WELCOME

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CLINICAL ECG
Presented by
Hemanth Das,
I MD Organon.
 ‘ECG’ stands for electrocardiogram,
or electrocardiograph. In some
countries, the abbreviation used is
‘EKG’. Electrocardiograph is a
sophisticated galvanometer, a
sensitive electromagnet, which can
detect & record changes in
electromagnetic potential.
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 The contraction of any muscle is
associated with electrical changes called
depolarization & these changes can be
detected by electrodes attached to the
surface of the body. Since all muscular
contractions will be detected, the
electrical changes associated with
contraction of the heart muscle will only
be clear if the patient is fully relaxed &
no skeletal muscles are contracting.
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 Although the heart has 4 chambers,
from the electrical point of view it
can be thought of as having only 2,
because the 2 atria contract together
& then the 2 ventricles contract
together.

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Electrical conduction of the Heart

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 Electrical conduction of the Heart
 Starts in the SA node.
 Depolarization then spreads through the atrial
muscle fibres.
 Delay while the depolarization spreads through
the AV node.
 Travels very rapidly down to the Bundle of His.
 Divides in the septum between the ventricles
into right & left bundle branches.
 Conduction spreads somewhat more slowly
through the Purkinje fibres.
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The Different Parts of The ECG

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 Times & Speeds
 ECG machines record changes in
electrical activity by drawing a trace on a
moving paper strip.
 Standard rate of 25 mm/s & use paper
with standard sized squares.
 Large square (5mm) represents 0.2
seconds, i.e. 200 ms.
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 There are 5 large squares /sec, &
300/min.
 So an ECG event, such as a QRS
complex, occurring once per large square
is occurring at a rate of 300/min.
 Heart rate= 1500÷ No. of small squares
between an R-R interval
OR
 Heart rate = 300÷ No. of large squares
between an R-R interval
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 The 12 lead ECG
 A lead is an electrical picture of the
heart.
 The electrical signal from the heart is

detected at the surface of the body

through electrodes, which are joined
to the ECG recorder by wires. 1
electrode is attached to each limb, &
6 to the front of the chest.
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 The ECG recorder compares the
electrical activity detected in the
different electrodes, & the electrical
picture so obtained is called a lead.
 The different comparisons ‘look at’

the heart from different directions.

 Each lead gives a different view of

the electrical activity of the heart, &

so a different ECG pattern.
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 The ECG is made up of 12
characteristic views of the heart, 6
obtained from the limb leads & 6
from the chest leads.

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 The standard limb leads
Lead Negative Positive
electrode electrode
I Right arm Left arm

II Right arm Left foot

III Left arm Left foot

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Augmented Unipolar limb leads
Lead Positive Negative
electrode electrode
aVR Right arm 0

aVL Left arm 0

aVF Left foot 0

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 Chest leads
V1 4th intercostal space immediately to the
right of the sternum
V2 4th intercostal space immediately to the left
of the sternum
V4 5th intercostals space in the midclavicular
line
V3 Midway between V2 & V4

V5 Same horizontal level as V4 but on anterior

axillary line
V6 Same horizontal level as V5 & V6 but on
midaxillary line
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 Frontal plane leads
 Leads I, II & VL look at the left lateral
surface of the heart, leads III & VF at
the inferior surface, & lead VR looks at
the right atrium.

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 Horizontal plane leads
 The Chest leads look at the heart in a
horizontal plane, from the front & left
side.
 V1 & V2 look at the right ventricle
 V3 & V4 look at the septum between the
ventricles & the anterior wall of the left
ventricle
 V5 & V6 look at the anterior lateral walls
of the left ventricle
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 The cardiac rhythm is identified from
whichever lead shows P wave most
clearly – usually lead II. When a
single lead is recorded simply to
show the rhythm, it is called a
‘rhythm strip’, but it’s important not
to make any diagnosis from a single
lead, other than identifying the
cardiac rhythm.
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Cardiac Axis

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 Leads VR & II look at the heart from
opposite directions. Seen from the
front, the depolarization wave
normally spreads through the
ventricles from 11 o’ clock to 5 o’
clock, so the deflections in lead VR
& normally mainly downward
(negative) & in lead II mainly
upward (positive).
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 The average spread of the
depolarization wave through the
ventricles as seen from the front
is called the cardiac axis. It is
useful to decide whether this axis
is in a normal direction or not.
This can be derived most easily
from the QRS complex in leads I,
II & III. www.similima.com 24
 When the cardiac axis is within
normal limits, there will be a
predominantly upward
deflection in leads I, II & III;
the deflection will be greater in
lead II than in I or III.

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 Right axis deviation
 If the right ventricle becomes
hypertrophied, it will have more effect on
the QRS complex than the left ventricle,
& the average depolarization wave- the
axis- will swing towards the right. The
deflection in lead I becomes negative
because depolarization is swinging away
from it, & the deflection in lead III
becomes positive because depolarization
is spreading towards it. This is called
Right axis deviation.
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 Causes of Right Axis Deviation
 Right ventricular dominance due to acquired
heart disease (Pulmonary embolism, c/c Cor
pulmonale) & congenital heart disease
mainly TOF.
 Anterolateral Myocardial Infarction
 WPW syndrome
 Left posterior hemiblock: When conduction
is interrupted or delayed in the
posteroinferior division of the left bundle
branch, it is termed left posterior hemiblock.
 Right ventricularwww.similima.com
hypertrophy. 27
 Left axis deviation
 When the left ventricle becomes
hypertrophied, it exerts more influence on
the QRS complex than the right ventricle.
Hence the axis may swing to the left, &
the QRS complex becomes
predominantly negative in lead III. Left
axis deviation is not significant until the
QRS deflection is also predominantly
negative in lead II.
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 Causes of Left Axis Deviation
 Inferior wall Myocardial Infarction.
 Left Anterior Hemiblock: When conduction
is interrupted or delayed in the
anterosuperior division of the left bundle
branch, it is termed Left anterior hemiblock.
 Ventricular tachycardia from a focus in the
apex of the left ventricle.
 Emphysema.
 WPW syndrome.
 Left ventricular hypertrophy
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 The cardiac axis is sometimes
measured in degrees though this
is not clinically useful. Lead I is
taken as looking at the heart from
0 degree; lead II from +60 deg.;
lead from +90 deg.; lead III from
+120 deg. Leads VL & VR look
from -30 & -150 degrees
respectively.
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 The normal cardiac axis is in the
range -30 deg. to +90 deg

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 If in lead II the S wave is greater than R
wave, the axis must be more than 90 deg
away from lead II. In other words, it must
be at a greater angle than -30 deg, &
closer to the vertical, & left axis deviation
is present. Similarly, if the size of the R
wave equals that of the S wave in lead I,
the axis is at right angles to lead I or at
+90 deg. This is the limit of normality
towards the right. If the S wave is greater
than the R wave in lead I, the axis is at an
angle of greater than +90 deg, & right
axis deviation is present.
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 QRS Complexes in chest leads
 Leads V1 & V2 look at the right
ventricle; leads V3 & V4 look at
the septum; & leads V5 & V6 at
the left ventricle.

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 In a right ventricular lead the deflection is
first upwards(R wave) as the septum is
depolarized. In a left ventricular lead the
opposite pattern is seen: there is a small
downward deflection (septal Q wave). In
a right ventricular lead there is then a
downward deflection (S wave) as the
main muscle mass is depolarized. When
the whole of the myocardium is
depolarized the ECG trace returns to base
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 The QRS complex in the chest leads
shows a progression from V1, where it is
predominantly downward, to V6, where it
is predominantly upward. The transition
point, where the R & S waves are equal,
indicates the position of the
interventricular septum. If the right
ventricle is enlarged, & occupies more of
the precordium than is normal, the
transition point will move from its normal
position of leads V3/V4 to V4/V5 or
sometimes V5/V6.www.similima.com 36
QRS is narrow[normal]

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Wide QRS

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Factors affecting the quality of ECG
 Poor electrode contact.
 Electrical interference.

 Over-calibration & under-calibration

 Altered paper speed.

 An unrelaxed & uncomfortable

subject.

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 A Normal ECG Report
 Rate
 Rhythm
 Conduction intervals
 Cardiac axis
 A description of the QRS complexes
 A description of the ST segments & T
waves
 Presence of U waves, if any.
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Normal ECG

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 Abnormalities of P waves

 P waves are best read in lead II &

V1. Normally P waves have duration
of 0.12 sec (3 small squares) & a
height of 2 mm.

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 Abnormalities of P waves
 Peaked P waves: They have an
amplitude greater than 2.5 mm & usually
indicate right atrial hypertrophy. Its
reflected by tall & peaked P waves in II,
III & aVF & is also called P pulmonale.
 Broad & notched P waves: Here the P
waves have duration greater than 0.12 sec
& appears notched (camel humped). They
usually indicate left atrial enlargement &
is also called P mitrale.
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 Absent P waves: P waves are
usually absent in the following
conditions:
 Junctional extrasystole
 Ventricular extrasystole
 Junctional tachycardia
 Supraventricular tachycardia
 Ventricular tachycardia
 Atrial fibrillation
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Ventricular Hypertrophy

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 Left Ventricular Hypertrophy
(LVH)
 General criteria to assess LVH are:
1. If the sum of the amplitude of S
wave in V1 & that of R wave in V6
exceeds 35 mm.
2. If R wave in V6 is taller than R
wave in V5.
3. Left axis deviation.
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 LVH

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 Right Ventricular Hypertrophy
(RVH)
 General criteria to assess RVH are:
1. Right axis deviation
2. Dominant R waves in right oriented leads namely,
aVR, V1 & V2.
3. RS or rS complexes in left oriented leads namely, I,
aVL, V5 & V6.
4. T wave inversion in the right oriented precordial
leads namely V1 to V4 & is most marked in V1 &
V2 & diminishes progressively in amplitude to
right, with associated minimal ST segment
depression with slightly upward convexity.
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 RVH

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Conduction Problems

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 First Degree Block

 One P wave per QRS complex.

 PR interval greater than 200 ms or

0.2 sec (1 large square)

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 Second Degree Block
 Mobitz type 2: PR interval of the
conducted beats is constant. One
P wave is not followed by a QRS
complex.

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Mobitz type II

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 Second Degree Block
 Wenckebach type: Progressive
lengthening of PR interval. One
non conducted P wave. Next
conducted beat has a shorter PR
interval than the preceding
conducted beat.
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Wenckebach type

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Wenckebach

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 Second Degree Block

 2:1 (or 3:1) block: 2 (or 3) P

waves per QRS complex, with
normal P wave rate.

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Third Degree (Complete) Block
 No relationship between P waves &
QRS complexes.
 Usually, wide QRS complexes.

 Usual QRS complex rate less than

50/min.
 Sometimes narrow QRS complexes,

rate 50-60/min.
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Third Degree (Complete) Block

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 Right Bundle Branch Block
 QRS duration > 120 ms (3 small
squares).
 RSR1 pattern.

 Usually dominant R1 wave in V1.

 Inverted T waves in V1, &

sometimes in V2-V3.
 Deep & wide S waves in V6.

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RBBB

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 Left Anterior Hemiblock

 Marked left axis deviation- deep S

waves in II & III, usually with a
slightly wide QRS complex.

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Left Bundle Branch Block
 QRS complex duration > 120 ms.
 M pattern in V6, & sometimes in V4-

V5.
 No septal Q waves.

 Inverted T waves in I, VL, V5-V6 &

sometimes, V4.
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LBBB

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 Bifascicular Block

 Left anterior hemiblock & RBBB

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Bifascicular block

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 Abnormalities of T wave

T wave inversion:
 Ischaemia
 Ventricular hypertrophy
 Bundle Branch Block
 Digoxin treatment
 Normally in aVR & V1.

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 Abnormalities of T wave
 T wave flattening: A low potassium
level causes T wave flattening & the
appearance of a hump on the end of the
T wave called a U wave.
 Peaked T waves: A high potassium
levels causes peaked T waves with the
disappearance of ST segment. QRS
complex may be widened.
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 Abnormalities of QT interval

 Normal QT interval is 450 ms

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 Abnormalities of QT interval
Prolonged QT interval: It is due to,
 Sleep
 Hypocalcemia

 a/c Myocarditis

 a/c MI

 Hypothermia

 Hypertrophic cardiomyopathy

 Complete AV block

 Cerebral injury
 Drugs- quinidine, Tricyclc antidepressants
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 Abnormalities of QT interval
 Shortened QT interval:
1. Digitalis
2. Hypercalcemia
3. Hyperthermia
4. Vagal stimulation
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 Infarction
 Accurate ECG interpretation in a patient with chest
pain is critical. Basically, there can be three types of
problems - ischemia is a relative lack of blood supply
(not yet an infarct), injury is acute damage occurring
right now, and finally, infarct is an area of dead
myocardium. It is important to realize that certain
leads represent certain areas of the left ventricle; by
noting which leads are involved, you can localize the
process. The prognosis often varies depending on
which area of the left ventricle is involved (i.e.
anterior wall myocardial infarct generally has a worse
prognosis than an inferior wall infarct).
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Ischemia Represented by symmetrical T wave
inversion (upside down) & ST
depression.

Injury Acute damage - look for elevated ST

segments. (Pericarditis and cardiac
aneurysm can also cause ST elevation;
remember to correlate it with the patient
Infarct Look for significant "patholgic" Q
waves. To be significant, a Q wave must
be at least one small box wide or one-
third the entire QRS height.
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 V1-V2 Anteroseptal wall

V3-V4 Anterior wall

V5-V6 Anterolateral wall

II, III, aVF Inferior wall

I, aVL Lateral wall

V1-V2 Posterior wall

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ST depression

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Inferior wall MI

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Anterolateral wall MI

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THANK
YOU
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