c 2017 First Edition

Ayalew Zewde (MD, Assistant Prof. Emergency Medicine)

2nd EDITION 2017

All Right RESERVED

REVIEWERS AND EDITORS

Professor Amal Mattu, MD ,

Emergency medicine physician
Vice Chairman at University of Maryland Medical center

Gelila Mengistu, MD, Assistant professor of Emergency medicine

Chief Executive Officer at AaBET hospital

Finot Debebe, MD, Assistant professor Emergency medicine

Department head at Tikur Anbesa Specialized Hospital, AAU

1
ACKNOWLEDGMENT

Thanks for the Almighty God and St Mary before everything.

I would like to thank my family and beloved wife.I want to thank all
emergency residents and staff of SPHMMC/Addis Ababa Burn, Emer-
gency and Trauma hospital (AaBET) and Tikur Anbesa specialized
hospital.
Special thanks go to professor Amal Mattu for his review and encour-
agement in publishing this guide; to Dr Finot Debebe, Dr Gelila Mengis-
tu ,and Dr Alegnta Gebreyesus for their valuable suggestions and
encouragements.

Finally i would like to thank Mr dejene Tagesse and Addisalem Mindaye

for there motivation and facilitating printing process

Ayalew Zewdie Assistant professor of Emergency Medicine

Chief of Academic Affairs at AaBET hospital

Addis Ababa, Ethiopia

Dec 15, 2017

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ACRONYMS AND ABBREVIATIONS

AMI Acute myocardial infarction

BBB Bundle Branch Block
BER Benign early repolarization
BPM Beats per minute
ECG Electrocardiogram
ECHO Echocardiography
LAD Left anterior descending artery
LBBB Left bundle branch block
LCX Left circumflex artery
LVH Left ventricular hypertrophy
PE Pulmonary embolism
RBBB Right bundle branch block
RCA Right coronary artery
RVH Right ventricular infarction
STD ST depression
STEMI ST segment elevation myocardi
al infarction
Vtac Ventricular tachycardia
WPW Wolff Parkinson White
syndrome

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TABLE OF CONTENTS

REVIEWERS AND EDITORS...............................................................1

ACKNOWLEDGMENT.........................................................................2
ACRONYMS AND ABBREVIATIONS.................................................3
1.ECG INTERPRETATION STEPS.......................................................5
2.ECG LEAD .........................................................................................9
3.RHYTHM SINUS OR NOT..............................................................13
4. RATE.................................................................................................23
5. AXIS..................................................................................................24
6. WAVES..............................................................................................26
6.1. P WAVE..........................................................................................26
6.2. QRS COMPLEX............................................................................27
6.2.1. QRS WAVES...............................................................................28
6.2.2. WIDE QRS..................................................................................29
6.2.3. VOLTAGE...................................................................................35
6.3. T WAVE..........................................................................................38
6.4. U WAVE..........................................................................................41
7. SEGMENTS......................................................................................41
7.1. ST SEGMENT................................................................................41
7.1.1. ST SEGMENT ELEVATION......................................................42
7.1.2. ST DEPRESSION........................................................................47
7.2.PR SEGMENT.................................................................................48
8. INTERVALS......................................................................................49
8.1. PR INTERVAL...............................................................................49
8.1.1 PR INTERVAL PROLONGATION..............................................49
8.1.2. SHORT PR INTERVAL...............................................................51
8.2. QT INTERVAL...............................................................................52
8.2.1 QT PROLONGATION.................................................................52
8.2.2 SHORT QT INTERVAL...............................................................53
9. MISCELLANEOUS..........................................................................53
REFERENCES......................................................................................58

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1. ECG INTERPRETATION STEPS

STEP 1: DETERMINE RHYTHM

1.1 IS IT SINUS?
1.2 IS IT REGULAR?
STEP 2: DETERMINE RATE
STEP 3: DETERMINE AXIS
STEP 4: ASSESS WAVES P, QRS, T, U
4.1 ASSESS P WAVE
4.1.1 P-MITRALE
4.1.2 P-PULMONALE
4.2 ASSESS QRS
4.2.1 WIDTH OF QRS- NARROW/WIDE
4.2.2 VOLTAGE OF QRS –LOW/LVH /RVH
4.3 ASSESS T WAVE
4.3.1 PEAKED T WAVE
4.3.2 T WAVE INVERSION
4.4 ASSESS U WAVE
STEP 5: ASSESS SEGMENTS PR, ST SEGMENTS
5.1 ASSESS PR SEGMENT
5.1.1 PR DEPRESSION
5.1.2 PR ELEVATION
5.2 ASSESS ST SEGMENT
5.2.1 ST SEGMENT ELEVATION
5.2.2 ST SEGMENT DEPRESION
STEP 6: ASSESS INTERVALS
6.1 ASSESS PR INTERVAL
6.1.1 SHORT PR INTERVAL -WPW
6.1.2 PR PROLONGATION ---AV BLOCKS
1ST DEGREE
2ND DEGREE MOBITZ TYPE 1
2ND DEGREE MOBITZ TYPE 2
3RD DEGREE BLOCK
FASICULAR BLOCK
BI/TRI FASICULAR BLOC

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 6.2 ASSESS QT INTERVAL
6.2.1 SHORT QT INTERVAL
6.2.2 PROLONGED QT INTERVAL
STEP 7: FINAL INTERPRETATION

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 SINUS YES REGULAR=NSR

NO IRREGULAR =S ARRYTHMIA

RHYTHM ARRYTHMIA

RATE

AXIS P WAVE –PEAKED –P PULMONALE =RA ENLARGMENT

-WIDE/BIFID/BIPHASIC-P MITRALE=LA ENLARGT

WAVES QRS - DURATION ASSESMENT NARROW

WIDE >0.12 -BBB

-VOLTAGE ASSESSMENT LOW VOLTAGE

LVH

RVH

T WAVES –PEAKED

-INVERTED /BIPHASIC

U WAVE

ST SEGMENT ELEVATION

SEGMENTS DEPRESSION

PR SEGMENT ELEVATION

DEPRESSION

INTERVALS PR INTERVAL PROLONGATION >0.2ms -AV BLOCKS

SHORT -WPW

QT INTERVAL SHORT-HYPERCALCEMIA

PROLONGED >0.5

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FIGURE 1.ECG interpretation steps

PATIENT ECG RCORD

i) PATIENT NAME ________________AGE___ SEX _______

ii) RHYTHM 1. SINUS NOT SINUS 2. REGULAR IRREGULAR
iii) RATE _____BPM
iv) AXIS A.NORMAL B.LEFT C. RIGHT D.EXTREME RIGHT
v) P WAVE A. NORMAL B. PEAKED C. WIDE/BIFID
D. BOTH PEAKED AND WIDE
vi) QRS 1. INTERVAL A. NARROW COMPLEX B. WIDE
2. VOLTAGE A. LOW B. LVH C. RVH D.NORMAL
vii) T WAVE A. NORMAL B. PEAKED C. INVERTED D. FLAT
viii) U WAVE A. YES B. NO
ix) ST SEGMENT A. ELEVATION ________ leads
B. DEPRESSION____________ leads C.NORMAL
x) PR SEGEMTNT A. ELEVATION __________ leads
B. DEPRESSION____________ leads C.NORMAL
xi) PR INTERVAL______ msc A. SHORT B. LONG C.NORMAL
xii) QT INTERVAL __________msc A. NORMAL B. LONG
C. SHORT
xii INTERPRETIATION
___________________________________________________________
___________________________________________________________
__________________________________________________

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2. ECG LEAD

LEADS PLACEMENT

Limb leads
Electrodes are placed on the right arm (RA), left arm (LA), right leg
(RL), and left leg (LL). With only four electrodes, six leads are viewed.
■ Standard leads and view of the heart: I-ateral, II and III-inferior
■ Augmented leads and : aVR-none, aVL-lateral, aVF -inferior

Figure 2. Limb leads and augmented leads

9
Chest leads placement and view of the heart
V1- 4th Intercostal space right of sternum-towards septum
V2 4th Intercostal space left of sternum-towards septum
V3 Directly between V2 and V4 -Anterior
V4 5th Intercostal space left mid-clavicular line-anterior
V5 Level with V4 at left anterior axillary line-lateral
V6 Level with V5 at left mid-axillary line-lateral
A 15-lead ECG, which includes the standard 12 leads plus leads V4R,
V8, and V9, increases the chance of detecting an MI in these areas.
V4R 5th Intercostal space in right anterior mid-clavicular line- Right
ventricle
V8 Posterior 5th intercostal space in left mid-scapular line of left ventri-
cle- Posterior wall
V9 Directly between V8 and spinal column at posterior 5th intercoastal
space of left ventricle- Posterior wall
The 12 'leads' that make up the standard ECG look at' the heart from
different directions. Each cycle of depolarization looks different in each
of the 12 leads because:
• depolarization spreading towards a lead causes an upward deflec tion
• depolarization spreading away from a lead causes a downward deflec
tion.

ECG PAPER

ECG paper is graph paper with horizontal and vertical lines at 1mm inter-
vals and a heavier line every 5mm. This creates 1mm and 5mm squares
used to measure the amplitude and duration of cardiac depolarizations and
repolarizations. Wave deflection (positive and negative) is measured
along the vertical axis and is expressed in millimeters. The usual calibra-
tion is that a 1mV signal produces a 10mm deflection. Time is measured
along the horizontal axis. With a paper speed of 25mm per second, 1 mm
= 0.04 seconds and 5mm = 0.2 seconds.

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 Figure 3. ECG paper

COMPONENTS OF ECG

The P wave represents atrial depolarization. The PR interval represents

the time needed for a sinus impulse to conduct through the atria and AV
node and reach the ventricles. Next, the depolarization of the ventricles
creates the QRS complex, followed by the ST interval and the T wave of
ventricular repolarization. Therefore, the QT interval is an indicator of
ventricular depolarization and repolarization. Atrial repolarization is
hidden within the QRS complex and cannot be visualized on an ECG.The
U wave represents late ventricular repolarization and is not always visual-
ized

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 Figure 4. The components of ECG

Important Normal ECG Intervals and Parameters

P waves <3 small squares (0.12 second) in duration, and amplitude <3
mm. Upright in lead I, II, inverted in aVR (if opposite, suspect reversed
arm leads or dextrocardia)

PR interval 0.12 to 0.2 second (up to 0.22 second in adults).

QRS duration 0.05 to 0.1 second;

≥0.1 second, consider incomplete LBBB, incomplete RBBB, or WPW
syndrome
Q waves Normally present in aVR; occasionally in V1 or in aVL(vertical
heart)
Often present in lead III: should be ≤0.04 second duration.
Other leads except lead I: <0.04 second duration and ≤3 mm deep; lead I
≤1.5 mm in patients older than age 30.
Q waves may be up to 5 mm deep in several leads in individuals age <30.

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R waves V1: 0 to 15 mm, age 12 to 20
0 to 8 mm, age 20 to 30.
0 to 6 mm, age >30.
V2: 0.2 to 12 mm, age <30
V3: 1 to 20 mm, age <30.

ST segment Isoelectric or <1 mm elevation in limb leads and <1 mm in

precordial leads except for normal variant

T wave Inverted in aVR; upright in I, II, and V3 through V6.

Variable in III, aVF, aVL, V1, and V2

3.RHYTHM SINUS OR NOT

SINUS

In order for a rhythm to be considered sinus, a P wave must precede each

QRS complex, each P wave must be followed by QRS with a normal P
axis (+30 to +90˚).P wave should be +ve in lead I,II and aVF and – ve
deflection in aVR
A sinus rhythm and the heart rate is within the normal range, the heart
rhythm is designated normal sinus rhythm (NSR).
If the heart rate is above the normal range for age, the patient is in sinus
tachycardia and if the rate is below the normal range for age, the patient
is in sinus bradycardia.
If the heart rate (RR interval) seems to vary from beat to beat, especially
with respiration, and the rhythm otherwise looks normal, the patient is
likely in sinus arrhythmia

Non-sinus Rhythms:
At times of SA node failure or conduction block, an atrial, AV junctional,
or ventricular pacemaker can exhibit automaticity and initiate cardiac
depolarization called ectopic rhythm

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ARRYTHMIA

Are normal P waves present?

Are the QRS complexes narrow or wide?
What is the relationship between the P waves and the QRS complexes?
Is the rhythm regular or irregular?
RYTHM

SINUS

YES NO

REGULAR IRREGULAR ARRYTHMIA

RATE

SINUS RHYTHM SINUS ARRYTHMIA TACHYARRYTHMIA BRADY ARRYTHMIA

Figure 5 . Tachycardia classification. AVnRT = atrioventricular nodal reentrant tachycardia;

AVRT = atrioventricular reentrant tachycardia; VT = ventricular tachycardia

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 1. ECTOPIC ATRIAL RHYTHMS

Atrial arrhythmias are characterized by an abnormal P wave axis and

morphology

1.1 WANDERING ATRIAL PACEMAKER

The P’ wave morphology and the PR interval will change with each cardi-
ac cycle.

Figure 6. WAP

1.2 PREMATURE ATRIAL CONTRACTION (PAC)

When a beat is initiated prematurely by atrial tissue before the regular

sinus beat is due the PP interval is shortened due to the early beat and the
P’ wave morphology will depend on the site of the ectopic atrial focus

Figure 7 . Premature atrial contractions in an atrial trigeminy pattern.

1.3 PSVT- PAROXYSMAL SUPRAVENTRICULAR TACHYCAR DIA

ECG Features of Paroxysmal Supraventricular Tachycardia

• Absence of normal (sinus-mediated) P waves with normal PR interval

• Rare retrograde P wave (usually inverted P wave and immediately adja
cent to QRS complex,pre or post)
• Narrow QRS complex, usually <100 ms in duration
• Ventricular rate usually 170–180 beats/min; the rate can range from as
low as 130 beats/min to as high as 300 beats/min

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Figure 8. PSVT

1.4 ATRIAL FLUTTER /ATRIAL FIBRILATION

The ECG hallmarks of atrial fibrillation

• the absence of discernible P waves
• narrow QRS and
• an irregularly irregular ventricular rhythm
Causes of atrial fibrillation
x Ischaemic heart disease x Hypertensive heart disease
x Rheumatic heart disease x Thyrotoxicosis
x Alcohol misuse (acute o rchronic) x Cardiomyopathy (dilated or
hypertrophic)
x Sick sinus syndrome x Post-cardiac surgery
x Chronic pulmonary disease x Idiopathic (lone)

Figure 9. Atrial fibrillation

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ECG Features of Atrial Flutter
• Identifiable P waves
• Single morphology
• Negative amplitude (“flutter waves” in “sawtooth
pattern”) best seen in inferior ECG leads and V1
• Atrial rate is regular, usually at 300 beats/min
• QRS complexes narrow unless preexisting bundle-branch block
• Ventricular rate regular although occasional irregularity can be seen
• Ventricular rate often 150 beats/min= atrial flutter with 2:1 conduction

Figure 10. Atrial flutter

1.5 MULTIFOCAL ATRIAL TACHYCARDIA

This is form of wandering atrial pacemaker (WAP) is associated with a

ventricular response of>100 bpm. MAT is commonly seen in patients
with COPD

ECG Features of Multifocal Atrial Tachycardia

• At least 3 distinct P-wave morphologies in a single ECG lead

• No consistent P to P, PR, or R to R intervals
• Irregularly irregular rhythm with rates usually 100–180 beats/min
• Normal QRS complex unless preexisting bundle-branch blocks
• Frequently confused with atrial fibrillation or flutter

Figure 11 . Multifocal atrial tachycardia. Note multiple P-wave morphologies with irregular
tachycardia rhythm.

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1.6 SICK SINUS SYNDROME

ECG Features of Sick Sinus Syndrome

• Intermittent combination of bradydysrhythmias and tachydysrhyth
mias
• Bradydysrhythmias
• Sinus bradycardia
• Sinus arrest
• SA block
• Tachydysrhythymias
• Atrial fibrillation
• Atrial flutter
• Paroxysmal supraventricular tachycardia

2. AV JUNCTIONAL RHYTHMS- Rhythms originating from the AV

junction

ECG Features of Junctional Rhythm

• Absence of normal (sinus-mediated) P waves with normal PR interval

• Rare retrograde P wave (usually an inverted P wave and immediately
adjacent to QRS complex, pre or post)
• Narrow QRS complex
• Regular rate

JUNCTIONAL RHYTHM =Ventricular rate between 40 and 60

beats/min for

ACCELERATED JUNCTIONAL RHYTHM = Ventricular rate

between 60 and 100 beats/min for

JUNCTIONL TACHYCARDIA = Ventricular rate >100 beats/min

for

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 Figure 12. Junctional rhythm with absent P waven and rate of 90

3. VENTRICULAR RHYTHMS- have large, wide QRS complexes

3.1 A PREMATURE VENTRICULAR CONTRACTION (PVC) is

characterized by a large amplitude, wide QRS complex that occurs before
the expected sinus beat in a regular rhythm. There is no P wave and the T
wave points in the opposite direction as the QRS.

If a PVC alternates with a normally conducted beat, the rhythm is called

ventricular bigeminy. If a PVC follows two regular QRS complexes, the
rhythm is called ventricular trigeminy.

Figure 13. Premature ventricular contractions producing ventricular bigeminy.

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THE RULES OF MALIGNANCY:PVCS

• Frequent PVCs
• Runs of consecutive PVCs, especially three or more in a row
• Multiform PVCs, in which the PVCs vary in their site of origin and
hence in their appearance
• PVCs falling on the T wave of the previous beat, called the “R-on-T”
phenomenon. The T wave is a vulnerable period in the cardiac cycle,
and a PVC falling there appears to be more likely to set off ventricular
tachycardia.
• Any PVC occurring in the setting of an acute myocardial infarction

Figure 14. Sinus rhythm in an ST-segment elevation myocardial infarction patient with a prema-
ture ventricular contraction (PVC) initiating ventricular tachycardia. Note the R wave (large
arrow) of a PVC falling on the T wave (small arrow) of the last sinus beat. This R-on-T event
produces ventricular tachycardia.

3.2 VENTRICULAR TACHYCARDIA- regular wide QRS tachycar-

dia, >3 PVCs at rate of 120-180
Surface ECG criteria for ventricular tachycardia include the following:
• Atrioventricular dissociation
• QRS axis between -90° and +180°
• Positive QRS concordance (positive QRS Vl-V6)
• QRS duration of 140 msec or more with right bundle branch block
pattern and 160 msec or more with left bundle branch block pattern
• Combination of left bundle branch block pattern and right axis
• Monophasic or biphasic QRS complex with right bundle branch block
pattern and slurred or prolonged S wave in V1 with left bundle branch
block morphology

20
• Fusion beats ,capture beats

Non sustained vs sustained Vtac

The term nonsustained designates spontaneous termination of ventricular

tachycardia in less than 30 seconds. The term sustained ventricular tachy-
cardia is used when the episodes are longer or require immediate interven-
tion for termination

ECG Features of Monomorphic and Polymorphic Ventricular Tachy-

cardia

•• Monomorphic
• No P waves associated with QRS complex, occasional dissociated
wave
• Rapid and regular rhythm
• Rate usually 140–180 beats/min (range, 120–300 beats/min)
• Widened QRS complex >100–120 ms with consistent beat-to-beat
morphology
•• Polymorphic
• No P waves associated with QRS complex; may have occasional
dissociated P wave
• Rapid and irregular rhythm
• Rate 140–180 bpm (range, 120–300 beats/min)
• Widened QRS complex >100–120 ms with inconsistent
beat-to-beat morphology

Figure 15. Ventricular tachycardia with a rate of 180 beats/min

21
Figure 16. Polymorphic ventricular tachycardia of the torsade de pointes subtype, with the charac-
teristic pattern of progressively changing QRS complex amplitude and direction

When in doubt, it is safer to assume a new and symptomatic wide-com-

plex tachycardia is ventricular in origin .

3.3 VENTRICULAR FIBRILLATION- an irregular pattern in which

the QRS complexes vary in size and configuration

Figure 17. Ventricular fibrillation

3.4 IDEOVENTRICULAR RHYTHM –wide QRS with rate of 20-40

,no P waves
ACCELERATED IDEOVENTRICULAR RHYTHM-Rates of
40-100 beats/min are usual.

Figure 18. Idioventricular rhythm with a ventricular rate of approximately 30 beats/min.

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Pathological causes of bradycardia

DIE-DRUGS, ISCHEMIA, ELECTROLYTES

x Acute myocardial infarction
x Drugs—for example, B blockers, digoxin, amiodarone
x Obstructive jaundice
x Raised intracranial pressure
x Sick sinus syndrome
x Hypothermia
x Hypothyroidism

4. RATE

For regular rhythm: start with a complex that lies on a bold vertical grid
line.The memorization of the sequence 300 – 1 50 – 100 – 75 – 60 – 50
between R-R interval on successive heavy black lines (5 mm intervals)

Figure 19.Rate based on boexes.

23
Rate = 300 bpm ÷ number of large boxes (0.2 second) in one RR interval.
= 1500÷number of small boxes in one RR interval
For irregular rhythm
Count the number of QRS complexes in two of 3-second periods (6
seconds) and multiply by 10 or Count the number of QRS complexes in 10
second period and multiply by 6

5. AXIS

Table 2. Axis determination

Axis Lead I Lead AVF

Normal axis Positive Positive
Left axis deviation Positive Negative
Right axis deviation Negative Positive
Extreme right axis deviation Negative Negative

Conditions for which determination of the axis is helpful in diagnosis

• Conduction defects—for example, left anterior hemiblock

• Ventricular enlargement—for example, right ventricular hypertrophy
• Broad complex tachycardia—for example, bizarre axis suggestive of
ventricular origin
• Congenital heart disease—for example, atrial septal defects
• Pre-excited conduction forexample, Wolff-Parkinson-White syndrome
• Pulmonary embolus

Conditions associated with right axis deviation

• Right ventricular hypertrophy

• Left posterior hemiblock
• Lateral myocardial infarction
• Acute right heart strain-Pulmonary embolus

Right axis deviation is normal in infants and children

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Conditions associated with left axis deviation

• Left anterior hemiblock

• Left ventricular hypertrophy
• Left bundle branch block
• Inferior MI
• Ventricular ectopy
• Paced rhythm
• WPW

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6. WAVES

6.1. P WAVE

Characteristics of the P wave

• Positive in leads I and II

• Best seen in leads II and V1
• Commonly biphasic in lead V1
• < 3 small squares in duration
• < 2.5 small squares in amplitude

Right atrial enlargement features:

• High amplitude, peaking : tall, pointed P waves, taller in lead III

than in lead I; high amplitude (≥2.5 mm), particularly in lead II, III,
or aVF
• The classic picture of right atrial enlargement has been called P
pulmonale, because it is often caused by severe lung disease.

Left atrial enlargement is characterized by the following:

• The amplitude of the terminal (negative) component of the P wave

may be increased and must descend at least 1 mm below the isoelec
tric line in lead V1.
• The duration of the P wave is increased, and the terminal (negative)
portion of the P wave must be at least 1 small block (0.04 seconds)
in width.
• No significant axis deviation is seen because the left atrium is
normally electrically dominant
• The electrocardiographic picture of left atrial enlargement has been
called P mitrale because mitral valve disease is a common cause of
left atrial enlargement

26
Large diphasic in V1: if the first half of the P wave is positive ≥1.5 mm
and the second half is negative ≥1 mm and wide, consider biatrial
enlargement
Absent P waves: consider SA block and AV junctional rhythms.If the
rhythm is irregular, consider atrial fibrillation

Figure 20.P wave abnormality approach

6.2. QRS COMPLEX

The QRS complex represents ventricular depolarization. It is usually

predominantly positive in most lateral and inferior leads. Across the
precordium, the R waves increase in size, progressing from V1 to V5. A
small initial Q wave, representing septal depolarization, can often be seen
in the left lateral and inferior leads.

27
6.2.1. QRS WAVES

Q WAVE

Normal Versus Pathologic Q Waves

Small Q waves can be seen in the left lateral leads (I, AVL, V5, and V6) and
occasionally in the inferior leads (especially II and III) of perfectly normal
hearts. These Q waves are caused by the early left-to-right depolarization
of the interventricular septum

Pathologic Q waves signifying infarction tend to be wider and deeper.

They are often referred to as significant Q waves.

The criteria for significance are as follows:

• The Q wave must be greater than 0.04 seconds in duration.
• The depth of the Q wave must be at least one third the height of
the R wave in the same QRS complex
• There are several Q wave equivalents seen in the precordial leads.
These include
(1) R wave diminution or poor R wave progression;
(2) reverse R wave progression, in which R waves increase then
decrease in amplitude across the precordial leads (although this
must be distinguished from precordial electrode misconnection); &
(3) Tall R waves in leads V1 and V2, representing ‘‘Q waves’’ of
posterior infarction

R WAVE

The height of the R wave is variable and increases progressively across the
precordial leads; it is usually < 27 mm in leads V5 and V6. The R wave in
lead V6, however, is often smaller than the R wave in V5, since the V6
electrode is further from the left ventricle.

28
Causes of Tall R Waves in V1 and V2

1. Thin chest wall or normal variant, age <20, early transition

2. Right bundle branch block
Note: Slurred S wave in leads I, V5, and V6
3. Right ventricular hypertrophy
No slurred S wave in leads I, V5, & V6
4. Wolff-Parkinson-White syndrome
5. True posterior infarction
Note: Associated inferior MI, no slurred S in V5 and V6, and T upright in
V1 and V2
6. Hypertrophic cardiomyopathy
7. Duchenne muscular dystrophy
8. Low placement of leads V1 and V2
9. Dextroposition
The S wave is deepest in the right precordial leads; it decreases in ampli-
tude across the precordium, and is often absent in leads V5 and V6

6.2.2. WIDE QRS

The common causes of a wide QRS complex are

(1) Aberrant ventricular conduction (bundle branch block);
(2) Ventricular ectopy/ventricular tachycardia;
(3) Ventricular paced beats;
(4) Ventricular pre-excitation syndromes (eg, Wolff Parkinson White
syndrome);
(5) Left ventricular hypertrophy;
(6) Nonspecific intraventricular conduction delay;
(7) Hypothermia;
(8) Hyperkalemia; and
(9) Drug toxicity (primarily sodium channel blockers, eg, cyclic antide
pressants, cocaine)

29
Figure 21. Approach to wide QRS interval

Left Bundle Branch Block

■ QRS >0.10 sec

■ QRS predominantly negative in leads V1 and V2
■ QRS predominantly positive in V5 and V6 and often notched
■ Absence of small, normal Q waves in I, aVL, V5, and V6
■ Wide monophasic R waves in I, aVL, V1, V5, and V6

30
 Figure 22 .Left bundle branch block

• A presumptive diagnosis of incomplete LBBB may be mad0e if the QRS

duration is 0.10 to 0.11 second with notching of the R wave in V5 or V6.

Right Bundle Branch Block

■ QRS >0.10 sec
■ QRS normal or deviated to the right
■ Slurred S wave in leads I and V6
■ RSR’ pattern in lead V1 with R’ taller than R
• The axis may be normal, right, or left. If left axis is present, consider
left anterior fascicular block (hemiblock)

Figure 23. An rSR′ in V 1 ; M-shaped complex in V1 and V 2 ; QRS duration≥0.12 second;

and wide, slurred S waves in V5 and V 6 indicate right bundle branch block (RBBB)

31
CONDITIONS ASSOCIATED WITH R IGHT BUNDLE BRANCH
BLOCK
x Rheumatic heart disease x Cor pulmonale/right ventric
ular hypertrophy
x Myocarditis or cardiomyopathy x Ischaemic heart disease
x Degenerative disease of the conduction system x Pulmonary embolus
x Congenital heart disease—for example, in atrial septal defects

BRUGADA SYNDROME

Typical features

Atypical, incomplete right bundle branch block with a curious (odd shape)
ST segment elevation / deformity in V1 to V 3 , described as the coved (in
V1 , V2 ) and saddle-back patterns (V3 )
Two types of STE morphologies have been described:
Convex upwards (coved)and
Concave upwards (saddle-type

32
 Figure 24 .Right bundle branch block

ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA,

Another rare condition that shows an atypical RBBB pattern, is a

marker for sudden cardiac death in younger individuals

Figure 25. Normal sinus rhythm in a patient with arrhythmogenic right ventricular dysplasia.The
arrowheads point to late right ventricular activation called an epsilon wave. (From Braunwald
E:Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed., Philadelphia, 2001, WB
Saunders, Elsevier Science.

HEMIBLOCK

LEFT ANTERIOR HEMIBLOCK

• Normal QRS duration and no ST segment or T wave changes

• Left axis deviation between -30° and +190°
• No other cause of left axis deviation is present.

33
 Figure 26.Left anterior fasicular block

LEFT POSTERIOR HEMIBLOCK

• Normal QRS duration and no ST segment or T wave changes

• Right axis deviation
• No other cause of right axis deviation is present.

Figure 27. Left posterior fasicular block

BIFASCICULAR BLOCK-refers to the combination of either left ante-

rior or left posterior hemiblock with right bundle branch block.

TRIFASCICULAR BLOCK -The combination of first degree block

and bifascicular block is sometimes called (perhaps inaccurately) trifas-
cicular block

34
Figure 28. Trifascicular block • PR interval 280 ms • Left axis deviation • Broad QRS complexes
• RSR1 pattern in V1]

6.2.3. VOLTAGE

Assess for right ventricular hypertrophy (RVH).

(1) R wave in V1 ≥7 mm†
(2) S wave in V5 or V6 ≥7 mm
(3) R/S ratio in V1 ≥1
(4) R/S ratio in V5 or V6 ≤1
(5) Right axis deviation ≥ +110°Any two of above = RVH likely
(6) Specificity increased if ST depression and T wave inversion in V1 to
V3 or right atrial hypertrophy

35
Figure 29 . Leads V1 through V6 : A tall R wave in V 1 , R/S ratio in V1 >1, and R/S ratio in V5
or V 6 <1 are features of right ventricular hypertrophy

Assess for left ventricular hypertrophy (LVH).*

Voltage Criteria
• R wave in lead IS wave in lead III 25 mm (2.5 mV)
• R wave in aVL 11 mm (1.1 mV)
• R wave in V6 26 mm (2.6 mV)
• R wave in V6 S wave in V1 >35 mm (3.5 mV)-49% sensitivity and a
specificity of approximately 90%.
• Left axis is supportive of LVH but is not necessary for the diagnosis.
• Onset of intrinsicoid deflection in V5 or V6 >0.05 second
• Specificity increased to ≈98% in presence of (a) Left atrial enlarge
ment or (b) ST segment depression and T wave inversion (strain
pattern) in V5 or V6

Figure 30.Note that the standardization at half voltage in V1 through V6 is markedly increased;
ST-T strain pattern in V5 and V6 and left atrial enlargement are typical features of left
ventricular hypertrophy

36
LOW VOLTAGE

Criteria for Low-Voltage QRS

• In all limb leads, the amplitude of the entire QRS complex (R + S) is <5
mm.
• In each of the precordial leads, the amplitude of the entire QRS complex
(R + S) is <10 mm
• Voltage sum of .I+II+III<15
• Voltage sum of V1+V2+V3< 30
Causes of Low-Voltage QRS
• Obesity • Pericardial effusion
• Constrictive pericarditis • Myxedema
• Amyloidosis and other restrictive cardiomyopathy and diffuse myocardial
diseases
• Pleural effusion • COPD

Figure 31.LOW VOLTAGE The ECG shows first-degree atrioventricular block. There is low
voltage of the P waves and the QRS complexes, with abnormal left-axis deviation. The T waves are
inverted in leads V1 through V3. (From Chou TC: Electrocardiography in Clinical Practice, 4th ed.,
Philadelphia, 1996, WB Saunders, Elsevier Science.)

37
6.3. T WAVE
The T wave represents ventricular repolarization.
The amplitude, or height, of a normal T wave is one third to two thirds that
of the corresponding R wave. The T wave is always upright (positive) in
leads I , II , and V4 through V6
The most important thing to remember about the T wave is in which leads
it may be inverted in normal people:
• aVR
• V1 and sometimes V2
• other chest leads in black people
T wave inversion in other leads may be associated with:
• Bundle branch block
• Ventricular origin of depolarization
• Ischaemia
• Ventricular hypertrophy
• Drugs .
Diffuse, deep T wave inversion in the absence of ST segment elevation or
significant depression is not diagnostic and can be associated with the
following:
• Ischemia • Post-MI evolutionary changes
• Left ventricular hypertrophy with or without ischemia
• Post–Stokes-Adams attack
• Post–supraventricular tachycardia or ventricular tachycardia
• Myocarditis • Pericarditis
• Apical cardiomyopathy (causes giant T wave inversion)
• Pulmonary embolism • Cardiomyopathies
• Primary or secondary cardiac tumors • Cocaine abuse
• Alcohol abuse

38
• Electrolyte imbalance
• Subarachnoid hemorrhage
• Acute pancreatitis and gallbladder disease
• Pheochromocytoma

Figure 32.T wave inversions

Wellen’s syndrome

Refers to history of recent angina with T-wave inversion in the LAD distri-
bution, particularly V2–V4, in the presence of persistent R waves =specif-
ic for critical stenosis of the LAD=High risk for extensive anterior wall MI
next few days and weeks
Type A=Biphasic, with initial positivity and terminal negativity (25%)
Type B=deeply and symmetrically inverted (75%)

Figure 33. Wellen’s syndrome

39
Peaked T waves are often normal, but can be due to Hyperkalemia,
ischemia
T waves that are >6 mm in the limb leads or >10 mm in the precordial
leads may occur as follows:
• In V2 through V5 in some normal individuals. Note the base of
normal peaked T waves is not narrow, as it is with hyperkalemia.
Peaked T waves occasionally may be associated with ST elevation
occurring as a normal variant
Hyperkalemic T waves tend to be tall, narrow, and peaked with a prom-
inent or sharp apex. Also, these T waves tend to be symmetric in mor-
phology. Conversely, the hyper acute T waves of early AMI are often
asymmetric with a broad base

Figure 34. Peaked T wave in hyperk

Severe myocardial ischemia or acute MI (hyper acute T waves may occur).

• Hyperkalemia
• Left ventricular overload, as in severe mitral regurgitation.
• Cerebrovascular accidents.

Figure 35.Causes for T wave abnormalities

40
De Winter’s T waves
- ST depression and peaked T waves in precordial leads
- is anterior STEMI equivalent that presents without obvious ST
segment elevation
ECG features
• Tall ,prominent ,symmetric T waves in precordial leads
• Upslopping ST depression >1mm at the J point in precordial leads
• ST segment elevation (0.5-1mm) in aVR
• Absence of ST elevation in other leads

6.4. U WAVE

The U wave is a small deflection that follows the T wave.It is generally

upright except in the aVR lead and is often most prominent in leads V2
to V4. U waves result from repolarisation of the mid-myocardial cells
that is, those between the endocardium and the epicardium and the
His-Purkinje system. Many electrocardiograms have no discernible U
waves. Prominent U waves may be found in athletes and are associated
with hypokalaemia and hypercalcaemia (See figure 49)

7. SEGMENTS

7.1. ST SEGMENT

The ST segment represents the time from the end of ventricular depolar-
ization to the start of ventricular repolarization. The QRS complex termi-
nates at the J point or ST junction Segments reference is the isoelectric
line which is the TP segment

41
Figure 36.ST segment and reference line TP segment

7.1.1. ST SEGMENT ELEVATION

ST elevation ≥1 mm (0.1 mV)

CAUSES OF STE

• STEMI Left ventricular aneurysm

• Cardiomyopathy BER - Benignearly repolarization Pacer
• Myocarditis Pericarditis
• Ventricular ectopy
• Post electrical cardio version LVH Brugada syndrome.
• Cardiac contusion BBB (LEFT, RIGHT)
OTHERS: PE, Hyperkalemia, Stroke, hypothermia STEMI VS BER VS
PERICARDITIS
• ST MORPHOLOGY,PR SEGMENT
• OLD ECG
• ECHO
• CATHLAB

STEMI

ST elevation ≥1 mm (0.1 mV) in two or more contiguous ECG leads in a

patient with chest pain indicates STEMI.
-Morphology – Convex
-Anatomical
-Associated reciprocal change

42
 Table 3. Location of MI by ECG leads

Table 4. ST elevation, Location of STEMI and corresponding artery

43
 Figure 37. Evolution of inferior STEMI ,lead III

INFERIOR FAMILY OF MI´S

• Inferior MI: Q waves and evolving ST-T changes in leads II, III, aVF
• True posterior MI: ECG changes are seen in anterior precordial leads
V1-3, but are the mirror image of an anteroseptal MI. Often seen with
inferior MI
• Right Ventricular MI (only seen with proximal right coronary occlu
sion). ECG findings usually require additional leads on right chest, V4R
Suspect if ST elevation III>II

STE in aVR-The “missed lead”

STE in aVR ≥1mm demonstrates
• Left main coronary artery occlusion= STE in aVR≥V1,wide
spread ST depression
• Proximal left anterior descending artery (LAD) occlusion
• Severe triple –vessel disease
• Diffuse sub endocardial ischemia
Prognostic features of ST segment elevation-decreasing order of impor-
tance
(1) anterior location, compared with inferior or lateral ;
(2) total ST deviation or the absolute sum of STE and STD ;
(3) ST score (the sum of all STE) greater than 1.2 mV (12 mm) (these last
two features each take into account the prognostic effects of greater
height of ST segments and greater number of leads involved) ; and

44
(4) distortion of the terminal portion of the QR S (loss of S-wave in leads
with RS configuration, or J point R 50% the height of the R wave)

The Sgarbossa criteria for acute ST segment myocardial infarction with

coexisting left bundle branch block are
(1) ST segment elevation ≥ 1 mm concordant to QRS complex; 5point
(2) ST segment depression ≥ 1 mm in leads V1, V2, or V3 (concordant to
QRS complex); and 3 point
(3) ST segment elevation ≥ 5 mm discordant to QRS complex.2 point –
Modified sgarbosa-ST segment elevation/S wave ≥0.25

Benign early repolarisation characteristic electrocardiographic features:

• Elevation of the J point above the isoelectric line, with high take-off
of the ST segment;
• A distinct notch at the junction of the R wave and S wave, the J point;
• An upward concavity of the ST segment; “smiley face” and
• Symmetrical, upright T waves, often of large amplitude

Figure 38-Benign early repolarization

PERICARDITIS

• The ST segment elevation is diffuse rather than localised

• The elevated ST segments are concave upwards,
• The absence of widespread reciprocal change,
• The presence of PR segment depression, and
• Absence of Q waves

45
The electrocardiographic abnormalities evolve through four classic stages
Stage I is characterized by STE, prominent T waves, and (in most cases)
PR segment depression.
Stage II is characterized by a normalization of the initial abnormalities,
namely a resolution of the STE.
Stage III involves T wave inversion, usually in the same distribution
where STE was encountered.
Stage IV is a normalization of all changes with a return to the baseline
ECG.
Persistent STE and pathologic Q waves are not encountered in patients
who have myopericarditis these electrocardiographic findings suggest
another etiology.

LV ANEURYSM

In patients who have ventricular aneurysm , significant Q waves are

observed in the same distribution as the STE. If the ratio of the amplitude
of the T wave /QRS complex exceed s 0.36 in any single lead, the ECG
likely reflects AMI. If this ratio is less than 0.36 in all leads, however, the
findings are likely caused by LV ANEURYSM

Figure 39. Features of LV aneurysm

46
7.1.2. ST DEPRESSION

Causes of ST Segment Depression

■ Myocardial ischemia ■ Left ventricular hypertrophy

■ Intraventricular conduction defects ■ Medication (e.g., digitalis)
■ Reciprocal changes in leads opposite the area of acute injuryPAILS
- Reciprocal STD is defined as depression in leads anatomically
opposite, or near-opposite, to those with STE

Causes of Nonspecific ST-T Wave Changes

Nonspecific ST-T wave changes can be caused by a number of conditions,

such as the following:
• Improper electrode contact
• Ischemia
• Electrolyte abnormalities
• Arrhythmias
• Myocarditis
• Pericarditis, constrictive pericarditis
• Intraventricular conduction defects
• Cardiomyopathy
• Pulmonary embolism
• Drink of cold water
• Hyperventilation
• Drug use, including ethanol abuse
• Digoxin
• Subarachnoid hemorrhage or cerebral hemorrhage

ISCHEMIA

Primary STD is ECG sign of subendocardial ischemia, and in the context

of ACS, indicates UA/NSTEMI
ST segment depression indicative of definite myocardial ischemia should
fulfill the following criteria:
• Greater than 1 mm depression.

47
• Present in two or more leads.
• Present in two or more consecutive QRS complexes.
• Flat (horizontal) or down-sloping with or without T wave inversion
• Abnormal convex coving of the ST segment in V1 through V3 or V2
through V4 associated with T wave inversion.

Figure 40. Flat (horizontal) and down-sloping ST segment depression greater than 1 mm in a
patient with proven angina and obstructive coronary artery disease

7.2. PR SEGMENT

PR segment depression except in aVR is associated with pericarditis.-

Look for associated features for pericardits

PR segement depression in inferior leads with reciprocal PR segment

elevation in lead I or aVR is used as one of diagnostic criteria for atrial
infarction

Diagnostic criteria for atrial ischemia or infarction-Liu’s criteria

• PR elevation>0.5 mm in V5 &V6 with recipirocal PR depression in

V1&V2
• PR elevation >0.5 mm in lead I with reciprocal PR depression in leads II
&III
• PR depression >1.5 mm in the precordial leads
• PR depression > 1.2 mm in leads I,II,&III
• Abnormal P wave morphology -M,W shaped

48
8. INTERVALS

8.1. PR INTERVAL

The PR interval represents the time from the start of atrial depolarization
to the start of ventricular depolarization.

8.1.1 PR INTERVAL PROLONGATION

AV BLOCK

The diagnosis of first-degree AV block requires only that the PR interval

be longer than 0.2 seconds,

Figure 41.First degree AV block

Mobitz type I second-degree AV block, more commonly called

Wenckebach block .What you see on the EKG is a progressive lengthen-
ing of the PR interval with each beat and then suddenly a P wave that is
not followed by a QRS complex (a dropped beat).

Figur 42.Second degree Mobitz type I AV block

49
Mobitz Type II Block requires the presence of a dropped beat without
progressive lengthening of the PR interval

Figure 43. Second degree Mobitz type II AV block

Figure 44. Second degree block (2:1)

Third-Degree AV Block

requires the presence of AV dissociation in which the ventricular rate is

slower than the sinus or atrial rate. A narrow QRS complex indicates that
the rhythm originates within the His bundle itself below the block, but a
wide QRS complex indicates that ventricular depolarization originates
in the Purkinje system
A

50
 B

Figure 45. A,B-3rd degree AV block.

8.1.2. SHORT PR INTERVAL

Criteria for WPW Syndrome

• PR interval less than 0.12 seconds
• Wide QRS complexes
• Delta wavseen in some leads.
In type A, the delta wave and QRS complex are predominantly upright in
the precordial leads. The dominant R wave in lead V1 may be misinter-
preted as right bundle branch block.
In type B, the delta wave and QRS complex are predominantly negative
in leads V1 and V2 and positive in the other precordial leads, resembling
left bundle branch block

Figure 46. WPW type A and type B .

51
Criteria for LGL Syndrome

• PR interval less than 0.12 seconds

• Normal QRS width
• No delta wave

8.2. QT INTERVAL

Represents the time from the start of ventricular depolarization to the end
of ventricular repolarization the QT interval varies inversely with the
cardiac rate.
As a general guide the QT interval should be 0.35- 0.45 s, and should not
be more than half of the interval between adjacent R waves (R-R inter-
val). Bazett developed the following formula for performing this correc-
tion:
QTc=QT/√RR interval (in seconds)
The upper limit of the duration of the QTc interval is approximately 0.46
s (460 ms).

8.2.1 QT PROLONGATION

Figure 47. Prolonged QT interval, QTc 550 millisec

A prolonged QT interval may be associated with:

• Electrolyte disturbance -hypokalemia,hypocalcemia,hypothermia
• Drugs
• A congenital abnormality

DRUGS CAUSING PROLONGATION OF QT INTERVAL

Amiodarone, astemizole, bepridil, bretylium, cisapride, cocaine, tricyclic

antidepressants,cyproheptadine, disopyramide, erythromycin, haloperi-
dol, flecainide,

52
thioridazine, pimozide, ibutilide,itraconazole, ketoconazole, phenothi-
azines, procainamide, propafenone, quinidine, quinine, sotalol, terfena-
dine, vasopressin

8.2.2 SHORT QT INTERVAL

Hypercalcmia-The main ECG abnormality seen is shortening of QT

interval .
Osborne waves (J waves)=severe hypercalcemia
Ventricular fibrillation=extreme hypercalcemia
Short QT syndrome-Genetically inherited cardiac channelopathy
- arrythmogenic disease associatd with paroxysmal atrial and
ventricular fibtilation ,syncope and sudden cardiac arrest.
- QTc intervals <330 ms in males,or<340 in females

ECG features of short QT syndrome

• Short QT interval
• Peaked T waves,
• Short or absent ST segments,
• Episodes of atrial or ventricular fibrillation

9. MISCELLANEOUS

ELECTROCARDIOGRAPHIC ABNORMALITIES FOUND IN

ACUTE PULMONARY EMBOLISM

• Sinus tachycardia
• Atrial flutter or fibrillation
• S1, Q3, T3 pattern
• Right bundle branch block (incomplete or complete)
• T wave inversion in the right precordial leads
• pulmonale
• Right axis deviation

53
Figure 48 –S1Q3T3 pattern and RBBB in patient with PE

Electrocardiographic features of hypokalemia

• Broad, flat T waves

• U wave
• ST depression
• QT interval prolongation
• Ventricular arrhythmias (premature ventricular contractions, torsades
de pointes, ventricular tachycardia, ventricular fibrillation)

Figure 49. Obvious U waves in leads V1 to V3 in patient with hypokalemia

Electrocardiog raphic features of hyperkalaemia

Ser um potassium (mmol/l) Major change
5.5-6.5 Tall peaked T waves
6.5-7.5 Loss of P waves
7.0-8.0 Widening of QRS complexes
8.0-10 Sine wave, ventricular arrhyth
mias, asystole

54
 Figure 50- serial changes in hyperkalemia

The QT prolongation seen in hypercalcaemia is primarily due to ST

prolongation
Hypocalcaemia is associated with shortening of the QT interval

ELECTROCARDIOGRAPHIC FEATURES OF HYPOTHERMIA

• Tremor artefact from shivering

• Atrial fibrillation with slow ventricular rate
• J waves (Osborn waves)
• Bradycardias, especially junctional
• Prolongation of PR, QRS, and QT intervals
• Premature ventricular beats, ventricular tachycardia, or ventricular
fibrillation
• Asystole

Figure 51- Sinus bradycardia ,with a J wave ,in a patient with hypothermia –core
temperature 29◦c(note the shivering effect)

55
Digitalis

EKG apperance with digitalis (digitalis effect)

• remember Salvador Dali.

• T waves depressed or inverted.
• QT interval shortened.

Digitalis Toxicity (blocks , irritable foci firing rapidly)

• SA Block
• Atrial Fibrillation
• P.A.T. with Block
• Junctional or Ventricular Tachycardia
• AV Blocks
• multiple P.V.C.’s
• AV Dissociation
• Ventricular Fibrillation

ECG MANIFESTATIONS: DEXTROCARDIA

• Negative P-QRS-T complex in lead I

• Reversed appearance of leads aVR and aVL
• Abnormal precordial QRS complex progression

Figure 52. DEXTROCARDIA

56
RA/LA LEAD REVERSAL.

Lead I features an upside-down P-QRS-T, and the major vector of its

QRS complex is uncharacteristically opposite to that seen in lead V6.
The waveforms in lead aVR appear normal and are actually those that
appear in aVL when the electrodes are placed properly.
Leads II and III also are reversed,

Figure 53. RA/LA LEAD REVERSAL

57
REFERENCES

1. Shirley A. Jones : ECG Notes Interpretation and Management Guide.

FA Davis, Philadelphia,2005
2. M. Gabriel Khan: Rapid ECG Interpretation ,Third Edition,
Totowa,2003
3. Braunwald E:Heart Disease: A Textbook of Cardiovascular Medicine,
6th ed., Philadelphia, 2001, WB Saunders, Elsevier Science
4. Malcolm S. Thaler: Only EKG Book You'll Ever Need,5th Edition,
2007 Lippincott Williams & Wilkins
5. Francis M.,June E.William J.,John C., ABC OF CLINICAL ELEC
TROCARDIOGRAPHY,1st edition, London,2003, BMJ Books
6. Richard A. William J. Brady, Theodore C The ECG in Emergency
Medicine, Emerg Med Clin N Am 24 (2006) xi–xii
7. Masood Akhtar, The Electrocardiogram Examination of the Heart
Part5
8. Chou TC: Electrocardiography in Clinical Practice, 4th ed., Philadel
phia, 1996, WB Saunders, Elsevier Science
9. Judith E. Tintinalli: Tintinalli’s Emergency Medicine A Comprehen
sive Study Guide,8th edition, 2016 , McGraw-Hill Education
10. www.lifeinthefastlane .com/ECG-library

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