ECG IN CONGENITAL HEART DISEASES

1. ECG IN CONGENITAL HEART
DISEASE

2. Significance of ECG
• ECG is a simple non invasive tool to assist in
the diagnosis of congenital heart disease.
• In arrhythmias-no substitute
• In CHD assists in –
1. Diagnosis
2. Severity of the condition
3. Complications
4. Associated conditions

3. OVERVIEW
• Normal ECG changes in children
• Situs & Ventricular position identification
• Common acyanotic heart disease
• Common cyanotic heart disease
• Others

4. NORMAL ECG CHANGES IN
CHILDREN
• A positive correlation between ECG and
hemodynamic findings has been
described.
• ECG changes appear to be determined
largely by the load imposed on the
ventricles

5. At birth –PVR > SVR; the pressure in both ventricles is
presumably equal.
With expansion of the lungs and ligation of the cord, PVR falls
rapidly ,SVR rises, right to left shunt across ductus ceases
Thus ,at birth Tall R waves are recorded in right and
especially mid-precordial leads and deep S waves in left leads
RV thickness remains higher than left
initially

6. Changes in hemodynamics at birth are better reflected by T wave
variability than changes in QRS complex
Positive on day 0 to Day 5-7,It becomes negative by
day 5 and remains so throughout infancy and early
childhood

7. During first 72 hrs – RV forces more prominent than LV.
Loop is usually clockwise
By 6 weeks to 2 months –loop changes to counterclockwise
loop
Loop is most anterior by 2 months age, by 1 – 2 yrs becomes
more posterior
ECG Change from RV dominance to LV dominance lags behind
the changes in ventricular weight ratio.
LV:RV weights = equal by 1 month age,2.5-3:1 by 3 to 6 months
age,
But ECG changes to normal adult LV dominance by 1 to 3 yrs age

9. • NEW BORN
• FIRST 72 hrs
• 1 WEEK TO 1
MONTH

10. • 1 MONTH TO 6
MONTHS
• 6 MONTHS TO 3 YRS
• 3 YRS TO 8 YRS
• 8 TO 16 YRS

11. IDENTIFICATION OF SITUS AND
VENTRICULAR POSITION BY
ECG

12. IDENTIFYING SITUS
• In situs solitus,Right atrial focus-P wave
axis is normal, approx +60 degrees
Positive P in I and AVF ,Inverted in avR
• In situs inversus,left atrial focus – P wave
axis is shifted Rightwards,approx +120
degrees
Negative in I,positive in avF

13. I
AVF
V1

14. • Situs solitus with ectopic left atrial focus –
negative P in I,dome and dart P in V1
• Situs inversus with ectopic left atrial
focus-normal P wave axis,dome and dart P
in V1

15. • Situs ambiguus –
• Asplenia syndrome – 2 sinus nodes may
occur,competition between them may
occur. 2 p waves,one positive in lead I and
other negative in Lead I
• Polysplenia syndrome-absent SAN,Low
atrial pacemaker,giving p wave axis of -90
degrees

16. VENTRICULAR POSITION
• Ventricular position is independent of
atrial situs
• 4 patterns –
1. Normal or levocardia
2. Mirror image dextrocardia
3. Dextro rotation
4. Ventricular inversion

19. Normal Dextrocardia Dextro
rotation
Ventricular
inversion
Biphasic
voltages
V3 or V4 One of the
right chest
leads(V3R,V4
R)
V1,V3R,V4R,
V3 resembles
V6
Initial forces Superior and
right(Q in
I,V6)
Superior &
left(No deep q
in I,AVF)
Same as
normal
Superior and
left (Q in
V1,absent Q in
I,AVL,V6)
Major forces Inferior &
left(tall R in
I,AVF,V6)
Inferior &
Right(rS or QS
in I,V6;tall R
in AVF)
Same as
normal
Terminal
forces
Superior &
left(small s in
AVF,Tall R in
I,V6)
Superior &
right (S in
I,AVF,V6)
Same as
normal

20. DEXTROCARDIA
AVR and AVL reversed
Lead I predominantly negative
Right precordial leads should be recorded in
suspected dextrocardia

21. • D loop of heart tube – RV to Right of LV
and septal depolarisation from left to right
• Thus,Q in left precordial leads
• L loop- Q in right precordial leads

22. Ventricular
Inversion

23. CARDIAC MALPOSITIONS
• 4 Combinations can occur-
• Situs solitus with levocardia
• Situs solitus with dextrocardia
• Situs inversus with dextrocardia
• Situs inversus with levocardia
• Mesocardia

24. Normal ECG
• Important in the identification of
• 1.atrial situs,2.ventricular position,3.D/L loop

25. SITUS INVERSUS WITH DEXTROCARDIA

26. ACYANOTIC CHD

27. ECG

28. With shunt
• ASD:
• Secundum Atrial Septal Defects:
• Clockwise loop with vertical axis. right
axis with pulmonary hypertension or
young females with pulmonary vascular
disease
• left-axis deviation is rare but has been
described in hereditary forms such as
Holt-Oram syndrome and in older adults
with presumably acquired left anterior
fascicular block

29. • Pwave-tall right atrial p wave
• P wave axis-inferior and to left with upright p in
inferior leads
• PR interval:may be prolonged, -intra-atrial and
H-V conduction delay-first-degree AV block

30. • QRS: duration may be prolonged
• terminal QRS is directed rightward
,superior and anterior-rsR’ in v1 and
widening of s in v6
• R’ In v1 and AVR is slurred
• Crochetage-specific for ASD if present in
all inferior leads

31. • Arrhythmias:
• SND occurs as early as 2 years of age
• Atrial fibrillation,flutter,PAT are common
in 4th decade

33. CROCHETAGE
• In inferior leads, a notch near the apex of the R
wave,coined “crochetage,” has been correlated with ASD
• Seen in 73.1%, specificity - 92% (all 3 inf
leads),86.1%(atleast 1 inf lead)

34. Evolution
• As PAH develops rsR’ gives way to R in v1
• Signs of PAH like RAD develop
• RVH signs develop
• After surgery R may revert to rsR’ in 40%
of patients

35. Sinus venosus ASD
• P wave axis is superior and left-inverted p
in inferior leads,isoelectric in v1 and
positive in AVR

37. TYPES OF ASD
OS OP Sinus venosus
P wave Axis Normal Normal Superior axis in
SVC type
QRS Axis Vertical
LAD – assoc
MVP/MR
LAD Vertical
Loop Clockwise Anticlockwise Clockwise
Crochetage + _ +
Notch in upstroke
of S in Inf leads
Arrhythmias First degree AV
block more
common,Atrial
arrhythmias more

38. Severity of shunt
Size of Shunt Mild Moderate Severe
Qp/Qs <1.4 1.4 – 2 >2
RAE No Yes Yes
RV volume
overload
No Yes Yes
N rsr’ rsR’/evidence of
PAH
Crochetage No No Yes
Evidence of PAH No No Yes
R’ > 7mm in V1

39. ASSOCIATED CONDITIONS
• Lutembacher’s syndrome – LAE,RVH
more common,Atrial arrhythmias more
common

41. • TAPVR-resembles OS ASD,PR prolonged,
AF in older persons
• PFO – no hemodynamic changes
ECG is normal or shows crochetage
• Common Atrium –
Absent atrial septum
ECG shows features of combination
of
OS, OP, Sinus venosus ASD

42. PRIMUM ASD
• Counterclockwise loop
• Left axis deviation(extreme in downs)
• PR prolongation
• RVH- tall R in v1,,deep s in v6-pul.htn –left
A-V valve regugitation
• Notching of s wave upstokes in inferior
leads

44. analysis
ASD-clockwise loop
with rsR’,right atrial
P wave
Clockwise loop
Secundum-pwave
axis
normal,crochetage
Sinus venosus-p
wave axis
superior,crochetage
counterclockwise
primum-leftaxis
Notching of s waves
LVH/LAE

45. GERBODES DEFECT
• Tall peaked p waves and RAE from infancy,
• PR prolongation
• rsr’ in v1,terminal r in avr and V3r –RV
volume overload
• LV volume overload
• Increased incidence of arrythmias
• Pathognomonic-RAE with LV volume
overload

47. VSD
• Site
• Hemodynamic status
• Associated anomalies
• Typical features are LV volume overload -
gradually progressing to BVH.

48. site
• Usually normal axis
Left axis deviation –seen in 3 – 15%
• Inlet VSD
• Large Peri membranous VSD with Inlet extension
• Ventricular septal aneurysm
• Multiple muscular VSDs
• DORV VSD
• L TGA VSD
• RAD-VSD with PAH

49. • L TGA with VSD-LAD Clockwise
• DORV with VSD-LAD Counter clockwise

50. hemodynamics
• Accurately reflects underlying
hemodynamics
• Restrictive,small-no changes,only deep s
in right precordial leads,R in v5,v6-Lv
volume overload

51. • Moderately restrictive-LVH+,LAE
• Non restrictive-BVH- katz wachtel , RAD
• EISENMENGER-moderately peaked
p waves, RAD , tall monophasic R in v1,
deep S in left precordial leads

54. • Katz- Wachtel phenomenon
• High amplitude RS complexes in mid
precordial leads
• R + S waves in mid precordial lead >
60mm
• Classically described in VSD

55. COMPLICATIONS
• PAH
• RAD
• RVH
• R/S >1 in V1
• ST depression,T inversion in Right leads

56. Conduction defects
• PR prolongation-inlet vsd
• ECDS
• DORV
• L-TGA
• Septal aneurysm-AF,AFLU,PAT,CHB
• POST OP-RBBB(ventricular approach)

58. • ARRHYTHMIAS
• First-degree AV block occurs in about 10% of
patients, with a 1% to 3% incidence of complete
heart block on long-term follow-up.
• PR interval prolongation – Inlet VSD,Endocardial
cushion defects, DORV, L TGA
• Right bundle branch block +/- LAFB is found in 30%
to 60% of patients, independent of whether the VSD
was repaired through an atrial or ventricular
incision
• CHB is a recognized complication of transcatheter
device closure.

59. • Isolated VPC, couplets, and multiform
premature ventricular contractions may be
noted.
• Nonsustained or sustained VT occurs in
5.7% of patients, particularly with higher
pulmonary artery pressures.

60. • Endocardial cushion defects – LAD,
prolonged PR interval
• RAE + LV & RV volume overload =
Gerbode defect
• DORV with VSD –LAD,Increased PR
interval, Notched and broad S in II III aVF,
notch R in I AVL,V5,V6,counterclockwise
loop
• L TGA – LAD, q in V1/V2 with absent q in
lateral leads, heart block

61. • Associated with PS – RVH dominates,
RAD, T inversion in right leads
• Associated with AR
• CoA LVH dominates
• PDA

62. GERBODES DEFECT
• Tall peaked p waves and RAE from infancy,
• PR prolongation
• rsr’ in v1,terminal r in aVR and V3R –RV
volume overload
• LV volume overload
• Increased incidence of arrythmias
• Pathognomonic-RAE with LV volume
overload

63. VSD CWLOOP
LAD
L-TGA
MULTIPLE
MUSCULAR
VSD CCWL
LAD
TRICUSPID
ATRESIA
INLET VSD
DORV

64. VSD RAD
SEVERE
PAH

65. CCTGA
• The atrial septum is mal aligned with the
inlet ventricular septum, the regular AV node
does not make contact with infra nodal right
and left bundle branches.
• The AV node is displaced outside of Koch’s
triangle, anterior and slightly more laterally.
• Anomalous anterior AV node with a bundle
penetrates the atrioventricular fibrous
annulus and descends onto the anterior aspect
of the ventricular septum.

66. • The long penetrating atrioventricular
bundle is well formed in the hearts of
young children, but in adolescence, the
conduction fibers are replaced by fibrous
tissue, which is responsible for
atrioventricular block

67. • The right bundle branch is concordant with
the morphologic right ventricle, and the left
bundle branch is concordant with the
morphologic left ventricle.
• An Ebstein anomaly of the left
atrioventricular valve with left-sided
accessory pathways provides the substrate
for pre-excitation between the morphologic
left atrium and the morphologic right
ventricle.

68. • 75% have AV conduction abnormalties
• 30% have complete heart block
• Incidence of complete heart block increases
by 2% /yr
• Long bundle length –difficult to localise site
of block
• 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.

69. 3 MAJOR ECG FEATURES OF
CCTGA
• (1) Disturbances in conduction and
rhythm
• (2) QRS and T-wave patterns that reflect
ventricular inversion
• (3) Modifications of the P wave, QRS, ST
segment, and T wave caused by coexisting
congenital heart disease

70. Typical features
• 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

71. • P wave usually normal.
• Occasionally broad in cases of non
restrictive VSD and left AV valve
regurgitation.
• Peaked p waves in cases of PAH/PS.

74. AV SEPTAL DEFECTS
• Extreme form is when atria and ventricles
are connected by a common opening-
called common AV canal.
• It permits shunt between –
• LA to RA
• LV to RA
• RV to LA
• LV to RV

75. AV SEPTAL DEFECTS
• Marked left to right
shunt
• Early development of
PAH
• Associated MR
determines outcomes

76. • Ostium primum ASD
• Cleft mitral valve-MR
• Cleft septal leaflet tricuspid valve-TR
• Malformation or lack of development of
left anterior fascicle-LAD
• Small high membranous vsd

77. AV SEPTAL DEFECTS
• Characteristic finding :
• - left axis deviation
• - QRS vector counter clockwise loop
Mech : due to posterior and inferior displacement
of the AV node and the left bundle
• S waves in leads II, III, and aVF have a
characteristically
notched upstroke
• QRS pattern in right leads resembles OS-ASD-Due
to longer than normal Rt bundle

78. • The atrioventricular conduction axis
penetrates only at the crux, and the
penetrating bundle is displaced posteriorly,
lying on the posteroinferior rim of the
ventricular component of the defect.
• The His bundle is shorter than normal and is
posteriorly positioned. The left bundle
branch is displaced posteriorly and arises
from the common bundle immediately after
it enters the ventricular septum.

79. The left anterior division of the left bundle
branch has fewer fibers than normal and is
increased in length. The left posterior
division is shorter than normal and
provides small branches to the
posterobasal wall of the left ventricle.
• The right bundle branch is abnormally
long.

80. • Short HV intervals are in accordance with
elaborate studies that show early
activation of the posterobasal left
ventricular wall in atrioventricular septal
defects.
• These anatomic and electrophysiologic
observations provide acceptable
explanations for left axis deviation and for
the depolarization Pattern.

84. COMPLICATIONS
• PAH –
1. Complete AV canal defects with marked
left to right shunt
2. Ostium primum ASD with left AV valve
regurgitation
3. Pulmonary vascular disease of down’s
syndrome

85. • ARRHYTHMIAS
• PR prolongation also commonly seen (>50%)
Mech: secondary to intra atrial and
atrioventricular nodal conduction delay
• Rarely CHB-in immediate post op in 1-
7%,~2% thereafter
• Atrial flutter/fibrillation-with increase in age,
after surgical repair in >5%
• VPC-30%,Complex ventricular arrhythmia-
those with LV dysfunction

86. ASSOCIATED CONDITION
• Extreme LAD,early development of PAH –
Down’s syndrome
• Sub aortic obstruction – further increases
left to right shunt,early PAH

87. PDA
• Diagnosis by -
• LV Volume overload
• LAE
• +/- RV pressure overload
• QRS axis – normal

90. SHUNT SEVERITY
• Small –normal
• Moderate – LAE + LV Vol overload
q & Tall R in V5-6,deep S in
V1-2,
T remain upright
• Large – Biatrial enlargement + BV
hypertrophy
• Eisenmenger – RAE + RVH

91. COMPLICATIONS
• PAH
• BUT Q IN V5-V6 PERSIST EVEN AFTER
DEVELOPMENT OF PAH
• PR interval prolongation -10 – 20%
• AF – in older persons with large shunt

92. ASSOCIATED CONDITIONS
• RAD – Neonates ,
LAD- Rubella,sometimes superior axis
• CoA – LVH with secondary ST- T changes

93. STENOTIC LESIONS

94. Without shunt:
normal or decreased pulmonary flow
• Right side of heart
Valvular PS
DCRV
Peripheral PS

95. Pulmonary stenosis
• Obstruction to RVOT increases afterload
on RV – RV systolic overload
• RVH With or without RAE
• Good correlation with hemodynamics and
ECG

96. • Normal ht of R in V1 =<8 mm in infancy,
<10 mm in children
• Persistent upright T waves in V1 & V2
after 4 days age indicates RVH

97. MILD MODERATE SEVERE
1 Normal in 30%-60%
of cases
2 Right axis
deviation<100°
3 R in v1<10-15mm
4 Upright right
precordial T waves
after 4 days of age
maybe only sign
5 Gradient of
40mmHg
6 RVSP<50% of LVSP
1 r/s in v1>4:1
2 rsR’ or a small r is
present on upstroke
of R’
3 R in v1 <20mm
4 50%-upright T
waves
5 Gradient>40 mm Hg
6 RVSP>50% of LVSP
1 RAD>150°
2 Monophasic R or Qr
3 R >20mm in V1
4 P in lead 2 tall and
peaked
5 RVSP=LVSP or more
6 Gradient >80 mm Hg
7 Deep inverted T
waves ,ST depression
beyond v2
-RVSP>LVSP

98. MILD PS -RVSP<50% of LVSP

99. MODERATE -RVSP>50% of LVSP

100. SEVERE – RVSP >LVSP

101. RVSP MEASUREMENTS
• Ht of R in V1/V4R x 5,between 2 – 20 yrs age, if
pure R wave is present.
• Ht of R in V1 x 3 + 47

102. TYPES OF PS
• Valvular PS – As described
• Sub/Supra valvular –same
• Sub infundibular PS/DCRV –Degree of RVH
in V1-3 less than anticipated,
Upright T in V3R may be the only finding in
40% cases
• Dysplastic Pulmonary valvular stenosis as a
part of Noonan syndrome –Extreme axis
deviation,QRS prolonged and splinteredQRS
in inferior and left precordial leads

103. ASSOCIATED CONDITIONS
• Extreme RAD –may indicate pulmonary
valve dysplasia
• LAD – PS + Rubella syndrome
• PS as a part of TOF – RV pressures less
than in pure PS
• PS with large ASD- resembles OS-
ASD+RVH

104. Pure PS
• RAD, marked
• Tall R in Rt precordial
leads
• Deeply inverted
symmetric T waves
TOF(VSD + PS)
• Not Marked RAD
• Tall R only in V1,with
sudden transition
• Less deeply inverted T
waves/upright T in V1 &
V2

105. • 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

106. CONGENITALAS
• LVOT OBSTRUCTION
• LVH with T inversions,ST depression and
absent q waves

108. SEVERITY OF AS
• ECG of valvular aortic stenosis is a poor
predictor of the severity of stenosis
• A completely or nearly normal ECG does
not exclude severe stenosis
• SCD can occur inspite of normal ecg
• Severity may progress without change in
ECG

109. TYPES OF AS
• ECG is similar in valvular,sub and supra
valvular AS

110. • Evidence of subendocardial ischemia –
Severe AS,Supravalvular AS with
coronary ostial narrowing

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

112. COARCTATION OF AORTA
• LV pressure overload
• LAE
• Normal Axis

114. ASSOCIATED CONDITIONS
• AS due to bicuspid aortic valve –
prominent ST depressions and deeply
inverted T waves
• AR due to bicuspid aortic valve –
Prominent q in left precordial leads
• RVH – Infants,Assoc PAH
• RV volume overload – Associated PFO
with left to right shunt

115. CONGENITAL MITRAL STENOSIS
• The electrocardiogram exhibits right atrial
P waves, right axis deviation,
and right ventricular hypertrophy.

116. Shones complex

117. COR TRIATRIATUM
• RAE, RVH,RAD are common
• LAE may be seen due to prolonged
conduction in proximal accessory chamber

119. Endocardial Fibroelastosis
• The electrocardiogram records a variety of
disturbances in rhythm and conduction,
including paroxysmal atrial, junctional or
ventricular tachycardia, and neonatal
atrial fibrillation.

121. • Complete heart block has been detected in utero and
raises the question of a relationship between maternal
antibodies.
• P waves show left atrial, biatrial, or right atrial
abnormalities.
• The QRS axis is normal, although rightward or
leftward axes occasionally occur.
• Left ventricular hypertrophy is an important
electrocardiographic feature of primary endocardial
fibroelastosis of the dilated type.

122. • An infarct pattern is a feature of
endocardial fibroelastosis associated with
anomalous origin of the left coronary
artery from the pulmonary trunk . If an
infarct pattern occurs in primary
endocardial fibroelastosis, the Q waves are
in right precordial leads, not in leads 1
and aVL

123. REGURGITANT LESIONS
• CONGENITAL PR
• Normal in mild-mod cases
• RV volume overload in severe cases
• CONGENITAL AR
• LV volume overload with LV q waves

124. ALGORITHM FOR ACYANOTIC
CHD:
STEP 1
Which chamber is enlarged
RV
volume
overload(rsr’/rs
R’)
Pressureoverload
(monophasic
R/qR
•ASD
•RSOV
PS
DCRV
Infantile
coarctation
Cortriatriatum-broad
left atrial P waves
Congenital MS-LAE
LV

125. LVH alone/BVH?
Nonrestrictive VSD
Large PDA
AP Window
RSOV
LTGA
volume overload
Moderately
restrictive VSD
PDA
Pressure overload
Coarctation of aorta
Congenital AS
Interrupted .aortic
arch
Critical PS of infancy

126. • q in lateral leads : -simple
VSD,PDA,RSOV
• q in v1,2:L TGA
• RA enlargement if present-RSOV

127. ACHD
CLOCKWISE LOOP
NORMAL AXIS
SMALL VSD
MILD PS
COA(ADULT)
AS
RIGHT AXIS
VSD WITH PAH
(MUSCULAR ,OULET)
ASD WITH PAH
PDA WITH PAH
CONGENITAL MS
CORTRIATRIUM
LEFT AXIS
MULTIPLE MUSCULAR
VSD
L TGA +VSD
COUNTERCLOCKWISE
LOOP
LEFT AXIS
INLET VSD
AV CANAL DEFECT

128. CYANOTIC HEART DISEASES

129. Cyanotic and ↓ PBF
• Dominant RV
TOF
DORV+VSD+PS
SINGLE VENTRICLE(RV)+PS

130. Cyanotic and ↓ PBF
• Dominant LV
Tricuspid atresia
Ebstein’ anomaly
Single ventricle –LV type with PS
• TGA (VSD and LVOTO), with restricted
PBF
• TGA (VSD and PVOD), with restricted
PBF

131. Cyanotic and ↑ PBF
 Transposition physiology
D-TGA
• DORV with sub pulmonary VSD with NO PS
Tausig Bing
• Admixture physiology
Common atrium
Truncus arteriosus
TAPVC

132. Cyanotic and ↓ PBF
• Dominant RV
TOF
DORV+VSD+PS
SINGLE VENTRICLE(RV)+PS

133. Tetralogy of fallot
• P waves usually normal.
• Duration of P wave may be narrow due to underfilled LA.
• The QRS axis is the same as the axis of a normal newborn.
• The QRS axis and the direction of ventricular
depolarization do not change as the neonate matures
because the functional demands on the right ventricle do
not change.
• RVH is characterized by a tall monophasic R wave
confined to lead V1 with an abrupt change to an rS pattern
in lead V2.

135. • Presence and depth of Q waves and the
amplitude of R waves in leads V5-6 are
sensitive signs of the magnitude of
pulmonary blood flow and left ventricular
filling.
• Reduced pulmonary flow with an
underfilled left ventricle is accompanied
by rS patterns in leads V2_6.

136. • RBBB is common after surgical repair of
tetralogy of Fallot, even when the repair is
performed from a transatrial approach.
• This is probably due to delayed activation
of the right ventricular outflow tract
caused by disruption of the right
ventricular conduction system during
resection of infundibular stenosis.

137. • All patients with ventricular
tachycardia or sudden death had QRS
duration >180 ms.

138. Cyanotic and ↓ PBF
• Dominant LV
Tricuspid atresia
Ebstein’ anomaly
Single ventricle –LV type with PS
• d-TGA (VSD and LVOTO), with restricted
PBF
• d-TGA (VSD and PVOD), with restricted
PBF.

139. ECG
• Counter clockwise loop
• LAD
• Left ventricular hypertrophy
• Little or No RV forces
• RAE

141. Type -2
• Usually non restrictive VSD
• Normal or vertical axis
• LAE and RAE

143. Ebsteins anomaly

145. Hypoplastic left heart
• 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

148. Single Ventricle
• RVH
• LVH
• Stereotype QRS

150. 90% are LV morphology inverted outlet
chamber
Non inverted outlet chamber include left
axis deviation, left ventricular
hypertrophy, QRS complexes of great
amplitude, and stereotyped precordial
patterns

151. • 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

152. • Right ventricular morphology:Precordial
QRS complexes are stereotyped with right
ventricular hypertrophy patterns of
increased amplitude

153. Cyanotic and ↑ PBF
 Transposition physiology
D-TGA
Tausig Bing
• Admixture physiology
Common atrium
Truncus arteriosus
TAPVC

154. TGA
• Typical feature is RAD with RVH/BVH
• one third of infants with large VSD have
normal QRS axis for age.
• Left-axis deviation - typical in TGA with
AV canal types of VSD

157. TGA with non restrictive ASD
• Initial normal ECG
• Developing into RAD with RVH
• LV not prominent

159. TGA nonrestrictive VSD
• RAD
• Biventricular hypertrophy
• As PAH increases it evolves into
pure RVH

161. DORV

162. DORV with subaortic VSD with no PS
• Left axis deviation with counterclockwise
depolarization is an important feature .
• PR interval prolongation is common -unusually
long course of the common atrioventricular
bundle.
• Peaked right atrial P waves are associated with
bifid broad left atrial P waves when pulmonary
blood flow is increased.
• Mechanism of left axis deviation is unknown.

164. • Right ventricular hypertrophy -obligatory and is
manifested by tall R waves in leads V1 and aVR
with deep S waves in left precordial leads .
• Left ventricular volume overload is indicated by
large RS complexes in mid-precordial leads and
by tall R waves in left precordial leads .
• Elevated pulmonary vascular resistance is
associated with right axis deviation and püre right
ventricular hypertrophy

165. DORV with sub aortic VSD with PS
• Peaked right atrial P waves
• Right ventricular hypertrophy
• Important
– Distinction from TOF is presence of
counterclockwise loop with slurred s in II III
aVF and broad R in aVR I V5 V6 and
presence of PR prolongation

167. Taussig bing anamoly

168. Truncus
• 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
• Biventricular hypertrophy

170. Common atrium

171. TAPVC
• Resembles secundum ASD
• Vertical/right axis
• RVH-common feature
• RAE-present only in non
obstructive type

173. CCHD
CLOCKWISE
LOOP
NORMAL
TOF(PINK
RIGHT AXIS
TOF,
D-TGA VSD PS ,
L-TGA VSD PS ,
SV(LV) INV
OULET
SV(RV)
TAPVC
EISENMENGERS
SEVERE PS WITH
ASD
LEFT AXIS ADULT TOF
COUNTERCLOCK
WISE LOOP LEFT AXIS
TA
SV(LV)NI OUT
AV CANAL/EISE
COMMON
ATRIUM
RIGHT AXIS
DORV VSD PS
NORMAL AXIS
TA TYPE II C