Main ECG from Basics to Essentials: Step by Step

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This brand new guide assists students, interns and residents in developing a functional understanding of the set-up, workings and interpretation of ECGs
  • Step-by-step graphics and short, bite-sized explanations
  • Covers all major cardiac abnormalities including hypertrophy, arrhythmias, conduction blocks, and pre-excitation syndromes
  • Begins with a section on physiology of the heart and the basic set up of ECG recording
  • Features top tips on what to look for, complete with illustrated examples
  • Supported by a companion website featuring additional practice tracings

Year:
2016
Edition:
1
Publisher:
Wiley-Blackwell
Language:
english
Pages:
440 / 442
ISBN 10:
1119066417
ISBN 13:
9781119066415
File:
PDF, 33.47 MB
Download (pdf, 33.47 MB)

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ECG from Basics to
Essentials
Step by Step

ECG from Basics to
Essentials
Step by Step
Roland X. Stroobandt
MD, PhD, FHRS
Professor Emeritus of Medicine
Heart Center, Ghent University Hospital
Ghent, Belgium

S. Serge Barold
MD, FRACP, FACP, FACC, FESC, FHRS
Clinical Professor of Medicine Emeritus
Department of Medicine
University of Rochester School of Medicine and Dentistry
Rochester, New York, USA

Alfons F. Sinnaeve
Ing. MSc
Professor Emeritus of Electronic Engineering
KUL – Campus Vives Oostende, Department of Electronics
Oostende, Belgium

This edition first published 2016 © 2016 by John Wiley & Sons, Ltd.
Registered office:

John Wiley & Sons, Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

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the copyright material in this book please see our website at www.wiley.com/wiley-blackwell
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The contents of this work are intended to further general scientific research, understanding, and discussion only and are not
intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by health
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changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment,
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or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the
author or the publisher endorses the information the organization or Website may provide or recommendations it may make.
Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when
this work was written and when it is read. No warranty may be created or extended by any promotional statements for this
work. Neither the publisher nor the author shall be liable for any damages arising herefrom.
Library of Congress Cataloging-in-Publication Data are available
ISBN 9781119066415
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in
electronic books.
Cover image: Courtesy of Alfons F. Sinnaeve
Set in 9/10 Helvetica LT Std by Aptara

1

2016

Contents

Preface, vi
About the companion website, vii
1 Anatomy and Basic Physiology, 1
2 ECG Recording and ECG Leads, 21
3 The Normal ECG and the Frontal Plane QRS Axis, 53
4 The Components of the ECG Waves and Intervals, 73
5 P waves and Atrial Abnormalities, 85
6 Chamber Enlargement and Hypertrophy, 99
7 Intraventricular Conduction Defects, 105
8 Coronary Artery Disease and Acute Coronary Syndromes, 123
9 Acute Pericarditis, 187
10 The ECG in Extracardiac Disease, 193
11 Sinus Node Dysfunction, 203
12 Premature Ventricular Complexes (PVC), 217
13 Atrioventricular Block, 227
14 Atrial Rhythm Disorders, 243
15 Ventricular Tachycardias, 279
16 Ventricular Fibrillation and Ventricular Flutter, 305
17 Preexcitation and Wolff-Parkinson-White Syndrome (WPW), 311
18 Electrolyte Abnormalities, 327
19 Electrophysiologic Concepts, 333
20 Antiarrhythmic Drugs, 351
21 Pacemakers and their ECGs, 359
22 Errors in Electrocardiography Monitoring, Computerized ECG, Other Sites of ECG Recording, 391
23 How to Read an ECG, 407

Index, 425

v

vi

Preface

Before deciding to write this book, we examined
many of the multitude of books on electrocardiography to determine whether there was a need for
a new book with a different approach focusing on
graphics. In our experience the success of our “step
by step” books on cardiac pacemakers and implanted
cardioverter-defibrillators was largely due to the
extensive use of graphics according to feedback we
received from many readers. Consequently in this
book we used the same approach with the liberal use
of graphics. This format distinguishes the book from
all the other publications. In this way, the book can
be considered as a companion to our previous “step
by step” books. The publisher offers a large number of PowerPoint slides obtainable on the Internet.

Based on a number of suggestions an accompanying set of test ECG tracings is also provided on
the Internet. We are confident that our different
approach to the teaching of electrocardiography will
facilitate understanding by the student and help the
teacher, the latter by using the richly illustrated work.
The authors would also like to thank Garant Publishers, Antwerp, Belgium /Apeldoorn, The Netherlands for authorizing the use of figures from the
Dutch ECG book, ECG: Uit of in het Hoofd, 2006
edition, by E. Andries, R. Stroobandt, N. De Cock,
F. Sinnaeve and F. Verdonck,
Roland X. Stroobandt
S. Serge Barold
Alfons F. Sinnaeve

About the companion website

This book is accompanied by a companion website, containing all the figures from the book for you to
download: www.wiley.com/go/stroobandt/ecg

vii

Chapter 1

ANATOMY
AND
BASIC PHYSIOLOGY
*
*
*
*

What is an ECG?
Blood circulation – the heart in action
The conduction system of the heart
Myocardial electrophysiology
° About cardiac cells
° Depolarization of a myocardial fiber
° Distribution of current in myocardium
* Recording a voltage by external electrodes
* The resultant heart vector during ventricular depolarization

ECG from Basics to Essentials: Step by Step. First Edition. Roland X. Stroobandt, S. Serge Barold and Alfons F. Sinnaeve.
Published 2016 © 2016 by John Wiley & Sons, Ltd. Companion Website: www.wiley.com/go/stroobandt/ecg

1

2

WHAT IS AN ECG?
atrial
electrical
activity P

time

R
T
time

Q S

ventricular
electrical
activity

3
The electrocardiogram (ECG) is the recording of
the electrical activity generated during and after
activation of the various parts of the heart. It is
detected by electrodes attached to the skin.

The ECG provides information on:

* the heart rate or cardiac rhythm
* position of the heart inside the body
* the thickness of the heart muscle or dilatation of heart cavities
* origin and propagation of the electrical activity and its possible
aberrations
* cardiac rhythm disorders due to congenital anomalies of
the heart
* injuries due to insufficient blood supply (ischemia, infarction, ...)
* malfunction of the heart due to electrolyte disturbances or drugs

History
The Dutch physiologist Willem Einthoven was one of the pioneers of electrocardiography and
developer of the first useful string galvonometer. He labelled the various parts of the electrocardiogram using P, Q, R, S and T in a classic article published in 1903. Professor Einthoven
received the Nobel prize for medicine in 1924.

4

BLOOD CIRCULATION – THE HEART IN ACTION
O2

CO2

VENTRICULAR
DIASTOLE

Lungs

Pulmonary
circulation

LA

Ao

RA

SVC
LA

PV

MV

RA

Systemic
circulation

Systemic
circulation

AoV

IVC

LV
TV RV

ATRIAL CONTRACTION
VENTRICULAR RELAXATION

BODY
low
pressure

high
pressure

VENTRICULAR
SYSTOLE
Lungs

PV

RV
RA

TV

HEART

LA
MV

LV

LV

AoV
RV

VENTRICULAR CONTRACTION
ATRIAL RELAXATION

BODY
low
pressure

high
pressure

Abbreviations : Ao = aorta ; AoV = aortic valve ; LA = left atrium ; LV = left ventricle ; MV = mitral valve ; PV = pulmonary
valve ; RA = right atrium ; RV = right ventricle ; TV = tricuspid valve ; IVC = inferior vena cava ; SVC = superior vena
cava ; O 2 = oxygen ; CO 2 = carbon dioxide

5
The heart is a muscle consisting of four hollow chambers. It is a double
pump: the left part works at a higher pressure, while the right part works on
a lower pressure.
The right heart pumps blood into the pulmonary circulation (i.e. the lungs).
The left heart drives blood through the systemic circulation (i.e. the rest of
the body).
The right atrium (RA) receives deoxygenated blood from the body via two
large veins, the superior and the inferior vena cava, and from the heart itself
by way of the coronary sinus. The blood is transferred to the right ventricle
(RV) via the tricuspid valve (TV). The right ventricle then pumps the deoxygenated blood via the pulmonary valve (PV) to the lungs where it releases
excess carbon dioxide and picks up new oxygen.
The left atrium (LA) accepts the newly oxygenated blood from the lungs via
the pulmonary veins and delivers it to the left ventricle (LV) through the mitral
valve (MV). The oxygenated blood is pumped by the left ventricle through the
aortic valve (AoV) into the aorta (Ao), the largest artery in the body.
The blood flowing into the aorta is further distributed throughout the body
where it releases oxygen to the cells and collects carbon dioxide from them.

The cardiac cycle consists of two primary phases:
1. VENTRICULAR DIASTOLE is a period of myocardial relaxation
when the ventricles are filled with blood.
2. VENTRICULAR SYSTOLE is the period of contraction when the
blood is forced out of the ventricles into the arterial tree.
At rest, this cycle is normally repeated at a rate of approximately
70–75 times/minute and slower during sleep.

6

THE CONDUCTION SYSTEM OF THE HEART

LEFT
ATRIUM

1

3
3

BUNDLE
of
HIS

SINUS
NODE
(SA)

LEFT
VENTRICLE
(LV)

RIGHT
ATRIUM
(RA)

2

4

AV
NODE

LEFT
BUNDLE
BRANCH

RIGHT
VENTRICLE
(RV)

5

4

RIGHT
BUNDLE
BRANCH

PURKINJE
NETWORK
(P. FIBRES)

Sinus node

AV
Node

His
Bundle

Atria

Left
Bundle
Branch

AV node
LBB
Main
Stem

Right
Bundle
Branch

Bundle of His
Left
Posterior
Fascicle
Left
Anterior
Fascicle

Right BB

Purkinje
fibers
Right
ventricle

Left BB
Left
anterior
fascicle

Left
posterior
fascicle

Purkinje
fibers

Purkinje
fibers

Left
ventricle

7
The contractions of the various parts of the heart have to be
carefully synchronized. It is the prime function of the electrical
conduction system to ensure this synchronization. The atria
should contract first to fill the ventricles before the ventricles
pump the blood in the circulation.

1. The excitation starts in the sinus node consisting of special
pacemaker cells. The electrical impulses spread over the right
and left atria.
2. The AV node is normally the only electrical connection between
the atria and the ventricles. The impulses slow down as they
travel through the AV node to reach the bundle of His.
3. The bundle of His, the distal part of the AV junction, conducts
the impulses rapidly to the bundle branches.
4. The fast conducting right and left bundle branches subdivide
into smaller and smaller branches, the smallest ones connecting to the Purkinje fibers.
5. The Purkinje fibers spread out all over the ventricles beneath
the endocardium and they bring the electrical impulses very
fast to the myocardial cells.
All in all it takes the electrical impulses less than 200 ms to travel
from the sinus node to the myocardial cells in the ventricles.

8

ABOUT CARDIAC CELLS 1
Cylindrical cells

intercalated disks

membrane potential
- 90 mV
Na+
MEMBRANE

EXTRACELLULAR

Na+

K+

INTRACELLULAR

micropipette
electrode

Na+

Na+

Na+

K+

POLARIZED RESTING CELL

K+

SO -4 -

Na+

Na+

PO -4 --

-Prot

K+

Na+

Na+
Na+

Na+

extracellular
electrode

Na+
ION CHANNELS

Na Cl Ca
ION

ion e
ion i
Extracellular
Intracellular
concentration in concentration in
mmol/liter, mM mmol/liter, mM
4

150

Na

145

10

Ca

1.8

10-4

Cl

120

20

K

Influx

CELL
Efflux

K

Cardiac muscle cells are more or less cylindrical. At their ends they may
partially divide into two or more branches, connecting with the branches
of adjacent cells and forming an anastomosing network of cells called a
syncytium. At the interconnections between cells there are specialized
membranes (intercalated disks) with a very low electrical resistance.
These “gap-junctions” allow a very rapid conduction from one cell to
another.

All cardiac cells are enclosed in a semipermeable membrane
which allows certain charged chemical particles to flow in and
out of the cells through very specific channels. These charged
particles are ions (positive if they have lost one or more electrons, such as sodium Na+, potassium K+ or calcium Ca++ and
negative if they have a surplus of an electron, e.g. Cl-).
The ion channels are very selective. Larger ions such as
---phos-phate ions (PO4 ), sulfate ions (SO4 ) and protein ions
are unable to pass through the channels and stay in the inside
making the inside of the cell negative. A voltmeter between an
intracellular and an extracellular electrode will indicate a
potential difference. This voltage is called the resting membrane potential (normally about –90 millivolts).

In the resting state, a high concentration of positively charged sodium ions (Na+)
is present outside the cell while a high concentration of positive potassium ions
(K+) and a mixture of the large negatively charged ions (PO4---, SO4--, Prot--) are
found inside the cell.
There is a continuous leakage of the small ions decreasing the resting membrane
potential. Consequently other processes have to restore the phenomenon. The
Na+/K+ pump, located in the cell membrane, maintains the negative resting
potential inside the cell by bringing K+ into the cell while taking Na+ out of the
cell. This process requires energy and therefore it uses adenosine triphosphate
(ATP). The pump can be blocked by digitalis. If the Na+/K+ pump is inhibited,
Na+ ions are still removed from the inside by the Na+/Ca++exchange process.
This process increases the intracellular Ca++ and ameliorates the contractility
of the muscle cells.

9

10

ABOUT CARDIAC CELLS 2
electrical
impulse

1

POLARIZED CELL
(RESTING)

2

INFLUX

local ionic current

Na+

propagation of
depolarization

moving depolarization front

EFFLUX

INFLUX
Ca

3

4

DEPOLARIZED CELL

propagation of
repolarization

moving depolarization front

voltage

Action potential

-60 mV
-90 mV

Depolarization

-30 mV

Resting
potential
voltage
+20

Phase 1

++

Phase 2

Ca

Phase 0

0 mV

OUT

IN
+

Na
IN

time

Repolarization

+30 mV

0 mV

K

Phase 3

IN

-20

+

Phase 0

K

-40
Phase 3
Phase 4

Phase 4

Action potential of
myocardial cells

Phase 4

++

OUT

Ca

+

K

Phase 4

-60
-80

Action potential of
pacemaker cells

11
An external negative electric impulse that converts the outside of
a myocardial cell from positive to negative, makes the membrane
permeable to Na+. The influx of Na+ ions makes the inside of the cellless
negative. When the membrane voltage reaches a certain value(called
the threshold), some fast sodium channels in the membraneopen
momentarily, resulting in a sudden larger influx of Na+.Consequently, a
part of the cell depolarizes, i.e. its exterior becomesnegative with respect
to its interior that becomes positive.Due to the difference in concentration
of the Na+ ions, a local ioniccurrent arises between the depolarized part
of the cell and its stillresting part. These local electric currents give rise
to a depolarizationfront that moves on until the whole cell becomes
depolarized.
As soon as the depolarization starts, K+ ions flow out from the cell
trying to restore the initial resting potential. In the meantime, some
Ca++ ions flow inwards through slow calcium channels. At first, these
ion movements and the decreasing Na+ influx nearly balance each
other resulting in a slowly varying membrane potential. Next the Ca++
channels are inhibited as are the Na+ channels while the open K+
channels together with the Na+/K+ pump repolarize the cell. Again local
currents are generated and a repolarization front propagates until the
whole cell is repolarized.

The action potential depicts the changes of the membrane potential during the depolarization and the subsequent repolarization of the cell. The intracellular
environment is negative at rest (resting potential) and
becomes positive with respect to the outside when the
cell is activated and depolarized.

The cells of the sinus node and the AV junction do not have fast
sodium channels. Instead they have slow calcium channels and
potassium channels that open when the membrane potential is
depolarized to about −50 mV.

12

ABOUT CARDIAC CELLS 3
voltage
+20

Action potential
of a sinus node cell
time

0 mV
IN

-20

++

Ca

OUT

K

-40
IN

-60
-80

If

Phase 4

I f = funny current

Dominant Pacemaker
time

Sinus Node (SAN)
60–80 /min

Latent or Escape
Pacemakers

steeper
slope of
phase 4

voltage normal

threshold

spontaneous
depolarization

cycle
shortening

voltage

+

AV Junction including
the His Bundle
40–60 /min

cycle
lengthening
time

Right and Left
Bundle Branches
30–40 /min
less
steep
slope

Purkinje Fibers
20–40 /min

Common myocardial cells only depolarize if they are triggered by an
external event or by adjacent cells.
However, cells within the sinoatrial node (SAN) exhibit a completely
different behavior. During the diastolic phase (phase 4 of their action
potential) a spontaneous depolarization takes place.
The major determinant for the diastolic depolarization is the so-called “funny current” If.
This particularly unusual current consists of an influx of a mix of sodium and potassium
ions that makes the inside of the cells more positive.
When the action potential reaches a threshold potential (about −50/−40mV), a faster
depolarization by the Ca++ ions starts the systolic phase. As soon as the action potential
becomes positive, some potassium channels open and the resulting outflux of K+ ions
repolarizes the cells. The moment the repolarization reaches its most negative potential
(−60/−70mV), the funny current starts again and the whole cycle starts all over.

The funny current If is most prominently expressed in the sinoatrial node (SAN),
making this node the natural pacemaker of the heart that determines the rhythm
of the heart beat. Hence If is sometimes called the “pacemaker current”.
Spontaneous depolarization may be modulated by changing the slope of the spontaneous
depolarization (mostly by influencing the If channels). The slope is controlled by the autonomic
nervous system.
Increase in sympathetic activity and administration of catecholamines (epinephrine,
norepinephrine, dopamine) increases the slope of the phase 4 depolarization. This results
in a higher firing rate of the pacemaker cells and a shorter cardiac cycle. Administration of
certain drugs decreases the slope of the phase 4 depolarization, reducing the firing rate and
lengthening the cardiac cycle.
Spontaneous depolarization is not only present in the sinoatrial node (SAN) but, to a lesser
extent, also in the other parts of the conduction system. The intrinsic pacemaker activity of the
secondary pacemakers situated in the atrioventricular junction and the His-Purkinje system is
normally quiescent by a mechanism termed overdrive suppression. If the sinus node (SAN)
becomes depressed, or its action potentials fail to reach secondary pace-makers, a slower
rhythm takes over.

Secondary pacemakers provide a backup if the activity of the SAN fails
Overdrive suppression occurs when cells with a higher intrinsic rate (e.g. the dominant pacemaker) continually depolarize or overdrive potential automatic foci with a lower intrinsic rate
thereby suppressing their emergence.
Should the highest pacemaking center fail, a lower automatic focus previously inactive
because of overdrive suppression emerges or “escapes” from the next highest level.
The new site becomes the dominant pacemaker at its inherent rate and in turn suppresses all
automatic foci below it.

13

14
DEPOLARIZATION OF A MYOCARDIAL FIBER

depolarizing
ionic currents
gap junctions
(nexus)

depolarized
refractory cell

active cell
resting cells

DISTRIBUTION OF CURRENT IN MYOCARDIUM
AND RAPID SPREAD OF ELECTRICAL ACTIVITY

I = injection point of
electrical impulse

gap junction

transversal

I

longitudinal

cell

15
A depolarization front can propagate through the fibers of the heart muscle in the
same way as the depolarization front moves through a single cylindrical cell. Local
ionic currents between active cells and resting cells depolarize the resting cells
and activate them.

Very rapid conduction of electrical impulses from one cell to another
is due to “gap junctions” with a low electrical resistance between the
cylindrical cells.
Cardiac cells partially divide at their ends, forming an anastomosing
network or “syncytium” causing fast depolarization of the whole myocardium.

Due to the intercalated disks with their gap junctions, a depolarizing electrical
impulse spreads out rapidly in all directions. However, the gap junctions with
their very low electrical resistance are only present at the short ends of the
myocardial cells. Hence, depolarization propagates very fast in the longitudinal
direction of the fibers and less fast in the transversal direction.

16

RECORDING A VOLTAGE BY EXTERNAL ELECTRODES
2 : negative pole
of the voltmeter

NO
potential
difference

1 : positive pole
of the voltmeter

NO
potential
difference

Voltmeter
90 mV

I

0 mV
2

1

2

I

voltage
vector

0 mV
1

2

1

resting part
of the cell

Depolarized part
of the cell
depolarization
front

Current

electrode 1

electrode 2
voltage
vector

+

noninverting
input (positive
connector)

inverting
input (negative
connector)

ECG machine

17
A voltage is always measured
between TWO electrodes.

A potential difference or voltage is only caused
by a propagating front (either depolarization or
repolarization). A resting cell or a depolarized
cell does not give rise to a deflection of the
voltmeter.
The voltmeter shows a positive deflection if the voltage vector points
towards its positive pole !
A very small current flows through the voltmeter from its positive pole
to its negative pole. The internal resistance of the voltmeter has to be
extremely high since the small current may not influence the condition
of the source, i.e this weak current may not affect the distribution of the
ions around the cell.

Due to the high degree of electrical interaction between the branched
cells, many cells are depolarizing simultaneously in different regions
of the ventricles during the ventricular activation process. The voltage
vectors of these many cells may be combined into one resultant vector.
When a depolarization front or a repolarization front moves rapidly
through a region of the heart it generates a voltage vector and a tiny
electrical current flows through the body (which is a good conductor).
The ECG recorder acts in the same way as a voltmeter and when the
voltage vector points to its positive connector, the ECG registers a
positive (+) deflection.

18
THE RESULTANT HEART VECTOR
DURING VENTRICULAR DEPOLARIZATION

Schematic model
of the ventricles
SPREAD OF THE
DEPOLARIZATION

plane of
cross
section

(only the resultant vector
at a given time is shown)
10 ms

20 ms

30 ms

40 ms

50 ms

1

2
50 ms

70 ms

60 ms

cross section of
ventricles and
depolarization
at 50 ms.

90 ms

resultant vector

2
RV and LV vectors
occurring simultaneously

1

19

Ventricular activation consists of a series of
sequential activation fronts. At each particular
time, the vectors of these activation fronts may be
combined to form one resultant vector. The
resultant vector changes continually as the
ventricles are being progressively depolarized.
However, at each point in time the multiple
activation fronts can be represented by a single
resultant vector.

THE RESULTANT HEART VECTOR IS NOT CONSTANT
* its direction in space changes continuously
* its magnitude changes all the time

End of
QRS
complex

Terminal
vector

VT

Initial VI
vector
Start of
QRS
complex

Peak of
R wave

Main
vector

VM

VI, VM and VT occur sequentially
The point of the resultant heart vector traces a closed loop in space.
The projection of this path is the vectorcardiogram.

20

Further Reading
Barold SS. Willem Einthoven and the birth of clinical electrocardiography a hundred years ago. Card Electrophysiol Rev.
2003;7:99-104.
Hurst JW. Naming of the waves in the ECG, with a brief account of their genesis. Circulation. 1998;98:1937-42.
Janse MJ, Rosen MR. History of arrhythmias. Handb Exp Pharmacol. 2006;171:1-39.
Kligfield P. The centennial of the Einthoven electrocardiogram. J Electrocardiol. 2002;35 Suppl:123-9.

Chapter 2

ECG RECORDING
AND
ECG LEADS
*
*
*
*
*
*
*
*
*
*
*
*
*

The ECG machine or electrocardiograph
The ECG grid
Time interval versus rate
Registration of an ECG
Standard leads according to Einthoven
Wilson central terminal
Augmented limb leads according to Goldberger
The precordial leads after Wilson
How to locate the 4th right and left intercostal spaces
The 12 leads put together
Understanding the hexaxial diagram and its importance
Common errors in recording the ECG from precordial leads
Lead reversals in frontal plane

ECG from Basics to Essentials: Step by Step. First Edition. Roland X. Stroobandt, S. Serge Barold and Alfons F. Sinnaeve.
Published 2016 © 2016 by John Wiley & Sons, Ltd. Companion Website: www.wiley.com/go/stroobandt/ecg

21

22

THE ECG MACHINE OR ELECTROCARDIOGRAPH

grounding
to prevent
EMI

feedback
circuit

pre-amplifiers
& filters

lead
selector
switch

µ-processor
(computer)

LA

RA
power
amplifier

battery

recorder
or
printer

power
supply
grounding
for patient
safety
mains plug
220 V

RL
LL

paper
speed

virtual grounding
for the suppression
of interference
(driven
right leg)

2010
battery powered
and portable

Abbreviations
EMI = electromagnetic interference ; µ = micro (Greek letter mu)
RA = right arm ; LA = left arm ; RL = right leg ; LL = left leg (frontal plane connections)

23
* A safety grounding prevents electrocution if a fault occurs in the power
supply of some ECG machines (class I). This protective wire is normally
incorporated in the mains cable. ECG machines with double insulation
(class II) do not need such connection. Of course, ECG machines working
on a battery and without a connection to the mains are not equipped with
a safety ground connection.
* Pre-amplifiers enhance the small signals picked up by the electrodes on
the patient. They also provide filters avoiding non-cardiac signals from
disturbing the ECG. An AC-filter counteracts 50 or 60 Hz interference (EMI)
and another filter cuts down the influence of myopotentials from
musculoskeletal sources.
* Contemporary ECG machines may contain an embedded microprocessor
(computer) that not only controls the proper functioning of the equipment,
but also provides an ECG diagnosis.
* A feed-back circuit combines all spurious signals (noise) of the limb leads
and is coupled to the right leg. This eliminates most of the unwanted noise
and provides a thin baseline so that small details of the ECG can be
observed.
* The power amplifier delivers the necessary power for the movement of the
mechanical parts in the recorder or printer which delivers a document on
paper.

1908
still a long way to go...

Cambridge Medical Instruments (London)

24

THE ECG GRID

PAPER

amp

lifier

electrode

–

+

electrode

5 mm = 200 ms

5 mm =
0,5 mV

Calibration

1 mm = 40 ms
10 mm
= 1 mV

1 mm =
0,1 mV
25 mm = 1 sec

MEASURING MAGNITUDES

14 mm

10 mm
= 1 mV

10 mm
= 1 mV

Baseline
7 mm

Baseline

Calibration : 10 mm for 1 mV
Height of deflection : 14 mm or 1.4 mV

Calibration : 10 mm for 1 mV
Depth of deflection : 7 mm or 0.7 mV

voltage
(mV)

25
Time is measured horizontally in s or ms
Magnitude is measured vertically in mV
time
(ms)

* Conventionally the sensitivity of the ECG machine is adjusted (i.e. calibrated) so that a 1 millivolt (1 mV) electrical
signal produces a 10 mm deflection on the ECG (i.e. two
large squares).
* The standard paper speed is 25 mm per second (i.e. 1 s or
1000 ms corresponds to five large squares)
Note:
* If the QRS complexes are too small (low voltage) or too large (tall voltage)
the voltage calibration can be doubled or halved accordingly by flipping a
switch in the ECG machine.
* The same grid is used in ECG monitoring where the electrical activity of
the heart is shown on a display such as on a laptop (or formerly on a
cathode-ray tube such as used in older oscilloscopes).

positive
deflection

Baseline

Baseline

Baseline

negative
deflection

There is no absolute or fixed zero voltage. All measurements of voltages
on ECG are relative to the baseline or isoelectric line.
Upward deflections on an ECG (above the baseline) are called positive.
Downward deflections (under the baseline) are called negative.

26

TIME INTERVAL VS RATE
5 mm

interval

interval

Large square = 5 mm = 0.2 s = 200 ms

Small square = 1 mm = 0.04 s = 40 ms
1200 ms
1000 ms
800 ms
600 ms
400 ms
200 ms

5 mm

1 mm

50

60

75

0
10

0
15

0
30

St

ar

t

m

bp

27
* The intervals are normally expressed in milliseconds (ms).
* The heart rate or frequency of the heart is expressed in
beats per minute (bpm).
* There are 1000 ms in one second and 60 seconds in a minute.
* Hence :

Heart Rate (in bpm) =

60,000
RR-interval (in ms)

No calculation needed for a quick estimation of the rate, just
count the number of squares between two consecutive R waves !

Heart rate (bpm) =

300
Number of large squares

or with more accuracy

Heart rate (bpm) =

1500
Number of small squares

For
determinationofofthe
therate,
rate,
For aa rapid
rapid determination
memorize the
memorize
thenumbers
numbers
300
300--150
150- -100
100- -75
75- -60
60- -5050

28

TIME INTERVAL VS RATE – EXAMPLES
Numbers to remember ! INTERVAL

RATE
R

R

300
bpm

RR interval
= 200 ms
1 large square

150
bpm

RR interval
= 400 ms
2 large squares
QS

R

QS

R

RR interval
= 600 ms
3 large squares

100
bpm

R

R

RR interval
= 800 ms
4 large squares

75
bpm

R

R

RR interval
= 1000 ms
5 large squares

60
bpm

50
bpm

R

R

RR interval
= 1200 ms
6 large squares

Methods for determining the heart rate during regular rhythm
1. Cardiac ruler method
Place the beginning point of a cardiac ruler over an R wave. Look at the
number on which the next R wave falls and read the heart rate.

R

R

300

175
120
90
75
65
55
100
80 70
60
200 150

50

45

40

35

30

25 mm/sec

2. The 300 method
Count the number of large squares (5 mm boxes) between 2 consecutive R
waves and divide 300 by that number.
3. The 1500 method
Count the number of small squares (1 mm boxes) between 2 consecutive R
waves and divide 1500 by that number.
4. The 6 seconds method
Obtain a 6 s tracing (30 large squares) and count the number of R waves that
appear in that 6 s period and multiply by 10 to obtain the heart rate in bpm.

Methods for determining the heart rate during irregular rhythm
When the heart rate is irregular (e.g. atrial fibrillation), a longer interval should be
measured to provide a more precise rate. “1 second time lines” may be used to
measure longer intervals. If no “1 s time lines” are marked on the ECG paper, they
can be created by counting 5 large squares (5 x 0.2 s = 1 s).
1. The 6 seconds method
Heart rate = number of QRS complexes in 6 s multiplied by 10
2. The 3 seconds method
Heart rate = number of QRS complexes in 3 s multiplied by 20
Example of the 6 s rule during irregular rhythm

* A 6 s strip is selected between the two blue arrows
* Number of QRS complexes in 6 s is 13
* Mean heart rate is 13 x 10 = 130 bpm

29

30
REGISTRATION OF AN ECG

electrode 1

electrode 2

lead
axis

positive pole
ECG machine

negative pole

z-axis

r
rio
ste

Po

Superior

horizontal or
transverse
plane

r
rio

te
An

y-axis
Right

x-axis
sagittal
plane

Left

Anterior

Inferior

frontal
plane

31

An ECG is the registration of the projection of
the resultant heart vector upon the lead axis.
A lead axis is the hypothetical line joining the
two electrodes or poles of that particular
lead.

The lead axis of a lead can theoretically be orientated in any direction
or plane relative to the heart. Obviously, this will depend upon
electrode placement.
Conventionally, however, there are 12 leads which may be divided
into two groups on the basis of their orientation. One group is
orientated in the frontal plane of the body, the other in the horizontal
plane.

In the frontal plane we have:
* 3 standard leads according to Einthoven
* 3 augmented leads according to Goldberger
In the transverse plane are situated:
* 6 precordial leads according to Wilson

32

STANDARD LEADS ACCORDING TO EINTHOVEN

LEAD II

LEAD I

RA

RA

LA

RA = right arm
LA = left arm
LL = left leg

LL

LEAD III
Einthoven’s
equilateral
triangle

LA

RA
LL

I

LA

I
II

7
mm

12
mm

III

5
mm

III

LL
lead
axis III

II

lead
axis I

lead
axis II

I + III = II or 7 mm + 5 mm = 12 mm

33
The standard leads are :
* Bipolar leads since the measurement occurs between two electrodes
(+ and −) attached to the body
* Limb leads or extremity leads since the electrodes are connected to
the extremities
Note : Arms and legs are good electrical conductors, hence the position of the
electrodes (hand or shoulder, foot or hip) is not critical.
The positive electrodes (+) of the standard limb leads are electrically at about the
same distance from a theoretical zero reference in the heart. Hence, the lead axes
form an equilateral triangle with the heart and its zero reference in the center. This
triangle is called Einthoven’s triangle. (Although in reality it is not exactly
equilateral, but it is a good approximation.)

Einthoven’s law
If : V
 LA is the potential at the left arm (LA)
VRA is the potential at the right arm (RA)
VLL is the potential at the left leg (LL)
then the potential difference or voltage in the frontal leads is given by :
   Lead I = VLA − VRA
   Lead II = VLL − VRA
   Lead III = VLL − VLA
It follows that (VLA − VRA) + (VLL − VLA) = (VLL − VRA)
or :

lead I + lead III = lead II

This equation can also be written as :

lead I + lead III – lead II = 0
which is the well-known form of Einthoven’s law!

The relationship between the standard limb leads is such that the
sum of the electric voltages recorded in leads I and III equals the
electric voltage recorded by lead II.

34
WILSON CENTRAL TERMINAL

amplifier of
electrocardiograph

exploring
electrode

P
RA

LA

WILSON
BOX

LL

VCT

Reference
potential

Equipotential
points

35
Wilson connected the three standard limb leads through
equal-valued resistors to a common point. The potential
at this point is the average of the potentials at each limb
electrode and is used as a reference potential.

This reference is known as the
central terminal potential (VCT)
and is used by physicians as
zero equivalent.

By linking the three limbs RA, LA and LL through large equal resistors a relatively
stable reference potential VCT is created. Although it is technically incorrect to label
VCT as the zero potential it may be considered as such because the electrocardiograph only registers variations of voltages and suppresses constant (or DC) voltages.

VCT =

VRA + VLA + VLL
3

Since the potential of the central terminal is essentially constant, the potential
difference or voltage recorded by the electrocardiograph only reflects the potential
variations at the exploring electrode - hence the term “unipolar lead”.

The hypothetical electrical center of the heart, having about the same
potential as the reference point in the central terminal (VCT), is located
somewhere left of the interventricular septum and below the AV junction.

36

AUGMENTED LIMB LEADS

ACCORDING TO GOLDBERGER
LEAD aVL

LEAD aVR

to ECG recording
circuitry

to ECG recording
circuitry

RA

LA

RA

LL

LA

reference in
ECG machine

reference in
ECG machine

LL

LEAD aVF
to ECG recording
circuitry

LA

RA

lead
axis
aVR

LA

RA
aV

L

R

reference in
ECG machine

LL
lead
axis
aVF

aVR
-8 mm

+6 mm

+2 mm
aVF

aV

aVF

LL

aVL

lead
axis
aVL

aVR + aVL + aVF = 0
or : aVL + aVF = –aVR
6 mm + 2 mm = – (–8) mm = 8 mm

This law is very useful to detect
lead misplacement !

With the Wilson box as a reference potential, additional lead axes were
created using one of the three limb electrodes (i.e. RA, LA and LL) as an
exploring electrode.
By using only two resistors and omitting the connection between the exploring
electrode and the reference point, Dr. Goldberger obtained an amplitude of
the deflecton that was 50% larger.
Therefore these leads are called “augmented” hence the letter “a” is applied
to the VR, VL and VF leads (aVR, aVL, aVF).

The augmented leads are:
* Limb leads because the exploring electrode (+ pole of the ECG
machine) is connected to a leg or an arm.
* Unipolar leads since only one exploring electrode is used
and the negative pole of the ECG machine is connected to the
reference point.
* Frontal plane leads like leads I, II and III.
The lead axis for any particular augmented lead is a straight
line drawn between the reference voltage point at the center
of the heart and its extremity electrode.

aVR + aVL + aVF = 0
For each lead, the potential of the neutral point is the mean of two other
limb potentials.
So if: VLA is the potential at the left arm (LA)
VRA is the potential at the right arm (RA)
VLL is the potential at the left leg (LL)
then the voltage of the neutral point for lead aVL is:

Vref =

VRA + VLL
2

and lead aVL becomes aVL = VLA – Vref or:
VRA + VLL
2VLA – VRA – VLL
aVL = VLA –
aVL =
or
2
2
It can be proven in the same way:
2VLL – VRA – VLA
2VRA – VLA – VLL and
aVF =
aVR =
2
2
Obviously, the sum of the three augmented leads is aVL + aVR + aVF = 0 beacause:
2VLL – VRA – VLA
2VRA – VLA – VLL
2VLA – VRA – VLL
=
+
+
2
2
2
2VLA - VRA - VLL + 2VRA - VLA - VLL + 2VLL - VRA - VLA
2

=0

37

38

THE PRECORDIAL LEADS
AFTER WILSON

Precordial electrode
(exploring electrode)

LA

RA

amplifier of
electrocardiograph

WILSON
BOX

VCT
LL

midclavicular
line

Reference
point

anterior
axillary
line
midaxillary
line

V1
V6

V2

V3 V4

V6
V1 V2 V3 V4

V5

V5

The Wilson leads are:
* Unipolar leads since the measurement occurs with only one exploring
or probing electrode (the negative pole of the ECG machine is connected
to the central terminal; the reference point VCT acts as a zero potential).
* Chest leads or precordial leads since the electrodes are placed on
the chest around the heart.
Anatomically the RV lies anteriorly and medially but the LV lies laterally and
posteriorly. Leads V1 and V2 are situated over the RV, leads V3 and V4 face the
interventricular septum and leads V5 and V6 clearly point towards the free lateral
wall of the LV. QRS changes emanating from the LV overshadow those from the
RV in the absence of a conduction delay involving the RV. Therefore, V1 and V2
reflect the electrical activity of the interventricular septum (pre-dominantly a leftsided structure), leads V3 and V4 point towards the anterior LV, while leads V5
and V6 reflect the lateral LV.

Normal position of precordial electrodes
V1 Right side of the sternum in the fourth intercostal space
V2 Left side of the sternum in the fourth intercostal space
V3 Midway between V2 and V4
V4 Midclavicular line in the fifth intercostal space
V5 Anterior axillary line at the same level as V4
V6 Midaxillary line at the same level as V4

Lead axes in the
horizontal plane

0° V6
+30° V5
+120°
V1

+60° V4
+90° +75°
V2 V3

39

40

HOW TO LOCATE THE 4TH RIGHT AND LEFT
INTERCOSTAL SPACES

Sternal angle
or angle of Louis

Start at the
suprasternal
notch

1st rib

midclavicular
line

1

2nd intercostal space
(between 2nd
and 3rd ribs)

2
3
4

4th intercostal
space
Place V1 at the
very edge of
the sternum

5
6
7
8
9
10

V1

V2

V3

V4

V5

41
Locating the 4th intercostal space.
It sounds easy but is not !

It can be difficult to locate the fourth intercostal space. The best
way is to run your fingers from the suprasternal notch starting at
the heads of the clavicles down the sternum, until you meet a
distinct bony horizontal ridge (the sternal angle or angle of Louis).
It is the anterior angle formed by the junction of the manubrium
and the body of the sternum. This structure is palpable and easier
to find in male patients. The second rib is continuous with the sternal angle. With your finger on this sternal ridge, slide to the
patient’s right and your finger will drop into an intercostal space
which is the second intercostal space, and then move down to the
third and then the fourth, where you place V1 at the very edge of
the sternum.
Lead V2 is placed in the same way on the other side.

42

THE 12 LEADS PUT TOGETHER
SUPERIOR

-150°
aVR

- 30°

aVL

0°

I

V6
V1

V5

V2 V3 V4

HORIZONTAL
PLANE

60°

120°

III

II

90°

aVF

INFERIOR

I
High Lateral

II
Inferior

III
Inferior

aVR
aVL
High Lateral

V1

V4

Anteroseptal

Anterior

V2

V5
Low Lateral

Anteroseptal

aVF

V3

Inferior

Anterior

V6
Low Lateral

LEFT LATERAL

RIGHT LATERAL

FRONTAL
PLANE

WHY DO WE NEED 12 LEADS?

If you want to check the quality of an apple you have to look
for weak spots from many directions  !
The same principle applies to the heart !

The
The 12-lead ECG provides 12 different views of the electrical
activity of the
outside
of of
activity
the heart,
heart,each
eachview
viewlooking
lookingfrom
fromthe
the
outside
the chest
chest toward
toward the
the reference
reference point
point within
within the
the heart.
heart.
the

Lead aVR is directed opposite to that of the other leads and is often
ignored (“the forgotten 12th lead”).
Lead aVR does not view any single surface of the heart as do other
lead systems. Yet, aVR can be very helpful in diagnosing a number
of different entities. Inverted aVR (or minus aVR) can improve the
diagnosis of inferior and lateral myocardial infarction.

43

44

The deflection on the ECG for a particular lead is proportional to
the projection of the resulting heart vector upon that lead axis. The
projection of the heart vector on a lead axis, and hence the deflection on the ECG, remains the same when the lead axis is shifted in
parallel to its original direction. Therefore, all lead axes can be
thought as going through the electrical center of the heart.

original
projection
of the heart
vector

original
position
of lead I
axis

electrode

electrode

LA

RA

HEART
VECTOR

SHIFT

parallel

theoretical
position
of lead I
axis

projection
of the heart
vector on
theoretical lead axis

Only positive directions

Parallel shift

I

I

II

III
III

II

I

III

II

Lead I is chosen as the reference direction and (0°). The position of the other
leads is expressed by the rotation (angle) from this reference. This rotation is
positive in clockwise direction and negative in the counter-clockwise direction.

45
THE LIMB LEADS IN THE FRONTAL PLANE
(HEXAXIAL REFERENCE FIGURE)
GOLDBERGER

EINTHOVEN

aV

L

aV

R

I

II

III

aVF
-90°
-120°

-150°

aV

-60°

-30°

L

R

aV

I

-180°
+180°

0°

30°

150°

120°

aVF

III

90°

II
60°

46

UNDERSTANDING THE HEXAXIAL DIAGRAM
AND ITS IMPORTANCE
-90°
-120°

lea

da

xis

aV

R-

-60°

150

-30°

°

-180°
+180°

30

°

150

°

II

lead axis aVF 90°

120

III

-aV

xis

xis

ion

da

da

rec
t

lea

lea

(di

R)

60°

re
(di

L

aV

0° lead axis I

°

ctio

n -a

)
VL

d

lea

s
axi

Advantages of the hexaxial diagram:
* Better understanding of the relationships of the various frontal
plane leads and their recording sites of myocardial electrical activity.
Leads II, III and aVF reflect the inferior surface of the heart, while
leads I and aVL reflect the lateral part of the LV.
* Format for the determination and calculation of the mean frontal
QRS axis (discussed later).
* Understanding the importance of minus aVR (−aVR)
Note: Lead minus aVL (−aVL) is not used in recording the standard ECG. It is
useful in estimating the frontal plane axis and understanding the configuration
of the QRS complex. Lead minus aVR (−aVR) is available in relatively few electrocardiographs. It may be used to identify a myocardial infarct (see further on).

A lead axis is selectable. An axis has only a direction and not a magnitude (or
amplitude). Therefore axes cannot be vectors and cannot be combined by the
parallelogram rule.
The leads themselves are real vector quantities having magnitude and direction.
They may be combined in the classical way.
All frontal leads are orthogonal projections of the heart vector upon their specific
axes (orthogonal means right angles or 90°). By combining these projections, the
heart vector can be reconstructed in a continuously changing format. By doing
so at many consecutive times a loop in the frontal plane is formed (i.e. the vectocardiogram).
lead I

lead axis I

90°

electric
center of
the heart

heart vector

lead II

90°

lead III

90°

lead axis III

lead axis II

Just by looking at the hexaxial diagram with all 6 lead axes originating at
the electrical center of the heart, it is quite clear that all frontal limb leads
can be considered to function in the same way !
However, it is obvious that they all look at the heart from different directions.

Since the direction of all lead axes is known, every two leads may be combined
by the computer in an ECG machine to find direction and magnitude of the heart
vector. Consequently, the resulting heart vector can be decomposed to determine
any other lead in the frontal plane. This gives only a good approximation since the
human body is not homogeneous and Einthoven’s triangle itself is an approximation.

47

48
COMMON ERRORS IN RECORDING
THE ECG FROM PRECORDIAL LEADS

The precordial electrodes require careful positioning by palpating
the bony structures of the chest. Common errors in placement of
a chest electrode include:
1. Placing an electrode directly on a rib, rather than on an intercostal space.
2. Placing it on the wrong intercostal space.
3. Placing V1 or V2 directly on the sternum.
4. Placing V1 to the left of the sternum.
5. The right precordial electrodes V1 and V2 are often too high
and too far apart.
6. The left precordial electrodes V4 to V6 are commonly placed
both too low and too far towards the back for serial ECG
recording.

Technicians are commonly trained to place the chest electrodes
under the breast of women. The effect of breast tissue on the ECG
is smaller than that of misplacement.Therefore it is recommended
by some experts to place the electrodes on the breast rather than
under the breast to facilitate the precision of electrode placement
at the correct horizontal level and at the correct lateral positions.
Others believe that there is insufficient evidence to support a switch
from traditional sites beneath the left breast to record V4 to V6.

Errors in the placement of the chest electrodes do not influence the morphology of the QRS complex of the limb leads
in the frontal plane.

An error in the placement of precordial leads may change the morphology
of the ECG and result in inadequate or even wrong diagnosis.
In the example below, the P wave changes from its normal equiphasic
ap­
pear­
ance to monophasic positive if the electrodes are placed
incorrectly too low or monophasic negative if they are placed too high:
Correct positioning of the precordial electrodes

V1

V2

Equiphasic

V3

V4

V5

V6

V3

V4

V5

V6

QS

2 IC lower than normal

V1

V2

Monophasic
positive
rS

2 IC higher than normal

V1

V2

V3

V4

V5

V6

Monophasic
negative

The right precordial leads can be placed deliberately too low in order to
make a differential diagnosis between left anterior hemiblock (LAH) and
an old anteroseptal infarction.
In the example above, there is a QS pattern in V1 and V2.
If the precordial electrodes are placed 2 intercostal places lower the QS
morhology changes to rS indicating LAH.
For an old anteroseptal infarction the QS would persist.

49

50

LEAD REVERSALS IN FRONTAL PLANE
Lead switches are a common mistake in ECG recording and can lead to wrong diagnoses. The
most common mistake in electrode positioning is reversal of the right and the left arm leads,
which occurs in about 3% of ECGs recorded in a hospital setting. Lead I becomes the mirror
image of the true lead I so that all deflections (P wave, QRS complex and T wave) are inverted.
Lead aVR shows reversed polarity with a positive P wave and QRS complex. Just looking at lead
I makes the diagnosis.
Right and left arm lead reversal can be distinguished from the much rarer dextrocardia (where the
heart is positioned on the right side) by examination of the precordial R wave progression. This
progression is normal with arm lead reversal but is reversed with dextrocardia.
Transposition of the arm and leg electrodes is much less common but quite complex to evaluate,
except reversal of the right leg lead with one of the arm leads. In this situation the reversal produces
“pseudo-asystole” (a straight line) in either lead II or III because the potential between the two
legs is zero. Lead II or III appears “collapsed” (very small voltage), but this sign occurs in only one
lead. Consider the switch of the right arm (RA) and the right leg (RL) electrodes. Lead II records
the potential difference between the left leg (LL) and RA electrodes (i.e. LL − RA). Now that RA
becomes RL as the result of the switch, the electrocardiograph will record lead II with LL − RL
which yields an essentially zero potential. The same argument applies to the left arm (LA) and
RL switch. Lead III is LL − LA but as LA is now RL, lead III records the difference between LL
and RL which is again essentially zero.

Always look at lead I to recognize arm lead reversal: P, QRS and T
are all inverted.
A straight line in leads II or III suggests arm lead and right leg reversal.

I

V1

II
V2

RA/LA reversal
P, QRS, T negative
in lead I
Normal R wave
progression in
precordial leads

III
V3
aVR
V4
aVL
aVF

V5
V6

V1

I
II

III

Dextrocardia

V2

P, QRS, T negative
in lead I

V3

Reversed R wave
progression in
precordial leads

aVR

V4

aVL

V5

aVF

51

V6

RA/RL
reversal

LA/RL
reversal
Pseudo-asystole
in lead III

Pseudo-asystole
in lead II

RA/RL
and LA/LL
reversal
Zero potential
in lead I
Both arm leads are on
the legs and both leg
leads are on the arms.
Lead I = LA – RA but
with reversal of arm
and leg electrodes
lead I now becomes
LL – RL = 0

I

I

II

II

II

III

III

III

I

52

Further Reading
Braun K, Cohen AM. A comparison of unipolar leads obtained with the methods of Wilson and Goldberger. Br Heart
J. 1952;14:462-4.
Burch GE. History of precordial leads in electrocardiography. Eur J Cardiol. 1978;8:207-36.
Goldberger E. Recent advances in the use of augmented unipolar extremity leads. Med Clin North Am. 1950;34:857-67.
Goldberger E. The relations of augmented unipolar extremity leads (aVL, aVR VF) to ordinary unipolar extremity leads
(VL, VR, VF). Arch Inst Cardiol Mex. 1948;18:68-72.
Herrmann GR, Heitmancik MR, Kopeck JW. The superiority of the Wilson leads and the value of unipolar limb and
precordial derivations in clinical electrocardiography. Am Heart J. 1950;40:680-95.
Wilson FN, Johnston FD, Rosenbaum FF, Barker PS. On Einthoven’s triangle, the theory of unipolar electrocardiographic
leads, and the interpretation of the precordial electrocardiogram. Am Heart J. 1946;32:277-310.

Chapter 3

THE NORMAL ECG
AND
THE FRONTAL PLANE
QRS AXIS
*
*
*
*
*
*
*
*
*

The origin of the ECG – projection of the heart vector
Neutral plane and hemisphere concept
The origin of the ECG – normal QRS complex
Normal QRS complex in the frontal plane
Summary of the frontal plane for a normal heart
Summary of the precordial plane for a normal heart
Rotation of the heart
Mean frontal plane electrical QRS axis
Determination of the mean QRS axis in the frontal plane

ECG from Basics to Essentials: Step by Step. First Edition. Roland X. Stroobandt, S. Serge Barold and Alfons F. Sinnaeve.
Published 2016 © 2016 by John Wiley & Sons, Ltd. Companion Website: www.wiley.com/go/stroobandt/ecg

53

54

THE ORIGIN OF THE ECG
voltage
vector

voltage
vector

voltage
vector

voltage
vector

θ

θ

Lead
projection

projection

projection

axis

perpendicular

projection

Lead
axis

perpendicular

time

2
1

90°

projection
zero

3

Lead

Lead

axis

axis

3
1
perpendicular

2

2

2
Biphasic
perpendicular

3

3

1

time

4

4

1

lead axis

lead axis

3

3
4

2

4
2

1

1

Predominantly positive

Predominantly negative

55
The ECG records the electrical activity of the heart.
Potential differences or voltages are created by depolarization and
repolarization wavefronts in the heart.
Voltages can be represented by vectors having a direction and a
magnitude.
The magnitude of the voltage vector is to a large extent determined by
the amount of myocardium that depolarizes simultaneously. Therefore,
the thick wall of the left ventricle is electrically dominant.
The deflection on the ECG paper corresponds to the projection of the
voltage vector on the lead axis.
The lead axis refers to one of the traditional 12 leads or any special
leads.

The deflection on the ECG will be positive if the projection of the
voltage vector points to the positive pole of the lead axis. The
deflection on the ECG will be negative if the projection of the voltage
vector points to the negative pole of the lead axis.
The magnitude of the deflection on the ECG is determined by the
angle between the voltage vector and the lead axis.
The resultant voltage vector of the heart is continuously changing
during the heart cycle causing ECG deflections to vary with the
passage of time. The tip of the resultant voltage vector describes a
closed loop in space.
No deflection is produced when the resultant heart vector is
perpendicular to the axis of a lead.
When the heart vector fluctuates at both sides of the perpendicular
(partly pointing towards the positive pole and partly towards the
negative pole) a biphasic deflection on the ECG is produced.
If the positive and negative deflections are equal in magnitude, an
equiphasic deflection is present and the sum of the deflections is
zero.
The perpendicular to an axis of a lead serves as a boundary
between the predominantly positive and the predominantly negative
deflections in any given lead.

56

NEUTRAL PLANE AND HEMISPHERE CONCEPT

No ECG deflection is produced when the resultant heart vector
is perpendicular to the axis of a lead: the perpendicular to
the lead axis is a “neutral line”, it is the boundary between the
positive and the negative deflections for any given lead.

When the perpendicular to a lead axis is rotated around that
lead axis, a neutral plane is created. Each heart vector lying in
that plane is projected on the axis as a single point and does
not generate a deflection on the ECG.
The neutral plane divides the space around the heart into two
halves. The half along the positive side of the lead axis is the
positive hemisphere. Any resultant heart vector in that hemisphere has a positive projection upon the lead axis and causes
a positive deflection on the ECG.

Obviously, there is a positive hemisphere for each lead, i.e. six
hemispheres for the frontal plane leads: aVL, I, II, aVF, III, aVR.
The same concept also applies to the horizontal plane.

57
rotation
perpendicular
zero
deflection

perpendicular

heart
vector
lead axis

90°
lead axis
projection
zero

neutral
plane

perpendicular

perpendicular

heart
vector

heart
vector

positive
deflection

negative
deflection

lead axis

negative
projection

lead axis

positive
projection

Neutral Plane

HEART
VECTOR

lead I
POSITIVE HEMISPHERE
for LEAD I
ECG deflections will be
positive if the resulting
heart vector is in this
hemisphere.

58

THE ORIGIN OF THE ECG

NORMAL QRS COMPLEX

Terminal
vector VT
dir
e
ro ctio
tat n
ion of

VI

Initial
vector
Main
vector

direc
ti
rotat on of
ion

VM

59

TO REMEMBER !

During the initial phase, depolarization takes place in the interventricular septum, the paraseptal and anteroseptal zones of
the left and right ventricles. The initial heart vector VI is
directed to the right, anteriorly and slightly superiorly or
inferiorly.
During the main phase ventricular depolarization occurs in the
anterolateral and slightly later in the posterolateral regions.
The main heart vector VM is directed to the left, posteriorly
and inferiorly.
Ventricular depolarization ends in the posterobasal zone of
the left ventricle, the upper part of the interventricular septum
and finally the outflow tract of the right ventricle. The terminal
heart vector VT is directed backwards and upwards and may
be directed to the left or to the right.a

60

NORMAL QRS COMPLEX
IN THE FRONTAL PLANE
perpendicular
to lead I
-90°
-120°

RIGHT

lead I

-60°

-150°

-30°

VT

LEFT
M

0°

-180°
+180°

axis of
lead I

VI

150°

T

I

VM 30°
60°

120°
90°

-120°

-90°

lead aVF

-60°

-150°

-30°

VT

RIGHT

0°

-180°
+180°

LEFT
perpendicular
to aVF

VI
VM

150°

120°

M
I
T

30°

60°
90°

aVF

lead aVR
-90°
-120°

-60°

I

-150°

aVR

-30°

VT

RIGHT

0°

-180°
+180°

VI

150°

perpendicular
to aVR

VM

30°

60°

120°
90°

White half: positive hemisphere
Dark half: negative hemisphere

LEFT

T

M

61

SUMMARY OF THE FRONTAL PLANE
FOR A NORMAL HEART

T

I

M

M

T

aVL

aVR

I

VT

M

I

VI

T
I

VM

III
I

II

M

aVF
M

T
I

M

I

T

I = initial ; M = main ; T = terminal

T

62

SUMMARY OF THE PRECORDIAL PLANE
FOR A NORMAL HEART

PRECORDIAL
PLANE
VT

VM

VI

V6
V1

V1

V2

V3

V2 V3 V4

V4

V5

V5

V6

63

In the normal ECG looking at the precordial leads, the r wave usually
progresses from showing an rS complex in V1, with an increasing R
and a decreasing S wave when moving towards the left side.
There is usually a qR complex in V5 and V6 (the q wave reflecting
septal activation) but the absence of q waves in V5 and V6 may be
normal. The R wave amplitude is usually taller in V5 (and occasionally
in V4) than in V6 because of the attenuating effect of the lungs.
The transition zone is the lead with equal R and S wave voltage (i.e.
R/S = 1) and occurs normally in V3 or V4. It may be normal to have
the transition zone at V2 (called “early transition”), and at V5 (called
“delayed transition”). It is normal to have a narrow QS or rSr’ pattern
in V1.

Normal progression in the precordial plane

V1

V2

V3

V4

V5

V6

64

ROTATION OF THE HEART
V1

Normal

Anterior

RV

V6

Right
LV

Left

Posterior

V1

V1

CW

Anterior

CCW

Anterior

RV

V6

Right
LV

Left

LV

Right

Posterior

V1

V6

RV

Left

Posterior

V2

V3

V4

V5

V6
A

N
O
R
M
A
L

L

R
P
A

L

R
P
A

CCW
rotation
Early
transition

R

CW
rotation
Late
transition

R

L
P

L
P

In cardiac rotation the heart is always visualized from under
the diaphragm looking up. Hence, the anterior and posterior
orientation of the body with its precordial leads is turned
upside down.

VIEW DIRECTION

LA
BASE

RA

LV

RV

APEX
SEPTUM

rotation possible in both directions

R WAVE PROGRESSION
In the normal ECG looking at the precordial leads, the r wave usually progresses
from showing an rS complex in V1, with an increasing R and a decreasing S wave
when moving towards the left side. There is usually an qR complex in V5 and V6 (the
q wave reflecting septal activation) but the absence of q waves in V5 and V6 may be
normal. The R wave amplitude is usually taller in V5 (and occasionally in V4) than in
V6 because of the attenuating effect of the lungs. The transition zone is the lead with
equal R and S wave voltage (R/S = 1) and occurs normally in V3 or V4. It may be
normal to have the transition zone at V2 (called “early transition”), and at V5 (called
“delayed transition”). It is normal to have a narrow QS or rSr’ pattern in V1.
The definition of poor R wave progression in the literature varies considerably. A
common definition relies on an R wave being less than 2-4 mm in leads V3 and V4.
In addition it requires one or more of the following criteria: R in V4 < R in V3, R in
V3 < R in V2, R in V2 < R in V1. If transition occurs at/or before V2 it is called CCW
rotation. If it occurs after V4 it is called CW rotation. Poor R wave progression is also
defined as a late transition seen in V5 or V6. In other words, poor R wave progression
is present when the R wave height does not become progressively taller from leads
V1 to V3 or V4, or even remains of low amplitude across the entire precordium. Poor
R wave progression is abnormal but is not a diagnosis provided faulty ECG technique
is ruled out, remembering that it can also be a normal variant.

65

66

MEAN FRONTAL PLANE ELECTRICAL QRS AXIS
end of
ventricular
depolarization

direction of
rotation
instantaneous
heart vectors
changing as
time proceeds
start of
ventricular
depolarization

ELECTRICAL
AXIS

The electrical QRS axis in the frontal plane refers to the
direction of a single vector representing the summation or mean
of all the instantaneous frontal plane vectors generated by
ventricular depolarization. It depicts the net overall direction of
the electrical activity in the frontal plane. The mean frontal plane
electrical QRS axis (abbreviated as “electrical axis”) usually
points to the left and inferiorly in the normal heart because of
left ventricular dominance.

The mean QRS axis in the horizontal plane is rarely, if ever, used clinically. Determining the
mean QRS axis in the horizontal plane may be useful for determining the origin of ventricular premature beats and ventricular tachycardias.

67

DETERMINATION OF THE MEAN
QRS AXIS IN THE FRONTAL PLANE 1
STEP 1 : LOOK AT LEADS I & aVF TO DETERMINE IN WHICH
QUADRANT THE FRONTAL PLANE AXIS IS SITUATED

Lead I
negative

(- 90°)
(- 120°)

Lead aVF
negative

Lead I
positive
(- 60°)
(- 30°)

(- 150°)

(0°)

(180°)

Lead I
negative
Lead aVF
positive

Lead aVF
negative

(30°)

(150°)
(120°)
(90°)

(60°)

I
Lead I
positive
Lead aVF
positive

aVF
Leads I and aVF divide the thorax into 4 quadrants equal in size. Examine the
direction of the QRS complex in leads I and aVF. The combination should place the
electrical axis in one of the 4 quadrants of the hexaxial diagram.
1. If leads I and aVF are both upright, the axis is in the left inferior quadrant (yellow
area). There is no point in going further to obtain the precise site of the mean axis
as it is always normal in this quadrant.
2. If lead I is upright and lead aVF is downward, the axis is in the left superior
quadrant (red area) where it may be normal or abnormal because the normal site
extends from 90° to −30° moving in a counterclockwise fashion. The site of the
axis can be more precisely determined by one step which involves looking at
lead II (discussed later). The axis in this quadrant is called left superior axis
deviation if it is more superior or more negative than −30°.
3. If lead I is downward and aVF is upright, the axis is in the right inferior quadrant
(green area). It is simply called right axis deviation.
4. If both leads I and aVF are downwards, the axis is in the right superior quadrant
(blue area). This quadrant has been described by a variety of names: no man’s
land, marked right axis deviation, marked left axis deviation, indeterminate axis,
right shoulder axis and northwest quadrant. It is best called a right superior axis.
Another method related to the quadrant technique involves determining the frontal
plane axis by seeking the QRS complex with the greatest amplitude. The axis is
parallel to this lead (see step 2).

68

DETERMINATION OF THE MEAN
QRS AXIS IN THE FRONTAL PLANE 2
STEP 2 : LOOK IN THE APPROPRIATE QUADRANT FOR THE
TALLEST R WAVE OR THE DEEPEST S WAVE
(0°)

(0°)

(30°)

(30°)
(60°)

(60°)

AXI

II

S

AXIS

(90°)

II

aVF

aVF

The lead nearest to (or parallel along) the QRS axis has the largest positive
deflection. If two leads have equal positive deflections, the axis is exactly in the
middle between these two leads.

STEP 3 : FIND THE LEAD WHICH IS PERPENDICULAR TO THE
ELECTRICAL QRS AXIS

(- 90°)
(- 120°)

(- 60°)

aVL is equiphasic
(- 30°)

(- 150°)

aVL Lead aVL is perpendicular

aVR

to the QRS axis

(180°)

I (0°)

(30°)

(150°)

III

(120°)

aVF

(90°)

II

(60°)

Lead I is positive, thus the
QRS axis is on the left

QRS axis in the frontal plane

QRS axis is along lead II. Note that
lead II has the largest positive deflection, confirming the direction of the
axis.

The electrical QRS axis is perpendicular to the lead with an isoelectric (equiphasic)
QRS complex or the lead with the smallest net amplitude (most equiphasic lead).
Since there are two perpendicular directions to each isoelectric lead, choose the
direction (positive or negative) that best fits to the adjacent leads.
This method can determine the axis within ± 10°−15°. If there is no isoelectric lead,
there are usually two leads that are nearly isoelectric, and these are always 30°
apart. Find the perpendiculars for each lead and choose an approximate QRS axis
within the 30° range.
Occasionally each of the 6 frontal plane leads is small and/or isoelectric. The axis
cannot be determined and is called indeterminate.

Normal & abnormal QRS axes of the heart
Right
superior
quadrant
axis

Left
(superior)
axis deviation

(- 90°)
(- 120°)

(- 60°)
(- 30°)

(- 150°)

aVL

aVR

(180°)
Right
axis deviation

I (0°)

(30°)

(150°)

Normal
axis
(- 90°)
(- 120°)

III

(120°)

aVF

(90°)

II

(60°)

(- 60°)

(- 150°)

AXIS
(- 30°)

aVR

aVL

(A)

I (0°)

(30°)

(150°)

QUADRANT METHOD
plus LEAD II

III

II

(90°)

aVF

(- 90°)

The normal axis resides between 90° and
–30° (yellow area)!
When lead I is positive and lead aVF is
negative, the axis cannot be determined
without looking at lead II.
A. If lead II is equiphasic, the axis is
directed along lead aVL. This is because
an equiphasic lead (lead II in this case) is
perpendicular to the aVL axis.
B. If lead II is more positive than negative,
the axis is below –30° and normal (yellow
area).
C. If lead II is more negative than positive,
the axis is more negative than –30° and is
in the left superior quadrant (red area).

(- 120°)

(- 60°)
(- 30°)

(- 150°)

aVL

aVR

AXIS

(B)

I (0°)

(30°)

(150°)

III

(90°)

II

AXIS

aVF
(- 90°)
(- 120°)

(- 60°)
(- 30°)

(- 150°)

aVL

aVR

(C)

I (0°)

(30°)

(150°)

III

(90°)

aVF

II

69

70

MEAN QRS AXIS IN THE FRONTAL PLANE
EXAMPLES 1
lead I

lead II

lead III

lead aVR

lead aVL

lead aVF

(- 90°)

Normal electrogram
QRS axis at + 60°

(- 120°)

(- 60°)
(- 30°)

(- 150°)

I and aVF both positive: left inferior quadrant
tallest R wave in II: QRS axis is along II
most equiphasic in aVL: perpendicular to aVL

aVL

aVR

(180°)

I

(30°)

(150°)

III
(120°)

lead I

lead II

lead III

lead aVR

aVF

lead aVL

II

(60°)

lead aVF

(- 90°)

Left Axis Deviation (LAD)
QRS axis at − 60°
I positive; aVF negative: left superior quadrant
tallest S wave in III: QRS axis is along III
most equiphasic in aVR: perpendicular to aVR

(- 120°)

((- 60°)
(- 30°)

(- 150°)

aVL

aVR

(180°)

I

(30°)

(150°)

III
(120°)

aVF

II

(60°)

71

MEAN QRS AXIS IN THE FRONTAL PLANE
EXAMPLES 2
lead I

lead II

lead III

lead aVL

lead aVR

lead aVF

(- 90°)
(- 120°)

Right Axis Deviation (RAD)
QRS axis at about + 110°

(- 60°)
(- 30°)

(- 150°)

aVF is + and lead I is −: QRS is in the right inferior
quadrant
tallest R wave in III: QRS axis is close to III
lead III > aVF: axis near III

aVL

aVR

(180°)

I

(30°)

(150°)

Note that the sum of R and S waves in lead I is
negative which places the axis in the right
inferior quadrant

lead I

lead II

lead III

III
(120°)

aVF

lead aVL

lead aVR

II

(60°)

lead aVF

(- 90°)
(- 120°)

Right Superior Axis
QRS axis at about −100°
aVF is negative: QRS is oriented superiorly
most equiphasic in lead I: QRS axis is nearly
perpendicular to lead I
Note that the largest QRS deflections are in
leads II and aVF. Therefore the axis is diametrically opposite the line that bisects the angle
between the lead II axis and the aVF axis.

(- 60°)
(- 30°)

(- 150°)

aVL

aVR

(180°)

I

(30°)

(150°)

III
(120°)

aVF

II

(60°)

72

Further Reading
Burchell HB, Tuna N. The interpretation of gross left axis deviation in the electrocardiogram. Eur J Cardiol. 1979;10:25977.
Pahlm US, O’Brien JE, Pettersson J, Pahlm O, White T, Maynard C, Wagner GS. Comparison of teaching the basic electrocardiographic concept of frontal plane QRS axis using the classical versus the orderly electrocardiogram limb lead
displays. Am Heart J. 1997;134:1014-8.
Perloff JK, Roberts NK, Cabeen WR Jr. Left axis deviation: a reassessment. Circulation. 1979;60:12-21.
Prajapat L, Ariyarajah V, Spodick DH. Utility of the frontal plane QRS axis in identifying non-ST-elevation myocardial
infarction in patients with poor R-wave progression. Am J Cardiol. 2009;104:190-3.
Spodick DH, Frisella M, Apiyassawat S. QRS axis validation in clinical electrocardiography. Am J Cardiol.
2008;101:268-9.
Stephen JM, Dhindsa H, Browne B, Barish R. Interpretation and clinical significance of the QRS axis of the electrocardiogram. J Emerg Med. 1990;18:757-63.

Chapter 4

THE COMPONENTS
OF THE ECG
WAVES AND INTERVALS
*
*
*
*
*

What can be seen on the normal ECG – waves and complexes
Intervals and segments
The QT interval and the U wave
T wave polarity and morphology
The QRS complex – designation of special cases

ECG from Basics to Essentials: Step by Step. First Edition. Roland X. Stroobandt, S. Serge Barold and Alfons F. Sinnaeve.
Published 2016 © 2016 by John Wiley & Sons, Ltd. Companion Website: www.wiley.com/go/stroobandt/ecg

73

74

WHAT CAN BE SEEN ON THE NORMAL ECG
Atrial
depolarization

QRS
complex

R

Junction
or “J” point

T
wave

P
wave

Heart at rest
no electrical
activity

U
wave

Q

S

Isoelectric line
or baseline

Ventricular
repolarization

Ventricular
depolarization

R

R wave
Purkinje fibers

His bundle

Sinus node

Start AV node

R

isoelectric
line

P
AV Node
delay

time

Q wave
Q

Q

S wave
S

*  Only electrical activity can be seen !
Mechanical action (contraction) is not registered by the ECG.
*  Atrial repolarization is not seen in the ECG.
*  The depolarization of sinus node, AV node, His bundle and
bundle branches is not marked on the normal ECG because
they do not contain sufficient cells to produce a voltage that
can be measured on the skin of the body.
* An obvious U wave is seldom seen on a normal ECG.

* The P wave represents the depolarization of both the
right and left atria.

* The QRS complex is the representation of ventricular
depolarization.
*  The Q wave is the first downward deflection of the
QRS complex and is followed by the upward R
wave.
*  The R wave is the first upward deflection of the
QRS complex and is followed by a downward
S wave.
*  The S wave is the downward deflection preceded
by an upward deflection.
Note: differentiation between downward Q and S
waves depends on whether the downward stroke
occurs before or after the R wave.

* The T wave represents the repolarization of both the
right and left ventricles.

75

76
ABOUT INTERVALS AND SEGMENTS
RR interval

R

R

J point

T

P
PR
interval

T

P

time

QT
interval

S

QRS
interval

isoelectric line

R

R
ST
segment

T

P

T

P

time

Q S

Q S

* Intervals are periods of time including waves and complexes.
Segments are always measured between waves but never
include them.
* The baseline or isoelectric line is a straight flat line seen when
no electric activity of the heart is detected.

77
PR interval
The PR interval begins at the onset of the P wave and ends at the onset of the
QRS complex. This interval represents the time taken by the cardiac impulse to
reach the ventricles starting from the sinus node and high right atrium. It is called
PR interval because the Q wave is frequently absent. Normal values are between
0.12 and 0.20 s ; prolongation defines 1st-degree atrioventricular block.
RR interval
The RR interval starts at the peak of one R wave to the peak of the next R wave
and represents the time between two QRS complexes.This measure-ment is
useful in calculating the heart rate.
QRS complex
The QRS complex represents the duration of ventricular depolarization. The short
duration of the QRS complex indicates that ventricular depolarization normally
occurs very rapidly (0.06 to 0.10 s). The QRS complex begins at the onset of the
Q wave and ends at the endpoint of the S wave. The deflections are still termed
QRS complexes even if one or more of the 3 waves (Q, R, S) are not visible.
Hence the traditional use of the term RR interval to indicate the time between two
QRS complexes regardless of their configurations.
The ventricles have a much larger muscle mass compared to the atria, causing the
QRS complex to exhibit a much larger amplitude than the P wave. The amplitude
of the QRS complex is increased secondary to a larger myo-cardial mass in left
ventricular hypertrophy.
If the QRS complex is prolonged (> 0.1 s) conduction is impaired within the
ventricles.
ST segment
The ST segment begins at the endpoint of the S wave and ends at the onset of
the T wave, lasting 0.08 to 0.12 s. During the ST segment, the atria are relaxed
and the ventricles are contracting but no electricity is noted. Electrical activity is
not visible so that the ST segment is normally isoelectric but ST eleva-tion with a
slight upward concavity may also be normal thereby complicating the diagnostic
value of the ST segment.
The length of the ST segment shortens with increasing heart rate. A change from
baseline producing ST segment depression or elevation occurs in pathological
situations.
QT interval
The QT interval represents the duration from depolarization to repolarization of
the ventricles. (See next page.)

78

THE QT INTERVAL
R-R interval
R

R

T

P
Q

time

S

Q S

QT interval
1

0 mV

time

2
3

0
- 90 mV

T

P

4
Action Potential
Duration

THE U WAVE
R

R

T

P
Q

S

U

P
Q

time

S

79
The QT interval represents the duration from depolarization to repolarization of
the ventricles. It is measured from the beginning of the QRS complex to the end of
the T wave. Therefore it roughly estimates the duration of an average ventricular
action potential. Ventricular action potentials shorten in duration at faster rates
which decrease the QT interval. The QT interval also varies according to gender
(longer in females), and age (increases slightly with age). The QT interval can
range from 0.2 to 0.4 s approximately depending upon the heart rate. Because
prolonged QT intervals can indicate susceptibility to certain types of ventricular
tachyarrhythmias and sudden death (see later), it is important to determine if a
given QT interval is truly excessively long, especially in patients receiving drugs
that lengthen the QT interval.
In practice, the QT interval is expressed as a “corrected QT interval” (QTc) by
taking the QT interval (in s) and dividing it by the square root of the RR interval
(in s). This is known as the Bazett formula:

QTc (in s) =

QT interval (in s)
R-R interval (in s)

The Bazett formula allows an assessment of the QT interval that is independent of
heart rate. The normal corrected QTc is < 0.44 s in men and < 0.46 s in women.
Easy to remember: at a heart rate of 60 bpm, the RR interval is 1 s and QTc = QT.
The QT interval should be determined as the average value obtained from 3 to 5
cardiac cycles.
Modern ECG machines give the QTc. However, the machines are not always
capable of making the correct determination of the end of the T wave. Therefore, it
is important to check the QT time manually. The methodology of QT measure-ment
has not been standardized!

The U wave is not always seen. It is typically low amplitude, and, by definition,
follows the T wave. The U wave may be seen in some leads, especially the right
precordial leads V2 to V4. U waves are associated with metabolic disturbances,
typically hypokalemia. Additionally, it may be seen closely following the T wave
and can make interpretation of the QT interval especially difficult.

T-WAVE POLARITY AND MORPHOLOGY
Repolarization

Depolarization

from epi- to endocardium

direction of
wavefront

Purkinje
fibers

equivalent
dipole
moving to
epicardium

endocardium

R
_ _
electrode

epicardium

direction of
wavefront
Purkinje
fibers

T

_ _

equivalent
dipole
moving to
endocardium

_

from endo- to epicardium

_

80

electrode

endocardium

epicardium
free wall

free wall

ACTION POTENTIAL of myocardial cells
time
REPOLARIZATION

ENDO

1/ EPI
2/ ENDO

EPI
DEPOLARIZATION
(nearly synchronous)
(A notch is seen only in epicardial action potentials)

SPREAD OF WAVEFRONTS in myocardial tissue
DEPOLARIZATION
near-simultaneous
activation

REPOLARIZATION

spread over
time

81
T wave
time

* The T wave represents the repolarization of the ventricles and roughly
corresponds to phase 3 of the action potential of an average myocardial cell.
* The T wave is broader and not as large as the R wave because ventricular repolarization is less synchronous than depolarization.

The T wave is the most variable wave in the ECG. T wave changes including lowamplitude T waves and abnormally inverted T waves may be the result of many
cardiac and non-cardiac conditions. The normal T wave is usually in the same
direction as the QRS except in the right precordial leads. In the normal ECG the T
wave is always upright in leads I, II, V3 to V6, and always inverted in lead aVR. The
other leads are variable depending on the direction of the QRS and the age of the
patient.The shape of the T wave is normally rounded and smooth. Also, the normal
T wave is asymmetric with the first half moving more slowly than the second half.
The action potential duration in epicardial cells is shorter than in endocardial cells.
Hence, the repolarization starts in the tissue that was depolarized last. Repolarization
occurs from epicardum towards endocardium, i.e. opposite to the direction of
depolarization. However, the voltage vector (the +/− dipole) is still pointing to the
epicardium and towards the recording electrode and again causes a positive deflection
(T wave) on the ECG. The heterogeneity of ventricular repolarization is in large part
due to the presence of M cells constituting 30% to 40% of the mid-myocardium
between the endocardial and epicardial layers of the heart. The hallmark of the M
cells is their different electrophysiologic properties that pro-long their action potential
duration even beyond those of epicardial and endocardial cells. Full repolarization of
the epicardial cells coincides with the peak of the T wave and repolarization of the M
cells corresponds to the end of the T wave.
Repolarization takes longer and is more diffuse than depolarization because the
process spreads from cell to cell so that the T wave has a lower amplitude and a
longer duration than the QRS complex.

82
THE QRS COMPLEX

Designation of special cases

s

q

R

R

R

s

q

R

R’

S

S

q

r’
S

S

r

R

s
Q

QS

r r’

R

r
S

r r’

S

Q

r

S

r

r
q

Q

R

R

R’

R’
r

r

s s’

Notched
R wave

s
Q

Slurred
S wave

Slurred
R wave

Notched
S wave

Delta wave

Osborn
wave

Epsilon
wave

The waves composing the QRS complex are usually identified by upper or
lower case letters depending on the relative size of the waves. The large waves
that form the major deflections are identified by upper case letters (Q, R, S,
QS). The smaller waves that are less than one-half the amplitude of the major
deflections are identified by lower case letters (q, r, s). Thus, the ventricular
depolarization complex can be accurately described by using combinations of
upper and lower case letters (qrS, rS, Qrs, ...).
A QS wave is a QRS complex that consists entirely of a single large negative
deflection.
A QS complex should not be called or equated to a Q or q wave especially when
comparing the significance of a QS complex with one showing a qR, QR or Qr
configuration.
More than one deflection in the same direction
Altough there may be only one Q wave, there can be more than one R wave and
S wave in the QRS complex. A second upward or downward deflection is indicated
by an accent (R’ = R prime or S’ = S prime). A rare subsequent deflection may be
indicated by a double accent (e.g. R’’ = R double prime).
Concordance
Positive or negative concordance indicates that the QRS complex in all 6 precordial
leads has the same polarity. The 6 leads are either all positive or all negative.
Notches
A notch is a change in direction of the QRS complex and may involve the Q, R and
S waves. A notch does not cross the baseline (causes and clinical significance will
be discussed later).
Slurring
Slurring reflects a change in the rate of rise or fall of a wave within the QRS complex.
Delta wave
The slow and slurred upstroke of the QRS complex is called a “delta wave” because
of its resemblance to the Greek capital letter delta (symbol Δ). Delta waves are due
to premature ventricular excitation caused by an accessory pathway between atrium
and ventricle (discussed later : WPW syndrome and preexcitation). The delta wave is
a form of slurring of the initial portion of the QRS complex.
Osborn wave
When the J point is exaggerated and the downward deflection resembles the
letter “h”, the QRS complex displays an Osborn wave (named after Osborn who
described the association of this wave with hypothermia). Osborn waves also occur
in hypercalcemia (discussed later).
Epsilon wave
Epsilon waves are often seen in patients with right ventricular dysplasia. The waves
are best seen as small wiggles in the ST segment of leads V1 and V2. They are
caused by late excitation of myocytes in the right ventricle and constitute postexcitation.

83

84

Further Reading
Isbister GK, Page CB. Drug induced QT prolongation: the measurement and assessment of the QT interval in clinical
practice. Br J Clin Pharmacol. 2013;76:48-57.
Johnson JN, Ackerman MJ. QTc: how long is too long? Br J Sports Med. 2009;43:657-62.
Malik M. Errors and misconceptions in ECG measurement used for the detection of drug induced QT interval prolongation. J Electrocardiol. 2004;37 Suppl:25-33.
Postema PG, Wilde AA. The measurement of the QT interval. Curr Cardiol Rev. 2014;10:287-94.
Surawicz B. U wave: facts, hypotheses, misconceptions, and misnomers. J Cardiovasc Electrophysiol. 1998;9:1117-28.
Surawicz B, Macfarlane PW. Inappropriate and confusing electrocardiographic terms: J-wave syndromes and early repolarization. J Am Coll Cardiol. 2011;57:1584-6.
Zareba W, Cygankiewicz I. Long QT syndrome and short QT syndrome. Prog Cardiovasc Dis. 2008;51:264-78.

Chapter 5

P WAVES AND
ATRIAL
ABNORMALITIES
*
*
*
*
*
*

Topographical anatomy of the heart
The normal P wave in the frontal plane
The normal P wave in the horizontal plane
Left atrial abnormality
Right atrial abnormalitiy
Biatrial abnormality

ECG from Basics to Essentials: Step by Step. First Edition. Roland X. Stroobandt, S. Serge Barold and Alfons F. Sinnaeve.
Published 2016 © 2016 by John Wiley & Sons, Ltd. Companion Website: www.wiley.com/go/stroobandt/ecg

85

86
TOPOGRAPHICAL ANATOMY OF THE HEART

Left Atrium

(LA)

Right Atrium

(RA)

Plane of
horizontal
section

Horizontal section

(POSTERIOR)
BACK
Esophagus

Branches of
L. Bronchus

Branches of
R. Bronchus

Left Ventricle

Left Atrium

(LA)

(LV)

Right Atrium

(RA)

Interventricular
septum

FRONT
(ANTERIOR)

Right Ventricle

(RV)

87

Due to rotation of the heart along its long axis the right
heart is located anteriorly with regard to the left heart.
The right atrium (RA) is located to the right, while the
right ventricle (RV) is the most anteriorly located
structure. The left ventricle (LV) lies behind the RV
and points towards the left. The LV is situated mostly
in the anterior part of the chest. The left atrium (LA) is
the most posteriorly (dorsally) located heart chamber.
The wall thickness of a cardiac chamber reflects the
amount of muscle tissue needed to produce its level
of pressure. Therefore a cross-section of the chambers shows that the atrial walls and the interatrial
septum (wall) are relatively thin. The right ventricular
wall is much thicker. The left ventricular wall is again
several times thicker than that of the right. The
increased thickness of the left ventricle enables it to
generate the high pressure required for the systemic
circulation. In contrast, the right ventricle is a low
pressure system sustaining the pulmonary arterial
circulation. The ventricular septum separates the two
ventricles. It is mostly muscular but partly membranous in its superior portion. The septum is directed
obliquely backward and to the right, and is curved
with the convexity toward the right ventricle.
Note: The anatomic heart axis differs from the
electrical axis.

88
THE NORMAL P WVE 1
THE FRONTAL PLANE
sum
P1 + P2

P2

P wave e.g. in lead II

P1

P2

< 2.5 mm
(< 0,25mV)

P1

time

< 110 ms

What is the sum P1 + P2 ?
P1+ P2

P1

P2

Lead aVR

P2

P1

P1+ P2

-90°
-120°

-60°

aVR-150°

-30°

-180°
+180°

aVL

0° I

150°

Lead II

30°
60°

120°

III

90°

aVF

II

Resultant
P wave
vector

Lead II is oriented nearly
parallel to atrial activation

SINUS
NODE
(SA)

RIGHT
atrium
(RA)

89

Schematic
representation
of the atria
P2
P1

LEFT
atrium
(LA)

The P wave represents
the depolarization
of both right
and left atria

AV NODE

The sinoatrial node is situated near the top of the right atrium near the
inlet of the superior vena cava.
Atrial depolarization starts at the sinus node and progresses from
right to left.
The right atrium depolarizes first and the wave front (P1) travels from
the top (superior) to the bottom (inferior).
Electrical activation is transmitted from the sinoatrial node to the high
left atrium via Bachmann’s bundle which serves as the only atrial
specialized conduction system or tract conducting electrical activity
to the high left atrium. This arrangement causes a slight delay in left
atrial compared to right atrial depolarization as the activation then
travels to the left and posteriorly (P2). This delay causes continuing
left atrial depolarization after right atrial depolarization has finished.

Since activation starts at the sinus node, the P wave is always negative
in lead aVR during normal sinus rhythm. The P wave vector is directed
towards lead II and hence the P wave is always positive in lead II during
sinus rhythm.
The mean frontal plane axis of the P wave is between 0° and 75°. It is
usually between 45° and 60°. The axis of the P wave is usually the first
measurement in ECG interpretation to determine whether normal sinus
rhythm is present. An abnormal P wave axis may suggest the presence
of a non-sinus rhythm, dextrocardia or reversal of the ECG limb leads.
The normal P wave has a smooth contour and is never peaked or
pointed.

90

THE NORMAL P WAVE 2
THE HORIZONTAL PLANE

Left Atrium

(LA)

P2
V6

P1

Right Atrium

(RA)

Lead V5
V5

P

wave

Lead V1

V4
V1

V2

V3

P

wave

Biphasic

Lead V1
P1
surface area of
negative deflection
< 1 mm2
(i.e. less than the
equivalent area of
small square on the
ECG paper)

P2
< 40 ms

depolarization
of RA
P1

< 1.5 mm
(< 0,15 mV)

P2
depolarization
of LA

91

The best two leads to examine the P wave are leads II and
V1 as they look at the atria in opposite directions (lead II
looks along the axis of the atria, while V1 looks across
the atria).
Lead V1 allows the easy separation of the two components of atrial depolarization.

The P wave consists of two components: the depolarization of the
right atrium (P1) and the depolarization of the left atrium (P2). The
first part of the P wave is positive in lead V1 as the depolarization
vector of the RA is directed towards lead V1 which is oriented to the
right and anteriorly. The terminal part of the P wave is negative in
V1 as the depolarization vector of the left atrium (P2) is directed
towards the left and posteriorly (i.e. in the opposite direction of lead
V1). Thus, the P wave in lead V1 is often biphasic as the mean P
wave vector travels perpendicular to the axis of lead V1.
Atrial depolarization generates a positive deflection in the leads
that look at the heart from below (frontal plane). The chest leads
(apart from V1) do not detect atrial depolarization well because
atrial depolarization is downwards (i.e. inferiorly). As five of the six
(excluding V1) chest leads are mostly on the left side of the body
and approximately at the same level in the horizontal plane, the P
wave will not exhibit the P wave variations typical of the frontal
plane leads.There will generally not be much difference in the P
wave in these leads with small positive deflections seen in each.
Lead V1 with its different view on the heart looks at the atrial depolarization passing across its axis.

92

LEFT ATRIAL ABNORMALITY
Look at leads where the P wave is most prominent:
usually lead II, but also leads III and aVF, and V1.
The P wave becomes broadened (P wave duration ≥ 0.11 s) because of prolonged
total atrial activation time. P wave amplitude generally remains unchanged. The P
wave may be notched, or double-peaked (M shape pattern) with an interpeak interval
≥ 0.04 s due to the delay in left atrial activity which also causes wider separation of
right and left atrial depolarization. These features are best seen in lead II. The left
atrial vector may increase toward the left and become more pronounced, resulting in a
negative terminal deflection of the P wave in leads III and aVF. Leads V1 and V2 may
show a deeply inverted or negative portion of the P wave reflecting left atrial activation
directed posteriorly. The terminal inverted P wave in V1 should be ≥ 1 mm in depth
and ≥ 1 mm (0.04 s) in duration. The product of amplitude and duration should have
an area greater than that of the initial upright portion of the P wave (reflecting right
atrial activation which is directed anteriorly) or greater than the area of a small square
on the ECG paper.

II

V1
isoelectric
line

I

V1

II

V2

III

V3

aVR

V4

aVL

V5

aVF

V6

25 mm/s

isoelectric
line

93

LEFT ATRIAL ABNORMALITY
“Atrial abnormality” (or delay of left atrial activation) is a term being used increasingly in
place of “atrial enlargement”, “atrial dilatation”, “atrial distention”, “atrial hypertrophy”,
“atrial overload”, and “P mitrale” or even in the presence of atrial conduction delay.

Schematic
representation
of the atria

SINUS
NODE
(SA)

P2

P1

RIGHT
atrium
(RA)

FRONTAL PLANE

AV NODE

aVL

aVR
P2

I

P1

LEFT
atrium
(LA)

Wide and notched
P wave
lead II

time

III

> 110ms

II

aVF

HORIZONTAL PLANE

P2

lead V1

> 1 mm

V6
P1

V1

V5
V2

V4

time

> 1 mm

94

RIGHT ATRIAL ABNORMALITY
Left atrial abnormality causes wider P waves with no significant change in amplitude.
RA abnormality does not cause a significant change in P wave
duration (though the P waves appear somewhat more narrow)
but it increases the P wave amplitude.
Right atrial (RA) abnormality refers to delayed activation of the right atrium as a
result of dilatation, hypertrophy, scarring or a conduction abnormality. RA abnormality is also known as P pulmonale because it is often the result of severe lung
disease. An RA abnormality is reflected in the early portion of the P wave.
RA abnormality leads to simultaneous activation of the two atria resulting in relatively narrow tall pointed and peaked P waves which are increased in amplitude
(> 2.5 mm in leads II, III and aVF). This reflects the summation of the enhanced
RA component with the left atrial component.
In leads V1 and V2 the positive part of a biphasic P wave may display prominent
positivity and be > 1.5 mm which is larger than the negative component.
The P wave axis in the frontal plane is deviated to 75° or greater. Therefore the
tallest P wave may be seen in lead III rather than lead II.

The criteria for the diagnosis of RA abnormality are
not specific nor sensitive

V1

II

I

aVR

C1

C4

II

aVL

C2

C5

III

aVF

C3

C6

25 mm/s

95

RIGHT ATRIAL ABNORMALITY
LEFT
atrium
(LA)

SINUS
NODE
(SA)

Schematic
representation
of the atria

P2
P1

RIGHT
atrium
(RA)
AV NODE

FRONTAL PLANE
aVL

aVR

I

Tall and symmetrically
peaked P wave
lead III
P

1

> 0,25mV

Mean
P wave
vector

III

sum

P2

II

aVF

time

< 110ms

HORIZONTAL PLANE

P2
V6

> 0,15mV

P1

V1

lead V1

V5
V2

V4

time

96

BIATRIAL ABNORMALITY
Biatrial or combined atrial abnormality demonstrates essentially some of the
features of both RA and LA abnormalities. The P wave in lead II is > 2.5 mm
and > 0.12 s in duration. The initial positive component of the P wave in lead
V1 is > 1.5 mm tall and the terminal portion of the P wave is prominent with a
negative amplitude > 1 mm. Little evidence is available regarding the accuracy
of the ECG in combined atrial abnormality.

INTERATRIAL CONDUCTION DELAY
The Bachmann Bundle (interatrial bundle) plays a fundamental role in interatrial
conduction as the preferential interatrial connection which ensures rapid interatrial conduction leading to physiologic near-simultaneous right and left atrial
contraction. Delay in this pathway causes an interatrial conduction delay (IACD)
manifested by the typical ECG pattern of left atrial abnormality but not all the features may be present. Typically there is widening of the P wave with one or two
notches. The ECG configuration is not surprising because the general features
of left atrial abnormality from a variety of causes are more dependent on IACD
than on actual atrial dilatation.
Isolated IACD due to atrial fibrosis or scarring is a diagnosis of exclusion and
should be suspected when there is no clinical suspicion or evidence of left atrial
enlargement. The situation is compounded by the fact that primary IACD may
be associated with left atrial enlargement as a result of the conduction disorder
itself. Furthermore, an ECG pattern of left atrial abnormality may be produced by
primary left atrial enlargement. IACD is not uncommun in patients with sick sinus
syndrome and is a precursor to atrial fibrillation. For patients undergoing dual
chamber pacemaker implantation, measurement of the electrocardiographic P
wave duration is essential. IACD may cause significant left atrial electromechanical dysfunction which may necessitate placement of an atrial pace-maker lead
at a site other than the traditional right atrial appendage.

97

BIATRIAL ABNORMALITY
Lead V1

Leads II, III or aVF
> 1.5 mm

> 2.5 mm

> 1.5 mm

> 2.5 mm

INTERATRIAL CONDUCTION DELAY
Diagrammatic representation of interatrial conduction
delay due to a lesion in Bachmann’s bundle

BLOCK
Bachmann’s
bundle

Sinus
node

LA

RA

AV node

His bundle

LV

Right
bundle
branch

RV

II

V1
isoelectric
line

Left
bundle
branch

isoelectric
line

98

Further Reading
Heikkilä J, Hugenholtz PG, Tabakin BS. Prediction of left heart filling pressure and its sequential change in acute myocardial infarction from the terminal force of the P wave. Br Heart J. 1973;35:142–51.
Kitkungvan D, Spodick DH. Interatrial block: is it time for more attention? J Electrocardiol. 2009;42:687-92.
Michelucci A, Bagliani G, Colella A, Pieragnoli P, Porciani MC, Gensini G, Padeletti L. P wave assessment: state of the art
update. Card Electrophysiol Rev. 2002;6:215-20.
Platonov PG. Atrial conduction and atrial fibrillation: what can we learn from surface ECG? Cardiol J. 2008;15:402-7.
Platonov PG. P-wave morphology: underlying mechanisms and clinical implications. Ann Noninvasive Electrocardiol.
2012;17:161-9.
Tereshchenko LG, Shah AJ, Li Y, Soliman EZ. Electrocardiographic deep terminal negativity of the P wave in V1 and Risk
of Mortality: The National Health and Nutrition Examination Survey III. J Cardiovasc Electrophysiol. 2014;25:1242-8.

Chapter 6

CHAMBER
ENLARGEMENT
AND HYPERTROPHY
* Left ventricular hypertrophy
* Right ventricular hypertrophy

ECG from Basics to Essentials: Step by Step. First Edition. Roland X. Stroobandt, S. Serge Barold and Alfons F. Sinnaeve.
Published 2016 © 2016 by John Wiley & Sons, Ltd. Companion Website: www.wiley.com/go/stroobandt/ecg

99

100

LEFT VENTRICULAR HYPERTROPHY
LEFT VENTRICULAR
HYPERTROPHY
DUE TO SYSTOLIC OVERLOAD

The left ventricular wall is much
thicker than normal

SOME CRITERIA TO DIAGNOSE LEFT VENTRICULAR HYPERTROPHY

In the horizontal plane

V5 or V6

V1 or V2

(Sokolow index)
S + R 35 mm

R

S

In the frontal plane
(for a horizontal heart axis)

Lead aVL

R

11 mm

In the frontal plane (if left axis deviation)
Lead aVL

Lead III

R

In the frontal plane

13 mm

AND

S

(R in I) + (S in III) > 25 mm
Lead III

Lead I

R

S

Lead V6

R
Delayed intrinsicoid deflection
(Time from QRS onset to peak R is > 50 ms)

> 50 ms

15 mm

101
Left ventricular hypertrophy (LVH) refers to an increase in the size
of myocardial fibers. Such hypertrophy is usually the response to
a chronic volume or pressure overload.
* The two most important pressure overload states are systemic
hypertension and aortic stenosis.
* The major conditions associated with LV volume overload are
aortic or mitral valve regurgitation and dilated cardiomyopathy.
Hypertrophic cardiomyopathy is an example of an inherited condition in which LVH
(usually with asymmetric septal hypertrophy) occurs in the absence of any apparent hemodynamic pressure or volume overload unless there is LV outflow tract
obstruction.
A physiologic type of hypertrophy with increase in wall thickness and diastolic volume overload may occur in trained athletes. The “athletic heart” is often associated
with ECG voltage criteria for LVH.
The electrocardiogram is a useful but imperfect tool for detecting LVH. The utility of
the ECG relates to its being relatively inexpensive and widely available. The limitations of the ECG relate to its poor sensitivity depending upon which of the many
proposed sets of criteria are applied. The ECG is often used as a screening test to
determine who should undergo further testing with an echocardiogram.

Commonly used ECG criteria for diagnosis of LVH :
* S in V1 + R in V5 or V6 (whichever is larger) ≥ 35 mm (or 3.5 mV)
* R in aVL ≥ 11 mm
or if left axis deviation R in aVL ≥ 13 mm plus S in III ≥ 15 mm
* R in I + S in III > 25 mm
* Delayed intrinsicoid deflection in V6 ≥ 50 ms
The ECG criteria for diagnosing LVH are very insensitive (about 20–50%) meaning that
many patients with LVH cannot be recognized by ECG (false negatives!). However,
the criteria are very specific (about 90%) which means it is very likely thatLVH is
present if the criteria are met.

The power of some of the more commonly used ECG criteria to
rule out the diagnosis of LVH in patients with hypertension is poor.

102

RIGHT VENTRICULAR HYPERTROPHY
The causes of RVH involve mostly congenital disease and lung disease.
Because the electrical activity of the RV is overshadowed by that of the
LV, RVH has to be significant to cause ECG abnormalities.
The diagnosis requires a QRS duration < 0.12 s and a right axis deviation of approximately 100° or larger. There are a number of criteria but the diagnosis is usually made on
the basis of a constellation of supportive findings.
R wave in lead V1.
As expected RVH increases the height of the R waves in the RV leads (V1 to V3).
1.  Lead V1 shows > 7 mm in height (with an s wave < 2 mm) and the R/S ratio is > 1.
2.  Lead V1 may show a qR pattern.
3.  If there is an rSR’ complex the R’ > 10 mm
In the normal ECG the S wave is dominant in lead V1. A dominant R wave can occasionally be a normal variant. A posterior myocardial infarction (MI) may cause a dominant R
wave in lead V1 but the T waves are often upright in the right precordial leads. Such a
posterior MI is commonly associated with an inferior MI which is easily recognizable on the
ECG.
Deep S waves in the left ventricular leads. The S wave > R wave.
ST - T wave changes in leads V1 to V3. There is T wave inversion in lead V1 and often in V2
and V3. The ST segment is depressed secondary to RVH. The changes are opposite in polarity
to the QRS complex. This pattern used to be called RV strain.
R wave in lead aVR. The R wave in lead aVR is > q wave in the same lead. The R > 5 mm.
Right axis deviation. At least 100°.
Right atrial enlargement provides indirect proof of RVH.
Delayed intrinsicoid deflection in lead V1. This is similar to the corresponding changes in
the left ventricular leads in left ventricular hypertrophy.

The specificity varies according to
the underlying pathology. The diagnosis of RVH can be made with an
ECG in only 50% of patients with
chronic obstructive pulmonary disease who have definite RVH documented echocardiographically.
However the specificity is higher.

V6

V5

V4

V3

V2

ECG at half standardization (1 mV = 5 mm) of a patient with primary pulmonary hypertension
showing right ventricular hypertrophy.
Note the tall 22 mm R wave in lead V1. The initial and remaining QRS vectors are directed
rightward and anteriorly. There is right axis deviation of +110° and ST segment depression
and inverted T waves in leads V1 to V4.

aVF

aVL

aVR

III

II

I

V1

Chest X-ray in a patient with primary pulmonary hypertension
showing marked prominence of the main pulmona