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A good ppt on Clinical congenital heart disease for Post Graduate
This document discusses clinical congenital heart disease (CCHD) and provides classifications and descriptions of various conditions. It classifies CCHD into cyanotic types with increased or decreased pulmonary blood flow, acyanotic stenotic types, and unclassifiable types. For each type, it describes symptoms, physical exam findings including auscultation findings, and chest x-ray appearances. It also discusses unusual causes of cyanosis, Fallot physiology, complications of CCHD with decreased pulmonary blood flow, and keys to clinical diagnosis including focusing on pulse characteristics and the second heart sound.
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A good ppt on Clinical congenital heart disease for Post Graduate
- 1. Clinical congenital heart disease ProfM S Ranjit MD DCH Senior consultant paed. Cardiologist Chennai.
- 2. Some clinical aspects “paediatricand adolescent accent” Classification (modified for simplicity) cyanotic - with ↑ pulm blood flow - with ↓ pulm blood flow - unclassifyiable – ebsteins/ TGA IVS acyanotic – largely shunt lesions stenotic - outflow & arterial obstructions
- 3. Cyanosis caused by >5gm/dl reduced Hb Clinical detection depends on - % arterial blood that is desaturated - Hb Concentration !! If art O2 satn is 60%, cyanosis is detectable if Hb > 12.5gm/dl ! but not if Hb < 10 gm/dl ! ie 4gm/dl insufficient for detection of cyanosis !
- 4. Detection of cyanosis Astute physician/ paed cardiologist detects when reduced Hb 3 gm/dl Others detect at 5gm/dl Better to overdiagnose than underdiagnose ! Clinical diagnosis of cyanosis is inaccurate M Tynan in Andersons Paediatric cardiology 2007
- 6. Cyanosis -some aspects Some CCHD with Rt to Lt shunt and ↑ P B flow UO TAPVR/ Truncus/ TGA-VSD/ Single ventr Physiol etc - may have low saturations - but undetectable cyanosis clinically i.e. 88-92% !! Polycythemic patients appear cyanosed Methhaemoglobinaemia !!
- 7. Hyperoxic test cyanosed ornot Pulse oximeter - not always reliable “a random number generator” Rt radial ABG in air and after 5-10 min O2 paO2 > 250mmHg -excludes CCHD paO2 > 160 -CCHD unlikely ( UO TAPVR False negative !) paO2 < 100 -CCHD likely (usually lower) (severe Lung disease (high paCo2), PPHN/PFC)
- 8. “Radial ABGmore useful than ECG or CXR in detection of cyanotic heart disease” Warburton 1981
- 9. C C HD in 3 major circumstances Pulmonary obstruction with avenue for right to left shunting Discordant AV connection i.e transpositions Common mixing situations i.e common atrium single ventricle etc
- 10. Unusual causes ofcyanosis without murmurs ! surviving to adolesc./ adult life Left SVC to LA IVC to LA Rt. SVC to LA Pulm. AV Fistulae (Ostler Rendu Weber syndr)
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- 12. Cyanosis – whichcategory? Symptomatology Clinical examination Chest X ray
- 13. Fallot physiology Systemicvenous return unable to reach lungs Shunted right to left away from pulm circulation ASD/VSD essential for this to occur; Or a common chamber ! PLUS
- 14. Fallot physiology Obstructionat - RA outlet - i.e Tric atresia - infund/valvar Pulm stenosis - rarely branch PA stenosis/ DCRV - High PVR – Eisenmenger ! obstructed pulm arterioles !!
- 15. CCHD with ↓pulm blood flow pulmonary oligaemia on CXR Symptomatology Inspection findings Auscultatory findings Chest Skiagram
- 16. CCHD with ↓PBF - symptoms Exertional dyspnoea Cyanosis, spells, seizures CNS complications No recurrent RTI/ no diaphoresis No breathlessness at rest except in extremes / anaemia
- 17. CCHD - ↓PBF - inspection /palpatory findings Cyanosis & clubbing polycythemia Quiet precordium to inspection & palpation No Harrisons sulcus or precordial bulge Apex well within limits if visible No palpable sounds or thrills
- 18. CCHD with ↓PB Flow auscultatory findings Normal first heart sound Single second heart sound Pulm component inaudible Stenotic pulmonary murmur slightly after S1 stops short of S2 Other murmurs – ductal/ MAPCA/ AR
- 19. Ejection murmur inFallot physiology Length & loudness inversely proportional to severity of stenosis In isolated PVS – the opposite ! Absent murmur – acquired pulm atresia - MAPCA murmur over back - soft ductal murmur (tortuous) To & Fro – Aortic regurg / Abs PV syndrome
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- 21. CCHD with Pulm.bloodflow Tetralogy of Fallot VSD - PS DORV – VSD – PS Tricusp. atresia - PS Single ventricle - PS TGA with VSD – PS Corr.transp.-VSD-PS ASD - PS
- 22. Chest skiagram inCCHD with ↓ PBF Small heart Pulmonary bay Pulmonary oligaemia Right aortic arch/ RA enlargement/ differential vascularity/ narrow pedicle in various defects
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- 24. Typical - FallotCXR Pulm bay RV apex Pulmonary oligaemia
- 25. Tricuspid atresia Normally relatedgreat arteries Restrictive VSD PFO / ASD VSD / PDA Fallot physiology
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- 27. Transposition of the Greatarteries With V S D and P S TGA-VSD-PS Fallot physiology
- 28. LV RA LA PA AO Double inlet Left ventricle WithPS CCHD with PB Flow Single ventricle with PS Fallot physiology
- 29. Atrial septal defectwith pulmonic stenosis ASD with PS Fallot physiology Fallot physiology S2 variable Pulm ESM
- 30. Corrected Transposition withVSD and PS Atrio-ventricular & ventriculo-arterial Discordance LV RVRA LA AO PA Fallot Physiology Fallot physiology Single S2 Loud A2 pulmonic ESM
- 31. CNS complications ofCCHD with ↓ PBF Paradoxic embolus Cerebral thrombosis Cerebral abcess Seizures Hypoxic damage Endocarditis & vegetations Postoperative strokes
- 32. CCHD with ↑pulm blood flow Transpositions with VSD/Duct/ASD Common mixing situations atrial level – TAPVR/Comm Atr Mixing at ventric level – DORV/Single ventric arterial level – comm art trunk Mild cyanosis, CCF, resp symptoms, ex dyspnoea
- 33. CCHD with ↑Pulm blood flow Seldom survive to adolescence/ adulthood UO TAPVR/ comm atrium- the exceptions Most have Eisenmenger by then and those features dominate
- 34. CCHD ↑ PB Flow easy diagnosis – rare Clinical differentiation not always possible (Tynan M, Andersons paed cardiology 2007) Brisk pulses, ej click, to& fro murmur – Truncus Sm. pulses, RV impulse, wide split S2,TV MDM – TAPVR AV regurg murmur, wide split, TV MDM – comm. atrium Sing S2, cont murmur over back – p atr / MAPCAS
- 35. CCHD with ↑P B Flow - symptoms Respiratory symptoms predominate Growth retarded – weight & height Scrawny, sick, dyspnoeic patient Recurrent LRTI/Pneumonias Chronic lung disease- bronchiectasis etc Diaphoresis/ breathlessness at rest Exertional dyspnoea, limited activity.
- 36. CCHD with ↑P B Flow inspection findings Sickly underweight individual Cyanosis & clubbing -mild to moderate Severe PHT, Eisenmenger – modifies findings Harrisson’s sulcus, precordial bulge Active precordium, RV, LV, PA pulsations Obvious cardiomegaly
- 37. CCHD with ↑P B Flow palpatory findings Active precordium RV impulse – DORV, TAPVR, TGA VSD PS LV Impulse – Single ventricle, AVSD-AV regurg Palpable second sound / Thrills rare
- 38. Eminently operable Operablebut PHT Eisenmenger
- 39. CCHD with ↑P B Flow auscultatory findings Single second heart sound Loud pulm component, if heard Ejection click – pulmonary/ truncal
- 40. CCHD with ↑P B Flow auscultatory findings -2 Pulm flow – ejection murmur MD murmur - if no severe PHT/ Eisenmenger PR/ TR murmurs may dominate To & fro murmurs in- Truncus/ abs PV syndr. MR murmur in complex AVSD /comm Atrium
- 41. Double outlet rightventricle with VSD & PAH Normally related great arteries DORV – VSD - PAHCCHD with P B Flow RV impulse Single S2 - loud Pulm ESM Mitral MDM
- 42. Common atrium CCHD withP B Flow Often complex venous anatomy VSD physiology RV impulse Wide split S2 Tricuspid MDM Pulm. ESM
- 43. Transposition of the Greatarteries With V S D
- 44. Truncus arteriosus CCHD withP B Flow Brisk pulses Ejection click Non specific ESM EDM if truncal regurg. Mitral MDM
- 45. Supra cardiac Cardiac Infra cardiac Totalanomalous pulmonary venous return TAPVR VSD physiology ASD on auscultation Mild cyanosis
- 46. CCHD with ↑P B Flow radiographic findings Cardiomegaly (unless sev. PHT/Eisenmenger) Dilated PA Pulmonary plethora Atrial enlargement RV/LV/ Biventric. -Depends on anatomy/age
- 51. Keys to clinicaldiagnosis Work in order Pulses,pulses, pulses Colour ie. Cyanosis, pallor, polycythemia Inspect – for chest form, pulsations Palpate to determine – which ventricle ? Forget the murmur !! Listen first to S1, and then to S2 Can you split the second sound ?? Then concentrate on the components Finally the murmurs – systolic – ejection or pansyst. Is there a diastolic murmur
- 52. The second heartsound the key to diagnosis of CHD Single Normal split Wide variable split Wide fixed split Reverse split Loud A2 Loud P2
- 53. Unclassifiable CCHD TGA–IVS– do not survive Ebsteins – may have features of CCF & ↓PBF cyanosis, cardiomegaly multiple sounds, wide split, soft P2, Sail sound TR murmur, MDM, scratchy sounds P Atresia IVS – seldom survive infancy
- 55. Acyanotic CHD Stenotic CHD Few issues ASD, VSD , PVS, AVS too well known to talk about
- 56. AAO ARCH DAO PA Coarctation ofaorta COA
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- 59. Cxr coarct adult– rib notching
- 61. Coarctation of aorta Asymptomatic adults – collaterals Hypertension ! Femorals !! Bicuspid AV in 80% - ejection click ! Collateral murmur over back AVS
- 64. DD of acontinous murmur With or without cyanosis ? Continous or a To & Fro murmur ?
- 65. Continous murmurs withoutcyanosis PDA (Patent arterial duct) AP Window Venous Hum Coronary AV Fistula ALCAPA RSOV Periph Pulm. Stenosis Systemic AV Fistula Collaterals in COA Mammary Souffle Aortico-LV tunnel
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- 70. Continous murmur withcyanosis Duct in Tetralogy Pulm Atresia with Duct MAPCAS in Pulm atresia Supracard. TAPVR Pulm AV Fistulae Post BT shunt (Thomas-Blalock-Taussig shunt) Post - Pott’s, Waterston, Central shunts
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- 72. To & FroMurmur without cyanosis with cyanosis VSD AR MR AR AS AR PS PR Post op Tetralogy MR AR TR PR etc Tetralogy with AR Truncus with regurg Absent PV syndrome
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- 75. VSD outcome CCF > FTT> marasmus pneumonias / death PHT / PVOD / Eisenmenger Infective endocarditis Aortic prolapse & regurg. Mitral regurgitation. LV to RA shunts RSOV Infundibular pulm. stenosis VSD gets smaller spontaneous closure Surgical closureArrhythmias LV dysfunction Subaortic membrane
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