This document discusses several types of cardiac dysfunction including atrial and ventricular septal defects, patent ductus arteriosus, atrioventricular septal defect, coarctation of the aorta, aortic stenosis, pulmonary stenosis, tetralogy of Fallot, tricuspid atresia, transposition of the great arteries, total anomalous pulmonary venous return, and truncus arteriosus. For each condition, it describes the pathophysiology, clinical manifestations, diagnostic evaluations, and management/treatment approaches.

1. Cardiac dysfunction
S.SINDHIYA RAJAKUMARI MSC (N)

7. Atrial Septal defect

11. Ventricular septal defect

13. Patent ductus artriosus

15. Atrioventricular septal defect

16.  It consist of a low ASD that is continuous with a high VSD
and clefts of mitral and tricuspid values which create a
central AV value that allows blood flow between all four
chambers of the heart.

17. Pathophysiology
 The alternation in hemodynamics depends on the
severity of the defects and the childs pulmonary
vascular resistance.
 Pulmonary resistance is high there is minimum
shunting of blood through the defects.
 Once resistance falls LF to RT shunting occurs and
pulmonary blood flow increases
 Pulmonary vascular enlargement predispose the
child to development of CHF.

18. CM
 Moderate to severe CHF
 Systolic murmur
 Mild cyanosis increase in crying

19. Complication
 Heart block
 CHF
 Mitral regurgitation
 Dysrhythmias and PHT

20. Management
 Surgical repair of septal closure

21. Coarctation of Aorta
 Narrowing of aortic arch,usually in juxtaductal
position.
 Incidence:
Three times more frequently in males than in
females

22. Types
 Preductus coarctation of Aorta

23. Pathophysiology
 Due to coarcted part blood unables to enter
 Dilation of aorta
 Due to major 3 blood vessels
 Coarcted
 Decreased blood supply

24. C/M
 Diminished or absent femoral pulses
 Pulse lag in lower extremities
 Blood pressure is greater in upper extremities that in
lower extremities
 Poor feeding
 Poor weight gain
 pallor

25. Diagnostic evaluation
 ECG – Lf or RT ventricular hypertrophy
 Echo
 Chest xray
 BP –all four extremities may reveal discrepancies

26. Management
 End to End anastomosis
 Subclavian flap aortoplasty
 Patch aortoplasty
 Balloon aortoplasty

27. Aortic stenosis

28. Types
 Valvular stenosis
 Supravalvular
 Subvalvular obstruction

29. Pathophysiology
 Due to aortic stenosis
 LV not ejaculated the blood into the aorta,LV will filled
and overload
 LV hypertrophy
 LV filled and back flow of blood into the pulmonary
vein
 Pulmonary overload
 Pulmonary edema

30. CM
 Asymptomic in infancy
 Systolic ejection murmur at upper right sternal border
 Thrill on carotid arteries
 Systolic click at the apex of the heart

31. Diagnostic Evaluation
 Chest xray
 Echo

32. Management
 Balloon angioplasty
 Value replacement
 Aortic valvotomy

33. Pulmonary stenosis

34. Pathophysiology
 High pressure of RA
 opens foramen ovale
 shunting occurs
 Mixing of de O2 RT to LF atrium systemic circulation
 Mild cyanosi

35. CM
 Cyanosis
 Poor feeding
 Dyspnea
 Activity intolerance
 Poor weight gain
 Growth retardation
 Severe cyanosis ccf

36. Diagnostic evaluation
 Chest X ray
 Echo

37. Management
 Pulmonary valvotomy
 Balloon angioplasty

38. Cyanotic
 Decreased pulmonary flow Mixed blood flow
Tetrology of fallot Transposition of great arteries
Tricuspid atresia Total anamolous pulmonary
venous return
Truncus arteriosis
Hypopladtic left heart syndrome

39. Tetralogy of fallot
 Pulmonary stenosis
 Right ventricular hypertrophy
 Over riding of aorta
 Ventricular sepal defect

41. Clinical features
 Cyanosis
 Tachypenia
 Clubbing of fingers
 Dyspnea
 Pansystolic murmur
 Blue spells
 Squating position

43. Diagnostic evaluation
 ECG
 Chest x ray
 Echo

44. Management
 Medical management

45. Surgical
 BT shunt
 Waterson shunt
 Potts procedure
 Brocks procedure

46. Tricuspid atresia
 Tricuspid valve fails to develop and no communication
exists between the right atrium and right ventricle.
 INCIDENCE
2-3% of congenital heart disease

48. Pathophysiology
 Tricuspid valve fails to develop
 Right ventricle is hypoplastic and ASD or patent foramen ovale present
 VSD is common
 Pulmonary arteries may be small in size
 Inn presence of tricuspid atresia,unoxygenated blood returning to the RA
cannot pass into the RV.

49. C/F
 Harsh murmur if vsd is present
 Clubbing of fingers
 Poor feeding
 Activity intolerance

50. D/E
 Cardiac examination
 ECG
 Chest xray
 Echo

51. Management
 Medical mgt
PGE1
surgical mgt
BT shunt
Balloon atrial septostomy
Fontan procedure 4-5 yrs of age

52. Post op complication
 Renal failure
 CHF
 Residual VSD
 Conduit obstruction
 Dysrhythmias
 Infective endocarditis

53. Transposition of Great Arteries

54. Incidence
 More common in males than females
 Usually seen in term babies

55. Pathophysiology

56. C/F
 Cyanosis
 Hypoxic spells during crying or exertion
 clubbing

57. Diagnostic evaluation
 Cardiac examination
 ECG
 Chest xray
 ECHO

58. Management
 Prostaglandin infusion IV to keep ductus arteriosus
open.
 O2 therapy
 Surgical mgt:
Rashkind procedure
Balock hanlon procedure

59. Corrective surgery
Atrial switch procedure
Mustard procedure
Senning procedure

60. Total Anamolous Pulmonary Venous
Correctoion

61. Types
 Supracardiac
 Cardiac
 Infradiaphargmatic

62. Pathophysiology

63. C/F
 Cyanosis early in life
 Children with unobstructed TAPVC may be
asymptomatic until pulmonary vascular resistance
decrease during infancy,increasing pulmonary blood
flow with resulting signs of CHF.

64. Surgical treatment
Corrective repair is performed in early infancy surgical
approach varies with theanatomical defect.

65. Truncus Arteriosus

66. Classification
 Type I II III
 Type IV