National ECG Workshop AIMST MMA 2015

Understanding the
ELECTROCARDIOGRAM
and
MYOCARDIAL INFARCTION
Dato’ Wira Prof Dr LR Chandran DGMK DSDK SDK BCK

MBBS(Monash) MRCP(UK) FRCP(Edin) FRCP (Lond) FRCP (Glasg)
Fellow of the Academy of Medicine of Malaysia [FAMM]
Thursday, 23 April 2015 Dato' Wira Prof Dr L R Chandran 1
Alor Star
Thursday, 23 April, 2015 Basic ECG Slides 2
Dato' Wira Dr L R Chandran
Dato' Wira Prof Dr L R Chandran 3
Alor Star
Thursday, 23 April 2015
ST
Elevation
Q Wave T
inversion

Dato' Wira Prof Dr L R Chandran Alor
Star
“J” point
= ST –T junction
Basic ECG Slides

Thursday, 23 April, 2015 5
“J” point
= ST –T junction
Basic ECG Slides

Basic ECG Slides
“J” point
= ST –T junction Dato'Basic
Thursday, 23 April, 2015
ECG Slides
Wira Dr L R Chandran
8
Basic ECG Slides
Basic ECG Slides
Basic ECG Slides
Basic ECG Slides
Basic ECG Slides
ST SEGMENT
IS IN
ISOELECTRIC
LINE
Basic ECG Slides
Basic ECG Slides
Basic ECG Slides
Basic ECG Slides
ST SEGMENT DEPRESSION
Basic ECG Slides

Basic ECG Slides

Basic ECG Slides
“Lossof R wave”
= “Q” wave
Sequence of changes seen during evolution of myocardial infarction

Thursday, 23 April 2015 21 Dato' Wira Prof Dr L R Chandran Alor Star
When is it SIGNIFICANT?
 subendocardial ischemia [NSTEMI] or infarction
Horizontal
Down-sloping Up-sloping
Basic ECG Slides Dato' Wira

Thursday, 23 April 2015 22
Prof Dr L R Chandran Alor Star
In exercise stress tests, horizontal or down-
sloping depression of ≥1 mm
POSITIVE SIGN OF ISCHEMIA
Up-sloping depression of the
same magnitude 80 ms beyond
the J point
POSITIVE SIGN OF ISCHEMIA

Up-sloping depression of <1 mm at
80 ms beyond the J point
J POINT DEPRESSION
(NOT A ST DEPRESSION)
The q (Q) must be
At least 0.03 sec The q (Q) must
wide= nearly be
1 SMALL SQUARE At least

1/3 of the height
of
Thursday, 23 April 2015 Dato' Wira Prof Dr L R Chandran Alor Star 26

Acute Myocardial Infarction
Basic ECG Slides
Dato' Wira Prof Dr L R Chandran Alor Star
Basic ECG Slides
r
NO r
Basic ECG Slides

r
Basic ECG Slides

Pathological Q waves
As the acute myocardial infarction evolves,
changes to the QRS complex include
loss of R wave height &

the development of
pathological Q waves.
Pathological Q
waves in
inferior and anterior leads
31
Basic ECG Slides
Pathological Q waves
As the acute myocardial infarction evolves,
changes to the QRS complex include
loss of R wave height &

the development of
pathological Q waves.
Pathological Q
waves in
inferior and anterior leads
32
Basic ECG Slides
Hyperacute T waves May be the FIRST change seen
Thursday, 23 April 2015 Basic ECG Slides 33
TALL T WAVES
Basic ECG Slides

Basic ECG Slides
Sometimes
 the QRS complex,
 the ST segment, and
 the T wave
fuse to form a
Single
monophasic
deflection,
called
a giant R wave or
“ tombstone”
Anterior myocardial infarction with gross ST segment elevation

(showing “tombstone” R waves)
Thursday, 23 April 2015 Dato' Wira Prof Dr L R Chandran Alor Star 36

Reciprocal changes are seen in up to
 70% of inferior and
 30% of anterior
infarctions.
reciprocal changes
very useful
when
there is doubt about
clinical significance
of
ST segment elevation.
Infero-Lateral myocardial infarction [ II, III, aVF & V5, V6 ST ELEVATION

reciprocal changes [ ST Depressions ] in
leads I, aVL, V1, V2 ST DEPRESSION
[ for Inferior II,III,aVF, & for lateral V5, V6
Alor Star
Reciprocal changes are seen in up to
 70% of inferior and
 30% of anterior
infarctions.
reciprocal changes
very useful
when
there is doubt about
clinical significance
of
ST segment elevation.
Infero-lateral
myocardial infarction
[ II, III, aVF & V5, V6 ST ELEVATION
reciprocal changes
[ ST Depressions ] in
leads I, aVL, for Inferior – II, III, aVF [ & reverse ]
ANTERIOR leads V1 –V4 cannot record from POSTERIOR leads – NO Reciprocal

Alor Star
Reciprocal change
strongly indicates acute infarction,
with a sensitivity &
+VE predictive value of
over 90%,
though its absence

does not rule out the diagnosis
Reciprocal changes:
widespread ST segment depression antero - lateral leads [ I, aVL, V5, V6 ] strongly

suggests that
the subtle inferior ST segment elevation [ II, III, aVF ] is due to acute infarction
Reciprocal changes are most frequently seen when the infarct is large, and
they may reflect an extension of the infarct or
occur as a result of coexisting remote ischaemia. Dato' Wira Prof Dr L R Chandran
OR, ?? a benign electrical phenomenon. Alor Star 39
Reciprocal change
strongly indicates acute infarction,
with a sensitivity &
+VE predictive value of
over 90%,
though its absence

does not rule out the diagnosis
Reciprocal changes:
widespread ST segment depression antero - lateral leads [ I, aVL, V5, V6 ] strongly

suggests that
the subtle inferior ST segment elevation [ II, III, aVF ] is due to acute infarction
Reciprocal changes are most frequently seen when the infarct is large, and
they may reflect an extension of the infarct or
occur as a result of coexisting remote ischaemia. Dato' Wira Prof Dr L R Chandran
OR, ?? a benign electrical phenomenon. Alor Star 40
Alor Star
aVF
ST elevation
can produce
aVL
ST depression

The
REVERSE
Is also TRUE
aVL
ST elevation
can produce
aVF
ST depression
Dato' Wira Prof Dr L R Chandran Alor Star 43 Thursday, 23 April 2015

Basic ECG Slides
Anterior AMI
Q waves ,
ST segment elevation,
T inversion
V1 –V4
NO reciprocal
changes
Basic ECG Slides

45 Thursday, 23 April 2015
STEMI vs. NSTEMI

NON ST
ELEVATION
MI
-1/5
Basic ECG Slides

Basic ECG Slides
Basic ECG Slides
Basic ECG Slides
Basic ECG Slides
Basic ECG Slides
INFARCTS
 Anterior
 Inferior
 Right ventricular
 Posterior
Basic ECG Slides

Basic ECG Slides 55
Thursday, April 23, 2015 55
Basic ECG Slides
Thursday, April 23, 2015
2015年4月23日 Dato' Wira Prof Dr L R Chandran Alor Star
Anterior
AMI
ST segment elevation
T inversion
Q waves ,
V1 –V4
NO
reciprocal changes
Basic ECG Slides
Acute Extensive Anterior Myocardial Infarction
ST elevation in the anterior Leads V1 - 6, I and aVL

Reciprocal ST depression in the inferior leads [ II, III, aVF ]
Basic ECG Slides 59
Acute Antero- Lateral myocardial infarction
ST elevation in the anterior leads:

V1 - 6, I and aVL
Basic ECG Slides 60

Acute Antero- Lateral myocardial infarction
•ST elevation in the anterior leads: V1 - 6, I and aVL
•reciprocal ST depression in the inferior

leads II, III , aVF
Basic ECG Slides 61

ST elevation & Q wave  V2-V5,
Anterior /
septal I & aVL
V1-V4 Reciprocal ST depression  Lead III
Basic ECG Slides 62

Q waves  V1-V2
ST elevation  V1-V4
Q waves  V1-V2
Reciprocal ST depression  lead III
Peaked T waves  V2-V4 ST elevation  V1-V4
Peaked T waves  V2-V4

Reciprocal ST depression  lead III
Basic ECG Slides 63

• Reciprocal ST depression  III ,aVF
• ST elevation  V2-6, I , aVL
Reciprocal ST depression  III ,aVF ST elevation  V2-6, I , aVL
Basic ECG Slides 64

ST elevation  precordial & inferior leads
Hyperacute T waves  V1-V3 Q waves V1-V3 , lead III and aVF
Q waves V1-V3 , lead III and aVF
ST elevation  precordial & inferior leads Hyperacute T waves  V1-V3
Basic ECG Slides 65

2015年4月23日 Dato' Wira Prof Dr L R Chandran Alor Star 66 66
R C Art
INFERIOR WALL  lead II,III, aVF

R C Art
ST elevation & Early Q wave II,III, aVF
ST Depression & T inversion  aVL
Basic ECG Slides 68

ST elevation & Early Q wave II,III, aVF • ST elevation & Early Q wave II,III, aVF
• ST Depression & T inversion  aVL
ST Depression & T inversion  aVL
Basic ECG Slides 69

Right
ventricular
infarction
Basic ECG Slides

Right ventricular infarction
Right ventricular infarction often missed,

standard 12 lead ECG not sensitive indicator of RV damage.
[ RV thin,1/6 of LV thickness]
 RV infarction associated with 40% of inferior infarctions.

 Occasionally with anterior infarctions but
 rarely occurs as an isolated phenomenon.
Clinically, THINK
RV Infarction IF
• History suggesting AMI,
LOW BP ,
• Raised JVP ,
• CLEAR Lung BASES
Right ventricular infarction
Right ventricular infarction often missed,
standard 12 lead ECG not sensitive indicator of RV damage.
[ RV thin, 1/6 of LV thickness]
 RV infarction associated with 40% of inferior infarctions.

 Occasionally with anterior infarctions but
 rarely occurs as an isolated phenomenon.
Standard 12 lead ECG

R C Art
RV infarction is indicated by
 signs of inferior infarction,
 ST segment elevation in Lead V1.
 Besides ST segment V1 is “looking” at the anterior wall of
the right ventricle.
 RARE for ST segment elevation in lead V1 to occur as an

isolated phenomenon .
“LOOKS”
at
RV
Right sided chest leads are much

more sensitive to the presence of Right Ventricular infarction.
The most useful lead is lead V4R (an electrode is placed over the right 5th intercostal space in the mid-
clavicularline).
Lead V4R should be recorded ASAP in all patients with inferior infarction, as ST segment elevation in
RV infarction may be short lived
R C Art
Reciprocal changes  lead I & aVL ST elevation in V1 RV infarction considered
ST elevation  lead II, III, aVF
Acute Inferior Myocardial Infarction which is often associated with a Right Ventricular Myocardial Infarction.
Inferior Infact :
ST elevation  lead II, III, aVF
Reciprocal changes  lead I & aVL
elevation in V1 RV infarction
ST2015年4月23日 considered
Dato' Wira Prof Dr L R Chandran Alor Star 74 74
V4R  ST elevation
Leads II, III, aVF  ST elevation + Biphasic T
Acute INFERIOR Dx of RV infarction  associated with hypotension.

myocardial infarction Rx : nitrates / diuretic Hypotension (can Rx with 200 titrate upto 1000cc
with associated Right normal saline )
Ventricular
infarction
2015年4月23日 Dato' Wira Prof Dr L R Chandran Alor Star 75
ST is elevated  Lead II, III, aVF [ INFERIOR AMI ]
Reciprocal ST depression Leads I, aVL [Reciprocal ] + V1R, V2R
ST is elevated  LeadsV4R, V5R, V6R [ RV AMI ]

Discussion 9 B 76
76
Electrical VECTOR points to LeadIII , so it will be TALLER than
Lead II [can ignore]
Reciprocal ST depression Leads I, aVL [Reciprocal]
ST is elevated  Lead V4R [ RV AMI ]

elevated  Lead V4R [ RV AMIDato'
ST is2015年4月23日 ] Wira Prof Dr L R Chandran Alor Star 79 79
ST is elevated in Leads? ST is depressed in Leads?
ST is elevated in Leads…II, III, aVF - Inferior AMI
ST is elevated in Leads…V4R –V6R – RV AMI
ST is depressed in Leads… I, aVL–Reciprocal Leads
I aVR V1 V4R
Right
Ventricular
Wall
II aVL V2 V5
Always make sure to

denote the leads III aVF V3R V6
you change.
82
RV infarction :
• inferior STEMI & ST elevation in lead III > lead II. C.O
• V1 is isoelectric
• V2 is significantly depressed.
• ST elevation  V3R-V6R.
POSTERIOR
INFARCTION

[POST INF-0]
R C Art
Lead V1 – Tall ‘R’ ; ST depression;

UPRIGHT ‘T’

Lead V1 – “INVERTED View”
[POST INF-0]
Lead V1 – Tall ‘R’ ; ST depression;

UPRIGHT ‘T’

Posterior myocardial infarction
Posterior myocardial infarction  infarction of the posterobasal wall of the left ventricle.
Isolated
posterior infarction
with no associated
inferior changes
[ RARE]
(note ST segment
depression in
leads V1 to V3 with
UPRIGHT T
[POST INF-1]

87
Posterior Infarct
R in V1
V2
Upright
T
ST
depressed

LEADS POSITION FOR RV & POSTERIOR AMI Dx
[POST INF-4]
POSTERIOR
Leads
&
RIGHT Leads
[POST INF-4]
ST segment POSTERIOR
Leads
elevation 
posterior chest leads
V8 & V9
[POST INF-5]
Lead V1 –
“INVERTED View”
Lead V1 –
Tall ‘R’ ; ST depression;
UPRIGHT ‘T’
[POST INF-4] Posterior infarct
Lead V1 –
Tall ‘R’ ; ST
depression;
UPRIGHT ‘T’
Inferior infarct
Lead II,III
ST elevation
93
A Fast Beating Heart
Narrow & Wide Tachycardias –
Ventricular Tachycardia
Dato’Wira Dr LR Chandran DGMK DSDK SDK BCK

MBBS(Monash) MRCP(UK) FRCP(Edin) FRCP(Glasg) FRCP (Lond)
Fellow of the Academy of Medicine Malaysia (FAMM)
Wide Complex Tachycardias Dato' Wira Prof LR 1
Thursday, April 23, 2015 Chandran Alor Star
The MOST famous WIDE complex = “Ventricular Ectopic”
Thursday, April 23, 2015 Wide Complex Tachycardias 2

Dato' Wira Prof LR Chandran Alor Star
Thursday, April 23, 2015 Wide Complex Tachycardias Dato' Wira 3
Prof LR Chandran Alor Star
Thursday, April 23, 2015 Wide Complex Tachycardias Dato' Wira 4
Prof LR Chandran Alor Star
Why FAST heart rates
are BAD for US

Basically
In a tachycardia, we need to know
If it is
WIDE or NARROW
If WIDE
About 80% are
VENTRICULAR TACHYCARDIA

Can often
Deteriorate into
Ventricular FLUTTER &
 Ventricular FIBRILLATION
 DEATH

VT rapidly becomes VF see ST elevation - AMI - in V5

VT rapidly becomes VF see ST elevation - AMI - in V5

Myths about
VT vs Narrow complex Tachycardias
 ALL VTs get LOW BP very fast
 If “SVT” ( narrow complex Tachycardias,
usually AVNRT )
‘BP will be stable with NO
haemodynamic problems’
BUT - “SVT”s can get LOW BPs
and VTs CAN remain stable for quite some time

Why FAST heart rates
are BAD for US
BOTH
VT S & “ SVTS”
Examples of NARROW & WIDE QRS complexes

NARROW
Can you see

1 -- 3 NARROW complexes
2 -- 6 BROAD ( WIDE ) complexes
3 -- 1 wide PJC
NARROW
1 2 3
Can you see

1 -- NARROW complex
2 -- BROAD ( WIDE ) complex
3 -- 1 wide PJC
Narrow / WIDE N W N Wide complex Tachycardia

Narrow / WIDE N W N Wide complex Tachycardia
IF conduction is FAST (as down B of HIS)

& NO delays = NARROW complex(es)
IF conduction is SLOWED ( AFTER B of HIS) OR

current STARTS in VENTRICLES
= WIDE QRS
Ventricular
Tachycardias
T R of V Ectopic on Previous T

Ventricular
Tachycardias
T R of V Ectopic on Previous T

The concept of
Ventricular Tachycardias
1 Onset of CHEST pain

2 Palpitations AFTER that
ECG - Wide QRS tachycardia
= Ventricular Tachycardia IF BP LOW or DROPPING
( If Palpitation same time / or
Treat as VT
before CHEST pain
CANNOT make this ( if WIDE QRS tachycardia)
assumption = DC cardioversion
19
Wide Complex Tachycardias Dato'
Wira Prof LR Chandran Alor Star Thursday, April 23, 2015
2015年4月23日
Arterial Supply of the Heart
 The arterial supply of the heart is provided by the right and left coronary arteries, which
arise from the ascending aorta immediately above the aortic valve.
 The coronary arteries and their major branches are distributed over the surface of the
heart, lying within subepicardial connective tissue.
Right coronary artery:
 The right coronary artery arises from the anterior aortic sinus of the ascending aorta
and runs forward between the pulmonary trunk and the right auricle.
 It descends almost vertically in the right atrioventricular groove, and at the inferior
border of the heart it continues posteriorly along the atrioventricular groove to
anastomose with the left coronary artery in the posterior interventricular groove.
 The following branches from the right coronary artery supply the right atrium and right
ventricle and parts of the left atrium and left ventricle and the atrioventricular septum.
Branches:
 The right conus artery supplies the anterior surface of the pulmonary conus
(infundibulum of the right ventricle) and the upper part of the anterior wall of the right
ventricle.
 The anterior ventricular branches are two or three in number and supply the anterior
surface of the right ventricle. The marginal branch is the largest and runs along the
lower margin of the costal surface to reach the apex.
 The posterior ventricular branches are usually two in number and supply the
diaphragmatic surface of the right ventricle.
 The posterior interventricular (descending) artery runs toward the apex in the
posterior interventricular groove. It gives off branches to the right and left ventricles,
including its inferior wall. It supplies branches to the posterior part of the ventricular
septum but not to the apical part, which receives its supply from the anterior
interventricular branch of the left coronary artery. A large septal branch supplies the
atrioventricular node. In 10% of individuals the posterior interventricular artery is
replaced by a branch from the left coronary artery.
2015 ECG WORKSHOP AIMST UNIVERSITY

ANATOMY –Compiled by Prof Dr.R. Arul Moli
 The atrial branches supply the anterior and lateral surfaces of the right atrium. One
branch supplies the posterior surface of both the right and left atria. The artery of the
sinuatrial node supplies the node and the right and left atria; in 35% of individuals it
arises from the left coronary artery.

Left coronary artery:
 The left coronary artery, which is usually larger than the right coronary artery, supplies
the major part of the heart, including the greater part of the left atrium, left ventricle,
and ventricular septum.
 It arises from the left posterior aortic sinus of the ascending aorta and passes forward
between the pulmonary trunk and the left auricle . It then enters the atrioventricular
groove and divides into an anterior interventricular branch and a circumflex branch.

Branches:
 The anterior interventricular (descending) branch runs downward in the anterior

interventricular groove to the apex of the heart. In most individuals it then passes
around the apex of the heart to enter the posterior interventricular groove and
anastomoses with the terminal branches of the right coronary artery. In one third of
individuals it ends at the apex of the heart. The anterior interventricular branch supplies
the right and left ventricles with numerous branches that also supply the anterior part
of the ventricular septum. One of these ventricular branches (left diagonal artery) may
arise directly from the trunk of the left coronary artery. A small left conus artery
supplies the pulmonary conus.
 The circumflex artery is the same size as the anteriorinterventricular artery. It winds
around the left margin of the heart in the atrioventricular groove. A left marginal artery
is a large branch that supplies the left margin of the left ventricle down to the apex.
Anterior ventricular and posterior ventricular branches supply the left ventricle. Atrial
branches supply the left atrium.
Variations in the Coronary Arteries:
 Variations in the blood supply to the heart occur and the most common variations affect
the blood supply to the diaphragmatic surface of both ventricles. Here the origin, size,
and distribution of the posterior interventricular artery are variable.
 In right dominance, the posterior interventricular artery is a large branch of the right
coronary artery. Right dominance is present in most individuals (90%).
 In left dominance, the posterior interventricular artery is a branch of the circumflex
branch of the left coronary artery (10%).
Coronary Artery Anastomoses:
 Anastomoses between the terminal branches of the right and left coronary arteries
(collateral circulation) exist, but they are usually not large enough to provide an
adequate blood supply to the cardiac muscle should one of the large branches become
blocked by disease.
 A sudden block of one of the larger branches of either coronary artery usually leads to
myocardial death (myocardial infarction), although sometimes the collateral circulation
is enough to sustain the muscle.

Summary of the Overall Arterial Supply to the Heart in Most Individuals:
 The right coronary artery supplies all of the right ventricle (except for the small area to
the right of the anterior interventricular groove), the variable part of the diaphragmatic
surface of the left ventricle, the posteroinferior third of the ventricular septum, the right
atrium and part of the left atrium, and the sinuatrial node and the atrioventricular node
and bundle. The LBB also receives small branches.
 The left coronary artery supplies most of the left ventricle, a small area of the right
ventricle to the right of the interventricular groove, the anterior two thirds of the
ventricular septum, most of the left atrium, the RBB, and the LBB.
Arterial Supply to the Conducting System:
 The sinuatrial node is usually supplied by the right but sometimes by the left coronary
artery.
 The atrioventricular node and the atrioventricular bundle are supplied by the right
coronary artery.
 The RBB of the atrioventricular bundle is supplied by the left coronary artery; the LBB is
supplied by the right and left coronary arteries.
****

Basic electrophysiology
Electrocardiogram ( ECG ) depicts summed up electrical activity of the cardiac muscle
recorded extracellularly.
Electrocardiography (ECG or EKG from Greek: kardia, meaning heart) is the process of
recording the electrical activity of the heart over a period of time using electrodes placed on
the surface of the body.
Principle underlying ECG:
During the generation and transmission of cardiac impulse electrical currents also
spread to the adjacent tissues surrounding the heart and small fluctuations of this current
spread all the way to body surface because body fluids are good volume conductors. The
electrical potentials generated by these currents can be recorded from the surface of the
body if appropriate electrodes and recorders are used. The record of these potential
fluctuations during the cardiac cycle is the electrocardiogram abbreviated as ECG or EKG
and the electronic machine that is used to obtain this record is called electrocardiograph.
Classically a wave of depolarization refers to when the muscle fiber under goes a reversal in
its resting membrane potential i.e. negative inside becomes positive (B in the Fig) and
repolarization is as the cell recovers its resting polarity (D in fig 1 ).
Note: No potential is recorded in the ECG when the muscle is either completely polarized or
depolarized, only when the muscle is partly polarized or depolarized the current flows from
one part to the next and it is picked up by the recording electrodes.
Prepared by Prof Dr Neena Bhattacharya & Dr Nasrin Habib

(Physiology Unit, FOM)
PHYSIOLOGY HANDOUT
( Fig. 1 )
Cardiac impulse generation its spread and ECG waves
The timing of discharge of the cardiac impulse as reflected in ECG is as shown in the Fig
below:

PHYSIOLOGY HANDOUT
The depolarization is initiated in the sinoatrial node (SAN, the pacemaker), the impulse then
spreads radially through the atria, then converges on the atrioventricular node (AVN). Atrial
depolarization leads to atrial contraction and scribes P wave on the ECG which is complete
within 0.1sec.
At AV node there is a delay of about 0.1sec (AV nodal delay) after which wave of
depolarization (excitation) passes to the bundle of His and purkinjee fibers and finally gives
rise to QRS complex. Depolarization leads to ventricular contraction and is followed by
ventricular repolarization (relaxation) which causes T wave in the ECG.
Depolarization of the ventricles start at the left side of the interventricular septum and then
moves to the right side across the mid portion of the septum. The wave of depolarization
then moves down the septum across the apex of the heart, returning to the AV groove
proceeding from endocardial to the epicardial surface. The last parts of the heart to be
depolarized are the posterior basal portion of the left ventricle, pulmonary conus and the
upper most part of the septum.
ECG Lead system:

PHYSIOLOGY HANDOUT
ECG lead system is an arrangement of the electrodes fixed on the body surface by which
electrical activity of the heart is recorded e. g. lead I consists of circuit between two
electrodes one fixed on the left arm and the other on the right arm.
Classically following lead systems are used internationally.
A. Standard Bipolar limb leads- Lead I, Lead II and Lead III.
B. Augmented unipolar limb leads--- aVR, aVL, aVF.
C. Unipolar Chest leads--- V1- V6
A. Standard Bipolar limb leads:
Lead I: Between left and right arms, with left arm connected to positive and right arm to
negative terminal.
Lead II: Between right arm and left leg, with left leg connected to positive and right arm to
negative terminal.
Lead III: Between left leg and left arm, with left leg connected to positive and left arm to
negative terminal.
B. Augmented Unipolar Limb Leads:
The augmented limb leads record between one limb as active electrode and the other two
made zero by connecting to the recorder through a high resistance (5000 ohms). This
increases the size of the potential by 50% without affecting the configuration of different
waves. The augmented limb leads are designated according to the position of active
electrode as:
 aVR active electrode on the right arm

 aVL active electrode on the left arm
 aVF active electrode on the left leg.

PHYSIOLOGY HANDOUT
C. Unipolar chest leads:
In this lead system all the three limb leads are connected to a high resistance( 5000 ohms)
to create a zero potential. An exploring electrode is placed at different standard positions in
precordial region as
 V1 - 4th intercostals space just right to the sternum

 V2 - 4th intercostals space just left to the sternum
 V3 - Midway between V2 & V4
 V4 - 5th intercostals space at mid clavicular line
 V5 - 5th intercostals space at anterior axillary line
 V6 - 5th intercostals space at mid axillary line.

PHYSIOLOGY HANDOUT
Each of the 12 ECG leads records the electrical activity of the heart from a different angle,
and therefore align with different anatomical areas of the heart. Two leads that look at
neighboring anatomical areas are said to be contiguous.
Category Leads Electrical activity from
Inferior leads' Leads II, III and aVF inferior surface of the heart
Lateral leads I, aVL, V5 and V6 lateral wall of left ventricle

PHYSIOLOGY HANDOUT
Septal leads V1 and V2 septal surface of the heart (interventricular septum)
Anterior leads V3 and V4 anterior wall of the right and left ventricles
Characteristics of the normal Electrocardiogram
The normal electrocardiogram is composed of a P wave, a QRS complex, and a T wave.
The P wave is caused by electrical potentials generated when the atria depolarize before
atrial contraction begins.
The QRS complex is caused by potentials generated as the depolarization wave spreads
through the ventricles before contraction. The QRS complex has often, but not always, three
separate waves: the Q wave, the R wave, and the S wave.
Therefore, both the P wave and the components of the QRS complex are depolarization
waves.
The T wave is caused by potentials generated as the ventricles recover from the state of
depolarization. This process normally occurs in ventricular muscle 0.25 to 0.35 second after
depolarization, and the T wave is known as a repolarization wave.
Diagrammatic representation of two cycles of ECG waves

PHYSIOLOGY HANDOUT
Interpretation of ECG:
 Rate and Rhythm

 Wave forms
The ECG Paper
Horizontally
 One small box - 0.04 s
 One large box - 0.20 s
Vertically
 One large box - 0.5 mV

PHYSIOLOGY HANDOUT
Paper speed is such that
 Every 3 seconds (15 large boxes) is usually marked by a vertical line.

 This helps when calculating the heart rate.
NOTE: the following strips are not marked but all are 6 seconds long.
3 sec 3 sec
ECG Rhythm Interpretation
Rhythm Analysis
Step 1: Calculate rate
 Option 1
 Count the number 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
Interpretation: 9 × 10 = 90 bpm

PHYSIOLOGY HANDOUT
 Option 2
 Find a R wave that lands on a bold line.
 Count the number 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
R wave
 Memorize the sequence: 300 - 150 - 100 - 75 - 60 – 50
OR
 Less than three boxes- Tachycardia
 More than four boxes- Bradycardia
OR
Measure RR interval in mm and divide 1500 by RR interval in mm
e.g. if RR interval is 15mm, HR= 1500 divided by 15 = 100
Step 2: Determine regularity
 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?
R R

PHYSIOLOGY HANDOUT
Interpretation---- Regular
Step 3: Assess the P waves
 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?
Interpretation--- Normal P waves (1 P wave for every QRS)
Step 4: Determine PR interval
 Normal: 0.12 - 0.20 seconds (3 – 5 small boxes)
P R
Interpretation --- 0.12 seconds
Step 5: QRS duration
 Normal: 0.04 - 0.12 seconds (1 - 3 boxes)
Interpretation ---- 0.08 seconds

PHYSIOLOGY HANDOUT
Rhythm Summary
 Rate 90-95 bpm

 Regularity regular
 P waves normal, 0.12 s
 QRS duration 0.08 s
Interpretation --- Normal Sinus Rhythm
NSR (Normal Strip Rthym) Parameters
 Rate 60 - 100 bpm

 Regularity regular
 P waves normal
 PR interval 0.12 - 0.20 s, QRS duration - 0.04 - 0.12 s
Rhythm #2
o Rate 130bpm
o Regularity regular
o P waves normal
o PR Interval 0.16s
o QRS Duration 0.08s
Interpretation ----Sinus Tachycardia

PHYSIOLOGY HANDOUT
ST Elevation:
One way to diagnose an acute MI is to look for elevation of the ST segment. Elevation of the
ST segment (greater than 1 small box--1 mm /0.1 mV) in 2 leads is consistent with a
myocardial infarction.
The current guidelines for the ECG diagnosis of the ST segment elevation type of acute
myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in the limb
leads, and at least 2 mm elevation in the precordial leads. These elevations must be present
in anatomically contiguous leads I, aVL, V5, V6 (lateral wall); V3-V4 (anterior wall) ; V1-V2
(septal wall); II, III, aVF ( inferior wall).
Note: Acute myocardial infarction is not the only cause of ST segment elevation in all chest
pain patients. Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation
in at least one precordial lead. ECG changes similar to those seen in MI can occur in:
 Left ventricular hypertrophy,
 Left bundle branch block,
 Paced rhythm,
 Early repolarization,
 Pericarditis,
 Hyperkalemia,
 Ventricular aneurysm.

PHYSIOLOGY HANDOUT
ST Depression:
ST segment depression is considered significant if the ST segment is at least one box below
baseline as measured two boxes after the end of the QRS. As with infarction, the location of
the ischemia is reflected in the leads in which the ST depression occurs.
It is significant if it is more than 1 mm in V5-V6, or 1.5 mm in aVF or lead III.
Causes of ST depression (below the isoelectric line)
 Acute myocardial ischemia

 Ventricular hypertrophy with strain
 Digoxin toxicity
 Acute true posterior myocardial infarction with dominant R and tall upright T wave.
Uses of the ECG
For determination of:
 Heart Rate
 Conduction in the heart
 Cardiac arrhythmia
 Direction of the cardiac vector
 Damage to the heart muscle ( MI or Myocardial ischemia)

PHYSIOLOGY HANDOUT
Coronary Circulation
&
ECG
Dr. Mohammed Shahjahan Kabir

MBBS
FCPS (Medicine)
MD (Cardiology)
Branches of Coronary Artery
1. Right Coronary Artery (RCA):

A. Rt conus A
B. Rt anterior & posterior ventricular
C. Rt marginal
D. Rt posterior descending
E. Septal
F. Artery to SA node
2. Left Coronary Artery (LCA):
A. LAD:
I. Diagonal branches
B. Lt circumflex (LCx):
I. Marginal branches
ECG Leads Representing Surface of the Heart
Area
Surface of the heart ECG leads
Supplied by
Inferior Surface LII, LII and aVF RCA
Lateral Surface LI and aVL LCx
V5, V6
High Lateral Surface V5, V6, aVL LCx
V5, V6, aVL and LI
Anterior surface V1, V2, V3, V4, V5 and V6 LAD
Antero-septal V1, V2, V3 and V4 LAD
Right Ventricle RV4 RCA
Poursterior Surface V7, V8 PDA
Right Coronary Artery (RCA)
Area of Supply Clinical Impact ECG Findings
 Right atrium ST elevation ±

 Inferior MI
 Right ventricle pathological Q wave in
 Right Ventricular
 Post-inferior part LII, LIII & aVF (Inferior
Infarction
of left ventricle leads)
 60% SA node Bradycardia HR < 60 bpm

RCA Occlusion Inferior MI
ST segment elevation in
II, II, aVF
Posterior Descending Artery (PDA)
Clinical
Area of Supply ECG Findings
Significance
 Posterior (Basal) & inferior Tall R & ST

 Posterior MI
2/3rd of septum depression in V1
 90% AV node
 Right bundle branch HR < 60 bpm
 Bradycardia
 Posterior part of left
bundle brunch
PDA Occlusion Posterior MI
Tall R & ST segment
depression in V1
Right Ventricular Infarction Acute INFERIOR myocardial
infarction with associated Right
Ventricular infarction
Reciprocal ST depression I, aVL V4R  ST elevation
Leads II, III, aVF  ST elevation
9
“LOOKS”
at RV
Right sided chest leads are much more sensitive to the presence of Right
Ventricular infarction.
The most useful lead is lead V4R (an electrode is placed over the right 5th
intercostal space in the mid-clavicular line).
elevated  Lead V4R [ RV AMI ]
2015年4月23日
ST is
Left Anterior Descending (LAD) Artery
Occlusion
Clinical
Significance
ST elevation ±
 Anterior wall of left ventricle  Anterior MI
pathological Q
 Anterior 2/3rd of septum  Antero-septal MI
wave in V1-V6 ;
 Apex of LV
V1-V4
LAD Occlusion Anterior MI ST segment elevation in
V1-V6
Left Circumflex Artery (LCx)
Clinical
Significance
ST elevation ±
Lateral / high
Left lateral part of left venricle pathological Q
lateral MI
wave in LI, aVL
Posterior (Basal) & inferior
2/3rd of septum
Posterior MI Tall R & ST
(when PDA arise from LCx –
depression in V1
Dominant Left coronary
artery)
ST segment elevation in
LCx occlusion Lateral MI
L1, aVL
PDA Occlusion Posterior MI
Tall R & ST segment
depression in V1
???
Thank You
National ECG Workshop: 2015
Basic relevant Physiology
 Genesis of ECG waves
 Mechanism underlying configuration
of different wave forms: reasoning the
upward & downward deflections
Basics
• The cardiac impulse as it passes
through the heart, electrical
current spreads from the heart
into the adjacent tissues
• When electrodes are placed on the
skin on opposite sides of the heart,
electrical potentials generated by
the current can be recorded, the
recording- (electrocardiogram)
depicts summed up electrical
activity of the cardiac muscle
recorded extracellularly.
Generation & Transmission of Cardiac
impulse & ECG waves
Potentials on the surface of a
depolarizing cardiac muscle
Normal ECG in different
Lead Systems
Why ECG waves in each Lead have
different configuration ?
Factors that influence Configuration
of waves
• Sequence in which, the parts of the heart are

depolarized & the direction of the mean
depolarization (vector) with respect to the
position of the electrode
Flow of current in a partially
depolarized heart
Important Rules
A wave of depolarisation travelling

• towards a +ive electrode→ a +ive (upward)
• away from a +ive electrode → a –ive
(downward) deflection.
A wave of repolarisation travelling
• towards a +ve electrode → a –ve (downward)
deflection.
• away from a +ve electrode → a +ve (upward)
deflection in the ECG trace.
Depolarization in relation to the
recording lead
Important Rules ( Cont. )
• A wave of depolarisation or repolarisation travelling

perpendicular to an electrode axis results in a
biphasic deflection of equal positive and negative
voltages
• The instantaneous amplitude of the measured

potentials depends upon the orientation of the
positive electrode relative to the mean electrical
vector & is directly related to the mass of tissue
undergoing depolarisation or repolarisation.
Lead versus Electrode
• ECG lead system is an arrangement of the
electrodes fixed on the body surface by which
electrical activity of the heart is recorded
• e. g.
Lead I consists of circuit between two
electrodes one fixed on the left arm and the
other on the right arm.
The 12-Leads
3 Limb leads LEAD I

(I, II, III)
3 Augmented leads
(aVR, aVL, aVF)
6 Precordial leads LEAD II LEAD III
(V1- V6)
ECG Lead System
Classical lead systems used internationally
A Standard Bipolar limb Lead I, Lead II and Lead III.

leads
B Augmented unipolar limb aVR, aVL, aVF.
leads
C Unipolar Chest leads v1- v6

ECG Lead Systems,
ECG Analysis & Interpretation
• For details- Please Refer Handout

Thank You
Cardiac Biomarkers
Dr. Veena Bhaskar S Gowda

MBBS,MD (Biochemistry)
Old Classification of MI
No ECG Aspect Pathological Aspect
1 Q wave MI Full thickness/ Transmural MI
2 Non Q wave MI Subendocardial MI
Full thickness MI
New Classification
Acute Coronary Syndrome
No ST segment elevation ST segment elevation
Markers of myocardial Markers of Elevated markers of

necrosis not elevated
myocardial necrosis myocardial necrosis
elevated
Unstable ST segment elevation

angina Non ST segment myocardial infarction
elevation myocardial
ischemia
Old Vs New Classification
Cardiac Biomarkers ?
Certain proteins, called serum cardiac

biomarkers
Released from necrotic heart muscle

after MI
Detectable in blood
Different Cardiac Biomarkers
Cardiac Biomarkers for ACS
1. Myoglobin
2. Creatine kinase [CK-MB (mass)]
3. Cardiac troponin I (cTnI) and cardiac troponin T
(cTnT)
4. Lactate dehydrogenase (LDH)
5. Aspartate amino transferase (AST)
Future Cardiac Biomarkers

• Ischemia modified albumin
• Fatty acid binding protein
• CD40 ligand binding protein
• Myeloperoxidase (MPO)
Release of Cardiac Biomarkers after AMI
Release of Cardiac Biomarkers after AMI
Kinetics of Cardiac Biomarkers after AMI
Time to
Time to Initial Time to Peak
Biomarkers Return to
Elevation Elevation
Normal
Myoglobin 1-4 hours 8-10 hours 24 hours
CK/CK-MB 4-8 hours 18 hours 2-4 days
Troponins 4-6 hours 12-48 hours Up to 10 days
LDH 10-12 hours 48-72 hours 7-10 days

Selection of Markers
Biomarkers Timing Advantage Disadvantage
Myoglobin We never Earliest Very nonspecific
assay this appearance Disappear early
Cardiac 1st day of Can’t rule out old
Troponins Very specific
symptoms MI
CK-MB 1st day of
Very specific
symptoms
AST 2nd day of
symptoms
LDH 3rd day of
symptoms
Serial Sampling of Cardiac
Biomarkers
• When initial results are negative

• Serial sampling at presentation, 6–9 h later, and
after 12 h is recommended if the earlier results
are negative and clinical suspicion remains high
MARKERS IN AMI ASSESSMENT OF REPERFUSION
• “Washout” phenomenon
 Enzymes & proteins have direct vascular access when
occluded coronary circulation becomes patent
 Peak concentrations earlier & at higher levels if
reperfusion successful
Successful
reperfusion
Marker Level
Unsuccessful
reperfusion
Time
Approach to a Patient with ACS
Understanding the ELECTROCARDIOGRAM
– CHEST PAIN
– MYOCARDIAL INFARCTION
Dato’ Wira Prof Dr LR Chandran DGMK DSDK SDK BCK

MBBS(Monash) MRCP(UK) FRCP(Edin) FRCP (Lond) FRCP (Glasg)
Fellow of the Academy of Medicine of Malaysia [FAMM]
Alor Star
CHEST
PAIN

Alor Star
PQRST assessment for chest pain
•P- Precipitating events
•Q- Quality of pain
•R- Radiation of pain
•S- Severity of pain
•T- Timing
Basic ECG Slides

• Initially the BP and pulse may be elevated.
•Later, BP will drop due to decreased cardiac output.
• Urine output will decrease
• Lung sounds will change to crackles
• Jugular veins may become distended and have obvious
pulsations.
Basic ECG Slides

Within the first 10 minutes upon arrival to the
hospital
• Give 300mg aspirin to chew and swallow [ GTN bite & under
tongue – if systolic > 100mmHg ]
• Establish IV access
• Check vital signs and evaluate oxygen saturation
• Obtain and review 12-lead ECG
• Take a brief focused history and perform a physical exam
• Obtain blood samples to evaluate initial cardiac markers,
electrolytes and coagulation
hospital
hospital
hospital
• Give 300mg aspirin to chew and swallow [ GTN bite &
under tongue – if systolic > 100mmHg ]
hospital
hospital
NSTEMI
• ST segment depressions
• T wave changes
• No Q wave development
• Mild enzyme elevations
• No reciprocals

NSTEMI
• T wave changes
• No reciprocals

NSTEMI
• T wave changes
• No reciprocals

NSTEMI
• T wave changes
• No reciprocals

NSTEMI
• T wave changes
• No reciprocals

Basic ECG Slides

“Loss of R wave” = “Q” wave

“Loss of R wave”
= “Q” wave

Elevated “T” wave “ST” elevation Onset of “Q”wave
Basic ECG Slides

“T” wave inverts “ST” back to baseline “Q” remains
Basic ECG Slides
Phases of a STEMI
• Hyperacute Phase
– Occurs within the first few hours of MI onset.
– Leads facing the infarcted surface: ST segment elevation.
– Leads facing the uninjured surface: ST segment depression
(reciprocals)
– T waves become tall, widened and might be taller than the R
wave.

Phases of a STEMI
• Fully Evolved Phase

– Q wave development
– ST elevation
– T waves start to become inverted
in leads facing the injury.

Phases of a STEMI
• Resolution Phase
– Weeks after there will be
a gradual return of
ST segments to baseline.
– T waves will gradually return to normal but are the
last to change back.

SERUM
CARDIAC
MARKERS

Serum Cardiac Markers
Myocardial cells produce
certain proteins and enzymes
associated with cellular functions.
When cell death occurs,
these cellular enzymes are released
into the blood stream.
 CPK and Troponin
CPK
 Creatine Phosphokinase
 Begin to rise 3 to 12 hours after acute MI.
 Peak in 24 hours
 Return to normal in 2 to 3 days
Basic ECG Slides

Thursday, 23 April, 2015 Dato' Wira Dr L R Chandran 31
Troponin
 Myocardial muscle protein released into circulation after injury.
 These are highly specific indicators of MI.
 Troponin rises quickly like CK

but will continue to stay elevated for 2 weeks.
 Myoglobin- NO cardiac specificity.

Basic ECG Slides
Serum
Cardiac
Markers


National ECG Workshop AIMST MMA 2015

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Understanding the

Dato’ Wira Prof Dr LR Chandran DGMK DSDK SDK BCK

Thursday, 23 April 2015

Basic ECG Slides

Basic ECG Slides

Basic ECG Slides

Basic ECG Slides

Sequence of changes seen during evolution of myocardial infarction

Basic ECG Slides Dato' Wira

POSITIVE SIGN OF ISCHEMIA

1 SMALL SQUARE At least

Thursday, 23 April 2015 Dato' Wira Prof Dr L R Chandran Alor Star 26

Basic ECG Slides

Basic ECG Slides

loss of R wave height &

loss of R wave height &

Basic ECG Slides

Anterior myocardial infarction with gross ST segment elevation

Thursday, 23 April 2015 Dato' Wira Prof Dr L R Chandran Alor Star 36

Infero-Lateral myocardial infarction [ II, III, aVF & V5, V6 ST ELEVATION

ANTERIOR leads V1 –V4 cannot record from POSTERIOR leads – NO Reciprocal

Thursday, 23 April 2015 Dato' Wira Prof Dr L R Chandran 38

though its absence

widespread ST segment depression antero - lateral leads [ I, aVL, V5, V6 ] strongly

though its absence

widespread ST segment depression antero - lateral leads [ I, aVL, V5, V6 ] strongly

Thursday, 23 April 2015 42 Dato' Wira Prof Dr L R Chandran Alor Star

Dato' Wira Prof Dr L R Chandran Alor Star 43 Thursday, 23 April 2015

Basic ECG Slides

Thursday, 23 April, 2015 Basic ECG Slides 46

Basic ECG Slides

Basic ECG Slides

ST elevation in the anterior Leads V1 - 6, I and aVL

ST elevation in the anterior leads:

Basic ECG Slides 60

•reciprocal ST depression in the inferior

Basic ECG Slides 61

Basic ECG Slides 62

Peaked T waves  V2-V4

Basic ECG Slides 63

Reciprocal ST depression  III ,aVF ST elevation  V2-6, I , aVL

Basic ECG Slides 64

ST elevation  precordial & inferior leads Hyperacute T waves  V1-V3

Basic ECG Slides 65

INFERIOR WALL  lead II,III, aVF

ST elevation & Early Q wave II,III, aVF

ST Depression & T inversion  aVL

Basic ECG Slides 68

ST Depression & T inversion  aVL

Basic ECG Slides 69

Basic ECG Slides

Right ventricular infarction often missed,

 RV infarction associated with 40% of inferior infarctions.

 RV infarction associated with 40% of inferior infarctions.

Standard 12 lead ECG

 RARE for ST segment elevation in lead V1 to occur as an

Right sided chest leads are much

Reciprocal changes  lead I & aVL ST elevation in V1 RV infarction considered

ST elevation  lead II, III, aVF

Leads II, III, aVF  ST elevation + Biphasic T

Acute INFERIOR Dx of RV infarction  associated with hypotension.

ST is elevated  LeadsV4R, V5R, V6R [ RV AMI ]

ST is elevated  Lead II, III, aVF [ INFERIOR AMI ]