This document discusses ECG findings in various congenital heart diseases: 1) Acyanotic CHDs like atrial septal defect (ASD) show findings of right or left ventricular hypertrophy depending on shunt direction, while ventricular septal defect (VSD) shows signs of left or bi-ventricular overload. 2) Cyanotic CHDs like transposition of the great arteries (TGA) show right axis deviation and ventricular hypertrophy initially, evolving to match pulmonary blood flow. Tricuspid atresia typically shows left axis deviation and ventricular hypertrophy. 3) Algorithms are provided to systematically analyze ECG patterns and identify the underlying CHD based on chamber

1. ECG IN CONGENITAL
HEART DISEASE

2. LEAVE SOME SPACE FOR GREEN

4. ECG IN CHD
• ACYANOTIC CHD
• CYANOTIC CHD

5. Acyanotic
CHD
Without
shunt(normal or
decreased
pulmonary flow)
Right side of heart Left side of heart
↑ PBF
Atrial
Ventricular
Aortic root
right side of heart
Aortopulmonary
level

6. II° ASD
• 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

7. • 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

8. CROCHETAGE SIGN:R WAVE NOTCH IN ALL INFERIOR LEADS

9. FOLLOW UP
• PAH
rsR’ gives way to R in v1
Signs of PAH: RAD/RVH
• After surgery R may revert to rsR’ in 40% of
patients

10. ORIGINAL AND MODIFIED METHODS OF
DEFINING THE BUTLER-LEGGETT SCORE

11. I°ASD
• 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

12. I° ASD

15. ASD ALOGARITHM
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

16. VSD
•Location
•Hemodynamic burden
•Associated anomalies
•Typical features
LV volume overload
Progressing to BVH

17. LOCATION
PERIMEMBRANOUS
VSD
INLET VSD MULTIPLE VSD
With septal aneurysm-left
axis deviation
Counterclockwise loop,
LAD and prolonged PR
interval
Clockwise loop with left
axis deviation

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

22. ASSOCIATED ANAMOLIES
• PS-early transition
• AR-marked LVH in presence of restrictive VSD-DEEP Tall Deeply
inverted T and coved ST segments in left precordial leads
• DORV,L-TGA-Similar to VSD

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

25. 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 arrhythmias
• Pathognomonic-RAE with LV volume overload

27. CONGENITALLY CORRECTED
TRANSPOSITION

28. • 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

29. • Conduction system
• QRS patterns
• Modifications of P,QRS,ST,T segments

30. TYPICAL
• 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

32. • 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
• In even in prescence of left AV valve regurgitation and volume
overload-no Q waves in left precordial leads

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-LTGA

38. PDA
• SIMILAR TO VSD
• QRS axis
• RAD- infants with respiratory distress
• Superior/extreme left-Rubella syndrome

39. AP WINDOW
• SIMILAR TO non restrictive VSD

40. D-MALPOSED GA
• P wave abnormality- if RA recieves shunt or TR develops
• PR prolongation is seen
• CHB can develop
• QRS axis is normal or rightward
• All 4 chambers enlarged-into RA
• RVH,LAE,LVH-into RV
• Only LA,LV-rupture into LA
• LVH is seen,RVH is seen ,but it occyurs alone it is due to RVOT
obstruction by unruptured aneurysm

42. WITHOUT SHUNT: NORMAL OR
DECREASED PULMONARY FLOW
• Right side of heart
Valvular PS
DCRV
Peripheral PS

43. VALVULAR PS
Tall monophasic R or qR in v1
Right axis deviation
Strain pattern in right precordial leads

44. SEVERITY OF PS
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 aves
 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 waves ,ST
depression beyond v2 and R
in v1 >20mm-RVSP>LVSP

49. PS SPECIAL
• 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

52. DCRV
• RVH can be present
• But in 40% of cases upright T in v3R can be the only finding

53. ASD WITH PS
• 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

54. NORMAL OR ↓ PBF
• Left side of heart
Coarctation of aorta
Cortriatriatum
Congenital MS
Congenital AS

55. COARCTATION
• 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
• LV strain pattern in infancy is indication for surgery

59. INTERRUPTION OF AORTIC ARCH
• Peaked right atrial p waves and RVH-infants
• BVH gradually develops

60. COR TRIATRIATUM

61. SHONES COMPLEX

62. ALOGARITHM FOR ACYANOTIC CHD:STEP I
• 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-ASD/RSOV
• Pressure overload-PS
DCRV
Infantile coarctation
• Cortriatriatum-broad left atrial P waves
• Cogenital MS-LAE

63. STEP II
 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

64. • BVH
Nonrestrictive VSD
Large PDA
AP window
RSOV
L-TGA
• q in lateral leads/v1 : lateral leads-simple VSD,PDA,RSOV
• q in v1,2:L TGA
• RA enlargement is present-RSOV

65. DORV

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

69. CYANOTIC AND ↑ PBF
 Transposition physiology
D-TGA
• D-TGA nonrestrictive VSD with tricuspid atresia
• DORV with sub pulmonary VSD with NO PS
• Tausig Bing
• Admixture physiology
Common atrium
Truncus arteriosus
TAPVC

70. 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

71. CYANOTIC AND ↑ PBF
• D-TGA: conal inversion
• right and anterior aorta
• TGA (IVS or small VSD) with increased PBF and small ICSa
• TGA (VSD large) with increased PBF and large ICS
• TGA (VSD and LVOTO), with restricted PBF
• TGA (VSD and PVOD), with restricted PBF

72. • 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

73. TGA WITH NON RESTRICTIVE ASD
• Initial normal ECG
• Developing into RAD with RVH
• LV not prominent

75. TGA NONRESTRICTIVE VSD
• RAD
• Biventricular hypertrophy
• As PAH increases it evolves into pure RVH

79. TGA WITH SUB PULMONIC OBSTRUCTION
• Pure RAD with RVH

81. 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 v5,6,1,avl and
broad R in avr and presence of PR prolongation

84. TAUSSIG BING ANAMOLY

85. 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

87. COMMON ATRIUM

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

91. TRICUSPID ATRESIA

92. VAN PRAAGH AND ASSOCIATES- 1971
 tricuspid atresia
 First classification
 morphology of the tricuspid valve
 (a) muscular type, (b) fibrous (membranous) type, and (c) Ebstein’s type
 modified by him”’ and by Weinberg
muscular type constituted 84%
membranous type n 8%
 The Ebstein’s type in 8%

93. TRIUSPID ATRESIA BY KUHNE

94. ECG
• Cyanotic child
• LAD
• Left ventricular hypertrophy
• Type1- adult pattern of progression
• RAE

96. TYPE -2
• Usually non restrictive VSD
• Normal or vertical axis
• LAE and RAE

98. 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

99. SINGLE VENTRICLE
• BVH common
• RVH
• LVH
• Stereotype QRS

100. 90% ARE LV MORPHOLOGY INVERTED OUT
LEFT CHAMBER
Non inverted outlet chamber include left axis deviation, left ventricular hypertrophy,
QRS complexes of great amplitude, and stereotyped precordial patterns
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
Right ventricular morphology:Precordial QRS complexes are stereotyped with right
ventricular hypertrophy patterns of increased amplitude

101. BVH
• Biventricular Hypertrophy (difficult ECG diagnosis to make)
• R/S ratio in V5 or V6 < 1
• S in V5 or V6 > 6 mm
• RAD (> 90 degrees)

102. ESTES CRITERIA FOR LVH
>5 SURE,>4 PROBABLY

103. I AM NOT BE 100% ENTERTAINING