Transcript Ventricular Septal Defect ( VSD )

Congenital heart disease
Dr. aso faeq salih
Pediatric cadiologist
2013-2014
Ventricular Septal
( VSD )
Defect
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
Muscular :
 mid portion of septum to the apex .
 Single or multiple (Swiss cheese septum )
Inlet :
At level of both Av valve s
 Size of defect :
 Small (restrictive ) :
 Trivial L  R shunt . (LV pressure > RV )
 Normal pulmonary arterial &RV pressure .
 Normal cardiac chambers .
 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
Pathophysiology :
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 .
 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 para sternal lift .
 Lateral displacement of apex beet , apical thrust .
 Holosystolic murmur ( less harsh , more blowing ).
 Pulmonary component of S2 may be increased 
pulmonary hypertension
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 .
Echocardiography :
Cardiac catheterization
Treatment :
Small VSD:
 Reassurance & encourage to live normal life
with no restriction of activities .
 Protection against infective endocarditis .
 Regular follow – up
Large VSD :
Aim of treatment :
 Control the symptoms of H.F .
 Prevent the development of pulmonary vascular
disease .
 Surgical closure of defect : Indications :
1. Patient at any age with large defect in whom clinical
symptoms , FTT cannot be controlled medically .
2. Supracristal VSD .
3. VSD complicated with AR or subvalvular PS
 Complication of surgery :
 Residual defect .
 Heart block .
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 .
 Moderate – Large VSD :
• Early & successful therapy may become smaller &
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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 .
Patent
Ductus
Arteriosus
( PDA)
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) .
•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
Pathophysiology :
Types &clinical manifestations :
 Small PDA :
 Usually asymptomatic .
 Normal cardiac size .
 Pressure within PA , RA & RV are normal .
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 .
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.
 Echocardiography :
Cardiac Catheterization :
Prognosis & complications :
 Small PDA :
 May live a normal span with a few or no
symptoms .
 Spontaneous closure after infancy is extremely
rare.
 Infective endocarditis .
 Large PDA :
 HF in early infancy , FTT .
 Infective endocarditis .
 Pulmonary or systemic emboli .
Treatment :
 Surgery :
Ligation & division of Ductus , preferably before
1st year of live .
 Trans catheter closure of defect.