2. • A recording of the electrical activity of the heart
over time
• Gold standard for diagnosis of cardiac
arrhythmias
• Helps detect electrolyte disturbances (hyper- &
hypokalemia)
• Allows for detection of conduction abnormalities
• Screening tool for ischemic heart disease during
stress tests
• Helpful with non-cardiac diseases (e.g. pulmonary
embolism or hypothermia )
3. Leads used:
• Limb leads are I, II, II. So called because at one
time subjects had to literally place arms and legs in
buckets of salt water.
• Each of the leads are bipolar; i.e., it requires two
sensors on the skin to make a lead.
• If one connects a line between two sensors, one
has a vector.
• There will be a positive end at one electrode and
negative at the other.
• The positioning for leads I, II, and III were first
given by Einthoven, form the basis of Einthoven’s
triangle
4. Correct Lead placement and good contact
Proper earth connection, avoid other gadgets
Deep inspiration record of L3, aVF
Compare serial ECGs if available
Relate the changes to Age, Sex, Clinical history
Consider the co-morbidities that may effect
ECG
Make a xerox copy of the record for future use
Interpret systematically to avoid errors
5. Bipolar leads record
voltage between
electrodes placed on
wrists & legs (right
leg is ground)
Lead I records
between right arm &
left arm
Lead II: right arm &
left leg
Lead III: left arm &
left leg
7. ECG Bipolar Limb Leads
Standard ECG is recorded in 12 leads
Six Limb leads – L1, L2, L3, aVR, aVL, aVF
Six Chest Leads – V1 V2 V3 V4 V5 and V6
L1, L2 and L3 are called bipolar leads
L1 between LA and RA
L2 between LF and RA
L3 between LF and LA
7
9. Precardial (chest) Lead Position
V1 Fourth ICS, right sternal border
V2 Fourth ICS, left sternal border
V3 Equidistant between V2 and V4
V4 Fifth ICS, left Mid clavicular Line
V5 Fifth ICS Left anterior axillary line
V6 Fifth ICS Left mid axillary line
9
13. ECG Complex
3 distinct waves are
produced during cardiac
cyc3 distinct waves are
produced during cardiac
cycle
P wave caused by atrial
depolarization
QRS complex caused by
ventricular
depolarization
T wave results from
ventricular repolarization
le
14. SA node -> atrial muscle -> AV node -> bundle
of His -> Left and Right Bundle Branches ->
Ventricular muscle
15. ECG Complex
Elements of the ECG:
• P wave: Depolarization of both atria;
• Relationship between P and QRS helps distinguish various cardiac
arrhythmias
• Shape and duration of P may indicate Atrial enlargement
• PR interval: from onset of P wave to onset of QRS
• Normal duration = 0.12-2.0 sec (120-200 ms) (3-4 horizontal boxes)
• Represents atria to ventricular conduction time (through His bundle)
• Prolonged PR interval may indicate a 1st degree heart block
• QRS complex: Ventricular depolarization
• Larger than P wave because of greater muscle mass of ventricles
• Normal duration = 0.08-0.12 seconds
• Its duration, amplitude, and morphology are useful in diagnosing cardiac
arrhythmias, ventricular hypertrophy, MI, electrolyte derangement, etc.
• Q wave greater than 1/3 the height of the R wave, greater than 0.04 sec
16. ECG Complex
ST segment:
• Connects the QRS complex and T wave
• Duration of 0.08-0.12 sec (80-120 msec
T wave:
• Represents Repolarization or recovery of ventricles
• Interval from beginning of QRS to apex of T is
referred to as the absolute refractory period
QT Interval:
• Measured from beginning of QRS to the end of the
T wave
• Normal QT is usually about 0.40 sec
• QT interval varies based on heart rate
17. 17
ECG Graph Paper
X-Axis represents time - Scale X-Axis – 1 mm = 0.04 sec
Y-Axis represents voltage - Scale Y-Axis – 1 mm = 0.1 mV
Runs at a paper speed of 25mm/sec
One big square on X-Axis = 0.2 sec (big box)
Two big squares on Y-Axis = 1 milli volt (mV)
Each small square is 0.04 sec (1 mm in size at a speed of
25mm/sec)
Each big square on the ECG represents 5 small squares
= 0.04 x 5 = 0.2 seconds
5 such big squares = 0.2 x 5 = 1sec = 25 mm
One second is 25 mm or 5 big squares
One minute is 5 x 60 = 300 big squares
17
19. No. of Big R – R Interval Rate Rate T
Boxes Cal. A
C
One 0.2 sec 60 0.2 300 H
Y
Two 0.4 sec 60 0.4 150
N
Three 0.6 sec 60 0.6 100 O
R
Four 0.8 sec 60 0.8 75 M
A
Five 1.0 sec 60 1.0 60 L
B
Six 1.2 sec 60 1.2 50 R
A
Seven 1.4 sec 60 1.4 43 D
Y
Eight 1.6 sec 60 1.6 37 19
21. To find out the heart rate we need to know
The R-R interval in terms of # of big squares
If the R-R intervals are constant
In this ECG the R-R intervals are constant
R-R are approximately 3 big squares apart
So the heart rate is 300 3 = 100
21
23. To find out the heart rate we need to know
The R-R interval in terms of # of big
squares
If the R-R intervals are constant
In this ECG the R-R intervals are constant
R-R are approximately 4.5 big squares apart
So the heart rate is 300 4.5 = 67
23
25. To find out the heart rate we need to know
The R-R interval in terms of # of Big
Squares
If the R-R intervals are constant
In this ECG the R-R intervals are not
constant
R-R are varying from 2 boxes to 3 boxes
It is an irregular rhythm – Sinus arrhythmia
Heart rate is 300 2 to 3 = 150 to 100
approx
25
27. The QRS electrical (vector) axis can have 4
directions
Normal Axis - when it is downward and to the
left – southeast quadrant – from -30 to +90
degrees
Right Axis – when it is downward and to the
right – southwest quadrant – from +90 to 180
degrees
Left Axis – when it is upward and to the left –
Northeast quadrant –from -30 to -90 degrees
Indeterminate Axis – when it is upward & to the
right – Northwest quadrant – from -90 to +180
27
28. 28
ALL UPRIGHT MEET LEAVE
NORMAL RIGHT
LEFT
28
29. Axis LI LIII aVF TIP
Normal Positive Positive Both Up
Right Negative Positive Meet
Left Positive Negative Leave
Indeterminae Negative Positive Meet
29
30. 30
What is the Axis ?
LEAD 1
aVR
LEAD 2 aVL
LEAD 3 aVF
30
31. Note the QRS voltages are positive
and upright in the leads - L1, L2, L3
and aVF
L2, L3 and aVF tell that it is
downward
L1, aVL tell that it is to the left
Downward and leftward is Normal
Axis
Normal QRS axis
31
32. 32
What is the Axis ?
LEAD 1 aVR
LEAD 2 aVL
LEAD 3 aVF
32
33. Note the QRS voltages are positive and upright
in leads L1and aVL
Negative in L2, L3 and aVF
L1, aVL tell that it is leftward
L2, L3, and aVF tell that it is not down ward -
instead it is upward
Upward and Leftward is Left Axis
See the Left - Leave criterion QRS in L1 and L3
leave each other
Left Axis Deviation - LAD
33
35. Standardization – 10 mm (2 boxes) = 1 mV
Double and half standardization if required
Sinus Rhythm – Each P followed by QRS, R-R
constant
P waves – always examine for in L2, V1, L1
QRS positive in L1, L2, L3, aVF and aVL. – Neg in
aVR
QRS is < 0.08 narrow, Q in V5, V6 < 0.04, < 3 mm
R wave progression from V1 to V6, QT interval < 0.4
Axis normal – L1, L3, and aVF all will be positive
ST Isoelectric, T waves ↑, Normal T↓ in aVR,V1, V2
35
37. This is the ECG of a 6 year old child
Heart rate is 100 – Normal for the age
See V1 + V5 R >> 35 – Not LVH –
Normal
T↓ in V1, V2, V3 – Normal in child
Base line disturbances in V5, V6 –
due to movement by child
37
39. 39
Normal Resting ECG – cannot exclude disease
Ischemia may be covert – supply / demand
equation
Changes of MI take some time to develop in ECG
Mild Ventricular hypertrophy - not detectable in
ECG
Some of the ECG abnormalities are non specific
Single ECG cannot give progress – Need serial ECGs
ECG changes not always correlate with Angio
results
Paroxysmal events will be missed in single ECG
39
40. May have slight left axis due to rotation of heart
May have high voltage QRS – simulating LVH
Mild slurring of QRS but duration < 0.09
J point depression, early repolarization
T inversions in V2, V3 and V4 – Juvenile T ↓
Similarly in women also T↓
Low voltages in obese women and men
Non cardiac causes of ECG changes may occur
40
42. This ECG has all normal features
The ST-T (J) Junction point is
elevated. T waves are tall, May be inverted in LIII, The ST
segment initial portion is concave. This does not signify
Ischemia 42
43. 43
T↓
Before
Chest pain
T↑
During
Chest pain
T↓
Chest pain
Relieved
43
47. Always examine V 1 and Lead 1 for LAE
Biphasic P Waves, Prolonged P waves
P wave 0.16 sec, ↑ Downward component
Systemic Hypertension, MS and or MR
Aortic Stenosis and Regurgitation
Left ventricular hypertrophy with dysfunction
Atrial Septal Defect with R to L shunt
47
50. Always examine Lead 2 for RAE
Tall Peaked P Waves, Arrow head P
waves
Amplitude is 4 mm ( 0.4 mV) - abnormal
Pulmonary Hypertension, Mitral Stenosis
Tricuspid Stenosis, Regurgitation
Pulmonary Valvular Stenosis
Pulmonary Embolism
Atrial Septal Defect with L to R shunt
50
51. 51
Ventricular Muscle
Hypertrophy
QRS voltages in V1 and
V6, L 1 and aVL
We may have to record to
½ standardization
T wave changes opposite
to QRS direction
Associated Axis shifts
Associated Atrial
hypertrophy
51
53. Tall R in V1 with R >> S, or R/S ratio > 1
Deep S waves in V4, V5 and V6
The DD is RVH, Posterior MI, Anti-clock wise
rotation of Heart
Associated Right Axis Deviation, RAE
Deep T inversions in V1, V2 and V3
Absence of Inferior MI
53
55. Criteria and Causes of RVH
Criteria of RVH
Tall R in V1 with R >> S, or R/S ratio > 1
Deep S waves in V4, V5 and V6
The DD is RVH, Posterior MI, Rotation
Associated Right Axis Deviation, RAE
Deep T inversion in V1, V2 and V3
Cause of RVH
Long standing Mitral Stenosis
Pulmonary Hypertension of any cause
VSD or ASD with initial L to R shunt
Congenital heart with RV over load
Tricuspid regurgitation, Pulmonary stenosis 55
57. Classical changes seen are
Right ventricular hypertrophy
Right axis deviation
Right Bundle Branch Block
P – Pulmonale - Right Atrial enlargement
P – Mitrale – Left Atrial enlargement
If Atrial Fibrillation develops – „P‟
disappears
57
59. High QRS voltages in limb leads
R in Lead I + S in Lead III > 25 mm
S in V1 + R in V5 > 35 mm
R in aVL > 11 mm or S V3 + R aVL > 24 , >
20
Deep symmetric T inversion in V4, V5 & V6
QRS duration > 0.09 sec
Associated Left Axis Deviation, LAE
Cornell Voltage criteria, Estes point scoring
59
61. Causes and Criteria of LVH
Causes of LVH
Pressure overload - Systemic Hypertension, Aortic Stenosis
Volume overload - AR or MR - dilated cardiomyopathy
VSD - cause both right & left ventricular volume overload
Hypertrophic cardiomyopathy – No pressure or volume
overload
Criteria of LVH
High QRS voltages in limb leads
R in Lead I + S in Lead III > 25 mm or S in V1 + R in V5 > 35
mm
R in aVL > 11 mm or S V3 + R aVL > 24 , > 20
Deep symmetric T inversion in V4, V5 & V6
QRS duration > 0.09 sec, Associated Left Axis Deviation, LAE
61
63. Atrial Ectopics
Note the premature (ectopic) beats
marked as
APC (Atrial Premature Contractions)
These occurred before the next expected
QRS complex (premature)
Each APC has a P wave preceding the
QRS of that beat – So impulse has
originated in the atria
The QRS duration is normal < 0.08, not
wide
63
66. Complete LBBB has a QRS duration > 0.12 sec
Prominent S waves in lead V1, R in L I, aVL, V6
Usually broad, Bizarre R waves are seen, M
pattern
Poor R progression from V1 to V3 is common.
The "normal" ST-T waves in LBBB should be
oriented opposite to the direction of the QRS
Incomplete LBBB looks like LBBB but QRS
duration is 0.10 to 0.12 sec, with less ST-T change.
This is often a progression of LVH changes.
68
68. Heart has four surfaces
Anterior surface – LAD, Left Circumflex (LCx)
Left lateral surface – LCx, partly LAD
Inferior surface – RCA, LAD terminal portion
Posterior surface – RCA, LCx branches
Rt. and Lt. coronary arteries arise from aorta
They are 2.5 mm at origin, 0.5 mm at the end
Coronary arteries fill during diastole
Flow - epicardium to endocardium –
poverty/plenty
70
69. 71
1. Ischemia produces ST
Myocardial segment depression with
Ischemia or without T inversion
2. Injury causes ST segment
elevation with or without
Myocardial loss of R wave voltage
Injury 3. Infarction causes deep Q
waves with loss of R
Myocardial wave voltage.
Infarction
71
73. Non ST ↑ MI or NSTEMI, Non Q MI
Or also called sub-endocardial Infarction
Non transmural, restricted to the sub-
endocardial region - there will be no ST ↑
or Q waves
ST depressions in anterio-lateral &
inferior leads
Prolonged chest pain, autonomic
symptoms like nausea, vomiting,
diaphoresis
Persistent ST-segment ↓even after
resolution of pain
75
75. STEMI and QWMI
ST ↑ signifies severe transmural myocardial
injury – This is early stage before death of the
muscle tissue – the infarction
Q waves signify muscle death – They appear late
in the sequence of MI and remain for a long time
Presence of either is an indication for
thrombolysis
77
76. 78
A – Normal ST segment and T
waves
B – ST mild ↑ and prominent T
waves
C – Marked ST ↑ + merging
upright T
D – ST elevation reduced, T↓,Q
starts
E – Deep Q waves, ST segment
returning to baseline, T wave
is inverted
F – ST became normal, T Upright,
Only Q+ 78
81. Note the hyper acute elevation of ST
The R wave is continuing with ST and the
complexes are looking rectangular
Some times tall and peaked T waves in the
precardial leads may be the only evidence
of impending infarct
Sudden appearance LBBB indicates MI
MI in Dextro-cardia – right sided leads are
to be recorded
83
82. Note the hyper acute elevation of ST
The R wave is continuing with ST and the
complexes are looking rectangular
Some times tall and peaked T waves in the
precardial leads may be the only evidence
of impending infarct
Sudden appearance LBBB indicates MI
MI in Dextro-cardia – right sided leads are
to be recorded
84
84. Note the marked ST elevations in
chest leads V2 to V5 and also ST↑ in
L1 & aVL
T inversions have not appeared as yet
R wave voltages have dropped
markedly in V3, V4, V5 and V6
Small R in L1 and aVL.
86
87. Due to occlusion of the distal Left
circumflex artery or posterior
descending or distal right coronary
artery
Mirror image changes or reciprocal
changes in the anterior precardial leads
Lead V1 shows unusually tall R wave (it
is the mirror image of deep Q)
V1 R/S > 1, Differential Diagnosis -
RVH
89
102. In common
Representation in culture:
• In TV medical dramas, an isoelectric ECG (no cardiac electrical
activity, aka, flatline, is used as a symbol of death or extreme
medical peril.
• Technically, this is known as asystole, a form of cardiac arrest,
with a partcularly bad prognosis.
• Defibrillation, which can be used to correct arrythmias such as
ventricular fibrillation and pulseless ventricular tachycardia,
cannot correct asystole.
103. To summarize:
1. Calculate RATE
2. Determine RHYTHM
3. Determine QRS AXIS
4. Calculate INTERVALS
5. Assess for HYPERTROPHY
6. Look for evidence of INFARCTION
