acyanotic chd

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  1. 1. 04/29/15 DR. M. S. PRASAD 1 Acyanotic Congenital Heart DiseaseAcyanotic Congenital Heart Disease Dr. M. S. Prasad Professor & HOD Dept. of Pediatrics SGT Medical College
  2. 2. 04/29/15 DR. M. S. PRASAD 2 ObjectivesObjectives By the end of this class, the students will be able to define Congenital Heart Disease (CHD), and to describe common types of Acyanotic CHD.
  3. 3. 04/29/15 DR. M. S. PRASAD 3
  4. 4. 04/29/15 DR. M. S. PRASAD 4 Diagram of Normal HeartDiagram of Normal Heart PAPA AortaAorta RA RV LA LV PVPVIVC & SVC
  5. 5. 04/29/15 DR. M. S. PRASAD 5
  6. 6. 04/29/15 DR. M. S. PRASAD 6
  7. 7. 04/29/15 DR. M. S. PRASAD 7 Cardiovascular DiseasesCardiovascular Diseases Congenital Heart Disease Acyanotic CHD (L R shunt) Cyanotic CHD (R L shunt). Acquired Heart Diseases: Kawasaki Disease, Myocarditis, Rheumatic Heart Disease.
  8. 8. 04/29/15 DR. M. S. PRASAD 8 Congenital Heart Disease (CHD)Congenital Heart Disease (CHD) Con = Together. Genitus = Born.
  9. 9. 04/29/15 DR. M. S. PRASAD 9 Definition A structural or functional deficiency in heart or its appendages which originates during foetal life is known as Congenital Heart DiseaseCongenital Heart Disease (CHD). It may or may not manifest at birth. Congenital Bicuspid Aortic Valve is normal at birth but may take 2, 3, or more decades to stiffen, calcify and present as overt Aortic Stenosis.
  10. 10. 04/29/15 DR. M. S. PRASAD 10
  11. 11. 04/29/15 DR. M. S. PRASAD 11 CLASSIFICATIO N ACYANOTIC CYANOTIC Physical Examination, or Pulse Oximetry.
  12. 12. 04/29/15 DR. M. S. PRASAD 12
  13. 13. 04/29/15 DR. M. S. PRASAD 13 Acyanotic CHDAcyanotic CHD Shunt Lesions (Left Right), Obstructive Lesions, Regurgitant Lesions, and Mixed (combination)
  14. 14. 04/29/15 DR. M. S. PRASAD 14 LL R Shunt LesionsR Shunt Lesions ASD (Atrial Septal Defect), AVSD (Atrio-ventricular Septal Defect), VSD (Ventricular Septal Defect), PDA (Patent Ductus Arteriosus).
  15. 15. 04/29/15 DR. M. S. PRASAD 15 Obstructive LesionsObstructive Lesions AS (Aortic Stenosis), COA (Coarctation of Aorta) HLHS (Hypoplastic Left Heart Syndrome), PS (Pulmonary Stenosis), Mitral Stenosis, Tricuspid Stenosis
  16. 16. 04/29/15 DR. M. S. PRASAD 16 Regurgitant LesionsRegurgitant Lesions AR (Aortic Regurgitation), MR (Mitral Regurgitation), MVP (Mitral Valve Prolapse), TR (Tricuspid Regurgitation), PI (Pulmonary Incompetence)
  17. 17. 04/29/15 DR. M. S. PRASAD 17 Patent Foramen OvalePatent Foramen Ovale (PFO)(PFO) && Atrial Septal DefectAtrial Septal Defect (ASD)(ASD)
  18. 18. 04/29/15 DR. M. S. PRASAD 18 PFOPFO An isolated patent foramen (PFO) is a common finding during infancy and it usually closes. It is not considered abnormal, even if it persists throughout life. It is usually of no hemodynamic significance and is not considered an ASD. May play an important role if other structural heart defects are present.
  19. 19. 04/29/15 DR. M. S. PRASAD 19 Atrial Septal Defect (ASD)Atrial Septal Defect (ASD) A defect in the wall between left and right atrium is known as Atrial Septal Defect (ASD). This is one of the Acyanotic CHD with L R shunt. More common in females than in males. [M:F = 1:2].
  20. 20. 04/29/15 DR. M. S. PRASAD 20
  21. 21. 04/29/15 DR. M. S. PRASAD 21 Types of ASDTypes of ASD Ostium Secundum Defect (5-10% of CHD) Sinus Venosus ASD. (10% of ASD) Ostium primum ASD
  22. 22. 04/29/15 DR. M. S. PRASAD 22 SVC IVC TV Ostium primum Ostium secundum Superior Sinus Venosus Inferior Sinus Venosus
  23. 23. 04/29/15 DR. M. S. PRASAD 23 Ostium secundum ASD constitutes 5-10% of CHD. Ostium Secundum Defect is 3 times more common in girls than in boys. PAPVR may be present.
  24. 24. 04/29/15 DR. M. S. PRASAD 24 Secundum ASDSecundum ASD Spontaneous closure up to 2-3 years may occur. Symptoms in childhood are rare. Life expectancy virtually normal if closure undertaken in childhood.
  25. 25. 04/29/15 DR. M. S. PRASAD 25 Sinus VenosusSinus Venosus Spontaneous closure does not occur. Natural history same as secundum ASD.
  26. 26. 04/29/15 DR. M. S. PRASAD 26 ASD History: Usually asymptomatic. Physical Examination: Thin built. There is absence of sinus arrhythmia. Wide & fixed splitting of 2nd Heart Sound. Ejection Systolic Murmur. ECG CXR Echocardiogram
  27. 27. 04/29/15 DR. M. S. PRASAD 27 ASD ECG: Features of RBBB rsR/ pattern V1 Mild RVH RAD CXR: Cardiomegaly Prominent Pulmonary Conus. Increased Pulmonary Vascular Markings. Echocardiography Diagnostic, shows exact location.
  28. 28. 04/29/15 DR. M. S. PRASAD 28 Atrio-ventricular Septal DefectAtrio-ventricular Septal Defect
  29. 29. 04/29/15 DR. M. S. PRASAD 29 Atrio-Ventricular Septal DefectAtrio-Ventricular Septal Defect Partial (ostium primum) AVSD Atrial Shunting, Mitral Valve is always defective, LV RA shunting may occur. Complete AVSD Strong association with Downs Syndrome, Atrial and Ventricular shunting, AV regurgitation.
  30. 30. 04/29/15 DR. M. S. PRASAD 30 Clinical FeaturesClinical Features FTT Clinical signs of CHF, Signs of the most prominent lesion (ASD, Regurgitation, others)
  31. 31. 04/29/15 DR. M. S. PRASAD 31 ManagementManagement Management of CHF, Corrective surgery.
  32. 32. 04/29/15 DR. M. S. PRASAD 32
  33. 33. 04/29/15 DR. M. S. PRASAD 33 Ventricular Septal Defect (VSD) VSD is the most common cardiac malformation and accounts for 32% of CHD
  34. 34. 04/29/15 DR. M. S. PRASAD 34
  35. 35. 04/29/15 DR. M. S. PRASAD 35 Types of VSD Membranous. Muscular. Swiss Cheese Septum.
  36. 36. 04/29/15 DR. M. S. PRASAD 36 VSD: PathopyhsiologyVSD: Pathopyhsiology LV pressure higher than RV. Blood passes through the defect to RV. RV load is increased. PA receives more volume than expected. This extremely large pulmonary blood flow results into Pulmonary Hypertension.
  37. 37. 04/29/15 DR. M. S. PRASAD 37 Clinical ManifestationsClinical Manifestations
  38. 38. 04/29/15 DR. M. S. PRASAD 38 Small VSDSmall VSD Asymptomatic. Cardiac lesion is usually found during routine physical examination. A loud, harsh, or blowing systolic murmur best heard over the lower left sternal border.
  39. 39. 04/29/15 DR. M. S. PRASAD 39 Large VSDLarge VSD Patients with large defects typically develop CHF. Excessive pulmonary blood flow and Pulmonary Hypertension Dyspnoea or effort intolerance. Poor Growth.
  40. 40. 04/29/15 DR. M. S. PRASAD 40 Large VSDLarge VSD (continued) Profuse Perspiration (Sweating). Recurrent RTI. Feeding difficulty, Systolic Murmur: less harsh, more blowing Loud P2
  41. 41. 04/29/15 DR. M. S. PRASAD 41 VSD:VSD: DiagnosisDiagnosis Most common Acyanotic CHD. CXR: Small VSD: Normal. Large VSD: Cardiomegaly. Increased Pulmonary Vascular Markings. ECG: Small VSD: Normal. Large VSD: Biventricular Hypertrophy. Echocardiogram Cardiac Catheterization.
  42. 42. 04/29/15 DR. M. S. PRASAD 42 Natural HistoryNatural History 65% of VSD present at birth close spontaneously. Remaining cases: FTT, Feeding difficulty, Signs of VSD and CHF.
  43. 43. 04/29/15 DR. M. S. PRASAD 43 ManagementManagement Manage CHF, Surgical closure.
  44. 44. 04/29/15 DR. M. S. PRASAD 44 Patent Ductus ArteriosusPatent Ductus Arteriosus (PDA)(PDA)
  45. 45. 04/29/15 DR. M. S. PRASAD 45 Patent DuctusPatent Ductus arteriosus (PDa)arteriosus (PDa) Patent DuctusPatent Ductus arteriosus (PDa)arteriosus (PDa) PA Aorta RA RV LA LV PVIVC & SVC
  46. 46. 04/29/15 DR. M. S. PRASAD 46
  47. 47. 04/29/15 DR. M. S. PRASAD 47
  48. 48. 04/29/15 DR. M. S. PRASAD 48 PDAPDA More in females [2:1] Maternal Rubella in early pregnancy. Common in premature infants. 10% of PDA is associated with other CHD.
  49. 49. 04/29/15 DR. M. S. PRASAD 49 PDA: Clinical ManifestationsPDA: Clinical Manifestations Wide Pulse Pressure. Bounding Peripheral Pulses. Cardiac Enlargement. Thrill. LSB & below left clavicle. Machinery Murmur. CHF
  50. 50. 04/29/15 DR. M. S. PRASAD 50 PDA: DiagnosisPDA: Diagnosis ECG: Normal/LVH/BVH CXR: Prominent PA & Increased PVM. Echocardiogram: from the suprasternal notch. Colour & Pulsed Doppler Examination. Cardiac Catheterization.
  51. 51. 04/29/15 DR. M. S. PRASAD 51
  52. 52. 04/29/15 DR. M. S. PRASAD 52 Coarctation of Aorta (COA)
  53. 53. 04/29/15 DR. M. S. PRASAD 53 COA COA is a localized or segmental constriction [narrowing] of aorta The size of constriction may vary.
  54. 54. 04/29/15 DR. M. S. PRASAD 54 COACOA It may be at one point or multiple points. It may involve a long segment continuously. Involvement of long segment is known as Tubular Hypoplasia. Sometimes, the the aorta becomes completely atretic and results in an Interrupted Aortic Arch.
  55. 55. 04/29/15 DR. M. S. PRASAD 55 COACOA The COA may occur at any point from the Transverse Arch to the iliac bifurcation. 98% occur just below the origin of the left subclavian artery at the origin of the ductus arteriosus [juxtaductal COA].
  56. 56. 04/29/15 DR. M. S. PRASAD 56 Coarctation of Aorta Two times more common in males. M:F = 2:1
  57. 57. 04/29/15 DR. M. S. PRASAD 57 Types of COATypes of COA o Infantile Type. COA associated with arch hypoplasia was referred to as Infantile Type because its severity led to its recognition in early infancy. o Adult Type. Adult Type referred to isolated juxtaductal COA, which if mild, was not usually recognized until later childhood.
  58. 58. 04/29/15 DR. M. S. PRASAD 58 COA: Clinical Manifestations Weakness and pain after exercise. Hypertension on routine physical examin