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Rawaa Hatif Abd
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EKG
RAJOOJ'S
Dr. Abdulhamza Rajooj Hmood CLINICAL
EKG
Dr. Rawaa Hatif Abd
Revised by:
Authors
Prof. Nasser Ghaly Yousif Rajooj Hmood
Dr. Abdulhamza
Dr. Rawaa
Faculty member at Colorado Hatif Abd
University
Revision
Prof. Nasser Ghaly Yousif
Faculty Member at Colorado University
Fourth Edition 2015

2015
ABOUT
B M - P U B L I S H E R, Inc
2006 FIRST EDITION
2009 SECOND EDITION
2012 THIRD EDITION
2015 ©All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any
means, electronically or mechanically, including photocopying, recording or any information storage or
retrieval system, without the prior permission from the BM-publisher.
Whilst the information in this book is believed to be true and accurate at the date of going to press, the BM-
publisher cannot accept any legal responsibility or liability for any errors or omissions that may be made.
RAJOOJ'S CLINICAL EKG® is a registered trademark of the BM-Publisher, Inc
ISBN 978-0-9864331-0-8
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USA
Email: bmpublisher@bmpublisher.net
PREFACE TO THE FOURTH EDITION
This book is specially designed to meet the need of undergraduate

students and resident doctors. It can however be read as a basic guide
by postgraduate students. This book explains the techniques,
indications and interpretations of the EKG. The aim of this book is to
help the medical undergraduates and resident doctors efficiently
acquire the practical means of the EKG interpretation and to provide
them with the sound-up-to date information about this interpretation
since the ability of doctors to accurately interpret the EKG is crucial.
A. RAJOOJ H.
RAJOOJ'S CLINICAL EKG 1
Revision: Prof. Nasser Ghaly Yousif
INTRODUCTION
Contraction of cardiac muscles is accompanied by electrical activity called depolarization that can be
detected by electrodes attached to the surface of the body via the EKG (ECG). EKG is used to detect
cardiac ischemia, infarction, heart block, and myocardial hypertrophy. It may also give information about
electrolyte disturbances and the toxicity of certain drugs.
RECORDING AN EKG
To obtain a 12-lead EKG, four wires (electrodes) are attached to the four limbs (FIGURE 1.1 The left view)
and six wires are attached at different locations on the chest (FIGURE 1.1 The right view).
FIGURE 1.1 ECG connections. RA refers to right arm, LA refers to left arm, RL refers to right leg, and LL
refers to left leg.
The total of ten wires provides 12 leads; six limb leads and six chest (precordial) leads. Limb wires are
placed on the right arm (usually red in color), left arm (usually yellow in color), right leg (usually black in
color), and left leg (usually green in color). With only these four electrodes, six leads are viewed. These are
the three bipolar limb leads (I, II, and III) and the three unipolar leads (VR, VL, and VF). The three unipolar
limb leads (FIGURE 1.2 A) are connected to a central terminal which is electrically neutral (connected to the
right leg). The signal recorded from the electrode on the left arm is augmented (designated by the letter a)
relative to the central terminal and is therefore designated lead aVL. Similarly augmented signals are
obtained from the right arm (aVR) and left foot (aVF). The bipolar leads; I, II and III (FIGURE 1.2 B) are
generated by subtraction of the signals from two adjacent leads. Lead I is the left arm minus the right arm,
lead II is the left leg minus right arm and lead III is the left leg minus left arm.
FIGURE 1.2 A and B

demonstrate positions of
limb leads. RA means
right arm, LA means left
arm, and LL means left
leg (foot)
A B
The six unipolar chest leads V1-V6 are attached to anterior chest wall (FIGURE 1.1 The right view) in the
following positions:
2 RAJOOJ'S CLINICAL EKG
V1 This lead is placed at the right fourth intercostal space

V2 This lead is placed at the left fourth intercostal space
V3 This lead is placed between V2 and V4
V4 This lead is placed at the apex beat (left fifth intercostal space, midclavicular line)
V5 This lead is placed at the left fifth intercostal space anterior axillary line
V6 This lead is placed at left fifth intercostal space mid axillary line
Thus leads V1 and V2 look at the right ventricle, V3-V4 look at the interventricular septum and the anterior wall
of the left ventricle, and V5 –V6 look at the anterior and lateral walls of the left ventricle.
TIME AND SPEED OF THE EKG

FIGURE 1.3
EKG machines record changes in electrical ECG speed
activity by drawing a trace on a moving paper and time.
strip. All EKG machines run at a standard rate
and use paper with standard sized squares
(FIGURE 1.3). The horizontal scale represents
time, such that, at a standard paper speed of 25
mm/sec, each small square (1mm) represents
0.04 second and each large square (5 mm)
represents 0.2 second. There are therefore five
large squares per second (25 small squares) and
300 per minute. The vertical scale represents
amplitude (10 mm = 1mV).
ORIGIN OF THE EKG DEFLECTIONS
P wave is the deflection produced by atrial activation; QRS complex is the complex of deflections produced
by ventricular activation; T wave is the deflection produced by ventricular repolarization (FIGURE 1.4).
FIGURE 1.4 Origin of the ECG deflections.

EKG WAVES NOMNECLATURE
Components of the QRS complex are designed as follows (FIGURE 1.5):
I Q wave is the initial downward deflection (if present) followed by an R wave

II R wave is the first upward deflection whether preceded by a Q wave or not
III S wave is the downward deflection following the R wave; S wave is only considered when it touches the
base line
IV R′ wave is the second upward deflection (if present)
V S′ wave is a subsequent negative deflection following the first S wave (if present)
VI QS is a single negative deflection represent the entire QRS complex
VII Capital letters (Q, R, and S) refer to relatively large waves (over 1 large square); small letters (q, r, s)
refer to relatively small waves (under 1 large square)
FIGURE 1.5 Names of the ECG waves.

QRS COMPLEXES IN LIMB LEADS
EKG is arranged so that when a depolarization wave spreads FIGURE 1.6

towards a lead, the stylus moves upwards i.e., R wave is Direction of
larger than S wave and when it spreads away from the lead, the normal
the stylus moves downwards that is to say S wave is larger depolarization
than R wave. If QRS complex is predominantly upward or waves in limb
positive (R wave > S wave), depolarization is mainly toward leads.
that lead. If the QRS complex is predominantly downward or
negative (S wave > R wave), depolarization is mainly away
from that lead. When depolarization wave is moving at right
angles to the lead, R wave and S wave are of equal size.
Seen from the front, depolarization wave normally spreads
through the ventricles from 11 to 5 o'clock (FIGURE 1.6) so
that the aVR is normally mainly downward (negative). Thus
when the cardiac axis is normal, the QRS complex are
predominantly upright in leads I, II, and III (FIGURE 1.6).
QRS COMPLEXES IN CHEST LEADS
Depolarization of the
interventricular septum FIGURE 1.7
occurs first (FIGURE 1.7) The phases of
and moves from the left to depolarization
the right thus generating and resultant
an initial negative electrical
deflection in V6 (Q wave) pictures.
and an initial positive
deflection in V1 (R wave).
The second phase of
depolarization causes an
activation of the body of
the left ventricle, which
creates a large positive deflection or R wave in V6 with reciprocal changes in V1. The third and final phase of
depolarization involves the right ventricle and produces a small negative deflection or S wave in V6. The
QRS complex in the chest leads shows progression from V1 where the QRS is predominantly downward
(negative) to V6 where it is predominantly upward (positive). The point at which R wave and S wave are of
equal size is called the transition point which indicates the position of the interventricular septum. This point
is normally at V3/V4 (FIGURE 1.7).
EKG DESCRIPTION AND INTERPRETATION
EKG should be read in two fundamental steps; description and then interpretation. The description of the
EKG should always be performed in an orderly fashion as shown in BOX 1.1.
BOX 1.1 Steps for EKG description

STEP 01 Technical quality STEP 07 PR interval
STEP 02 Cardiac rhythm STEP 08 QRS complex
STEP 03 Heart rate STEP 09 ST segment
STEP 04 Cardiac axis STEP 10 T wave
STEP 05 P wave STEP 11 QT interval
STEP 06 PR segment STEP 12 Additional waves
STEP 01 TECHNICAL QUALITY OF THE EKG
This step is undertaken under three headings. Look first at the speed which should be 25 mm/s and look
then to the amplitude which is normally 10 mm/s. Both these data are usually provided in the bottom of the
EKG paper although some devices provide them in the upper part of the EKG paper (FIGURE 1.8). The third
step involves looking at the aVR lead. The depolarization wave normally spreads through the ventricles from
11 o'clock to 5 o'clock thus the deflections in aVR are normally mainly downward i.e., negative. Negative,
neutral and positive aVR leads are shown in FIGURE 1.9.
FIGURE 1.8 Normal ECG speed and FIGURE 1.9 Calculation of the QRS net area. The area
amplitude. You can slow the speed of the below the isoelectric line (hatched) is subtracted from the
ECG machine and reduce the amplitude. area above the line.
If the aVR deflections are upward (positive), you should think about three possibilities; reversed limb leads
placement (limb leads have been incorrectly attached to the limbs), dextrocardia, and right ventricular
hypertrophy/strain or right bundle branch block.
FIGURE 1.10 Reversed limb leads (A) and proper lead placement (B). Look at the aVR in view A and
look again at view B when the limb leads are properly placed. Lead aVR is interchanged with lead aVL;
lead II is interchanged with III; lead I become negative; and lead aVF is unchanged. All these changes
are reversed when the leads are properly placed (view B).
In both reversed limb leads and dextrocardia, lead I will show negative P wave and negative QRS and T
wave, aVR is reversed with aVL (aVR becomes aVL i.e. positive aVR and negative aVL), lead III is reversed
with lead II, and lastly the aVF is unchanged. The difference between the two conditions is that in reversed
limb lead (FIGURE 1.10) the precordial leads remain normal (progression from predominantly negative QRS
complexes to positive QRS complexes) while in dextrocardia (FIGURE 1.11) the precordial leads will show
poor R wave progression from V1 through V6 (precordial leads remain negative). Moreover, if the EKG of a
patient with dextrocardia is repeated with the limb leads reversed and the chest leads are placed to the right
side of the chest, the EKG becomes like that of a normal person. The approach to a positive aVR is shown in
FIGURE 1.12.
FIGURE 1.11 A case of dextrocardia. Look at aVR which is positive, P wave in V1 which is inverted, and
lack of normal chest leads progression.
FIGURE 1.12
Approach to a positive
aVR.
STEP 02 THE RHYTHM
When an EKG is described, the rhythm could be either regular or irregular depending on the R-R interval
(FIGURE 1.13). Causes of irregular rhythm are shown in BOX 1.2.
BOX 1.2 Causes of irregular rhythm

Sinus arrhythmia Atrial fibrillation
Frequent ectopic beats Atrial flutter with variable response
Frequent escape beats Second degree heart block with variable response
Infrequent escape beats and extra systoles do not disorganize the EKG pattern therefore the only cause for
completely irregular rhythm is atrial fibrillation (AF). Extreme form of sinus arrhythmias and atrial rhythm can
cause irregular rhythm, however both of these conditions have P wave while in AF there is no P wave.
RAJOOJ'S CLINICAL EKG
Revision: Prof. Nasser Ghaly Yousif 7
FIGURE 1.13 Look at the regularity of the RR interval in the first example and the irregularity of RR
interval in the second example.
ARRYTHMIAS
When the depolarization is begun at atrial muscle (atrial rhythm), the region around atrioventricular node
(nodal or junctional rhythm) or ventricular muscle (ventricular rhythm), an arrhythmia is said to be present
(FIGURE 1.14). In supraventricular rhythm, depolarization spreads normally into the ventricles, whether it
has begun in the sinoatrial node, atrial muscle or the AV node. The QRS complex is thus normally shaped.
Ventricular repolarization is also normal so the T wave is of a normal shape (FIGURE 1.14).
In ventricular rhythm, depolarization spreads relatively slowly through the ventricular muscle, so the QRS
complex is wide and abnormal. Repolarization is also abnormal so the T wave is often inverted (FIGURE
1.14). When the activation of the atria or ventricles is totally disorganized, fibrillation is said to occur.
FIGURE 1.14 Origin and configuration of cardiac beats.
Arrhythmia can occur singly earlier than it should and is called single early beat (extra-systole, ectopic beat,
or premature beat), or singly later than it should and is called late beat, or as sustained early beats
(tachycardia or tachyarrythmia), or as sustained late beats (escape rhythm). Thus arrhythmia includes:
I. SINGLE EARLY BEAT (ECTOPIC BEAT)

Any part of the heart can be depolarized earlier than it should and the accompanying heart beat is called
extrasystoles or ectopic beat or premature contraction. Ectopic beats can be classified according to their
origin into supraventricular (atrial or junctional) or ventricular (FIGURE 1.14). As mentioned above
supraventricular extra-systoles have normally shaped QRS and T waves, but ventricular extrasystoles have
abnormally shaped QRS complex and T waves. Atrial ectopic beat had abnormal P wave; junctional (mid-
junctional) ectopic beat had no P wave (it is usually buried inside the QRS and is difficult to be seen). The
QRS complex and the T wave are the same of those of the sinus rhythm. Ventricular ectopic beat had no P
wave, abnormal QRS complex and abnormally shaped T wave. The difference thus between
supraventricular and ventricular beats is simply realized by the shape of that beat.
FIGURE 1.15 Nomenclature of ectopic and escape beats.

These ectopic beats can be unifocal that is identical in morphology, arising from a single ectopic focus or
multifocal that is of varying morphology arising from multiple foci. When two successive ectopic beats had
been arisen, they called couplet ectopic beats (FIGURE 1.15) and called triplet ectopic beats if they are
three. When more than three successive ectopic beats are present, the resultant electrical activity is called
rhythm. Moreover bigeminy means alternate ectopic and sinus beat while trigeminy means alternate ectopic
and two sinus beats. The same principle can be applied for quadrigeminy. R on T phenomenon means
occurrence of an ectopic beat at the peak of T wave of the preceding beat (FIGURE 1.16).
FIGURE 1.16 Examples of ectopic beat.
II. SINGLE LATE BEAT (ESCAPE BEAT)

The EKG appearance of an escape beat arising in either the atrial muscle, the nodal or junctional region, or
the ventricular muscle, is the same as that of the corresponding extra-systole. The difference is that ectopic
beat comes early (than expected next sinus beat) and escape beat comes late (than expected next sinus
beat). This is shown in FIGURE 1.17.
FIGURE 1.17 An example

showing the difference
between the ectopic beat and
the escape beat. The shape is
similar but the time of
occurrence is different.
III. SUSTAINED EARLY BEATS (TACHYCARDIA/TACHYARRHYTHMIA)

Tachyarrhythmia means sustained repetitive premature beats that can be supraventricular or ventricular.
Foci in the atria, the junctional (AV nodal) region, and ventricles may fire repeatedly, causing a sustained
tachycardia. The criteria already described for ectopic or escape beats can be used to decide the origin of
the arrhythmia. Sustained tachycardia can be classified into two type according to the origin of the beats;
supraventricular and ventricular tachycardia. The mechanism is illustrated in FIGURE 1.18.
FIGURE 1.18 Mechanism of tachyarrhythmia.
1 SUPREVENTRICULAR TACHYCARDIA (NARROW COMPLEX TACHYCARDIA)
The rhythm here is originated from a region above the ventricles and therefore called supraventricular. This
tachycardia includes sinus tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation, and junctional (AV
nodal) tachycardia. Because QRS complexes are normal in all these types, the term narrow complex
tachycardia is sometimes used. Sinus tachycardia (FIGURE 1.19) is characterized by normally shaped P
wave, QRS complex, T wave and regular RR interval as well as normal PR interval.
FIGURE 1.19
Sinus tachycardia.
Look at the RR
interval which is
regular and the
normally shaped
P wave, QRS
complexes, and
the T wave.
The frequency of depolarization of the SA node is affected by the vagus nerve and inspiration causes its rate
to increase and expiration causes its rate to decrease. The normal heart thus is little irregular and the term
sinus arrhythmia is applied (FIGURE 1.20). This vagal effect diminishes with increasing age and lost in
autonomic neuropathy.
FIGURE 1.20
Sinus arrhythmia.
Look at the RR
interval which is
irregular and the
normally shaped
P wave, QRS
complexes, and
the T wave.
In contrast to sinus rhythm, sinus arrhythmia had markedly variable RR interval, but the shape of the P wave,
QRS complexes, and T wave is normal. The duration of the PR intervals are constant in both (FIGURE 1.21).
FIGURE 1.21 Look at the regular RR interval in the first example (sinus rhythm) and also look at the
second example that had irregular RR interval (sinus arrhythmia).
Atrial tachycardia (FIGURE 1.22) is characterised by abnormally shaped P waves, normal shapes of the
QRS complexes and the T waves.
FIGURE 1.22
Atrial
tachycardia.
Look at the
abnormally
shaped P
wave, normal
QRS
complexes,
and normal T
wave.
Any tachycardia arising above the AV junction that has a P wave configuration different from sinus rhythm is
called atrial tachycardia. In general, impulses arising in the superior portion of the right or left atrium produce
a positive P wave in the inferior leads (i.e., leads II, III, and aVF), whereas impulses arising in the lower or
inferior portions result in negative P waves in the same leads. When the P wave configuration is uniform from
beat to beat, the tachycardia is unifocal atrial tachycardia (FIGURE 1.22). Multifocal atrial tachycardia (MAT)
is characterized by at least three distinct P wave morphologies and often at least three different PR intervals
(FIGURE 1.23). Heart rate in atrial tachycardia is typically between 100-150 beats/min.
FIGURE 1.23 The differences between unifocal atrial tachycardia (A) and multifocal atrial tachycardia (B)
is the presence of different shaped P waves (> 3) and different PR intervals. In both the P wave shape is
different from that of sinus rhythm.
In junctional tachycardia (FIGURE 1.24), the atria contract faster than 120 beats per minute. It is
characterized by absence of P waves, normal QRS complexes and T waves. This type of arrhythmia is
called supraventricular tachycardia (SVT), or junctional tachycardia, or nodal tachycardia, or more recently
AV nodal re-entry tachycardia (AVNRT).
FIGURE 1.24 Junctional tachycardia (SVT) is characterised by absence of P wave and normal QRS
complexes and T waves.
In junctional tachycardia, the P waves are frequently absent because they are buried in the preceding QRS
complexes or the T waves. Some times however, the P wave may be seen within the QRS (FIGURE 1.25).
FIGURE 1.25 Two examples of junctional tachycardia (SVT). In the first example the P wave can not be
seen and this is the usual clinical setting while in the second example, the P wave is seen after the QRS
i.e. retrograde conduction.
Junctional tachycardia is termed high–junctional tachycardia when there are P waves that appear
immediately before each QRS complexes and termed mid–junctional when these P waves appear within the
QRS complexes and termed low–junctional tachycardia if these P waves appear after the QRS complexes
as in FIGURE 1.25.
In atrial flutter (FIGURE 1.26), the atrial rate is greater than 250 beats per minute; the P waves form
continuous saw-tooth line with normal QRS complexes and T waves.
FIGURE 1.26 Atrial flutter with variable response i.e. the relation between F wave and QRS complex is
variable.
Atrial flutter circuit rotates in a clockwise or counterclockwise direction in the right atrium around the tricuspid
valve annulus. Common atrial flutter (counterclockwise 80%), with a negative “saw-tooth” appearance in
leads II, III, and aVF and positive in V1, has a fairly uniform route of impulse propagation localized to the right
atrium. Incidental left atrial activation produces a negative saw-tooth flutter wave in the inferior leads. A
reverse of this direction in the circuit could cause a positive flutter wave in the same leads (uncommon or
clockwise). As the AV node usually fails to conduct all the P waves, the relationship between P waves and
QRS complexes is usually 1:1, 2:1, 3:1, or 4:1 (FIGURE 1.27); these P waves are called flutter waves. If the
Ventricular rate is rapid and P waves can not be seen, carotid sinus pressure will usually increase the block
in the AV node and make the saw tooth more obvious (FIGURE 1.28).
FIGURE 1.27 Atrial flutter

with fixed response 4:1.
Look at the regular rhythm,
flutter waves, and normal
shape of QRS and T
waves.
FIGURE 1.28 Atrial flutter becomes more apparent with carotid sinus massage.
In atrial fibrillation (FIGURE 1.29), the atrial muscle fibers independently contract (fibrillating) to produce no P
wave and totally irregular base line. In atrial fibrillation, in contrast to atrial flutter, the QRS complexes are
totally irregular. At certain times, atrial activity may become sufficiently synchronized to produce flutter waves
pattern. This finding is called atrial flutter-fibrillation which behaves likes atrial fibrillation. Again carotid sinus
pressure will usually make the saw-tooth appearance more obvious. Carotid sinus pressure may affect some
of supraventricular tachycardia as shown in BOX 1.3.
14 RAJOOJ'S CLINICAAL EKG
FIGURE 1.29 Atrial fibrillation. Look at the base line which lacks the P waves and at the rhythm which is
irregular.
BOX 1.3 Effect of carotid sinus pressure on arrhythmia

TYPES OF ARRHYTHMIAS EFFECTS OF CAROTIS SINUS PRESSURE
Sinus tachycardia Slows
Atrial tachycardia Abolished or no effect
Junctional tachycardia Abolished or no effect
Atrial flutter Increased AV block and reveal the flutter wave
Atrial fibrillation No effect
Atrial fibrillation (AF) is described as rapid AF when the heart rate is fast or as slow AF when the heart rate is
slow. Moreover, AF is described as fine (FIGURE 1.29) or coarse (FIGURE 1.30).
FIGURE 1.30 An
ECG showing
coarse atrial
fibrillation.
2 VENTRICULAR TACHYCARDIA (WIDE COMPLEX TACHYCARDIA)
The rhythm here is originated from the ventricles and therefore called ventricular. Because of the widening in
the QRS complexes, this tachycardia is called wide complex tachycardia. It includes ventricular tachycardia
(VT), Torsades des pointes (TdP), and ventricular fibrillation (VF). In ventricular tachycardia (FIGURE 1.31)
there is no P wave, abnormal wide QRS complexes, and abnormal T wave (as with the corresponding
ventricular ectopic beat). Ventricular tachycardia is called monomorphic when all the QRS complexes have
the same appearance, and polymorphic when they vary (FIGURE 1.32). A twisting polymorphic ventricular
tachycardia is called torsade des pointes. The EKG (FIGURE 1.33) shows rapid irregular complexes that
oscillate from an up right to an inverted position and seem to twist around the baseline as the mean QRS
complex axis changes. This arrhythmia is usually non-sustained, but may degenerate into ventricular
fibrillation. When the ventricular muscle fibers contract independently, no QRS complexes can be identified
and the EKG is totally disorganized (FIGURE 1.34). This type of tachycardia is called ventricular fibrillation.
The need to recognize and treat ventricular fibrillation (VF) quickly is one of the main foundations on which
the policy of acute coronary care unit is built. If you realized such changes in the EKG, look at the patient as
he /she may have lost consciousness.
FIGURE 1.31 Ventricular tachycardia. Look at the regularity in the RR interval, absence of P wave,
widening of the QRS complexes, and abnormality in T wave.
FIGURE 1.32 Ventricular tachycardia; monomorphic and polymorphic.
FIGURE 1.33
Torsade de
Pointes.
FIGURE 1.34 Ventricular fibrillation. Look at the end of the strip where VF started after an R on T
phenomenon.
Ventricular tachycardia is easily recognized and differentiated from supraventricular tachycardia because VT
had wide QRS complex (more than 3 mm) while SVT had normal (or narrow) QRS complexes. When the
heart rate exceeds 180 bpm, there will be physiological widening in the QRS complexes (bundle branch
block) or when the underlying basic EKG has wide QRS complexes, one should differentiate the rhythm
whether it is SVT with block or VT. If you can not differentiate between the two, treat the patient as he/she is
having ventricular tachycardia. The problem can be analyzed by looking at the following points:
01 Broad complex tachycardia occurring in the course of an acute myocardial infarction is almost always
ventricular tachycardia
02 Response to the carotid sinus pressure or to intravenous adenosine infavor SVT with block
03 Presence of atrioventricular node dissociation is a pathognomonic feature for wide complex tachycardia
to be ventricular tachycardia
04 The presence of one P wave per QRS complex suggest sinus rhythm and bundle branch block while if P
waves are seen at a slower rate than QRS complex, the rhythm is ventricular
05 QRS complex duration if more than 160 ms (> 4 small squares), it is probably ventricular
06 QRS complex regularity. Ventricular tachycardia is usually regular; an irregularity means atrial fibrillation
with block
07 QRS complex configuration. If the QRS complex in the chest leads all point either upward or downward
(concordance), it is probably VT, but twisting QRS complexes indicate torsade de pointes
08 When the QRS complex show right bundle branch block (RBBB) pattern, abnormal conduction is more
likely if the second R peak is higher than the first; VT is likely if the first R is higher
09 Presence of fusion and capture beats is a pathognomonic for ventricular tachycardia (FIGURE 1.35). In
VT, there is independent atrial and ventricular activity. Occasionally a P wave is conducted to the
ventricles through AV node. This may produce a normal sinus beat in the middle of the tachycardia
(capture beat). However, more commonly the conducted impulse fuses with an impulse from the
tachycardia (a fusion beat).
FIGURE 1.35 Ventricular tachycardia; capture and fusion beats.
IV. SUSTAINED LATE BEATS (ESCAPE RHYTHM)

It is important not to try to suppress escape rhythm, because without it the heart might stop altogether.
Normally the SA node controls the heart rate because it has the highest frequency of discharge, but if for any
reason this fails, the region with the next highest intrinsic depolarization frequency will emerge as the
pacemaker and set up an escape rhythm. The atria and the junctional region have automatic depolarization
frequencies of about 50/min. If both the SA node and the nodal region fail to depolarize or if conduction to
the ventricles fails, a ventricular focus may emerge, with a rate of 30-40/min. There are three escape
rhythms (FIGURES 1.36, 1.37, and 1.38); atrial escape (idioatrial) rhythm, nodal or junctional (idionodal)
rhythm, and ventricular (idioventricular) rhythm. The EKG appearance is the same for that of atrial,
junctional, and ventricular tachycardia, but the difference is in the heart rate. Escape rhythms are not primary
disorder, but are the response to problems higher in the conducing pathway. They are commonly seen in the
acute phase of a heart attack. Atrial escape rhythm (FIGURE 1.39), also called idioatrial rhythm or wandering
atrial pacemaker, has the same features of that of atrial tachycardia; the difference is in the heart rate.
Junctional escape rhythm (FIGURE 1.39), also called idionodal rhythm, has the same features of that of
junctional tachycardia; the difference is in the heart rate. It is usually associated with a rate of 40–60/minute
and narrow QRS complexes. The heart rate may be enhanced and increased to 100/minute; in this stage it is
called “accelerated junctional rhythm”. Ventricular escape rhythm (FIGURE 1.39), also called idioventricular
rhythm, has the same features of that of ventricular tachycardia; the difference is in the heart rate.
Ventricular escape rhythms are usually associated with rates 20–40/minute. The heart rate may be
enhanced and increased to 100/minute; in this stage it is called “accelerated idioventricular rhythm”.
FIGURE 1.36 Idioatrial rhythm. It is also called wandering atrial pacemaker. The difference between atrial
tachycardia and this rhythm is in the heart rate.
FIGURE 1.37 Idionodal rhythm. It is also called junctional escape rhythm. The difference between SVT
and this rhythm is in the heart rate.
FIGURE 1.38 Idioventricular rhythm. It is also called ventricular escape rhythm. The difference between
VT and this rhythm is in the heart rate.
FIGURE 1.39 Tachycardia versus escape rhythm.

REVIEW OF ARRHYTHMIA
Narrow complex rhythm (in which the QRS complex is normal in width) includes sinus rhythm (and sinus
arrhythmia), atrial rhythm (atrial tachycardia, atrial flutter, atrial fibrillation, atrial escape rhythm) and
junctional rhythm (junctional tachycardia (SVT) and junctional escape rhythm). Wide complex rhythm (in
which the QRS is more than three small squares) includes ventricular rhythm (ventricular tachycardia and
Torsade de pointes) and narrow complex rhythm when the EKG is basically wide (e.g. bundle branch block).
The following two approaches are recommended in assessing the heart rhythm:
20 Revision: Prof. Nasser Ghaly Yousif
STEP 03 HEART RATE
Heart rate can be estimated with regard to the regularity of the rhythm as follows:
I. Regular rhythm
Heart Rate = 300 ÷ number of large squares between beats.
Or
Heart Rate = 1500 ÷ number of small squares between beats.
II. Irregular rhythm
Heart Rate = number of R waves in 15 large X 20 squares
Heart rate above 100/minute is called tachycardia while below 60/minute is called bradycardia. If the rhythm
is irregular heart rate is estimated (FIGURE 1.40) and the result should be given as a range. The commonest
cause for irregularly irregular rhythm is atrial fibrillation.
FIGURE 1.40 Heart rate estimation.
STEP 04 CARDIAC AXIS
The average deflection of depolarization waves in the ventricle spreads from 11 o'clock to 5 o'clock. It is
therefore moving a way from aVR and towards other limb leads. This is called the cardiac axis (or cardiac
vector) and in the normal heart the QRS complex is predominantly downward in aVR (that is, the S wave
exceeds the R wave), but predominantly upward in the other limb leads (the R wave is bigger than any S
wave that may be present). The direction of the QRS complex in leads I and aVF determines the cardiac axis
as follows:
Lead I Lead aVF Interpretation

Positive Positive Normal
Positive Negative Left axis deviation
Negative Positive Right axis deviation
Negative Negative Extreme right axis deviation
Left axis deviation (FIGURE 1.41) is usually seen in short obese healthy individuals and right axis deviation
(FIGURE 1.41) is usually seen normally in tall thin healthy individuals however other causes for left and right
axis deviations (BOX 1.4) should also be sought.
BOX 1.4 Causes of axis deviation

LEFT AXIS DEVIATION RIGHT AXIS DEVIATION
Normal in obese and short individuals Normal in tall and thin individuals
Left ventricular hypertrophy Right ventricular hypertrophy
Left anterior hemiblock Left posterior hemi block (rare)
Anterior myocardial infarction Anteriolateral myocardial infarction
Wolff-Parkinson-White syndrome (type A) Wolff-Parkinson-White syndrome (type B)
Pregnancy Pulmonary embolism
FIGURE 1.41 Normal and abnormal cardiac axis.
STEP 05 P WAVE
The normal P wave has a width of less than 3 small squares and amplitude of less than 2.5 small squares. In
sinus rhythm, the P wave is normally upright in all leads except aVR. When the QRS complex is
predominantly downward in lead aVL, the P wave may also be inverted normally. When you would like to
identify the P wave look first at leads II, III, aVF, and leads V5 and V6. In these leads, the P waves should be
upright. If the P wave is difficult to be seen in these leads, look then at other leads.
Abnormalities of P wave may take one of the following fashions:
Absence of P wave This occurs in atrial fibrillation, atrial flutter, junctional ectopic beat, junctional
escape beat, junctional tachycardia (SVT), idionodal rhythm, ventricular ectopic
beat, ventricular escape beat, ventricular tachycardia, and idioventricular rhythm.
It may also occur in hyperkalemia and in sinoatrial block (discussed later)
Inverted P wave in lead I This may indicate dextrocardia or improper lead placement
Abnormal P wave shape This may indicate atrial ectopic beat, atrial tachycardia, atrial escape beat, and
atrial escape rhythm
Widened P wave (more This may occur in atrial infarction, intra-atrial conduction defect, and left atrial
than 2.5 small squares) enlargement
Now look especially at leads II and V1 to diagnose atrial enlargement (FIGURE 1.42). Because the sinus
node is located in the right atrium, the right atrium begins to depolarize before the left atrium and finishes
earlier as well. Therefore, the first part of the P wave predominantly represents right atrial depolarization and
the second part represents left atrial depolarization. The P wave should be upright in lead II and biphasic in
lead V1 when you are looking at these leads. The criteria designed to diagnose atrial enlargement via the
EKG are as follows:
Peaked tall P wave This indicates right atrial enlargement. In this condition, the P waves has an amplitude
exceeding 2.5 mm in the inferior leads (P-pulmonale) with no change in the duration
of the P wave i.e. < 3 mm
Bifid notched P wave This indicates left atrial enlargement. The amplitude of the terminal (negative)
component of the P wave may be increased and must descend at least 1 mm below
the isoelectric line in lead V1 giving the appearance of notched P wave (P-mitrale).
The duration of the P wave is increased, and the terminal (negative) portion of the P
wave must be at least one small square in width.
FIGURE 1.42
Atrial
enlargements.
STEP 06 PR SEGMENT
The PR segment is the straight line running from

the end of the P wave to the start of the QRS
complex. It therefore measures the time from the
end of atrial depolarization to the start of
ventricular depolarization. It should be
isoelectrical (FIGURE 1.43). Depressed PR
interval is a sensitive sign for acute pericarditis. It
may also encounter in ventricular hypertrophy
and chronic lung disease.
FIGURE 1.43 PR segment and interval.
STEP 07 PR INTERVAL
The PR interval is measured from the start of the P wave to the beginning of the QRS complex (FIGURE
1.43). In sinus rhythm, the PR interval ranges from 120-200 ms (represented by 3 – 5 mm or 3 – 5 small
squares). A PR interval of less than 3 small squares indicates pre-excitation syndrome (i.e. electrical
conduction occurs more quickly than usual) and that of more than 5 small squares indicates a conduction
block (i.e. electrical conduction occurs more slowly than usual).
SHORT PR INTERVAL: PRE-EXCITATION SYNDROME
The depolarization normally starts at the SA node and then spreads through atrial muscle fibers. While
depolarization spreads through AV node, there is a physiological delay represented by the 3 – 5 small
squares (i.e. the PR interval). In pre-excitation, there is an accessory (or extra) conduction pathway which
connects the atria with the ventricles or the atria with the His bundle and these are Wolff-Parkinson-White
(WPW) syndrome and Lown-Ganong-Levine (LGL) syndrome respectively. In both syndromes, the
accessory conduction pathways act as short circuits, allowing the atrial wave of depolarization to bypass the
AV node and activate the ventricles prematurely.
FIGURE 1.44 Mechanism of WPW and LGL syndrome origin.

FIGURE 1.45 WPW syndrome type A.
FIGURE 1.46 WPW syndrome type B.
In WPW syndrome there is an accessory conducting pathway (called bundle of Kent) which connects either
right atrium with right ventricle (WPW type B) or left atrium with left ventricle (WPW type A), by passing the
normal delay at AV node, thus ventricular depolarization occurs early and the PR interval is short. Early
ventricular depolarization causes a slurred upstroke of the QRS complex called delta wave (FIGURE 1.44).
WPW syndrome type A has a dominant R wave in V1 (FIGURE 1.45) while WPW type B has no such
(FIGURE 1.46). LGL syndrome is due to an AV node bypass that connects the atrium to the His bundle
(FIGURE 1.44) and is called James fibers. The EKG reveals only short PR interval with normal shape QRS
complex (FIGURE 1.47). Both syndromes can be associated with the development of tachyarrhythmia. In
WPW syndrome, depolarization can spread down the normal pathway and back (retrogradely) up through
the accessory pathway to reactivate the atria and so cause a tachycardia. The ventricles are therefore
depolarized in the normal way, producing narrow QRS complexes with P waves sometimes visible just after
each QRS complexes. This is called orthodromic tachycardia which is the most common form of tachycardia
in WPW syndrome (FIGURE 1.48) and is similar to junctional tachycardia. Alternatively, depolarization can
pass down the accessory pathway and retrogradely upward the His bundle. The ventricles are then
depolarized through the accessory pathway; producing broad complex tachycardia with P waves may or may
not be seen. This is called an antidromic tachycardia (FIGURE 1.48). This type of tachycardia is similar to
ventricular tachycardia described earlier. The onset of atrial fibrillation may produce very rapid ventricular
rates because the by pass pathway lacks the rate limiting properties of the normal AV node (FIGURE 1.48).
When re-entry and therefore tachycardia occurs in LGL syndrome, the QRS complexes remain narrow, with
appearance similar to that of a junctional tachycardia. Tachycardia due to the WPW and LGL are grouped
together under the term atrioventricular re entrant (AVRT) tachycardia.
FIGURE 1.47 Lown-Ganong-Levine syndrome.
FIGURE 1.48 WPW syndrome. When the ventricles are depolarized through the AV node (1) the ECG is
normal. When the ventricles are depolarized through the accessory conducting tissue (2) the ECG shows
a very short PR interval and a wide QRS complex.
PROLONGED PR INTERVAL: CONDUCTION BLOCK
If the PR interval is more than 200 ms (i.e. > 5 small squares) it indicates a conduction defect (block) e.g.
first degree heart block. Conduction defect may take one of the following forms:
01 SINOATRIAL BLOCK
In sinoatrial block, the SA node depolarizes normally, but the depolarization fails to penetrate the atrium. The
EKG appearance reveals no P QRS T, but the atrium must have been depolarized because the next P wave
appears at the predicted time. This should be differentiated from sinus arrest (sinus pause) that means loss
of SA node activity. In sinus arrest the expected P wave does not appear until after two or three normal
intervals and then not at the predicated time (FIGURE 1.49).
FIGURE 1.49 Sinoatrial block and sinoatrial arrest.
02 CONDUCTION PROBLEMS IN THE AV NODE AND HIS BUNDLE
I. FIRST DEGREE HEART BLOCK (FIGURE 1.50)

When each atrial depolarization is followed by ventricular depolarization, but atrioventricular conduction is
slow, the PR interval on the surface EKG is prolonged (> 5 ss) and the first degree heart block is said to be
present. First degree heart block had fixed prolonged PR interval.
FIGURE 1.50 First

degree heart block.
FIGURE 1.51 Second degree heart block.

II. SECOND DEGREE HEART BLOCK (FIGURE 1.51)

When atrial depolarization intermittently fails to induce ventricular depolarization, second degree heart block
exists. There are three varieties. Mobitz type I (Wenckebach phenomenon) describes progressive
lengthening of the PR interval with each beat till a P wave is not conducted and is not followed by a QRS
complex; Mobitz type II is present when most beat are conducted, but occasionally a P wave is not followed
by a QRS complex; Type 2:1 is present when alternate P waves are not conducted. This block may be 2:1 or
3:1 depending on the relation between P wave and QRS complex.
III. THIRD DEGREE (COMPLETE) HEART BLOCK (FIGURE 1.52)

Complete heart block is said to occur when atrial contraction is normal, but no beats are conducted to the
ventricles. Complete heart block results either from His bundle disease or from bilateral bundle branch block.
A narrow QRS complexes indicate that the rhythm originates within the His bundle itself below the block, but
a wide QRS complex indicates that ventricular depolarization originates in the Purkinje system. The EKG in
third-degree heart block shows P waves marching across the rhythm strip at their usual rate (60 to 100
waves per minute) but bearing no relationship to the QRS complexes that appear at a much slower escape
rate (30 to 40 waves per minute). The QRS complexes appear either narrow or wide.
FIGURE 1.52 Third

degree heart block.
Look at the P wave
which has no relation
to the QRS
complexes i.e. it
comes before, within,
or after.
It is important to remember that AV dissociation is not synonymous with complete heart block. AV
dissociation refers to any circumstance in which the atria and ventricles beat independently of each other.
This situation occurs in heart block, ventricular tachycardia, and sometimes junctional escape rhythm.
IV. BUNDLE BRANCH BLOCK

When the His bundle conducts normally, but one of the bundle branches is blocked, the PR interval is
normal, but QRS complex is widened because of the late depolarization of the part of the ventricle normally
supplied by the bundle branch which is blocked. The characteristic appearances of right bundle branch block
(RBBB) include (FIGURE 1.53) dominant R wave in V1, wide QRS complexes (greater than 0.12 seconds or
three small squares), an RSR′ pattern in V1 and V2 (rabbit ears) with ST segment depression and T wave
inversion, and lastly deep and wide S waves in V6.
FIGURE 1.53
Right bundle
branch block.
The characteristic appearance of left bundle branch block (LBBB) includes (FIGURE 1.54) wide QRS
complex (wider than 0.12 seconds or wider than three small squares), loss of septal Q waves, broad or
notched R wave (M shape) with prolonged upstroke of the QRS complex in the lateral leads (I, II, VL, and V5-
V6) with ST segment depression and T wave inversion, reciprocal changes in V1 and V2, and lastly left axis
deviation may be present.
FIGURE 1.54 Left bundle branch block.
Remember that a dominant R wave in V1 (i.e. longer R wave than S wave in V1) is the most discriminative
feature and it indicates right bundle branch block. Both right and left bundle branch block can be intermittent
or fixed. In some individuals, the ventricles conduct normally at slow heart rates, but, above when the heart
rate accelerates, bundle branch block develops. This occurs because the descending impulse in tachycardia
finds one of the branches is still in its refractory period. This is called rate-dependant bundle branch block.
Causes of bundle branch block are shown in BOX 1.5.
BOX 1.5 Causes of bundle branch block

RIGHT BUNDLE BRANCH BLOCK LEFT BUNDLE BRANCH BLOCK
Coronary artery disease Coronary artery disease
Right ventricular hypertrophy or strain pattern e.g. Hypertension
pulmonary embolism
Congenital heart disease e.g. ASD Aortic valve disease
Normal variant Cardiomyopathy
When there is QRS widening greater than 0.12 seconds (three small squares) without any other criteria for
either bundle branch block, the term used is nonspecific intraventricular conduction delay. Partial or
incomplete RBBB is characterized by normal QRS complex duration, but with an RSR′ pattern in V1. It is
quite common in healthy people. A diagnosis of incomplete LBBB may be made if the QRS duration is
greater than 0.10 with notching of the R wave in V5 or V6.
V. FASCICULAR BLOCK
The right bundle branch block is a single structure, but the left bundle branch divides into two fascicles;
anterior and posterior. Block at the anterior fascicle (left anterior fascicular block or left anterior hemi block)
causes extreme left axis deviation while block at the posterior fascicle (left posterior fascicular block or left
posterior hemi block) may cause extreme right axis deviation. Because of this anatomy, LBBB can be called
bifascicular block and RBBB is called monofascicular block. Bifascicular block includes RBBB and left
anterior fascicular block (FIGURE 1.55) or RBBB with left posterior fascicular block, or LBBB. If first degree
heart block is added to the bifascicular block, trifascicular block is said to be present (FIGURE 1.56). When
RBBB is present with LBBB (or left anterior and posterior hemi block), complete heart block is likely to occur.
FIGURE 1.55 RBBB and left anterior hemiblock. This combination is called bifascicular block.
FIGURE 1.56 RBBB, left anterior hemiblock, and first degree heart block. This combination is called
trifascicular block.
An approach to suspected bundle branch block is shown here:

STEP 08 QRS COMPLEX
In the normal chest leads, the QRS complexes start as a negative wave in lead V1 and V2 and then ended as
a positive lead in V5 and V6; the transition point where R and S waves are equal in the chest lead over the
interventricular septum is normally at V3 or V4; an RSR′ pattern in V1 is a normal acceptable variant provided
that the duration is less than three small squares (partial RBBB); the normal width of the QRS is less than
three small squares; R wave is smaller than S wave in V1; R wave in V6 is less than five large squares; R
wave in V5 or V6 plus S wave in V1 or V2 is less than seven large squares. There may be small thin Q waves
(less than 1 small square in width and less than 3 small squares in depth or less than 1/4 of the
corresponding height of R wave) in the lateral leads: I, VL, V5-V6 or in lead III, but not VF. These Q waves
are called septal Q waves. More than this value one should consider them pathological until proves
otherwise. Abnormalities in the precordial QRS leads may take one of the following forms:
1. Wide QRS (more than three > small squares) may indicate bundle branch block, WPW syndrome,
hyperkalemia, and ventricular source (e.g. ventricular ectopic beats and tachycardia, ventricular escape
beat and rhythm), or wide complex tachycardia.
2. Tall (dominant) R wave in V1 may occur in right ventricular hypertrophy, WPW syndrome type A, right
bundle branch block, or true posterior myocardial infarction. This finding could be normally seen in
certain individuals. An approach to dominant R wave in V1 is shown here
Right ventricular hypertrophy (FIGURE 1.57) is seen in leads V1 – V4. The Sokolow-Lyon criteria for right
ventricular hypertrophy adds the R wave amplitude in V1 to the S wave amplitude in lead V5 or V6; a sum of
1.1 (11 small squares) mV or greater implies right ventricular hypertrophy (RVH). There is thus dominant R
wave in V1 and in severe cases there is inversion of T waves (with/without ST depression) in V1 and V2 and
sometimes V3 or even V4. This is called right ventricular strain pattern.
FIGURE 1.57 Right ventricular hypertrophy with strain pattern.

3. Tall R wave in V5 or V6 may indicate left ventricular hypertrophy (LVH). It is significant when there is
voltage criteria (R waves in V5 or V6 is greater than 5 large squares or R wave in V5 or V6 plus S waves
in V1 or V2 is greater than 7 large squares). Strain pattern is said to be present when inverted T waves
(with/without ST depression) are seen in the lateral leads of I, VL, V5-V6 (FIGURE 1.58).
FIGURE 1.58 Left ventricular hypertrophy with strain pattern.
4. Low voltage QRS complex is present when QRS height is less than one large square in limb leads and
less than two large squares in chest leads. This (FIGURE 1.59) may result from incorrect standardization
of the EKG device, emphysema, obesity, pericardial effusion, hypopituitarism, and myxoedema. In
pericardial effusion, QRS complexes are small and there may be an electrical alternans that is a
changing axis with alternate beats caused by heart moving in a bag of fluid (FIGURE 1.60).
FIGURE 1.59 Low voltage QRS complex.
FIGURE 1.60 Electrical alternans. The

arrows point to each QRS complex.
5. Shifting of the transition point from its normal site at V3-V4 to further point e.g., V4-V5 or V5-V6 may
indicate chronic lung disease. This is called clockwise rotation of the heart and shown in FIGURE 1.61.
FIGURE 1.61
Shifting of the
transition point.
This is called
clockwise
rotation of the
heart.
STEP 09 ST SEGMENT
ST segment is measured from the end of the QRS to the beginning of the T wave (FIGURE 1.4). It should be
isoelectric (the same level as the EKG trace between beats that is between the T wave to the next P wave).
Abnormalities of the ST segment may include elevation or depression.
ST SEGMENT ELEVATION FIGURE 1.62

Localization of
A raised ST segment may indicate acute the main
myocardial infarction, left ventricular myocardial
aneurysm, Prinzmetal's angina, brugada walls.
syndrome or pericarditis. It can be however
a normal variant.
Horizontal ST segment elevation more than
two small squares in chest leads and/or
more than one small square in limb leads
indicate acute myocardial infarction. The
infracted (and even ischemic) areas of the
myocardium can be localized through the
leads showing EKG changes (FIGURE
1.62 and BOX 1.6).
BOX 1.6 EKG localization of myocardial wall affected by infarction or ischemia

MYOCARDIAL INFARCTION EKG CHANGES CORONORY TERRITORY
Anterolateral V4 to V6, lead I, and aVL Left main stem
Septal V1 and V2 Left anterior descending artery
Anterior V3 and V4 Left anterior descending artery
Anteroseptal V1 to V4 Left anterior descending artery
Lateral I, aVL and V1-V6 Left circumflex
High lateral Lead I and aVL Left circumflex artery
Posterior Dominant R wave in V1 Usually left circumflex, also right coronary
Inferior II, III and aVF Right coronary artery
Right ventricular ST segment elevation in V4R Right coronary artery
Persistent ST segment elevation is quite common after an anterior myocardial infarction. It may indicate the
development of a left ventricular aneurysm, but it is not a reliable evidence of this. The upward concave
shape of the ST segment and unusual distribution of changes in pericarditis may help to distinguish
pericarditis from myocardial infarction (FIGURE 1.63). The EKG in acute pericarditis typically evolves
through four stages. In stage 1, there is widespread elevation of the ST segments, often with upward
concavity (sometimes called smiling face), involving two or three standard limb leads and V2 to V6, with
reciprocal depressions only in aVR and sometimes V1, as well as PR-segment depression. Usually there are
no significant changes in QRS complexes. In stage 2, after several days, the ST segments return to normal
and only then, or even later, do the T waves become inverted (stage 3). Ultimately, weeks or months after
the onset of acute pericarditis, the EKG returns to normal in stage 4.
FIGURE 1.63 Stage 1 acute pericarditis. There are ST segment elevation in inferior and some of the
anterior leads with reciprocal changes at the aVR and PR segment depression.
Prinzmetal's angina (FIGURE 1.64) occurs as a result of coronary artery spasm. It may be associated with
reversible ST segment elevation without myocardial infarction. These EKG abnormalities can be transient at
time of pain.
FIGURE 1.64 Prinzmetal's angina. It is characterized by reversible ST segment elevation.
The EKG appearance of Brugada syndrome (FIGURE 1.65) between attacks superficially resembles that
associated with partial RBBB, with an RSR′ pattern in leads V1 and V2. However the ST segment in these
leads is raised and there is no wide S wave in V6 as there in RBBB.
FIGURE 1.65 Brugada syndrome.
Myocardial infarction can be divided into two types on the basis of their associated EKG findings into:
1 ST segment elevation myocardial infarction

2 Non ST segment elevation myocardial infarction
ST SEGMENT ELEVATION MYOCARDIAO INFARCTION (STEMI)
This type is also called full thickness myocardial infarction, transmural myocardial infarction, or Q – wave
myocardial infarction. The serial evolutions of EKG changes (FIGURE 1.66) in this type include:
1. Symmetrically peaked (hyperacute) T waves that resolve after several minutes as the characteristic ST
segment elevation develops (WITHIN SECONDS).
2. Acute ST segment elevation that indicates the current of injury (WITHIN MINUTES).
3. Progressive loss of R wave, development of Q wave, resolution of the ST segment elevation and
terminal T wave inversion (WITHIN HOURS).
4. Deep Q wave and T wave inversion (WITHIN DAYS).
5. Old or established myocardial infarction is characterized by persistent Q waves and less marked T
waves (WITHIN WEEKS OR MONTHS).
6. In the setting of acute MI there may be ST segment depression in some leads, and these are called
reciprocal changes.
FIGURE 1.66
Serial evolution
of STEMI.
During the initial stage, total occlusion of an epicardial coronary artery produces ST-segment elevation. Most
patients initially presenting with ST-segment elevation ultimately evolve Q waves on the EKG. However, Q
waves in the leads overlying the infarct zone may vary in magnitude and even appear only transiently
depending on the reperfusion status of the ischemic myocardium. A small proportion of patients initially
presenting with ST-segment elevation will not develop Q waves when the obstructing thrombus is not totally
occlusive, obstruction is transient, or if a rich collateral network is present. A minority of patients who present
initially without ST-segment elevation may develop a Q-wave myocardial infarction. For these reasons terms
such as Q-wave myocardial infarction, non-Q-wave myocardial infarction, transmural myocardial infarction,
and nontransmural myocardial infarction, have been replaced by STEMI and NSTEMI. Examples of STEMI
are shown in FIGURES 1.67, 1.68, and 1.69.
FIGURE 1.67
Inferior wall
STEMI. There
are ST
segment
elevation in
leads II, III,
and aVF with
reciprocal
changes in
V1-V4.
FIGURE 1.68
Anterior wall
STEMI. There
are ST
segment
elevation in
leads V3 and
V4 with Q
waves.
FIGURE 1.69
Anterolateral
STEMI with
old inferior
STEMI. There
is ST segment
elevation in V1
– V6.
Infarction of the posterior wall of the left ventricle does not cause ST segment elevation or Q waves in
standard leads, but can be diagnosed by presence of the reciprocal changes in the form of ST segment
depression and a tall R wave in leads V1-V4 (FIGURE 1.70).
FIGURE 1.70 Probable posterior wall myocardial infarction.
Moreover, posterior infarction can be diagnosed by placing the chest leads on the back of the left side of the
chest to obtain V7, V8, and V9 (FIGURE 1.71).
FIGURE 1.71 Posterior leads are placed as follows:
V7 is placed at the fifth intercostal space posterior axillary line.
V8 is placed at the posterior fifth intercostal space in left midscapular
line.
V9 is placed directly between V8 and spinal column at posterior fifth of
left ventricle intercostal space.
Inferior infarction may involve the right ventricle. This may be identified by recording from right ventricular
leads (FIGURE 1.72). The classic clinical presentation involves a triad of hypotension, clear lung fields, and
elevated JVP. The diagnosis is assisted by obtaining right precordial EKG leads (FIGURE 1.72), which are
routinely indicated for inferior acute myocardial infarction. Acute ST segment elevation of at least 1 mm (0.1
mV) in one or more of leads V4R to V6R is both sensitive and specific (>90%) for identifying acute right
ventricular injury, and Q or QS waves effectively identify right ventricular infarction.
FIGURE 1.72 Right precordial leads are placed at sites

corresponding to left precordial leads as follows:
V1R is placed at the fourth intercostal space to left of
sternum.
V2R is placed at the fourth intercostal space to right of
sternum.
V3R is placed directly between V2R and V4R.
V4R is placed at the fifth intercostal space at right
midclavicular line.
V5R is placed level with V4R at right anterior axillary line.
V6R is placed level with V5R at right midaxillary line.
Sometimes it is perfectly normal for the ST segment to be elevated following an S wave in leads V2-V5
(FIGURE 1.73). This is called high take off ST segment and represent an early repolarization of the
ventricles. As always, normal variety should be diagnosed by exclusion of other serious causes.
FIGURE 1.73. High take – off ST segment elevation.
NON ST SEGMENT MYOCARDIAL INFARCTION (NSTEMI)
This type is called non ST segment elevation myocardial infarction (NSTEMI), non Q wave myocardial
infarction, partial thickness myocardial infarction, or subendocardial myocardial infarction. This type is
characterized by deep symmetrical T wave inversion together with a reduction in the height of the R waves in
leads facing the infracted area (FIGURE 1.74).
FIGURE 1.74 Anterior wall NSTEMI.
Sometimes one may encounter more than one infarction which may imply multi-vessel disease. This type of
presentation is called double wall infarction (FIGURE 1.75).
FIGURE 1.75 Acute anterolateral myocardial infarction and inferior ischemia.
STEMI AND BBB
The presence of RBBB usually does not mask typical ST-T wave or Q wave changes, except for rare cases
of isolated true posterior acute myocardial infarction. LBBB usually causes disorganized EKG pattern and
makes changes due to myocardial infarction more difficult. However a patient admitted with ischemic chest
pain and EKG shows LBBB that is known to be new; it can be assumed that an acute infarction has
occurred. Certain EKG patterns, although relatively insensitive, suggest acute myocardial infarction if present
in the setting of LBBB. These are:
1. ST segment elevation of 1 mm or more in leads with a positive QRS complex.
2. ST segment elevation of 5 mm or more associated with a negative QRS complex.
3. R wave regression from V1 to V4.
4. ST segment depression of 1 mm or more in leads V1, V2, or V3.
5. Q waves in two of leads I, aVL, V5, V6.
ST SEGMENT DEPRESSION
Normally ST segment may be depressed in lead III, but not aVF and often the segment slopes upward. On
the other hand, digoxin causes down sloping depression of the ST segment (FIGURE 1.76). This finding of
down slopping ST segment depression is called reverse tick sign.
FIGURE 1.76 Varieties of ST

segment depression.
A. Planar ST depression is
usually indicative of
myocardial ischemia.
B. Down-sloping depression
usually indicates myocardial
ischemia or digoxin therapy.
C. Up-sloping depression
may be a normal finding.
Horizontal (Planar) depression of the ST segment more than two small squares indicates ischemia or even
more than one small square in patient with chest pain. The EKG changes are best seen in the leads which
face the ischemic area (FIGURES 1.77 and 1.78).
38 Revision: Prof. Nasser Ghaly Yousif
FIGURE 1.77 Anterolateral myocardial ischemia. There is horizontal ST segment depression involving
the anterior leads and down sloping of the lateral leads. Lead aVF shows up – slopping ST segment
depression.
FIGURE 1.78 Severe anterolateral ischemia.
STEP 10 T WAVE
T wave is the most variable part of the EKG. Normally the T wave has the following characteristics:
1 Inverted in aVR
2 Inverted in aVL provided that the P wave is also inverted
3 Inverted in lead III, but not aVF
4 Inverted in V1, V2 in young and V3 in black people
The T wave could be inverted, flattened or peaked according to the pathology. One should consider the
following clinical settings:
Acute myocardial infarction Hyperacute (peaked) T wave

Established STEMI Terminal T wave inversion
NSTEMI Deep symmetrical T wave inversion
Ischemia Inverted T wave
Left or right ventricular hypertrophy T wave inversion (strain pattern)
Bundle branch block T wave inversion
Pulmonary embolism T wave inversion
Hyperkalemia Peaked T wave
Hypokalemia Flat and prolonged
Hypertrophy cardiomyopathy Deep T wave inversion mimics infarction called (pseudoinfarct pattern)
Subarachnoid hemorrhage T wave inversion (cerebral T wave)
Many minor degrees of ST segment and T wave abnormalities such as T wave flattening are usually of no
great significance and are best reported as non specific ST–T changes. However if these T wave changes
are associated with ischemic chest pain, or elevated cardiac enzymes, or are new and deep (more than
three small squares) one should considered them significant (FIGURE 1.79).
FIGURE 1.79 Anterior and inferior wall ischemia.
The EKG in pulmonary

FIGURE 1.80 S1Q3T3
embolism is non specific and
of massive pulmonary
may show sinus tachycardia
embolism.
(most common) or features of
right axis deviation, right
ventricular hypertrophy, or right
bundle branch block. A large S
wave in lead I and a deep Q
wave in lead III as well as
inverted T wave in lead III may
also be seen (FIGURE 1.80).
This pattern is called S1Q3T3.
Unlike an inferior infarction, in
which Q waves are usually seen in at least two of the inferior leads, the Q waves in an acute pulmonary
embolus are generally limited to lead III.
Hyperkalemia produces a progressive evolution of changes in the EKG that can culminate in ventricular
fibrillation and death. As the potassium begins to raise, the T waves across the entire 12-lead EKG begin to
peak (FIGURE 1.81 A). This effect can easily be confused with the peaked T waves of an acute myocardial
infarction. One difference is that the changes in an infarction are confined to those leads overlying the area
of the infarct, whereas in hyperkalemia, the changes are diffuse. With a further increase in the serum
potassium, the PR interval becomes prolonged, and the P wave gradually flattens and then disappears
(FIGURE 1.81 B). Ultimately, the QRS complex widens until it merges with the T wave, forming a sine wave
pattern (FIGURE 1.81 C). Ventricular fibrillation may eventually develop.
FIGURE 1.81 Changes of hyperkalemia.
With hypokalemia, the EKG may show ST FIGURE 1.82

segment depression, flattening of the T wave, Changes of
and appearance of a U wave (FIGURE 1.82). hypokalemia.
In hypertrophic cardiomyopathy, EKG usually
shows left ventricular hypertrophy, often with
prominent septal Q waves that can be
misdiagnosed as indicative of infarction
(FIGURE 1.83).
FIGURE 1.83 Hypertrophic cardiomyopathy.

The EKG in subarachnoid hemorrhage frequently shows ST-segment and T-wave changes similar to those
associated with cardiac ischemia (FIGURE 1.84). Prolonged QRS complex, increased QT interval, and
prominent "peaked" or deeply inverted symmetric T waves are usually secondary to the intracranial
hemorrhage. There is evidence that structural myocardial lesions produced by circulating catecholamines
and excessive discharge of sympathetic neurons may occur after subarachnoid hemorrhage, causing these
EKG changes and a reversible cardiomyopathy sufficient to cause shock or congestive heart failure. The
sympathetic nerves themselves appear to be injured by direct toxicity from the excessive catecholamine
release. An asymptomatic troponin elevation is common. Serious ventricular dysrhythmias are unusual.
FIGURE 1.84 Subarachnoid hemorrhage.
STEP 11 QT INTERVAL
The QT interval is measured from the start of the QRS complex to the end of the T wave. It varies with heart
rate (the faster the heart rate, the shorter is the QT interval), gender and time of day. There are several
different ways of correcting for heart rate, but the simplest one is Bazett's formula. In this, the corrected QT
interval, QTc, is calculated as (QTc = QT interval / √R-R interval)
Corrected QT intervals are considered long if greater than 440 msec in men (11 small squares) and 450–460
msec in women (11.5 small squares), but in practice long QT is considered when the QT interval is more
than two large squares (FIGURE 1.85).
FIGURE 1.85 Markedly prolonged QT interval.
Short QT syndrome is considered when QT interval is less than 300 msec (7.5 small squares). Causes of
abnormal QT are shown in BOX 1.7.
BOX 1.7 Causes of abnormal QT interval

PROLONGED QT INTERVAL
1. Congenital 2. Drugs
Jervell-Lange-Nelson syndrome Disopyramide Procainamide
Romano-ward syndrome Amiodarone Tricyclic antidepressant
Sotolol Erythromycin
3. Electrolyte abnormalities
Hypokalemia Hypocalcemia Hypomagnesemia
SHORT QT INTERVAL
Hyperkalemia Hypercalcemia Digoxin therapy
STEP 12 ADDITIONAL WAVES
The normal U wave is a small, rounded deflection ≤1 mm that follows the T wave and usually has the same
polarity as the T wave. It is thought to be due to depolarization of the interventricular (Purkinje) conduction
system. It is commonly seen in normal subjects in the anterior chest leads. It may be seen with bradycardia
and left ventricular hypertrophy. An abnormal increase in U-wave amplitude is most commonly due to drugs
(e.g., amiodarone, sotalol, procainamide, and disopyramide) or to hypokalemia (FIGURE 1.82). Very
prominent U waves are a marker of increased susceptibility to the torsades de Pointe type of ventricular
tachycardia. Inversion of the U wave in the chest leads is abnormal and may be a subtle sign of ischemia.
Osborne or J wave is a small hump seen at the end of the QRS complex and is a characteristic of
hypothermia (FIGURE 1.86). It may however be seen in normal subjects.
FIGURE 1.86 Osborne waves.
An epsilon wave (e wave) refers to the

terminal notching of the QRS complexes in
V1–V3. When it is distinct and appears
separated from the QRS complex, it is
referred to as an epsilon wave (FIGURE 1.87)
and suggests right ventricular dysplasia.
FIGURE 1.87 Epsilon waves.

Another random document with
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spelling, manifestly the attempt would be to measure the changes
which have been brought about in any group in terms of units which
are comparable. If group one shows ability ten, having advanced
during the year from ability seven, it will be considered just as
satisfactory as the advance which has been made in group two,
which has moved from ability eight to ability eleven. In other words,
the purpose of measurement is never to attempt to make all alike. It
is rather to discover differences and the reason for their existence;
but most of all to give us some adequate means of determining
progress or change.
Let us suppose again, in a matter of business administration, that
one school shows a much higher per capita cost than another. This
does not prove that one school is more efficiently managed than
another. What it does do is to suggest that some adequate reason is
to be found for the difference which exists. In like manner, one city
may show a much higher cost for janitors’ salaries than does
another. This may suggest investigation, but it does not prove that
the city with the higher cost for janitors’ service is inefficiently
managed or extravagant in its expenditures. It may be that the city
that spends a relatively large amount for janitorial service actually
gets more per dollar for the money which it spends than does the city
with the smaller cost. It is always a purpose of measurement to
discover discrepancies and to raise problems.
It has been contended that it is not important to derive scales or
units of measurement on the ground that the scientific study of
education is significant only in so far as it has to do with a careful
investigation of the processes involved in growth. Those who make
this contention seem to feel that a careful study of the way in which
children come to form habits, to grow in power of reasoning, or in
ability to appreciate, will give us the final answer concerning the
methods to be employed in teaching. The difficulty with this point of
view is that human beings, even though they be trained in
investigation, are fallible. The only final test of the success of any
method, however carefully derived, and however much of it may
depend upon a knowledge of the processes involved in growth in the
particular aspect of mental life which is involved, is to be found in the
result achieved. Theoretically a method may seem to be perfect, and
yet in terms of the results which are secured it may prove to be a
failure. If the results are not accurately measured, if we do not derive
scales of measurement, we can never be certain of our conclusions
with regard to the method to be employed in bringing about any
particular type of mental growth or development.
Possibly the one element in the situation which has operated to
retard development in the direction of accurate measurement of
results, more than any other, is the tendency in education to appeal
to authority, and the corresponding lack of devotion to scientific
investigation. It is, of course, much easier to solve the problems
which one meets by taking the opinion of those who have had
experience in the field. No one would deny the value of the judgment
of our great educational leaders. The fact remains, however, that
these same leaders would be the last ones to place their own
opinion in opposition to the results obtained from a careful scientific
investigation. Indeed, it is in no small measure due to the insistence
of these leaders that we are coming to have adequate investigations
with regard to our educational practice.
It has seemed necessary to discuss at some length the objections
which have been made against the attempt to measure results in
education, rather than to devote more space to a discussion of the
work which has already been done. All students of education are
familiar with the early work of Rice, and with the later contributions of
Thorndike, Ayres, Cornman, and many others who have contributed
to the literature of educational investigation. Possibly the most
significant piece of work that has been done is Thorndike’s scale for
measuring handwriting.[32] We may reasonably hope to have scales
derived for the measurement of abilities in other subjects.
In administration, considerable work has already been done with
reference to the cost of education, both as regards the relationship of
expenditure for education to other expenditures, the question of a
proper distribution of money within the educational budget, and of
the proper distribution of state school funds.[33] We can, of course,
hope for much more significant work in this field as more adequate
systems of accounting are introduced and more satisfactory reports
are issued. It is noteworthy that in those school systems in which an
attempt has been made to check up expenditures carefully,
remarkable savings have been made. We have not yet reached the
limit of possible reduction of expenditure without the sacrifice of our
present efficiency. Much work has been done on problems of school
organization, yet the problems of retardation and elimination will be
satisfactorily treated only as we secure more accurate records
concerning attendance, scholarship, health, promotions, and
demotions, such as are provided for by the genetic records now kept
in some of our more progressive school systems. The problems of
departmental work and individual instruction can never be
satisfactorily solved until we measure accurately the results secured
under different systems of organization.
Implicit in all of the argument which has been advanced in favor of
measuring results is the contention that education means change. If
changes are brought about in the children who are being educated,
then there must be the possibility of measurement. These changes
may take place in habit, in knowledge, in methods of work, in
interests and ideals, and in power of appreciation. Probably no one
would question the possibility of measuring the change which takes
place in the formation of habits. We have quite commonly been
willing to measure growth in knowledge by tests which demand that
students not only remember facts, but that they show some ability to
apply them. Whether or not a student commands a particular method
of work can be determined by observation of his method of
procedure as well as by the results that he secures. If interests or
ideals are changed, there necessarily follows a change in activity.
Any real power of appreciation will be accompanied by some change
in expression.
The fact that we do not yet have scales or units of measurement
which will enable us to evaluate accurately the results obtained in all
of the different forms of school activity is not an argument against the
possibility of measurement. In any field the development of units of
measurement is dependent upon careful investigation, and upon a
realization of the imperfection of the units already used. It is only as
we insist upon measurement that we can hope to have our units
refined. Take for example the problem of grades or marks which are
commonly assigned to students as a measure of their efficiency in
doing school work. Any investigation of these units will show that
there is very great variation in their application by different members
of the teaching corps.
The way to bring about a remedy is not to abolish all marks or
grades, but rather to study the problem of the proper distribution of
marks, and, if necessary, to weigh differently the marks of different
instructors. The more imperfect the unit of measure which we now
apply, the greater the need for insisting upon accurate measurement.
The first step in the development of scientific inquiry in any field is
found in accurate description of the phenomena involved. The
demand that we measure results in education is simply a demand
that the basis for scientific investigation be made available by means
of this accurate description of the situation as it exists. Some
investigators in education have already been able to take the further
steps in scientific inquiry which have enabled them to foretell with
considerable accuracy the results which might be expected in
education under given conditions. Further progress is, however,
dependent upon that sort of measurement which will discover
problems which are not now clearly defined or which have not yet
been thought of. Of course, as inferences are made in the light of the
problems suggested, there will be still further necessity for accurate
measurement. When those who are charged with the responsibility
of determining educational policy appeal to fact rather than to
opinion, when we are able to evaluate accurately that which we
achieve, educational progress will be assured and a profession of
education will have been established.
We shall always have most excellent work in teaching done by
those for whom scientific investigation, as such, means little. The
investigations made will, however, modify the practice of these same
teachers through changed demands and because of the
demonstration of the validity of the new method of work by those
who can appreciate the significance of results achieved by
investigators. It is certainly to be expected that open-minded
teachers will experiment for themselves and will aid in the work of
the expert who must use the schools as his laboratory. Much
depends upon the coöperation and good will of all who are engaged
in teaching. It is not too much to expect that the spirit of investigation
will be found in large measure to characterize those whose privilege
it is to provide the situation in which intellectual development is
stimulated.
An example of a study involving the coöperation of the pupils,
teachers, and supervisory officers of twenty-six separate schools or
school systems is Dr. C. W. Stone’s study on Arithmetical Abilities
and Some of the Factors Determining them. The following quotations
from Dr. Stone’s study indicate the type of result which we may hope
to get from such investigations.
In Reasoning
The scores for the reasoning problems were determined from the results of two
preliminary tests—one, giving one hundred 6th grade pupils all the time they
needed to do the problems as well as they could in the order as printed (see page
11); and another, giving one hundred 6th grade pupils all the time they needed to
do the problems as well as they could in the reverse order from that as printed.
The results as tabulated below in table II show that scores for reasoning problems
of Grade VI pupils can be very definitely arranged in a scale on the basis of
relative difficulty. Just what the scale should be can only be determined by
determining the form of distribution and the location of the zero point. From what is
known of these the scale of weighting shown in the last column of table II is
believed to be the best, and this is the one employed in the computations of this
study. However, in order to enable the reader to satisfy himself as to which is the
best method, the scores of the twenty-six systems were calculated on each of
three other bases—(1) counting each problem reasoned correctly a score of 1; (2)
counting each problem reasoned correctly a score based on the ratio of its
difficulty as shown in the next to the last column of table II; and (3) counting the
scores made on only the first six problems for which presumably all pupils of all
systems had ample time. See Appendix, p. 98.
In both reasoning and fundamentals the scores used as a measure of the
achievement of a system were computed by combining the scores of one hundred
pupils. Where more than one hundred pupils were tested, the papers used were
drawn at random, the number drawn from each class being determined by the ratio
of its number to the total number tested in the system. Where less than one
hundred pupils were tested, the combined scores made were raised to the basis of
one hundred pupils.
TABLE II
PRELIMINARY TESTS
Reasoning—Unlimited Time
100 Different Pupils Tested Each Time
% Reasoned % Reasoned Average % Weight According

Number of Weight Used as
Correctly as Correctly as Reasoned to Average %
Problems Probably the Best
Printed Reversed Correctly Correct
1 95 92.6 93.8 1 1
2 86 82.2 84.1 1.1 1
3 94 89 91.5 1 1
4 80 83 81.5 1.5 1
5 88 86 87 1.1 1
6 69 57.4 63.2 1.5 1.4
7 70 80 75 1.25 1.2
8 29 44 36.5 2.6 1.6
9 19 15.5 17.2 5.45 2
10 24 27.4 25.7 3.6 2
11 17 7.5 12.3 7.6 2
12 7 16.4 11.7 8 2
Precautions observed to make the Scoring Accurate

The simplicity of the tests made the scoring comparatively easy; and with the
observance of the following precautions it is believed that a high degree of
accuracy was attained. (1) In so far as practicable, all the papers were scored by a
single judge—only two persons being employed on any phase of the work for the
entire twenty-six systems; (2) each problem was scored through one hundred or
more papers, then the next followed through, etc.; (3) the score for each part of
each problem, the errors, etc., were entered on a blank provided with a separate
column for each item; (4) where there was doubt as to how the score should be
made, the scorer made a written memorandum of how the case was finally
decided and this memorandum served as the guide for all future similar cases.
What the Scores Measure

As used in this study the words achievements, products, abilities, except where
otherwise qualified, must necessarily refer to the results of the particular tests
employed in this investigation. That some systems may achieve other and possibly
quite as worth-while results from their arithmetic work is not denied; but what is
denied is that any system can safely fail to attain good results in the work covered
by these particular tests. Whatever else the arithmetic work may produce, it seems
safe to say that by the end of the sixth school year, it should result in at least good
ability in the four fundamental operations and the simple, everyday kind of
reasoning called for in these problems. It does not then seem unreasonable, in
view of the precautions previously enumerated, to claim that the scores made by
the respective systems afford a reliable measure of the products of their respective
procedures in arithmetic.
The Data
The source of the data used to help answer the above questions is some six
thousand test papers gathered from twenty-six representative school systems.
Copies of the tests may be found in Part I, pages 10 and 11; as may also a
statement of conditions under which the tests were personally given by the author,
page 13; and the method of scoring, pages 15 to 18.
The achievements are considered from two standpoints—(1) the scores and
mistakes of the systems as systems, (2) the scores of individual pupils as
individuals.
Table III gives the scores made in reasoning by each of the twenty-six systems,
counting all the problems that were solved, and weighting them according to the
last column of table II. The Roman numerals used in the left-hand column to
designate the systems are those that fell to each system by lot. As seen by the
column headed scores made, the systems are arranged according to number of
scores, i.e. system XXIII made three hundred fifty-six points, the lowest score, and
is placed first in the table; system XXIV made four hundred twenty-nine points, and
is placed second, etc. System V, having made the highest score, is placed last in
the table.
ACHIEVEMENTS OF THE SYSTEMS AS SYSTEMS
Measured by Scores Made
TABLE III[34] TABLE IV
Scores of the Twenty-six Systems in Reasoning with Scores of the Twenty-six Systems in Fundamentals
Deviations from the Median. Scores from all with Deviations from the Median. Scores from all
Problems Problems
M[35] = 551 M = 3111
Devia- Devia- Devia- Devia-
Systems in Scores tions from tions in Per Systems in Order Scores tions from tions in Per
Order of [36] the Cent of the of Achieve- ment Made the Cent of the
Achieve- ment Made
Median Median Median Median
XXIII 356 -195 -35 XXIII 1841 -1270 -41
XXIV 429 -122 -22 XXV 2167 -944 -30
XVII 444 -107 -19 XX 2168 -943 -30
IV 464 -87 -16 XXII 2311 -800 -26
XXV 464 -87 -16 VIII 2747 -364 -12
XXII 468 -83 -15 X 2749 -362 -12
XVI 469 -82 -15 XV 2779 -332 -11
XX 491 -60 -11 III 2845 -266 -8
XVIII 509 -42 -8 I 2935 -176 -6
XV 532 -19 -3 XXI 2951 -160 -5
III 533 -18 -3 II 2958 -153 -5
VIII 538 -13 -2 XVII 3042 -69 -2
VI 550 -1 -2 XIII 3049 -62 -2
I 552 1 2 VI 3173 62 2
X 601 50 9 XI 3261 150 5
II 615 64 12 IX 3404 293 9
XXI 627 76 14 XII 3410 299 10
XIII 636 85 15 XXIV 3513 402 13
XIV 661 110 19 XIV 3561 450 14
IX 691 140 20 IV 3563 452 14
VII 734 183 33 V 3569 458 15
XII 736 185 34 XXVI 3682 571 18
XI 759 208 38 XVI 3707 596 19
XXVI 791 240 44 XVIII 3758 647 21
XIX 848 297 54 VII 3782 671 22
V 914 363 66 XIX 4099 988 31
The middle column gives the deviations from the median, which is that measure
above and below which one half the cases lie. In this table the median is five
hundred fifty-one. These deviations serve to show the differences in scores made;
and they are also employed in computing the measures of variability and
relationship. The third column is the deviations in per cent of the median. It affords
another expression of the difference in size of scores made by the systems.
Table IV reads exactly as III, the scores[37] being those made on all problems of
the test in fundamentals. These two tables give some general help on the nature of
the product of the first six years of arithmetic work. One very evident fact is the
lack of uniformity among systems; another is the lack of correspondence of relative
position among the systems in the two tables. With the exception of systems XXIII
and XIV, no system occupies the same relative position in the two tables, e.g.
system XXIV stands second from the lowest in reasoning and eighteenth from the
lowest in fundamentals. This fact is more accurately summarized in the coefficients
of correlation, table XV, p. 37.
As seen from its heading, table XXII gives the systems in order of achievements.
These serial standings are derived from tables III and IV. Reading from the top,
system XXIII has an average serial standing of one, being lowest in both reasoning
and fundamentals; system XXV ranks three in average serial standing, being
fourth from lowest in reasoning and second from lowest in fundamentals; the
readings for the other systems are similar.
Column Heading Keys:
Sys = Systems
A = Average serial standing
B = Serial standing in reasoning
C = Serial standing in fundamentals
D = Serial standing in time expenditure
E = Week minutes devoted to arithmetic
F = Week minutes devoted to all subjects
G = % of time to arithmetic
TABLE XXII TABLE XXIII TABLE XXIV
Time Distribution among Grades

Comparative Comparative Time
Lower numbers show week minutes devoted to
Sys Achievements Expenditure
arithmetic; upper show % of school time devoted to
arithmetic in each grade
A B C D E F G I II III IV V VI
7 6 12 15 15 15
XXIII 1 1 1 14 1150 9675 12 100 100 200 250 250 250
7 9 10 9 13
XXV 3 4 2 2 722 8700 8 .. 100 140 155 130 197
8 8 8 7 11
XXII 4½ 5 4 1 507 7200 7 .. 90 90 90 90 147
7 10 12 14 15 15
XX 5 7 3 15 1161 8200 14 80 113 210 240 265 253
2 12 20 20 24 23
XVII 7½ 3 12 21 1283 7500 17 27 158 250 258 300 290
2 14 15 15 15 15
VIII 8 11 5 18 1258 9600 13 25 233 250 250 250 250
11 15 20 17 18
XV 8 9 7 16 1173 8025 15 .. 147 213 292 250 271
10 9 11 11 12 16
III 9 10 8 6 944 8025 12 125 125 150 150 165 229
14 17 17 17
XXIV 10 2 18 7 950 8775 11 .. .. 200 250 250 250
7 12 12 14 18
X 10 14 6 5 921 8550 11 .. 88 154 184 216 279
9 13 14 14 15
I 11 13 9 9 1068 9375 11 .. 130 213 238 238 249
28 20 20 24 20 23
IV 12 4 20 26 1854 8400 22 249 300 306 361 300 338
8 12 14 14 15 16
II 13 15 11 17 1247 9900 13 121 192 217 225 233 259
8 10 10 12 14 13
XXI 13 16 10 4 865 7650 11 80 100 100 180 210 195
8 12 18 18 19
VI 13 12 14 11 1126 9000 13 .. 127 177 266 266 290
5 8 13 18 17 16
XVI 14½ 6 23 12 1127 9000 13 75 113 187 263 251 238
26 23 18 19 19
XIII 15 17 13 25 1626 8475 19 .. 388 350 288 300 300
XVIII 6 5 15 20 20 19
16 8 24 19 1265 8700 15 75 75 225 300 300 290
13 15 18 18 18 21
IX 17½ 19 16 22 1559 9000 17 200 225 275 275 275 309
11 15 18 18 18
XI 18½ 22 15 10 1130 8575 13 .. 157 216 250 250 257
15 16 18 19 19 19
XIV 18½ 18 10 23 1560 8850 18 225 245 270 280 270 270
6 18 16 19 19
XII 19 21 17 13 1148 8400 14 .. 81 226 255 288 298
7 10 10 13 13 17
XXVI 22½ 23 22 3 837 7200 12 80 125 125 150 150 207
13 19 22 22 22 17
VII 22½ 20 25 24 1573 7800 20 175 262 300 300 300 236
8 10 11 12 13 13
V 23 25 21 8 971 8700 11 113 154 167 175 183 179
8 10 17 17 13 20
XIX 25 24 26 20 1276 9000 14 125 150 250 250 250 301
.. = no time assigned.
Tables XXIII and XXIV keep the same order of systems and show the time
expenditure. The first line of table XXIII reads,—system XXIII ranks fourteenth
from the lowest in time expenditure, with 1150 week minutes devoted to arithmetic,
9675 week minutes devoted to all subjects, the 1150 week minutes devoted to
arithmetic being 12 per cent of the 9675 week minutes devoted to all subjects.
Similarly for the other systems, e.g. system XXV with a serial standing in abilities
of three, and a serial standing in time expenditure of two, spends 722 week
minutes on arithmetic, and 8700 week minutes on all subjects, arithmetic costing 8
per cent of all the school time. The reader will recognize that the third column,
which gives the time devoted to all subjects for one week of each of the first six
years, gives the only new data of this table, column two being the same as given in
table XXI and the first and fourth columns being derived from the others.
Probably the first essential shown by this table is the lack of correspondence
between the serial standing in time cost and the serial standing in abilities; e.g. the
system with the lowest time cost is found by referring to table XIII to be system
XXII, which is seen in table XXII to rank four and one-half in average abilities.
Similarly, the system that ranks fifteenth in time cost, ranks fifth in abilities, etc.
Another noticeable showing is the wide variability in the school time of the
systems. It will be seen to vary from 7200 to 9900 week minutes. This time
includes recesses, and it means that lengths of school days vary from an average
of four hours to five and one-half hours. And if the names of the systems were
given, it would be recognized that almost invariably the longer school hours are
accompanied by the least amount of variation in program, such as physical
education, field trips, assemblies, etc. Perhaps the other most striking fact of this
table is the wide variation in the per cent of time devoted to arithmetic. It varies
from 22 per cent for system IV to 7 per cent for system XXII, a difference of more
than three to one.
As table XXIV is part of the discussion of factors in time expenditure, its sample
readings are given under that heading, page 62.
The Relation of Time Expenditure to Abilities Produced

The reader found one indication of the relation, or lack of relation, between time
cost and products in tables XXII and XXIII. Each of the three following tables
expresses these same facts.
TABLE XXV
Comparison of the Achievements of the Systems having Less than
Median Time Cost with those having More
Combined Scores of the Thirteen Systems

With less than With more With less than With more
median time than median median time than median
cost time cost cost time cost
Including home study Without home study
Reasoning 7,519 7,893 7,277 8,135

Fundamentals 40,751 40,273 37,165 43,859
TABLE XXVI
Ratio of Time Expenditures to Abilities[38]
Average Ratios Reasoning Ratios Fundamental Ratios

Time Cost to
Systems Serial Serial Serial
Reasoning and Time Cost to Time Cost to
Standing of Standing of Standing of
to Reasoning Fundamentals
Systems Systems Systems
Fundamentals
IV 1 2.26 1 3.99 4 .520
XXIII 2 1.92 2 3.22 1 .624
XVII 3 1.65 3 2.88 7 .421
XIII 4 1.54 4 2.55 3 .533
XX 5 1.45 7 2.36 2 .535
XVIII 6 1.41 5 2.48 13 .336
XIV 7 1.40 7 2.36 6 .438
VIII 8 1.39 8 2.33 5 .457
IX 9 1.353 9 2.25 5 .457
XVI 10 1.352 6 2.40 18 .304
XV 11 1.31 11 2.20 8 .422
VII 12 1.28 12 2.14 9 .415
XXIV 13 1.24 10 2.21 21 .270
II 14 1.22 14 2.02 7 .421
VI 15 1.20 13 2.04 11 .354
I 16 1.15 15 1.93 10 .363
III 17 1.05 16 1.77 16 .331
XII 18 0.943 17 1.55 13 .336
XXV 19 0.941 17 1.55 15 .333
X 20 0.93 18 1.53 14 .335
XI 21 0.913 20 1.48 12 .346
XIX 22 0.91 19 1.50 17 .311
XXI 23 0.83 21 1.37 19 .293
V 24 0.67 23 1.06 20 .272
XXII 25 0.65 22 1.08 23 .219
XXVI 26 0.64 24 1.05 22 .227
The above details are compiled from the scores of individual systems as given in
tables III and IV, the median cost being that given in table XXI. As measured by the
time used in school, the thirteen systems with less than the median cost stand
slightly the better; and as measured by the time including home study, the thirteen
systems with more than the median time cost stand somewhat the better. The time
used in school is doubtless the more exact measure, but, as shown in table XXI,
some systems depend on home study to a considerable extent. Hence both
measures are used. The lack of relation indicated in this general way is shown
more accurately in the table, page 263, in terms of coefficients of correlation.
The order of systems in this table is determined by the first column, which gives
the average serial standing as determined by the ratios of time to products. The
right-hand column under each heading gives the ratio of time expenditure to
abilities produced, and the left-hand column gives the serial order of that system
as measured by the highness of the ratio, i.e. highness of cost per unit of product;
e.g. in system IV the ratio of time to reasoning is 3.99 (see fourth column), the
highest ratio in reasoning (determined by dividing the time cost, 1854 week
minutes, by 464, the points made in reasoning). The ratio of time to fundamentals
in this system is .52; giving an average ratio of 2.26. That is to say, the ratio of time
to abilities in system IV is as 2.26 to 1, the highest among the twenty-six systems.
That there is no direct ratio between time expenditure and abilities is again
shown by this table. For example, system XXII, which spends the least amount of
time (see table XXI), ranks fourth from the lowest in abilities (see table XXII), ranks
25th, that is, next to the highest, in ratio of time cost to abilities produced; and,
what is even more striking, system XXVI, which spends third from the least amount
of time, ranks third from the highest in abilities and 26th or highest in the ratio of
time cost to abilities produced.
That a large amount of time expended is no guarantee of a high standard of
abilities may again be convincingly seen by comparing the ratios of the five
systems spending the smallest amount of time with the five spending the largest.
Of the five spending the least time, the average ratio is .80, which corresponds
with the 23d or the 3d from the best in ratio; and of the five spending the greatest
amount of time, the average ratio is 1.57, which corresponds with the 4th poorest
in ratio.
The last three tables have each shown the decided lack of relationship between
time cost and abilities produced, and hence for these systems it is evident that
there is practically no relation between time expenditure and arithmetical abilities;
and, in view of the representative nature of these twenty-six systems, it is probable
that this lack of relationship is the rule the country over.
This is not to say that a certain amount of time is not essential to the production
of arithmetical abilities; nor that, given the same other factors, operating equally
well, the product will not increase somewhat with an increased time expenditure.
What is claimed is that, as present practice goes, a large amount of time spent on
arithmetic is no guarantee of a high degree of efficiency. If one were to choose at
random among the schools with more than the median time given to arithmetic, the
chances are about equal that he would get a school with an inferior product; and
conversely, if one were to choose among the schools with less than the median
time cost, the chances are about equal that he would get a school with a superior
product in arithmetic.[39]
So far, then, as ability in arithmetic means ability to handle such foundation work
as is measured by the tests in this study, this “essential” has not necessarily
suffered by the introduction of other subjects and the consequent reduction of its
time allotment.
One would need to read the whole study to appreciate fully the
nature of the investigation. From the pages quoted, however, it must
be apparent that: (1) schools and school systems vary greatly in the
results which they secure in arithmetic; (2) the excellence of the work
done is not directly proportional to the time expended. We will find it
necessary to revise our opinions with regard to the organization of
school subjects, the allotment of time, the methods of teaching, and
the like, in proportion as we have careful investigation in these
several fields.
For Collateral Reading

E. L. Thorndike, The Principles of Teaching, Chapter XVI.
APPENDIX
I . T H E T E A C H I N G O F E N G L I S H I N E L E M E N TA RY S C H O O L S
By Franklin Thomas Baker, A.M.
I. Historical View of the Subject
1. The Choice of Reading Matter.

1. The school reader an expression of social ideals.
2. German primers and readers of the sixteenth and seventeenth centuries.
3. The “moral tales” of the eighteenth century.
4. The New England Primer.
5. The oratorical and patriotic selections of the early nineteenth century.
6. The school readers of to-day; their general characteristics.
2. Method.
1. The alphabetic method in use until modern times.
2. New ideas in the sixteenth century and later. Work of Ickelsamer, Basedow,
Pestalozzi, Comenius, and Jacotot.
3. Gradual ascendency of the analytic over the alphabetic (or synthetic)
method.
4. Recognition of the importance of phonetics, of association of ideas, etc.
References: Kehr, Geschichte des Lese-Unterrichts in der Volksschule, Gotha,
1889. Fechner, Geschichte des Volksschullesebuches, Gotha, 1889. Ford, The
New England Primer, New York, 1897. Reeder, Historical Development of the
School Reader, New York, 1900. Hall, How to Teach Reading, New York, 1886.
American Journal of Education, Vol. V., Hartford and London, 1858. Russell,
German Higher Schools, New York, 1900. Carpenter, Baker, and Scott, The
Teaching of English, New York, 1903. Huey, Psychology and Pedagogy of
Reading, New York, 1908.
II. First Steps in Instruction
1. Material.
1. Material should be (1) interesting, (2) literary, so far as possible, (3)
adapted to the capacities and tastes of children, (4) of enough difficulty and
sufficiently above their own ordinary thoughts to have value as instruction.
2. The best material (1) folk stuff, such as the classic fairy tales, Mother
Goose, etc., (2) tales of heroism and sacrifice, (3) poetry of the simpler type, like
that of Stevenson and Christina Rossetti.
3. Much of the language work should be free conversation between the
teacher and the children about their ordinary experiences.
2. Method.
1. During the first years much of the literary material must be given orally by
the teacher. Oral work is to be held of great importance.
2. Children to be encouraged to commit good things to memory.
3. All reading aloud by the pupils to be done as naturally as possible.
Importance of reading by phrases and sentences, rather than word by word.
4. Value of the dramatic element in early work.
5. The conflict between the “word method” and the “sentence method” over.
Modern teaching eclectic in method. If any name can be given to the best way, it
might be, perhaps, “thought method.”
6. Use of script and print: advantages of each as a first form. Value of printed
cards and other devices for drill.
7. Form of type for beginners’ books: not too large; letters to have all
differentiating marks distinct. Importance of right kind of paper, width of columns,
etc. Kinds of pictures most serviceable.
8. When shall writing begin? In general not to be forced on the child in the first
year. Arguments for and against this arrangement. Should there be any fixed
standard of accomplishment for the first year?
9. Phonetic drill. How many words must be known before it begins? Various
plans equally successful. The main thing, perhaps, is to have drill enough to give
the pupils certainty in their work, but to keep the drill subordinated to their
interest in reading.
10. The order of such drill. “Normal words,” chosen for their meaning, their
frequency of occurrence, and their similarity in form to other words either at their
beginning or at their end. Many words, however, must be learned without
relation to such a scheme.
11. “Normal sentences” those that partially help the reader to the recognition
of words; as, “The sun rises in the east, and sets in the west.” For young
children, sentences involving the use of repetitive phrases must also be
regarded as normal, as in “The House that Jack Built.”
12. In general, both analysis and synthesis to be used in word drill.
13. Importance of securing good habits as to intelligent reading, correct
spelling, etc., in the early years. Children can usually do better than they or their
elders think they can.
14. Emphasis to be placed upon reading many of the good things over and
over, until they are known in whole and in part.
References: Bryant, How to tell Stories to Children. Carpenter, Baker, and
Scott, The Teaching of English. Chubb, The Teaching of English. Colby, Literature
in Life and in School. Hall, How to teach Reading. Hinsdale, Teaching the
Language Art. Huey, Psychology and Pedagogy of Reading. Arnold, Reading, How
to teach it. Laurie, Language and Linguistic Method. Dewey, “The Primary
Education Fetich,” in The Forum, May, 1898. Dewey, The School and Society.
Dye, Story-Teller’s Art.
III. The Teaching of Literature
1. General Problems.
1. Can literature be taught? Or can pupils “be taught through literature”?
Examples of such educational use of literature.
2. Present aims in teaching literature: entertainment, portrayal of life,
acquaintance with the world of thought and feeling as presented in books,
cultivation of imagination and sense of beauty.
3. True interpretation implies grasping the central purpose, idea, or feeling of
the piece.
4. Various types of literature demand various treatment. Necessity of adapting
the treatment to the class.
5. Taste (sense of beauty) developed mainly by contact with good models.
Instruction plays a minor part. The love of good reading fostered by judicious
selection of material, and by example and influence.
6. How can the habit of good reading be cultivated?
2. Material.
1. The literature chosen must be suitable in its themes, its action, its feeling,
its simplicity.
2. Literary histories and biographies: their limited value in elementary work.
3. Scientific and historical material in literature. Literary use of such material
not to be confounded with science and history.
4. Pictures and other illustrative material: Sometimes give intuitive basis for
desired concepts; sometimes interfere with the imagination.
3. Method.
1. Reading aloud: its value. Means of securing good results; interest, sense of
reality, consciousness of an audience.
2. Analytic study, of content, form, and general literary effects.
a. Must be adapted to the pupil’s interest and his stage of development.
b. Must yield results of value appreciable by the pupil.
c. Effects of too much or too little such study.
3. Correlation of literature with other work possible in limited degree. A matter
of class treatment rather than of the general arrangement of the course of study.
A problem for the teacher rather than the principal.
4. Treatment of allusions, historical, literary, etc. The need of judicious
selection.
5. Treatment of figures of speech, verse forms, new words, etc.
6. Lesson plans: their function and value.
a. An outline should control and direct the work, yet be flexible enough to
allow freedom on the part of teacher and pupil.
b. Introductions: their nature and function. When necessary.
References: Carpenter, Baker, and Scott, Laurie, Chubb, Hinsdale, Arnold and
Hall, as cited. Scudder, Literature in Schools. C. A. McMurry, Special Method in
Reading. Bates, Talks on the Study of Literature. Colby, Literature in Life and in
School. Adler, Moral Instruction of Children.
IV. Study of Certain Typical Books
1. Nursery Rhymes (as Mother Goose, Stevenson’s Child’s Garden of Verses).

a. The nature of their appeal to children in sound, imagery, and ideas.
b. Their value in training the ear, the powers of speech, etc.
2. Grimm’ “Fairy Tales.”
a. Their source and relation to other folklore.
b. The marvelous, and its effect on children.
c. Action, logical sequence, local color.
d. Various types of myth.
e. The ideal element, poetic justice, etc. Need the harsher elements be
omitted?
f. Typical lessons.
3. “Alice in Wonderland.”
a. Its origin and its place in literature.
b. The nature of its reality: based upon things in the child’s world of
imagination.
c. Its value as humor, as a means of quickening the power of thought.
d. What preparation is needed for the appreciation of it?
e. Typical lessons.
4. “Robinson Crusoe.”
a. Its origin and place in literature.
b. Fundamental characteristics as a piece of fiction.
c. Elements in it that appeal to children, or fail so to appeal.
d. Justification of the abridged editions.
e. Its relation (1) to the world of romance, (2) to real life.
f. How best presented. Typical lessons.
5. Longfellow’s “Hiawatha.”
a. Its origin, form, popularity.
b. Its qualities, epic and romantic.
c. Its treatment of the myth.
d. Its value as school reading; parts best suited for this.
e. General value of reading about primitive life.
f. Relation to handwork, etc.
6. Hawthorne’s “Wonder Book” and “Tanglewood Tales.”
a. Their origin and general literary qualities.
b. Romantic coloring given to classic stories; compare Kingsley’s The
Heroes, and Bulfinch’s Age of Fable, and other versions of the
myths.
c. Different types of myth and fairy story represented.

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FIGURE 1.2 A and B

V1 This lead is placed at the right fourth intercostal space

TIME AND SPEED OF THE EKG

ORIGIN OF THE EKG DEFLECTIONS

FIGURE 1.4 Origin of the ECG deflections.

EKG WAVES NOMNECLATURE

Components of the QRS complex are designed as follows (FIGURE 1.5):

I Q wave is the initial downward deflection (if present) followed by an R wave

FIGURE 1.5 Names of the ECG waves.

QRS COMPLEXES IN LIMB LEADS

EKG is arranged so that when a depolarization wave spreads FIGURE 1.6

QRS COMPLEXES IN CHEST LEADS

EKG DESCRIPTION AND INTERPRETATION

BOX 1.1 Steps for EKG description

STEP 01 TECHNICAL QUALITY OF THE EKG

STEP 02 THE RHYTHM

BOX 1.2 Causes of irregular rhythm

FIGURE 1.14 Origin and configuration of cardiac beats.

I. SINGLE EARLY BEAT (ECTOPIC BEAT)

FIGURE 1.15 Nomenclature of ectopic and escape beats.

FIGURE 1.16 Examples of ectopic beat.

II. SINGLE LATE BEAT (ESCAPE BEAT)

FIGURE 1.17 An example

III. SUSTAINED EARLY BEATS (TACHYCARDIA/TACHYARRHYTHMIA)

FIGURE 1.18 Mechanism of tachyarrhythmia.

1 SUPREVENTRICULAR TACHYCARDIA (NARROW COMPLEX TACHYCARDIA)

FIGURE 1.27 Atrial flutter

BOX 1.3 Effect of carotid sinus pressure on arrhythmia

2 VENTRICULAR TACHYCARDIA (WIDE COMPLEX TACHYCARDIA)

FIGURE 1.32 Ventricular tachycardia; monomorphic and polymorphic.

FIGURE 1.35 Ventricular tachycardia; capture and fusion beats.

IV. SUSTAINED LATE BEATS (ESCAPE RHYTHM)

FIGURE 1.39 Tachycardia versus escape rhythm.

STEP 03 HEART RATE

FIGURE 1.40 Heart rate estimation.

STEP 04 CARDIAC AXIS

Lead I Lead aVF Interpretation

BOX 1.4 Causes of axis deviation

FIGURE 1.41 Normal and abnormal cardiac axis.

The PR segment is the straight line running from

SHORT PR INTERVAL: PRE-EXCITATION SYNDROME

FIGURE 1.44 Mechanism of WPW and LGL syndrome origin.

FIGURE 1.45 WPW syndrome type A.

FIGURE 1.46 WPW syndrome type B.

FIGURE 1.47 Lown-Ganong-Levine syndrome.

PROLONGED PR INTERVAL: CONDUCTION BLOCK

FIGURE 1.49 Sinoatrial block and sinoatrial arrest.

02 CONDUCTION PROBLEMS IN THE AV NODE AND HIS BUNDLE