The document provides a comprehensive overview of electrocardiogram (ECG) interpretation, detailing its history, the recording process, and the significance of various waveforms and intervals. It covers standard ECG leads, normal and abnormal wave characteristics, and practical tools for determining heart rate and rhythm patterns. Additionally, the document emphasizes the importance of accurate interpretation in identifying cardiac conditions such as hypertrophy and arrhythmias.

1. Maj Neamatullah Ahmed, PBGMS , MBBS, MPH
Electrocardiogram & It’s Interpretetion

2. OUTLINE
 HISTORY
 INTRODUCTION
 ECG LEADS AND RECORDING
 ECG WAVE FORMS AND INTERVALS
 ECG INTERPRETATION
 ARTIFACTS IN ECG
 NORMAL VARIANTS IN ECG

3. History
 1895 - William Einthoven , credited for the invention
of ECG.
 1924 - the noble prize for physiology or medicine is
given to William Einthoven for his work on ECG.
 1942- Goldberger increased Unipolar lead voltage by
50% and made Augmented leads

5. MODERN ECG INSTRUMENT

6. Introduction
 Ecg is defined as graphic recording of electric
potentials generated by the heart.
 Electric currents that spread through the heart are
produced by three components:cardiac pacemaker
cells,specialized conduction tissue & heart muscle
itself.
 Ecg however records only the depolarisation &
repolarisation potentials generated by the atrial &
ventricular myocardium.

7. Recording of ECG
ECG graphs:
– 1 mm squares
– 5 mm squares
Paper Speed:
– 25 mm/sec standard
Voltage Calibration:
– 10 mm/mV standard

8. ECG Paper: Dimensions
5 mm
1 mm
0.1 mV
0.04 sec
0.2 sec
Time
Voltage

9. 9
 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
 aVR, aVL, aVF are called unipolar leads
 aVR – from Right Arm Positive
 aVL – from Left Arm Positive
 aVF – from Left Foot Positive
ECG Unipolar Limb Leads

10. ECG Leads
Leads are electrodes which measure the difference in
electrical potential between either:
1. Two different points on the body (bipolar leads)
2. One point on the body and a virtual reference
point with zero electrical potential, located in
the center of the heart (unipolar leads)

11. ECG Leads
The standard ECG has 12 leads: 3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads
The limb leads record potentials transmitted on to the frontal
plane & chest leads record potentials transmitted on to the
horizontal plane.
The axis of a particular lead represents the viewpoint from
which it looks at the heart.

12. Summary of Leads
Limb Leads Precordial Leads
Bipolar I, II, III
(standard limb leads)
-
Unipolar AVR, AVL, AVF
(augmented limb leads)
V1-V6

13. Localising the arterial territory
Inferior
II, III, AVF
Lateral
I, AVL,
V5-V6
Anterior /
Septal
V1-V4

14. Standard Limb Leads

15. Precordial Leads

16. 16
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
ECG Chest Leads

18. 18
ECG Graph Paper
X- Axis time in seconds
Y-
Axis
Amplitude
in
mill
volts

19. 19
19
 X-Axis represents time - Scale X-Axis – 1 mm = 0.04
sec
 Y-Axis represents voltage - Scale Y-Axis – 1 mm = 0.1
mV
 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)
 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
ECG Graph Paper

20. ECG Wave forms & Intervals

21. 21
ECG Complex
P wave
PR Interval
QRS complex
ST segment
T Wave
QT Interval
RR Interval

22. Normal P wave
 Atrial depolarisation
 It is best seen & studied in lead II because the frontal P
wave axis is usually directed to the positive pole of this
lead.
 Duration 80 to 100 msec
 Maximum amplitude 2.5 mm
 Axis +45 to +65
 Biphasic in lead V1

23. Normal QRS complex
 Produced due to ventricular depolarization
 It corresponds to phase ‘0’ of ventricular action
potential
 Completely negative in lead aVR , maximum positivity
in lead II
 rS in right oriented leads and qR in left oriented leads
 Transition zone commonly in V3-V4
 RV5 > RV6 normally
 Normal duration 50-110 msec, not more than 120 msec
 Physiological q wave in frontal leads is not > 0.03 sec
in duration

24. Amplitude of QRS
 Depends on the following factors
 1.electrical force generated by the ventricular
myocardium
 2.distance of the sensing electrode from the ventricles
 3.Body build :a thin individual has larger complexes
when compared to obese individuals
 4.direction of the frontal QRS axis

25. J Point
• It refers to the point on ECG which coincides with
the end of depolarization and start of repolarization
of ventricles, i.e.it occurs at the end of QRS
complex.
• At this point since all parts of ventricles are
depolarized, so no current is flowing around the
heart.
• Therefore, at J point the potential of ECG exactly
zero voltage.

26. ST Segment
• It is an isoelectric period between the
end of QRS complex and beginning of T
wave.
• It corresponds to phase ‘2’ of ventricular
action potential.

27. Normal T wave
 Produced due to active ventricular repolarization.
 It corresponds to phase ‘3’ of ventricular action
potential
 Same direction as the preceding QRS complex
 Smooth contours ,blunt apex with asymmetric limbs
 The T wave in V6 is greater than T wave in V1 normally
 Relatively tall T waves are seen in V2 toV4 leads
 Height < 5mm in limb leads and <10 mm in precordial
leads
 May be tall in athletes

29. Normal u wave
 Genesis of U wave is uncertain
 Best seen in midprecordial leads
 Isoelectric in lead aVL
 Height < 10% of preceding T wave
 Rarely exceeds 1 mm in amplitude
 May be tall in athletes (2mm)

30. PR Interval
 It starts from the beginning of the P wave to
starting of QRS cmplex.
 Normal duration is 0.12-0.2osec.
 It includes atrial depolarisation & AV nodal delay.

31. Normal ECG

32. ECG INTERPRETATION
 Standardization & technical features(including lead
placement &artifacts)
1) Heart rate
2) Rhythm
3) Axis
4) P wave
5) PR interval
6) QRS interval
7) T wave
8) QT interval
9) U wave
10) Precordial R wave progression
11) Abnormal Q waves
12) ST segment

33. Determining the Heart Rate
•Rule of 300/1500
•6 Second Rule

34. Rule of 300
Count the number of “big boxes” between
two QRS complexes, and divide this into
300. (smaller boxes with 1500)
for regular rhythms.

35. The Rule of 300
It may be easiest to memorize the following table:
No of big
boxes
Rate
1 300
2 150
3 100
4 75
5 60
6 50

36. 6 Second Rule
ECGs record 6 seconds of rhythm per page,
Count the number of beats present on the ECG
Multiply by 10
For irregular rhythms.

37. 37
 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
What is the Heart Rate ?

38. 38
38
What is the Heart Rate ?
Answer on next slide

39. 39
 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
What is the Heart Rate ?

40. 40
40
What is the Heart Rate ?
Answer on next slide

41. 41
 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
What is the Heart Rate ?

42. 42
QRS Axis
 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

43. 43
43
Normal ECG

44. 44
Normal ECG
 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

45. 45
45
Be aware of normal ECG
 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

46. 46
46
Pseudo Normalization
Before
Chest pain
During
Chest pain
Chest pain
Relieved
T↓
T↓
T↑

47. 47
47
Atrial Waves

48. 48
48
Left Atrial
Enlargement

49. 49
49
Left Atrial
Enlargement
P wave duration is 4 boxes-0.04 x 4 = 0.16

50. 50
 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
Left Atrial
Enlargement

51. 51
 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
Right Atrial Enlargement

52. 52
52
Right Ventricular Hypertrophy

53. 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
Right Ventricular Hypertrophy

54. 54
54
Is there any hypertrophy ?

55. 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

56. 56
56
What is in this ECG ?

57. 57
ECG OF MS with RVH, RAE
 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

58. 58
58
Left Ventricular Hypertrophy

59. 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
Left Ventricular Hypertrophy

60. 60
60
What is in this ECG ?

61. 61
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
Causes and Criteria of LVH

62. 62
62
Atrial Ectopics
APC
APC
APC
APC

63. 63
 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
Atrial Ectopics

64. 66
66
Complete RBBB

65. 67
Complete RBBB
 Complete RBBB has a QRS duration > 0.12 sec
 R' wave in lead V1 (usually see rSR' complex)
 S waves in leads I, aVL, V6, R wave in lead aVR
 QRS axis in RBBB is -30 to +90 (Normal)
 Incomplete RBBB has a QRS duration of 0.10
to 0.12 sec with the same QRS features as
above
 The "normal" ST-T waves in RBBB should be
oriented opposite to the direction of the QRS

66. 68
68
Complete LBBB

67. 69
Complete LBBB
 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. 70
70
Blood Supply of Heart
LCA
RCA
LAD
LCX
RCA

69. 71
 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
Blood Supply of Heart

70. 72
72
Ischemia, Injury & Infarction
Myocardial
Ischemia
Myocardial
Injury
Myocardial
Infarction
1. Ischemia produces ST segment
depression with or without
T inversion
2. Injury causes ST segment
elevation with or without loss
of R wave voltage
3. Infarction causes deep Q waves
with loss of R wave voltage.

71. 73
73
Ischemia and Infarction
TRANSMURAL Injury
ST Elevation

72. 74
Ischemic Heart Disease (IHD)
Blood supply Sub-
endocardial
Transmural
Ischemia
Transient loss
Stable
Angina
Variant
Angina
Infarction
Persistent loss
NSTEMI
ACS
STEMI
ACS
ST Segment Depressed Elevated

73. 75
75
Interpret this ECG

74. 76
NSTEMI
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. 77
77
What are these ECGs

76. 78
STEMI and QWMI
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. 79
79
Evolution of Acute MI
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. 80
80
Critical Narrowing of LAD

79. 81
81
Normal Q waves
Notice the small
Normal Q in Lead I

80. 82
82
Pathological Q wave
Notice the deep & wide
Infarction Q in Lead I

81. 83
83
Very Striking

82. 84
Hyper Acute MI
 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. 85
85
Severe Chest Pain – Why ?

84. 86
 Note the ST elevations in
Inferior leads- namely L2, L3
and aVF
 T inversions yet to appear
 aVL lead shows complimentary
ST↓and T inversion
Acute Inferior wall MI

85. 87
87
Acute True Posterior MI

86. 88
 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
Acute True Posterior MI

87. RHYTHM
 The word rhythm of heart is used to refer part of the
heart which is controlling activation sequence.
 Normal heart rhythm,with electrical activation
beginning in SA node ,is called sinus rhythm.

88. Sinus Rhythms
Sinus Bradycardia
Sinus Tachycardia

89. Rhythm #1
30 bpm
• Rate?
• Regularity? regular
normal
0.10 s
• P waves?
• PR interval? 0.12 s
• QRS duration?
Interpretation? Sinus Bradycardia

90. Sinus Bradycardia
Deviation from NSR
- Rate < 60 bpm

91. Sinus Bradycardia
 Etiology: SA node is depolarizing slower than normal,
impulse is conducted normally (i.e. normal PR and
QRS interval).

92. Rhythm #2
130 bpm
• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.16 s
• QRS duration?
Interpretation? Sinus Tachycardia

93. Sinus Tachycardia
Deviation from NSR
- Rate > 100 bpm

94. Sinus Tachycardia
 Etiology: SA node is depolarizing faster than normal,
impulse is conducted normally.
 Remember: sinus tachycardia is a response to physical
or psychological stress, not a primary arrhythmia.

95. Premature Beats
Premature Atrial Contractions
(PACs)
Premature Ventricular Contractions
(PVCs)

96. Rhythm #3
70 bpm
• Rate?
• Regularity? occasionally irreg.
2/7 different contour
0.08 s
• P waves?
• PR interval? 0.14 s (except 2/7)
• QRS duration?
Interpretation? NSR with Premature Atrial
Contractions

97. Premature Atrial Contractions
Deviation from NSR
 These ectopic beats originate in the atria
(but not in the SA node), therefore the
contour of the P wave, the PR interval,
and the timing are different than a
normally generated pulse from the SA
node.

98. Premature Atrial Contractions
 Etiology: Excitation of an atrial cell forms an impulse
that is then conducted normally through the AV node
and ventricles.

99. Teaching Moment
 When an impulse originates anywhere in the atria
(SA node, atrial cells, AV node, Bundle of His) and
then is conducted normally through the ventricles,
the QRS will be narrow (0.04 - 0.12 s).

100. Rhythm #4
60 bpm
• Rate?
• Regularity? occasionally irreg.
none for 7th QRS
0.08 s (7th wide)
• P waves?
• PR interval? 0.14 s
• QRS duration?
Interpretation? Sinus Rhythm with 1 PVC

101. PVCs
 Deviation from NSR
 Ectopic beats originate in the ventricles resulting in
wide and bizarre QRS complexes.
 When there are more than 1 premature beats and look
alike, they are called “uniform”. When they look
different, they are called “multiform”.

102. PVCs
 Etiology: One or more ventricular cells are
depolarizing and the impulses are abnormally
conducting through the ventricles.

103. Teaching Moment
 When an impulse originates in a ventricle, conduction
through the ventricles will be inefficient and the QRS
will be wide and bizarre.

104. Ventricular Conduction
Normal
Signal moves rapidly
through the ventricles
Abnormal
Signal moves slowly
through the ventricles

105. Artifacts in ECG

106. REVERSAL OF LEADS
 Reversal of arm leads is the most common lead
placement error and is the easiest to recognize because of
negative P wave in L1.
 In patients with AF or unrecognizable P waves, if the
polarity of QRS in L1 is different from that of left
precordial leads V5 and V6, arm lead reversal is
suspected.

107. ECG

108.  In case of reversal of arm leads the morphology of
complexes in the limb leads resembles dextrocardia.
 However dextrocardia and reversal of arm leads can be
differentiated on the basis of QRS complexes in the
precordial leads.
 In dextrocardia as we progress from V1 to V6 QRS
complex becomes progressively smaller and displays
mostly QS or rS in V5 or V6.
 In reversal of arm leads the progression of QRS from
V1 to V6 is normal.

109. Normal variants of ECG
 Sinus arrhythmia
 Early repolarisation syndrome
 Persistent juvenile pattern
 Non specific T wave changes

110. Sinus arrhythmia
 Characterized by alternating periods of slow and rapid
rates.
 It is due to irregular fluctuating discharge of SA node.
 Mostly associated with phases of respiration(respiratory
sinus arrhythmia)
 The period of faster rate occur during end of inspiration,
slower rate towards end of expiration.
 The mechanism is mediated by reflex stimulation of
vagus nerve from receptors in lungs.
 It is accentuated by vagotonic procedures like carotid
sinus compression and abolished by vagolytic procedures
like exercise,atropine.

111. One P wave for one QRS complex
Constant PR interval
Normal P,QRS,T complexes with alternating periods
of gradually lengthening and shortening of P-P
intervals.
Respiratory sinus arrhythmia is normal physiological
phenomenon and most marked in young persons.

112. Early repolarisation syndrome
 Also called athletes heart
 Characterized by
1. Prominent j(junctional) waves
2. concave upward minimally elevated,ST segments
3. Relatively tall and frequently symmetrical T waves
4. Occasionally inverted T waves
5. Prominent but narrow initial Q waves in left oriented leads
6. Tall R waves in left precordial waves
7. Prominent mid precordial U waves
8. Rapid precordial transition
9. A tendency to counterclockwise electrical rotation
10. Sinus bradycardia or normal but slow sinus rates

114. Persistent Juvenile pattern
 Characterized by inversion of T waves in right
precordial leads V1 to V4.
 T wave inversions in V1toV4 are common in infancy
and childhood
 If it persists in adults also then called persistent
juvenile pattern.
 More common in negroes.

116. Non specific T wave variants
 Inversion of T waves may occur as non specific
manifestation in leads where T waves are normally
upright.
 They may be found in following circumstances
1. Anxiety and fear
2. As an orthostatic response
3. As a postprandial response
4. As result of hyperventilation
5. Idiopathic

117. 119