This document discusses the interpretation of electrocardiograms (ECGs) in pediatric patients, particularly those with congenital heart disease. It covers normal variations in ECG findings with age from neonatal to adolescent periods. It then discusses ECG patterns associated with various congenital heart defects, including septal defects, obstructive lesions, cyanotic conditions and miscellaneous defects. Key findings are described for interpreting ECGs and correlating them with specific heart conditions. The document emphasizes that while not diagnostic, the ECG can provide important clues to the presence of chamber enlargement, conduction abnormalities and help classify certain congenital heart diseases.

1. DR RAHUL C

2. 1. Introduction
2. The Normal Electrocardiogram
3. Classification of Congenital Heart
Diseases
4. Acyanotic Congenital Heart Diseases
5. Cyanotic Congenital Heart Diseases
6. Miscellaneous Conditions
7. Conclusion

3.  Interpretation of pediatric electrocardiograms
(ECGs) can be challenging.
 Part of this difficulty arises from the fact that
the normal ECG findings, including rate,
rhythm, axis, intervals and morphology,
change from the neonatal period through
infancy, childhood, and adolescence.

 These changes occur as a result of the
maturation of the myocardium and
cardiovascular system with age.

4.  Congenital heart disease (CHD) occurs in 8 of every
1000 live births, and the clinical presentation of these
patients can vary in terms of both symptomatology and
timing.
 The ECG, although not diagnostic, can provide
important clues in patients suspected of having CHD.
 In particular, the ECG can show the presence of
chamber enlargement or conduction abnormalities that
may be associated with specific CHDs.
 A number of ECG findings can be associated with
specific congenital heart diseases .
 Although abnormalities on the ECG are found in the
majority of cases, it is important to remember that with
some CHDs (such as PDA), the ECG can appear age
appropriate and normal.

5. Electrocardiogram : Utility
 Identify cardiac malposition.
 Atrial and ventricular hypertrophy
- specific dx.
- assess severity
 Pericardial and myocardial disease.
 Electrolyte imbalance.
 Atriovent. & intravent conduction abn.
 Arrhythmias.
5

6. In congenital heart disease interpretation of
the ECG is useful only on the patient’s
bedside.
6

8.  Both Quite Different
 Most remarkable – RV Dominance in Infants.
 Most noticeable in New born.
 By 3 years resemble that of Adult.
 Adult type R/S progression rare in 1st month.
 Complete Reversal of R/S progression ≤ 1
month.
 Partial Reversal b/w 1month-3 years with
dominant R in both V1,V2 & V5,V6.
 Absence of Normal Right Ventricular
Dominance in infants is indicative of LVH.

9. Electrocardiogram
from a normal 1-
week-old infant-
RAD(+140),Dominan
t R wave(V1,V2),-ve
T wave in V1.
Electrocardiogram from a normal
young adult.- +60 axis,Dominant
R in L leads,+ve T V2-V6.

10. At Birth : RAD (+90 to +120) RVH
At 2 to 5 years :-
Normal axis (+30 to +75)
Normal LV dominance
Transitional period (Unstable ECG)
10

11.  P wave
 Situs Solitus with Levo/Dextrocardia
 P wave - +ve in I,aVL, -ve in aVR.
 Situs Inversus with Dextro/Levocardia
 P wave - -ve in I,aVL, +ve in aVR
 Left Atrial Rhythm – Dome & Dart P in V1/V2 irrespective
of atrial situs.

12.  Ventricle activation and Repolarisation reverse of normal.
 In lead I major QRS –ve & T wave inverted
 Septal Q waves +nt in Right lat.precordial leads as septal
depolarisation from right to left.
 Situs Solitus with Dextrocardia n D-loop
 Q waves in I,Avl n left precordial leads.
 Prominent R in V1,V2 & R/S in rest preordial leads.
 L-loop SS Dextrocardia
 Q waves absent in left but +nt in right leads.

13. ECG Crucial data
 Age
 Cyanotic or acyanotic
 Heart size – x-ray
13

14. CLASSIFICATION
L  R shunts Obstr. lesions Cyanotic pts
• Atrial level Right sided With PS
• Vent. Level Left sided With PAH
• PA level
14

16. 1. Left to Right Shunts
 Atrial Level(ASD Secundum & Primum)
 Ventricular Level(VSD small/large,PS/without PS,PAH/without
PAH)
 Great Arterial Level(PDA,AP Window)
1. Obstructive Lesions
 Pure Pulmonary Stenosis
 Aortic Stenosis
 Coarctation Of Aorta

17.  Sinus arrhythmia
 Clockwise loop with vertical axis
 Right axis with PAH
 Left-axis deviation : Holt-Oram syndrome
/LAHB
 RAE
 P wave axis- inferior and to left with upright p
in inferior leads
 PR interval: may be prolonged, intra-atrial /H-
V conduction delay-first-degree AV block

18. Wide QRS
RBBB
R’ In v1 and AVR is slurred
Crochetage-specific for ASD if
present in all inferior leads
SND occurs as early as 2 years of age
Atrial fibrillation, Atrial flutter
PAT

22.  PAH
rsR’ gives way to R in v1
Signs of PAH: RAD/RVH
 After surgery R may revert to rsR’ in
40% of patients

23. Counterclockwise loop
LAD
PR prolongation
RVH- tall R in v1,deep s in v6
Left A-V valve regurgitation: LVH
Notching of s wave upstrokes in
inferior leads

25. ASD
Clockwise loop
II° ASD
P -wave axis
normal
Crochetage+
SV ASD
P- wave axis
superior
Crochetage+
Counterclockwise
Loop
I° ASD
LAD/Notching of s
in inf leads
LVH/LAE

26. ECG changes in VSD
depends on
Location
Hemodynamic burden
Associated anomalies
Typical features
LV volume overload
Progressing to BVH

27. PERIMEMBRANO
US VSD
INLET VSD MULTIPLE VSD
With septal
aneurysm-
left axis deviation
Counterclockwise
loop,
LAD and
prolonged PR
interval
Clockwise loop
with left axis
deviation

28.  Accurately reflects underlying hemodynamics
 Restrictive & small VSD -
 no changes
 Deep s in right precordial leads, R in v5,v6-LV volume overload
 Moderately restrictive VSD-
 LVH+LAE
 Non restrictive VSD-
 BVH and
 Katz -Wetchel,RAD
 EISENMENGER -
 Moderately peaked p waves,
 RAD,
 tall monophasic R in v1,
 deep S in left precordial leads

32. VSD with PS-
early transition of QRS
VSD with AR :
marked LVH in presence of restrictive
VSD
Tall Deeply inverted T and coved ST
segments in left precordial leads

34.  PR prolongation
Inlet VSD
ECDS
DORV
L-TGA
 Septal aneurysm- AF,AFLU,PAT,CHB/Axis
change
 POST OP- RBBB (ventricular approach)

35. VSD
LEFT AXIS
Clockwise loop-
L-TGA
MULTIPLE
MUSCULAR
Counter clockwise-
DORV
INLET VSD
TRICUSPID ATRESIA
RAD
Severe PAH

36. VSD
LVH
MODERATELY
RESTRICTIVE
WITH RAE-
GERBODES
BVH
NONRESTRICTIVE

37. NONRESTRICTIVE-
BVH
Q IN LATERAL
LEADS
PRESENT-simple
VSD ABSENT-L-TGA

39.  The AV node is displaced outside of Koch’s
triangle, anterior and slightly more laterally
 An elongated His bundle extends toward the
site of fibrous continuity between the right-
sided mitral valve and pulmonary
artery(posterior)
 It courses across the anterior rim of the
pulmonary valve and continues along the
superior border of VSD

40. Conduction system
QRS patterns
Modifications of P,QRS,ST,T
segments

41. Reversal of the normal Q-wave pattern in
the precordial leads: Q waves are present
in the right precordial leads but are absent
in the left precordial leads
Clockwise loop
Left axis deviation
Upright T waves in all precordial leads –
side by side orientation of both ventricles

43. 75% have AV conduction abnormalties
 30% have complete heart block
Incidence of complete heart block
increases by 2% /yr
Sub pulmonic stenosis develops- axis will
be right
Even in prescence of left AV valve
regurgitation and volume overload- no Q
waves in left precordial leads

44. SIMILAR TO VSD
QRS axis
• RAD :
• infants with respiratory distress
• Superior/extreme left :
• Rubella syndrome

45.  Moderately restrictive – LA n LV volume overload.
 QRS Axis normal
 Left in Rubella Syndrome.
 Bifid prolonged left atrial P waves.
 LV volume overload – V5,V6-Tall R ,Prominent q
waves,Tall peaked T waves.
 Non Restrictive – Biatrial P waves n Combined
Ventricular Hypertrophy.

48.  Right side of heart
Valvular PS
DCRV
Peripheral PS

49. Tall monophasic R or qR in v1
Right axis deviation
Strain pattern in right precordial
leads

50. MILD MODERATE SEVERE
 Normal in 30%-60%
of cases
 Right axis
deviation<100°
 R in v1<10-15mm
 Upright right
precordial T waves
after 4 days of age
maybe only sign
 Gradient of 40mm
mmHg
 RVSP<50% of LVSP
 r/s in v1>4:1
 rsR’ or a small r is
present on upstroke
of R’
 R in v1 <20mm
 50%- upright T
waves
 Gradient>40 mm Hg
 RVSP>50% of LVSP
 RAD>150°
 Monophasic R or Qr
 R >20mm
 P in lead 2 tall and
peaked,in v1
terminal force is
written by right atrial
dilatation
 P maybe negative
 RVSP=LVSP or
more
 Gradient >80 mm
Hg
 Deep inverted T

54. PS with extreme right axis deviation with
splintered QRS and QS in inferior leads-
dysplastic PS of Noonan syndrome.
Infants with severe stenosis, in whom the
right ventricle may be hypoplastic, have a
more leftward axis than expected (in the
range of +30 to +70 degrees) as well as
evidence of left ventricular hypertrophy

55.  Non restrictive ASD and mild PS
• like ASD
• RVH will be disproportionate
• QRS axis is vertical or rightward
• rsR’ in v1-R’will be taller than that due to isolated ASD
 Severe PS with PFO- resembles isolated
severe PS

56. Left side of heart
Coarctation of aorta
Cor-triatriatum
Congenital MS
Congenital AS

57. LAE in adults,
LVH- tall R waves and low flat inverted T
waves
Deeply coved ST segments with AS –
bicuspid aortic valve
Q waves in left precordial leads suggests
AR
Symptomatic infants- RAE ,RAD with
RVH

60.  Which chamber is enlarged
 Step -2-suppose it is RV
 Step-3-
 is it volume overload(rsr’/rsR’) or
 pressure overload(monophasic R/qR)
 Step-4-
 volume overload-1)ASD 2)RSOV
 Pressure overload-1)PS
2)DCRV
3)Infantile coarctation
 Cortriatriatum-broad left atrial P waves
 Cogenital MS-LAE

61.  Suppose it is LV
 Is it LVH alone/BVH?
 LVH alone?
 volume/pressure?
 volume overload
 Moderately restrictive VSD
 PDA
 Pressure overload
 Coarctation of aorta
 Congenital AS
 Interrupted .aortic arch
 Critical PS of infancy

62.  BVH
Non-restrictive VSD
Large PDA
AP window
RSOV
L-TGA
 q in lateral leads/v1 :
 q wave in lateral leads-
 simple VSD,PDA,RSOV
 q in v1,2: L-TGA
 RA enlargement is present-RSOV

64. CYANOTIC : Subgroups
 PS, no VSD, R to L at atrial level
 PS with VSD (TOF physiology).
 pulm flow (Transposition physiol.)
 PA pr ,  pulm. flow (Eisenmenger
physiol).
 Pulm. ven. obst.
 PA pr. normal, No PS, No PAH.

66. Left axis deviation with
Counter clockwise loop
QRS duration is normal
RVH is obligatory- tall R in v1,Deep s in
V6
DORV with LV volume overload – tall RS
complexes in mid precordial leads and tall
R in v5/v6
DORV with PAH- clockwise loop with right
axis deviation

69.  ECG in DORV (double outlet right ventricle) varies with
the clinical type.
 In DORV, right ventricle is connected to the aorta and
faces systemic pressure.
 Hence features of right ventricular hypertrophy is almost
uniformly present in all types of DORV.
 Since both great vessels arise from the right ventricle, a
ventricular septal defect is obligatory.
 If the ventricular septal defect is small we can expect
pressure overloading of the left ventricle.
 When the ventricular septal defect is large, in the
absence of pulmonary stenosis or pulmonary vascular
obstructive disease, pulmonary blood flow is increased
and there will be left ventricular volume overload.

70.  In tetralogy like DORV which has a subaortic ventricular
septal defect with pulmonary stenosis, the ECG shows right
axis deviation.
 TGA like (transposition like) DORV has a subpulmonic VSD
without pulmonary stenosis.
 In this type, ECG shows left ventricular volume overload and
right axis deviation.
 Left ventricular volume overload is manifest as tall R waves
with deep narrow Q waves lateral leads.
 VSD like DORV has subaortic ventricular septal defect with no
pulmonary stenosis. This condition has left ventricular volume
overload on the ECG with left axis deviation.

71.  Peaked right atrial P waves
Right ventricular hypertrophy
Important
• Distinction from TOF is presence of
• counterclockwise loop with
• slurred s in v5,6,1,avl and
• broad R in avr and
• presence of PR prolongation

76.  Initial normal ECG
 Developing into RAD with RVH
 LV not prominent

77.  RAD
 Biventricular hypertrophy
 As PAH increases it evolves into pure RVH

80. Tall peaked right atrial p waves
Bifid left atrial p waves
Left axis deviation- increased pulmonary
blood flow
Right axis deviation- decreased pulmonary
blood flow ( with PS or PAH)
Biventricular hypertrophy

82. Resembles secundum ASD
Vertical/right axis
RVH-common feature
RAE-present only in non
obstructive type

86. Cyanotic child
LAD
Left ventricular hypertrophy
Type1- adult pattern of progression
RAE

88. Usually non restrictive VSD
Normal or vertical axis
LAE and RAE

90.  Always RVH
 qR pattern
 Left precordial R waves are
diminutive
 Deep S waves are usually seen in
lead V6
 Right atrial enlargement
 Right axis deviation
 ST segment changes
may reflect inadequate coronary perfusion from
restriction of retrograde flow through a
hypoplastic ascending aortic arch.

92. BVH common
RVH
LVH
Stereotype QRS

93.  Non inverted outlet
chamber include
 left axis deviation,
 left ventricular
hypertrophy,
 QRS complexes of great
amplitude, and
 stereotyped precordial
patterns

94.  90% ARE LV morphology
inverted out left chamber
 Inverted outlet chamber
include
 PR interval prolongation,
 an inferior or rightward
QRS axis,
 absent left precordial Q
waves,
 RS complexes of great
amplitude, and
 stereotyped precordial
patterns

95. Dominant RV
• Normal posterior
AV node and
HIS bundle
• RAD
• Tall stereotyped
R in precordial
leads.

97. 97
Arrhythmias and conduction
defects suggest specific
congenital cardiac anomalies

98. SSS
 ASD in Holt Oram synd.
 Sinus venosus ASD.
 AV canal defects
 Ebstein’s anomaly.
 Asplenia, polysplenia synd.
98

99. Narrow QRS tachycardia
 Ebstein’s disease.
 Cong. CTGA
 LV – RA shunt
 AV canal defects
 Older pts of TA and ASD 2°.
99

100. Wide QRS tachycardia
 ALCAPA
 Coron. arterio-ven. fistula
 Arrhythmogenic RV dysplasia.
10
0

101. Atrioventricular conduction defects
and pre-excitation syndrome
• Ebstein’s disease.
• Cong. CTGA
10
1

102.  EKG rarely reflects the anatomy of the lesion but
the physiological derangements due to the lesion.
 Do not try to diagnose anatomy based on EKG
alone.
 “Probable” anatomical lesion based on Clinical
features,EKG n X Ray findings.
 Some exceptions – Arrythmias,Electrolytes:Classic
EKGs.