Ecg in congenital heart disease
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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
Ecg in congenital heart disease
- 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
- 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
- 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
- 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
- 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