Ventricular septal defect (VSD) is a defect in the wall separating the left and right ventricles of the heart. There are four main types of VSD based on location. A VSD allows blood to flow from the left ventricle to the right ventricle, overloading the right ventricle and lungs. Symptoms depend on the size of the shunt but can include heart failure, pulmonary hypertension, and abnormal heart sounds. VSDs are typically diagnosed via echocardiogram and may close on their own, though large defects often require surgical closure to prevent complications later in life. With treatment, long-term prognosis is excellent.

1. V E N T R I C U L A R
S E P T A L D E F E C T
By: Shayan Fatima Azad 1

2. By: Shayan Fatima Azad 2

3. WHAT IS VSD?
• VSD is a defect in interventricular
septum that allows a left to right
shunting of blood.
• Approximately 2-8 out of 1000 live
births are affected withVSD.
• They may occur separately.
• They may also occur as complex
set of cardiac abnormalities.
By: Shayan Fatima Azad 3

4. By: Shayan Fatima Azad 4

5. ANATOMICAL TYPES
Four main anatomical types based upon anatomical subsections of the interventricular septum.
VSDType Name Synonym Occurance Description/Location
Type 1 Peri membranous defect ConoventricularVSD 70-80%
Most common
Usually located within the
membranous septum and may extend
to tricuspid valve annulas or base of
the aortic valve.
Type 2 Muscular defect TrabecularVSD 10% Located within the membranous
septum and often multiple.
Type 3 Atrioventricular defect Atrioventricular canal
type
5% Located in atrioventricular canal
beneath the tricuspid valve.
Type 4 Sub arterial defect Infundibular or sub
arterialVSD
5-10% Lies with in the canal septum
immediately subaortic.
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7. PATHOPHYSIOLOGY
• A defect in the interventricular septum allows communication between the systemic and pulmonary circulations.
• As a result, flow moves from a region of high pressure to a region of low pressure—that is, from the LV to the RV (a
left-to-right shunt).
• The pathophysiologic effects of aVSD derive from the hemodynamic effects secondary to a left-to-right shunt and
from changes in the pulmonary vasculature.
• A left-to-right shunt at the ventricular level has following hemodynamic consequences:
1. Increased LV volume load
2. Excessive pulmonary blood flow (may lead to progressive edema and congestive cardiac failure).
3. Reduced systemic cardiac output
4. Elevated pulmonary artery pressures (due to persistent elevated pulmonary blood flow and pulmonary vascular
resistance lead to irreversible pulmonary hypertension)
They may also result in reversal of flow across the defect called as Eisenmenger’s syndrome
By: Shayan Fatima Azad 7

8. PATHOPHYSIOLOGY OF SHUNTING
The pressure generated during
contraction by the left
ventricle is higher than that
generated by the simultaneous
contraction of the right
ventricle. Blood will thus be
pushed through the VSD (also
called "shunted") from the left
ventricle to the right ventricle.
The right ventricle has to do
extra work to handle the
additional blood volume. It
may have trouble keeping up
with the load and enlarge,
affecting its ability to pump
efficiently.
In addition, the lungs receive
too much blood under too
much pressure.
The arterioles (small arteries)
in the lungs thicken in
response to the excess blood
under excess pressure. If this
extra pressure persists,
permanent damage can be
done to the lungs.
It makes a considerable
difference whether the size of
the VSD is small or large
By: Shayan Fatima Azad 8

9. CLINICAL
PRESENTATION
Depends upon:
• The magnitude of the left-to-right shunt
• Also depend upon size of shunt
• Pulmonary and systemic resistance
In first five years 30-50%VSD closes spontaneously
Clinically:
• A loud pan systolic murmur can be detected at left
sternal border
• Congestive cardiac failure (in first 2 months of life)
• Pulmonary hypertension
• Eisenmenger’s syndrome (in second decade of life)
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10. SIZES OF VSD
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11. RISK FACTORS
Factors affecting the
developing fetal heart can
be associated with
development ofVSDs.
Genetic conditions
(chromosomal, single gene
or polygenic), like trisomy
(Edward’s, Patau,Turner’s,
Down’s syndrome)
Environmental influences
Fetal alcohol syndrome
Gestational Diabetes
Mellitus
By: Shayan Fatima Azad 11

12. DIAGNOSIS
ECG
Chest X-Ray
Echocardiography
(degree of shunting)
Cardiac catheterization
(quantify various pressures
between chambers and to assess
the degree of pulmonary HTN
and Oxygen saturation)
By: Shayan Fatima Azad 12

13. WHAT TO DO??
Medical therapy
Surgical closure
(in case of failure of medical therapy)
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14. COMPLICATIONS
Aortic
regurgitation
Progressive
infundibular
stenosis
Infective
endocarditis
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15. PROGNOSIS
• Long term prognosis is excellent
• If treated within 1-2 years of life
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16. HOPE YOU HAVE NO QUESTION
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