Congmal (1)

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ACYANOTIC HEART DEFECTS Ms. Sandeep Kaur M.Sc (N)2 nd year

Transcript of Congmal (1)

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ACYANOTIC

HEART

DEFECTS

Ms. Sandeep Kaur M.Sc (N)2nd year

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Objectives:

At the end of 2 hours of active learning discussion, the

students will be able to:

1. Define acyanotic heart defects

2. Understand atrial septal defect and ventricular septal

defect in terms of:

a. anatomical defect

b. clinical manifestations

c. diagnostics

3. Formulate nursing diagnoses and appropriate nursing

care

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Definition:

Acyanotic Heart Defects – a

congenital disorder manifested

with left to right shunting and

obstructive lesions. Clinical

signs are not always apparent

at birth, they manifest anytime

during infancy or early

childhood.

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Defects:

a. Left to right shunting lesions, increased pulmonary

blood flow

• The blood is shunted through an abnormal opening

from the left side of the heart to the right side of the

heart

• Pulmonary blood flow increases because of the extra

volume in the right side. There is a “step-up” 02

saturation in the right side of the heart (abnormal

increased) because of the addition of more highly

saturated blood. Physiologic effects include increased

pulmonary blood flow, increased cardiac workload

(including ventricular strain, dilation, and hypertrophy).

Examples: Atrial Septal Defect (ASD), Ventricular Septal

Defect (VSD), Patent Ductus Arteriosus (PDA), and

Atrioventricular Septal Defect (AVSD).

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b. Obstructive or stenotic lesions – stenosis of an

opening can occur in a valve or vessel constricting or

obstructing blood flow through the area. Pressure rises

in the area behind the obstruction; blood flow distal to

the obstruction may be decreased or absent.

Physiologic effects of obstructive or stenotic lesions

include increased cardiac workload and ventricular

strain, clinical consequence of CHF, decreased CO

and pump failure.

Example: Pulmonary stenosis, aortic stenosis, Coarctation

of Aorta, and interrupted aortic archs.

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Atrial Septal Defect (ASD)

Incidence and Pathophysiology:

● ASD accounts for approximately 10% of all CHDs. It is seen more frequently in females than males.

● The lesion consists of an abnormal opening between the atria

Types of Lesions:

1. Ostium Secundum – located at the middle of the atrial septum (fossa ovalis), the most common type.

2. Ostium Primum – located low in the atrial septum, results from a defect in endocardial tissue formation and is often associated with a left mitral valve malformation.

3. Sinus Venosus – which is located high in the septum close to the SVC

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Atrial Septal Defect

(ASD)

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Atrial Septal Defect (ASD)

Altered Hemodynamics:

● Lower right ventricular compliance which is the ease of

ventricular diastolic filling, compared with left ventricular

compliance leads to left to right shunting at the atrial level

through the ASD. This increased blood flow through the

ASD leads to an enlarge RA and RV and increased

pulmonary blood flow.

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Manifestations:

● Most infants and children are asymptomatic but over years to decades

may experience:

1. Fatigue and SOB

2. Palpitations or atrial dysrythmias – result of atrial enlargement

3. Recurrent respiratory infections can occur when there is a large amount

of pulmonary blood flow

4. Systolic murmur is produced by increased blood flow across the

pulmonary valve.

5. Diastolic murmur is present with large shunts

6. Stroke or major organ damage can occur because of embolization of

thrombus, air or other materials – PARADOXIMAL EMBOLISM

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Diagnostics:

1. Echocardiogram

2. EKG

3. CXR

4. Cardiac Catheterization

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Atrial Septal Defect Therapeutic Management:

1. Asymptomatic child is followed by cardiologist. Spontaneous closure can occur in the first years of life for smaller size secundum ASDs.

2. Elective surgical repair is performed around 2-5 years of age

3. Surgical repair is recommended for all sinus venosus and ostium primum defects.

Medical Management:

1. Asymptomatic patients with moderate size secundum ASDs are monitored for spontaneous closure in the first years of life with medication.

2. Symptomatic infants and children are treated with diuretics and digoxin as indicated

3. Atrial dysrythmias are treated with appropriate antidysrythmics

Surgical Management:

● Surgical closure using either sutures or a pericardial prosthetic patch is performed on an elective basis early in childhood. This is an open heart procedure, through a sternal incision.

● Mortality rate is <2%, with most centers near 0%. For the young adult with ventricular dysfunction or pulmonary, the risk can be significantly higher.

● Complications include sinus node and atrial dysrythmias

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Ventricular Septal Defect (VSD)

Incidence and Pathophysiology:

● VSDs account for approximately 25% of all CHDs.

● VSD is the most common congenital cardiac lesion and is

often accompanied by other cardiac defects.

● The lesion consists of an abnormal opening between the

right and left ventricles which may vary in size from a

miniscule hole to complete absence of the septum, resulting

in a common ventricle.

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Altered Hemodynamics:

● The degree of left to right shunting through the VSD

depends on the size of the defect and the pulmonary

vascular resistance compared with the systemic vascular

resistance. The pulmonary vascular system is high in the

newborn. Over the first few weeks of life, the resistance

decreases. As this occurs, an increased amount of blood

shunts left to right of the VSD level. The pulmonary

vascular circulation receives increased pulmonary blood

flow. With large defects the pulmonary arteries are

exposed to systemic pressures, causing pulmonary

hypertension, and over time, progressive pulmonary

vascular disease.

Ventricular Septal Defect (VSD)

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Ventricular Septal Defect (VSD)

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Ventricular Septal Defect (VSD)

Manifestations:

● Signs and symptoms vary with the size of the defect and

the presence of associated cardiac lesions. Clinical

symptoms are usually not seen at birth because of

continued high pulmonary vascular resistance in the

newborn. Infants with moderate to large defects will

become symptomatic within the first few weeks of life.

● Children with small defects will remain asymptomatic.

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Clinical Manisfestations

• Tachypnea, dyspnea

• Poor growth

• Palpable thrills

• Systolic murmur at left lower sternal border

• Shortness of breath

• Failure to gain weight

• Fast heart rate

• Pounding heart

• Frequent respiratory infections

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Complications:

• Congestive heart failure.

• Growth failure, especially in infancy.

• Bacterial endocarditis

• Irregular heartbeat or rhythm

• Pulmonary artery hypertension

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Diagnostics:

• Chest x-ray -- looks to see if there is a large heart with

fluid in the lungs

• ECG -- shows signs of an enlarged left ventricle

• Echocardiogram -- used to make a definite diagnosis

• Cardiac catheterization (rarely needed, unless there are

concerns of high blood pressure in the lungs, in which

case surgery to close the defect is generally not

recommended)

• MRI of the heart -- used to find out how much blood is

getting to the lungs

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Ventricular Septal Defect (VSD)

Therapeutic Management:

● From 20%-80% of all VSDs closed spontaneously.

1. Many small lesions do not require surgical intervention.

2. If there is aortic valve regurgitation related to VSD position near the valve and even if the defect is small, surgery is indicated to reduce the progression of valve insufficiency.

3. Antibiotic prophylaxis is indicated for all VSDs.

Medical Management:

1. Infants who develop CHF- digoxin diuretics, ACE inhibitors to reduce afterload.

2. Nutritional supplements are added to infant formula to increase caloric intake.NGT feeding or gastrostomy tube feeding for infants who are unable to obtain adequate calories orally

3. Avoid exposure to respiratory infections.

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Ventricular Septal Defect (VSD)

Surgical Management:

1. Pulmonary artery banding for children with multiple muscular

VSDs. In this palliative procedure, a band is placed around

the main pulmonary artery, decreasing blood flow, reducing

the severity of CHF and decreasing the risk of pulmonary

vascular disease.

● The current trend is to perform corrective surgery earlier in

life, and consequently, pulmonary artery banding is

performed less frequently than in the past.

3. Total correction is accomplished by placing sutures to close

small defects or by placing a pericardial or prosthetic patch

over moderate to large defects.

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● The surgical approach is usually through the RA to avoid a

right ventricular incision which could impair the contractility

of the ventricle.

● VSDs just below the pulmonary valve are closed through

an incision in the main pulmonary artery. Mortality is 5%-

8%, depending on the age and type of VSD.

● Complications include residual VSDs, pulmonary

hypertension in the postoperative period, heart block that

may require a pacemaker and an abnormal rhythm called

junctional ectopic tachycardia.

●CO can be significantly decreased if dysrythmias are

persistent. Post pericardiotomy syndrome can also occur.

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Nursing Diagnosis and Care of the

Child with Left-to-Right Shunting

(Acyanotic)

Impaired gas exchange

• Monitor intake and output

• Limit fluids as ordered

• Administer diuretics as ordered

• Position changes every 2 hours or as

ordered

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Nursing Diagnosis and Care of the

Child with Left-to-Right Shunting

(Acyanotic)

Risk for impaired growth and development

• Treat child as normally as possible

• Teach parents that children are more comfortable

when they know what to expect

• Promote age-appropriate activities as condition

allows

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Nursing Diagnosis and Care of the

Child with Left-to-Right Shunting

(Acyanotic)

Altered nutrition: less than body

requirements

• Offer small, frequent feedings

• Use soft nipple for infant to ease the

stress

of sucking

• Organize care to allow for rest

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Nursing Diagnosis and Care of the

Child with Left-to-Right Shunting

(Acyanotic)

Risk for infection

• Limit exposure to individuals with infections

• Promote good pulmonary hygiene

• Prophylactic antibiotics when undergoing

surgical or dental treatment to prevent

subacute bacterial endocarditis

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