electrocardiogram (Ecg) in CONGENITAL HEART DISEASES

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 – Diagnosis Severity of the condition Complications 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

8. NEW BORN FIRST 72 hrs 1 WEEK TO 1 MONTH

9. 1 MONTH TO 6 MONTHS 6 MONTHS TO 3 YRS 3 YRS TO 8 YRS 8 TO 16 YRS

10. IDENTIFICATION OF SITUS AND VENTRICULAR POSITION BY ECG

11. 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

12. I AVF V1

13. 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

14. 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

15. VENTRICULAR POSITION Ventricular position is independent of atrial situs 4 patterns – Normal or levocardia Mirror image dextrocardia Dextro rotation Ventricular inversion

16. Normal Dextrocardia Dextro rotation Ventricular inversion Biphasic voltages V3 or V4 One of the right chest leads(V3R,V4R) 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

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

18. 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

19. Ventricular Inversion

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

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

22. Situs solitus , dextrocardia

23. SITUS INVERSUS WITH DEXTROCARDIA

24. ACYANOTIC CHD

25. ECG

26. 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

27. P wave -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

28. 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 lea ds

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

30. 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)

31. 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

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

33. 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 PAH More common

34. 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

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

36. 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

37. 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

38. analysis

39. 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

40. VSD LV volume overload +/- RV pressure overload Normal Axis

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

42. 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

43. site Inlet vsd-counterclockwise loop,left axis deviation,prolonged PR interval Perimembranous vsd with septal aneurysm-left axis deviation Multiple muscular vsds-clockwise loop with left axis deviation

44. 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

45. L TGA with VSD- LAD Clockwise DORV with VSD- LAD Counter clockwise

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

47. 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

48. SIZE OF SHUNT Restrictive defects – Normal RV systolic pressure Moderately Restrictive VSD : RV systolic pressure increased,but less than systemic pressure. Non restrictive VSD – RV systolic P equal to systemic(Sub systemic) Eisenmenger syndrome – RV systolic pressure more than systemic( Suprasystemic )

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

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

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

52. VSDs , however large it may be,  usually spares the conduction system . This is simply due to the fact , developmentally the two systems  ventricular septum and the electrical  system  of the heart comes from different embryological focus and and are simply anchored together.

53. If the IVS is not formed properly ,the bundle  of His and it ‘ s major right and left branches  are  simply displaced  and not are  destroyed  ,  they  tend to occupy  one of the rims of VSD *Further, a VSD located peripherally and distally towards the apex - little impact on the conduction tissue

54. Membranous VSD Migration  of  A-V node   posteriorly toward crux of heart * His bundle  courses  along  the  postero inferior rim of defect * This makes sure the compact AV node never comes into picture of VSD . It  also explains the  rairty of   complete heart block  due to mechanical damage  to the  AV node  by the  VSD jet.

55. Location of conduction defect in various  VSDs Membranous VSD  –  Conduction tissue runs along  posteroinferior  border of defect Muscular VSD (Especially with Inlet extension)  – conduction tissue is  anterosuperior  to defect AV canal defects . This is the only type of VSD where serious defects of conduction occur  .Interruptions can also occur in the AV node.

56. 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.

57. 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.

58. ASSOCIATED ANAMOLIES PS-early transition AR-marked LVH in presence of restrictive VSD-Deep Q,tall R, deeply inverted T and coved ST segments in left precordial leads

59. ASSOCIATED CONDITIONS Minor anomalies of the tricuspid valve- associated with perimembranous defects in the form of extra septal leaflet tissue or pouches that can partially or completely occlude the defect . These pouches have been called aneurysms of the ventricular septum Associated with increase in arrhythmias and heart block Associated with LAD

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. Congenitally corrected transposition

64. 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.

65. An elongated His bundle extends toward the site of fibrous continuity between the right-sided mitral valve and pulmonary artery. It courses across the anterior rim of the pulmonary valve and continues along the superior border of a ventricular septal defect (VSD )

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. Complete heart block that is present at birth results from discontinuity between the anterior atrioventricular node and the ventricular septum. A cord­like right bundle branch extends leftward to the morphologic right ventricle, and a left bundle branch descends down the septal surface of the morphologic left ventricle.

68. 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.

69. 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.

70. 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

71. 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

72. 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.

73. 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

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

75. 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

76. 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

77. 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.

78. 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.

79. 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.

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

81. 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

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

83. A parachute type or double-orifice “mitral ” valve may be present and may have prognostic implications . Depending on the severity of dysfunction of the left AV valve, patients with ostium primum ASDs may become symptomatic at a much younger age than patients with other types of ASDs

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

85. 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

86. 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

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

88. STENOTIC LESIONS

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

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

91. 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

92. SEVERITY OF PS MILD MODERATE SEVERE P Wave Sharp pointed/peaked P waves <2.5 mm in II & V1 Sharp pointed/peaked P waves >2.5 mm in II & V1 Sharp pointed/peaked P waves >5 mm in II & V1 QRS Axis 40 to 60(N) 100 to 120 120 to 150 QRS voltage Tall R in V1/V2,but R/S <1 <10 – 15mm Tall R in V1/V2,but R/S >4:1,<20mm or rsR ’/Notched R’ Shift of transition zone to left Tall R / qR in V1/V2,but R/S >>4,with ht >20mm Shift of transition zone to left QR in V1 T wave Inverted in V1/V2 only Upright T in V1 –V2 after 4 days may be only sign Inverted upto V4-V5, In 50% cases upright in right leads Deep symmetric inversions,upto V6 T inversions II,III,AVF ST depression No No Yes

93. 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

94. MILD PS - RVSP<50% of LVSP

95. MODERATE -R VSP>50% of LVSP

96. SEVERE – RVSP >LVSP

97. 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

98. 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

99. 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

100. 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

101. 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

102. CONGENITAL AS LVOT OBSTRUCTION LVH with T inversions,ST depression and absent q waves

103. 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

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

105. ASSOCIATED CONDITIONS P is usually normal,LAE – significant co existing MR RVH – Neonates with pin point AS Assoc PAH Small LV cavity Left to right shunt through PFO

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

107. 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

108. COARCTATION OF AORTA LV pressure overload LAE Normal Axis

109. In Neonates –RVH + RAD After Infancy – LVH

110. 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

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

112. Shones complex

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

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

115. 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.

116. 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

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

118. APPROACH

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

120. 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

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

122. CYANOTIC HEART DISEASES

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

124. 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

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

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

127. 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 V 2.

128. Presence and depth of Q waves and the amplitude of R waves in leads V 5-6 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 V 2 _ 6.

129. 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 .

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

131. 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.

132. Tricuspid atresia

133. Tricuspid atresia by Kuhne

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

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

136. Ebsteins anomaly

137. 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

138. Single Ventricle RVH LVH Stereotype QRS

139. 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

140. 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

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

142. 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)

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

144. 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

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

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

147. DORV

148. DORV with subaortic VSD with no PS Left axis deviatio n 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. M echanism of left axis deviation is unknown .

149. Right ventricular hypertrophy - obligatory and is manifested by tal l R waves in leads V 1 and aVR with deep S w aves in left precordial leads . Left ventricular volume overload is indicated by large RS complexes in mid-precordial leads and by tal l R waves in left precordial leads . Elevated pulmonary vascular resistance is associated with right axis deviation and püre right ventricular hypertrophy  

150. 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

151. Taussig bing anamoly

152. Taussig bing anamoly

153. 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

154. Common atrium

155. Common atrium

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