ALL ABOUT ECG

NIU H.M
ADCV(S)2/2016-2662
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
 Location of Myocardial Infarction
• Septal :V1, V2
• Anterior :V3, V4
• Anterior Septal : V1, V2, V3, V4
• Lateral : LI, aVL and V5, V6 (or both)
• Anterior Lateral : LI, aVL, and V3,V4,V5,V6
• Extensive Anterior : LI,aVL and V1-V6
• Inferior : LI, LII, aVF
• Posterior : in reciprocal lead V1, V2 or V7, V8
• Right Ventricular : LII, LIII, aVF, and V4R

25
26
27
28
• Caused by failure to discharge an impulse.
• This failure in the automaticity of the SA node
upsets the timing of the sinus node discharge
resulting in a pause on ECG which bears no
relationship to the predominant cycle length. 29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
 Premature Ventricular Contractions

• Rate -Variable
• P wave -Usually obscured by the QRS, PST or T wave of the PVC
• QRS - Wide > 0.12 seconds; morphology is bizarre with the ST
segment and the T wave opposite in polarity. May be multifocal
and exhibit different morphologies.
• Conduction - Impulse originates below the branching portion of
the Bundle of His; full compensatory pause is characteristic.
• Rhythm - Irregular. PVC's may occur in singles, couplets or
triplets; or in bigeminy, trigeminy or quadrigeminy. 45
46
47
48
49
50
51
52
Left Anterior Fascicular Block
Criteria for LAFB
• Left axis deviation
• Small Q waves with tall R
waves (= ‘qR complexes’) in
leads I and aVL
• Small R waves with deep S
waves (= ‘rS complexes’) in
leads II, III, aVF
• QRS duration normal or
slightly prolonged (80-110
ms)
• Prolonged R wave peak time
in aVL > 45 ms
• Increased QRS voltage in
the limb lead
53
Left Posterior Fascicular Block
Criteria for LPFB
• Right axis deviation
• rS complexes’in leads I & aVL
• qR complexes’ in leads II, III & aVF
• QRS duration normal or slightly
prolonged (80-110ms)
• Prolonged R wave peak time in aVF
• Increased QRS voltage in the limb
leads
• No evidence of right ventricular
hypertrophy
• No evidence of any other cause
for RA deviation
54
 Multifascicular Block
• Refers to conduction delay
in more than one of the
structural components of
the specialized conduction
system, that is ,the LBBB,
the left anterior and
posterior fascicles and
the RBBB.
• Conduction delay in any
two is called bifascicular
block , and delay in all
three fascicles is called
trifascicular block.
55
 Bifascicular Block
• Combination with RBBB
with either LAFB or LPFB
• Conduction to ventricles
via single remaining
fascicle.
• ECG show typical RBBB
plus either left of right
axis deviation
• RBBB & LAFB most
common
56
Trifascicular Block
• Refers presence of
conducting in all
three fascicles:
– RBB
– LAF
– LPF
• Can be incomplete or
complete depend
whether all three
have completely
failed or not.
57
Incomplete Trifascicular Block
Can be inferred from one or Criteria
two ECG pattern: • Bifascicular block + 1st degree
• Fixed block of two fascicles AV block (most common)
(i.e. bifascicular block) with
evidence of delayed • Bifascicular block + 2nd
conduction in the remaining degree AV block
fascicle(i.e. 1st or 2nd degre
e AV block).
• Fixed block of one fascicle • RBBB +
(i.e. RBBB) with intermittent alternating LAFB / LPFB
failure of the other two
fascicles (i.e.
alternating LAFB / LPFB).
58
 Complete Trifascicular Block
• Bifascicular
block + 3rd degree
AV block

• RBBB , LAD, Third

degree AV block

• Treatment of BBB
require a
pacemaker
59
60
Left Atrial Hypertrophy
• Consequence of atrial
overload

• Result of mitral valve

disease ( stenosis or
insufficiency ), aortic
valve disease, or
hypertension in
systemic circulation.

61
 Right Atrial Hypertrophy
• Consequence of
right atrial overload
• Result form
tricuspid valve
disease ( stenosis or
insufficiency ),
pulmonary valve
disease,pulmonary
hypertension.
• Large P wave( ≥ 0.25
mV ) is seen in lead
II and aVF.
62
Left Ventricular Hypertrophy

63
64
Right Ventricle Hypertrophy
• Right axis deviation.
• Dominant R wave in V1 (> 7mm tall or R/S
ratio > 1).
• Dominant S wave in V5 or V6 (> 7mm deep
or R/S ratio < 1).
• QRS duration < 120ms (i.e. changes not due
to RBBB).
• RA enlargement (P pulmonale).
• RV strain pattern = ST depression
• T wave inversion in the right precordial
(V1-4) inferior (II, III, aVF) leads.
• Deep S waves in the lateral leads (I, aVL,
V5-V6)
65
 Generalized Low Voltage
QRS is said to be low
voltage when :
• The amplitudes of all
the QRS complexes in
the limb leads are < 5
mm; or
• The amplitudes of all
the QRS complexes in
the precordial leads
are < 10 mm

66
Pulmonary Embolism
Criteria
• Sinus tachycardia
• RV strain pattern
• S1 QIII TIII pattern, with an S
wave in lead I and a new Q
wave in lead III with T wave
inversion in that lead (This
pattern, which may simulate
that produced by acute inferior
wall MI, is probably due to
acute right ventricular dilation)
• An incomplete or complete
right bundle branch block
(RBBB) pattern (wide rSR' in
lead V1 )
67
Pericarditis Criteria
• Widespread concave ST
elevation and PR depression
throughout most of the
limb leads (I, II, III, aVL, aVF)
and precordial leads (V2-6).
• Reciprocal ST depression
and PR elevation in lead aVR
(± V1).
• Sinus tachycardia is also
common in acute
pericarditis due to pain
and/or pericardial effusion. 68
 Pericarditis in 4 Stage

Pericarditis is classically associated with ECG changes that

evolve through four stages.
• Stage 1 – widespread STE and PR depression with
reciprocal changes in aVR (occurs during the first two
weeks)
• Stage 2 – normalization of ST changes; generalized T wave
flattening (1 to 3 weeks)
• Stage 3– Flattened T waves become inverted (3 to several
weeks)
• Stage 4 – ECG returns to normal (several weeks onwards)
69
 Drug Toxicity Digitalis
• Treat heart failure and
certain arrhythmias
• Shorten repolarization time
in the ventricles
• Shorten QT interval cause
ST segment and T wave
fused together
• Most common T wave
abnormality is biphasic T
Characteristic scooping of the ST-T
complex produced by digitalis wave with negative
deflection and terminal
positive deflection
70
71
 Antiarrhythmic
Drug Toxicity • E.g Quinidine, procanaimide,
• Prolong ventricular
repolarization therefore
prolong QT interval and flatten
the T wave.
• Cause fainting or event
sudden death due to torsade
de pointes type of VT
• This proarrhythmic effect is
most likely to occur with
prolonged QT intervals and/ or
prominent U waves.

72
73
74
75
76
77
78
79
80
81
82
83
84
/

85
86
87
88
89
90
91
92