1 / 29

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 .

rue
Download Presentation

Congenital heart disease

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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.

More Related