ECG made easy early book-compressed (1) .pdf

This book entails detail description aboit ecg

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BY DR. FAWAD FAROOQ

2. Dedication

Dedicated to My Mother an honest & hard working
teacher who dedicated all her life to my education
and setting me on a noble path but unfortunately
left me on May 10th 2016, leaving unforgettable
memories, may Allah grant her higher place in
Jannah, to my Father who sees my carrier as his
first priority, may Allah help me in keeping him
please, to my wife and Children for their love and
understandings of my commitments to patient care
and academics, to my teachers key in achieving my
professional excellence, to my colleagues for their
support and last but not the least to my patients a
constant source of learning and encouragement.

3. Authors Introduction: Dr. Fawad Faroog is an Interventional
Cardiologist serving at National Institute of Cardiovascular
Diseases (NICVD). He did his MBBS from Sindh Medical

College in 1995, passed FCPS in Cardiology in 2005 after that
did training of Interventional Cardiology from NICVD and joined
Karachi Institute of Heart Diseases as Senior Registrar in 2006
worked there up to 2009 after which He joined NICVD as Senior
registrar and presently working there as Associate Professor of
Cardiology.

A AN mern

4. Preface

Health Care professionals are chosen by Almighty Allah, to take care of
its most precious creation. Acquiring knowledge and skills to fulfill this
responsibility is mandatory for them.

‘Managing patient is a team work which needs different level of compe-
tency at different levels but knowledge of Electrocardiogram (ECG)
reading is needed at every level. It’s a cheap and easily available investi-
gation which has a pivotal role in diagnosing and managing number of
acute and chronic illnesses.

Considering this need I started workshops on ECG reading about 10
years back, done multiple sessions till today, used to give handouts of
presentation as well to consolidate the knowledge of the participants,
now formulated a small booklet and recorded a teaching session on
ECG reading which will be uploaded on my YouTube Chanel so that it
will serve as a constant source of enhancing ECG reading skills for the
reader in future.

May Allah guide and help us to acquire right path and make this effort
as Sadqa-e-Jariah for better patient care.

Dr. Fawad Farooq

Dhrranaruon

5. Content

Introduction 07
Axis determination 21
Rhythm Analysis 2
Ischemia 69
Chamber enlargement 79
Practice Cases 87

7. What is a 12 lead ECG?

Records the electrical activity of
the heart (depolarisation and
repolarisation of the myocardium)

Views the surfaces of the left
ventricle from 12 different angles

Why do a 12 lead ECG?

Monitor patients heart rate and rhythm
Evaluate the effects of diseases or
injury on heart function

Detect presence of electrolyte and
other disturbances

8. Introduction

Electrocardiography (ECG) is a net electrical
activity of the heart recorded on paper with the
help of twelve electrical leads placed on chest and
limbs at 12 different points to record the electrical
activity from 12 different angles, details of
recording principle will be discussed in subsequent
text.

ECG is a cheap and easily available investigation
helps in diagnosing multiple acute conditions, like
acute coronary syndrome, arrhythmias and
electrolyte disorders. It also helps in providing
clues towards many chronic cardiac and
non-cardiac conditions.

9. Anatomical Position of the Heart

Impulse Conduction & the ECG

Sinoatrial node
y
AV node
y
Bundle of His
Bundle Branches

y
Purkinje fibers

10. As we know that heart is placed beneath the
sternum with atria forming the top and ventricles
bottom, with its apex pointing towards left, ECG is
generated by specialized conduction system
embedded with in heart muscles.

Conduction system comprises of sinoatrial SA
node which lies on the upper part of Right atria
which is connected to Atrioventricular AV node
through Internodal pathways which lies almost
between Atria and Ventricles AV node then
connects to Bundle branches through bundle of His
and these bundle branches generate Purkinji fibers
which ends within ventricular endocardium.

11. The “PQRST”

+ P wave - Atrial
depolarization

+ QRS - Ventricular
depolarization

+ T wave - Ventricular
repolarization

12. In normal conduction, SA node generates the
electrical activity and depolarized the atrias
forming P wave after that conduction delays for a
while in AV node and then enters into ventricles
through His bundle, Right and Left bundle
branches and Purkinji fibers to depolarize
ventricles and forming QRS complex and
subsequent ventricular repolarization generates T
waves.

This above mentioned electrical activity is recorded
on paper with the help of twelve different leads
placed on all four limbs and chest, remembering
their exact position is important for proper ECG
recording and interpretation as shown in page 12 &
13.

13. Limb Leads

3 Unipolar Leads

savR - right arm (+)
eavL - left arm (+)
«avF - left foot (+)

note that right foot is a ground lead

Limb Leads
3 Bipolar Leads
from (Einthovens Triangle)

Lead I - measures electrical potential
between right arm (-) and arm (+)

Lead II - measures electrical potential
between right arm (-) and left leg (+)

Lead III - measures electrical potential

between left arm (-) and left leg (+)

14. Chest Leads

6 Unipolar leads
Precordial leads V1, V2, V3, V4, V5 and V6 - all positive

VI 4th intercostal (right)
V2 4th intercostal (left)
V3 Betwwen V2 & V4
V4 Midclavicular
(mid-collarbone)
V5 Sth intercostal space
(anterior axillary
line)
V6 Sth intercostal
(midaxillary line)

Chest Leads

15. Net

P vector’s
direction
Net
ORS vector's
direction

Think of the positive electrode as an ‘eye’...
the position of the positive electrode on
the body determines the area of the
heart ‘seen’ by that lead.

16. Configuration of different ECG waves like ‘P’ ,
“QRS” and “T” is different in different leads
depending on the relation of direction of their net
vector to the positive terminal of that leads, as net
vector of P wave is directed from SA node to AV
node i.e. from right upper quadrant to the left lower
quadrant so it is positive in lead II and negative in
lead avR.

Same applies to “QRS” because of its direction
towards apex of the heart, it is also upright or
positive in lead II and downward or negative in lead
avR.

17. ECG Waveforms

+ When an electrical impulse travels
towards a positive electrode, there
will be a positive deflection on the
ECG

+ If the impulse travels away from
the positive electrode, a negative
deflection will be seen

The Normal EKG

Right Arm ‘Lead I”

Ventricular muscle VEN

depolrization Mais

18. So remembering positive electrode as an eye,
principle is simple, if net electrical activity’s
direction is towards positive of a lead it will be
upright in that lead and if towards negative end it
will be downward and if perpendicular it will be
biphasic, but if more towards positive then more
positive and less negative.

We commonly take lead II as rhythm strip
because in normal axis both P and QRS waves are
assumed to be most upright and best seen in this
lead considering ECG recording Principle as
their net vector is towards positive end of lead
ILMany pathological conditions like chamber
enlargement, Ischemia, degenerative changes and
pre-excitation can affect the normal direction of
net QRS electrical axis.

19. Positive electrodes of limb leads

-90°
-120° 60°
avR -150° -30° ave
180° & œ 1
150° N 30°
60°
120° o
un 1
avF
Limb leads
1=+00
II = +600
TI = +1200
Augmented
leads
avL

avR = -1500

20. The concept of ECG waves recording and their
relation to positive terminals of different leads is
important for recognizing false abnormalities like
newly developed Q waves or change in axis due to
wrongly placed leads.

As for example lead II and lead avR are exactly
opposite to each other in terms of their positive
terminals so it’s almost impossible to have upright
*P and ‘QRS’ waves in both of these leads
simultaneously unless and until the leads are
wrongly placed.

21. AXIS
Axis refers to the mean QRS axis (or vectors
direction) during ventricular
depolarization.

The QRS Axis

By near-consensus, the normal QRS
axis is defined as ranging from -30° to
+90".

-30° to -90° is referred to as a left axis |-#
deviation (LAD)

+90° to +180° is referred to as a right
axis deviation (RAD)

22. Axis determination

Correlating QRS configuration and net QRS
direction in different leads help in identifying the
direction of net vector which is called axis,
although complete concept of axis determination
needs knowing of positive end of each lead and
correlating it with QRS direction. As a beginner if
we simply remember this very basis that.

Normal QRS axis is between -30° to +90", if it is
between -30" and -90° it is left axis deviation, if
490° to +180” it is right axis and between +180" to
-90° it is indeterminate or extreme right axis.
Looking at QRS configuration in specific leads
helps in determining the axis.

23. Normal, left, right or right
superior axis deviation

QRS Complexes
I II Axis

Extreme right / determinate

+ + Normal

= + Left axis deviation

- + Right axis deviation 180° ~

- - Right superior axis 150%
deviation

AXIS

Is the QRS axis normal in this ECG?

Fig: 19

24. To get an idea about these quadrants we have to
look for lead I & II so if QRS is upright in both lead
1 & IL its normal axis, if upright in I and downward
in IL its left axis deviation, if downward in I and
upright in Its right axis deviation and if downward
in both I and II its extreme right or indeterminate
axis.

Figure 19 showing an ECG where if you are starting
with axis you should be looking at lead I and II and
in this ECG, QRS is upright in I and downward in IT
so the axis will be , fill this blank by your-
self. Since axis determination has a correlation with
lead positioning so I covered it with the description
of leads.

25. The ECG Paper

+ Horizontally if
- One small box - 0.04 s
- One large box - 0.20 s

Vertically

- One large box - 0.5 mV

lee

od EE

un rn nn
The standard 12 Lead ECG
6 Limb Leads 6 Chest Leads (Precordial leads)
avR, avL, avF, I, I, IIT VI, V2, V3, V4, V5 and V6

eye

LE EEE EIS EERGI ERS JE

Rabe A A ee
Rhythm Strip

26. Now you can move on to standardization. As you
know, ECG is a graph in which time is on X-axis
and voltage on Y-axis and for time and interval
measurement, the stander is 25mm/second, i.e.
25mm passes through stylus of ECG machine in 1
second or 1 seconds activity recorded in 25mm of
paper and this is why one large square is 0.2second
and 1 small square is 0.04 second but you can
change the speed to SOmm/sec or 12.5mm/sec ,
similarly stander for voltage is 10mm/millivolt ie.
1 millivolt generated by heart moves stylus 10mm
and you can increase or decrease this response
with changing your calculations accordingly.
Sometimes an inexperience operator may alter
these standards as he may record ECG on
50mm/sec which lead to false impression of
bradycardia, bundle branch block and increase PR
interval in ECG as same activity recording in
double the length of paper, similarly if decrease
stander to 12.5mm/sec it leads to false impression
of tachycardia, same happens with change in
voltage standers as well if you increase it to
20mm/mv you got false increase amplitudes and
decreasing voltage decreases amplitude.

27. 69 year old man without symptoms. What is the rhythm?

28. Rhythm analysis

Before starting discussion on rhythm analysis I
would like you to go through this rhythm quiz and
come up with your conclusion regarding rhythm in
this ECG, correct anwser of this rythm strip can be
found in video lecture. For proper rhythm
assessment one should be looking ECG features to
get an idea of origin of rhythm that is from Sinus
node or somewhere else and then its normal
sequential conduction pattern.

ECG rhythm description:

29. Normal Impulse Conduction

Sinoatrial node $
À nu reef
AV node
y Av me
Bundle of His Bir

Bundle Branches

y
Purkinje fibers

Impulse Conduction & the ECG

Sinoatrial node
AV node
Bundle of His

Bundle Branches

y
Purkinje fibers

30. We know that conduction system normally originate
rhythm from sinus node at standard frequency in
regular pattern recognized by presence of similar P
wave before each QRS complex at a regular rhythm
with a rate of 60-100/min, then there is a delay at
AV node about 120-200millisecond showing a
PR interval of 0.12second to 0.2second ie. 3-5
small squares and then conduction passes through
bundle of His into right and left bundle branches at
almost similar speed and depolarized both left and
right ventricle from endocardium to epicardium
through Purkinje fibers giving a narrow QRS in
ECG which is less then 120 millisecond or <3 small
squares.

Seeing this normal pattern of rhythm origin from
sinus node ie. P wave with a normal conduction
through AV node that is PR interval and normal
conduction through ventricles i.e. narrow QRS at a
rate of 60-100 is important in every complex of
rhythm strip.

31. The “PQRST”
+ P wave - Atrial
depolarization

+ QRS - Ventricular
depolarization

+ T wave - Ventricular
repolarization

Rhythm analysis
HE SC Cal ns DN Bae a
Step 1: Calculate rate.
Step 2: Determine regularity.
+ Step 3: Assess the P waves.
+ Step 4: Determine PR interval.
+» Step 5: Determine QRS duration

32. As already discussed that similar P waves show
atrial depolarization originating from sinus node,
narrow QRS represent ventricular depolarization
through proper conduction, T wave ventricular
repolarization looking at PR and QT interval is also
important for rhythm assessment.

Analyzing rhythm needs a sequential approach to
see ECG finding first and then contemplate about
final rhythm abnormality, we usually do this
mistake to conclude with seeing just one obvious
abnormality, without going through whole rhythm
strip and without looking at every complex in step
wise fashion.

33. Step 1: Calculate Rate
<— 3 se — <——-3 sec —>

| 1 | 1 N
HAUS Po ELA]

+ Option 1
- Count the # of R waves in a 6 second rhythm
strip, then multiply by 10.
- Reminder: all rhythm strips in the Modules are
6 seconds in length.

ion?

Interpretation? 9 10-00 bpm

Step 1: Calculate Rate
Ps aa

ASS er

R wave

+ Option 2

- Find a R wave that lands on a bold line.
- Count the # of large boxes to the next R wave.
If the second R wave is 1 large box away the
rate is 300, 2 boxes - 150, 3 boxes - 100, 4

boxes - 75, etc. (cont)

Fig: 28
®

34. First step of analyzing rhythm is to calculate rate. It
gives you an idea about patient’s stability as well
and in case of severe tachycardia or bradycardia you
may have to offer management before further
assessment according to patients clinical status.

Better way of calculating rate is to mark a six
second strip, as we know that 5 large squares are
equal to one second so you have to mark 30 large
boxes and see how many QRS complexes are there
and multiply them with 10 to get the rate. This
applies to both regular and irregular rhythms.

Other easy method of calculating rate is to see
number of large squares between 2 QRS complex
in a regular rhythm and then give rate with formula
given in Fig. 28.

Limitations of this method is that you cannot apply
it to irregular rhythm and sometimes you may not
get exact numbers of large squares between two
QRS which leads to approximation of rate
calculation rather than exact rate.

35. Step 1: Calculate Rate

165
500
| 1 al | 1 } f { 1

nah Deh NEN 0 SEEN ed

-

KR

Option 2 (cont)
- Memorize the sequence:
300 - 150 - 100 - 75 - 60 - 50

A
o | ox dl box leas ti

100 =95 bpm
Step 2: Determine regularity

RR

herum brand Weta brand baum bead |
rame uud: | iba Er di

+ Look at the R-R distances (using a caliper or
markings on a pen or paper).

+ Regular (are they equidistant apart)? Occasionally
irregular? Regularly irregular? Irregularly
irregular?

Interpretation?

Regular

36. As if there is 1 large square between 2 QRS the rate
will be 300/min, 2 large squares between QRS the
rate will be 150/min and every small square from 1
large to 2 large squares will reduce the rate by 30 as
for example if you have 1 large and 1 small square
between 2 QRS the rate will be 270/min, 1 large
and 2 small squares the rate will be 240 and so
forth. Similarly when you have 3 large squares
between 2 QRS rate is 100/min and adding every
small square from 2 large to 3 large will reduce the
rate by 10 as if you have 2 large and 1 small
between 2 QRS the rate will be 140/min, 4 large
squares between 2 QRS will give rate of 75/min and
adding small squares from 3 to 4 large square will
reduce the rate by 5/min, 5 large squares between 2
QRS will give rate of 60 and adding 1 small square
from 4 to 5 will reduce the rate by 3.

Second step is to see regularity of QRS that is
whether all QRS complexes in rhythm strip are
equidistance or not. If equidistant then you can
label this rhythm as regular.

37. Lil

Step 3: Assess the P waves

ll,

|

Wt u
em PMA ADA DAD EN NEN

Are there P waves?
+ Do the P waves all look alike?

+ Do the P waves occur at a regular rate?
+ Is there one P wave before each QRS?

Interpret

A
tation? Normal P waves with 1 P

wave for every QRS

Step 4: Determine PR interval

j À
de LH (OSE aie ES en Be

+ Norm:

Interpret

al: 0.12 - 0.20 seconds.
(3 - 5 boxes)

tation?
0.12 seconds

38. Third step is to look for P waves and four points
about it, whether present or absent if present similar
or dissimilar which means you have to march
through every P wave very carefully then P rhythm
for which you have to assume that if there is no
QRS orT in strip where do you expect the P wave in
the strip because in sinus rhythm they always found
between T and PR segments but in abnormal
rhythms you may found them within QRS or T
waves, lastly you have to look very carefully is
there one P wave before each QRS or more than that
or P missing before any QRS. I personally feel
assessing P wave is the back bone of rhythm
assessment.

Fourth step is PR interval which is normally 0.12 to
0.2 second measured from start of P to start of QRS
complex, it should be measured in every complex of
rhythm strip with a view of progressive
prolongation and variability.

39. Step 5: QRS duration

| | | | | |
ee

+ Normal: 0.04 - 0.12 seconds.
(1 -3 boxes)

ion?
Interpretation? 6 08 seconds

Rhythm Summary
| { 1 t t [ 1
Unia NEN DEN
+ Rate 90-95 bpm
+ Regularity regular
+ P waves normal
+ PR interval 0.125
© QRS duration 0.08 s
Interpretation?
Normal Sinus Rhythm
Fig: 34

40. Final step of rhythm assessment is QRS duration,
that is whether it’s narrow (normal) or wide
(20.12seconds / >3 small squares).

Let's analyze rhythm in Fig. 34 rate around 90-95
with regular QRS complexes with ‘P’ waves of
similar shape, originating regularly before each
QRS with fix PR interval of 0.12-0.2 second and a
narrow QRS complex, these all features are
characteristics of normal sinus rhythm and anything
deviated from them is arrhythmia, so by applying
these five steps you can easily and confidently say
whether you are dealing with normal sinus rhythm
or arrhythmia.

41. ARRYTHMIAS

Fig: 35

42. Now we will discuss different arrhythmias, now 1
will request you to go through rhythm in step wise
approach and write your findings in the blanks,
after looking at figure: 35 and all of subsequent
ECG strips of different arrhythmias it will help you
in memorizing and applying steps of rhythm assess-
ment and serve as practice exercise for you.

Rate: Rhythm:

P waves: Present/Absent Similar/Dissimilar

One before each QRS: yes / No

PR Interval: QRS duration: Narrow/Wide

Going through all these steps you will found everything
similar to sinus rhythm except the rate so conclusion of
this rhythm is.

43. Fig: 37

44. In figure 37 Rate: Rhythm:
P waves present or absent, here P is absent so that
means rhythm is not originating from sinus and you
don’t have to look for other features of P and PR
interval as well, QRS is narrow that means, rhythm
is originating from AV node and following normal
passage through His bundle left and right bundle
branches, to depolarize ventricles, fast rate and
absence of ‘P’ wave is the major abnormality
making it supraventricular tachycardia.

In Fig. 38 Rate: Rhythm: P
waves are again absent because you may see some
waves without fulfilling the criteria of normal P
waves probably fibrillatory waves, QRS is narrow
so conclusion will be and deviation
from sinus rhythm is absent P waves with
irregularly irregular rhythm, whenever you found
an irregular rhythm you have to further classify it in
to regularly irregular, irregularly irregular or
occasional irregular rhythm.

46. In Fig. 39, Rate: Rhythm: „In this strip
we have multiple P waves of similar shapes around
4 in between each QRS called flutter waves PR is
short or normal with narrow QRS conclusion will
be „in this rhythm atria is generating very
fast rate from focus other than sinus node, atrial
rate is about 300/min and ventricular rate depends
on how fast the conduction is through AV node as
some time 2:1 conduction in which ventricular rate
increases to 150 similarly, if its 3:1 then around 100
and 4:1, conduction of flutter waves across of AV
node gives a normal ventricular rate of arround
75/min.

In figure 40, you have to pick the rhythm conceptu-
ally applying all steps of rythm assessment. Rate is
around 70-80/min, rhythm is occasional irregular
that is all regular but 2nd and 7th QRS complexes
are premature means before expected sinus beat P
present and one before each QRS but 2nd and 7th
Ps are premature and different from other Ps which
are similar, PR interval is normal except short in
2nd and 7th QRS. Now conclusion is sinus rhythm
with atrial premature, so in this rhythm second and
7th complexes are originating from focus with in
atria but other than sinus and slightly before the
expected sinus beat, making it sinus rythm with
Atrial premature beats.

©

47. Fig: 41

Fig: 42

48. Figure 41 is showing sinus rhythm with bizarre
looking 4th complex which is premature and broad
as well and its premature ventricular contraction
similarly figure 42 is showing two( 3rd & Sth)
dissimilar Broad, bizarre looking QRS which are of
different morphology and coming prior to expected
sinus beat again ventricular premature beats but
polymorphic i.e. from two different foci.

Ventricular premature beats are actually ventricular
depolarization prior to expected sinus beat
originating from an abnormal focus within the
ventricles with an abnormal cell to cell conduction,
Ventricles sometime also generates beat in case of a
prolong sinus pause which is a lifesaving escape
ventricular beat due to fault in sinus node.

49. Ventricular Conduction

Normal Abnormal
Signal moves rapidly Signal moves slowly
through the ventricles through the ventricles

Fig: 43
ef E
Fig: 44

50. Figure 43, is showing concept of PVC by looking
first at normal conduction through ventricle which
is through bundle of His, left and right bundle and
finally Purkinji fibers to depolarize ventricles
generating normal narrow QRS but in PVCs any
one focus with in the ventricles starts
depolarization prior to next coming sinus beat and
this conduction travels through cell to cell to
depolarize ventricle which gives a broad bizarre
QRS and its shape depends on its site of origin and
conduction it may originates from apex and travel
to base or originate from base to apex or right to left
or left to right.

So finally PVC as shown in figure 44 is a broad
QRS which is without P wave and comes before
expected sinus beat.

51. Fig: 45

Fig: 46

52. Figure 45 is showing same PVC pattern of QRS at
fast rate, around 170-200 regular without P and
broad QRS called Broad complex tachycardia or
ventricular tachycardia (VT). By definition 3 or
more than 3 consecutive ventricular beats at a rate
of more than 100 is said to be VT, otherwise two
consecutive PVCs are called couplets. An alternate
rhythm of 1 Normal QRS and 1 PVC for a longer
period is called Bigeminy, 2 Normal QRS and 1
PVC Trigeminy and so forth.

Figure 46 showing broad QRS with changing
morphology and irregular rhythm, without any
proper pattem which happens in ventricular
fibrillation.

54. Let’s move on to the other side of spectrum, applying
rhythm assessment points to Figure 47 will give you a
finding of a rate of around 50/min, regular rhythm with
normal features of P wave and PR interval and a
narrow QRS complex so conclusion is

because rate is slow with all other features of normal
sinus rhythm.

In figure 48, again rate is slow, rhythm is regular, P
present, similar, regular P rhythm and one P before
each QRS but PR interval is prolong and fix with
narrow QRS, so along with sinus bradycardia there is
first degree heart block as well.

55. Fig: 49

Fig: 50

56. In Figure 49. Ist 3 complexes are showing progres-
sive PR prolongation while the 4th P wave is unable
to conduct and fifth P is starting the cycle again,
which is consistent with second degree type I AV
block in which you have progressive prolongation of
PR interval followed by a non-conducted P wave, a
transient pause after that P and then restart of cycle
again.

In second degree type II you have fix PR interval and
abruptly there is a drop beat as shown in Figure 50,
after every two beats with normal PR interval third P
is without QRS complex so beat dropping with fix
PR interval. To pick this rhythm abnormality its
important to march through PR interval of every
QRS complex sequentially.

57. 2nd Degree AV Block

pe |

Hi M
N (Wenckebach)
EB PUR GENE Re

EKG Characteristics: Progressive prolongation of the PR interval
until a P wave is not conducted.

As the PR interval prolongs, the RR interval
actually shortens

Type 2
EKG Characteristics: Constant PR interval with intermittent
failure to conduct
Fig: 51

Second-Degree AV Block, 2:1 Conduction
(2:1 AV Block)

+. ji

58. So let's revise again first degree AV heart block just
shows prolong PR interval with all conducting P
wave. Second degree further divided into Type I
called Wenceback where you have progressive PR
prolongation and a drop beat as shown in figure 51,
Sth P is without QRS, this usually present as group
beating and if rate is fast then you may have some
difficulty differentiating P from T wave and second
degree type II is one, where you have a drop beat
with fix PR as shown in Figure 51 which may be
normal or prolong.

‘There is one more category of 2nd degree called 2:1
block as shown in Figure 52 where one *P? wave is
conducting and second successive nonconducting
and you can't make out whether its type I or type IL
because you don’t have enough complexes before
dropping beat to differentiate. so it may be type I or
type IL Actually the pathological difference
between these two types is that type I is nodal block
and type II is infra-nodal so more dangerous.

59. Fig: 54

60. Figure 53 is showing another variety called high
degree AV block it is somewhere between 2nd and
3rd degree 3:1 block where every third beat is
conducting while two beats are non-conducting, fix
PR interval in every conducting beat make this
rythm diferrent from 3rd digree AV block.

Lastly figure 54 is showing 3rd degree AV block, in
which P waves are more than QRS with variable
PR interval and both P and QRS have their own
independent rhythm without any association
pathologically a condition where impulse
generated by sinus node in the form of P is not
conducting through AV node and ventricular
depolarization is done by impulse generated by
either AV node or ventricles and QRS configuration
& escape rate gives an idea about origin of escape
rythm ie. if narrow with rate 40-60/minutes it’s
from AV node and if broad with rate 20-40/ minute
then it’s from ventricles.

Both ‘P’ and ‘QRS’ rhythm is usually regular in 3rd
degree AV Block.

61. Remember
+ When an impulse originates in a ventricle, conduction through

the ventricles will be inefficient and the QRS will be wide and
bizarre.

E

Sinoatrial node
y
AV node
Bundle of His
y
Bundle Branches

y
Purkinje fibers

62. Actually when ventricles are depolarized by an
impulse generated within ventricles showed a
broad bizarre QRS as in PVCs because the impulse
conduction is not through normal conduction
system, this depolarizes ventricles through cell to
cell transfer.

In conclusion rhythm assessment needs a very
careful screening of ECG under already described
five steps to pick abnormalities and finally
correlating these abnormalities to different
arrhythmias.

63. Bundle Branch Blocks

So, depolarization of the
Bundle Branches and
Purkinje fibers are seen as
the QRS complex on the
ECG.

Therefore, a conduction
block of the Bundle
Branches would be
reflected as a change in
the QRS complex.

Left Bundle Branch Block
Criteria

+ QRS duration > 120ms

+ Broad R wave in I and V6

+ Prominent QS wave in V1

+ Absence of q waves (including physiologic
q waves) in I and V6

64. In bundle branch block after bundle of His one of
the bundle, either right or left is unable to conduct
so conduction beyond that point occurs through
cell to cell while other bundle conducts normally
and ECG features are normal P wave , PR interval
but a broad QRS with a specific pattern showing
either right or left bundle branch block.

‘As for example in left bundle branch block
(LBBB) the conductions blocks at the start of left
bundle beyond which it travels cell to cell on left
but continue normally to right bundle and right
purkinji fibers giving a broad R waves in I and V6
with prominent QS in VI and absence of Q, in I
and V6.

65. Left Bundle Branch Block

Fig: 59

Right Bundle Branch Block
Criteria

+ QRS duration > 110ms
+ rSR’ pattern or notched R wave in VI
+ Wide S wave in land V6

Fig: 60

66. Figure 59 is showing an ECG with sinus rhythm but
a wide QRS and if you match it with previously
defined features you will found it to be consistent
with left bundle branch block.(LBBB) .

In right bundle branch block the conduction blocks
just at the starting point of right bundle beyond
which conduction travels cell to cell in right side
but left bundle conducts normally to left sided
purkinji fibers and ECG shows rsR’ pattern or a
notched R wave in VI and S wave in I and V6 as
described in figure 60 .

67. Right Bundle Branch Block

PE

hr IE BIENEN.

AHA AN ART

Ml EST UL a REA

Fig: 61

Rhythm Analysis

HN

+ Step 1: Calculate rate.

+ Step 2: Determine regularity.

+ Step 3: Assess the P waves.

+ Step 4: Determine PR interval.

+ Step 5: Determine QRS duration.

Fig: 62

68. Fig 61 showing an ECG with sinus rhythm but a
broad QRS complex which if we match with
characteristics shown in Fig 60 found it to be
consistent with Right bundle branch block.

Some times broad QRS are not exactly following
either RBBB or LBBB pattern so labeled
nonspecific intraventricular conduction delay. Here
I would like you to write a comprehensive report on
analyzing rhythm of figure 61 by applying and
revising the summary of rhythm analysis shown in
figure 62.

ECG report:

69. ISCHEMIC CHANGES

One way to
diagnose an
acute ML is to
look for
elevation of the
ST segment.

+ S-T segment elevation

+ S-T segment depression

+ Hyper-acute T-waves

+ T-wave inversion

+ Pathological Q-waves
Left bundle branch block

Fig: 63

ST ELEVATION

70. Ischeamia

Ischemia theoretically can generate any ECG change
and its diagnosis is predominantly depends on com-
bining patient symptoms with ECG findings but there
are some changes as shown in Figure 63, which helps
in diagnosing acute ischemia. As for example ST-T
changes are not only important for diagnosing
ischemia but also helps in diagnosing trans mural
infarction and deciding about reperfusion therapy.

Before looking at ST elevation its very important to
understand “J” point, a point where QRS meet ST
segments or in other words where QRS ends and ST
segment starts, for a definitive shift of ST segment one
has to compare this J point with preceding “TP”
segment to see whether it is elevated or depressed
along with ST segment and ideally ECG should be
recorded in straight line to diagnose true ST elevation
or depression.

71. ST-ELEVATION

ST elevation’ ST elevation|

KT
LH

Evolution of Acute MI
Fig: 66

72. As shown in Figure 65 that J point along with ST
segment is elevated in chest leads in comparison to
“TP” segment and this is a feature or trans mural
infarction. Timely identification of these changes
along with symptoms is very helpful in offering
definitive treatment as early as possible which
helps in reduction of mortality and morbidity in
these patients.

The evolution of these findings as shown in figure
66 are hyper acute T wave leading to ST elevation,
Q wave formation, settling of ST segments that is
coming back to normal plane and T wave inversion
with T wave sometimes uprights again but leaving
a Q wave if not properly perfused at the time of
infarction.

73. Be,
E

hn rn PESE
E

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Fig: 67

RIGHT

74. Just for sake of practice I would like you to go
through figure 67 and tell exactly the extent of
elevation and depression in millimeters in all leads
that is you have to write exact height and depth of
elevation and depression in every lead you found.

ST elevation
ST depression:

When you are looking for ST elevation to diagnose
myocardial infarction (ML) then you should be aware
of leads representing different territories because for
diagnosing trans mural M1. for reperfusion you need
ST segment elevation in at least two leads of a territory.
Combination of various leads representing different
territories are shown in figure 68.

75. ST-DEPRESSION

Can be characterised as:-
+ Downsloping

+ Upsloping

+ Horizontal

Horizontal ST depression

Figure 28

76. For seeing ST depression again J point is important
but depression can be up slopping, down slopping
and horizontal, diagnosing ischemia needs symptoms
correlations and dynamic changes so one need old
ECG and further serial ECGs in ST depression to
diagnose patient and finally need cardiac markers to
diagnose Non ST elevation MI. or unstable angina.

Dynamic horizontal ST depression as shown in
figure 70 in multiple leads is very categorical of
ischemia. For calculating exact amplitude of ST
depression one has to compare ST segments along
with J point with TP segment, looking at depth in
terms of small squares which co-relates with
millimeters.

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Fig: 71
Q Waves

Non Pathological Q waves
Q waves of less than 2mm are normal

Pathological Q waves
Q waves of more than 2mm

indicate full thickness myocardial
damage from an infarct i
Late sign of MI (evolved)

78. Again I would like you to go through figure 71 and
write down exactly amplitude of ST depression
and ST elevation marching through every lead.
Identify J point and compare it with preceding TP
segment to calculate exact depression and
elevation.

ST depression:

ST Elevation:

Lastly Q waves, without other acute changes is an
evidence of old trans mural infarction but there are
other reasons as well but a significant is one which
is at least 2mm deep and 0.04 second wide and
should be present in two leads of a territory. There
are other non-specific changes like T inversions
and sometimes bundle branch blocks can happen
in ischemia as well.

79. Left Atrial Enlargement

Criteria Lead
Mm
P wave duration in I > ! FS oes (aac
120ms
or Lead Vi
Negative component of

biphasic P wave in V1 > eo fame
1 “small box” in area 2

Right Atrial Enlargement
a Lead II
Criteria aE
P wave height in I> } Ala
24mm

ee Re er Lead Y,
sitive component of 1, pig
biphasic Pwave in Vlz 4 7171

1 “small box” in area

80. Chamber Enlargement

Looking for Atrial and Ventricular enlargement you
have to look for specific criteria as described for
Atrial Enlargement P waves in lead V1 and lead II
are important. In V1, if 2nd downward component
of ‘P’ wave is >Imm deep and >Imm wide or in
lead II “P” wave is =120ms or 3 small square, it is
consistent with left Atrial enlargement.

If upper and Ist component of P wave in lead VI is
=1 small box in area that is Imm of height and 1
small square width or P wave in lead II has height of
224mm, it shows right Atrial enlargement.

81. Left Ventricular Hypertrophy

Many sets of criteria for diagnosing LVH have been
proposed:

Sensitivity | Specificity
The sum of the S wave in V, and
the R wave in either V, or V, > 35 43% 95%
mm
Sum of the largest precordial R
wave and the largest precordial S 45% 93%
wave > 45 mm
Romhilt-Estes Point System 50-54% 95-97%
Left Ventricular Hypertrophy
pray

ES

fl
ne

82. Regarding left ventricular hypertrophy there are
multiple criterion as shown in figure 75 but simple
to remember for adults is S wave in V1 plus R wave
in VS or V6, if >35mm it is consistent with LVH.
Remember ECG is less sensitive but specific in
diagnosing LVH.

Now it’s time to write a comprehensive ECG report
of Fig. 76 mentioning axis, rhythm, ischemia and
chamber enlargement to have a revision.

ECGreport:

83. RVH

+ V1 Lead:
- RS ratio > 1 and negative T wave

+ VS or V6
- R/S ratio in V5 or V6 < 1

Fig: 77

Right Ventricular Hypertrophy

En

hr a tL N.
le

LE
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Fig: 78

84. For right ventricular hypertrophy you have to look
for QRS in Leads V1 or V6 if in Lead VI R wave
height is more than the depth of S wave that is R/S
ratio greater than 1 or in Lead VS R wave height is
less than S wave depth that is R/S ratio <1 it favors
RVH as shown in figure 77.

There are some other ECG differentials of R wave
in V1 along with RVH so this finding needs clinical
co-relation.

Again its time to write a comprehensive ECG
report on Figure 78

ECG Report:

85. Conclusion

Reading ECG is not difficult but
mastering needs persistent reading
with sequence.

+ For diagnoses and management
one has to combine ECG findings
with patients clinical status

86. With that we have completed tips for basic
screening of ECG which will help a beginner to
at least be able to see major abnormalities in
ECG . In conclusion I will again stress on the fact
that reading ECG is not difficult but mastering
need persistent sequential reading, so one has to
see at least 5-10 ECGs daily as a beginner to
consolidate the skills of ECG reading and
secondly using ECG for diagnosis need
combining of ECG findings with patients clinical
status, that means just ECG findings is not
enough to make final diagnosis.

In the next segments you will found some case
scenarios with ECG abnormalities which I want
you to go through by yourself in terms of making
diagnosis and management strategies and write it
on blank space then see the complete discussion
on these cases in video, which is there on
YouTube.

Elremesireug

87. ECG - 1

A.60 year old man with 2 hours of “crushing” chest pain suddenly collaps.

ECG -2
50 yrs well controled hypertensive female on amlodipine
5mg having palpitation for last 1 week
a =

88. Practice Cases

Case 1:60 years man with two hours of crushing chest pain suddenly
collapse.

ECG report:

Management:

Case 2: 50 years well controlled hypertensive female on Amlodipine
‘Smg having palpitation for last 1 week.
ECG report:

Management:

89. ECG—3

A 70 year old man with exercise intolerance.

ECG-4
55 yrs male H/O of Inf. MI 10 yrs back lost to follow up came to ER
with 2 hours of palpitations

90. Case 3: 70 years old man with weakness lethargy and Exercise
intolerance
ECG report:

Management:

Case 4 : 55 years male with history of Inferior M.I. 10 years back
lost to follow up came to ER with 2 hours of palpitation.
ECG report:

Management:

91. 72 yrs male having H/O two episodes of syncope in
last two weeks.

po

E ac cde

(A 40 year old woman with pleurkic chest pain and breathlessness.

92. Case 5 : 72 years male having history of two episodes of syncope in
last two weeks.
ECG report:

Management:

Case 6: 40 years female with 2 hours of pleuritic chest pain and
breathlessness.
ECG report:

Management:

93. 63 yrs diabetic male with no other co-morbids going
for cataract surgery.

Art eee
Fee aie
ie RTE cit ag at Ris
BEER

94. Case 7: 76 years male with shortness of breath for few months
severe for last two days with palpitation.
ECG report:

Management:

Case 8 : 63 years Diabetic male with no other co-morbid going for
cataract surgery
ECG report:

Management:

95. ECG -9
À 56 year old man with bröathiesanas and aisé JVP:
ars
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ECG - 10

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96. Case 9: A 56 years male with breathlessness and raised JVP.
ECG report:

Management:

Case 10 : A 55 years old man with four hours of crushing chest pain.
ECG report:

Management:

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98. Case 11 : 58 yrs diabetic female sudden severe central chest discom-
fort for last 15 minutes.
ECG report:

Management:

Case 12 : 66 yrs male with SOB on minimal exertion since last 1
month.
ECG report:

Management:

99. ECG - 13

ECG - 14

RDA

Seen JE

ML away ltl ded
| |

eee Pica ¿hd

100. Case 13: 22 yrs male visited ER for the first time with headache
found to have BP of 190/110.
ECG report:

Management:

: 55 years male, smoker with prolong history of SOB and
cough , increased in last three month.
ECG report:

Management:

101. ECG - 15

À 58 year old man on haemodialysis presents with profound weakness

102. Casel5: 58 years male on hemodialysis presented with profound
weakness.
ECG report:

Management:

103. Final Words

Dear reader Experts have done wonderful work in
propagating ECG knowledge and this small booklet
is just few drops from that Ocean of existing
knowledge available.

My only objective in compiling this booklet was to
present things in simple easy way for beginner who
along with seeing video should at least be able to start
seeing and reading ECG. ECG reading is something
you need at every stage in any discipline of Medicine
to timely diagnose and treat or refer life threatening
situations. I hope this book along with video will help
you in doing so. You may found mistake in it if so feel
free to communicate.

[email protected]

A TAPA Darren

o

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ae PrermEvo vt) LS.

RBI: ARBI-D ron ree tnt dame it

105. MyPro /bnorecnon

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A safer option in diabetes’ )

Reduces upto 47% cholesterol”

SOON

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|
|
Reno protective than other statins” y
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