CYANOTIC
Increased pulmonary Mixed
bloodflow blood flow
1. TOF 1. Transposition of great arteries
2. Tricuspid atresia 2. Total anomalous pulmonary
3. Epstien anomaly venous return
3. Truncus arteriosus
4. Hypoplastic left heart
syndrome
9.
INCIDENCE
.
CHD affects 8to 12 of every 1,000 neonates
In spontaneously aborted and stillborn fetus,
the incidence is much higher
10.
ETIOLOGY
90% of theetiology of congenital cardiac
defects is unknown.
Most are thought to be a result of
multifactorial inheritance.
11.
Risk factors
Fetal exposureto drugs such as phenytoin, lithium and
radiation.
Maternal viral infections such as rubella.
Maternal metabolic disorders such as phenylketonuria
and insulin-dependent diabetes mellitus.
Maternal complications of pregnancy such as increased
age and ante partal bleeding.
Maternal dietary deficiencies.
Genetic factors
Chromosomal abnormalities like Turner syndrome,
Down syndrome and Trisomy 13 and 18.
13.
LEFT TO RIGHTSHUNT
(ACYANOTIC)
RIGHT TO LEFT SHUNT
(CYANOTIC)
1. Acyanotic heartdisease is a congenital heart defect that
occurs when blood is pumped abnormally around the
body, but still contains enough oxygen.
DEFINITION
DEFINITION
• Ventricular SeptalDefect is a congenital
disorder in which blood moves from left
ventricle to right ventricle through a
defective ventricular septum. It may vary in
size from very small defects (Roger’s defect)
to very large defect.
19.
INCIDENCE
It is themost common congenital heart defect, occurring
in approximately 30% to 40% of all children with
congenital heart disease.
Many VSDs (20 – 60%) are thought to close
spontaneously.
Spontaneous closure is most likely to occur during the
first year of life in children having small or moderate
defects.
20.
CLASSIFICATION
1. Membranous VSD-The most common type, accounting
for about 80% of cases, and occurring in the upper
section of the ventricular septum.
2. Muscular VSD- These defects are surrounded by
muscular tissue and may occur anywhere in the septum
Accounts for about 20% of VSDs in infants, and often
involves more than one hole.
3. Inlet VSD - Occurs just below the tricuspid valve in the
right ventricle and the mitral valve in the left ventricle.
4. Outlet (conoventricular) VSD - Creates a hole just
before the pulmonary valve in the right ventricle and
just before the aortic valve in the left ventricle
22.
ETIOLOGY
•Ventricular Septal Defect(VSD) occurs
when the wall that separates the heart's
left and right ventricles doesn't fully form
during a baby's development.
23.
The cause ofVSD is often unknown, but it can be due to:
1. Developmental abnormalities: During the heart's
development, the interventricular septum may not form
properly.
2. Genetic syndromes: Changes in chromosomes or genes
can cause VSDs.
3. Environmental factors: A combination of genes and
environmental factors, such as what a mother eats,
drinks, or takes, may increase the risk of VSD.
ETIOLOGY
24.
Left to rightshunt
Portion of oxygenated blood from left ventricle enters the right ventricle
Magnitude of shunt is determined by the size of VSD and amount of pulmonary vascular
resistance (PVR) present
High PVR in newborn
It will elevate right ventricular pressure (approximate to left ventricular pressure)
Decrease shunting across VSD
Child may be asymptomatic
As PVR decreases over the first 1-2 months of life
Child become symptomatic
PATHOPHYSIOLOGY
25.
CLINICAL MANIFESTATIONS
Only 15%of VSDs are large enough to cause symptoms.
Small VSD usually asymptomatic; high spontaneous
closure rate during the first year of life.
Large VSDs.
CHF: tachypnea, tachycardia, excessive sweating associated
with feeding
Frequent Upper Respiratory Infections.
Poor weight gain, failure to thrive.
Feeding difficulties.
Decreased exercise tolerance.
MANAGEMENT
It has beenestimated that, about 70-80% of all VSD
become smaller in size or disappear entirely, and is
known as spontaneous closure.
In almost 90% of the patient with spontaneous closure
occurs by the age of 3yrs, though it may occur as late as
25 yrs or more.
Treatment is conservative when no signs of congestive
heart disease or pulmonary hypertension are present.
28.
MANAGEMENT
• Infants withsmall VSDs require no surgery, except
antibiotics.
• Infants with moderate to large VSDs who are symptomatic
are usually medically managed with a combination of
Digoxin and Diuretics.
• If the infant continues to show signs of congestive heart
failure, early surgical repair is indicated.
29.
SURGICAL MANAGEMENT
• Surgicalrepair of VSD is an Open heart procedure.
• Moderate to small size VSDs are closed by Purse
string sutures.
• Large defects, a synthetic Dacron patch is used to
close the defect.
30.
NURSING MANAGEMENT
1. Regularcheckups
• Children with VSDs should have regular checkups with a
cardiologist. The frequency of checkups depends on the size
of the VSD and the child's age.
2. Medications
• Children with VSDs may need medications to treat
symptoms or help the heart work better.
3. Surgery
• Nurse should give pre-operative and post operative care.
31.
NURSING MANAGEMENT
4. Nutrition
•Children with VSDs may need extra nutrition to help them
grow. Babies who are failing to thrive may need a high-
calorie formula or fortified breast milk.
5. Antibiotics
• Children with VSDs may need antibiotics before certain
dental or surgical procedures to prevent infection.
6. Hygiene
• Children with VSDs should maintain good hygiene to
minimize the risk of infection
7. Vaccines
• Children with VSDs should get all the recommended
vaccines .eg. Influenza vaccine
32.
NURSING MANAGEMENT
8. Avoidsmoke
• Children with VSDs should be kept away from smoke.
9. Monitor potassium levels
• Children with VSDs should be monitored for potassium
levels, as low levels can lead to digoxin toxicity.
10. Monitor heart rhythm
• Children with VSDs should be monitored for heart
rhythm, as dysrhythmia(irregular hearbeat) is an early
sign of problems.
33.
PROGNOSIS
Highest risk associatedwith surgical repair is in the
first few months of life.
Children respond well to surgery and experience
substantial “catch up” growth
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