A ventricular septal defect (VSD) is a type of heart defect (congenital heart disease) in which there is a hole in the wall
(septum) between the heart's lower chambers (ventricles). The hole may be as small as a pinpoint, or as large as the space
where the entire septum should be (i.e., the total absence of the septum). Small holes may close on their own during the first
years of life without any symptoms or harmful effects. About 50 percent close by the age of three. However, small holes that
do not close on their own could lead to the production of blood clots that may be carried to the brain and cause a stroke.
Larger holes allow more blood to pass through, increasing the risk of symptoms and other harmful effects. For example, they
may cause other conditions, including arrhythmias (abnormal heart rhythms).

Oxygen-rich blood in the left ventricle normally leaves the heart through the aorta. However, a VSD causes some of the blood
from the left ventricle to be diverted (shunted) through the VSD and into the right ventricle, where it mixes with blue, oxygen-
poor blood. The right ventricle of the heart is then receiving blood from two different places: from the right atrium, as it
should, and from the left ventricle (through the VSD). This results in too much blood flow to the right side of the heart and
lungs. The more blood that is diverted to the right side of the heart, the harder the lungs and right ventricle must work to
compensate for the problem.

Eventually, the stress on the overworked right ventricle may cause it to weaken and/or enlarge. Also, the lungs can become
congested from constantly receiving more blood than is needed. Eventually, the congestion and overwork could lead to
arrhythmias (abnormal heart rhythms) or heart failure.

A VSD is a type of left-to-right shunt - a condition in which blood is diverted (shunted) from the left side of the heart to the
right. Left-to-right shunts, which also include atrial septal defect (ASD) and patent ductus arteriosus (PDA), account for over
half of all heart diseases that are present at birth (congenital heart disease).

There are a number of different types of VSDs, which include the following:

1.Membranous VSD. Located near the tricuspid valve, and making up 75 percent of all VSDs, this is the type of VSD
most likely to close on its own.

2.Muscular VSD. This type is less common. Physicians must be careful when diagnosing a muscular VSD, because just
one of them can sometimes look like several.

3.Gerbode defect. Often misdiagnosed, this involves a direct connection between the left ventricle and right atrium when
the tricuspid valve and mitral valve are somewhat displaced.

4.Outflow tract VSD. This is a more rare form of VSD. An outflow tract VSD is unlikely to close on its own.

5.Endocardial cushion VSD. This is a rare form of VSD, and an electrocardiogram (EKG) may also show another
problem that is sometimes associated with it: superior axis deviation.

A VSD may be present by itself, or it may be one of a number of heart conditions, including:

a.Atrial septal defect (ASD). This defect refers to a hole in the septum between the upper chambers of the heart (atria).

b.Total anomalous pulmonary venous connection. Instead of the pulmonary veins connecting with the left atrium, as
they should, they connect to the right atrium.

c.Mitral valve abnormalities. These valvular defects affect the blood flow, often causing it to leak back out from where it
came instead of flowing forward.

What are the symptoms of a VSD?

Although a physician can often find a VSD by listening for a heart murmur (abnormal heart sound), the majority of VSD
patients have no symptoms. Therefore, the defect may be found when a person is three or four years old, or when a person is
30 or 40 years old. If symptoms do appear, they may include frequent chest colds and infections that, if severe enough, can
stunt a young child's growth. Furthermore, the more congested the lungs become, the more susceptible a person is to
pulmonary hypertension - a condition in which blood pressure in the lung's blood vessels is high.

Symptoms of pulmonary hypertension include the following:

a.Bluish skin (cyanosis)

b.Chest pain

c.Coughing (sometimes with blood)

d.Distended neck veins

e.Dizziness

f.Enlarged liver

g.Fainting (syncope)

h.Shortness of breath

i.Swelling (edema) in the ankles or feet

j.Swollen abdomen

k.Tiring easily

How is a VSD diagnosed?

Because children with a VSD often have no symptoms, the VSD is usually first noticed during routine testing or medical
check-ups. Most commonly, it is found when a physician uses a stethoscope to listen for a heart murmur. However, not all
heart murmurs are signs of a VSD. Therefore, the physician will often listen to the patient's heart a number of times over a 6-
to 12-month period before ordering further testing.

An echocardiogram of the heart and major arteries is often the next test to find a possible VSD. This test uses sound waves to
visualize the structure and function of the heart. A moving image of the patient's beating heart is played on a video monitor,
where a physician can study the heart's thickness, size and function. The image also shows the motion pattern and structure of
the four heart valves, revealing any potential leakage (regurgitation). During this test, a Doppler ultrasound may also be done to
evaluate blood flow in the coronary arteries, the blood vessels of the arms and legs, and the carotid arteries in the neck.

What is the treatment for a VSD?

Physicians may wish to wait long enough to see if the VSD will close on its own, particularly if it is a membranous VSD
(which has the highest chance of self-closing). A VSD that does not close on its own after birth will need treatment. The
physician may wish to try to treat the VSD with medications, which may include the following:

a.Afterload reducing agents. Reduce the amount of blood that passes through the VSD from the left ventricle to the
right.

b.Diuretics. Promote the formation of urine in the kidneys, causing the body to flush out fluids and minerals.

c.Inotropes. Increase the heart's pumping efficiency, so it needs less energy to pump harder.

If the medications are not working, or the VSD is too large, or the child has already passed the age at which the VSD would
have closed, the physician will often choose to do surgery. Most often this surgery involves a (sternotomy), an operation in
which the breastbone (sternum) is divided in two to open the chest and expose the heart. The strategy for closing a defect
during surgery depends on the size of the hole. Smaller holes are closed by stitches (sutures). Larger holes are patched with a
large "swatch" made of either a synthetic material or the patient's own tissue (often from the fluid-filled sac around the heart
called the pericardium). When a VSD occurs along with other defects, the surgery becomes more complicated. However, the
surgery to treat a VSD alone has a relatively low risk, high rate of success and short hospital stay (three to five days).

Minimally invasive techniques are being tested to repair septal defects. Researchers are evaluating a method to squeeze a patch
into a catheter and snake it through the body up to the heart. Once in place, the physician can place the patch over the hole,
sealing it. The patch eventually becomes covered with the body's tissues.

Can a VSD be prevented?

While certain types of congenital heart disease may be diagnosed in-utero, the reason for their developing in the first place is
frequently unknown. This is true for VSD. With this in mind, prevention is not always a possibility. However, it has been
shown that any type of congenital heart disease in either the mother or father increases the risk of a defect in the developing
foetus. The risk of inheriting a congenital heart condition from the father increases by up to 3 percent; from the mother up to
18 percent. For this and other "higher risk" situations, experts recommend genetic counselling and access to an experienced
obstetrician and paediatric cardiologist to help ensure a healthy pre- and postnatal course.

Genetic research continues to make progress in identifying proteins involved in heart structure and function, and how
abnormal (mutated) forms of those proteins influence congenital heart defects. For example, scientists have uncovered
mutations in genes responsible for a normal heart septum. It is hoped that DNA testing will allow for early diagnosis (and,
therefore, early treatment) for many types of septal defects.

Ventricular Septal Defect