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
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
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
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
19.
20.
21.
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
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
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
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
31.
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
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
41.
42. WITHOUT SHUNT: NORMAL OR
DECREASED PULMONARY FLOW
• Right side of heart
Valvular PS
DCRV
Peripheral PS
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
45.
46.
47.
48.
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
50.
51.
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
56.
57.
58.
59. INTERRUPTION OF AORTIC ARCH
• Peaked right atrial p waves and RVH-infants
• BVH gradually develops
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
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
67.
68.
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
74.
75. TGA NONRESTRICTIVE VSD
• RAD
• Biventricular hypertrophy
• As PAH increases it evolves into pure RVH
76.
77.
78.
79. TGA WITH SUB PULMONIC OBSTRUCTION
• Pure RAD with RVH
80.
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
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%
94. ECG
• Cyanotic child
• LAD
• Left ventricular hypertrophy
• Type1- adult pattern of progression
• RAE
95.
96. TYPE -2
• Usually non restrictive VSD
• Normal or vertical axis
• LAE and RAE
97.
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
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)