Download to read offline
More Related Content
Presentation
- 1.
- 7.
- 11.
- 13.
- 15.
- 16. It consistof 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 alternationin 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 tosevere CHF Systolic murmur Mild cyanosis increase in crying
- 19. Complication Heart block CHF Mitral regurgitation Dysrhythmias and PHT
- 20. Management Surgical repairof 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 coarctationof Aorta
- 23. Pathophysiology Due tocoarcted part blood unables to enter Dilation of aorta Due to major 3 blood vessels Coarcted Decreased blood supply
- 24. C/M Diminished orabsent 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 toEnd anastomosis Subclavian flap aortoplasty Patch aortoplasty Balloon aortoplasty
- 27.
- 28. Types Valvular stenosis Supravalvular Subvalvular obstruction
- 29. Pathophysiology Due toaortic 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 ininfancy Systolic ejection murmur at upper right sternal border Thrill on carotid arteries Systolic click at the apex of the heart
- 31. Diagnostic Evaluation Chestxray Echo
- 32. Management Balloon angioplasty Value replacement Aortic valvotomy
- 33.
- 34. Pathophysiology High pressureof RA opens foramen ovale shunting occurs Mixing of de O2 RT to LF atrium systemic circulation Mild cyanosi
- 35. CM Cyanosis Poorfeeding Dyspnea Activity intolerance Poor weight gain Growth retardation Severe cyanosis ccf
- 36. Diagnostic evaluation ChestX ray Echo
- 37. Management Pulmonary valvotomy Balloon angioplasty
- 38. Cyanotic Decreased pulmonaryflow 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.
- 45. Surgical BT shunt Waterson shunt Potts procedure Brocks procedure
- 46. Tricuspid atresia Tricuspidvalve fails to develop and no communication exists between the right atrium and right ventricle. INCIDENCE 2-3% of congenital heart disease
- 48. Pathophysiology Tricuspid valvefails 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 murmurif vsd is present Clubbing of fingers Poor feeding Activity intolerance
- 50. D/E Cardiac examination ECG Chest xray Echo
- 51. Management Medical mgt PGE1 surgicalmgt 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 GreatArteries
- 54. Incidence More commonin males than females Usually seen in term babies
- 55.
- 56. C/F Cyanosis Hypoxicspells during crying or exertion clubbing
- 57. Diagnostic evaluation Cardiacexamination ECG Chest xray ECHO
- 58. Management Prostaglandin infusionIV to keep ductus arteriosus open. O2 therapy Surgical mgt: Rashkind procedure Balock hanlon procedure
- 59. Corrective surgery Atrial switchprocedure Mustard procedure Senning procedure
- 60. Total Anamolous PulmonaryVenous Correctoion
- 61. Types Supracardiac Cardiac Infradiaphargmatic
- 62.
- 63. C/F Cyanosis earlyin 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 repairis performed in early infancy surgical approach varies with theanatomical defect.
- 65.
- 66. Classification Type III III Type IV