ECG

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Ventri-
cular
depola-
rization

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Ventri-
cular
depola-
rization
(cont’d)

Heri Fadjari
Ventri-
cular
depola-
rization
(cont’d)

Heri Fadjari
Ventri-
cular
depola-
rization
(cont’d)

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Ventri-
cular
repola-
rization
- +
- +
+
- + - -
- + - -+
- + - +
-
- + - +
-
- + - +
- + - -
+
- + - -
+
+ +
- +
-
+

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Lead I

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Lead II

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Lead III

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Limb
Leads Lead I
(bipolar)

Lead II

Lead III

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aVR

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aVL

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aVF

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Uni- aVR
polar
Lead

aVL

aVF

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Normal Intrinsicoid
deflection
values < 0.05”
QT segment
Men < 0.39”
Wo < 0.40”

ST segment
Std: > 1mm
Pre : > 2mm
PR interval
0.12-0.20” U wave

P wave QRS duration T wave

0.8-0.11” 0.06-0.12”
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Pre-
cordial
leads

V6
V5
V1 V4
V2 V3

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Hori-
zontal
vs
Verti-
cal
heart

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Hori-
zontal
vs
Verti-
cal
heart

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Clock-
wise
vs
Counter
clock-
wise 4
2
rotation
3

Viewed from below the heart looking towards the apex in vertical hea

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P wave

V1

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Atrial
Enlarge
ment

Left atrial
enlargement
P mitral
Wide and notch

Biphasic with
(-) terminal
component
V1

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Atrial
Enlarge
ment
(cont’d)

Right atrial
enlargement
Tall and peaked
P wave

Tall and peaked

P wave

V1

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Elec-
trical
axis Σ qRS = +3

Lead I

Σ qRS = +1

aVF
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The
QRS
Bundle of His

LBB

Anterosuperior
division

Posteroinferior
division

RBB

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The QRS vectors:
1. Initial depolarization
QRS 2. Terminal depolarization
3. S-T segmen
4. Re-polarization

4
2
V6
1
3

V1

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Myo- Electrical forces are directed away from a injured area
cardial
A B C
injury

Normal Minimal Subendocard Transmural

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Myo- ST segment deviated towards the surface of injured tissue
cardial
A B C D
injury

Normal Minimal Subendocard Transmural Subepicard

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Myo- Zones of myocardial infarction:
cardial • Necrosis
infarction • Injury
• Ischaemia

4 3

2 1 4
2
2
1 1
3 3

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Myo- ECG parameters of myocardial infarction:
cardial • Necrosis
infarction • Injury
(cont’d) • Ischaemia

4
2
1 V6
3

V1

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Myo- Phases of myocardial infarction:
cardial
infarction • Hyperacute phase
(cont’d) - Slope elevation of the ST sement
- Tall widened T wave
- Increased ventr. activation time

• Fully evolved phase

- Pathological Q wave
- Coved, elevated ST segment
- Inverted symetrical T wave

• Old infarction
- Pathological Q wave
- ST segment and T wave return to normal

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AMI
The hyperacute phase
There are four main features of
early myocardial infarction (as per
Schamroth):
• increased VAT
• increased R wave amplitude (!)
• ST elevation which is sloped
upwards!
• Tall, widened T waves (The ST
segment
often merges with these)
Heri Fadjari Note that Q waves are not seen
early on.
The features of `full blown' MI
may be:
• prominent Q waves;
• elevated ST segments;
• Inverted `arrowhead' T waves.
Remember, that a significant
proportion of people having an
acute MI will have a normal
ECG, so do not rely on any of
these features to exclude MI.
Myo- Localization of infarcted areas
cardial
infarction
(cont’d)

2 I
1 aVL
3 V4
V1 V5
V2 V6
V3

II, III, aVF

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Right
ventri
cular
hyper
trophy
4
2
V6
1
3

V1

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RVH

A number of ECG abnormalities have been associated with RVH.

These include:
• Right axis deviation;
• Tall R wave (bigger than the S) in V1; R/S >1
• R wave in V1 >7mm
• An initial slur of the QRS, or a small r, or a tiny q;
• Increased VAT in V1
• left-sided RS or rS complexes in V6

Whenever you see a tall R in V1, consider the following

differential:
• posterior myocardial infarction
• Right bundle branch block
Heri Fadjari • Dextrocardia, Duchenne muscular dystrophy
• Incorrect lead placement!
RVH
Supporting ECG criteria
• ST segment depression and T wave inversion in leads V1 to V4
• Deep S waves in leads V5, V6, I, and aVL

Other causes of tall R wave in V1

• Posterior myocardial infarction
• Wolff-Parkinson-White syndrome
• Right bundle branch block
• Some normal children and young adults

Other causes of right axis deviation

• Left posterior hemiblock
• Lateral myocardial infarction
• Acute right heart strain
• Normal in infants and childr

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Left Diatolic overload
ventri
cular
hyper
trophy
4
2
V6
1
3

V1

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Left Systolic overload
ventri
cular
hyper
trophy
4
2
V6
1
3

V1

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LVH

The absence of LVH on ECG means nothing, as the features are

insensitive. Because the criteria were formulated on white
males. However, if they are present, LVH is very likely.
A criterias have been proposed. Useful are:
• The sum of the S in V1 and the R in V5 or V6 over 35mm
• R in I over 15mm
• R in AVL over 11mm

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LVH
Left ventricular hypertrophy Voltage criteria

Voltage criteria (less accurate among patients less than age

40)
• Limb leads
- R wave in lead 1 plus S wave in lead III >25 mm
- R wave in lead aVL >11 mm
- R wave in lead aVF >20 mm
- S wave in lead aVR >14 mm

• Precordial leads
- R wave in leads V4, V5, or V6 >26 mm
- R wave in leads V5 or 6 plus S wave in lead V1 >35
mm
- Largest R wave plus largest S wave in precordial
leads >45 mm

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LVH

Left ventricular hypertrophy non-voltage

criteria

• May be confused with ischemic changes

• Delayed ventricular activation time 0.05 s in
leads V5 or V6
• ST segment depression and T wave inversion
in
the left precordial leads

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LVH Scoring system – LVH if points are 5 or more

• More specific, less sensitive

Amplitude (any of the following) 3

• Largest R or S wave in limb leads 20 mm
• S wave in leads V1 or V2 30 mm
• R wave in leads V5 or V6 30 mm
• ST-T wave segment changes typical for LVH in
the
absence of digitalis 3
• Left atrial involvement 3
• Left axis deviation 2
• QRS duration of 0.09 s 1
• Delayed ventricular activation time in leads V5
and
V6 of 0.05 s 1

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RBBB

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RBBB
Diagnostic criteria for RBBB

• QRS 0.12 seconds or greater

• Secondary R’ in lead V1 or V2
• Wide, slurred S wave in leads I, V5 and V6
• Secondary inversion of T waves in right precordial leads

Causes of RBBB

• Rheumatic heart disease

• Right ventricular hypertrophy
• Myocardial disease
• Ischemic heart disease
• Degeneration of the conduction system
• Pulmonary embolism
• Atrial septal defects

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LBBB

1b

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LBBB
Diagnostic criteria for LBBB

• QRS duration 0.12 seconds or greater

• Broad, monophasic R waves in leads I, V5 and V6
• Absent Q waves in V5 and V6

Associated features for LBBB

• Displacement of ST segment and T wave
deflections opposite
to major QRS vector
• Poor R wave progression across precordium
• RS, rather than monophic R wave complex in V5
and V6
• Left axis deviation is common

Poor R wave progression:

• Hypertension
Heri Fadjari • Old anteroseptal wall infarction
• Cardiomyopathy
QT Prolonged QTc
interval • Hypocalcemia
•Acute rheumatic carditis

Shortened QTc
• Hypercalcemia
• Digitalis effect
• Hyperthermia
• Vagal stimulation

Normal QT does not exclude the diagnosis of

• Acute myocardial infarction
QT • Acute myocarditis of any causes
QTc= • Sympathetic stimulation
R-R • Procain effect

Heri Fadjari
Atrial Disturbances of impulse formation
Septal Sinus rhythms
Ectopic atrial rythms
• Atrial extrasystole
Activa- • Sinus arrythmia
• Sinus tachycardia
• PAT
• Atrial fibrilation
tion • Sinus bradycardia • Atrial flutter

AV nodal rythms
• AVn extrasystole
• Paroxysmal AVn tachycardia
• Idionodal tachycardia
Ventricular rhytms
• V-extrasystole
• V-tachycardia
• V-flutter
• V-fibrilation
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• Idioventricular tachycardia
Arrhyth Disturbances of impulse conduction
mias
A-V block
S-A block

Reciprocal rythms
WPW syndrome
(Wolf-Parkinson-White)
LGL syndrome
(Lawn-Ganong-Levin)

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Arrhyth 2nd disorders of rythms
mias
A-V dissociation
AVn escape
Atrial escape

Aberrant ventricular Ventricular

conduction escape

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Arrhyth
mias

There is normally a slight degree of chaotic variation in heart

rate, called sinus arrhythmia

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Arrhyth
mias

The ectopic beat usually discharges the SA node, so subsequent

beats of SA origin are not in synchrony with the previous sinus
rhythm.

If the extrasystole occurs early on, it may find the His-Purkinje

system not quite ready to receive an impulse, and a degree of
block may be seen. This is termed `aberration'.

Heri Fadjari
Arrhyth
mias

Irregular SVT

The commonest cause of irregular SVT is atrial fibrillation, where

the atrial rate is in the region of 200 to 400/min, and the atria
really do not contract rhythmically at all.

The conventional view of the pathogenesis of AF is that there are

multiple re-entrant `wavelets' moving through the atrial muscle,
but recent evidence suggests that much AF actually arises from
ectopic activity in the muscular cuff surrounding the pulmonary
veins where they enter the left atrium ("electrical remodelling“).

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Arrhyth
mias

Atrial tacycardia

Although it looks like atrial fibrillation, the above image

actually shows multifocal atrial tachycardia. Note how there
are at least three different P wave configurations!

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Arrhyth
mias

Atrial flutter

The atrial rate is commonly 300/min, and there is usually a 2:1

block, resulting in a ventricular response rate of 150/min. Other
ratios are possible, and sometimes the ratio varies. This rhythm
is often unstable, and the heart may flip in and out of sinus
rhythm, or there may be runs of atrial fibrillation.
In the above ECG the clue is the rate. A rate of 150 should
always engender the suspicion of atrial flutter with 2:1 block.
The commonest cause of regular SVT is AV nodal re-entrant
tachycardia

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Arrhyth
mias

Wolff-Parkinson-White pattern

WHO criteria for the WPW pattern on ECG are:

• PR interval under 0.12s
• A delta wave
• QRS duration of 0.12s (or more)
• A normal P-wave axis
The WPW syndrome is a combination of the WPW pattern, and
tachycardias

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Arrhyth
mias

Ventricular extrasystoles

Because these arise within an ectopic focus within the

ventricular muscle, the QRS complex is wide, bizarre, and
unrelated to a preceding P wave.

Rarely, the ventricular beat may be conducted retrogradely

and capture the atrium (resulting in a P wave after the QRS,
with an abnormal morphology as conduction through the atrium
is retrograde)
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Arrhyth
mias

Ventricular tachycardia

Three or more ventricular extrasystoles are a bad sign, and are

termed ventricular tachycardia (VT). There is usually severe
underlying myocardial disease.
Sustained VT (more than about 30 b.p.m) often degenerates
into ventricular fibrillation, resulting in death.
The atrial rate is different from the ventricular rate, and
there is dissociation between atria and ventricles  the P
waves occur at any time in relation to the QRS complexes.
There is also a capture beat later on, where the P wave has
managed to sneak through and transiently take over

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Arrhyth
mias

Ventricular flutter

Ventricular 'flutter' is a bizarre sine-wave like rhythm, and

usually degerates into ventricular fibrillation.
You won't see it often (or for long).

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Arrhyth
mias

Ventricular fibrillation

This is a chaotic ventricular rhythm that rapidly results in

death.
It is often precipitated by a critically timed extrasystole, that
occurs during the relative refractory period of the myocardial
fibres.

VF is a dire emergency. If unsynchronised DC countershock is

applied within 30s of the onset of VF, there is an approximately
97% chance that sinus rhythm will be restored, and the person
will survive. Survival decreases exponentially thereafter, with
every minute of delay.
Heri Fadjari
Arrhyth
mias

The P wave

Normal atrial activation is over in about 0.10s, starting in the

right atrium.
A good place to look at P waves is in II, where the P shouldn't be
more than 2.5mm tall, and 0.11 seconds in duration.
A tall P wave (3 blocks or more) signifies right atrial enlargement,
a widened bifid one, left atrial enlargement

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Arrhyth
mias

First degree block

Simply slowed conduction.

This is manifest by a prolonged PR interval

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Arrhyth
mias
Second degree AV block

Conduction intermittently fails completely.

This may be in a constant ratio (more ominous, Mobitz -
Type II second degree block), or progressive (The
Wenckebach phenomenon) characterised by progressively
increasing PR interval culminating in a dropped beat --- this
is otherwise known as Mobitz Type I second degree heart
block

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Arrhyth
mias

2:1 AV block
Cannot determine Mobitz type from rhythm,
alone. Usually due to Wenckebach
phenomenon
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Arrhyth
mias

Third degree block:

There is complete dissociation of atria and ventricles.

Clearly a bad thing, requiring temporary or even permanent
pacing.

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Arrhyth
mias

Sinus bradycardia

Pathologic causes of sinus bradycardia

• Acute myocardial infarction especially inferior
• Drugs like digoxin, beta-blockers and
amiodarone
• Increased intracranial pressure
• Obstructive jaundice
• Hypothermia
• Hypothyroidism
• Sick sinus syndrome

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Arrhyth
mias

Sinoatrial block

Pauses are a multiple of the PP interval

Sinus arrest

Prolonged absence of atrial activity

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Arrhyth
mias

Escape rhythms

Junctional – Narrow QRS with rate of 40 to 60 BPM

Ventricular – Wide QRS with rate of 15 to 40 BPM

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Arrhyth
mias

J point marks the junction between the end of the QRS

and the beginning of the ST segment
ST segment duration is measured from the j point to the
beginning of the T wave
The ST segment is normally isoelectric with respect to
the preceding PT segment.
ST segments may appear elevated in leads V1 through V3
because the transition between the end of the QRS and
beginning of the ST segment is so gradual as to prevent
identification of a j point
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T wave
Normal T wave size:
• 1/8 size of R wave
• < 2/3 size of R wave
• Height < 10 mm

Tall
Very tall, symmetrical, T waves can occur hyperacutely
during ischemia, infrction or hyperkalemia

Inverted
Deep, symmetrical, “arrowhead”, inversion highly
suggestive of ischemia

Biphasic
Biphasic T waves that progress to inversion strongly
suggest ischemia

Normal inversion
III, aVR, V1 (and sometimes V2)
T wave negativity in association with predominantly negative
QRS
Heri Fadjari
COPD

Hyperinflation & depressed diaphragms lead to long-axis,

clockwise rotation of the heart

Diagnostic ECG criterias:

• rS pattern of normal right precordial leads moves
across precordium
• “Poor R wave progression”
• Transition zone (rS to qR) moves to V5 or V6
• QRS voltage may be reduced
• RVH suggests cor pulmonale
• Atrial arrhythmias are common
• PACs, atrial fibrillation
• Multifocal atrial tachycardia

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Pulmo
nary
embo
lism

Small emboli may produce sinus tachycardia

Large emboli may produce acute RV
dilatation

S1, Q3, T3 pattern

S wave in I; Q wave in III; T wave
inversion in III

Occurs in about 12% of patients with

massive pulmonary embolism
Heri Fadjari
Pulmo
nary
embo
lism

Another ECG findings of pulmonary embolism

• Sinus tachycardia
• Atrial flutter or fibrillation
• Right bundle branch block (incomplete or complete)

Heri Fadjari
Pulmo
nary
embo
lism

• T wave inversion in the right precordial leads

• P pulmonale
• Right axis deviation
• Right heart “strain”
Heri Fadjari
Hyper
tension ECG is normal in about 50%
Minimal ECG changes are present in about 20%
Voltage changes precede non-voltage changes
Poor R wave progression is sometimes seen

Heri Fadjari
Cardio
Hypertrophic cardiomyopathy
myo - Left ventricular hypertrophy
pathy -
-
Left atrial abnormality
Abnormal Q wavers in inferior, anterior and/or
lateral leads [*]
- QRS mimics of pre-excitation or bundle branch block

Dilated cardiomyopathy [*]

- Left bundle branch block
- Left atrial abnormality
- Abnormal Q waves in leads V1 to V4
- Left ventricular hypertrophy (about one-third). May
be obscured
by concomitant right ventricular enlargement.
- Ventricular arrhythmias and atrial fibrillation

Restrictive cardiomyopathy
- Infiltrative diseases: amyloidosis [*], sarcoidosis,
and
hemochromatosis
- Low QRS voltage
Heri Fadjari - Conduction abnormalities
- Ventricular and supraventricular arrhythmias
Valvu
Findings in all conditions are inconsistent
lar
heart Severe aortic stenosis
- LVH in 75%
disease - Left atrial abnormality
- Left axis deviation
- Left bundle branch block

Aortic regurgitation
- Left ventricular hypertrophy
- Strain pattern common

Mitral stenosis
- Left atrial abnormality (or atrial fibrillation)
- Right ventricular hypertrophy

Mitral regurgitation
- Atrial fibrillation or left atrial abnormality
- Left ventricular hypertrophy

Heri Fadjari
ECG

Questions?

Heri Fadjari