CONGENITAL HEART DISEASE (C.H.D.

)
Introduction
The problem of cardiovascular system consist of those associated with the heart and major blood vessels such
as the aorta.it as also important to note that the cardiovascular disease that affect children are different from
those seen in adult .many of the pediatric cardiovascular problems are caused by congenital heart disease ,
which may further be classified as acyanotic and cyanotic. acquired heart disease account for a smaller
percentage of cardiovascular in disease in children.

Epidemiology of CHD
Incidence - 8/1000 live births

- 3-4/100 still born

- 2/100 premature infants excluding PDA

-10-25/100 abortuses

• Most congenital defects are well tolerated during fetal life.

Incidence: 8: 1000 births.

Etiology of Congenital heart diseases (CHD):

The etiology of most CHD is not known, but several factors are associated with a higher than normal incidence
of the disease. These include:

1. Maternal rubella during pregnancy.

2. Maternal alcoholism, age over 40 years and insulin dependant diabetes.
3. Several genetic factors.
4. Exposure to radiation
FETAL CIRCULATION

The characteristics of fetal circulation ensure that the most vital organs and tissues receive the maximum
concentration of oxygenated blood. The fetal brain requires the highest oxygen concentration. The lungs are
essentially nonfunctional, and the liver is only partially functional, therefore less blood is needed in these
organs in fetal life.
Heart is completely developed in the first eight weeks of intra-uterine life.
During fetal life, blood carrying oxygen and nutritive materials from the placenta enters the fetal system
through the umbilicus via the large umbilical vein. Oxygenated blood enters the heart by the inferior vena cava
because of the higher pressure of the blood entering the right atrium and through the foramen ovale to the left
atrium. In this way, the better-oxygenated blood enters the left atrium and ventricle to be pumped through the
aorta to the head and upper extremities. Blood from the head and upper extremities entering the right atrium
from the superior vena cava is directed downward through the tricuspid valve into the right ventricle.
From the right ventricle, it is pumped through the pulmonary artery, where the major portion is shunted to the
descending aorta via the ducts arteriosus to supply the trunk and lower extremities. Only small amount flows to
the non-functioning fetal lungs for the purposes of nutrition.
CIRCULATION CHANGE AT BIRTH
With cessation of placental blood flow from clamping of the umbilical cord the expansion of the lungs at birth,
the hemodynamis of the fetal vascular system undergo abrupt changes. With the first breath, the lungs are
expanded and oxygen causes pulmonary vasodilatation, pulmonary pressure start to fall, a systemic pressures
given the removal of the placenta start to rise. Normally, the foramen ovale closes as the pressure in the left
atrium exceeds the pressure in the right atrium and it closes completely at third month of infant life. The ducts
arteriosus starts to close in the presence of increased oxygen concentration in the blood and other factors and it
closes completely at fourth month of infant life.

CIRCULATORY CHANGES AT BIRTH

Fetal structure Adult remnant

Foramen ovale Fossa ovalis
Ductus arteriosus Ligamentum arteriosum
Ductus Venousus Ligamentum venousum
Umblical vein Ligamentum teres
Umblical arteries Internal iliac artery umblical ligament

TYPES OF DEFECTS
Congenital heart defects have been divided into 2 categories:
 1. Traditionally, a physical characteristics, cyanosis has been used as distinguishing feature, dividing the
anomalies into:
 Cyanotic defects
 Acyanotic defects
2. Another classification system based on Hemodynamic characteristics also is used. The defining
characteristics is blood flow patterns:
o Increased pulmonary blood flow
o Decreased pulmonary blood flow
o Obstruction of blood flow out of the heart
o Mixed blood flow in which saturated and desaturated blood mix within the heart or great arteries.
Classification of Congenital Heart Disease:

Classification Of Congenital Heart Disease

Acyanotic Cyanotic

Pulmonary Obstruction to Pulmonary Mixed blood

blood flow blood flow from blood flow flow
ventricles

o ASD
o VSD o CoA o ToF o TGA
o PDA o Aortic Stenosis o Tricuspid Atresia o TAPVC
o AVC o Pul. stenosis o Truncus Arteriosus

Most acyanotic defects involve primarily left to right shunting through an abnormal opening. Others result from
obstructive lesions that reduce the flow of blood to various areas of the body.
MAJOR ACYANOTIC DEFECTS:

 Patent ductus arteriosus (PDA).

 Atrial septal defect (ASD).
 Ventricular septal defect (VSD).
 Pulmonic stenosis (PS).
 Aortic stenosis (AS).
 Coarctation of aorta (COA).

PATENT DUCTUS ARTERIOSUS (PDA)

introduction:
Patent ductus arteriosus is a common congenital heart disease particularly in premature neonates.it has account
for 10 to 12 % of all congenital heart disease .it is a communication between the pulmonary artery and the
aorta. The aortic attachment of the ductus arteriosus in just distal to the left subclavian artery .the ductus
arteriasus is present in the fetal life of all .its close functionally and anatomically soon after birth .persistence of
ductus arteriosus is called patent ductus arteriosus.
Incidence:
More common in females (2:1), Higher incidence among premature and commonly associated with maternal
rubella.
Pathophysiology
At birth the resistance pulmonary and systemic circulation is almost identical

That systemic pressure exceed the pulmonary pressure

Lead to blood begin to shunt from the aorta, across the duct, to the pulmonary artery (left to right shunt)

Due to increase workload on the left side of the heart, increase pulmonary vascular congestion

That result possibly resistance & potentially increases right ventricular pressure and hypertrophy

Assessment:
Clinical manifestation will depend on the size of duct and amount of shunting. Small PDA: asymptomatic
and discovered on a routine examination.
Large PDA:
イClassic machinery murmur, which is continuous from systole into diastole.
ロDyspnea on exertion and easy fatigability.
ハUnder weight thin child.
ニRepeated chest infections.
ホHeart rate over 150 b/m, gallop rhythm due to rapid filling of the ventricle.
ヘBounding pluses due to increased systolic pressure.
トLeft heart failure may develop in infancy in severe cases.
チEnlarged heart size in large PDA.
Diagnosis
 Clinical examination and history taking
 Chest X-ray may show cardiomegaly
 ECG show the ventricular hypertrophy
 Echocardiography may show the suprasternal and high parasternal views can demonstrate the
ductus
 Cardiac catheterization
Management
1. Supportive: fluid restriction with diuretics and digitalization for congestive heart failure CHF.
 2. Indomethacin ,a prostaglandin synthesis inhibitor can be given orally to close the ductus.anti
prostaglandin agent ,aspirin and mefanemic acid also be used
3. Surgical: surgery can be performed at anytime, although it is preferably done at about 6 months
of age, surgery maybe done earlier if the child is in difficulty to prevent complications and
growth retardation caused by PDA.
Outcome:
The prognosis is good with less than 1% mortality.
Complications:
 Infective Endocarditis/Endarteritis
 Embolization
 Congestive heart failure.
 Pulmonary hypertension.
ATRIAL SEPTAL DEFECT (ASD)

INTRODUCTION

Atrial septal defect is an abnormal opening between right and left atria resulting left to right shunting of blood .
the two main varieties are the ostium secundum and ostium primum defect .the ostium secundum type of atrial
septal defect is generally anatomically located at the fossa ovalis. it can also be superior and posterior to the
fossa ovalis .The ostium primum type of defect (endocardial cushion defect ) is situated inferior to the fossa
ovalis.it is associated with a cleft in the anterior leaflet of the mitral valve ,with or without a cleft in the septal
tricuspid leatlet .

Incidence:

7% of all CHD, more common in females.

Pathophysiology

Left to right shunt

Increase pulmonary blood flow

Endothelial dysfunction & vascular remolding

(Smooth muscle cell proliferation, increase in extracellular matrix, intravascular thrombus)

Increase pulmonary vascular resistance

Reversed shunt ,right to left

Ebstien syndrome

cyanosis

Assessment:
  The clinical manifestations depend on the location and size of the defect. The infant with small
defects may be asymptomatic.

 If there is a large left to right shunt and severe mitral incompetence cardiac

 enlargement and pericardial bulge are seen. These children are easily fatigued and have recurrent
pneumonitis.

 In atrial septal defect, pulse and venous pressure are normal and the heart size is normal or
slightly enlarged.

 Systolic murmur is present.

 The ausculatory finding of a widely split second heart sound is so unusual in complicated atrial
septal defects that the diagnosis is not made without it.
Diagnosis

 Clinical examination and history taking

 CXR - Right. V & A enlargement - Large pulm. artery- ↑ed pulm. vascularity (marking)

 ECG - volume overload, right axis deviation - minor right ventricular conduction delay

 Echocardiography

 Cardiac Catheterization
Management:

1. Supportive: same as that of the VSD.

2. Surgical: surgery is done on affected children before they enter school even if no symptoms are
present. If surgery is not done during childhood pulmonary hypertension, atrial arrhythmias and
cardiac failure make operation more hazardous in adult life.

Complications –

 Pulmonary hypertension,
 Eismenger syndrome

VENTRICULAR SEPTAL DEFECT (VSD)

Introduction

Ventricular septal defect is an abnormal opening between the right and left ventricles. The defects vary in size
and may occur in either the membranous or muscular portion of the ventricular septum. Due to higher pressure
in the right and left ventricles. A shunting of blood from the left to right ventricle occurs during systole. If
pulmonary vascular resistance produces pulmonary hypertension, the shunt of the blood is then reversed from
the right to the left ventricle, with resulting cyanosis.
Incidence:

Commonest (30% of all cases of CHD)

Pathophysiology
 Due to high pressure in left ventricle

Systemic arterial circulation more resistance than pulmonary circulation left to right shunt

That is blood volume is pumped in to the result in the pulmonary vascular resistance

Lead to increase pressure in right ventricle

Reversed of shunt right to left

That is right to left shunting & pulmonary resistance cause left ventricle hypertrophy

Ebstien syndrome

cyanosis

Clinical finding
 Small defects with trivial Lt to Rt Shunt
- Most common
- Asymptomatic
- Loud, harsh holosystolic M at LLSB
 Large defects
- Excessive pulmonary blood flow
- Pulmonary hypertension
- Dyspnea, feeding difficulties, poor growth,
- Perspiration, recurrent plum. infection, heart failure
- Less harsh but more blowing holosystolic murmur
- Accentuated 2nd heart sound
- Mid-diastolic apical M when shunt ratio > 2:1
Diagnosis
 Clinical examination and history taking
 CXR - Cardiomegaly - Plethoric lung
 ECG - may show biventricular hypertrophy
 Echocardiography –
Management:
 If the defect is small and asymptomatic, treatment is conservative because spontaneous closure may
occur before 1 or 2 years of age.
 If the defect is larger, medical care is given for CHF when it occurs: oral diuretics and digoxin.
 Surgical repair requires open-heart surgery and cardiopulmonary bypass.
Complications
 Infective endocarditis
 Recurrent lung infection
 Heart failure
 Pulmonary HTN
 Acquired pulmonary stenosis
 aortic valve regurgitation
COARCTATION OF THE AORTA
Introduction:-

Conginital coarctation of the aorta is located at the junction of the arch with the descending aorta.it is a sharp
intentation involving the anterior lateral and the posterior wall of the aorta.the medial wall is spread in the
narrowing .it may be distal or proximal to the ductus or ligamentum anteriosus and also the left subclavian
artery . The most common site of coarctation is near the aortic attachment of the ductus arteiosus or
ligamentum ateriosum. The coarctation may be preductal , juxtaductal ,or postductal .

Clinical finding

 Blood pressure is higher than normal in the upper part of the body, resulting in headache, dizziness
fainting, epistaxis, and later cerebrovascular accidents. In the leg, it is relatively low, resulting in
absence or diminishing of the femoral pulse.

 The legs may be cooler than the arms.

 If the child exercises muscle cramps in the legs may be due to tissue anoxia.
Diagnosis

 Clinical examination and history taking

 CXR - cardiomegaly & pulm. congestion - Notching of ribs
 ECG
 Echocardiography
 Angiocardiography
Management and Outcome:

 Surgical: repair consists of resection and anastomosis by aortic graft or subclavian flap angioplasty.

 Medical management of the condition is done with PGI 1 infusion ,antibiotics and prevention and
treatment of complication

 If blood pressure is not elevated and heart failure is not a problem, it is wise to postpone the operation
until the operation descending aorta is at least 50% of adult size (age of child 3-6 years) to avoid re-
stenosis
.Out come:
Surgery should be done if only a minor defect is present to avoid complication, e.g. hypertension, intracranial
hemorrhage and stroke.

AORTIC STENOSIS

INTRODUCTION
Congenital aortic valve stenosis is a obstructive cardiac lesion constitute of 8 percent of all CHDs .
pathologically the obstruction may be at the valve level ,above the valve (supravalvular) and below the valve
(subvalvular). At the valve level the aortic stenosis resulting from either an unicuspid and bicuspid aortic
valve.The unicuspid aortic valve is stenosis from its design and the patient become symptomatic early in life
.the bicuspid aortic valve stenosis resulting in the significant obstruction when the valve become thicker and
relatively immobile.

PATHOPHYSIOLOGY

AORTIC STENONSIS

Due to narrow in the aortic valve

That causes obstruction in the flow from the left ventricle

Leads to extra workload & causes hypertrophy on the left ventricle

That causes increase pressure in pulmonary vein

Resulting pulmonary vesicular congestion & pulmonary edema

CLINICAL FINDING

 Most patient with aortic stenosis have no manifestation except easy fatigability ,exercise intolerance
,dizziness and syncope .
 Symptomatic neonates present with severe CCF tachypnea .faint peripheral pulse ,poor perfusion ,poor
capillary refill ,cold skin ,poor feeding and metabolic acidosis.
 Older children manifestation are chest pain on exertion ,decreased exercise tolerance, dyspnea
,pulmonary edema, shortness of breath ,fatigue ,dizziness light head ache, palpitation .

DIAGNOSIS

 Physical examination and history taking

 Chest x ray
 ECG may show the ventricular hypertrophy
 Echocardiography
 Cardiac catheterization
 Graded exercise testing

MANAGEMENT

 Medical –aortic stenosis of neonate is done with PGE1 infusion ,

 Surgical treatment in indicated if significant aortic stenosis is associated .the two main operation is done
at present are valvotomy and aortic valve replacement .balloon aortic valvuloplasty is a new technique
for non operative relief of aortic obstruction .

PULMONIC STENOSIS
Introduction

Anatomically pulmonic stenosis is located at the valvular and subvalvular level.the pulmonic stenosis is called
infundibular pulmonic stenosis .uncommonly pulmonic stenosis may be in the pulmonary artery above the
valve or in the main right or left branches or the peripheral branches .

Clinical finding

 Patient with mild and moderate pulmonic stenosis are asymptomatic .with severe pulmonic stenosis
dysnea on effort appear
 If the foramen ovale is patent is right to left shunt at the atrial level may occur in severe pulmonic
stenosis and result in cyanosis
 Mild to moderate - asymptomatic
 Critical stenosis
 Systolic ejection murmur
 Heart failure in neonates & infants
 Rarely cyanosis

Diagnosis

 Physical examination and history taking

 Chest x ray
 Electrocardiography
 Echocardiography
 Cardiac catheterization

Management

Surgical balloon pulmonary valvuloplasty is a treatment of choice for isolated valvar pulmonic stenosis

Complications

 CHF in severe Ps
 rarely IE

CYANOTIC CONGENITAL HEART DISEASE

The common cause of cyanotic congenital heart disease is a communication between the pulmonary and a
systemic circulations through which venous (unoxygenated) blood enters the systemic circulatiory system (right
to left shunts or obstruction of pulmonary blood flow or obligatory mixing of venous and arterial blood).
Cyanosis may be seen at first year of life. It increases, as the child grows older.
cyanotic defects:

 Tetralogy of Fallot
 Tricuspid atresia
 Total anomalous pulmonary venous connection
 Hypoplastic left heart syndrome
 Truncus arteriosus
 Transposition of the great arteries
TETRALOGY OF FALLOT
The classical tetralogy consists of:
1. Pulmonary stenosis.
2. Ventricular septal defect.
3. Overriding of the aorta or dextroposition of aorta
4. Right ventricular hypertrophy.
In tetralogy of fallot, the blood normally returns from the systemic circulation to the right atrium and right
ventricle. The out flow of the blood from the right ventricle resisted by the pulmonary stenosis so that the blood
flows through the ventricular septal defect into the aorta. This is a right to left shunt.
Hypertrophy of the right ventricle occurs as a result of the pressure exerted against the pulmonary stenosis,
because the blood from the right ventricle is unoxygenated, cyanosis result.
Polycythemia develops because the body attempts to compensate for the unoxygenated blood. The resulting
increased viscosity of the blood causes slowing of the circulation and possible thrombophlebitis emboi and
vascular disease.
Pathophysiology
VSD is large
Pressure is equal in right & left ventricle
Shunt direction depends on the difference between pulmonary & systemic vascular resistance
Pulmonic stenosis
Decrease blood to the left side of heart

Clinical finding

 The neonate who has tetralogy of fallot is not cyanotic because of the presence of the patent
ductus arteriosus; cyanosis becomes evident after the ductus closes during the first months of
life.
  Clubbing of the fingers and toes (in long standing cases )

 Stunted growth.

 Intolerance to effort: exercise usually causes severe dyspnea. Infant and toddlers
may be able to play for a short time, but then they mustres infants assure a knee chest position
rather than extending their extremities when they lie down. Older children, learn that the
squatting position relieves dyspnea because:

 Flexing the legs decrease venous return from the lower extremities which have a very low
oxygen content, especially after exercise.

 Squatting position increase systemic vascular resistance, which diverts right ventricular blood
from the aorta into pulmonary artery increasing pulmonary blood flow. This increases the
amount of oxygenated blood in the left side of the heart and eventually into systemic circulation.
 Cyanotic spells. (Hypoxic, blue spells).
 Apansystolic murmur: it is usually associated with thrill.
 These children don’t develop congestive heart failure because the overload of the blood in right
ventricle flows freely through the septal defect and the overriding aorta into the systemic circulation.
 Pink tets (acyanotic) and blue tets (cynanotic)
Management:
Medical:
o Antibiotic prophylaxis before tooth extraction or GIT and urinary procedures.
o Treatment of cyanotic spells:
 Oxygen therapy
 Put the child in knee- chest position.
o Give morphine sulfate.
 I.V. beta- adrenergic inhibitor.
 If acidosis is present give I.V. sodium bicarbonate.
o Surgical: palliative and total corrective surgery is being done on infants and children of all ages.

TRANSPOSITION OF GREAT VESSELS

Introduction

Transposition of great artery occurs when the pulmonary artery originate from the left ventricle .it is a
embryologic defect caused by a straight division of the bulber trunk with out normal spiring. transposition of
the great vessels is a congenital heart defect in which the 2 major vessels that carry blood away from the heart
-- the aorta and the pulmonary artery -- are switched (transposed). Transposition of the great vessels is a
cyanotic heart defect. This means there is too little oxygen in the blood that is pumped from the heart to the rest
of the body. Low blood oxygen leads to cyanosis (a bluish-purple color to the skin) and shortness of breath.

Pathophysiology

Systemic VR to normally positioned Rt atrium


 Through bicuspid (Mitral) valve

Right sided left ventricle

Pulmo. artery  pulm. venous return

Normally positioned Lt atrium

Through tricuspid valve

Left sided Right ventricle  Aorta
Clinical finding

The clinical manifestation of cyanosis varies in degree depending on the type and size of the associated defects.
Children with minimal communication are severely cyanotic at birth. Those with large septal defects or a patent
ductus arteriosus may be less severely cyanotic but have symptoms of congestive heart failure usually before 4
months of age. In these infants the only signs at birth may be cyanosis after crying or feeding and progressive
hyperpnea in an attempt to compensate for decreased arterial oxygen saturation.

A murmur usually indicates the presence of septal defect or a patent ductus arteriosus cardiomegaly.

Management:

Palliative and corrective treatment used for the treatment of transposition of the great vessels.

TRICUSPID ATRESIA

Tricuspid atresia is the congenital absence of tricuspid valve resulting no communication between to right
atrium and right ventricles .so total systematic venous return enters the left heart by means of foramen ovale or
an ASD , resulting cyanosis.

PATHOPHYSIOLOGY

Patent foramen ovale/ASD

RA LA
 Patent ductus arteriosus

Blood flow to the pulmonary artery to lungs

VSD

LV RV pulmonary artery for oxygenation

Pulmonary blood flow

Clinical feature

 Cyanosis

 Tachycardia

 Dyspnea

 Clubbing

 Risk for bacterial endocarditis, brain abscess & stoke.

Management
• Pulmonary-to systemic artery anastomosis to increase blood flow to the lungs.
• Atrial septostomy to close ASD
• Pulmonary artery banding to lessen the blood to the lungs.
• Bidirectional Glenn shunt
• Modified Fontan procedure

TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION (TAPVC)

Introduction
Failure of the pulmonary veins to join the left atrium. The abnormal attachment results in mixed blood being
returned to the RA & shunted from the right to the left through an ASD
Type

 Supracardiac-attachment above the diaphragm, such as SVC. Commonest type.

 Cardiac-direct attachment to the heart, such as RA or coronary sinus.
 Infracardiac-attachment below the diaphragm, such as IVC. severe form

Pathophysiology
RA receives all blood that normally flow to LA
RA hypertropies
If there is associated ASD
 RA RV
Obstruction to pulmonary venous drainage
Pulmonary venous pressure rises
Pulmonary edema
CHF
Management
Common pulmonary vein is anastomosed to the left atrium,the ASD is closed,& the anomalous pulmunary
venous connection is ligated.
TRUNCUS ARTERIOSUS
Introduction
Uncommon anomaly 2°failure of primitive common truncus arteriosus to divide into aorta and pulmonary
artery.
Types

 Type I-A single pulmonary trunk arises near the base of the truncus & divides into the left & right
pulmonary arteries
 Type II-The left & right pulmonary arteries arises separately but in close proximity & at the same level
from the back of the truncus
 Type III-The pulmonary arteries arise independently from the sides of the truncus
Pathophysiology
Blood ejected from RV & LV
Common trunk
Mix up pulmonary & systemic circulation
Resistance to pulmonary blood flow is less than systemic vascular resistance
Blood flow to the lungs
Management
• Closing VSD so that truncus arteriosus receives the outflow from the LV, excising the pulmonary
arteries from the aorta,& attaching them to the right ventricles by means of a homograft

NURSING CARE OF A CHILD WITH CONGENITAL HEART DISEASE

Assessment:
Nursing care of the child with congenital heart disease begins soon as the diagnosis is suspected. However in
many instances symptoms that suggest cardiac anomaly is not present at birth or if manifested is so subtle that
they are easily overlooked.
Infants:
 Cyanosis generalized, especially mucous membranes, lips and tongue. Conjunctiva, cyanosis
during exertion such as crying, feeding, straining, or when immersed in water.
 Dyspnea, especially following physical effort such as feeding, crying or straining.
 Fatigue, paroxysmal hyperpnea, poor growth and development (failure to thrive).
 Frequent respiratory tract infection.
 Feeding difficulties.
 Hypotonia.
 Excessive sweating.

Older Children:

 Impaired growth.
 Fatigue.
 Orthopnea.
 Headache.
 Leg fatigue.
 Delicate body build.
 Effort dyspnea.
 Digital clubbing.
 Epistaxis.
NURSING CARE PLAN FOR CHILD WITH CONGENITAL HEART DISEASE:

1. Decreased cardiac output R/T structural defect.

Goal:
The patient will: exhibit improved cardiac output.
Intervention:
 Administer digoxin as ordered.
 The child’s apical pulse is always checked before administrating digoxin (as general rule the drug is not
given if the pulse is below 90-100 b/m in infants and young children or below 70 b/m in older children).
Expected Outcome: Heart rate and volume indicate satisfactory cardiac output.
2. Activity intolerance related to imbalance between oxygen supply and demand.
Goal:
The patient will: Maintain adequate energy levels.
Intervention:
 Allow for frequent of rest.
 Encourage quite games and activities.
 Help child to select activities appropriate to age, condition and capabilities.
 Avoid extremes of environmental temperature.
Expected Outcome:
Child determines and engages in activities commensurate with capabilities.
3. Altered growth and development related to inadequate oxygen, nutrients to tissue and social isolation.
Goal:
The patient will: Achieve normal growth.
Intervention:
 Provide well balanced highly nutritive diet.
Expected Outcome:Child achieves normal growth
Goal: (2)
The patient will: Exhibit adequate iron level.
Intervention:
 Administer iron preparation as prescribed.
 Encourage iron rich foods in diet.
Expected Outcome:
Child assimilates sufficient iron.
Goal: (3)
The patient will: Have opportunity to participate in activities.
Intervention: Encourage age appropriate activities.
Expected Outcome:
Child engaged in age appropriate activities.
4. High risk for infection related to debilitated physical status.
Goal:
The patient will: Exhibit no evidence of infection.
Intervention:
 Avoid contact with infected persons.
 Provide for adequate rest.
 Provide optimum nutrition.
Expected Outcome:
Child remains free from infection.
5. Altered family process related to having a child with a heart condition.
Goal:
The patient will: Experienced reduction of fear and anxieties.
Intervention:
 Discuss with parents their fears regarding child symptoms.
Expected Outcome:
Family discusses their fear and anxieties.
Goal: (2)
The patient will: Exhibit positive coping behavior.
Intervention:
 Encourage family to participate in care of child while hospitalized.
 Encourage family to include others in child’s care to prevent their own exhaustion.
 Assist family in determining appropriate physical activity and disciplining methods for child’s anorexia.
Expected Outcome:
Family copes with child’s symptoms in a positive way.
Goal: (3)
The patient will: Demonstrate knowledge of home care.
Intervention:
 Teach skills for home care.
 Administration of medications.
 Feeding techniques.
 Signs that indicate complications.
 Where and whom to contact for help and guidance.
Expected Outcome:
Family demonstrates ability and motivation for home care.
6. High risk for injury (complications) related to cardiac condition and therapies.
Goal:
The patient’s family will: Recognize signs of complications early.
Intervention:
 Teach family to intervene during hypercyanotic spells, place child in knee chest position with head and
chest elevated.
 Teach family to recognize signs of complications such as:
- Digoxin toxicity (vomiting, bradycardia, dysrhythmias).
- Increased respiratory effort (tachypnea, retraction, grunting, cough, cyanosis).
- Hypoxemia (cyanosis, restlessness, tachycardia).
- Cerebral thrombosis (compensatory polycythemia is particularly hazardous when child is
dehydrated).
- Cardiovascular collapse (pallor, cyanosis and hypotonia).
Expected Outcome:
Family recognizes signs of complications and institutes appropriate action.

BIBLIOGRAPHY

Books reference
  Achar ‘s text book of paediatric nursing 4th edition edited by swarna rekha bhat

 Basavanthappa, B.T. (2006). Child Health Nursing: Ahuja publication.

 Datta, Parul.(2009).Paediatric Nursing. New Delhi:Jaypee Brothers publisher.
 Gupta, Piyush. (2007).Essential Paediatric Nursing. New Delhi: Satish kumar Jain publication.
 Hockenberry, Marilyn and Wilson David. (2010). Essential of paediatric Nursing. New Delhi: Elsevier
publication.
 Jacob, Alphonsa. (2009). Paediatric Nursing. Indore: N.R Brothers.
 Marlow,R.Doroth and Redding, A.Barbara.(2002).Textbook of paediatric .New Delhi: Harcourt India
Private Limited.
 Mickinney,slone.Emiley et.all.(2000). Maternal child Health nursing.Saunders publisher
Internet reference

 www.FloridaHealthFinder.gov.com
 www.medscape.com
 MamasHealth.com