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Ventricular septal defect

From Wikipedia, the free encyclopedia

A Ventricular septal defect

ventricular
septal Classification and external resources
defect
(VSD) is a
defect in the
ventricular
septum, the
wall
dividing the
left and
right
ventricles of
the heart.

The Echocardiographic image of a moderate ventricular septal defect in the mid-muscular part of the
ventricular septum. The trace in the lower left shows the flow during one complete cardiac cycle and the red
septum mark the time in the cardiac cycle that the image was captured. Colours are used to represent the
consists of
velocity of the blood. Flow is from the left ventricle (right on image) to the right ventricle (left on
an inferior
muscular image). The size and position is typical for a VSD in the newborn period.
and superior ICD-10 Q21.0 (http://apps.who.int/classifications/apps/icd/icd10online/?gq20.htm+q210)
ICD-9 745.4 (http://www.icd9data.com/getICD9Code.ashx?icd9=745.4)
DiseasesDB 13808 (http://www.diseasesdatabase.com/ddb13808.htm)

eMedicine med/3517 (http://www.emedicine.com/med/topic3517.htm)

MeSH C14.240.400.560.540 (http://www.nlm.nih.gov/cgi/mesh/2008/MB_cgi?
mode=&term=Ventricular+Septal+Defects&field=entry#TreeC14.240.400.560.540)

membranous portion and is extensively innervated

with conducting cardiomyocytes.

The membranous portion, which is close to the

atrioventricular node, is most commonly affected in
adults and older children.[1][2]

Muscular ventricular septal defect is the most

common type, and may lie in four locations:
anterior, midventricular, posterior, apical[3]
Congenital VSDs are collectively the most common
congenital heart defects.[4]

Ventricular septal defect

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Diagnosis
A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holo- or
pansystolic murmur. Auscultation is generally considered sufficient for detecting a significant VSD. The
murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right
ventricle. If there is not much difference in pressure between the left and right ventricles, then the flow
of blood through the VSD will not be very great and the VSD may be silent. This situation occurs a) in
the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after
birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired
VSD. Confirmation of cardiac auscultation can be obtained by non-invasive cardiac ultrasound
(echocardiography). To more accurately measure ventricular pressures, cardiac catheterization, can be
performed.

Pathophysiology
During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right
ventricle, 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 left ventricle normally has a much higher systolic pressure (~120 mm Hg)
than the right ventricle (~20 mm Hg), the leakage of blood into the right ventricle therefore elevates
right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms.
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. Four
different septal defects exist, with perimembranous most common, outlet, atrioventricular, and muscular
less commonly.[5]

Signs and symptoms

Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.

Symptoms
VSD is an acyanotic congenital heart defect, aka a Left-to-right shunt, so there are no signs of cyanosis.

Signs
■ Pansystolic (Holosystolic) murmur (depending upon the size of the defect) +/- palpable thrill
(palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a
parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the
heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoiec
(breathe faster) with feeds [Textbook of Paediatric Emergency Medicine. p116-117 eds Cameron
P. et al. Elsevier 2006].

CAUSES: The cause of VSD ( ventricular septal defect) includes the incomplete looping of the heart
during days 24-28 of development. Faults with NKX2.5 gene can cause this.

Treatment

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Most cases don't need treatment and heal at the first

years of life. Treatment is either conservative or
surgical. Smaller congenital VSDs often close on
their own, as the heart grows, and in such cases may
be treated conservatively. Some cases may
necessitate surgical intervention, i.e. with the
following indications:
A nitinol device for closing muscular VSDs, 4 mm
1. Failure of congestive cardiac failure to respond to
diameter in the centre. It is shown mounted on the
medications
catheter into which it will be withdrawn during
2. VSD with pulmonic stenosis insertion.

3. Large VSD with pulmonary hypertension

4. VSD with aortic regurgitation

For the surgical procedure, a heart-lung machine is required and a median sternotomy is performed.
Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only
suitable for certain patients. Repair of most VSDs is complicated by the fact that the conducting system
of the heart is in the immediate vicinity.

Ventricular septum defect in infants is initially treated medically with cardiac glycosides (e.g., digoxin
10-20mcg/kg per day), loop diuretics (e.g., furosemide 1–3 mg/kg per day) and ACE inhibitors (e.g.,
captopril 0.5–2 mg/kg per day).

Surgical technique for Repair of Perimembranous VSD

a) Surgical closure of a Perimembranous VSD is performed on cardiopulmonary bypass with ischemic
arrest. Patients are usually cooled to 28 degrees. Percutaneous Device closure of these defects is rarely
performed in the United States because of the reported incidence of both early and late onset complete
heart block after device closure, presumably secondary to device trauma to the AV node.

b) Surgical exposure is achieved through the right atrium. The tricuspid valve septal leaflet is retracted
or incised to expose the defect margins.

c) Several patch materials are available, including native pericardium, bovine pericardium, PTFE
(Goretex(tm) or Impra(tm), or dacron.

d) Suture techniques include horizontal pledgeted mattress sutures, and running polypropylene suture.

e) Critical attention is necessary to avoid injury to the conduction system located on the left ventricular
side of the interventricular septum near the papillary muscle of the conus.

f) Care is taken to avoid injury to the aortic valve with sutures.

g) Once the repair is complete, the heart is extensively deaired by venting blood through the aortic
cardioplegia site, and by infusing Carbon Dioxide into the operative field to displace air.

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h) Intraoperative transesophageal echocardiography is used to confirm secure closure of the VSD,

normal function of the aortic and tricuspid valves, good ventricular function, and the elimination of all
air from the left side of the heart.

i) The sternum, fascia and skin are closed, with potential placement of a local anesthetic infusion
catheter under the fascia, to enhance postoperative pain control.

j) A video of Perimembranous VSD repair, including the operative technique, and the daily
postoperative recovery, can be seen here: VSD Repair, Perimembranous Ventricular Septal Defect
(http://www.youtube.com/watch?v=Uf_tRlG1nMc)

Epidemiology and Etiology

VSDs are the most common congenital cardiac anomalies. They are found in 30-60% of all newborns
with a congenital heart defect, or about 2-6 per 1000 births. During heart formation, when the heart
begins life as a hollow tube, it begins to partition, forming a septa. If this does not occur properly it can
lead to an opening being left within the ventricular septum. It is debatable whether all those defects are
true heart defects, or if some of them are normal phenomena, since most of the trabecular VSDs close
spontaneously.[6] Prospective studies give a prevalence of 2-5 per 100 births of trabecular VSDs that
closes shortly after birth in 80-90% of the cases.[7][8]

Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome.[9]

A VSD can also form a few days after a myocardial infarction[10] (heart attack) due to mechanical
tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart
tissue.

See also
■ Atrial septal defect
■ Atrioventricular septal defect
■ Cardiac output
■ Congenital heart disease
■ Heart sounds
■ Pulmonary hypertension

Additional images

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