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LECTURE - 2 Learning objectives

LECTURE - 2 Learning objectives. CONGENITAL HEART DISEASE 1. Introduction 2. Incidence 3. Pathogenesis 4. Types. Age of innocence ! ‏.

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LECTURE - 2 Learning objectives

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  1. LECTURE - 2Learning objectives CONGENITAL HEART DISEASE 1. Introduction 2. Incidence 3. Pathogenesis 4. Types

  2. Age of innocence !‏ A little boy, after being shouted at by his mum was sitting sad alone in a corner. Dad asked: "What happened, son?" “Boy : Dad, I can't handle your wife any more ! I want my own wife ! "

  3. 40 year after Club

  4. Abnormalities of heart/vessels at birth • Faulty embryogenesis during 3 – 8 wk • Major defects - septation, connections of great vessels/chambers, muscular • After surgery ht not normal; change - hypertrophy, remodelling pose problem INTRODUCTION

  5. INCIDENCE • Most common heart dis. in children • 1 % all live births, incidence higher in premature infants & stillbirths • 12 disorder account for 85% cases • Incidence increased due to better diagnostic methodologies – doppler echocardiography, MRI and others

  6. Frequency of Congenital Cardiac Malformation

  7. PATHOGENESIS • Heart among 1st organ to develop, multiple cell lineage/ genes involved • Cause – genetic ; placental infection;maternal disease like diabetes; drug; chemical; irradiation, multifactorial • 10% identifiable, some genes /CH identified, trisomy 21 (Down synd)

  8. CLINICAL FEATURE • R-L shunt; cyanosis, paradoxical embolism, polycythemia, clubbing • L-R shunt; ↑ pulmonary flow and hypertension, late cyanosis - tardive • Obstruction; abnormal narrowing of chambers, valves or blood vessels Malformations

  9. LEFT TO RIGHT SHUNTS • ↑ pulmonary flow / hypertension • Late cyanosis(tardive), months/ yrs after birth, reversal of shunts • Example – ASD, VSD, AVSD, PDA – all contain the letter ‘D’ in titles R L

  10. Abnormal opening atrial septum, communication left & right atria, 10% • 3 major type; secondum(90%), primum (51%), sinus venosustype: 5% • L to R shunt, higher pressure in left atrium ASD

  11. Well tolerated, usually not symptomatic before 30 years • Murmur, irreversible pulmonary hypertension 10%, eventually volume hypertrophy of right ht • Surgical correction, survival comparable to normal population CLINICAL FEATURE

  12. VENTRICULAR SEPTAL DEFECT • Incomplete VS formation, communication – LV / RV • Most common anomaly (40%), 30% isolated • 90% membranous part, rest in muscular septum • Large manifest at birth - signs of cardiac failure, small close spontaneously VSD

  13. R L

  14. Pediatric Cardiologist

  15. Umblical cord

  16. PATENT DUCTUS ARTERIOSUS • Ductus open after birth, 90% isolated • Length/diameter vary widely, narrow PDA no effect on growth • Obstructive pulmonary disease, shunt reversal • Machinery murmur, closed surgically early • May be life saving in anomalies like aortic valve atresia PDA

  17. RIGHT TO LEFT SHUNTS • Early cyanosis in postnatal life • Tetralogy of Fallot, transposition of great arteries, triscupidatresia, patent truncusarteriosus • Each category begins with letter T R L

  18. TA • Four (4)features : • Ventricular septal def • Pulmonary stenosis • Aorta overriding VSD • Right ventricular hypertrophy • Anterosuperior displacement of infundibulum septum in truncus • Some pts may survive into adult life even untreated 8.5 : 7.5 8 : 7

  19. CLINICAL FEATURE • RV hypertrophy, heart boot shaped, VSD , aortic valve at sup. border of VSD • Severity of obstruction of RV flow determines direction of blood flow • Some children are cyanotic at birth • Complete surgical repair possible now

  20. Patent truncus arteriosus TRANSPOSITION OF GREAT ARTERIES • Ventricular arterial discordance (partition – TA) • Incompatible with life unless shunt exists for mixing of blood, TGA with VSD or PDA • Right ventricular hypertrophy • No surgery, death in 1 month

  21. TGA with VSD

  22. OBSTRUCTIVE CONGENITAL ANOMALIES • Obstruction of blood flow at the level of heart valve or within a great vessel • Coarctation of the aorta , pulmonary stenosis/ atresia, aortic stenosis and atresia

  23. COARCTATION OF AORTA • Common anomaly (5%), male effected twice, Turner synd • Two forms; infantile form - tubular hypoplasia of arch proximal to PDA, adultform – discrete ridge like infolding opposite ductusarteriosus

  24. Types Adult Infantile

  25. CLINICAL FEATURE • Clinical features depend on severity • Coarct & PDA; early manifestation, no survival without surgical intervention • Coarct without PDA; asymptomatic; hypertension upper limb, weak pulse in lower, collateral circulation, LVH

  26. Summary

  27. Don’t fight a battle if you don’t gain anything by winning

  28. THANK YOU

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