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Congenital heart disease

Congenital heart disease. Dr. aso faeq salih Pediatric cadiologist 2013-2014. Ventricular Septal Defect ( VSD ). Most common cardiac malformation  25-30 %. Types of VSD : According to position  perimembranous , inlet , muscular .

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Congenital heart disease

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  1. Congenital heart disease Dr. asofaeqsalih Pediatric cadiologist 2013-2014

  2. Ventricular Septal Defect ( VSD )

  3. Most common cardiac malformation  25-30 % Types of VSD : • According to position  perimembranous , inlet , muscular . • According to size  small , medium , large . Membranous : most common , are usually single ,( called peri membranous ) may extend into adjacent muscle

  4. Muscular : • mid portion of septum to the apex . • Single or multiple (Swiss cheese septum ) Inlet : At level of both Av valve s

  5. Size of defect : • Small (restrictive ) : • Trivial L  R shunt . (LV pressure > RV ) • Normal pulmonary arterial &RV pressure . • Normal cardiac chambers .

  6. Large (non restrictive ) : • > aortic annulus • RV, LV pressure equalizes . • Direction & magnitude of shunt determined by ratio of pulmonary to systemic vascular resistance . • RV , pulmonary arterial hypertension . • Main pulmonary artery , LA , LV are enlarged • Medium will be in between

  7. Pathophysiology :

  8. Clinical features : Varies according to : size of defect , pulmonary blood flow & pressure . • Small VSD : • Most often asymptomatic . • Loud , harsh , blowing , holosystolic murmur heard best over LLSB frequently accompanied by thrill .

  9. Large VSD : • Dyspnea , feeding difficulties , poor growth , profuse perspiration , recurrent chest infection & cardiac failure in early infancy . • Cyanosis usually absent , duskiness noted during crying or infection . Physical signs : • Prominent L precordium , palpable parasternal lift . • Lateral displacement of apex beet , apical thrust . • Holosystolic murmur ( less harsh , more blowing ). • Pulmonary component of S2 may be increased  pulmonary hypertension

  10. Investigations : • CXR : • Small VSD : normal or minimal cardiomegaly . borderline increase in pul. Vasculature . • Large VSD : gross cardiomegaly ( RV , LV, LA PA ). prominent pulmonary vascularity . • ECG: • Small VSD : normal or may suggest LV hypertrophy • Large VSD: biventricular hypertrophy P- wave notched or peaked .

  11. Echocardiography : Cardiac catheterization

  12. Treatment : • Small VSD: • Reassurance & encourage to live normal life with no restriction of activities . • Protection against infective endocarditis . • Regular follow – up

  13. Large VSD : Aim of treatment : • Control the symptoms of H.F . • Prevent the development of pulmonary vascular disease . • Surgical closure of defect : Indications : • Patient at any age with large defect in whom clinical symptoms , FTT cannot be controlled medically . • Supracristal VSD . • VSD complicated with AR or subvalvular PS

  14. Complication of surgery : • Residual defect . • Heart block .

  15. Prognosis & complications : • Small VSD : • Spontaneous closure : 30 – 50 % most often during first 2 years of live ( small muscular are > likely to close ( up to 80 % ) than membranous (up to 35 % ) . • Most often asymptomatic . • Infective endocarditis .

  16. Moderate – Large VSD : • Early & successful therapy may become smaller & up to 8 % may close completely . • Repeated episodes of chest infection . • H.F & FTT . • Pulmonary HT & evidence of pulmonary vascular disease . • Eisen menger complex . • Aortic valve regurgitation • Acquired infundibular pulmonary stenos is .

  17. Patent DuctusArteriosus ( PDA)

  18. 6 – 8 % of CHD , F:M  2 : 1 • Ass. With maternal rubella infection in early pregnancy . • Common problem in premature infants . • Ductus Arteriosus : • Fetal life , patency of Ductus is maintained by : • Relaxant effect of low O2 tension . • Prosta glandines (E2) .

  19. In full term neonates , once Po2 passing through Ductus reaches 50 mmHg Ductal wall constricts . Functional closure of Ductus  10 – 15 hrs. in normal neonate , anatomical occlusion 4 m of age Ligamentum arteriosum

  20. Pathophysiology :

  21. Types &clinical manifestations : • Small PDA : • Usually asymptomatic . • Normal cardiac size . • Pressure within PA , RA & RV are normal .

  22. Large PDA : • PA pressure may be elevated to a systemic pressure . • Risk of pulmonary vascular disease . • Often symptomatic ( HF & growth retardation ). • Bounding peripheral pulsations . • Wide pulse pressure . • Moderate – gross cardiomegaly . • heaving apical impulse. • Thrill (systolic ) max. in 2nd L ICS +/_ radiation . • Machinery continuous murmur max. in 2nd L ICS .

  23. Investigations : • CXR : • Small PDA : normal . • Large PDA : moderate – gross cardiomegaly ( LV , LA ). Prominent intra pul. Vascular marking . normal or prominent aortic knob . • ECG : Small  normal. Large  LV or biventricular hypertrophy.

  24. Echocardiography : • Cardiac Catheterization :

  25. Prognosis & complications : • Small PDA : • May live a normal span with a few or no symptoms . • Spontaneous closure after infancy is extremely rare. • Infective endocarditis .

  26. Large PDA : • HF in early infancy , FTT . • Infective endocarditis . • Pulmonary or systemic emboli .

  27. Treatment : • Surgery : Ligation & division of Ductus , preferably before 1st year of live . • Trans catheter closure of defect.

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