ACYNOTIC

HEART DISEASE
VENTRICULAR SEPTAL DEFECT
 DEFINITION
“A hole in the wall between the two lower
chambers is called a ventricular septal defect.”
 RISK FACTORS
• Down syndrome
following conditions during pregnancy can
increase risk of having a newborn with a heart
defect.
• Rubella infection.
Becoming infected with rubella (German
measles) while pregnant can increase the risk
of fetal heart defects. The rubella virus crosses
the placenta and spreads through the fetus'
circulatory system damaging blood vessels and
organs, including the heart.
• Poorly controlled diabetes.
Uncontrolled diabetes in the mother in turn affects the
fetus' blood sugar, causing various damaging effects
to the developing fetus.
• Drug or alcohol use or exposure to certain
substances.
Use of certain medications, alcohol or drugs or
exposure to chemicals or radiation during pregnancy
can harm the developing fetus.
 CLASSIFICATION
May be classified according to location:
membranous (accounting for 80%) or
muscular. May vary in size from a small
pinhole to absence of the septum, which results
in a common ventricle.
 Pathophysiology:
Congenital causes

Abnormal opening between the RV &LV

Pressure in the LV is higher than RV

Blood is shunted from left to right ventricle

 Increase blood flow to the PA

Increase blood flow to the lungs.

Increase pulmonary vascular resistance

Increase pressure in right ventricle.

Right ventricular hypertrophy

cardiac failure
 CLINICAL MANIFESTATION
• Signs and symptoms of serious heart defects
often appear during the first few days, weeks
and months of a life.
• Signs and symptoms of a large ventricular
septal defect may include:
• A bluish tint to the skin, lips and fingernails
(cyanosis)
• Poor eating, failure to thrive.
• Fast breathing or breathlessness.
• Easy tiring
• Swelling of legs, feet or abdomen
• Rapid heart rate
• Sometimes a ventricular septal defect isn't
detected until a person reaches adulthood and
develops signs or symptoms of heart failure,
such as shortness of breath.
 TESTS AND DIAGNOSIS
Ventricular septal defects often cause a heart
murmur that doctor can hear using a
stethoscope. If doctor hears a heart murmur or
finds other signs or symptoms of a heart
defect, he or she may request one or more of
these tests:
• Chest X-ray
• Electrocardiogram (ECG)
• Echocardiogram
• Cardiac catheterization
 TREATMENT
• Spontaneously close
• Antibiotics
• Digoxin and Diurretics
• Surgery
Management of VSD:
1.GENERAL:
a) Treat iron deficiency if present
b) Ineffective endocarditis prophylaxis
c) Treat chest infection promptly
d) Follow up
2.TREATMENT OF CHF
3.SURGICAL TREATMENT:
Indication: Uncontrolled CHF
A) Small Defect : Conservative treatment
Large Defect : Open heart
surgery\Cardiopulmonary bypass.
B) Septal defect are patched up by
a)Prosthetic dacron
b)Direct suture
 C).Pulmonary artery banding:
Placing band around the main PA to decrease PBF.
D) Complete repair by:
Small defect : Purse string approach.
Large defect : Knitted Dacron patch seen over opening
Prognosis:
1.Membranous defect : Low mortality < 5%
2.Multiple muscular defects: High mortality >20%
Complication:
“THE GOOD” “THE BAD”
1.Spontaneous closure 1.CHF.
2.Reduction in size 2.Ineffective endocarditis
3.Growth failure
4.Recurring pneumonia
PULMONARY ARTERY BANDING AND PURSE STRING
APPROACH:
Other complication:
1.Pulmonary hypertension
2.CCF
3.Ineffective endocarditis.
 NURSING MANAGEMENT
Nursing management of infant with acyanotic heart disease
includes helping family members to adjust to the child’s
care &both preoperative &post operative care.
1.General nursing care:
a) Helping family members to adjust
b) During episodes \ Dyspnoea
c) Need for comfort & rest
e) Nutrional needs
f) Psychosocial needs
g) Continuing care
h) Family relationship
i) Financial support
 2.Preoperative care:
It includes
a) Pre operative assessment
b) Pre operative teaching
A)PRE OPERATIVE ASSESSMENT:
1.Admission history &physical examination
2.Pre operative studies
3.Baselines vital status.
4.Anthropometric measurement
5.Additional nursing observation.
B)PRE OPERATIVE TEACHING:
1. Introduction to environment.
2. Introduction to equipment
3.Introduction to postoperative procedures
3.Post operative care:
1. Transfer to ICU
2.Monitor vital signs.
3.Assist in restoring the optimal functioning of the
-Cardiopulmonary
-Gastro intestinal
-Renal
-CNS.
PATENT DUCTUS ARTERIOSUS
(PDA)
 DEFINITION
patent ductus arteriosus (PDA) the vessel does
not close and remains "patent" resulting in
irregular transmission of blood between two of
the most important arteries close to the heart,
the aorta and the pulmonary artery.”
Pathophysiology
 left to right shunt

blood flows from aorta to pulmonary artery

pulmonary overload

oxygenated blood of systemic circulation flows back to

pulmonary circulation

increased vascular pressure in the pulmonary tree

volume load on left heart

PDA and pulmonary hypertension may occur.

CLINICAL MANIFESTATION
PDA is usually diagnosed after age 6 to 8 wk on the basis of a
continuous murmur at the upper left sternal border. The
peripheral pulses are full, with a widened pulse pressure.
While some cases of PDA are asymptomatic, common
symptoms include:
• tachycardia
• shortness of breath
• Cardiomegaly
• Left subclavicular thrill
• Bounding pulse
• Widened pulse pressure
• Patients typically present in good health, with normal
respirations and heart rate. If the ductus is moderate
or large, widened pulse pressure and bounding
peripheral pulses are frequently present, reflecting
increased left ventricular stroke volume and diastolic
runoff of blood into the initially lower-resistant
pulmonary vascular bed. Prominent suprasternal and
carotid pulsations may be noted secondary to
increased left ventricular stroke volume.
• Poor growth
• Differential cyanosis, i.e. cyanosis of the lower
extremities but not of the upper body.
 TREATMENTS
• Medical management
Administration of
indomethacin(prostaglandin inhibitor) has
proved successful in closing a PDA in
preterm infants and some newborns
before the age of 10 days.
Orally dose 0.2mg /kg tds at an interwal of 12 to
24 hours.
 Surgical management
• Transection or ligation of patent ductus arteriosus via a
lateral thoracotomy, a closed heart intervention is
performed. It is done preferably between 3 and 10 years of
age in asymptomatic patients and in symptomatic patients,
it should be done irrespective of age and in the presence of
pulmonary hypertension. The result of surgery is excellent.
Preoperative and post operative care for thoracic surgery
to be provided with all precautions.
 Complications

• A child with PDA can have complications like CCF,

• infective endocarditis,
• pulmonary hypertension and pulmonary vascular occlusive
disease.
• Rarely, calcification of ductus,
• thromboembolism,
• rheumatic heart disease and
• eisenmenger syndrome may develop.
COARCTATION OF THE AORTA
DEFINITION
“Coarctation of the aorta or aortic
coarctation is defined by narrowing
of the aorta, the large blood vessel
that branches off heart and delivers
oxygen-rich blood to body. When this
occurs, heart must pump harder to
force blood through the narrow part of
aorta."
 CAUSES
• Idiopathic cause
• genetic conditions, such as Turner syndrome. .
Women and girls with this syndrome have 45
chromosomes, with one missing or incomplete X
chromosome, instead of 46. About 10 percent of
women and girls with Turner syndrome have aortic
coarctation.
• Coarctation of the aorta usually occurs beyond the
blood vessels that branch off to upper body and
before the blood vessels that lead to lower body. This
often means high blood pressure in arms, but low
blood pressure in legs and ankles.
 PATHOPHYSIOLOGY
• Narrowed aorta produces
increased left ventricular
afterload and wall stress,
left ventricular
hypertrophy, and
congestive heart failure.
• Systemic perfusion is
dependent on the ductal
flow and collateralization
in severe coarctation
 CLINICALMANIFESTATION
• The patient may have high blood pressure and
bounding pulses in the arms
• weak or absent femoral pulses, and cool lower
extremities with lower blood pressure
• signs of congestive heart failure (CHF) in infants.
• critical coarctation
• Hemodynamic condition may deteriorate rapidly with
severe acidosis and hypotension.
• Pale skin
• Irritability
• Profuse sweating
• High blood pressure
• Shortness of breath, especially during exercise
• Headache
• Muscle weakness
• Leg cramps or cold feet
• Nosebleeds
• Left untreated, aortic coarctation in babies may
lead to heart failure and death.
 COMPLICATIONS
• Rupture of the aorta
• Premature coronary artery disease narrowing
of the blood vessels that supply the heart
• Weakened or bulging artery in the brain
(cerebral aneurysm)
In addition, if the coarctation of the aorta is
severe, heart may not be able to pump
adequate blood to the organs of body, resulting
in the failure of organs such as kidneys or
liver.
 TESTS AND DIAGNOSIS
The age at which people with coarctation of the aorta are
diagnosed depends on the severity of the condition. If the
aortic coarctation is severe, it's usually diagnosed during
infancy.
Adults and older children tend to have milder cases and usually
appear healthy until a doctor detects:
• High blood pressure in the arms
• A blood pressure difference between arms and legs
• A weak or delayed pulse in the legs
• A heart murmur — an abnormal whooshing sound caused by
turbulent blood flow
 Diagnostic tests
Tests to confirm a diagnosis of coarctation of the aorta
include:
• Chest X-ray.
• Echocardiogram.
• Electrocardiogram (ECG). If the coarctation of the aorta is
severe, the ECG will show that might have a thickened heart
muscle (ventricular hypertrophy).
• Magnetic resonance imaging (MRI). An MRI of chest will
reveal the location of the coarctation of the aorta and
determine whether it affects other blood vessels in body.
• Cardiac catheterization
 TREATMENTS
Treatment options for coarctation of the aorta
depend on age of child. when diagnosed and
how narrowed aorta is. Other heart defects
may be repaired at the same time as aortic
coarctation. Treatment approaches usually
consist of surgery or a procedure called
balloon angioplasty.
 MEDICATION
• Medication isn't used to repair coarctation of the
aorta, but it may be used to control blood pressure
before surgery. Although repairing aortic coarctation
improves blood pressure, many people will still need
to take medication, even after a successful surgery.
• Child with severe coarctation of the aorta may
receive a drug called prostaglandin E. This drug helps
keep the ductus arteriosis open, providing a bypass
for blood flow around the constriction, until the
coarctation is repaired.
 TREATMENT
Surgery is usually recommended
The narrowed part of the aorta will
be removed.

• If the problem area is small, the

two free ends of the aorta may
be reconnected. This procedure
is called Anastomosis.

• If a large part of the aorta is

removed, a Dacron Graft
(synthetic material) is used to
fill the gap.

In some cases, balloon

angioplasty may be done instead
of surgery.
 EXPECTATIONS
Coarctation of the aorta can be cured with surgery.
Symptoms quickly get better after surgery.

There’s an increase risk for death due to heart problems

among those with aorta repaired.

Without treatment, death occurs before age 40

PULMONARY VALVE STENOSIS
 Pulmonary Stenosis
• No symptoms in mild or moderately severe
lesions.
• Cyanosis and RVH, right-sided heart failure in
patients with severe lesions.
• High pitched systolic ejection murmur maximal in
second left interspace.
• Ejection click often present.
• Oligaemic lung fields(Reduced pulmonary
vascular marking)
AORTIC STENOSIS
 Aortic Stenosis
• Aortic valve stenosis (AS) is a disease of
the heart valves in which the opening of the
aortic valve is narrowed.

• This narrowing prevents the valve from

opening fully, which obstructs blood flow
from the heart into the aorta and onward to
the rest of your body.
 Etiology
 Congenital heart defect:
 Normal aortic valves have three
leaves (tricuspid), but some
individuals are born with an aortic
valve that has two leaves
(bicuspid).
• Calcium buildup on the valve:
 In old age, Caused by accumulation
of calcium in the valve
• Rheumatic fever:
 More in males
 Pathophysiology
1. Pressure overload causes
obstruction to LV
outflow, which results in
left ventricular
hypertrophy (LVH).
2. With long standing as, the
left ventricle dilates,
causing progressive lv
dysfunction.
3. This end with heart
failure due to pressure
overload
 Clinical Picture
Symptoms:
• Dyspnea on exertion.
• Angina.
• Fainting, weakness, or
dizziness with activity.
• Palpitations.
• Syncope.
 Clinical Picture
Signs:
• Low pulse pressure.
• Sustained apex.
• Systolic thrill.
• Ejection systolic murmur
• Soft delayed aortic component
 Imaging Studies
• ECG
• Chest radiography
• Echocardiography
• Dobutamine echocardiography
• Cardiac catheterization
 Pharmacological Management
• Medical treatment has no role in preventing
the progression of the disease process
• But with the onset of LV systolic dysfunction,
the use of inotropic agent may be advocated
 Surgical Management
• AVR is indicated for symptomatic patients
• AVR improves survival in patients with
depressed as well as normal LV function
• The risks of surgery and prosthetic valve
complications outweigh the benefits of
preventing sudden cardiac death and prolonged
survival in asymptomatic patient
ATRIOVENTRICULAR CANAL DEFECT
 Treatment
• Baloon valvuloplasty
• PG1 administration
• Resection of hypertrophied muscle
• For supravascular stenosis the area of
obstruction is incised and a patch graft is
inserted,
Thank you.