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Congenital Heart Defects

Congenital Heart Defects. Craig T. Carter, D.O. Assistant Professor – EM/Peds University of Kentucky. A nurse approaches you - “Doctor, Doctor” - a kid just checked in with a history of Hypoplastic Left Heart syndrome – What is that again??” You reply ….

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Congenital Heart Defects

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  1. Congenital Heart Defects Craig T. Carter, D.O. Assistant Professor – EM/Peds University of Kentucky

  2. A nurse approaches you - “Doctor, Doctor” - a kid just checked in with a history of Hypoplastic Left Heart syndrome – What is that again??” You reply …..

  3. “ I need to go to the bathroom, as soon as I get back, I will tell you all about it....”

  4. So you sit and think…..

  5. And think some more….

  6. Back to Basics-Fetal Circulation • Four shunts of blood flow : placenta, ductus venosus, foramen ovale and ductus arteriosus

  7. Back to Basics-Fetal Circulation

  8. Changes after birth: • Shift of blood flow for gas exchange, from the placenta to the lungs. • Closure of ductus venosus :no placenta • increase in pulmonary blood flow • functional closure of foramen ovale (increased LA pressure) • Closure of ductus arteriosus (^O2)

  9. Newborn Cardiac Exam • Vital signs: RR, HR, BP • respiratory effort • color • palpate point of maximal impulse (PMI) of heart • palpate pulses of all extremities • auscultate

  10. Case 1: 2 day old infant • 2 day old baby girl is being examined for discharge physical. • Vitals: HR:120 RR:40 BP: r arm 75/40 • Gen : low hairline, webbed neck, edemetous dorsum of feet

  11. Case 1: cardiac exam • Normal PMI, no thrill • No hepatosplenomegally • unable to palpate pulses in lower extremities • BP’s all four extremities: both legs systolic BP lower 40/30

  12. Case 1: Auscultation • S2 splits normally • ejection click • systolic ejection murmur III/VI at the URSB and LLSB • systolic murmur radiates to the back • early diastolic decrescendo murmur at 3LICS

  13. Case 1: • What do you think is the congenital defect?

  14. Case 1: • What further evaluation do you need?

  15. Coarctation of Aorta (COA)

  16. Incidence: 8% of all congenital heart defects Turner’s syndrome: 30% have COA Preductal: 40% associated with other cardiac defects,symptomatic early in life Postductal: less likely to have symptoms early Coarctation of Aorta (COA)

  17. EKG: LVH (but may be normal in 20%) X-rays: heart size may be normal or slightly enlarged Rib notching in older children Echo: can see narrowing Bicuspid aortic valve Doppler:disturbed flow COA

  18. COA complications • COA can cause CHF, HTN (intracranial bleeding,hypertensive encephalopathy) • Bicuspid aortic valve: stenosis or regurg • LV failure • infective endocarditis

  19. Preductal COA in Newborn • 80% of infants with preductal COA develop CHF by 3 months of age! • Symptoms of CHF: poor feeding, poor weight gain, dyspnea in first 2-6 weeks of life.

  20. Case 2: Two week old with murmur • Two week old infant, who you saw as a newborn with normal exam, now is noted to have a heart murmur. • PMI LSB, not hyperdynamic • pulses equal all extremities • No HSM

  21. Case 2: Cardiac exam • Grade III/VI holosystolic murmur at LLSB

  22. Case 2: What would you like to do next? • EKG: LVH,LAH • Blood pressures all four extremities • Xray: look for cardiomegally and increase in pulmonary vascularity • oxygenation • Echo: VSD

  23. Ventricular Septal Defect (VSD) • The most common form of congenital heart disease: 20-25% • may be located in different anatomical locations • may be associated with many other cardiac defects ( in many cases essential for survival) • may be small or large (can cause CHF)

  24. Case 3: One day old infant • One day old infant with tachypnea and cyanosis • Gen: cyanotic • RR:65, HR 140, BP 40/20 • pulse ox on RA: less than 80

  25. Case 3: Respiratory and Cardiac • Lungs clear, no retractions, RR rapid • Cardiac: PMI at LSB • pulses palpable all extremities • S2 single and loud. No heart murmur.

  26. What would you like to do? • ABG: before oxygenation • Give 100% O2 and then repeat ABG • EKG, 4 extremity BP • CXR

  27. Results of ABG • Before O2: PH: 7.15,PaCO2 30 and Pa O2 40 • After 100% O2: PH: 7.12, PaCO2 25 and PaO2 50

  28. Transposition of Great Arteries

  29. Transposition of Great Arteries • 5% of all congenital heart defects • Aorta arises anteriorly from RV, PA arises posteriorly from LV • defects (VSD,ASD,PDA) that permit mixing of the two circulations are necessary for survival

  30. ABG:hypoxemia is unresponsive to O2 EKG: RVH X-rays: egg-on-a-string silhouette cardiomegally with increased pulmonary vascularity Echo: PA from LV associated anomalies:VSD,ASD,PDA TGA:

  31. Immediate Treatment • Prostaglandin E1 to reopen PDA • Oxygen • cardiology/surgery referral

  32. DDX of Cyanotic Heart Dz • Transposition of the Great Arteries • Tetralogy of Fallot • Total Anomalous Pulmonary Venous Return • Tricuspid Atresia • Pulmonary Atresia • Truncus Arteriosus

  33. Other congenital cyanotic defects • Ebstein’s anomaly • single ventricle • Double-outlet right ventricle (depends on associated defects…if cyanotic or not)

  34. Tetralogy of Fallot

  35. Tetralogy of Fallot (TOF) • Large VSD • RV outflow obstruction • right ventricular hypertrophy • overriding of the aorta

  36. Tetralogy of Fallot • 10% of all congenital heart defects • The MOST COMMON CYANOTIC cardiac defect beyond infancy

  37. TOF: physical exam • Varying degrees of cyanosis and clubbing • systolic thrill LSB • S2 single with ejection click • loud III-V/VI SEM LSB • continuous murmur of PDA

  38. EKG: RAD, RVH Xray: “boot-shaped” heart (hypoplastic MPA) Echo: image of four defects associated TOF

  39. Tetralogy of Fallot

  40. TOF complications • Hypoxic spells • growth retardation with severe cyanosis • brain abscess and CVA • infective endocarditis • polycythemia

  41. Hypoxic Spell ( “TET Spell” • Paroxysm of hyperpnea (rapid and deep) • irritability and prolonged cry • increasing cyanosis • decreased intensity of heart murmur • (may lead to limpness, convulsion,CVA or death)

  42. Treatment of “TET Spell” • Knee-chest (squat )position • morphine sulfate • treat acidosis • oxygenation

  43. Total Anomalous Pulmonary Venous Return • One percent of all congenital heart defects • Defect: no direct communication between the pulmonary veins and the left atrium (they can drain: supracardiac,cardiac,infracardiac or mixed)

  44. Total Anomalous Pulmonary Venous Return

  45. S2 widely split and fixed S3 or S4 gallop SEM: III-IV/VI middiastolic rumble at LLSB Xrays: cardiomegally “Snowman” Echo can define anatomy EKG:RAD TAPVR findings

  46. Tricuspid Atresia • 1-2% of all congenital heart disease in infancy • tricuspid valve is absent and RV is hypoplastic • associated defects of VSD,ASD or PDA are necessary for survival

  47. Tricuspid Atresia

  48. Tricuspid Atresia: findings • Exam: cyanosis • S2 single, often syst murmur of VSD, and occ of PDA present • early CHF

  49. EKG: superior QRS between O and -90 LVH Pulmonary vascularity is decreased Echo: defines minimal RV, and large LV Tricuspid Atresia

  50. Pulmonary Atresia • Less than 1% of congenital heart diseases • valve is atretic, RV cavity is hypoplastic • need other defects: ASD,PDA for survival

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