VENTRICULAR SEPTAL DEFECTS

NORMAL HEART

 has four chambers

 two upper chambers are atriums
 atriums are separated by IVS Membranacea
 two lower chambers are called ventricles
 ventricles are seperated by IVS Muscularis
 RV pumps blood to the lungs (pulmonary
circulation)
 LV pumps blood throughout the body (systemic
circulation)
 ETIOLOGY of VCD

 GENETICS :chromosomes abnormalities

(trisomies 13,15,18,21 & Turner
syndrome)
 ENVIRONMENT :congenital rubella
infection
 90% are idiopathic
 ABNORMAL HEART

 If there is a hole in the septum that

separates the two ventricles (VSD), blood
from the left ventricle can enter the right
ventricle
 This blood recycles through the lungs
before returning to the left ventricle.
 This results in less oxygenated blood
reaching the body.
 If the hole is sufficiently large, lack of
oxygen being delivered to the body
 NORMAL HEMODYNAMIC

Un oxygenated returns to RA Then RV pumps

blood from the body the blood to the lungs

to exchange for
the oxygenated Blood
oxygen
blood returns to LA leaving the lungs

then into LV provide oxygen

Blood is pumped
to all the
out
tissues of the body
 PATHOPHYSIOLOGY VSD

Right to left shunt Eisenmenger’s syndrome

Ventricular septal
defect

RV Pa >> LV Pa cyanosis
LV Pa >> RV Pa

LV volume
Pulmonary
overloaded
hypertension
Pan systolic murmur

↑ vessel LV hypertrophy to
Left to right shunt resistance maintain cardiac o/put

↑ pulmonary blood 3rd heart

↑ volume at RV flow sound
 During systole, some of the blood from LV leaks intoRV,
passes through the lungs and reenters the left ventricle
via the pulmonary veins and left atrium.
 This has two net effects.
 First, the circuitous refluxing of blood causes volume
overload on the left ventricle.
 Second, because the LV normally has a much higher
systolic pressure (~120 mm Hg) than the RV (~20 mm
Hg), the leakage of blood into the RV therefore elevates
RV pressure and volume, causing pulmonary
hypertension
 This effect is more noticeable in patients with larger
defects, who may present with breathlessness, poor
feeding and failure to thrive in infancy. Patients with
smaller defects may be asymptomatic.
 SIGNS AND SYMPTOMS

 Poor weight gain/ slowing of weight gain in the first

months of life

 Unusual behavior

 Shortness of breath

 breathing difficulty of any type, or worsening of an

existing breathing problem

 Bluish color of the skin, lips, or under the nails

 Unusual/ unexplained sweating

Exams and Tests

 echocardiogram (an ultrasound picture of

the heart)
 chest x-ray
 blood tests
 physical examination
ECHOCARDIOGRAPHY
 The presence of a hole in the heart can be
confirmed by echocardiogram. This painless
test uses ultrasound waves to construct a
moving picture of the heart. It can quantitate
the size of the left-to-right shunt
 enlargement of the left ventricle, pressure in
the lungs, and actually estimate the degree
of shunting by an empirical formula
 The trace in the lower left shows the flow during
one complete cardiac cycle and the red mark the
time in the cardiac cycle that the image was
captured. Colours are used to represent the
velocity of the blood. Flow is from the left
ventricle (right on image) to the right ventricle
(left on image).
X-RAY
 Chest x-ray is useful to see if
 the overall heart size is enlarged
 plus evidence of fluid in the lungs or
pulmonary congestion
ECG
 An electrocardiogram is helpful in
checking to see if the left ventricle is the
dominant working muscle
 the more of right ventricular enlargement
or hypertrophy seen
 the more the physician must worry about
pulmonary hypertension, and therefore
operate sooner.
PHYSICAL EXAMINATION
 A ventricular septal defect is detected on
physical examination by a systolic murmur
audible with a stethoscope along the lower
left sternal or breast bone border
 It is related to the oxygenated blood
“swishing” through the hole or VSD into
the right ventricle.
 TREATMENT

 Surgical Therapy
They often close on their own in childhood or adolescence. But if the
opening is large, even in patients with few symptoms, closing the hole in the
first two years of life is recommended to prevent serious problems later.
 Usually the defect is closed with a patch. Over time the normal heart lining
tissue covers the patch, so it becomes a permanent part of the heart. Some
defects can be sewn closed without a patch. Repairing a VSD restores the
blood circulation to normal. The long-term outlook is good.

 Medical
After their VSD is closed, patients should be examined regularly. Make sure
that the heart is working normally.

 Activity Restrictions
Most patients won't need to limit their activity. However, if you have
pulmonary hypertension or your heart doesn't pump as well as it used to,
you may need to limit your activity to how much you can endure. Your
cardiologist will help determine if you need to limit your activity.

 Endocarditis Prevention
Unclosed VSDs require endocarditis prophylaxis. After the VSD is
successfully closed, preventive treatment is needed only during a six-month
healing period.