An overview of paediatric ECG

All you need to know about Paediatric Electrocardiogram.
How to systematically analyse a paediatric ECG.

1. An Overview of
Paediatric
Electrocardiogram
Sid Kaithakkoden
MBBS,DCH,DipNB,MD.MRCPCH,FCPS
[email protected]

2. 2
The Electrocardiogram:
Basics

3. 3
The Cardiac Conduction System
Sino-atrial node
Purkinje fibresRight & left
bundle branches
Atrioventricular bundle
(bundle of His)
Atrioventricular
node
3.3
RA
LA
RV
LV

4. 4

5. 5
Conventional Placement for
3-lead Monitoring

6. 6
Rough Direction of
Depolarisation

7. 7
It’s all about being able to
relate……
This…. To this!

8. 8
ECGWaveform…
P
R
Q
S
T

9. 9

10. 10
Sequence of Electrical Activity in the
Heart Forming the P-Q-R-S-T Waves
•P wave:
–Atrial depolarization
–Axis: 0-90
–P wave is upright in I
& AVF

11. 11
The P Wave:
Spread of Electrical Activity
through the Atria
P

12. 12
The P Wave
•Represents atrial depolarisation and
activation
–Either from the SA node (sinus rhythm)
–Or from somewhere else in atria (ectopic)
•In sinus rhythm P wave rate is regular
•The only normalexception where P
wave rate varies is sinus arrhythmia–
usually only seen in people under40

13. 13
The P Wave: Characteristics
•P waves should be present!
•If absent, atrial activity may be:
–Truly absent (No coordinated atrial activity)
–Present but not visible on ECG
•No more than 0.12 secs duration
•No more than 2.5 mm high in lead II
•Upright in lead II (usually upright in all
leads except aVR)

14. 14
Analysis of P waves:
•Are the P waves regular?
•Is there one P wave for every QRS?
•Is the P wave normal and upright in
Lead II?
•Are there more P waves than QRS
complexes?
•Do all of the P waves look alike?

15. 15
•PR interval:
–Slow AV node
conduction
–No electrical activity
recorded by ECG
–PR interval is flat

16. 16
The PR Interval
•Measures the time from the beginning of
atrial depolarisation to the beginning of
ventricular depolarisation
–i.e. from beginning of P wave to beginning of QRS
complex
•A major portion of the PR interval is the slow
conduction through the AV node
•AV nodal conduction under autonomic control

17. 17
PR interval analysis:
•Normal PR interval (PRI) is 0.12 -0.2
secs in adults (age dependant in
children)
•Is the PRI measurement within the
normal range?
•Are all of the PRI’s the same?
•If the PRI varies, is there a pattern to
the changing measurements?

18. 18
•Q wave:
–Depolarization of
the ventricular
septum
–Axis: 180-270
–Negative deflection
in I & AVF

19. 19
•R Wave:
–Depolarization of
the ventricles
–Axis: 0-90
–Upright in I & AVF

20. 20
•S Wave:
–Depolarization of
the heart base
–Axis: 180-270
–Negative deflection
in I & AVF

21. 21
The QRS Complex
•Represents ventricular depolarisation
and activation
•Usually much bigger than P and T wave
as much larger muscle mass
•NB. TheQRS complex may comprise of
a Q, R and S wave –but often not all
three in same complex!

22. 22
The QRS Complex
•Q waves usually absent from most
leads of the 12-lead ECG
•The duration of the QRS complex is
termed the “QRS Interval” (Normal
range for is 0.07 –0.11 secs)
•QRS amplitude (on 12-lead ECG) varies
considerably –up to 3.0 mV (30mm)
may be normal

23. 23
QRS Waveform Nomenclature
R r qR qRs Qrs QS
Qr Rs rS qs rSr’ rSR’
7.1

24. 24
Analysis of QRS Complex
•What is the duration of the QRS complex?
•Are all of the QRS complexes of equal
duration?
•Do all of the QRS look alike?
•Are the unusual QRS complexes associated
with ectopic beats?
•Is the QRS complex preceded by a P wave?

25. 25
The ST Segment
•The ST segment lies between the end
of the S wave and the start of the T
wave
•It represents the time between end of
depolarisation and beginning of
repolarisation

26. 26
Analysis of the ST Segment
•The ST segment is normally
isoelectric
•Can be abnormal in two ways:
–Are the ST segments elevated?
•May indicate myocardial infarction
–Are the ST segments depressed?
•May indicate myocardial ischaemia

27. 27
ECG complex with isoelectric ST
segment

28. 28
12-lead ECG showing ST
Segment Depression

29. 29
12-lead ECG showing ST
Segment Elevation

30. 30
•T Wave:
–Repolarization of the
Ventricles
–upright deflection in
I & AVF

31. 31
The T Wave
•Represents repolarisation (“recharging”)
of the ventricular muscle to its resting
electrical state
•Analysis of the T wave would examine:
–Its direction
–Its shape
–Its height

32. 32
Repolarisation of Ventricle
The T wave:
Repolarisation of the ventricle
T
3.6

33. 33
The QT Interval
•The QT interval measures the total time
taken for depolarisation and
repolarisation of the ventricles
–Beginning of the QRS complex to the end
of the T wave
•Usually measured rather than the
duration of the T wave alone
•Varies with heart rate, age and sex

34. 34
The U Wave
•The U wave is normally either absent or
present as a small rounded wave
following the T wave
•Normally oriented in the same direction
as T wave
•Origin of U wave is uncertain
•More prominent in hypokalaemia,
hypercalcaemia or hyperthyroidism

35. 35
Age HR
bpm
QRS
Axis
degrees
PR
interval
seconds
QRS
interval
seconds
R
in V1
mm
S
in V1
mm
R
in V6
mm
S
in V6
mm
1st week 90-160 60-180 0.08-0.15 0.03-0.08 5-26 0-23 0-12 0-10
1-3wks 100-180 45-160 0.08-0.15 0.03-0.08 3-21 0-16 2-16 0-10
1-2 mo 120-180 30-135 0.08-0.15 0.03-0.08 3-18 0-15 5-21 0-10
3-5 mo 105-185 0-135 0.08-0.15 0.03-0.08 3-20 0-15 6-22 0-10
6-11 mo 110-170 0-135 0.07-0.16 0.03-0.08 2-20 0.5-20 6-23 0-7
1-2 yr 90-165 0-110 0.08-0.16 0.03-0.08 2-18 0.5-21 6-23 0-7
3-4 yr 70-140 0-110 0.09-0.17 0.04-0.08 1-18 0.5-21 4-24 0-5
5-7 yr 65-140 0-110 0.09-0.17 0.04-0.08 0.5-14 0.5-24 4-26 0-4
8-11 yr 60-130 -15-110 0.09-0.17 0.04-0.09 0-14 0.5-25 4-25 0-4
12-15 yr 65-130 -15-110 0.09-0.18 0.04-0.09 0-14 0.5-21 4-25 0-4
> 16 yr 50-120 -15-110 0.12-0.20 0.05-0.10 0-14 0.5-23 4-21 0-4
Normal Values

36. 36
QT interval:
•the duration from the beginning of the
QRS complex to the end of the T wave
•count the number of small squares,
then multiply by 0.04 seconds, that the
QT in seconds
•Corrected QT interval
–Normal QT is determined by the HR
–QTc = QT / square root of RR interval

37. 37

38. 38
Reading and Interpreting
Electrocardiograms
•Age: unless the patient’s age is known, the
paediatric ECG cannot be interpreted
•Is the ECG "full standard"?
•Is the ECG "standard speed"?
•The standard speed of paper is 25 mm/sec
•Occasionally it is made to run at a double speed (50
mm/sec) in cases of tachyarrhythmia to enable the
visualization of an otherwise hidden p waves
•Additional clinical information :
•Indication
•Clinical diagnosis: cardiac and other
•Medications: cardiovascular drugs, others eg. cisapride,
tricyclics
•Electrolytes

39. 39
Systematic reading of ECG:
1.Heart rate
2.P wave axis
3.Rhythm
4.QRS axis
5.Intervals PR, QRS, QT/QTc
6.P wave amplitude and duration
7.QRS amplitude, R/S ratio, Q waves
8.ST segments and T wave

40. 40
Heart Rate

41. 41
Heart Rate -Basics
•The standard UK and USA speed for
ECG recording is 25mm / second
•Before you measure the heart rate
always check that this speed has been
used!
•At this speed, a one-minute ECG
tracing covers 300 large squares

42. 42
ECG Paper: Dimensions
5 mm
1 mm
0.1 mV
0.04 sec
0.2 sec
Speed = Rate
Voltage
~ Mass

43. 43
Method 1
•Count the number of large squares
between two consecutive R waves and
divide into 300.
–Quick
–Not very accurate with fast rates
–Used ONLY with regular rhythms

44. 44
Method 2
•Count the number of small squares
between two consecutive R waves and
divide into 1500.
–The most accurate method
–Time-consuming
–Used only with regular rhythms

45. 45
Rhythms Arising From
the Sinoatrial Node

46. 46
Rhythms Arising From
the Sinoatrial Node
•(Normal) sinus rhythm
•Sinus tachycardia
•Sinus bradycardia
•Sinus arrhythmia
•Sick sinus syndrome

47. 47
Normal Sinus Rhythm
•Sinus rhythm is the normal cardiac
rhythm
•The sinoatrial node is acting as the
natural pacemaker
•Heart rate is between 60-100 / min
•P wave upright in lead II
•PR interval 0.12 –0.2 secs
•Each P wave followed by QRS complex

48. 48
Normal Sinus Rhythm

49. 49
Sinus Bradycardia
•Sinus bradycardia is sinus rhythm with a
heart rate of less than 60 / min
•P wave upright in lead II
•PR interval 0.12 –0.2 secs
•Each P wave followed by QRS complex
•It is unusual for sinus bradycardia to be
slower than 40 / min
–Consider alternative e.g. Heart block

50. 50
Sinus Bradycardia

51. 51
Sinus Bradycardia & Escape
Beats
•If sinus bradycardia is severe, escape
beats or rhythms may occur
•While these beats and rhythms may
look abnormal, they are protective
mechanisms

52. 52
Sinus Tachycardia
•Sinus tachycardia is sinus rhythm with a heart
rate of more than 100 / min
•P wave upright in lead II
•PR interval 0.12 –0.2 secs
•Each P wave followed by QRS complex
•Unusual for sinus tachycardia to be faster
than 180 beats / min, except in fit athletes
–Consider alternative eg. Nodal tachycardia

53. 53
Sinus Tachycardia

54. 54
Sinus Arrhythmia
•Sinus arrythmia is the variation of heart
rate seen with inspiration & expiration
•Each P wave followed by QRS complex
•Uncommon in age over 40 years
•Harmless
•Cause: heart rate increases during
inspiration as reflex response to more
blood returning to heart

55. 55
Sinus Arrhythmia

56. 56
Sick Sinus Syndrome
•This refers to a collection of impulse
generation and conduction problems related
to the sinus node
•Any or all of the following may be seen:
–Sinus bradycardia
–Sinus arrest
–Sinoatrial block
•May be associated with paroxysmal
tachycardias (“tachy–brady syndrome”)

57. 57
Sick Sinus Syndrome
Sinus arrest
•This is when the sinus node fails to discharge
on time,
•P wave fails to appear as expected, causing a
variable-length gap
Sinoatrial block
•Sinus node depolarises normally, but impulse
doesn’t reach the atria
•P wave fails to appear, but next one appears
in exactly the right place

58. 58
Sinus Arrest

59. Ectopics & Escape Beats:

60. 60
Ectopics
•The word “ectopic” implies “outside”
–(eg. ectopic pregnancy outside the uterus)
•Ectopic beatstherefore could be defined as
beats arising from outside the normal cardiac
conduction pathway ie. not starting at the
sinoatrial node
•Ectopic beats are also called:
–Extrasystoles
–Premature beats (or complexes)

61. 61
Ectopics
•Ectopic beats appear earlier than the
next expected beat
•They can arise from any region of the
heart, but are normally classified into:
–Atrial
–AV junctional
–Ventricular

62. 62
Ectopics
•Ectopic beats may occur as:
–Isolated single beats
–Multiple beats
–The dominant rhythm (usually defined as
three or more successive ectopic beats)
having “taken over” from the SA node

63. 63
Cardiac Conduction System:
Inherent Rates
Sino-Atrial (SA) Node:
•60-100 / min
Atrioventricular (AV) Node:
•40-60 / min.
Ventricles:
•20-40 / min.
Escape rhythms generated by the AV node and
ventricles will therefore be at the above
respective rates

64. 64
Beats & Rhythms Arising From
the Atria
•Atrial ectopics
•Atrial tachycardia
•Atrial flutter
•Atrial fibrillation

65. 65
Atrial Ectopics
•Atrial ectopics are identified by a P wave
which appears earlier than expected and has
an abnormal shape
•They will usually be conducted through to the
ventricles giving a QRS complex
–A normal QRS complex meaning normal
ventricular conduction
–Wide (>0.12 sec or 3 small squares) QRS
complex indicating aberrant ventricular conduction

66. 66
Atrial Ectopics
•Atrial ectopics are also known as:
–Premature atrial complexes (PAC’s)
–Atrial extrasystoles
•They may occur as:
–Isolated single beats
–Two beats together (a pair or couplet)
–As a run of ectopics (ie. more than 3) becoming a
tachycardia
–One ectopic for every sinus beat (bigeminy)

67. 67
Atrial Ectopics
•Atrial ectopics may all arise from the
same focus in the atria (unifocal)
–All the abnormal P waves would look the
same
•Atrial ectopics may arise from different
foci in the atria (multifocal)
–Abnormal P waves would vary in shape

68. 68
Atrial Ectopic –Single

69. 69
Atrial Bigeminy

70. 70
Atrial Tachycardia
•Atrial tachycardia is a tachycardia
originating from impulses generated in
the atrial myocardium
–From an ectopic focus
–Via a “re-entry” mechanism
•Characteristics:
–Heart rate greater than 100 / min
–Abnormally shaped P waves

71. 71
Atrial Tachycardia
•Atrial (P wave) rate is usually 120-250 /
min
•Above atrial rates of 200 / min, the AV
node struggles to keep up with
conduction so AV block may occur

72. 72
Atrial Tachycardia

73. 73
Atrial Flutter
•Differs from atrial tachycardia in that the atrial
(P wave) rate is higher
•Results from:
–Either an ectopic focus
–Or depolarization circling the atrium (“Circus
Movement”)
•Atrial rate is usually 250-350 / min, but often
almost exactly 300 / min
•The rapid rate gives it a classic “sawtooth”
appearance

74. 74
Atrial Flutter
•AV node cannot keep up with that rate,
so AV block occurs
•Most common is 2:1 block, giving
ventricular rate of around 150 / min
•3:1 = ventricular rate of 100 / min
•4:1 = ventricular rate of 75 / min
•AV block may also be variable

75. 75
Atrial Flutter

76. 76
Atrial Flutter –Variable Block

77. 77
Atrial Fibrillation
•Much more common than atrial flutter
•Affects 5-10% of elderly people
•Can be permanent
•May be transient or paroxysmal –
particularly in younger people
•Caused by rapid, chaotic depolarisation
of the atria (350 -650 impulses / min)

78. 78
Atrial Fibrillation
•Characteristics:
–No P waves seen
–Baseline consists of high frequency, low amplitude
oscillations (fibrillation or “f” waves)
–Conduction through AV node is erratic, therefore
ventricular (QRS) rate is irregular (often described
as “irregularly irregular”)
–Ventricular rate usually 120 –180 / min
•Unless patient medicated eg. digoxin

79. 79
Atrial Fibrillation

80. 80
Atrial Fibrillation

81. 81
•The term “supraventricular tachycardia”
(SVT) is frequently misused
•Literally, it refers to any heart rhythm over
over 100 / min that originates above the
ventricles, including:
–Sinus tachycardia
–Atrial fibrillation
–Atrial tachycardia
–AV re-entry tachycardia
Supraventricular Tachycardia
(SVT)

82. 82
Rhythms Arising From
The Ventricles

83. 83
Beats & Rhythms Arising From
the Ventricles
•Ventricular ectopics
•Ventricular escape beats & rhythms
•Accelerated idioventricular rhythm
•Ventricular tachycardia including
Torsade de Pointes
•Ventricular fibrillation

84. 84
Ventricular Ectopics
•Ventricular ectopics are also known as:
–Premature ventricular complexes (PVC’s)
–Ventricular extrasystoles
•They may occur as:
–Isolated single beats
–Two beats together (a pair or couplet)
–As a run of ectopics (ie. more than 3) becoming a
tachycardia
–One ectopic for every sinus beat (bigeminy)

85. 85
Ventricular Ectopics
•They activate the ventricles early, giving
rise to an early and wide QRS complex
–Wide QRS because the ventricular
conduction does not follow the specialised
pathways for fast conduction (bundle
branches)
•They may retrogradely conduct to &
activate the atria

86. 86
Ventricular Ectopics
•Characteristics:
–Early & wide QRS complex
–Compensatory pause
–No P wave (or inverted P wave)
•Ventricular ectopics may:
–All look the same if there is just one ectopic
focus (unifocal)
–Vary in morphology if there is more than
one ectopic focus (multifocal)

87. 87
Ventricular Ectopics -Unifocal

88. 88
Ventricular Ectopics -Multifocal

89. 89
Ventricular Bigeminy

90. 90
Ventricular Ectopics:
The “R-on-T” Phenomenon

91. 91
Ventricular Tachycardia
•Ventricular tachycardia (VT) is a broad-
complex tachycardiadefined as three or more
successive ventricular ectopic beats at a
heart rate above 120 / min
•Normally occurs at a rate of 150 –250 / min
•Symptoms of VT can range from mild
palpitations only, through to cardiac arrest

92. 92
Ventricular Tachycardia
Ventricular tachycardia may be described
as:
•Monomorphic
–Where all the ventricular complexes look
the same
•Polymorphic
–Where the ventricular complexes vary in
morphology (eg. Torsade de Pointes)

93. 93
Ventricular Tachycardia:
Torsade de Pointes
•Torsade de Pointes is a polymorphic
variant of VT associated with a long QT
interval
•Can cause significant haemodynamic
disturbance, and can also precipitate
ventricular fibrillation
•Establishing the causeof the long QT
interval is very important in its treatment

94. 94
Ventricular Tachycardia:
Monomorphic

95. 95
Ventricular Tachycardia:
Torsade de Pointes

96. 96
“Broad Complex Tachycardias”
(Not everything that looks like
VT is VT!)

97. 97
“Broad Complex
Tachycardias”
•Broad complex tachycardias are often
ventricular tachycardia
•However,sometimes supraventricular(ie
arising from above the ventricles) rhythms
can produce broad complexes if there is
abberant conduction (e.g. bundle branch
block or an accessory pathway)

98. 98
“Broad Complex
Tachycardias”
•Distinguishing between VT and SVT
with abberant conduction is not always
easy (even if you are a cardiologist!)
•It is important, however, to tell the
difference for correct management
•Luckily, in an emergency –both can be
treated with DC shock!

99. 99
“Broad Complex
Tachycardias”
Atrial Fibrillation with Abberant Conduction (Accessory Pathway)
Ventricular Tachycardia

100. 100
Ventricular Fibrillation
•Ventricular fibrillation (VF) can be defined as
rapid and totally disorganised ventricular activity
without discernible QRS complexes or T waves
in the ECG
•Untreated VF is a rapidly fatal arrhythmia
–Requires immediate DC shock
•Sometimes described as “coarse” or “fine” VF
depending on amplitude & frequency
–Fine VF can sometimes look like asystole –check
monitor gain

101. 101
Ventricular Fibrillation

102. 102
Asystole
•Asystole implies the absence of
ventricular activity
•P waves may still be seen (P wave
asystole or “ventricular standstill”)
•Characterised by a flat(tish) line
–Don’t forget a completely straight line is
often a loose lead
–Clue –check the patient!!

103. 103
Asystole

104. 104
“Heart Block”
(Or to be more correct Atrioventricular Block!)

105. 105
Atrioventricular (AV) Block
•Atrioventricular (AV) block refers to an
abnormality in electrical conduction
between the atria and the ventricles
•Caused by conduction abnormality in
one or more of the below:
–The AV node
–Bundle of His
–Both the right and left bundle branch

106. 106
Atrioventricular (AV) Block
The term degreeis used to describe the
severity of AV block:
•First degree (minor):
–All impulses conducted with delay
•Second degree (moderate):
–Some impulses are not conducted
•Third degree (complete):
–No impulses conducted

107. 107
First-Degree AV Block
•First-degree AV block is defined as a
prolongation of AV conduction to longer
than 0.2 secs (5 small squares)
–ie. PR interval is greater than 0.2 secs
•Can be:
–A normal variant
–Pathological due to cardiac problem or
drug interaction (eg beta blockers)

108. 108
First-Degree AV Block

109. 109
Second-Degree AV Block
•Second degree AV block is when one or
more, but not all, atrial impulses reach
the ventricles
•It may be intermittent or continuous
•Commonly described as two types:
–Mobitz Type 1 AV block (or Wenkebach
phenomenon)
–Mobitz Type 2 block

110. 110
Mobitz Type 1 AV block
(Wenkebach phenomenon)
Characteristics of this type of second
degree AV block are:
•Progressive lengthening of the PR
interval until one P wave fails to be
conducted and fails to produce a QRS
complex
•The PR interval then “resets” to normal
and the cycle repeats

111. 111
Mobitz Type 1 AV block
(Wenkebach phenomenon)

112. 112
Mobitz Type II AV block
Characteristics of this type of second
degree block are:
•Most P waves are followed by a QRS
complex
•The PR interval is normal and constant
•Occasionally a P wave is not followed
by a QRS complex

113. 113
Mobitz Type II AV block
•Mobitz Type II AV block is thought to
result from abnormal conduction below
the AV node
•It is considered more serious than
Mobitz Type I as it can progress without
warning to third degree (complete) AV
block

114. 114
Mobitz Type II AV block

115. 115
Third-Degree AV Block
(Complete Heart Block)
•There is complete interruption of conduction
between the atria and the ventricles
•The atria and the ventricles therefore are
working independently
•Any atrial rhythm may co-exist with 3
rd
degree
block
•The QRS complexes are usually the result of
a ventricular escape rhythm

116. 116
Third-Degree AV Block
(Complete Heart Block)
Main characteristics are therefore:
•P wave (atrial) activity may be normal,
abnormal or absent
•QRS complexes are slower & usually
broad
•No relationship between P waves and
QRS complexes

117. 117
3
rd
Degree AV block
(Complete Heart Block)

118. Axis Determination

119. 119
•Axis is perpendicular
to a lead where QRS
complex is isoelectric
( equal parts positive
& negative)

120. 120
•Mean QRS axis calculated in the frontal plane
•Looking at lead I (0 degree) and lead aVF(90 degree)
•if net QRS deflection is positive in leads I & aVF
-axis is normal
•if net QRS deflection is positive in leads I but
negative in aVF -LAD
•if net QRS deflection is negative in leads I but
positive in aVF –RAD
•if net QRS deflection is negative in leads I & aVF
–axis is indeterminate
How to determine QRS axis?

121. 121
Net QRS deflection
Lead I Lead aVF
Normal axis positive positive
LAD positive negative
RAD negative positive
Indeterminate negative negative
Axis Determination

122. Atrial Enlargement

123. 123
Right Atrial Enlargement (RAE)
•The P wave is taller than two small squares
in infants and small children
and more than three small squares in older
children and adults

124. 124
Left Atrial Enlargement (LAE)
•The P waves are wide, more than two small
squares (> 0.08 sec) in infants and small
children and more than three small squares
(> 0.12 sec) in older children and adults

125. Chamber Hypertrophy

126. 126
LVH
•R in V6 taller than 95% of normal and S in V1
deeper than 95%

127. 127
Age HR
bpm
QRS
Axis
degrees
PR
interval
seconds
QRS
interval
seconds
R
in V1
mm
S
in V1
mm
R
in V6
mm
S
in V6
mm
1st week 90-160 60-180 0.08-0.15 0.03-0.08 5-26 0-23 0-12 0-10
1-3wks 100-180 45-160 0.08-0.15 0.03-0.08 3-21 0-16 2-16 0-10
1-2 mo 120-180 30-135 0.08-0.15 0.03-0.08 3-18 0-15 5-21 0-10
3-5 mo 105-185 0-135 0.08-0.15 0.03-0.08 3-20 0-15 6-22 0-10
6-11 mo 110-170 0-135 0.07-0.16 0.03-0.08 2-20 0.5-20 6-23 0-7
1-2 yr 90-165 0-110 0.08-0.16 0.03-0.08 2-18 0.5-21 6-23 0-7
3-4 yr 70-140 0-110 0.09-0.17 0.04-0.08 1-18 0.5-21 4-24 0-5
5-7 yr 65-140 0-110 0.09-0.17 0.04-0.08 0.5-14 0.5-24 4-26 0-4
8-11 yr 60-130 -15-110 0.09-0.17 0.04-0.09 0-14 0.5-25 4-25 0-4
12-15 yr 65-130 -15-110 0.09-0.18 0.04-0.09 0-14 0.5-21 4-25 0-4
> 16 yr 50-120 -15-110 0.12-0.20 0.05-0.10 0-14 0.5-23 4-21 0-4
Normal Values

128. 128
Right Ventricular Hypertrophy (RVH)
•R in V1 taller than 95% of normal PLUSS in
V6 deeper than 95%

129. 129
•rsR’ in V1 & V2 without widening of QRS
complex as in bundle branch block.

130. 130
•qR in V1 & V2

131. 131
•Pure R wave in V1 & V2 , with or without ST & T
changes indicative of strain

132. Age related ECG progression

133. 133
•Full Term Newborn infant
–Right axis deviation (up to +180)
–RV dominance in praecordial leads:
–tall R in V1 ( >10mm suggests RVH)
–deep S in V6
–R/S ratio >1 in right chest leads, relatively small in
left
–QRS voltages in limb leads relatively small
T waves –low voltage
–T wave in V1 maybe upright for < 48 hours
(>48 hours suggests RVH)

134. 134
•1 week -1 month
–Right axis retained
–R waves remain dominant across to V6,
although dominant S maybe normal
–T wave negative V1
–T wave voltage higher in limb leads

135. 135
•1 –6 months
–QRS axis rotates to leftward (less than +120)
R wave remains dominant in V1
R/S ratio in V2 close to I but maybe >1 in V1
RSR’ pattern in V1 not abnormal
–Large voltages in praecordial leads suggestive of
BVH
–T waves negative across right chest leads

136. 136
•6 months –3 years
–QRS axis usually < +90
–R wave dominant in V6
–R/S ratio in V1 close to or less than 1
Large voltages in praecordial leads persist

137. 137
•3 -8 years
–Adult QRS progression in praecordial
leads:
•dominant S in V1
•dominant R in V6
•Large praecordial voltages persist
q waves in left chest leads may be large (<
5mm)
•T waves remain negative in right praecordial
leads

138. Normal Variants

139. 139
Normal variants
•T wave inversion:
–Infants older than 48 hours of age should have inverted T
waves in the right praecordial leads
–T inversion persist throughout childhood with inversion to
V4 being accepted as normal
–There is a progressive change to an upright T wave across
the praecordial leads from left to right as the child grows
older
–Until 8 years of age an upright T wave in V1 is considered
a sign of right ventricular hypertrophy
–Many children will show persistence of an inverted T
wave in V1 until their late teens

140. 140
References
•Houghton A.R., Gray D. Making Sense of the ECG. A Hands-on
Guide. Arnold. London. 1999. (If you only buy one book on
ECGs make it this one! Simple to read but still comprehensive,
pocket-size, not too expensive)
•Hampton J.R. 1992. The ECG Made Easy. 4
th
Ed. Churchill
Livingstone. Edinburgh.
•Hampton J.R. 1992. The ECG in Practice. 2
nd
Ed. Churchill
Livingstone. Edinburgh
•Wagner G.S. Marriott’s Practical Electrocardiography. 10
th
Ed.
Lippincott. Philadelphia. 2001. (Very good book for those
wanting to study ECGs in more depth)
•Hatchett R., Thompson D. Cardiac Nursing. A Comprehensive
Guide.Churchill Livingstone. Edinburgh
•“ECG Learning Centre”: http://medlib.med.utah.edu/kw/ecg/
(Excellent website -loads of example ECGs)