Ecg in congenital heart disease

ECG in congenital heart diseases

1. ECG IN CONGENITAL HEART DISEASE

2. Leave some space for green

3. ECG IN CHD ACYANOTIC CHD CYANOTIC CHD

4. 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

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

6. Crochetage sign:R wave notch IN ALL INFERIOR LEADS

7. 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

8. Original and modified methods of defining the Butler-Leggett score

9. 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

10. I° ASD

11. ASD ALOGARITHM

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

13. 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

14. 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

15. 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

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

17. 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

18. Congenitally corrected transposition

19. 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

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

21. 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

22. 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

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

24. AP WINDOW SIMILAR TO non restrictive VSD

25. 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

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

27. Valvular PS Tall monophasic R or qR in v1 Right axis deviation Strain pattern in right precordial leads

28. 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

29. 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

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

31. 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

32. normal or ↓ PBF Left side of heart Coarctation of aorta Cortriatriatum Congenital MS Congenital AS

33. 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

34. Interruption of aortic arch Peaked right atrial p waves and RVH-infants BVH gradually develops

35. Cor triatriatum

36. Shones complex

37. 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

38. 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

39. 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

40. DORV

41. 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

42. 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

43. 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

44. Cyanotic and ↑ PBF D-TGA: conal inversion right and anterior aorta TGA (IVS or small VSD) with increased PBF and small ICS a TGA (VSD large) with increased PBF and large ICS TGA (VSD and LVOTO), with restricted PBF TGA (VSD and PVOD), with restricted PBF

45. 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

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

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

48. TGA with sub pulmonic obstruction Pure RAD with RVH

49. 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

50. Taussig bing anamoly

51. 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

52. Common atrium

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

54. Tricuspid atresia

55. 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 %

56. Triuspid atresia by Kuhne

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

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

59. 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

60. Single Ventricle BVH common RVH LVH Stereotype QRS

61. 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

62. 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)

63. ESTES Criteria for LVH >5 sure,>4 probably

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