Congenital Heart Disease

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crod2424
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104884
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Congenital Heart Disease
Updated:
2011-09-28 13:24:15
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Congenital Heart Disease
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Congenital Heart Disease
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  1. What congenital defect(s) may be detected at birth if hemodynamic consequences are significant?
    • Patent ductus arteriosus (PDA)
    • Transposition of great vessels
  2. What congenital defect(s) may not be apparent until adulthood?
    Bicuspid aortic valve
  3. What are some congenital defects that may go undetected throughout life or resolve without intervention?
    • Small atrial septal defect (ASD)
    • Small muscular ventricular septal defect (VSD)
  4. In fetal circulation the left ventricle supplies:
    the upper body
  5. In fetal circulation the lower body and placenta are supplied by:
    thoracic aorta blood + ductus arteriosus
  6. At what age does the functional and anatomic ductus arteriosus closure occur?
    Functional DA closure at about 72 hrs and anatomic closure in 4–8 wks
  7. Presentation for coarctation of the aorta:
    • Localized narrowing of arch usually distal to left subclavian artery in area of DA so not present in fetus
    • “3” sign on CXR
  8. What is the most common cardiac defect associated with coarctation of the aorta?
    bucuspid aortic valve
  9. Presentation for coarctation of the aorta:
  10. Coarctation of the Aorta can be associated with:
    cerebral berry aneurysms and some patients have Turner's syndrome (XO karyotype) with webbed neck
  11. Physical Findings:
    Coarctation of Aorta
    • Delayed femoral pulses
    • Reduced blood pressure in lower extremities
    • Findings associated with bicuspid aortic valve
    • Pressure difference between upper and lower extremities considered significant if > 20 mm Hg – intervention considered
  12. Presentation on Electrocardiogram:
    Coarctation of Aorta
    LV hypertrophy
  13. Chest Radiogram:
    Coarctation of Aorta
    • Post-Stenotic aortic dilation
    • Prominent ascending aorta
    • LV enlargement
  14. Collaterals in coarctation of aorta
  15. What is the life span of someone with coarctation of the aorta if it goes untreated?
    Most untreated patients die < 50 yo from complications
  16. What is the most common heart defect in children?
    Tetralogy of Fallot
  17. What are the four characteristic features associated with Tetralogy of Fallot?
    • RV outflow obstruction – 2° to pulmonic valve or infundibular stenosis
    • VSD – usually membranous and large
    • RVH – 2° to RV outflow obstruction
    • Overriding aorta – across VSD
  18. In Tertralogy of Fallot what is the degree of right-to-left shunt dependent upon?
    Degree of right-to-left shunt depends on degree of RV outflow obstruction
  19. Acyanotic vs. Cyanotic
    • Acyanotic (pink tetralogy) – mild so shunting small
    • Cyanotic – more common so shunting large and “blue” blood shunted into systemic circulation
  20. Complications found with Tetralogy of Fallot:
    Complications include arrhythmias (usually ventricular, especially if QRS > 0.18 sec when patients are more at risk for sudden death), paradoxical emboli, bacterial endocarditis (prophylaxis a must in these patients), and severe erythrocytosis
  21. Physical Findings:
    Tetralogy of Fallot
    • Usually cyanotic
    • Possible clubbing
    • Prominent ejection murmur at left sternal border
    • Soft or absent P2
  22. Presentation on Electrocardiogram:
    Tetralogy of Fallot
    • RV hypertrophy
    • RA abnormality
  23. Chest Radiogram:
    Tetralogy of Fallot
    • Boot-shaped heart
    • Small pulmonary artery
    • Normal pulmonary vasculature
  24. Types of treatment for Tetralogy of Fallot
    Surgical (3):
    • Blalock-Taussig or similar procedure
    • Total repair
    • Palliative surgery
  25. Tetralogy of Fallot:
    Blalock-Taussig procedure
    procedure in infancy to alleviate RV outflow obstruction and improve pulmonary blood flow
  26. Tetralogy of Fallot:
    Total Repair
    includes VSD patch, enlarging RV outflow tract patch, and removing Blalock shunt
  27. Tetralogy of Fallot:
    Palliative surgery
    may be needed to create a shunt between the systemic and pulmonary circulations – ↑ pulmonary blood flow to ↑ O₂of systemic blood and improve cyanosis
  28. True or False:
    Hemodynamically stable women with Tetralogy of Fallot who reach adulthood can carry a preganancy.
    True
  29. Presentation of Tertalogy of Fallot:
  30. What is the most common congenital defect in adults?
    • Atrial Septal Defect
    • More frequent in women than in men - 3:1
  31. ASD
    Ostium secundum:
    most common and involves fossa ovale and may include mitral valve prolapse (MVP)
  32. ASD
    Ostium primum:
    involve AV junction, abnormalities in tricuspid and mitral valve leaflets, and high VSD’s
  33. ASD
    Sinus venosus defects:
    superior septal defect that can go with partially anomolous pulmonary drainage into SVC or RA
  34. Complications of ASD:
    Complications include paradoxical emboli as shunt reverses with worsening and one of most common causes of cryptogenic stroke in people < 55 yo, cardiac arrhythmias especially atrial fibrillation (AF), and heart failure due to chronic right heart overload
  35. True or False:
    ASD is usually asymptomatic until adulthood.
    • True
    • Most asymptomatic until adulthood when symptoms may develop due to RV dysfunction causing fatigue, dyspnea, and poor exercise tolerance
  36. Physical Findings:
    Atrial Septal Defects
    • Parasternal RV impulse
    • Wildly and fixed split S2
    • Ejection murmur across pulmonic valve
  37. Presentation on Electrocardiogrm:
    ASD
    • Right bundle branch block
    • Left axis deviation with ostium primum defect
  38. Chest Radiograph:
    ASD
    • Large pulmonary artery
    • Increased pulmonary markings
  39. Presentation of ASD:
  40. Ventricular Septal Defects:
    • An opening in the septum between the ventricles that allows blood to shunt between the left and right ventricles.
    • Common congenital abnormality – 1 in 500 normal births
    • About half close spontaneously as the septum grows and hypertrophies during childhood – both membranous and muscular
  41. In VSDs do smaller or larger defects have a greater left to right gradient?
    Smaller defects have a greater left to right gradient and a louder murmur (loud, harsh, holosystolic in 3rd and 4th left sternal interspaces) but may be asymptomatic
  42. Eisenmenger physiology
    pulmonary hypertension due to pulmonary vascular disease from high pressure and volume effects caused by large shunts and reversal of shunt flow as a consequence leading to cyanosis and clubbing
  43. Complications of VSDs:
    • endocarditis – more common in smaller shunts due to higher velocity of blood damaging tricuspid septal leaflet or RV free wall so must give antibiotic prophylaxis
    • CHF – if shunts large and uncorrected
  44. Physical Findings:
    VSDs
    • Hyperdynamic precordium
    • Holosystolicleft parasternal mumur, with or without thrill
  45. Presentation on Electrocardiogram:
    VSDs
    • LV and RV hypertrophy
    • EKG and CXR may not help – depends on size of VSD and sequela
  46. Usefulness of Echo/Doppler in viewing VSDs:
    can show size, anatomy, and magnitude of shunt
  47. VSDs treatment:
    • About half close spontaneously as the septum grows and hypertrophies during childhood – both membranous and muscular
    • Most large ones are surgically corrected early
    • Treatment, if needed, is surgical by closing VSD with graft or percutaneously with closure devices
  48. Presentation of VSD:
  49. What is the result from the failed closure of the ductus arteriosus?
    Failure to close results in persistent communication between aorta and PA near origin of left subclavian but most patients asymptomatic if defect small or moderate until middle age
  50. Physical Findings:
    PDA
    • Loud continuous, rough machinery-like murmur louder in late systole and best heard in 1st and 2nd intercostal spaces at left sternal border (LSB) with thrill
    • If large enough, Eisenmenger physiology (↑ PVR and pulmonary HTN) can develop followed by reversal of flow and LV volume overload – will see cyanosis and clubbing of lower extremities with normal upper extremities
  51. Echo/Doppler:
    PDA
    can determine chamber size as well as blood flow in PDA
  52. Complications associated with PDA:
    Complications include CHF and endocarditis (prophylaxis a must)
  53. Treatment for PDA:
    Treatment is surgical with closure of PDA either by ligation or occluder devices – only done if no pulmonary HTN or right to left shunting
  54. Presentation of PDA:

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