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Group I - Acyanotic CHDs

  1. Atrial septal defect [ASD]
    1. ASD is an abnormal communication between the two atria
    2. The ostium secundum type of atrial septal defect is generally anatomically located at the fossa ovalis (common) Q
    3. Ostium primum type of the defect (Partial endocardial cushion defect) is situated inferior to the fossa ovalis (seen in Down's syndrome)
    4. Clinical feature:
      1. Asymptomatic, picked up at routine clinical examination
      2. Subtle effects like FTT, varying degree of exercise intolerance
      3. Clinical evidence of RV enlargement - precordial bulge, parasternal impulse , cystotic thrill at second Intercostal space
      4. S1 normal or increased  
      5. S2 is widely split and fixed*
      6. Ejection systolic murmur at second or third left I/C space. 
      7. CXR - shows increase pulmonary blood flow with right ventricular and right atrial enlargement 
  • Presence of a pansystolic murmur of MR at apex in a patient with other finding of ASD- suggests possibilities of:
  1. If ECG reveals left axis deviation > -30°- it suggests ostium primum type
  2. Floppy mitral valve
  3. A secundum ASD c rheumatic mitral regurgitation
  4. A secundum ASD c cleft mitral valve resulting in regurgitation 
  • ECG:
    Ostium secundum ASD RT axis deviation with Rt VHT
    Ostium primum left axis deviation beyond -30° ** 
  • Natural history
    < 3 mm 100% spontaneous closure
    3-8 mm 80%
    8 mm rarely close spontaneous 
  • Treatment:
  1. Medical                                                        
  2. Exercise restriction unnecessary
  3. Prophylaxis for infective endocarditis is not necessary                    
  4. Treat CHF if occurs
  5. Surgery - risk of operation - 1%                                  
  6. Ideal age - 2-5 years 
  1. Ventricular septal defect (VSD)

  1. Shunt depends upon:
    1. Size of VSD
    2. Pulmonary vascular resistance - Small VSD < 0.5 cm2 - RV pressure is normal— called Restrictive 



- Large VSD > 1 cm2 are Non-restrictive -Rt and Lt ventricular pressure are equal and shunting depend upon pulmonary   vascular resistance


Clinical features:


Small VSD - Usually asymptomatic and detected on routine physical examination

Murmur is loudQ, harsh, blowing and pansystolic.


Large VSD- Symptomatic when PBF increase and manifests as;

  1. Dyspnea
  2. Feeding difficulty
  3. Poor growth
  4. Perspiration
  5. Recurrent chest infection
  6. Congestive heart failure
  7. Precordium is prominent, pansystolic murmur is less harsh than that of small VSDQ
  8. Loud P2 vindicates pulmonary artery hypertension          
  9. CXR - Cardiomegaly (LV type ) With increased pulmonary vascular marking 


  1. CHF in infancy - high mortality
  2. 70-80% become smaller in size or closes
  3. 90% of closures - Ist 3 yr may be but closure may occur upto 25 yrs.
  4. Closure more common in membranous type
  5. VSD in the commonest congenital lesion complicated by infective endocarditis 

Medical management:

  1. Treatment of chest infection
  2. To control heart failure 

If early treatment is successful the shunt may diminish in size with spontaneous improvement during 1st yr of life Indication for surgical closure:

  1. Any age with large VSD in whom clinical symptoms is not controlled medically
  2. Infant between 6 m -12 m of age with large VSD associated with PAH 
  1. Patent Ductus Arteriosus (PDA):
    1. PDA is a communication between the pulmonary artery and aortaQ
    2. The aortic attachment of the ductus arteriosus is just distal to the left subclavian artery
    3. PDA in fetal life R L flow occur as lungs are collapsed
    4. Functional closure occurs soon afterbirth
    5. If patency continues after birth then shunt is L R
    6. Female > male [2:1] Q
    7. Sounds
      1. S1 loud
      2. S2 normal split or paradoxical split (with large L-R shunts)
      3. S3 with small L-R


  1. Shunt murmur continuous (machinery) Q
  2. Flow murmur
    1. Mitral delayed diastolic
    2. Aortic ejection systole

D/D of continuous murmur:

  1. Coronary AV fistula                      
  2. Rupture sinus of Valsalva *
  3. Aortic- pulmonary septal defect            
  4. Bronchial collateral                      
  5. Venous hum 

Term newborn PDA - wall is deficient in mucoid endothelial layer as well as muscular media and it does not close spontaneously


Premature baby PDA-Has normal histology and closes spontaneously Q


Clinical features:

  1. Small PDA asymptomatic
  2. Large PDA
    1. CHF with growth retardation
    2. Wide pulse pressure
    3. Bounding arterial pulses
    4. Cardiac enlargement may be seen 


  1. Continuous murmur is described as machinery murmur & best heard at High second LICS and also well heard below left clavicle.
  2. With large shunt mitral delayed diastolic murmur heard at apex.
  3. CXR shows prominent pulmonary artery with increased pulmonary vascular marking 

Prognosis and complications:

  1. Spontaneous closure is rare.
  2. CHF in early infancy if shunt is large
  3. Infective endocarditis
  4. Pulmonary and systemic emboli may occur 



Indomethacin -3 doses in premature babies


C/I -         Hepatic insufficiency


Renal insufficiency


Low platelet count

Irrespective of age patient with PDA requires surgical or catheter closure

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