Ventricular septal defect is an abnormal communication through the septum separating the right and left ventricles. It can be single or multiple, located in different areas of the septum. Most are asymptomatic at birth but may later cause failure to thrive and heart failure as pulmonary resistance decreases. Diagnosis is via echocardiogram. Small VSDs often close spontaneously but large defects require closure to prevent long term effects like pulmonary hypertension. Surgical patch closure is standard treatment for large unclosed VSDs.

1. Ventricular septal defect

2. DEFINITION
• Abnormal communication through the septum that separates the
right and left ventricles of the heart.

3. Classification
• Number
• may be large or small, single or multiple.
• Location
• Membranous (75% to 80%)
• Muscular or trabecular (5% to 20%) / Spontaneous closure is common.
• Canal or inlet (8%): This defect commonly lies beneath the septal leaflet of
the tricuspid valve; associated with Down syndrome.
• Subarterial, outlet, infundibular, or supracristal (5% to 7%): This is the least
common type of defect. It is usually found beneath the aortic valve, and it
may lead to aortic regurgitation. High prevalence in Asian population.

4. EPIDEMIOLOGY/DEMOGRAPHY
• 30% of all CHD
• 25% of all CHD in children and 10% of defects in adults
• 3 to 3.5 infants per 1000 live births and 0.5/1000 adults.
• M=F
•

5. Associated
• Atrial septal defect (35%)
• Patent ductus arteriosus (22%)
• Coarctation of the aorta (17%)
• Subvalvular aortic stenosis (4%)
• Subpulmonic stenosis, usually associated with progressive aortic
regurgitation caused by prolapse of the aortic cusp through the defect
• Multiple VSDs are more prevalent among patients with tetralogy of
Fallot and double-outlet right ventricular defects.

6. Hemodynamic

7. CLINICAL
• Dictated by the size of the defect and the ratio of the PVR/SVR
• Defects
• of ≤25% of the aortic annulus diameter- small
• 25% to 75% of aortic annulus diameter are considered to be moderate in size
• ≥75% of the aortic annulus diameter
• Infants
• Asymptomatic at birth because of elevated PVR. During the first few weeks of life, pulmonary arterial
resistance decreases, thereby allowing for more left-to-right shunting through the VSD. This results in a
the left atrium, and the left ventricle, which can potentially cause left ventricular volume overload.
Tachypnea, failure to thrive, and congestive heart failure may then ensue.
• Adults
• Eissenmenger
• Physical findings
• Holosystolic murmur, Systolic thrill, Mid-diastolic rumble ,S3 , Rales
• PAH-P2 loud,Cyanosis, clubbing, right ventricular heave, and signs of right heart failure

8. ETIOLOGY
• Usually congenital but can be acquired.
• Acquired VSD may result from postsurgical residual leak, trauma, or
myocardial infarction.
• Post infarct ventricular septal defect (PIVSD) typically occurs 1 to 5
days after the event in 0.2% of patients in the current fibrinolysis,
primary angioplasty era.

9. . DIAGNOSIS
• ECHO
• LAB
• SAT DATA

10. IMAGING STUDIES
• Ecg
• Echo
• Cath
• MRI

11. CARE
• Closure
• Infants with CHF . Unrestrictive VSDs require surgical intervention within the first 2 yr of life
to prevent pulmonary hypertension.
• A Children between the ages of 1 and 6 yr with persistent VSD and a pulmonary-to-systemic
blood flow ratio (Qp/Qs) of >2:1
• Adults with a Qp/Qs of ≥2 and clinical evidence of left ventricular volume overload (class I):
• Positive history of infective endocarditis (IE) (class I)
• Adults with a Qp/Qs of >1.5 with pulmonary artery pressure that is less than two thirds of
the systemic pressure and pulmonary vascular resistance that is less than two thirds of the
systemic vascular resistance (class IIa)
• Adults with a Qp/Qs of >1.5 in the presence of left ventricular systolic or diastolic failure
(class IIa)
• Surgical closure is not indicated for VSD with severe irreversible PAH.
• Surgical closure with Dacron or Gore-Tex patches or primary surgical closure has
long been the gold standard of therapy. It has low operative mortality (<2%) at
experienced centers.

12. Triage
• 75% to 80% of small VSDs close spontaneously by the time the patient reaches the age of 10 yr.
• Only 10% to 15% of large VSDs will close spontaneously.
• Large VSDs that are left untreated may lead to arrhythmias, congestive heart failure, pulmonary
hypertension, and Eisenmenger’s complex.
• Eisenmenger’s complex carries a poor prognosis, with most patients dying before the age of 40
yr.
• Follow
• AR/CAD/TR/ degree of L-R shunting/LVSD/PAH/PS/DCRV/Gasul/SAM/Arrhythmia/CHB/Embolism/IE

13. REFERRAL
• All

14. Conclusion
• A Small VSDs cause loud murmurs.
• Eisenmenger complex-No audible murmur.
• The risk of patients with unrepaired VSD developing infective endocarditis is 4%. The risk is higher if aortic insufficiency is present.
• Endocarditis
• routine antibiotic prophylaxis for dental or surgical procedures is no longer indicated for isolated VSDs, except in the following circumstances:
• In the presence of complex congenital heart disease with cyanosis
• In the presence of a residual VSD after surgical closure
• During the first 6 mo after surgical patch or percutaneous transcatheter closure
• Myocardial infarction with murmur-? VSD.
• Pregnancy
• tolerated in women with small VSDs, no pulmonary artery hypertension, and no associated lesions
• severe pulmonary artery hypertension or Eisenmenger’s physiology should be counseled against
• Risk
• Maternal use of valproic acid and phenytoin has also been suggested to cause structural defects.
• Closure
• Device, periventricular device closure of VSD without cardiopulmonary bypass and surgical

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