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This book is designed to teach healthcare professionals how to interpret electrocardiograms, presenting this information with numerous illustrations, solid practical content, questions to prompt critical thinking, case presentations, and plentiful practice ECG tracings to promote the application of skills.

Interpreting ECGs in Clinical Practice is practical book rather than a “theoretical book.” Although there is plenty of detail, the coverage is to the point, telling the reader the salient points and then showing what needs to be taken away. The breadth of information ranges from simple to complex, but regardless of how advanced the material, the explanations and visuals make the concepts easy to understand, making this a critical resource for all cardiology professionals.

Year:
2018
Edition:
1st ed.
Publisher:
Springer International Publishing
Language:
english
Pages:
119
ISBN 13:
9783319905570
Series:
In Clinical Practice
File:
PDF, 9.13 MB

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In Clinical Practice

Sercan Okutucu
Ali Oto

Interpreting
ECGs in
Clinical
Practice

In Clinical Practice

Taking a practical approach to clinical medicine, this series of
smaller reference books is designed for the trainee physician,
primary care physician, nurse practitioner and other general
medical professionals to understand each topic covered. The
coverage is comprehensive but concise and is designed to act
as a primary reference tool for subjects across the field of
medicine.
More information about this series at http://www.springer.
com/series/13483

Sercan Okutucu • Ali Oto

Interpreting ECGs
in Clinical Practice

Sercan Okutucu
Department of Cardiology
Memorial Ankara Hospital
Ankara
Turkey

Ali Oto
Department of Cardiology
Memorial Ankara Hospital
Ankara
Turkey

In Clinical Practice
ISSN 2199-6652	    ISSN 2199-6660 (electronic)
ISBN 978-3-319-90556-3    ISBN 978-3-319-90557-0 (eBook)
https://doi.org/10.1007/978-3-319-90557-0
Library of Congress Control Number: 2018943841
© Springer International Publishing AG, part of Springer Nature 2018
This work is subject to copyright. All rights are reserved by the Publisher, whether
the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on
microfilms or in any other physical way, and transmission or information storage
and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service
marks, etc. in this publication does not imply, even in the absence of a specific
statement, that such names are exempt from the relevant protective laws and
regulations and therefore free for general use.
The publisher, the authors, and the editors are safe to assume that the advice and
information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors;  give a warranty,
express or implied, with respect to the material contained herein or for any errors
or omissions that may have been made. The publisher remains neutral with
regard to jurisdictional claims in published maps and institutional affiliations.
This Springer imprint is published by Springer Nature, under the registered
company Springer International Publishing AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Preface

Electrocardiography has been a very useful clinical diagnostic tool for more than a century. It has been a first step after
clinical evaluation of the cardiac patients and in many situations for non-cardiac patients as it is widely available, easy to
reach, of low cost and reproducible. To learn how to read the
ECG however is a challenge and one should start from the
basics and relentlessly review large number of ECGs to make
the best use of it.
This book has been prepared for the medical students,
physicians in training and allied professionals who would like
to begin learning ECG. The format is to start with a short
explanation of the basics of ECG and the ABC of “How to
read an ECG?” followed by the typical real-life examples for
the most frequently encountered situations. The ECG tracings are kept as they are; therefore, the reader will see the
tracings as they will meet in their practice. This small book is
designed to be carried in the pocket as an everyday reference
and easy to reach. A short explanation is provided for each
ECG example. However, for further details any textbook can
be used. At the end ECG case studies are added for selfassessment; brief explanations are also provided to increase
benefits.
As a final note we express our gratitude to those who gave
energy and efforts into this book from the digital arrangement to printing.
Ankara, Turkey
Ankara, Turkey 
March 2018

Sercan Okutucu
Ali Oto

Contents

1	Fundamentals of ECG . . . . . . . . . . . . . . . . . . . . . .  1
1.1 Basics for ECG Interpretation . . . . . . . . . . . .   1
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  18
2	ECG Rhythm Interpretation . . . . . . . . . . . . . . . . .  19
2.1 Normal Rhythm and Arrhythmia  . . . . . . . . .  19
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  42
3	ECG in Conduction Disturbances . . . . . . . . . . . .  45
3.1 Normal Electrical Conduction
and Disturbances . . . . . . . . . . . . . . . . . . . . . . .  45
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  55
4	ECG in Cardiac Chamber Enlargement . . . . . . .  57
4.1  Cardiac Chamber Enlargement . . . . . . . . . . .  57
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  63
5	ECG in Coronary Artery Disease  . . . . . . . . . . . .  65
5.1 ECG Changes in Spectrum of Coronary
Artery Disease . . . . . . . . . . . . . . . . . . . . . . . . .  65
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  75
6	ECG in Miscellaneous Conditions . . . . . . . . . . . . 
6.1 Acute Pericarditis . . . . . . . . . . . . . . . . . . . . . . . 
6.2 Electrolyte Abnormalities . . . . . . . . . . . . . . . . 
6.3 Drug Effects and Miscellaneous Situations . 
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 

77
77
80
83
89

viii

Contents

7	Eponymous ECGs  . . . . . . . . . . . . . . . . . . . . . . . . .  91
7.1 Eponymous ECG Concepts  . . . . . . . . . . . . . .  91
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  96
Appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  99
ECG Cases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  99
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  113

Chapter 1
Fundamentals of ECG

1.1 Basics for ECG Interpretation
Electrocardiography (ECG) is the process of recording the
electrical activity of the heart over a period using electrodes
placed on the skin. These electrodes detect the subtle electrical changes on the skin that arise from the heart muscle’s
electrophysiologic pattern of depolarization and repolarization during each heartbeat [1, 2].
The electrocardiograph defines one electrode as exploring
(positive) and the other as reference (negative) electrode. A
vector heading towards the exploring electrode yields a positive wave/deflection and vice versa (Fig. 1.1).
The ECG waves are recorded on special ECG paper that
is divided into 1 mm2 grid-like boxes. The ECG paper speed
is ordinarily 25 mm/s. As a result, each 1 mm (small) horizontal box corresponds to 0.04 s (40 ms), with dark lines forming
larger boxes that include five small boxes and hence represent 0.20 s (200 ms) intervals (Fig. 1.2).
On occasion, the paper speed is increased to 50 mm/s to
better define waveforms. In this situation, the heart rate
appears to be one-half of what is recorded at 25 mm/s, and all
the ECG intervals are twice with respect to standard recording. Other paper speeds are occasionally used. Vertically, the
ECG graph measures the height (amplitude) of a given wave
© Springer International Publishing AG, part of Springer
Nature 2018
S. Okutucu, A. Oto, Interpreting ECGs in Clinical Practice,
In Clinical Practice, https://doi.org/10.1007/978-3-319-90557-0_1

1

Chapter 1. Fundamentals of ECG

2

Reference
electrode

–

Exploring
electrode

Reference
electrode

–

+

Vector

Exploring
electrode
Vector

Electrical vector is oriented towards the
exploring electrode and therefore
causes a positive deflection.

ECG

Electrical vector is oriented away from
the exploring electrode therefore
causes a negative deflection.

ECG

+

Figure 1.1 ECG Acquisition of electrical signal in different vectors
with opposite orientation is shown
1 mm =
0.04 s

5 mm =
0.2 s

10 mm =
1.0 mV
1 mm =
0.1 mV

Figure 1.2 ECG tracings are recorded on grid paper. The horizontal
axis of the ECG paper records time, each large block equals 0.2 s.
The vertical axis records ECG amplitude (voltage). Two large blocks
equal 1 millivolt (mV). Each small block equals 0.1 mV

1.1

Basics for ECG Interpretation

3

or deflection, as 10 mm (10 small boxes) equals 1 mV with
standard calibration. On occasion, particularly when the
waveforms are small, double standard is used (20 mm equals
1 mv). When the wave forms are very large, half standard may
be used (5 mm equals 1 mv). Paper speed and voltage are
usually printed on the bottom of the ECG [1, 2].
ECG leads are obtained according to the localization of
electrodes. Standard bipolar leads are recorded with one
positive (+) and one negative (−) electrodes. Whereas, unipolar leads are obtained with only one positive electrode. Three
standard bipolar leads are I, II and III. Altogether these 3
leads form the Einthoven’s Triangle. Among 3 bipolar leads
in; lead I, positive electrode is placed on left arm, negative
electrode is placed on right arm; lead II, positive electrode is
placed on left leg, negative electrode is placed on right arm;
lead III, positive electrode is placed on left leg, negative electrode placed on left arm (Fig. 1.3) [1, 3].
II

I

III

+

+

+

–

–

–

–

+

–
–

–

–

I
III

II

Einthoven’s
Triangle
+

+

III

II

Figure 1.3 Three standard bipolar leads and Einthoven’s triangle

Chapter 1. Fundamentals of ECG

4

Unipolar leads are named according to the placement of
positive electrode. If positive electrode is placed on right arm
in aVR, left arm in aVL and left leg in AVF. In these 3 derivations voltage is low therefore special augmentation if
performed. Because of this process lowercase ‘a’ letter is
­
added (a = augmented) before the name of unipolar lead. I,
II, III, aVR, aVL and aVF are named as standard extremity
leads (Fig. 1.4) [1, 3].
The unipolar chest (precordial) leads (V1, V2, V3, V4, V5
and V6) have the exploring electrodes located anteriorly on
the chest wall and the reference point located inside the chest
(Fig. 1.5). Precordial leads and their localization on chest wall
are summarized in Table 1.1. Chest leads are excellent for
detecting vectors traveling in the horizontal plane. In standard ECG recordings, there are 6 extremity leads and 6 chest

aVL
aVR

I

III
II
aVF

Figure 1.4 Standard extremity leads and its orientation with cardiac
frontal axis

1.1

Basics for ECG Interpretation

5

4

V1

V6
V5

V2
V3

V4

Figure 1.5 Chest leads and its orientation with cardiac horizontal
axis
Table 1.1 Precordial leads and their localization on chest wall
Lead
Localization
V1
Fourth intercostal space, to the right of sternum
V2

Fourth intercostal space, to the left of sternum

V3

Placed diagonally midway between V2 and V4

V4

Between rib 5 and 6 (fifth intercostal space) in the
midclavicular line

V5

Placed on the same level as V4, but in the anterior
axillary line

V6

Placed on the same level as V4 and V5, but in the
midaxillary line

6

Chapter 1. Fundamentals of ECG

leads. Therefore, it is usually expressed as standard 12-lead
electrocardiogram [1–3].
There are 6 limb leads (I, II, III, aVF, aVR and aVL) which
have the exploring electrode and the reference point placed
in the frontal plane. These leads are therefore excellent for
detecting vectors traveling in the frontal plane. Leads II, aVF
and III are called inferior limb leads and they primarily
observe the inferior aspect of the left ventricle. Leads I and
aVL are called lateral limb leads and they primarily observe
the lateral aspect of the left ventricle. aVR observes the heart
from the right arm. Therefore, it does not enface myocardium.
Because of this, it is called as cavity lead [1–3]. Anatomic relations of the limb leads with the cardiac frontal axis are shown
in Fig. 1.6.
Among the chest (precordial) leads; V1–V2 (“septal
leads”), primarily observe the ventricular septum but may
occasionally display ECG changes originating from the right
ventricle. V3–V4 (“anterior leads”), observe the anterior wall
of the left ventricle. V5–V6 (“anterolateral leads”): observe
–90º
aVL

aVR
–150º

–30º

–180º
+180º

0º

III

+120º

+60º
+90º

I

II

aVF

Figure 1.6 Anatomic relations of the limb leads with the cardiac
frontal axis

1.1

Basics for ECG Interpretation

7

the lateral wall of the left ventricle [2, 3]. Anatomic relations
of the chest (precordial) leads with horizontal cardiac section
are shown in Fig. 1.7. Please note that none of the leads in the
12-lead ECG are adequate to detect vectors of the right
ventricle.
The 12-lead ECG displays, as the name implies, 12 leads
which are derived by means of 10 electrodes (Fig. 1.8). The
12-lead ECG offers outstanding possibilities to diagnose
abnormalities. Importantly, most of the recommended ECG
criteria have been derived and validated using the 12-lead
ECG. At any given instant during the cardiac cycle all ECG
leads analyze the same electrical events but from different
angles [2, 3].
Standard 12-lead ECG provide insufficient information
for the accurate diagnosis of posterior and/or right ventricular disease. Posterior chest leads (V7–V9) and/or right-sided
precordial leads (V3R–V5R) provide important information
from those specific areas (Fig. 1.9) [2, 3].

V1

V2
+90º

+120º

V3
+60º
+30º V4

+150º

±180º

0º

V5

–30º V6

–150º
–60º

–120º
–90º

Figure 1.7 Anatomic relations of the chest (precordial) leads with
horizontal cardiac section

Chapter 1. Fundamentals of ECG

8

V6
V7

V5R
V8

V9

V6R

Angle of Louis

Mid-clavicular line

Anterior axillary line

b
Mid-axillary line

Left paraspinal line

Mid-scapular line

Mid-axillary line

a

Posterior axillary line

Figure 1.8 12-lead ECG displays 12 leads which analyze the same
electrical events but from different angles

V3R
V4R

V1

V2

Figure 1.9 Placement of posterior leads (a) and right ventricular
leads

1.1

Basics for ECG Interpretation

9

Among the posterior leads; V7 is placed on posterior axillary line, in the same horizontal level as V6; V8 is placed on
mid-scapular line, in the same horizontal level as V6; V9 is
placed on midway between mid-scapular line and spine (left
paraspinal line), in the same horizontal level as V6 [2, 3].
Right ventricular leads are V3R–V6R. V3R is placed on
midway between V1 and V4R; V4R is placed on 5th right
intercostal space, mid clavicular line; V5R and V6R are not
usually taken, unless there is dextrocardia. Their positions will
be corresponding opposite side of the left chest leads [2, 3].
Each portion of a heartbeat produces a different deflection on the ECG. These deflections are recorded as a series
of positive and negative waves. On a normal ECG, there are
typically up to five visible waveforms: P wave, Q wave, R
wave, S wave, and T wave. Portions between 2 waves are
called as segment. Distance between 2 waves are called as
interval [1–4]. ECG waves, basic intervals, points and segments are shown in Fig. 1.10.
ECG interpretation traditionally starts with assessment of
the P-wave. The P-wave reflects atrial depolarization (activation). P-wave is a small, positive and smooth wave. In normal
conditions, action potentials generated by the sinus node
spread throughout the atria. Initially right atrium then left
atrium are depolarized. Because of this initial portion of P
RR interval (distance between R-waves)
R

R
PP interval (distance between P-waves)

PR segment

ST-T segment

P-wave
duration

ST segment

T

TP interval

U
P

P
PR interval
0,12 – 0,22 s

Q

S

QRS duration
≤0,12 s

J-60 point: measurement of ST-segment
depression in exercise stress testing

Q

S

J point: measurement of ST-segment elevation and
ST segment depression in most instances

QT duration
Corrected QT duration men: ≤ 0,45 s
Corrected QT duration women: ≤ 0,47 s

The reference level for measuring ST-segment
deviation (depression or elevation) is not the
TP interval. The correct reference level is the
PR segment. This level is also called baseline
level or isoelectric level

Figure 1.10 ECG waves, basic intervals, points and segments

10

Chapter 1. Fundamentals of ECG

LA
RA

RA

LA

II

RA
LA

RA: Right atrium
LA: Left atrium
V1

Figure 1.11 P wave and its right atrial and left atrial components

wave reflects right atrial depolarization, latter part reflects
left atrial depolarization (Fig. 1.11). In presence of sinus
rhythm, P waves are positive in I, II, aVF and V3–V6 leads
(both right and left atrial depolarization vectors are towards
them) and negative in aVR. Lead V1 might display a biphasic
(diphasic) P-wave, meaning that the greater portion of the
P-wave is positive, but the terminal portion is slightly negative (the vector generated by left atrial activation heads away
from V1). Occasionally, the negative deflection is also seen in
lead V2. P-wave duration should be ≤0.12 s. P-wave amplitude should be <2.5 mm in the limb leads [1–4].
The PR interval is the distance between the onset of the
P-wave to the onset of the QRS complex. The PR interval is
assessed to determine whether impulse conduction from the
atria to the ventricles is normal. The flat line between the end
of the P-wave and the onset of the QRS complex is called the
PR segment and it reflects the slow impulse conduction
through the atrioventricular node (Fig. 1.12). The PR segment
serves as the baseline (also referred to as reference line or
isoelectric line) of the ECG curve. The amplitude of any
deflection/wave is measured by using the PR segment as the
baseline. The PR interval is assessed to determine whether
impulse conduction from the atria to the ventricles is normal
in terms of speed. A normal PR interval ranges between
0.12 s and 0.20 s [1–4].

1.1

Basics for ECG Interpretation

11

R

AV
node

Sinoatrial
node

J
T
P

U

P

Q
QRS S
duration
PR
segment
PR
interval

ST
segment
QT
interval

TP
interval

Figure 1.12 PR interval and PR segments. Please note the other
intervals and segments

The QRS complex represents the depolarization (activation) of the ventricles. It is always referred to as the “QRS
complex” although it may not always display all three waves.
The following rules apply when naming the waves: a deflection is only referred to as a wave if it passes the baseline. If
the first wave is negative, then it is referred to as Q-wave. If
the first wave is not negative, then the QRS complex does not
possess a Q-wave, regardless of the appearance of the QRS
complex. All positive waves are referred to as R-waves. The
first positive wave is simply an “R-wave” (R). The second
positive wave is called “R-prime wave” (R’). If a third positive
wave occurs (rare) it is referred to as “R-bis wave” (R”). Any
negative wave occurring after a positive wave is an S-wave
(Fig. 1.13). Large waves are referred to by their capital letters
(Q, R, S), and small waves are referred to by their lower-case
letters [1–4].
Ventricular depolarization consists 3 major vectors
(Fig. 1.14).
The first vector: the ventricular septum receives Purkinje
fibers from the left bundle branch and therefore depolarization

12

Chapter 1. Fundamentals of ECG

R

T
P

Q

S

Figure 1.13 ECG waves and components of QRS complex

Sinus
node

3

V5

R
g

2

2

Ex

plo

1

rin

Horizontal plane

V1

P
1

Exploring

3

q S

V1

V6

Figure 1.14 Formation of QRS complex and 3 major vectors of
ventricular depolarization

1.1

Basics for ECG Interpretation

13

proceeds from its left side towards its right side. The vector is
directed forward and to the right. The ventricular septum is
relatively small, which is why V1 displays a small positive wave
(r-wave) and V5 displays a small negative wave (q-wave). Thus,
it is the same electrical vector that results in an r-wave in V1
and q-wave in V5 [1, 2].
The second vector: the vectors resulting from activation of
the ventricular free walls is directed to the left and downwards. The vector resulting from activation of the right ventricle does not come to expression, because of the larger
vector generated by the left ventricle. Activation of the ventricular free wall proceeds from the endocardium to the epicardium. Lead V5 detects a very large vector heading towards
it and therefore displays a large R-wave. Lead V1 records the
opposite, and therefore displays a large negative wave called
S-wave [1, 2].
The third vector: the final vector stems from activation of
the basal parts of the ventricles. The vector is directed backwards and upwards. It heads away from V5 which records a
negative wave (s-wave). Lead V1 does not detect this vector
[1, 2]. Because of these 3 different major vectors of ventricular depolarization there are different shaped QRS complexes
in 12 leads of standard ECG (Fig. 1.15).
Normally the R wave amplitude increases from V1 to V5.
Around V3 or V4 the R waves become larger than the S
waves and this is called the ‘transitional zone’. If the transition
occurs at or before V2, this is called counterclockwise rotation. If the transition occurs after V4, this is called clockwise
rotation. Clockwise and counterclockwise rotation refer to a
change in the electrical activity in a horizontal plane through
the heart. While the observer standing at the feet of the
patient who is in bed. If the electrical activity of the heart has
turned more to the right side of the patient this is called counterclockwise rotation. If the electrical activity of the heart has
turned more to the left side of the patient this is called clockwise rotation [1, 2].

14

Chapter 1. Fundamentals of ECG
aVL

aVR
V6

I

V5
II
III
aVF

V1

V2

V3

V4

Figure 1.15 Orientation of major vectors of ventricular depolarization and different shaped QRS complexes in 12 leads of standard
ECG

The amplitude (depth) and the duration (width) of the
Q-wave dictate whether it is abnormal or not. Normal
Q-waves have duration <0.04 s and/or amplitude <25% of the
R-wave amplitude. Pathological Q-waves must exist in at
least two anatomically contiguous leads to reflect an abnormality. The QRS duration is generally <0.10 s but must be
<0.12 s. If QRS duration is ≥0.12 s (120 ms) then the QRS
complex is abnormally wide [4, 5].
The ST segment is the flat, isoelectric section of the ECG
between the end of the S wave (the J point) and the beginning
of the T wave. It represents the interval between ventricular
depolarization and repolarization. There are two types of ST
segment deviations. ST segment depression implies that the
ST segment is displaced, such that it is below the level of the
PR segment. ST segment elevation implies that the ST segment is displaced, such that it is above the level of the PR
segment. The magnitude of depression/elevation is measured
as the height difference (in millimeters) between the J point
and the PR segment. The J point is the point where the ST

1.1

Basics for ECG Interpretation

15

segment starts. If the baseline (PR segment) is difficult to discern, the TP interval may be used as the reference level [4, 5].
The T wave is the positive deflection after each QRS complex. It represents ventricular repolarization. The normal
T-wave in adults is positive in most precordial and limb leads.
The T-wave amplitude is highest in V2–V3. The T-wave should
be concordant with the QRS complex, meaning that a net
positive QRS complex should be followed by a positive
T-wave, and vice versa. Positive T-waves are rarely higher than
6 mm in the limb leads (typically highest in lead II). In the
chest leads the amplitude is highest in V2–V3, where it may
occasionally reach 10 mm in men and 8 mm in women [4, 5].
The ‘U’ wave is a wave on an electrocardiogram (ECG). It
is the successor of the ‘T’ wave and sometimes may not be
observed as a result of its small size. ‘U’ waves are thought to
represent repolarization of the Purkinje fibers. It is a positive
wave occurring after the T-wave. Its amplitude is generally
one fourth of the T-wave’s amplitude. The U-wave is most
frequently seen in leads V2–V4. Individuals with prominent
T-waves, as well as those with slow heart rates, display
U-waves more often [4, 5].
QT interval reflects the total duration of ventricular depolarization and repolarization (Fig. 1.16). It is measured from
the onset of the QRS complex to the end of the T-wave. The
QT duration is inversely related to heart rate; QT interval
increases at slower heart rates and decreases at higher heart
rates. Therefore, to determine whether the QT interval is
within normal limits, it is necessary to adjust for the heart
rate. The heart rate adjusted QT interval referred to as the
corrected QT interval (QTc interval). Bazett’s formula has
traditionally been used to calculate the corrected QT d
­ uration.
Normal values for QTc interval is ≤0.450 s for men
and ≤ 0.470 s for women [5, 6].
Assessment of the electrical axis is an integral part of ECG
interpretation. The electrical axis reflects the average direction of ventricular depolarization during ventricular contraction on frontal view (Fig. 1.17). The direction of the
depolarization (and thus the electrical axis) is generally

16

Chapter 1. Fundamentals of ECG
R

J
T

P

QT duration

QTc =

Bazett’s formula

U wave
U

RR interval

P

Q
S
QT
interval

Figure 1.16 QT, QTc interval and Bazett’s formula

Normal
axis

Left axis
deviation
I

III

II

I

III

II
–90º

aVR
Right
axis
deviation

–30º

–150º

I

III

–180º
+180º

0º

II
IIl

+120º

+90º
aVF

Figure 1.17 Normal cardiac axis and axis deviations

+60º

Il

l

1.1

Basics for ECG Interpretation

17

alongside the longitudinal axis of the heart (to the left and
downwards). Normal heart axis is between −30° and +90°. If
the axis is more positive than +90° it is referred to as right
axis deviation. If the axis is more negative than −30° it is
referred to as left axis deviation [5, 6].
According to basic information for ECG interpretation
and practical key points stated above, basic steps during
evaluation of ECG are summarized in Table 1.2. Calculation
of heart is demonstrated in Fig. 1.18.
Table 1.2 Basic steps of ECG evaluation
How to interpret ECG?
• Name on ECG and date?
• Standard recording?
• Calibration and sweep rate?
• Quality of recording, artifacts?
• Rhythm?
• Heart rate?
• QRS axis?
• P
 R interval (0.12–0.20 s), P wave duration and amplitude
(<0.12 s, <2.5 mm)?
• Q
 RS duration and amplitude (Q wave duration <0.04 s,
amplitude <1/4 R; QRS duration 0.06–0.11 s)?
• QT interval
• P wave duration and amplitude (<0.12 s, <2.5 mm)
• ST segment morphology
• T wave morphology, U wave morphology
• P
 and QRS waves relationship, R–R interval and regularity,
P–P interval and regularity
• Comments

18

Chapter 1. Fundamentals of ECG
1 small square 0.04
second (40 ms)

1 big square 0.2
second (200 ms)

R-R interval
5 big squares (1 second)
R-R interval (big squares)

Heart rate
300 / number of big squares or
1500 / number of little squares

Heart rate, bpm (beats per Minute)

1
2
3

300
150
100

4

75

5
6

60
50

Figure 1.18 Calculation of heart rate

References
1. Mirvis DM, Goldberger AL. Electrocardiography. In: Mann DL,
Zipes DP, Libby P, Bonow RO, Braunwald E, editors. Braunwald’s
heart disease: a textbook of cardiovascular medicine. 10th ed.
Philadelphia: Elsevier Saunders; 2015.
2. Rowlands DJ. Clinical electrocardiography. Philadelphia: J. B.
Lippincott; 1991.
3. Surawicz B, Knilans T, Chou TC. Chou’s electrocardiography in
clinical practice: adult and pediatric. 5th ed. Philadelphia: W. B.
Saunders; 2008.
4. Coviello JS. ECG interpretation made incredibly easy! 6th ed.
Philadelphia: Wolters Kluwer; 2016.
5. Mirvis DM, Goldberger AL. Electrocardiography. In: Zipes DP,
Libby P, Bonow RO, Mann DL, Tomaselli GF, editors. Braunwald’s
heart disease e-book: a textbook of cardiovascular medicine. 11th
ed. Philadelphia: Elsevier Saunders; 2018.
6. Goldberger AL, Goldberger ZD, Shvilkin A. Goldberger’s clinical electrocardiography: a simplified approach. Philadelphia:
Elsevier; 2017.

Chapter 2
ECG Rhythm Interpretation

2.1

Normal Rhythm and Arrhythmia

Normal cardiac rhythm, also known as sinus rhythm, arises
from the sinoatrial node (SA node) but pacemaker impulses
can come from ectopic foci in the atria, the atrioventricular
(AV) junction, and the ventricles under abnormal conditions.
When an ectopic impulse occurs singly, it generates a beat;
when the beat repeats itself, it becomes a rhythm (more than
3 beats) [1, 2]. Cardiac conduction system and its basic components are shown in Fig. 2.1.
Sinus rhythm implies that the SA node is the pacemaker
and normal sinus rhythm (NSR) is simply sinus rhythm with
heart rate in the normal range of 60–100 beats/min (Fig. 2.2).
The P waves in sinus rhythm have normal axis and are positive in lead II and negative in lead aVR. The QRS width in
sinus rhythm is normal because the ventricles are activated
rapidly by impulses conducted down the His bundle and
bundle branches (Figs. 2.3 and 2.4). Sinus bradycardia is a
sinus rhythm with a rate of 40–60 bpm (Figs. 2.5 and 2.6).
Sinus tachycardia is a normal sinus rhythm but with a heart
rate over 100 bpm (Fig. 2.7) [1, 2].
An escape beat is a heartbeat arising from an ectopic focus
in the atria, the AV junction, or the ventricles when the sinus

© Springer International Publishing AG, part of Springer
Nature 2018
S. Okutucu, A. Oto, Interpreting ECGs in Clinical Practice,
In Clinical Practice, https://doi.org/10.1007/978-3-319-90557-0_2

19

20

Chapter 2. ECG Rhythm Interpretation

Sinoatrial
node
His bundle

Atrioventricular
node

Left bundle branch

Right bundle branch

Figure 2.1 Simplified drawing of nodal and conduction systems

SA node
60-100 bpm

AV node
40-60 bpm

Purkinje system
20-40 bpm

Figure 2.2 Cardiac impulse formation and conduction system.
Please note different impulse rate of SA node, AV node and Purkinje
system

2.1 Normal Rhythm and Arrhythmia

21

Figure 2.3 Normal sinus rhythm. Heart rate is 80 bpm and regular.
P waves are positive in lead II and aVF, negative in aVR

Figure 2.4 Normal sinus rhythm. Heart rate is 80 bpm and regular.
Each P wave of atrial contraction is followed by a QRS complex of
ventricular contraction. P waves are positive in lead II and aVF,
negative in aVR

22

Chapter 2. ECG Rhythm Interpretation

Figure 2.5 Sinus bradycardia. Heart rate is 50 bpm and regular.
Each P wave is followed by a QRS complex. P waves are positive in
lead II and aVF, negative in aVR. In this ECG, U waves can be easily seen because of bradycardia. This ECG fulfills the properties of
sinus rhythm but heart rate is less than 60 bpm

Figure 2.6 Sinus bradycardia. Heart rate is 54 bpm and regular.
Each P wave is followed by a QRS complex. P waves are positive in
lead II and aVF, negative in aVR. In this ECG, U waves can easily
be seen particularly in precordial leads. The causes of sinus bradycardia include the following: sick sinus syndrome, inferior myocardial infarction, metabolic and environmental causes (such as
hypothyroidism and electrolyte disorders), medications (such as
beta-blockers, digitalis, ivabradine and amiodarone), infection (such
as myocarditis), increased intracranial pressure, and toxic exposure,
while it can sometimes be a normal phenomenon, especially during
sleep and in athletes

2.1 Normal Rhythm and Arrhythmia

23

Figure 2.7 Sinus tachycardia. Heart rate is 110 bpm and regular.
Each P wave is followed by a QRS complex. P waves are positive in
lead II and aVF, negative in aVR. Often sinus tachycardia is a normal response to certain situations such as exercise, anxiety, distress,
or fever. Certain disorders such as heart failure, thyroid disease,
anemia, and low blood pressure are also associated with sinus
tachycardia

node fails in its role as a pacemaker or when the sinus impulse
fails to be conducted to the ventricles as in complete heart
block. In junctional beat or rhythm, the atrial depolarization
current points cephalad and to the right, away from lead II
and toward lead aVR. Therefore, the P wave, if seen, would be
negative in lead II and positive in lead aVR. However, this P
wave is usually buried by the QRS complex and not visible.
On less common occasions when the P wave is visible, it may
be either immediately before or immediately after the QRS
complex [1, 2].
QRS complex of junctional beats is narrow and looks
exactly like the QRS complex of the sinus beat. The inherent
rate of atrial or junctional escape rhythm is 40–60 bpm. In
ventricular escape beat or rhythm, QRS complex is wide
(>120 ms) and has a shape different from that of the sinus
beat. The inherent rate of ventricular escape rhythm is
between 20 and 40 bpm [1, 2].
Sinus arrhythmia is a normal physiological phenomenon,
most commonly seen in young, healthy people (Fig. 2.8). The
heart rate varies due to reflex changes in vagal tone during

24

Chapter 2. ECG Rhythm Interpretation

Figure 2.8 Sinus arrhythmia. Heart rate is 80 bpm and mildly
irregular. Each P wave is followed by a QRS complex. P waves are
positive in lead II and aVF, negative in aVR. In this rhythm, there is
a sinus rhythm with a beat-to-beat variation in the P–P interval (the
time between successive P waves), producing an irregular ventricular rate. Variation in the P–P interval of more than 120 ms (3 small
boxes)

the different stages of the respiratory cycle. Inspiration
increases the heart rate by decreasing vagal tone. “Non-­
respiratory” sinus arrhythmia (not linked to the respiratory
cycle) is less common, typically occurs in elderly patients and
is more likely to be pathological (e.g. due to heart disease or
digoxin toxicity). Ventriculophasic sinus arrhythmia is a
­phenomenon commonly observed in patients with complete
AV block. Typically, the PP intervals which contain a QRS
complex are shorter than the PP intervals which do not
­contain it [3, 4].
Junctional rhythms occur when the AV node takes over as
the primary pacemaker site in the heart either because the SA
node has failed, or the AV node is going faster and over takes
the SA node (Fig. 2.9). In junctional beat or rhythm the atrial
depolarization current points cephalad and to the right, away
from lead II and toward lead aVR. Therefore, the P wave, if
seen, would be negative in lead II and positive in lead
aVR. However, this P wave is usually buried in the QRS

2.1 Normal Rhythm and Arrhythmia

25

Figure 2.9 There is junctional rhythm and heart rate is 55 bpm and
regular

c­ omplex and not visible. On less common occasions when the
P wave is visible, it may be either immediately before or immediately after the QRS complex. Since the impulse is ­conducted
to the ventricles via the His bundle and bundle branches, the
QRS complex of junctional beats is narrow and looks exactly
like the QRS complex of the sinus beat. The inherent rate of
junctional escape rhythm is 40–60 beats/min [3, 4].
Accelerated junctional rhythm (AJR) occurs when the
rate of an AV junctional pacemaker exceeds that of the sinus
node (Fig. 2.10). This situation arises when there is increased
automaticity in the AV node coupled with decreased automaticity in the sinus node. Common causes of AJR are digoxin
toxicity (the classic cause of AJR), beta-agonists, e.g. isoprenaline, adrenaline, myocardial ischemia, myocarditis, cardiac surgery, DC cardioversion, acute rheumatic fever and
electrolyte abnormalities [3, 4].
Accelerated idioventricular rhythm (AIVR) is a ventricular rhythm with a rate of between 40 and 120 beats/min
(Fig. 2.11a). Idioventricular means “relating to or affecting
the cardiac ventricle alone” and refers to any ectopic ventricular arrhythmia. There are multiple causes of AIVR
including: reperfusion phase of an acute myocardial infarction (most common cause); beta-sympathomimetics such as

26

Chapter 2. ECG Rhythm Interpretation

Figure 2.10 Accelerated junctional rhythm. Heart rate is 110 bpm
and regular. Each P wave is followed by a QRS complex. Retrograde
P waves may be present and can appear before, during or after the
QRS complex. Retrograde P waves are usually inverted in the inferior leads (II, III, aVF), upright in aVR and V1. AV dissociation may
be present with the ventricular rate usually greater than the atrial
rate. There may be associated ECG features of digoxin effect or
toxicity

a

b
Figure 2.11 (a) Accelerated idioventricular rhythm). In this ECG
tracing there is a wide QRS complex rhythm with a 60 bpm. This
ECG was obtained after primary percutaneous coronary intervention in a patient with anterior myocardial infarction. (b)
Idioventricular rhythm. The rate is usually 20–40 bpm

2.1 Normal Rhythm and Arrhythmia

27

Figure 2.12 PAC (fourth beat) has normal QRS duration and the
same morphology as that of the sinus beat

isoprenaline or adrenaline; drug toxicity, especially digoxin,
cocaine and volatile anesthetics such as desflurane; electrolyte abnormalities, cardiomyopathy, congenital heart disease,
myocarditis, return of spontaneous circulation following cardiac arrest, athlete heart. In idioventricular rhythm. The rate
is usually 20–40 bpm (Fig. 2.11b) [5, 6].
Premature atrial contractions (PACs), also known as atrial
premature complexes (APC) or atrial premature beats
(APB), are a common cardiac dysrhythmia characterized by
premature heartbeats originating in the atria (Fig. 2.12). It
depolarizes the atria prematurely (premature to the next
timely sinus beat) and produces a P wave that looks different
from a sinus-node generated P wave because the direction in
which the atria depolarize is abnormal (abnormal P wave
axis). Since the premature atrial impulse is conducted in a
normal fashion via the AV node, the His bundle, and the
bundle branches to depolarize the ventricles, the QRS complex associated with a PAC has normal QRS duration and the
same morphology as that of the sinus beat (Fig. 2.13) [1, 2].
A premature ventricular contraction (PVC)—also known
as a premature ventricular complex, ventricular premature
contraction (or complex or complexes) (VPC), ventricular
premature beat (VPB), or ventricular extrasystole (VES)—is
a relatively common event arises from a focus in the ventricles. Ventricular premature impulse is not transmitted to the
rest of the ventricles along the His bundle and bundle
branches. It is conducted along abnormal pathway in the

28

Chapter 2. ECG Rhythm Interpretation

Figure 2.13 Premature atrial contraction. In this ECG, there is sinus
rhythm, heart rate is 85 bpm. Tenth beat (shown with asterisk *) is an
atrial premature beat. P wave morphology and PR intervals are different from usual. QRS complex associated with a PAC has normal
QRS duration and the same morphology as that of the sinus beat.
The duration of the interval following a premature complex can help
in the differentiation of an atrial or ventricular premature complex.
In atrial premature beat, there is incomplete compensatory pause

v­entricular myocardium. This slow process produces an
abnormally wide QRS and bizarre looking T wave. Being a
ventricle-generated beat, there is no P wave. Activity before
the QRS complex (Fig. 2.14) [7, 8].
The duration of the interval following a premature complex can help in the differentiation of an atrial or ventricular
premature complex. There is a full compensatory pause, following the ventricular premature complex. A complete compensatory pause occurs when the sum of the coupling interval
and the compensatory pause is equal to twice the sinus cycle
length. In atrial premature beat, there is incomplete compensatory pause [1–4].
If more than one PVC is present on the ECG, they can be:
monomorphic: all VPBs have the same configuration and
thus have a mutual focus of origin; multiforme: the complexes

2.1 Normal Rhythm and Arrhythmia

29

Figure 2.14 Premature ventricular contraction. In this ECG, there is
sinus bradycardia and right bundle branch block. Heart rate is
53 bpm. Eighth beat (shown with asterisk *) is a ventricular premature beat. There is a wide QRS beat and ST–T alterations. There is
no P wave activity before the QRS complex. The QRS width is at
least >0.12 s, but often very broad at around 0.16–0.20 s. The VPB is
usually followed by a compensatory pause

Figure 2.15 Premature ventricular contraction. In this ECG, there is
sinus rhythm with a bigeminy PVCs

have different configurations; bigeminy: every sinus beat is
followed by a PVC; trigeminy: every second sinus beat is
­follow by a PVC (Fig. 2.15) [1–4].

30

Chapter 2. ECG Rhythm Interpretation

Figure 2.16 Atrial tachycardia). In this ECG, there is atrial tachycardia with a ventricular rate of around 60 bpm. Atrial rate was
230 bpm in electrophysiological study. Atrial activities are shown
with asterisks

Atrial tachycardia (AT) is defined as a regular atrial
rhythm originating from the atrium at 100–240 bpm. There is
an isoelectric baseline between the atrial P wave deflections
(Fig. 2.16).
Multifocal atrial tachycardia (MAT) is a cardiac arrhythmia caused by multiple sites of competing atrial activity. It is
characterized by an irregular atrial rate greater than 100 bpm.
Atrial activity is well organized, with at least 3 ­morphologically
distinct P waves, irregular P–P intervals, and an isoelectric
baseline between the P waves (Fig. 2.17). Most commonly
seen in patients with severe chronic obstructive pulmonary
disease or heart failure.
Tachyarrhythmias are divided into supraventricular tachycardia (SVT) and ventricular tachycardia (VT). SVT originates either from sinus node, atria, AV node or His bundle.
Focus of SVT lies above the ventricle whereas focus of VT

2.1 Normal Rhythm and Arrhythmia

31

Figure 2.17 Multifocal atrial tachycardia. This ECG shows MAT in
a patient with chronic obstructive pulmonary disease and adenocarcinoma of the lung. Three morphologically distinct P waves are
shown above with numbers

located in ventricle itself. Then depending upon the QRS
duration tachycardia are divided into narrow complex
(QRS ≤ 120 ms) tachycardia or (QRS ≥ 120 ms) tachycardia.
The narrow complex tachycardia is always supraventricular
in origin, whereas wide complex tachycardia is mostly ventricular tachycardia [1, 2].
Supraventricular tachycardia (excluding atrial fibrillation
or flutter and multifocal AT) refers to rapid rhythms that
originate and are sustained in atrial or atrioventricular node
tissue above the bundle of His (Figs. 2.18, 2.19, 2.20, and 2.21).
SVTs can be classified based on site of origin (atria or AV
node) or regularity (regular or irregular). Atrioventricular
nodal reentrant tachycardia, or AVNRT, causing about 60%
of all SVTs [1–6]. Atrioventricular reentrant tachycardia, or
AVRT, a type of SVT which includes Wolff-Parkinson-White
Syndrome (WPW). AVRT causes about 30% of all SVTs.
Sinus nodal reentrant tachycardia, or SNRT, causes less than
5% of SVTs. Intra-atrial reentrant tachycardia, or IART, is
also less than 5% of SVTs [1–6].

32

Chapter 2. ECG Rhythm Interpretation

Figure 2.18 Supraventricular tachycardia. In this ECG, there is SVT
with a heart rate of 180 bpm. It is a narrow QRS tachycardia (QRS
duration is 82 ms). P waves are not easily differentiated among the
QRS complexes. This patient had atrioventricular nodal reentrant
tachycardia (AVNRT) in electrophysiologic study. This is the commonest cause of palpitations in patients with structurally normal
hearts. It is more common in women than men (~75% of cases
occurring in women) and patients will typically complain of the sudden onset of rapid, regular palpitations. The tachycardia typically
ranges between 140 and 280 bpm and is regular in nature

Figure 2.19 Supraventricular tachycardia. This ECG presents SVT
with a heart rate of 220 bpm. It is a narrow QRS tachycardia (QRS
duration is 90 ms). Retrograde P waves can be differentiated after
the QRS complexes (shown with asterisk)

2.1 Normal Rhythm and Arrhythmia

33

Figure 2.20 Supraventricular tachycardia. This ECG presents a
SVT with narrow QRS tachycardia (heart rate is 240 bpm). This
patient had AVRT in electrophysiologic study. In AVRT accessory
pathways are fibers that connect the atrium or AV node to the ventricle outside the normal AV nodal–His-Purkinje conduction system.
These pathways can conduct impulses in the forward (anterograde
from the atrium to the ventricle) or reverse (retrograde from the
ventricle to the atrium) direction and are potential substrates for
AVRT. Tachycardia rate is usually 200–300 bpm P waves may be
buried in QRS complex or retrograde. QRS Complex usually
<120 ms unless pre-existing bundle branch block, or rate-related
aberrant conduction. QRS Alternans—phasic variation in QRS
amplitude associated with AVNRT and AVRT, distinguished from
electrical alternans by a normal QRS amplitude. T wave inversion
common and ST segment depression might be observed

Atrial flutter is a cardiac arrhythmia characterized by
atrial rates of 240–400 beats/min, usually with some degree of
conduction block at the AV node (Figs. 2.22 and 2.23). Atrial
flutter is the prototype of a macro-reentrant atrial rhythm.
The macro-reentrant circuit depends on cavotricuspid i­ sthmus
and is further divided into clockwise typical flutter and counter clockwise typical flutter. In the most common form of
atrial flutter (typical atrial flutter), ECG demonstrates a
negative sawtooth pattern in leads II, III, and aVF [1, 2].

34

Chapter 2. ECG Rhythm Interpretation

Figure 2.21 Supraventricular tachycardia. In this ECG, there is SVT
with narrow QRS tachycardia (heart rate is 160 bpm. This patient
had AVNRT in electrophysiologic study. In typical AVNRT, frequently, P waves are buried in the QRS complexes because of simultaneous activation of atria and ventricles and it is most common
presentation of AVNRT seen in most cases. If not synchronous then
pseudo S wave in inferior leads, pseudo R’ wave in lead V1 seen in
30% of the cases, resulting in subtle alteration of QRS complex. In
this case, pseudo R’ wave can be seen in V1 and V2. Pseudo S waves
can be seen in leads II, III or aVF

Figure 2.22 Atrial flutter. ECG demonstrates atrial flutter with
atrial rate of 300 bpm. Saw tooth pattern of flutter waves is seen in
leads II, III, aVF. Ventricular rate is fixed and is fraction of atrial
rate. There is 2:1 AV block and ventricular rate is 150 bpm

2.1 Normal Rhythm and Arrhythmia

35

Figure 2.23 Atrial flutter. ECG demonstrates atrial flutter with
atrial rate of 300 bpm. Saw tooth pattern of flutter waves is seen in
leads II, III, aVF. Ventricular rate is fixed and is fraction of atrial
rate. There is 4:1 block and ventricular rate is 75 bpm

Atrial fibrillation (AF) is a supraventricular arrhythmia
electrocardiographically characterized by low-amplitude
baseline oscillations (fibrillatory or F waves) and an irregularly irregular ventricular rhythm (irregular R–R intervals)
(Figs. 2.24 and 2.25). The F waves have a rate of 300–
600 beats/min and are variable in amplitude, shape, and timing. The ventricular rate during atrial fibrillation in the
absence of AV node blocking agents is typically 100–160 bpm.
AF is often described as having ‘rapid ventricular response’
once the ventricular rate is >100 bpm. ‘Slow’ AF is a term
often used to describe AF with a ventricular rate <60 bpm.
Causes of ‘slow’ AF include hypothermia, digoxin toxicity,
medications, and sinus node dysfunction [1–6].
The presence of a short PR interval, frequently with a delta
wave, defines the preexcitation syndrome. The Wolff-­Parkinson-­
White (WPW) pattern results from an accessory pathway, the
Kent bundle, which directly links the atria to the ventricles,
bypassing the atrioventricular (AV) node. The ­
ventricular
myocardium is activated early because of this bypass tract,
prior to activation via the normal AV node/His-Purkinje pathway. ECG demonstrates a short PR interval (<0.12 s) and a
delta wave (slurred and broad upstroke of the QRS complex),

36

Chapter 2. ECG Rhythm Interpretation

Figure 2.24 Atrial fibrillation. In this ECG, there is an irregularly
irregular rhythm. P waves are not seen. There is fibrillatory F waves
having small amplitudes. Please note the absence of an isoelectric
baseline. Ventricular rate is around 140 bpm

Figure 2.25 Atrial fibrillation. There is no P wave on ECG. There
are fibrillatory waves and irregular R–R intervals. Heart rare is
around 100 bpm. There are T wave inversions in chest leads suggesting ischemia

2.1 Normal Rhythm and Arrhythmia

37

representing early ventricular activation via the abnormal
accessory pathway. The QRS complex is wide (>0.12 s) and
bizarre appearing (Figs. 2.26, 2.27, and 2.28) [1–6].
Sustained ventricular tachycardia (VT) is a ventricular
rhythm faster than 100 bpm lasting at least 30 s or requiring
termination earlier due to hemodynamic instability. VT is
defined as a wide QRS complex tachycardia (QRS 120 ms or
greater) that originates from one of the ventricles, and is not
due to aberrant conduction (e.g., from bundle branch block),
at a rate of 100 bpm or greater (Figs. 2.29 and 2.30). Ventricular
tachycardia may impair cardiac output with consequent hypotension, collapse, and cardiac arrest. Prompt recognition and
initiation of treatment is required in all cases of VT [1–6].
Common cause of VTs are prior MI, active ischemia, cardiomyopathy, valvular diseases, arrhythmogenic right ventricular cardiomyopathy, left ventricular non-compaction, or
other disorders of the myocardium, known channelopathy
(e.g., long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, short QT syndrome), drug toxicity, or
electrolyte imbalance. VT can be described as monomorphic
or polymorphic. Torsades de pointes is a polymorphic VT
with a characteristic twisting morphology occurring in the
LEFT
ATRIUM

SINUS
NODE

ATRIOVENTRICULAR
NODE

1 2

2

LEFT
VENTRICLE

FUSION

ACCESSORY
CONNECTION

3

PWAVE

1

DELTAWAVE

3
RIGHT
ATRIUM

RIGHT
VENTRICLE

Figure 2.26 Short PR interval (<0.12 s) and a delta wave (slurred
and broad upstroke of the QRS complex), representing early ventricular activation via the abnormal accessory pathway

38

Chapter 2. ECG Rhythm Interpretation

Figure 2.27 Pre-excitation. ECG demonstrates short PR interval,
broad QRS with slurred upstroke of QRS the delta wave (shown
with *). Delta wave is formed because of myocardial activation
directly through the ventricular myocardium fusing with myocardial
activation using the His-Purkinje system. Thus, the QRS complex in
WPW represents a fusion beat; the initial part results from slow
ventricular activation via the accessory pathway, while the terminal
portion of ventricular activation is via the normal conduction system. Often there are associated ST segment and T wave abnormalities reflecting abnormal ventricular repolarization

Figure 2.28 Pre-excitation. In this ECG, there is short PR interval.
Please note the delta waves (shown with *). This patient had right
lateral accessory pathway which was diagnosed during EP study

2.1 Normal Rhythm and Arrhythmia

39

Figure 2.29 Ventricular tachycardia. This ECG shows a wide QRS
tachycardia with a heart rate of 185 bpm. There is AV dissociation (P
and QRS complexes at different rates)

Figure 2.30 Ventricular tachycardia. In this ECG, there is wide QRS
tachycardia with a heart rate of 164 bpm. There is extreme axis
deviation (“northwest axis”)—QRS is positive in aVR and negative
in I + aVF. There are broad QRS complexes (>160 ms). There is
fusion beat (shown with *) AV dissociation (P and QRS complexes
at different rates). Fusion beats occur when a sinus and ventricular
beat coincide to produce a hybrid complex. Capture beats occur
when the sinoatrial node transiently captures the ventricles, in the
midst of AV dissociation, to produce a QRS complex of normal
duration

40

Chapter 2. ECG Rhythm Interpretation

setting of QT interval prolongation. ‘Idiopathic’ VT occurs in
the absence of apparent structural heart disease [5–8].
Ventricular fibrillation (VF) is the major immediate cause
of sudden cardiac death. Traditionally, VF has been defined as
turbulent cardiac electrical activity, which implies a large
amount of irregularity in the electrical waves that underlie
ventricular excitation. During VF, the heart rate is too high
(>500 excitations/min) to allow adequate pumping of blood
(Fig. 2.31). In the electrocardiogram (ECG), ventricular
­complexes that are ever-changing in frequency, contour, and
amplitude characterize VF. Ventricular fibrillation is the most
important shockable cardiac arrest rhythm. Unless advanced
life support is rapidly instituted, this rhythm is fatal [5–8].
The pacemaker rhythm can easily be recognized on the
ECG. It shows pacemaker spikes: vertical signals that represent the electrical activity of the pacemaker (Figs. 2.32, 2.33,
and 2.34). Usually these spikes are more visible in unipolar
than in bipolar pacing [5–8].

High-frequency,
disorganized
excitation

Figure 2.31 Ventricular fibrillation. ECG demonstrates ventricular
fibrillation in a patient with frequent PVCs causing R on T phenomenon. There are chaotic irregular deflections of varying amplitude.
No identifiable P waves, QRS complexes, or T waves. During VF
amplitude of the waves decreases with duration (coarse wave VF
turns to fine wave VF and asystole)

2.1 Normal Rhythm and Arrhythmia

41

Figure 2.32 Pacemaker rhythm. Heart rate is 80 bpm and after each
wide QRS there is a pacemaker spike. Wide QRS is because of typical
right ventricular apical pacing from pacemaker ventricular electrode

Figure 2.33 Pacemaker rhythm. Heart rate is 70 bpm and after each
QRS complex there is a pacemaker spike. Different from previous
ECG, QRS is positive in V1 and V2. Furthermore, QRS complexes
are not wide. This is because of biventricular pacing with a cardiac
resynchronization therapy device

42

Chapter 2. ECG Rhythm Interpretation

Figure 2.34 Pacemaker rhythm. ECG demonstrates pacemaker
spikes before the P waves. Heart rate is 75 bpm with narrow QRS
complex. Different from previous two ECGs atrial pacemaker
stimulus reaches to ventricles via the atrioventricular nodal tracts.
Therefore, QRS complexes are narrow

References
1. Rowlands DJ. Clinical electrocardiography. Philadelphia: J. B.
Lippincott; 1991.
2. Mirvis DM, Goldberger AL. Electrocardiography. In: Mann DL,
Zipes DP, Libby P, Bonow RO, Braunwald E, editors. Braunwald’s
heart disease: a textbook of cardiovascular medicine. 10th ed.
Philadelphia: Elsevier Saunders; 2015.
3. Surawicz B, Knilans T, Chou TC. Chou’s electrocardiography in
clinical practice: adult and pediatric. 5th ed. Philadelphia: W. B.
Saunders; 2008.
4. Coviello JS. ECG interpretation made incredibly easy! 6th ed.
Philadelphia: Wolters Kluwer; 2016.
5. Mirvis DM, Goldberger AL. Electrocardiography. In: Zipes DP,
Libby P, Bonow RO, Mann DL, Tomaselli GF, editors. Braunwald’s
heart disease e-book: a textbook of cardiovascular medicine. 11th
ed. Philadelphia: Elsevier Saunders; 2018.
6. Goldberger AL, Goldberger ZD, Shvilkin A. Goldberger’s clinical electrocardiography: a simplified approach. Philadelphia:
Elsevier; 2017.

References

43

7. Shenasa M. ECG masters’ collection: favorite ECGs from master
teachers around the world. Minneapolis: Cardiotext; 2017.
8. Shenasa M. ECG masters’ collection: favorite ECGs from master teachers around the world volume 2. Minneapolis: Cardiotext;
2018.

Chapter 3
ECG in Conduction
Disturbances

3.1

 ormal Electrical Conduction
N
and Disturbances

Normal electrical conduction through the heart muscle takes a
predefined pathway. It travels from the Sinoatrial node (SA
node) to the Atrioventricular node (AV node) to the Bundle of
His and then onto the left and right bundle branches (­ usually in
a left to right pattern), ultimately ending up in the Purkinje
fibers. Additionally, the Left bundle branch has an anterior and
posterior component called a fascicle (Fig. 3.1) [1, 2].

Left bundle
branch

Sinoatrial
node

Left anterior fascicle

His bundle
Atrioventricular
node

Left bundle
branch

Right bundle branch

Left posterior fascicle
Right bundle branch

Figure 3.1 Components of cardiac conduction system

© Springer International Publishing AG, part of Springer
Nature 2018
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In Clinical Practice, https://doi.org/10.1007/978-3-319-90557-0_3

45

46

Chapter 3. ECG in Conduction Disturbances

Figure 3.2 Sinus arrest. There is a sudden cessation in electrical
activity of SA node lasting 4 s

Heart block can occur anywhere in the specialized conduction system beginning with the sino-atrial connections, the
AV junction, the bundle branches and their fascicles, and ending in the distal ventricular Purkinje fibers. Disorders of conduction may manifest as slowed conduction (first degree),
intermittent conduction failure (second degree), or complete
conduction failure (third degree). In addition, second degree
heart block occurs in two varieties: Type I (Wenckebach) and
Type II (Mobitz) [1, 2].
In sinus arrest, there is a sudden cessation in electrical
activity of SA node. This results in a pause in the electrical
activity seen on the tracing (Fig. 3.2). Sinus arrest can be
observed in healthy individuals up to 2 s. However, pauses
lasting more than 3 s, especially in awake period, is a marker
of sick sinus syndrome. If sinus arrest lasts long enough, then
atrial, nodal or ventricular escape beat may be seen [1, 2].
Sino-atrial (SA) exit block is due to failed propagation of
pacemaker impulses beyond the SA node (Fig. 3.3). The sino-­
atrial node continues to depolarize normally. However, some
of the sinus impulses are blocked from penetrating atrial tissue leading to intermittent failure of atrial depolarization
(dropped P waves). In sinus arrest (sinus standstill), the pause
is not a multiple of the P–P interval that preceded the pause.
In sinoatrial exit block, the pause is a multiple of the P–P
interval that preceded the pause. Sinoatrial exit block can be
divided into three types: first, second, and third degrees. The
second-degree exit block is further classified into type I (SA
block with Wenckebach conduction) and type II (SA Mobitz
II). SA block is included in a broader clinical scenario called

3.1 Normal Electrical Conduction and Disturbances
07:29:25(2)
I

.95

.83

.78

.80

1.472

HR: 65
.95

47

.88

II

III

Figure 3.3 Sinoatrial exit block

“sick sinus syndrome” (SSS) that may consist in inappropriate sinus bradycardia, SA exit block or sinus arrest, prolonged
sinus arrest with failing ectopic pacemaker, persistent atrial
or atrioventricular escape rhythm, episodes of alternating
supraventricular tachyarrhythmias with bradyarrhythmia,
long pause following cardioversion of atrial tachyarrhythmia,
or chronotropic incompetence [2, 3].
First-degree AV block is diagnosed when the PR interval
exceeds 0.2 s (5 small squares on the ECG) (Fig. 3.4). It
occurs because of disease in the AV node and is common in
older patients. Increased vagal tone, rheumatic fever, athletic
training, inferior myocardial infarction, valvular surgery, electrolyte disturbances and AV nodal blocking drugs (beta-­
blockers, calcium channel blockers, digoxin, amiodarone) are
the possible cause of the first-degree AV block. It may be a
normal variant, too [2, 3].
Wenckebach Phenomenon is the progressive prolongation
of the PR interval culminating in a non-conducted P wave.
The PR interval is longest immediately before the dropped
beat. The P–P interval remains relatively constant. The greatest increase in PR interval duration is typically between the
first and second beats of the cycle. The Wenckebach pattern
tends to repeat in P: QRS groups with ratios of 3:2, 4:3 or 5:4.
Mobitz I is usually due to reversible conduction block at the
level of the AV node (Fig. 3.5). Mobitz type I is usually a
benign rhythm, causing minimal hemodynamic disturbance
and with low risk of progression to third degree heart block.

48

Chapter 3. ECG in Conduction Disturbances

Figure 3.4 First degree atrioventricular block. ECG demonstrates a
tracing with 70 bpm and PR interval of 400 ms. There is significantly
prolonged PR interval

Figure 3.5 Second degree atrioventricular block, Mobitz Type I,
Wenckebach Phenomenon. ECG demonstrates progressive prolongation of the PR interval culminating in a non-conducted P wave
(shown with *)

Asymptomatic patients do not require treatment. Symptomatic
patients usually respond to atropine. Permanent pacing is
rarely required [2, 3].

3.1 Normal Electrical Conduction and Disturbances

49

Mobitz type II is usually due to failure of conduction at the
level of the His-Purkinje system (i.e. below the AV node). In
Mobitz type II, there is intermittent non-conducted P waves
without progressive prolongation of the PR interval (compare this to Mobitz type I). Mobitz type II is more likely to be
due to structural damage to the conducting system (e.g.
infarction, fibrosis, necrosis). There may be no pattern to the
conduction blockade, or alternatively there may be a fixed
relationship between the P waves and QRS complexes, e.g.
2:1 block, 3:1 block. The PR interval in the conducted beats
remains constant. The P waves ‘march through’ at a constant
rate. The RR interval surrounding the dropped beat(s) is an
exact multiple of the preceding RR interval (Fig. 3.6) [2, 3].
Third-degree atrioventricular (AV) block, also referred to
as third-degree heart block or complete heart block, is a disorder of the cardiac conduction system where there is no conduction through the atrioventricular node (Figs. 3.7 and 3.8).
Therefore, complete dissociation of the atrial and ­ventricular

Figure 3.6 Second degree atrioventricular block, Mobitz Type
II. Heart rate is 40 bpm and there is Mobitz type II block. In Mobitz
type II, there are alternate conducted and non-conducted P waves
without progressive prolongation of the PR interval. This ECG demonstrates twice as many P waves as QRS complexes. This is termed
2:1 conduction

50

Chapter 3. ECG in Conduction Disturbances

Figure 3.7 Third degree atrioventricular block, complete heart
block. ECG demonstrates complete heart block is represented by
QRS complexes being conducted at their own rate and totally independent of the P waves. Please note that escape rhythm is 30 bpm
with wide QRS complex. There is complete dissociation of the atrial
and ventricular activity

Figure 3.8 Third degree atrioventricular block, complete heart
block. ECG demonstrates complete heart block is represented by
QRS complexes being conducted at their own rate and totally independent of the P waves. Please note that escape rhythm is 40 bpm
with narrow QRS complex (different from previous ECG). Narrower
escape rhythm means escape focus is more proximal than the previous ECG. There is complete dissociation of the atrial P waves and
ventricular QRS complexes

3.1 Normal Electrical Conduction and Disturbances

51

activity exists. The ventricular escape mechanism can occur
anywhere from the AV node to the bundle-branch Purkinje
system. It is important to realize that not all patients with AV
dissociation have complete heart block. For example, patients
with ventricular tachycardia have AV dissociation, but not
complete heart block; in this example, AV dissociation is due
to the ventricular rate being faster than the intrinsic sinus rate.
The most common causes of AV block are idiopathic fibrosis
and sclerosis of the conduction system (about 50% of patients),
ischemic heart disease (40%). The remaining cases of AV
block are drugs (beta-blockers, calcium channel blockers,
digoxin, amiodarone), myocarditis, cardiac surgery (mitral
valve repair, tetralogy of Fallot repair), congenital and genetic
diseases [1–4].
A bundle branch block is a conduction defect of the
bundle branches or fascicles in the electrical conduction
system of the heart. Bundle branch block can be observed
on right or left branches. Criteria for differentiation of
bundle branch blocks are summarized in Table 3.1. During a
right bundle branch block, the right ventricle is not directly
activated by impulses travelling through the right bundle
branch (Fig. 3.9). The left ventricle however, is still normally
activated by the left bundle branch. In LBBB, activation of
the left ventricle of the heart is delayed, which causes the
left ventricle to contract later than the right ventricle
(Figs. 3.10 and 3.11) [3, 4].
A left anterior fascicular block (LAFB), also known as left
anterior hemiblock, occurs when the anterior fascicle of the
left bundle branch is no longer able to conduct action potentials (Fig. 3.12). The criteria to diagnose a LAFB on ECG
include the following: left axis deviation (usually between
−30 and −90°), QRS duration <120 ms and small Q waves
with tall R waves (qR complexes) in leads I and aVL. Other
criteria are small R waves with deep S waves in inferior leads
and prolonged R wave peak time in aVL >45 ms [3, 4].
In left posterior fascicular block (left posterior hemiblock), impulses are conducted to the left ventricle via the
left anterior fascicle (Fig. 3.13). The criteria to diagnose left
posterior fascicular block on ECG include the following:

Left

• QRS duration ≥120 ms
• Presence of RSR’ in left precordial
leads
• Absence of q waves in I, V4–V6;
absence of initial r wave in V1
• QRS discordant ST segment and T
waves

Table 3.1 Criteria for differentiation of bundle branch blocks
Bundle branch
V1
V6
Criteria
Right
• QRS duration ≥120 ms
• Presence of rSR’ in right precordial
leads
• Wide and deep S waves in left
precordial leads

52
Chapter 3. ECG in Conduction Disturbances

3.1 Normal Electrical Conduction and Disturbances

53

Figure 3.9 Right bundle branch block. ECG demonstrates right
bundle branch block with a heart rate of 75 bpm. There are rSR’
complexes in right precordial leads and wide and deep S waves in
left precordial leads. QRS duration is ≥120 ms. In lead V1 (which has
a good view of the right ventricle, the delay in the depolarization of
the right ventricle leads to the aptly-named “bunny ears”

Figure 3.10 ECG demonstrates left bundle branch block with a
heart rate of 80 bpm. QRS duration is 148 ms (≥120 ms) and there
are RSR’ complexes in left precordial leads. Absence of q waves in I,
V4–V6; absence of initial r wave in V1 and QRS discordant ST segment and T waves are other hallmark features of left bundle branch
block

54

Chapter 3. ECG in Conduction Disturbances

Figure 3.11 ECG demonstrates left bundle branch block with a
heart rate of 90 bpm. QRS duration is 156 ms (≥120 ms) and there
are RSR’ (notching or bunny ears) complexes in left precordial
leads. Absence of q waves in I, V4–V6; absence of initial r wave in
V1 and QRS discordant ST segment and T waves are other hallmark
features

Figure 3.12 ECG demonstrates left anterior fascicular block (QRS
duration <120 ms, left axis deviation and qR pattern in AVL) with
heart rate of 100 bpm

References

55

Figure 3.13 Left posterior fascicular block. ECG demonstrates left
posterior fascicular block (right axis deviation, rS patterns in leads I
and aVL and qR patterns in leads II, III and aVF. QRS duration is
<120 ms with a heart rate of 60 bpm

right axis deviation (>+90°), small R waves with deep S waves
in leads I and aVL and small Q waves with tall R waves in
leads II, III and aVF. QRS duration is <120 ms and prolonged
R wave peak time in aVF. There should be no evidence of
right ventricular hypertrophy and any other cause for right
axis deviation [3, 4].

References
1. Surawicz B, Knilans T, Chou TC. Chou’s electrocardiography in
clinical practice: adult and pediatric. 5th ed. Philadelphia: W. B.
Saunders; 2008.
2. Coviello JS. ECG interpretation made incredibly easy! 6th ed.
Philadelphia: Wolters Kluwer; 2016.
3. Mirvis DM, Goldberger AL. Electrocardiography. In: Zipes DP,
Libby P, Bonow RO, Mann DL, Tomaselli GF, editors. Braunwald’s
heart disease e-book: a textbook of cardiovascular medicine. 11th
ed. Philadelphia: Elsevier Saunders; 2018.
4. Goldberger AL, Goldberger ZD, Shvilkin A. Goldberger’s
­clinical electrocardiography: a simplified approach. Philadelphia:
Elsevier; 2017.

Chapter 4
ECG in Cardiac Chamber
Enlargement

4.1

Cardiac Chamber Enlargement

If an atrium becomes enlarged (typically as a compensatory
mechanism) its contribution to the P-wave will be enhanced.
Enlargement of the left and right atria causes typical P-wave
changes in lead II and lead V1 (Fig. 4.1) [1–3].
Left atrial enlargement; Prolonged P wave duration in I, II
and aVL (≥0.12 s) and notched or bifid wave (P mitrale),
increased depth and duration of terminal negative P wave in
V1 (>1 mm depth and >40 ms duration) (Fig. 4.2).
Right atrial enlargement; Presence of a peaked P wave (P
pulmonale) with amplitude >2.5 mm in the inferior leads (II,
III and AVF) and >1.5 mm amplitude in V1 (Fig. 4.3).
Biatrial enlargement; is diagnosed when criteria for both
right and left atrial enlargement are present on the same
ECG. The diagnosis of biatrial enlargement requires criteria
for right and left atrial enlargement to be met in either lead
II, lead V1 or a combination of leads [1–3].
The left ventricular hypertrophy (LVH) results in increased
R wave amplitude in the left-sided ECG leads (I, aVL and
V4–V6) and increased S wave depth in the right-sided leads

© Springer International Publishing AG, part of Springer
Nature 2018
S. Okutucu, A. Oto, Interpreting ECGs in Clinical Practice,
In Clinical Practice, https://doi.org/10.1007/978-3-319-90557-0_4

57

58

Chapter 4.

ECG in Cardiac Chamber Enlargement

Right atrium
Right atrium

Left atrium

Left atrium

NORMAL

Left atrial
enlargement

Right atrial
enlargement
V1

II

Figure 4.1 Normal P wave, left and right atrial enlargement

II

V1

Figure 4.2 ECG demonstrates sinus tachycardia (110 bpm) and left
atrial enlargement. There is prolonged P wave duration (≥0.12 s)
and notched or bifid wave (P mitrale). In addition there is increased
depth and duration of terminal negative portion of P wave in V1
(>1 mm depth and >40 ms duration)

(Figs. 4.4 and 4.5) [1–3]. Different criteria for LVH are
­summarized in Table 4.1.
Besides voltage criteria, thickened LV wall leads to prolonged depolarization (increased R wave peak time) and
delayed repolarization (ST and T-wave abnormalities) in the

4.1

Cardiac Chamber Enlargement

59

II

V1

Figure 4.3 There is prominent P wave (≥0.25 mV, P pulmonale) in
lead II and increased amplitude of initial positive portion P wave in
V1 (>1.5 mm amplitude)

Figure 4.4 Left ventricular hypertrophy. ECG demonstrates a sinus
rhythm with a heart rate of 70 bpm. There are increased R wave
amplitude in the left-sided ECG leads (I, aVL and V4–V6) and
increased S wave depth in the right-sided leads (III, aVR, V1–V3).
Prominent R in V5 (24 mm) + deepest S wave in V2 (28 mm) = 52 mm.
There are ST–T wave alterations in lateral precordial leads which is
called as strain pattern. In addition, fourth beat in this tracing is a
PAC (shown with *)

lateral leads. In addition, presence of left axis deviation and
left atrial enlargement supports the diagnosis of LVH. There
are 2 patterns of LVH: pressure overload and volume overload (Fig. 4.6) [1–3].

60

Chapter 4.

ECG in Cardiac Chamber Enlargement

Figure 4.5 Left ventricular hypertrophy. ECG demonstrates sinus
rhythm with a heart rate of 65 bpm. There is increased R wave
amplitude in the left-sided ECG leads (R waves in V5 and V6 are
greater than 27 mm)
Table 4.1 Different diagnostic criteria for LVH
Extremity leads
1. R wave in I + S wave in III >25 mm
2. R wave in aVL >11 mm
3. R wave in aVF >20 mm
4. S wave in aVR >14 mm
Chest leads
1. Tallest R wave in V4–V6 >27 mm
2. Tallest R wave in V4–V6 + Deepest S wave in V1–V3 >40 mm
3. Deepest S wave in V1–V3 >30 mm
Sokolow-Lyon index
S wave in V1 + R wave in V5 or V6 >3.5 mV; R wave in aVL
>1.1 mV
Cornell voltage criteria
S wave in V3 + R wave in aVL ≥2.8 mV (♂)
S wave in V3 + R wave in aVL ≥2.0 mV (♀)

4.1

Cardiac Chamber Enlargement

61

Patterns of left ventricular Hypertrophy
Pressure overload
Tall R wave with slurred ST segment and
inverted T wave (strain pattern)

Volume overload
Tall R wave with upright T wave
Deep Q wave
Inverted U wave

V6

V6

Figure 4.6 Two major patterns of left ventricular hypertrophy

Figure 4.7 Right ventricular hypertrophy. ECG demonstrates sinus
tachycardia with a rate of 140 bpm. There is dominant R wave in V1
(>7 mm tall or R/S ratio >1), dominant S wave in V5 or V6 (>7mm
deep or R/S ratio <1) and QRS duration <120 ms (i.e. changes not
due to RBBB). In this ECG there is right ventricular strain pattern,
ST depression/T wave inversion in the right precordial (V1–V4)
leads and S1 S2 S3 pattern

Right ventricular hypertrophy occurs mainly in lung disease or in congenital heart disease. The ECG shows a negative QRS complex in I (and thus a right heart axis) and a
positive QRS complex in V1 (Fig. 4.7). ECG criteria for right
ventricular hypertrophy are summarized in Table 4.2.

62

Chapter 4.

ECG in Cardiac Chamber Enlargement

Table 4.2 ECG criteria for right ventricular hypertrophy
Diagnostic criteria
• Right axis deviation of +110° or more
• Dominant R wave in V1 (>7 mm tall or R/S ratio >1)
• Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio <1)
• QRS duration <120 ms (i.e. changes not due to RBBB)
Supporting criteria
• Right atrial enlargement (P pulmonale)
• R
 ight ventricular strain pattern = ST depression/T wave
inversion in the right precordial (V1–V4) and inferior (II, III,
aVF) leads
• S
 1 S2 S3 pattern = far right axis deviation with dominant S
waves in leads I, II and III
• Deep S waves in the lateral leads (I, aVL, V5–V6)

Figure 4.8 Low voltage. In this ECG, rhythm is sinus rhythm with a
70 bpm. There is low voltage on ECG because of pericardial effusion. QRS amplitude is less than 5 mm in the limb leads and less
than 10 mm in the precordial leads

References

63

Dominant R-wave in V1/V2 implies that the R-wave is
larger than the S-wave, and this may be pathological. If the
R-wave is larger than the S-wave, the R-wave should be
<5 mm, otherwise the R-wave is abnormally large. This may
be explained by right bundle branch block, right ventricular
hypertrophy, hypertrophic cardiomyopathy,
posterolateral ischemia/infarction (if the patient experiences chest pain), preexcitation, dextrocardia or misplacement of chest electrodes [1–3].
Low voltage on ECG is defined as a peak-to-peak QRS
amplitude of less than 5 mm in the limb leads and/or less than
10 mm in the precordial leads (Fig. 4.8). Low voltage may be
present in the following situations: obesity, chronic obstructive pulmonary disease, pericardial effusion, amyloidosis and
hypothyroidism [1–3].

References
1. Rowlands DJ. Clinical electrocardiography. Philadelphia: J. B.
Lippincott; 1991.
2. Mirvis DM, Goldberger AL. Electrocardiography. In: Zipes DP,
Libby P, Bonow RO, Mann DL, Tomaselli GF, editors. Braunwald’s
heart disease e-book: a textbook of cardiovascular medicine. 11th
ed. Philadelphia: Elsevier Saunders; 2018.
3. Goldberger AL, Goldberger ZD, Shvilkin A. Goldberger’s clinical electrocardiography: a simplified approach. Philadelphia:
Elsevier; 2017.

Chapter 5
ECG in Coronary Artery
Disease

5.1

 CG Changes in Spectrum of Coronary
E
Artery Disease

There are wide variety of ECG changes in coronary artery
disease spectrum. ECG changes in spectrum of coronary
artery disease are summarized in Table 5.1. Ischemia usually
alters T waves (Figs. 5.1 and 5.2). In subendocardial ischemia,
there are symmetrical giant and peaked T waves. In addition,
prolongation of QT interval might be observed. Whereas, in
subepicardial ischemia, there are symmetrical deep T wave
inversions [1, 2].
Table 5.1 ECG changes in
spectrum of coronary artery
disease

• T wave inversion
• ST segment depression
• ST segment elevation
• P
 seudonormalization of T
waves
• T wave flattening
• Peaked T wave
• U wave inversion

© Springer International Publishing AG, part of Springer
Nature 2018
S. Okutucu, A. Oto, Interpreting ECGs in Clinical Practice,
In Clinical Practice, https://doi.org/10.1007/978-3-319-90557-0_5

65

66

Chapter 5.

ECG in Coronary Artery Disease

Figure 5.1 Myocardial ischemia. ECG demonstrates sinus rhythm
with a heart rate 60 bpm. There are deeply inverted T waves
(Wellens Type B) on left precordial leads and inferior leads. There
are PACs on fifth beat and tenth beat (shown with *)

Figure 5.2 Myocardial ischemia. ECG demonstrates sinus rhythm
with a heart rate 75 bpm. There are diffuse down sloping ST segment
depression and ST elevation in aVR and V1. This is due to the diffuse subendocardial ischemia. The ST elevation in aVR is reciprocal
to the ST depression vector that is directed anterior, lateral, and
inferior (towards leads II and V5). This pattern is usually observed
in patients with left main coronary artery or proximal left anterior
descending coronary artery stenosis

5.1 ECG Changes in Spectrum of Coronary Artery Disease

67

Myocardial injury is usually reflected by ST segment
changes on ECG. In subendocardial injury, there is ST segment depression. However, there is ST segment elevation in
subepicardial injury in leads oriented to this region. There is
usually reciprocal ST depression in the electrically opposite
leads [1, 2]
The cardiomyocytes in the subendocardial layers are especially vulnerable for a decreased perfusion. Subendocardial
ischemia manifests as ST depression and is usually reversible.
Causes of ST segment depression are summarized in Table 5.2.
Causes of T wave inversions are summarized in Table 5.3 [3, 4].
In the first hours and days after the onset of a myocardial
infarction, several changes can be observed on the ECG. First,
large peaked T waves (or hyperacute T waves), then ST elevation, then negative T waves and finally pathologic Q waves
Table 5.2 Causes of ST
segment depression

Coronary artery disease
Left ventricular hypertrophy
Cardiomyopathies
Drugs (digoxin)
Hypokalemia, hypomagnesemia
Stroke
Bundle branch blocks (RBBB, LBBB)

Table 5.3 Causes of T
wave inversions

Normal variant
Myocardial ischemia
Myocarditis, pericarditis
Stroke
Left or right ventricular overload
Idiopathic diffuse T wave inversions
Secondary T wave changes: bundle
branch blocks, pre-­excitation
Ventricular pacing

68

Chapter 5.

ECG in Coronary Artery Disease

develop (Fig. 5.3). Causes of ST segment elevation are summarized in Table 5.4 [3, 4].
Pathologic Q waves are the signs of previous myocardial
infarction. They are the result of absence of electrical activity

Normal

Seconds

Minutes

Hours

Days after an acute myocardial infarction

Figure 5.3 ECG changes in acute myocardial infarction
Table 5.4 Causes of ST segment elevation
Myocardial ischemia, myocardial infarction
• Non-infarct transmural ischemia (vasospastic angina)
• Acute myocardial infarction
• Post-myocardial infarction (ventricular aneurysm)
Acute pericarditis
Normal variant (early repolarization)
Left ventricular hypertrophy /left bundle branch block (V1–V2
or only V3)
Myocardial injury: myocarditis, tumor invasion
Trauma
Hypothermia (J wave/Osborn wave)
DC cardioversion
Stroke
Hyperkalemia
Brugada’s syndrome (right precordial leads)
Class IC antiarrhythmic drugs (especially V1–V2)
Hypercalcemia (especially V1–V2)

5.1 ECG Changes in Spectrum of Coronary Artery Disease

69

in the related area. A myocardial infarction can be thought of
as an electrical ‘hole’ as scar tissue is electrically dead and
therefore results in pathologic Q waves [3, 4].
The early and accurate identification of the infarct-related
artery on the ECG can help predict the amount of myocardium at risk. The specificity of the ECG in acute MI is limited
by individual variations in coronary anatomy as well as by the
presence of preexisting coronary artery disease, particularly
in patients with a previous MI, collateral circulation, or previous coronary artery by-pass surgery. The ECG is also limited
by its inadequate representation of the posterior, lateral, and
apical walls of the left ventricle. Despite these limitations, the
electrocardiogram can help in identifying proximal occlusion
of the coronary arteries, which results in the most extensive
and most severe myocardial infarctions [4, 5]. Different
examples of ECG in different stages of MI are shown in next
11 figures (Figs. 5.4, 5.5, 5.6, 5.7, 5.8, 5.9, 5.10, 5.11, 5.12, 5.13,
and 5.14). Localization of MI according to involved ECG
leads are summarized in Table 5.5.

Figure 5.4 Acute anterior wall myocardial infarction. There are ST
segment elevations in V1–V4 leads. Reciprocal ST segment depression can be easily noticed in inferior leads. There is sinus rhythm
with a heart rate of 100 bpm. There are q waves in V1–V3 suggesting
evolving anterior infarction

70

Chapter 5.

ECG in Coronary Artery Disease

Figure 5.5 Acute extensive anterior wall myocardial infarction.
There are ST segment elevations in V1–V6, I and aVL. Reciprocal
ST segment depression can be easily noticed in inferior leads. There
is sinus tachycardia with a heart rate of 120 bpm. This pattern of ST
elevation frequently called as tombstoning ST elevation

Figure 5.6 Acute anteroseptal wall myocardial infarction. There are
ST segment elevations in V1–V3. There is a mild sinus tachycardia
with a heart rate of 102 bpm

5.1 ECG Changes in Spectrum of Coronary Artery Disease

71

Figure 5.7 Subacute anterior wall myocardial infarction. There are
ST segment elevations in V3–V5 leads and are q waves in V1–V5
suggesting a subacute anterior myocardial infarction. There is also
prominent loss of R waves and T wave inversions in precordial leads

Figure 5.8 Old anterior wall myocardial infarction. There are q
waves in V1–V6 because of anterior infarction. Please note, there is
prominent loss of R waves and T wave inversions in precordial leads

72

Chapter 5.

ECG in Coronary Artery Disease

Figure 5.9 There are ST segment elevations in leads II, III and
aVF. Reciprocal ST segment depression can be easily noticed in I
and AVL

Figure 5.10 Acute inferoposterior wall myocardial infarction. There
are ST segment elevations in inferior leads. Reciprocal ST segment
depression can be noticed in lateral leads. There is ST segment
depression in V1 and particularly in V2. This pattern of ST depression is mirror like changes of posterior myocardial infarction

5.1 ECG Changes in Spectrum of Coronary Artery Disease

73

Figure 5.11 Subacute inferior wall myocardial infarction. There are
ST segment elevations in inferior leads. There are pathological q
waves in II, III and aVF suggesting inferior myocardial infarction
and prominent loss of R waves and T wave inversions in inferior
leads. Please also note PR interval prolongation and first degree AV
block

Figure 5.12 Old inferior wall myocardial infarction. The tracing
shows q waves in II, III and aVF suggesting inferior myocardial
infarction. There is prominent loss of R waves and T wave inversions
in inferior leads. Please note the marked left axis deviation because
of myocardial infarction

74

Chapter 5.

ECG in Coronary Artery Disease

Figure 5.13 Acute lateral myocardial infarction. ECG demonstrates
ST segment elevations in leads I and aVL. Reciprocal ST segment
depression can be easily noticed in inferior leads

Figure 5.14 Acute inferior myocardial infarction with right ventricular infarction. In upper tracing, there are ST segment elevations in II,
III and aVF. Reciprocal ST segment depression can be seen in I and
aVL leads. In lower and left tracings, there are ST segment elevations
in the right-sided leads (V3R–V6R). In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence
of ST elevation in V1. Usually, ST segment elevation in lead III > lead
II. Right ventricular infarction is confirmed by the presence of 1 mm
ST segment elevation in the V3R–V6R. The most sensitive lead for
right ventricular myocardial infarction is V4R [1, 4]

References

75

Table 5.5 Localization of MI according to involved ECG leads
Localization of MI
Involved leads
Anterior wall
Anteroseptal

V1, V2, V3

Anterior

V1–V3 + V4–V6

Anterolateral

V4, V5, V6, aVL and I

Extensive anterior

V1–V6, aVL and I

Lateral

aVL and I

Inferior wall
Inferior

II, III and aVF

Inferolateral

II, III, aVF, V5–V6, sometimes I, aVL

Inferoseptal

II, III, aVF, V1–V3

Posterior wall

V1, V2 (mirror like changes)

Subendocardial

Any

References
1. Rowlands DJ. Clinical electrocardiography. Philadelphia: J. B.
Lippincott; 1991.
2. Surawicz B, Knilans T, Chou TC. Chou’s electrocardiography in
clinical practice: adult and pediatric. 5th ed. Philadelphia: W. B.
Saunders; 2008.
3. Coviello JS. ECG interpretation made incredibly easy! 6th ed.
Philadelphia: Wolters Kluwer; 2016.
4. Mirvis DM, Goldberger AL. Electrocardiography. In: Zipes DP,
Libby P, Bonow RO, Mann DL, Tomaselli GF, editors. Braunwald’s
heart disease e-book: a textbook of cardiovascular medicine. 11th
ed. Philadelphia: Elsevier Saunders; 2018.
5. Goldberger AL, Goldberger ZD, Shvilkin A. Goldberger’s clinical electrocardiography: a simplified approach. Philadelphia:
Elsevier; 2017.

Chapter 6
ECG in Miscellaneous
Conditions

6.1

Acute Pericarditis

The most sensitive ECG characteristic of acute pericarditis is
ST-segment elevation, which reflects the abnormal repolarization that develops secondary to pericardial inflammation.
There may also be ST-segment depression in leads aVR and
V1. Depression of the PR segment is very specific of acute
pericarditis and is attributed to subepicardial atrial injury and
occurs in all leads except aVR and V1. These leads may
exhibit PR-segment elevation [1, 2]. Electrocardiographic differences between pericarditis and myocardial infarction are
summarized in Table 6.1.
The pattern of ST-segment elevation is important in the
diagnosis of acute pericarditis (Figs. 6.1 and 6.2). The
ST-segment elevation that occurs during acute pericarditis is
usually concave compared with the convex appearance of the
ST segment that occurs during the acute myocardial infarction. Another important feature of acute pericarditis is the
widespread ST-segment elevation not corresponding with any
specific arterial territory, which usually occurs in association
with acute myocardial infarction. Also, reciprocal changes are
absent in acute pericarditis, although they are frequently
found with acute myocardial infarction [2–4].

© Springer International Publishing AG, part of Springer
Nature 2018
S. Okutucu, A. Oto, Interpreting ECGs in Clinical Practice,
In Clinical Practice, https://doi.org/10.1007/978-3-319-90557-0_6

77

78

Chapter 6.

ECG in Miscellaneous Conditions

Table 6.1 Electrocardiographic differences between pericarditis
and myocardial infarction
Acute myocardial
Pericarditis
infarction
ST segment
Diffuse concave ST
Localized, convex,
elevation, absence of
reciprocal changes
reciprocal changes
PR depression

Common

Absent

Q wave

Absent (if no
infarction)

Common (Q wave
MI)

T wave

T wave inversion seen
after J point turned to
isoelectric

T wave inversion
starts when ST
segment is still
elevated

Arrhythmia

Rare

Frequent

Conduction
abnormalities

Rare

Frequent

Figure 6.1 Acute pericarditis. ECG demonstrates widespread concave ST-segment elevation secondary to pericardial inflammation.
There are ST-segment depressions in leads aVR and V1

6.1 Acute Pericarditis

79

Figure 6.2 Acute pericarditis. ECG demonstrates widespread concave ST-segment elevation secondary to pericardial inflammation.
There are ST-segment depressions in leads aVR and V1. Depression
of the PR segment is very specific of acute pericarditis and is attributed to subepicardial atrial injury and occurs in all leads except aVR
and V1. These leads may exhibit PR-segment elevation
Table 6.2 Four major ECG stages in acute pericarditis
Stage
ST segment
T wave
PR segment
I
Elevation
Positive
Isoelectric or
depression
II
early

Isoelectric

Positive

Isoelectric or
depression

II late

Isoelectric

Reduced/flat/
negative

Isoelectric or
depression

III

Isoelectric

Negative

Isoelectric

IV

Isoelectric

Positive

Isoelectric

Electrocardiographic changes in acute pericarditis are different during the clinical evolution of acute pericarditis.
There are 4 major ECG stages in acute pericarditis [3–5].
These stages are summarized in Table 6.2.

80

Chapter 6.

ECG in Miscellaneous Conditions

Figure 6.3 Early repolarization. In this ECG there is widespread
concave ST elevation, most prominent in the precordial leads (V2–
V5). Notching or slurring at the J-point are present

Early repolarization is another situation with ST elevation,
most prominent in the precordial leads or inferior leads
(Fig. 6.3). Notching or slurring at the J-point are usually present. ST changes are relatively stable over time (no progression on serial ECG tracings). ST elevation is usually <2 mm
in the precordial leads and <0.5 mm in the limb leads,
although precordial ST elevation may be up to 5 mm in some
instances. No reciprocal ST depression to suggest STEMI
(except in aVR) [3–5].

6.2

Electrolyte Abnormalities

ECG can give valuable information in electrolyte abnormalities and drug effects (Fig. 6.4). Narrow and tall peaked T
wave is an early sign of hyperkalemia. It is unusual for T
waves to be taller than 5 mm in limb leads and taller than
10 mm in chest leads (Fig. 6.5). Hyperkalemia should be suspected if these limits are exceeded in more than one lead. As
serum potassium concentration continues to rise, the PR
interval becomes longer, the P wave loses its amplitude and

6.2 Electrolyte Abnormalities

81

T

P

Normal
QRS
QT prolongation

u

Hypokalemia

Peaked T wave

Hyperkalemia
QT prolongation

Hypocalcemia
QT shortening

Hypercalcemia

Figure 6.4 ECG changes in common electrolyte abnormalities

Figure 6.5 Hyperkalemia. ECG from a patient with hyperkalemia
demonstrates tall peaked T wave both in limb leads and chest leads.
T waves are taller than 5 mm in limb leads and taller than 10 mm in
chest leads

may disappear, and the QRS complex widens. When hyperkalemia is very severe, the widened QRS complexes merge with
their corresponding T waves and the resultant ECG looks
like a series of sine waves [4, 5].

82

Chapter 6. ECG in Miscellaneous Conditions
HYPERKALEMIA
Tall, peaked
T wave

Decreased
R wave
amplitude
Wide, flat
P wave
Prolonged
PR interval

Depressed
ST segment
Widened QRS

HYPOKALEMIA
Slightly
prolonged
PR interval
Slightly
peaked
P wave

ST depression

Shallow
T wave

Prominent
U wave

Figure 6.6 Hypokalemia. ECG of a patient with severe hypokalemia (serum K = 2.1 mEq/L) demonstrates widespread ST segment
depression. T wave becomes flattened together with appearance of
a prominent U wave. On right side of the tracing, typical ECG
changes in potassium perturbations were summarized

With hypokalemia, the T wave becomes flattened together
with appearance of a prominent U wave (Fig. 6.6). The ST
segment may become depressed and the T wave inverted.
Unlike hyperkalemia, these additional changes are not
related to the degree of hypokalemia. ECG signs of
­hypercalcemia and hypocalcemia may not be obvious even in
patients who have deranged plasma calcium concentrations
that are clinically significant. If they are present, hypercalcemia is associated with short QT interval and hypocalcemia
with long QT interval. Interval shortening, or lengthening is
mainly in the ST segment [4, 5].
In hypomagnesemia, there are similar ECG changes is
hypokalemia. T wave flattening, and ST depression are common. The primary ECG abnormality seen with hypomagnesaemia is a prolonged QTc. Atrial and ventricular ectopy,
atrial tachyarrhythmias and torsades de pointes are seen in
the context of hypomagnesemia [4, 5].

6.3

6.3

Drug Effects and Miscellaneous Situations

83

 rug Effects and Miscellaneous
D
Situations

Digitalis effect refers to the presence on the ECG of
downsloping ST depression with a characteristic “Salvador
Dali sagging” or “reverse tick” appearance, flattened, inverted,
or biphasic T waves and shortened QT interval (Fig. 6.7).
Additional ECG Features are mild PR interval prolongation
of up to 240 ms (due to increased vagal tone), prominent U
waves, peaking of the terminal portion of the T waves and J
point depression (usually in leads with tall R waves) (Fig. 6.8).
Digitalis toxicity can induce literally every arrhythmia except
for rapidly conducted atrial arrhythmias (atrial fibrillation
and atrial flutter). The classic arrhythmias seen during digitalis toxicity include atrial tachycardia with a 2:1 conduction,
bidirectional ventricular tachycardia and atrial fibrillation
with a slow ventricular response [4, 5].
The ECG is a vital tool in the prompt diagnosis of poisoning with sodium-channel blocking medications such as
­tricyclic antidepressant (TCA) overdose. Features consistent
Digitalis Effect

ST depression with a
characteristic “Salvador
Dali sagging” or “reverse
tick” appearance

Figure 6.7 Digitalis effect. Downsloping ST depression with a characteristic “Salvador Dali sagging” or “reverse tick” appearance, T
waves and shortened QT interval

84

Chapter 6.

ECG in Miscellaneous Conditions

Figure 6.8 Digitalis effect. ECG demonstrates atrial fibrillation and
typical digitalis effect. There are downsloping ST segment depressions with a reverse tick appearance, flattened T waves and shortened QT interval

with sodium-channel blockade are: interventricular conduction delay—QRS >100 ms in lead II, right axis deviation,
terminal R wave >3 mm in aVR, R/S ratio >0.7 in
aVR. Patients with tricyclic overdose will also usually demonstrate sinus tachycardia secondary to muscarinic (M1)
receptor blockade [4, 5].
Quinidine, phenothiazines and tricyclic antidepressants may
cause low voltage T waves (or T wave inversion), ST segment
depression, prolonged Q-T interval, increased height of U
wave, widening and notching of P waves. Toxic doses of quinidine may cause widened QRS complexes, heart block, VT and
VF. Vaughan- Willams class IA and III (amiodarone, dofetilide,
ibutilide, sotalol) drugs may prolong QT interval. Beta blockers results sinus bradycardia and PR prolongation [4, 5].
The heart rate adjusted QT interval referred as the corrected QT interval (QTc interval). Bazett’s formula has
traditionally been used to calculate the corrected QT duration (QTc = QT/√RR). QTc is prolonged if >450 ms in
men or >470 ms in women (Fig. 6.9). QTc >500 is associated with increased risk of torsades de pointes. QTc is
abnormally short if <350 ms [4, 5]. Causes of long QT are
summarized in Table 6.3 and Table 6.4.

6.3

Drug Effects and Miscellaneous Situations

85

Figure 6.9 Long QT. ECG demonstrates sinus rhythm with a rate of
70 bpm. QTc interval is 540 ms which is significantly prolonged

Table 6.3 Causes of long QT
Drug effects
Hypokalemia
Hypomagnesemia
Hypothermia
Myocardial ischemia
Stroke, intracranial hypertension
Congenital long QT syndrome

ECG findings in patients with hypothermia can include
Osborn wave (also referred to as the J wave), prolongation of
the PR, QRS and QT intervals, T wave inversions, and various
dysrhythmias including atrial fibrillation, sinus bradycardia,
atrioventricular block, and ventricular fibrillation. Fatal ventricular fibrillation or asystole can occur in hypothermic patients
when core body temperature falls below 28 °C (Fig. 6.10) [4, 5].
Most common stroke-associated abnormalities in ECG
are T-wave abnormalities, prolonged QTc interval, and
arrhythmias (Fig. 6.11). Other ECG changes in stroke might

• Quinidine

• Procainamide

• Disopyramide

• Chlorpromazine

• Haloperidol

• Droperidol

 – Erythromycin
 – Clarithromycin

• Citalopram

• Escitalopram

• Venlafaxine

• Bupropion

• Moclobemide

• Imipramine

• Nortriptyline

• Desipramine

• Terfenadine

• Loratadine

• Astemizole

– Cisapride

 – Fluoroquinolones

• Macrolides

• Quinine

• Hydroxychloroquine

• Chloroquine

• Doxepin

• Diphenhydramine

• Mianserin

• Amitriptyline

Other

• Ibutilide

• Dofetilide

• Amiodarone

• Sotalol

Class III antiarrhythmics

Other antidepressants

Antihistamines

• Encainide

• Flecainide

Type IC antiarrhythmics

Tricyclic antidepressants

• Thioridazine

• Amisulpride

• Olanzapine

• Quetiapine

Type IA antiarrhythmics

Antipsychotics

Table 6.4 Drugs causing QT prolongation

86
Chapter 6. ECG in Miscellaneous Conditions

6.3

Drug Effects and Miscellaneous Situations

87

Figure 6.10 Hypothermia. ECG demonstrates sinus bradycardia
with shivering artifacts and prominent J waves which is eponymously called as Osborn waves. Hypothermia is defined as a core
body temperature of <35 °C. Hypothermia may produce the following ECG abnormalities: bradyarrhythmia, Osborne J Waves (shown
on right side with arrow), prolonged PR, QRS and QT intervals,
shivering artifacts, PVCs, cardiac arrest due to VT, VF or asystole

Figure 6.11 Stroke (cerebrovascular accident). ECG demonstrates
atrial fibrillation (possible stroke etiology for this case), widespread
ST segment depression and mild QTc prolongation

be pathologic Q-wave, ST-segment depression, ST-segment
elevation, and prominent-U wave [4, 5].
Artifacts on the ECG can result from a variety of internal
and external causes (Fig. 6.12). Loose lead artifact may be
encountered when dealing with patients who are diaphoretic

b

c

Figure 6.12 (a) Electromagnetic interference (EMI) artifact. (b) Wandering baseline artifact. (c) Motion artifact

a

88
Chapter 6. ECG in Miscellaneous Conditions

References

89

because the electrodes simply will not stick to the patient’s
body. You may also see this type of artifact when placing the
electrode over hair. Wandering baseline artifact presents as a
slow, undulating baseline on the electrocardiogram. It can be
caused by patient movement, including breathing.
Electromagnetic interference (EMI) artifact usually results
from electrical power lines, electrical equipment, and mobile
telephones. Motion artifact usually occurs because of movements of patient, tremor or shivering [4, 5].

References
1. Rowlands DJ. Clinical electrocardiography. Philadelphia: J. B.
Lippincott; 1991.
2. Surawicz B, Knilans T, Chou TC. Chou’s electrocardiography in
clinical practice: adult and pediatric. 5th ed. Philadelphia: W. B.
Saunders; 2008.
3. Coviello JS. ECG interpretation made incredibly easy! 6th ed.
Philadelphia: Wolters Kluwer; 2016.
4. Mirvis DM, Goldberger AL. Electrocardiography. In: Zipes DP,
Libby P, Bonow RO, Mann DL, Tomaselli GF, editors. Braunwald’s
heart disease e-book: a textbook of cardiovascular medicine. 11th
ed. Philadelphia: Elsevier Saunders; 2018.
5. Goldberger AL, Goldberger ZD, Shvilkin A. Goldberger’s clinical electrocardiography: a simplified approach. Philadelphia:
Elsevier; 2017.

Chapter 7
Eponymous ECGs

7.1 Eponymous ECG Concepts
There are many eponymous ECG concepts in current cardiology practice. Ashman phenomenon, also known as Ashman
beats, describes a wide QRS complex, often seen isolated that
is typically seen in atrial fibrillation [1, 2]. It is more often
misinterpreted as a premature ventricular complex (Fig. 7.1).
In Brugada Syndrome, ECG demonstrates typical ST segment elevation >2 mm in V1–V3 followed by a negative T
wave (Fig. 7.2). Brugada Syndrome is an ECG abnormality
with a high incidence of sudden death in patients with structurally normal hearts. Brugada syndrome is due to a mutation
in the cardiac sodium channel gene. This is often referred to
as a sodium channelopathy. Type 1 (Coved ST segment elevation >2 mm in >1 of V1–V3 followed by a negative T wave) is
the only ECG abnormality that is potentially diagnostic. This
has been referred to as Brugada sign. Brugada Type 2: has
>2 mm of saddleback shaped ST elevation. Brugada type 3:
can be the morphology of either type 1 or type 2, but with
<2 mm of ST segment elevation [1, 2].
Crochetage’ sign if the presence of notch near the apex of
the R wave in inferior limb leads [3]. This pattern of ECG
suggests ostium secundum atrial septal defect (Fig. 7.3).

© Springer International Publishing AG, part of Springer
Nature 2018
S. Okutucu, A. Oto, Interpreting ECGs in Clinical Practice,
In Clinical Practice, https://doi.org/10.1007/978-3-319-90557-0_7

91

92
V1

Chapter 7.

Eponymous ECGs

The underlying rhythm is atrial fibrillation

Similar RR intervals

Long RR

Aberration

Short RR

Figure 7.1 Ashman’s phenomenon. Presence of aberrantly conducted beats, usually of RBBB morphology, due a long refractory
period as determined by the preceding R–R interval

Figure 7.2 Brugada syndrome. Typical ST segment elevation >2 mm
in V1–V3

The de Winter ECG pattern is an anterior STEMI equivalent that presents without obvious ST segment elevation [4–
6]. Key diagnostic features include ST depression and peaked
T waves in the precordial leads (Fig. 7.4). The de Winter pattern is seen in nearly 2% of acute LAD occlusions and is
under-recognized by clinicians [4–6].
Wellens’ syndrome is a pattern of deeply inverted or
biphasic T waves in V2–V3, which is highly specific for a critical stenosis of the left anterior descending artery (Fig. 7.5).
Diagnostic criteria for Wellens’ syndrome are deeply-inverted

7.1

Eponymous ECG Concepts

93

Figure 7.3 Crochetage sign. The ECG demonstrated sinus rhythm,
incomplete right bundle branch block and ‘Crochetage’ sign (notch
near the apex of the R wave) in inferior limb leads

Figure 7.4 De Winter’s T waves. ST depression and peaked T waves
in the precordial leads

or biphasic T waves in V2–V3 (may extend to V1–V6), isoelectric or minimally-elevated ST segment (<1 mm), no precordial Q waves, preserved precordial R wave progression.
There are two patterns of T-wave abnormality in Wellens’
syndrome: Type A = Biphasic, with initial positivity & terminal negativity (25% of cases), Type B = Deeply and symmetrically inverted (75% of cases) [4–6].

94

Chapter 7.

Eponymous ECGs

Figure 7.5 Wellens’ syndrome. There are deeply inverted or biphasic T waves in V2–V3, which is highly specific for a critical stenosis
of the left anterior descending artery

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/ARVC) is an inherited cardiomyopathy characterized by structural and functional abnormalities in the right
ventricle resulting in ventricular arrhythmia. Epsilon wave is
a small positi