in 2nd and 3rd ICS
and/or with class Ic drug challenge test.

- To identify r' of type 2 BrP compared with other types of r', there is a new
technique of using the duration of the base triangle of r' at 5 mm from the high take-
off ……if it is ≥ 4 mm, the type 2 BrP is suggested.

- Other ECG findings

• QT generally is normal. May be prolonged in right precordial leads.
• Conduction disorders: Sometimes, prolonged PR interval (long HV interval).
RBBB, the conduction delay located in RV explains the r' and longer QRS
duration in right precordial leads compared with mid/left precordial leads
(mismatch between QRSd in V1 and V6).
• Supraventricular arrhythmias. Mostly atrial fibrillation.
• Some other ECG findings may be seen: the presence of r' wave in aVR > 3mm,
ER pattern in inferior leads, fragmented QRS, alternans of T wave after ajmaline
injection etc.

ECG diagnostic criteria of Brugada pattern (BrP)

1. BrP is definitively diagnosed if a coved type 1 ECG is observed in V1 or V2, either
spontaneously or induced by Na+ channel blockade (e.g., using ajmaline). The precordial
leads V1 and V2 may be placed in the standard position or higher, up to the second
intercostal space (ICS).
2. The saddle-back type 2 ECG are suspicious for, but not diagnostic of BrP. When
encountering a type 2 ECG the diagnosis of BrP may only be made after drug- induced
conversion to a type 1 ECG.
- In the presence of the ECG criteria of BrP, BrS is diagnosed if one/more of the following
clinical factors
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……Survivors of SCD
……,Presence of PMVT
…….History of non vagal syncope
…….Family Hx of unexplained SCD in patients younger than 45 years or
…….BrP type 1 in relatives.
N.B. - A unique feature of J wave is that it may not be present all the times and actually
as been seen to emerge just before onset of VF and also to disappear in survivors of VF.

Causes of ST elevation in lead aVR

1. Acute coronary syndrome: Predictive Value of ST-Segment Elevation in aVR
In the context of widespread ST depression + symptoms of myocardial ischemia:
- ST-segment elevation in aVR greater than or equal to 1 mm indicates proximal LAD/LMCA
occlusion or severe TVD.
- ST-segment elevation in aVR greater than or equal to 1 mm predicts the need for CABG.
- ST-segment elevation in aVR greater than or equal to V1 differentiates LMCA from proximal
LAD occlusion.

In the context of anterior ST-elevation MI:

- ST elevation in aVR greater than or equal to 1 mm is highly specific for LAD occlusion
proximal to the first septal branch.

N.B. - Magnitude of ST elevation in aVR is correlated with mortality in patients with ACS. Some
case of Acute RV infarction ….usually also have STE in V1 and ST depression in V2-V3 from
association with posterior wall MI because of proximal RCA occlusion (the occlusion of conus
branch from RCA make basal septum infarction which cause STE in aVR and occlusion of PDA
branch which cause posterior wall MI.

2. Takotsubo CM (LV Apical ballooning, TTC )

Because involving of the apical area of LV so the STE in lead I, II, III, aVF and V2 to V6 also
detected.

ECG findings in TTC

- Abnormal Q waves: occurred in only 10%, Q waves often tend to regress afterwards along
with R wave reappearance, suggesting electrical stunning.
- Inverted T wave in I, aVL, V5-V6 + STE in aVR
- STE in aVR without STE in V1
- STE in aVR with STE in inferior leads
- STE in aVR with STE in anteroseptal or anterior leads
- STE in anterior lead without reciprocal ST depression in inferior leads
- Diffuse T-inversion in TTC patients, especially in anterior and lateral leads. These
repolarization changes were also documented after reperfusion of prolonged myocardial
ischemia and were referred to stunned as well as viable but sympathetically denervated
myocardium.
N.B. - Clues for suspicious of Takotsubo CM are the absence of reciprocal change and the
ratio of ST-segment elevation in leads V4–6 to V1–3 ≥ 1

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3. Acute pulmonary embolism

- Due to acute RV overload, transient hypoxia from impaired coronary flow or increased
myocardial oxygen demand.
4. Orthodromic AVRT: retrograde P wave commonly superimpose onto ST segment of aVR lead

Causes of prominent R wave in aVR

1. Right-Left arm lead reversal
2. Dextrocardia
3. LAFB
4. Acute pulmonary embolism
5. Severe RVH
6. Left tension pneumothorax
7. LV aneurysm: Goldberger’s sign
8. Brugada syndrome: prominent R wave in lead aVR – also known as the ‘aVR sign’ – portends a
greater risk for arrhythmic events.
9. TCA poisoning: the amplitude of the terminal R wave (3 mm or greater) in aVR and the ratio of
the R wave to the S wave in aVR > 0.7 are also good predictors of seizures and arrhythmias.
10. Class I AADs intoxication esp. Class Ic
11. Hyperkalemia
12. Ventricular Tachycardia

Causes of T wave abnormalities

Tall upright T Waves

1. Ischemic causes
- Hyperacute phase of myocardial infarction
- Acute transient transmural ischemia (Prinzmetal’s angina)
- Chronic (evolving) phase of myocardial infarction (tall positive T waves reciprocal to primary
deep T wave inversions esp.in posterior wall MI)
2. Non ischemic causes
- Hyperkalemia (Tall, peak and tented T wave in early phase)
- LVH or LBBB (in right precordial leads have normal discordant ST-T pattern with preceding
QRS complex).
- Upright T waves in right precordial leads are reciprocal with left precordial ST depression
and inverted T wave.
- Diastolic load pattern of LVH (eccentric LVH from chronic severe AR, MR) in left precordial
leads.

N.B. - Diastolic load pattern of LVH will has ST-T changes which looked like early repolarization

- Systolic load pattern of LVH (concentric LVH from HT, AS, HCM etc.) in left precordial
leads will has ST depression and inverted or biphasic T wave (known as strain pattern).

- Benign early repolarization (BER)

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In ACS setting…...Loss of precordial T-wave balance occurs when the upright T wave in other precordial
leads is larger than that in V6. This is a type of hyperacute T wave.

……The normal T wave in V1 is inverted. An upright tall T wave in V1 is considered

abnormal especially if it is new implies acute ischemia.

……Tall T wave only in V1-V3 should be considered of acute posterior wall MI

Causes of Global T wave Inversion

T wave inversions in all standard leads except the aVR lead

1. LM coronary artery disease

2. Takotsubo cardiomyopathy
3. Myocarditis
4. Advanced AV block
5. Apical hypertrophic cardiomyopathy
6. Acute pericarditis
7. Acute cerebrovascular event
8. Pheochromocytoma
9. Cocaine use
10. Kounis syndrome
11. Hypokalemia
12. Pulmonary edema
13. Pulmonary embolism (rare)

Causes of Deep T Wave Inversion

Giant inverted T wave ≥ 10 mm, deep T wave inversion ≥ 5 mm and mild T wave inversion 1-4 mm

1. Myocardial ischemia/infarction
2. Takotsubo cardiomyopathy
3. Cerebrovascular accident (especially intracranial bleeds) and related neurogenic patterns
4. Left or right ventricular overload
- Typical patterns (“strain” patterns)
- Apical hypertrophic cardiomyopathy (Yamaguchi syndrome)
5. Secondary T wave alterations (secondary to depolarization abnormalities e.g. LVH, BBB, non-
specific IVCD, Pacing, WPW): T wave move discordant to QRS.
6. Memory inverted T waves: appear after pacing, after RF ablation of bypass tract (esp. right
posteroseptal BT), transient LBBB, or transient tachycardia.
7. Normal variants e.g. Juvenile T wave pattern, benign early repolarization (BER).

N.B. - New T-wave inversion (compared with prior ECGs) is always abnormal. Pathological T wave
inversion is usually symmetrical and inverted ≥ 3mm.

- Previously inverted T-waves can appear normal and upright in the setting of acute vessel
occlusion. This is known as pseudonormalization of T waves.

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Typical inverted T waves changes in LVH (systolic overload pattern)

- Asymmetrical inverted T with more steep of upslope
- Terminal T wave positive (overshoot of terminal portion above isoelectric baseline)
- T wave inversion in V6 > 3 mm
- T wave inversion in V6 > V4

Mild rapidly reversible T-wave abnormalities

- T-wave inversion occurs with standing, with hyperventilation, or after a meal

Causes of Biphasic T waves

There are two main causes of biphasic T waves: The two waves go in opposite directions.

1. Myocardial ischemia: Ischemic T waves go up then down

2. Hypokalemia: T waves go down then up

Important!!!!!…….Down-Up T-waves in V2 and V3 have only two causes.

- Hypokalemia (in which case the upright component is really a U-wave)

- Posterior MI with some reperfusion (reciprocal to Up-Down T-waves of the posterior wall,
analogous to Wellens' of the posterior wall as recorded from the anterior wall).

.……Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the
territory underlying aVL STEMI

Less common causes of biphasic T waves

1. LVH
2. Cardiomyopathy
3. Benign early repolarization in some patient esp. Black people

‘Camel Hump’ T waves: “camel hump T waves” and the “Tee-Pee sign”.

There are two causes for camel hump T waves:

1. Prominent U waves fused to the end of the T wave, as seen in severe hypokalemia.
2. Hidden P waves embedded in the T wave, as seen in ST/AT and various types of heart block.

Causes of Flattened T waves

1. Ischemia (Flattened T waves are a non-specific finding, but may represent ischemia if dynamic)
2. Hypokalemia
3. Cardiomyopathy
4. Pericarditis
5. Hypothyroidism
6. Normal variants

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Causes of Pseudo MI pattern from pseudo Q wave or loss of R wave amplitude

1. Ventricular preexcitation
- Depend on location of bypass tract (BT), the delta wave can simulate QS wave of old MI
- Might be falsely diagnosed as old inferior, old lateral, anteroseptal and posterior wall MI
2. HCM
- Abnormal Q waves are often seen and mimic varying MI location depend on q wave location
3. LVH and CLBBB
- QS deflection or poor R-wave progression in the right precordial leads that suggests anterior
or Anteroseptal wall MI
4. Left anterior hemiblock
- Occasionally associated with small Q waves in the precordial leads and rS in II, III, aVF
- Mimic anterior or inferior wall MI.
5. In COPD/Cor pulmonale
- R waves in the right precordial and sometimes mid-precordial leads become quite small or
are absent, suggesting Anteroseptal wall MI
- If RVH may mimic posterior or inferior wall MI
6. DCM: any MI
7. Chest deformity or abnormal intrathoracic disease
- Mimic inferior, posterior, anterior or Anteroseptal wall MI
8. Acute pulmonary embolism
- Mimic inferior, anterior or Anteroseptal wall MI
9. Dextrocardia or left pneumothorax (loss of lateral R wave progression)
- Mimic lateral wall MI
10. Normal variant septal Q or normal variant Q waves in leads V1, V2, aVL, III, and aVF
- Mimic septal ,inferior or inferolateral wall MI

Causes of Long QT (QTc ≥ 0.45 sec in men and ≥ 0.46 sec in women)
1. Congenital LQTS
2. Acquired long QT syndrome
2.1 Drug induce QT prolongation
- AADs: Class IA, Class III
2.2 Non-AADs
- Antibiotics: Erythromycin, Clindamycin, Clarithromycin, Quinolones (especially
sparfloxacin), Trimethoprim- sulfamethoxazole, Chloroquine, Pentamidine, etc.
- Antifungals: Itraconazole, Ketoconazole, Fluconazole, Voriconazole
- Psychotropics: Antidepressants; TCA (i.e., Amitriptyline, Desipramine), tetracyclic
agent, Lithium, Haloperidol, Droperidol, Doxepin, Risperidone, Phenothiazines,
Thioridazine
- Antihistamines: Astemizole, Terfenadine, Diphenhydramine
- Gastrointestinal: Cisapride, Domperidone, ondansetron
- Others: Methadone, Arsenic, Organophosphate insecticides
2.3 Cardiac abnormalities: Myocardial ischemia/MI, Myocarditis, CHF, severe LVH
2.4 Metabolic factors: Hypokalemia, Hypomagnesemia, Hypocalcemia, Hypoglycemia,
Hypothermia, Hypothyroidism
2.5 Bradyarrhythmias: Sinus bradycardia, Atrioventricular block
2.6 Cerebrovascular abnormalities: Intracranial hemorrhage, Subarachnoid hemorrhage, Stroke
2.7 Miscellaneous: Liquid protein diets, starvation, Autonomic neuropathy, HIV

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 Chula EP Team

N.B. – The QT measurement should be made in leads II and V5 or V6 with the longest value
being used

- Higher risk for developing TdP during QT prolongation if the ECG shows High QT
dispersion interval, High TpTe interval, T waves alternans.

QT dispersion

- QT dispersion is simply defined as the difference between the longest (QTmax) and the shortest
(QTmin).
- The normal range of QT dispersion is 40-50 msec.
- High levels of Q-T dispersion (e.g., greater than 100 msec) may be a risk factor for life-
threatening ventricular arrhythmias.

T-peak-to-T-end interval (TpTe interval)

- The interval from the peak to the end of the T wave provides a measure of transmural dispersion
of repolarization (TDR).
- TpTe values >100 msec predicts higher risk for life-threatening ventricular arrhythmias.

Causes of short QT (QTc ≤ 0.36 sec in men and QTc ≤ 0.37 sec in women)

1. Hypercalcemia
2. Hyperkalemia
3. Hyperthermia
4. Acidosis
5. Effect of catecholamine
6. Activation of KAch
7. Activation of KATP
8. Effects of drugs such as digitalis, lidocaine
9. Short QT syndrome

N.B. - QTc intervals ≤ 0.33 sec in men or ≤ 0.34 sec in women should be considered diagnostic of
SQTS.

- QTc intervals ≤ 0.36 sec in men or ≤ 0.37 sec in women should only be considered diagnostic
of SQTS when supported by symptoms or family history.

Causes of prominent U waves (taller than 25% of preceding T wave height or ≥ 1.5 mm)

1. Bradycardia
2. Long QTS
3. Hypokalemia
4. LVH
5. HCM
6. Mitral valve prolapse
7. Hyperthyroidism
8. Following exercise
9. Hypomagnesemia
10. Hypocalcemia
11. Hypercalcemia

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12. Hypothermia
13. Raised intracranial pressure
14. Drug effect : Class IA, III AADs, Digoxin

Causes of inverted U waves

1. Coronary artery disease
2. Hypertension
3. Valvular heart disease usually with LVH
4. Congenital heart disease
5. Cardiomyopathy
6. Hyperthyroidism

N.B. - In patients presenting with chest pain, inverted U waves are a very specific sign of myocardial
Ischemia. May be the earliest marker of unstable angina and evolving myocardial infarction.

- In the appropriate clinical context, an increase in U-wave amplitude in the precordial leads may
raise suspicion of posterior ischemia. This could be considered the mirror image of a negative U-
wave.

Causes of low voltage

1. Increase fluid: Pericardial effusion, Pleural effusion, anasarca
2. Increase fat: Obesity
3. Increase air: Emphysema, Left Pneumothorax
4. Infiltrative/Connective Tissue Disorders
- Myxedema
- Infiltrative myocardial diseases due to amyloidosis, sarcoidosis, hemochromatosis
- Constrictive pericarditis
- Scleroderma
5. Loss of viable myocardium: previous massive MI, end-stage dilated cardiomyopathy
6. Massive pericardial effusion
7. Artifactual or spurious e.g, unrecognized standardization of the ECG (decrease sensitivity)
8. Normal variant

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VI. Interesting Eponymous ECG and ECG signs

Bayés syndrome

- Bayés’ syndrome refers to the association between interatrial block and supraventricular
arrhythmias mainly the occurrence of AFL or AF. It is also a risk factor for cardio-embolic stroke.

Bachmann bundle

- A branch of the anterior internodal tract that resides on the inner wall of the left atrium. It is a
broad band of cardiac muscle that passes from the right atrium, between the superior vena cava
and the ascending aorta to the upper part of left atrium. Bachmann's bundle is, during normal
sinus rhythm, the preferential path for electrical activation of the left atrium. It is therefore
considered to be part of the "atrial conduction system" of the heart.

Brugada sign

- During regular WCT, the interval from the onset of the QRS complex to the nadir of the S-wave in
precordial leads ≥ 100 msec….suggestive of VT.

Cabrera sign

- Cabrera sign is used originally to diagnose an anterior wall MI (old > acute) in the setting of a
LBBB and consists of notching (fQRS) of ≥ 0.040 sec in the ascending limb of the S wave in lead
V3 to V5.

Chapman sign

- Chapman sign is used for diagnosis of an anterior wall MI (old > acute) in the setting of a LBBB
and consists of notching (fQRS) of ≥ 0.050 sec in the upslope of the R wave in lead I, aVL or V6.

Camel hump T waves

- Camel hump T waves and also call “Tee-Pee sign” is used when T wave morphology has two
humps (like camel back) or looked like an Indian tent (teepee), these T waveform could be found
in patients who have QT-U prolonged or have P wave after T wave.

Coumel law

- During PSVT, aberration may develop due to rate dependent bundle branch block in either
bundle branch. When the development of BBB is linked with PSVT rate slowing, it implies that the
blocked bundle was part of the PSVT circuit, and therefore the arrhythmia mechanism must be
orthodromic AVRT using a bypass tract that is ipsilateral to the blocked bundle branch.

Crochetage sign
- A notch near the apex of the R wave in inferior leads of ASD (mostly secundum) has been called
‘crochetage’ because the notch resembles the work of a crochet needle.
- Its incidence increases with larger anatomical defect or greater left-to-right shunt.

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- Early disappearance of this pattern was observed in 35% after ASD closure although the RBB
pattern persisted.

Dagger Q waves

- Describe the deep and narrow (‘dagger like’) Q waves in the lateral (V5-6, I and aVL) and inferior
(II, III and aVF) leads, due to asymmetrical septal hypertrophy.

Dressler beat

- Occurs during ventricular tachycardia and is also known as a fusion beat. This occurs when sinus
node impulse conducts through the normal conduction pathway during an episode of ventricular
tachycardia, resulting in a QRS complex which made from fusion of the normal QRS morphology
and that of the ventricular morphology from the ventricular tachycardia.

Dome and dart P waves

- The dome and dart P waves pattern in V1 is suggestive of left atrial in origin.

de Winter’s T waves

- Tall, prominent, symmetric T waves in the precordial leads

- Upsloping ST segment depression > 1 mm at the J-point in the precordial leads
- Absence of ST elevation in the precordial leads
- ST segment elevation (0.5 mm – 1 mm) in aVR
- Classical STEMI morphology may precede or follow the de Winter pattern

N.B. - The de Winter ECG pattern is an anterior STEMI equivalent that presents without obvious ST
segment elevation. Key diagnostic features include ST depression and peaked T waves in the
precordial leads. The de Winter pattern is seen in ~2% of acute proximal LAD occlusions and is
under-recognized by clinicians. Unfamiliarity with this high-risk ECG pattern may lead to under-
treatment. The explanation of this ECG pattern remains unclear. Hypothetically an anatomical variant
of the Purkinje fibers, with endocardial conduction delay, could be present. An alternative explanation
is that the absence of ST elevation may be related to the lack of activation of sarcolemmal ATP-
sensitive potassium channels by ischemic ATP depletion.

El-Sherif Sign

- El-Sherif Sign is an rsR’ complex, or its variants (rSr’ or rSR’), in the left anterior precordial leads
that is observed in patients with apical ventricular aneurysm. The rsR’ pattern in V6 with
prolonged QRS was mentioned in the ’50s by many researchers that tried to relate it with
ventricular aneurysms.

Fish Hook Pattern

- Another clue that suggests benign early repolarization (BER) is the presence of a notched or
irregular J point: the so-called “fish hook” pattern. This is often best seen in lead V4-V6.

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Goldberger Sign

ECG abnormalities described in patients with Left Ventricular Aneurysm (LVA).

1. Persistent ST segment elevation

2. Fragmented QRS complex (El-Sherif Sign)
3. Prominent R wave in lead aVR (Goldberger sign)

Their presence suggest the presence of an LVA.

N.B. - Absence of the above ECG abnormalities does not exclude the presence of LVA.

Haissaguerre Syndrome

1. Patients (mostly male) with idiopathic VF and ER pattern (one of two type of J wave syndrome).
2. Normal or slightly short QT interval
3. Have recurrent arrhythmic storm more frequently than idiopathic VF patients with a normal ECG
4. High-amplitude J waves conferred a higher risk for arrhythmic storm, and transient augmentation
of the J-wave amplitude preceded the onset of VF.

Josephson sign

- Notching near the nadir of the S-wave in V1 in V1 negative WCT…..suggestive of VT.

Kounis Syndrome

- The hypersensitivity reactions such as angioedema or anaphylactoid which induce allergic angina
or allergic MI secondary to mast cell degranulation with a surge in the serum concentration of
inflammatory mediators. This may present as…
• Unstable angina with normal ECG
• Non–ST-segment elevation MI with ST-segment depression, or symmetrical deep T-wave
inversions or STEMI

Lev's disease

- Lev's disease (or Lev-Lenegre syndrome) is an acquired complete heart block due to idiopathic
fibrosis and calcification of the electrical conduction system of the heart. Lev's disease is most
commonly seen in the elderly and is often described as senile degeneration of the conduction
system.

Marriott sign

- Notched downslope of the R wave in V1 in V1 positive WCT (the taller left rabbit
ear)….suggestive of VT.

McGinn-White Sign

- The McGinn-White Sign is the S1Q3T3 pattern seen on the ECG in the setting of acute
pulmonary embolism or other causes of acute right heart strain (cor pulmonale). A large S wave
in lead I, a Q wave in lead III, and an inverted T wave in lead III is the finding and only occurs in
about 10% of people with pulmonary embolism.

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Osborn Waves (J Wave)

- The Osborn wave (J wave) is a positive deflection at the J point.

- Characteristically seen in hypothermia (typically body temp < 32°C and are usually first seen in
leads II and V6)

Causes of Osborn waves in normothermic patients

- J wave syndrome (BrS or ERS)

- Hypercalcemia
- ACS including vasospastic angina
- After resuscitation of cardiac arrest
- Cocaine use
- Neurological insults such as intracranial hypertension, severe head injury and SAH
- Haloperidol or sedative drugs overdose
- Benign early repolarization(BER)

Pardee sign

- Upsloping convex STE during the acute phase of AMI, as described by Harold E.B. Pardee in his
original paper in 1920 is considered the typical morphology of a STEMI (“Pardee's sign”).

N.B. - In some STEMI case the STE segment may be seen as Tombstone-like or Shark fin-like
appearance

Spodick sign

- Appears in Stage I of Pericarditis and is a downsloping of the TP segment. It is said to be present

in up to 80% of cases of acute pericarditis and is best visualized in lead II and the lateral
precordial leads.

Wellens syndrome

Diagnostic criteria for Wellens syndrome:

- Deeply-inverted or biphasic T waves in V2-3 (may extend to V1-6)

- Usually has an upright T-wave in lead III
- Isoelectric or minimally-elevated ST segment (< 1mm)
- No precordial Q waves
- Preserved precordial R wave progression
- Recent history of angina and ECG pattern present in pain-free state
- Normal or slightly elevated serum cardiac markers
- There are two patterns of T-wave abnormality in Wellens’ syndrome:
• Type A = Biphasic, with initial positivity & terminal negativity (up and down pattern)
• Type B = Deeply and symmetrically inverted (75% of cases)

Yamaguchi syndrome

- The classic ECG finding in apical HCM is giant T-wave inversion in the precordial leads.

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V. References

Mattu, A. ECG’s for the Emergency Physician

Wagner, GS. Marriott’s Practical Electrocardiography

Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric

Goldberger, A. Goldberger's Clinical Electrocardiography

Bayés de Luna, A. Textbook of Clinical Electrocardiography

https://lifeinthefastlane.com/

http://hqmeded-ecg.blogspot.com/

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