Download - Cardio Vascular Disorders

7/30/2019 Cardio Vascular Disorders

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CARDIO VASCULAR DISORDERS

Congenital Heart Disease

1. Atrial septal defect (ASD)

2. Ventricular septa! detect (VSD)

3. Pulmonary stenosis (PS)

4. Patent ductus Arteriosus (FDA)

5. Coarctation of aorta

6. Aortic stenosis (AS)

7. Tetralogy of Fallot (TOF)

8. Transposition of the great vessels.

Rheumatic Heart Disease

Acute Rheumatic fever

Kawasaki disease (or) mucocutaneous lymph node syndrome

Congestive heart failure

a) Congenital Heart Disease

It is most common birth defects, 30% of the total congenital malformation.

The heart is developed during the period of embryogenesis from a primitive

muscles wrapped tube to a four chambered muscular organ with septa, valves,

conduction system and major vessels originating and terminating in the heart

If it is present any defect in this order and developmental leads to structural (or)

functional malformation.

Incidence of C H D:

1) 5-8 per 1000 live births have significant structural cardiac malformation

2) 2-3 in 1000 infants will be symptomatic during the first year of life (cardiac

anomaly)


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Common & Congenital Heart Lesions:

Acyanotic Cyanotic

1. VSD 32%

2. PDA 12%

3. Pulmonary stenosis 8%

4. ASD 6%

5. Coarctation of aorta 6%

6. Aortic Stenos's 5%

1) TetratOgy of Fa110:6%

2) Transposition of great vessels

5%

Causes:

Chromosomal abnormalities 8% Incidence Type of defect

21 Trisomy down syndrome60% A-V canal defect

18 Trisorny 90% VSD, PDA, DORA

13 Trisorny 90% Dextrocardia

Xo-Toners syndrome. 15% Coarctation of aorta


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Environmental Teratogen:

Intravenous infection Tyes of defect

Mumps PDA,SD,ASD endocardial

fibroelastosis

Maternal drugs:

Phenytoin Variable supra valvular aortic stenosis

Vitamin D Supra valvular aortic stenosis

Alchohol ASD,VSD

Maternal disease:Diabetes Transposistion of great vessels

Systematic lumps erythimatus Congenital heart block

Common Clinical Features in Congenital Heart Disease:

1. Mixing of systemic and pulmonary circulation leading to cyanosis

2. Inadequate blood reaching to lungs for oxygenation leading to cyanosis

3. The body growth is affected due to inadequate blood supply of the body

4. Increased in volume and pressure load over the ventricles leading to

congestive heart failure

5. Abnormal situs leading to positional malformation dextrocardia

6. Dysfunction of intrinsic conduction leading to arrhythmias.

7. While routine examination in older children and infant through

continuous murmur can identify the problem ex: FDA, VSE), ASO,

pulmonary stenosis in congenital absence of pulmonary valve.

8. Shock

9. Hyper cyanotic spells

10.Stridor

11.Chest pain


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12.Recurrent respiratory tract infection

13.Growth failure

Diagnostic Evaluation

Physical examination, history collection,

Chestradiograpy:

To evaluate cardiac size, classical

Cardiac contours lung musculature individual cardiac chamber, aortic arch,

abdominal situs.

Electrocardiogram:

To evaluate homodynamic status of defect, seventh of defect, suggestive of

certain lesions.

Echocardiography:

To evaluate homodynamic data regarding pressure differences across aortic

and pulmonary valves.

Cardiac catheterization.

Cineradiography

Cardiac MRI

Management of CHD: Diuretics:

Chlorothiazide (Diucii)

Frusemide (lasix)

Cardiac glycosides:

Digoxin (lanoxin)


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to prevent (or) treat CHF

Interventional Management

Nutritional support

Treatment of stroke seen in cyanotic heart disease

Prevention and treatment of hyper cyanotic spells

Anti arrhythmic treatment in arrhythmias

Complete congenital heart block

Paroxysmal SVT

Use of prostaglandin E, in shunt dependent congenital heart defects

Surgical Treatment:

Palliative surgeries mitigate symptoms (or) extend life without addressing

basic patho physiology of cardiac lesion.

1). Atrial Septal Defect (ASD)

It is abnormal opening between the atria, allowing blood flow from the

high pressure in left atrium to the lower pressure in right atrium.

Types of ASD :

1. Ostium primum (ASD1):

Opening of lower end of septum may be associated with mitrel valve

abnormalities

2. Ostium secundam: (ASD2) :

opening near to center of septum

3. Sinus venosus defect:

Opening near superior venacava (SVC) and right atrium, may be associated

with parietal anamolus pulmonary venous connection.


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ASD

Increased left atrial pressure

Blood flow from left to right atrium because increased oxygenated blood goes

to the right side of the heart

Low pressure difference and high rate of blood flow occur

(Low pulmonary vascular resistance, distensibiliy of the right atrium)

Reduced Flow resistance

(blood volume tolerated by the right ventricle)

Right Atrial and ventricular Enlargement

Cardiac failure (uncomplicated ASD)

Pulmonary vascular changes

Pathophysiology:


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Clinical Features:

Usually asymptomatic

May have audiable systolic ejection murmur at left sternal border


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Mild exercise intolerance

Mild to moderate Cardiomegaly with pulmonary vascular

disease gradually increasing

Diagnostic Evaluation:

1. ECG may reveal atrial arrhythmias (prolonged P-R interval) and RVH

2. Chest x-ray reveals pulmonary vasculature Prominent pulmonary

artery and right ventricular hypertrophy (RVH)

3. Echocardiogram: reveals abnormal septal motion, dilated right atriumand right ventricle

4. Angiography shows ASD.

5. Cardiac catheterization reveals increased 02 saturations in right atrium.

Complications:

Adult hood:

Atrial arrhythmias

Emboli

Heart failure

Left ventricular failure

Medical Management:

1. Right or left ventricular failure can be treated by administering

Digitalis (Digoxin) and Diuretics (Frusemide)

2. Post operatively it can be treated by administering antibiotic

to prevent complication

3. Monitor for signs of complication


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Surgical Management:

Open heart surgery (or) cardiopulmonary bypass:

The detective septum is closed with a purse string suture.

If the defect is large means need a knitted Dacron patch sewn over the

openings.

This surgery is contraindicated for right to left shunt

Females should always undergo surgical repair due to the high risk

of paradoxical emboli in pregnancy.

Nursing Management:

1. Maintain the nutritional status

2. Instruct to avoid sports and exercise

3. Antibiotic should be administered to prevent infection and to minimize

the risk of Bacterial endocarditis

4. Assess any complication

5. Note the child's colour, vital sings and blood pressure

6. Incision and dressing should be checked for bleeding and haematoma

7. Maintain intake and out put chart.

2). Ventricular Septa' Defect (VSD)

Ventricular septal defect is the most common congenital cardiac anomaly.

This anomaly is frequently occurs with both the cyanotic and acyanotic types.

Ventricular septal defect is an opening present in the septum between two

ventricles. It consists of an abnormal communication between the right and left

ventricle,


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Incidence:

About 3 in thousand live birth.

Causes:

Hereditary

The mother having mumps, measles , rubella and jaundice during the

time of pregnancy

T he m ot he r t ak in g A nt id ia be ti c, Antihypertensive,

Chemotherapy and Radiation therapy.

The mother having the habits of smoking and alcoholism.

Environmental factors

Idiopathic, hyperkalemia

Pressure in the left ventricle is higher then in the right ventricle

So, blood is shunted through the defect from left to right


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Then, the blood enter in to the pulmonary artery

Pulmonary hypertension

Due to increased pressure in the right ventricle muscular hypertrophy

occurs

Atrium may also enlarge

If pulmonary vascular resistance increases Left to right shunt reduces and

right to left shunt result

Un oxygenated blood crosses the defect to the left ventricle and enters to the

systemic circulation (Eisenrnenger syndrome)

Pathophysiology:


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Clinical Features:

Breathlessness due to decreased oxygenated blood


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Difficulty in feeding due to breathlessness

Congestive cardiac failure

Small peripheral pulse because of poor systemic blood flow

Para systolic murmur sound due to increased blood flow through the

chambers of heart

Thrusting apical pulse

Collapsing pulse

Narrow pulse pressure

Low diastolic pressure

Chillness of fingers and toes

Clubbing of fingers

Endocarditis (late)

Decreased exercise tolerance

Cyanosis (Due to pulmonary vascular disease)

Recurrent chest infection

Physical Signs:

Parasternal thrill

Heart murmur at lower left sternal edge

1. Loud Para systolic murmur when a small defect

2. Unimpressive ejection murmur from flow across the pulmonary valve

when a large defect

Variable pulmonary component of second sound

1. Normally when small defect

2. Loudly when large defect with pulmonary hypertension


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Left ventricular hypertrophy , pulmonary edema

Tachypnea, tachycardia and enlarged liver from heart failure

Delayed growth and development


History collection about congenital defect

Physical examination through this pulse rate, murmurs, abnormal chest

movement can be assessed.

Chest x-ray it shows hypertrophy of right and left ventricle

ECG

In this hypertrophy of right ventricle, right axis deviation can be seen

Echocardiography

It helps to demonstrate the site of ventricular septa' defect and the

presence of multiple defects

Ultrasonography

A For the direct visualization of the blood flow.

Cardiac catheterization.

The diagnosis of ventricular septal defect is confirmed by cardiac

catheterization the sings Include the presence of an abnormal

communication between the ventr icle, increased blood

oxygenation, precursor in the ri ght ventr icl e and abstr act ion at

the pulmonary artery (Infundibula stenosis)

Management:

Medical management:

1. Cardiac Drugs-Digoxin syrup 0.35mg/kg to decrease the workload of the 175


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heart

2. Diuretics-lasix 1.3 mg/kg

3. Prophylactic Antibiotics

4. Potassiom chloride syrup 3-5 ml


Purse String Suture:

Small defects are repaired with pursestring approach.

Open heart surgery.

Knitted Dacron Patch

Large defects usually require a knitted Dacron patch sewn over the opening

After this procedure heart size return to normal and murmurs disappear.

Cardiac Pulmonary Bypass Surgery

In a surgical correction can be achieved at any age using cardiopulmonary

bypass under deep hypothermia for the very young infant and to heart, lung

bypass in older child.

Nursing Management:

1. Maintain the nutritional status

2. Instruct to avoid sports and exercise

3. Antibiotic therapy should be administered to prevent infection and to

minimize the risk of Bacterial endocarditics

4. Assess any complication

5. Note the child colour, vital sings and blood pressure

6. Incision and dressing should be checked for bleeding and haematoma

Maintain intake and out put chart


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3). Pulmonary Stenosis (PS)

Pulmonary stenosis is the obstruction of flow of blood from the right

ventricle to lungs.

It may be associated with other defects such as atrial defect, ventricle

septal defect and patent ductus arieriousus,

Incidence:

It occurs 8% of congenital heart defects.

90% of obstruction occurs at the level of the pulmonary value

Pulmonary valve is obstructed by fusion of the cusps

Right ventricle hypertrophy in early stage

In Later stage the blood flow from right ventricle to right atrium

1) If baby have foramen vale, at that time the blood shunted from right atrium to

left atrium and left ventricle

2) If baby have ductus arteriousus the systemic circulation mixed with centre

circulation so cyanosis can occur

Pathophysiology:


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Clinical Features:

Mild to moderate pulmonic stenosis are asymptomatic

Palpitation

Chest pain

In severe pulmonary stenosis results in a further widening of the split

Delayed second heart sound

Pulmonary ejection murmur

Systolic murmur

Cyanosis

Cardiac failure

Dyspnoea


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On physical examination

Patients are characteristically described as having a round face and

hyperpeorism

Port-wine angiomatous malformation may be present over the skin

Turner's phenotype without chromosomal abnormalities (Noonan syndrome)


History Collection

Physical Examination:

Auscultation reveals a systolic ejection murmur over pulmonic area often

an ejection click and a widely split second sound can be heard

Chest x-ray shows enlargement of right ventricle and main pulmonary

artery

ECG: Moderate or severe cases demonstrate right ventricular hypertrophy

Two-dimensional echocardiography and Doppler study with colour flow

mapping can enhance visualization of the level of obstruction

Cardiac catheterization

Management:

Children having mild and perhaps even moderate pulmonic stenosis may

be no need of treatment

Children having a more severe defect require surgical pulmonary

valvotomy

If the obstruction is at the valvular level

The leaflets of the valve are separated by incisions at the fused

commissures

If the stenosis is infundibulam, resection of the excess muscle or fibrous

tissue is done


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If present of patent foramen ovale or atrial septal defect it is closed


Open heart surgery is necessary

In infants valve transventricular (closed) valvotomy (Brock) procedure

In children, pulmonary valvotomy with cardiopulmonary by pass

Non-Surgical Treatment:

Ba ll oo n an gi op la st y in th e ca rd ia c catheterization of laboratory to

dilate the valve

4). PATENT DUCTUS ARTERIOSUS (PDA)

Patent ductus arteriousus is a communication between the pulmonary

artery and the aorta. The aortic attachment of the ductus arteriosus is just distal

to the left subclavian artery. The ductus arterious is present in the fetal

life in all. It closes functionally and anatomically soon after birth

persistence of ductus is called patent ductus arteriousus.

Incidence:

It is twice as frequent in female as in male infants

Pathophysiology:

In fetal life the blood directly enter the descending aorta from thepulmonary artery through the ductus arteriosus

After the birth expansion of lungs takes place for increased blood pressure in

pulmonary artery.

It should dilate same time ductus arteriosus should be closed patent ductus

arteriosus.


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Clinical Features:

Murmur is heard at the middle to the upper left sternal border.

Pulse pressure is increased

Enlargement of left atrium, left ventricle, and right ventricle. If the

volume overload of left ventricle occurs, it causes pulmonary venous

engorgement resulting in congestive cardiac failure

Respiratory distress

Increased respiratory infection

Gallop rhythm due to rapid filling of ventricle

Dyspnoea decreased physical developement

Increased heart rate over 150/minute

Bounding pulses due to increased systolic pressure

Machinery murmur


1.Auscultation:

Continuous murmur is heard at the left intraclavicular area. A thrill

may be palpable.S1 is loud and the S2 is narrowly or paradoxically split

2. Chest x-ray reveals Cardiomegaly and left ventricular enlargement.

Aorta is prominent lung fields are plethoric.

3. ECG reveals left ventricular hypertrophy

4. 2-D echocardiography: study with colour flow are helpful for

visualization of PDA and blood flow across PDA.

Complications:

Before surgery:

Pulmonary Oedema

Pneumonia

Systemic emboli


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Pulmonary hypertension


Postoperatively:

Infective endocarditis

Pneumothorax

Death

Management:

Medical management:

Indomethacin:

(Inhibits the prostaglandins synthesis)

Diuretics:

Chlorothiazide 20mg/kg/24hour5.

Frusemide:

1.3mg/kg/dose/oral Digitalis:

Digoxin

0.35mg/kg

Surgical Treatment:

Surgical division or ligation of the patent vessels via a left thoracotomy.

(A newer technique, visual assisted thoracic scopic surgery (VATS), uses a

thoracoscope and instruments placed through small incisions on the left side of the

chest to place a clip on the ducts. It is used in some centers and eliminates the

need for a thoracotomy there by speeding post operative recovery.

Non-Surgical Treatment:

Use of coils to occlude the PDA in the catheterization laboratory is done in


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many centers. Small infants (with small diameter femoral arteries) and those

patients with large or unmusical PDAs may require surgery.

5) COARCTATION OF THE AORTA

It is the narrowing of the lumen with in the area of aortic arch.

Incidence:

This defect s seen more frequently in males and is commonly seen in

association with Turner's syndrome.

Causes:

Narrowing causes decreased blood flow distal to the structure, and the back-up of

blood flow in the heart.

Clinical features:

Usually depend up on severity.

Hypertension in arterial branches proximal to the defect and hypotension

distal to the defect has a symptomatic until adolescence if presents of mild

narrowing area.

Decreased / absent femoral pulses with a brachial femoral leg.

Systolic murmur audiable in left upper side of the axillae.

Blood pressure: - Upper extremities > lower extremities.

Poor feeding

Poor weight gain

Pallor

Respiratory distress etc..


1. X-ray shows enlargement in portion of aorta proximal to stricture,


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Cardiomegaly & pulmonary oedema

2.ECG shows evidence of slight left ventricular hypertrophy.

3.Echo shows visualization of Coarctation site, dilated right ventricle &

hypoplastic left ventricle.

Complications:

1. 1. Death from heart failure.

2. Renal shutdown(postoperative(y)

3. Recoarctation

4. Death

Medical management:

Administer digitalis, dopamine, diuretics, and prostaglandin-E

(in newborn to keep ductus arteriosis open.

Provide fluids & electrolytes monitoring andrenal monitoring.

Balloon angioplasty can be used as a primary non-surgical procedure.

Surgical management:

Surgical repair of narrowed aortic area and reanastamosis (subclavian

flap aortoplasty) of the resected area usually occurs with in the first to two

years of life.

6). Aortic stenosis

Narrowing or stricture of the aortic valve causing resistance to

blood flow in the left ventricle, decreased cardiac output in the left

ventricular hypertrophy & pulmonary vascular congestion.

Incidence:

Aortic stenosis is more common in males than females


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Causes:

Congenital anomalies

A stricture in the aortic outflow tract

Resistance to ejection of blood from the left ventricle

Hypertrophy of the left ventricle

Blood backs up in the left atrium

Increased pressure in the left atrium


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Increased pressure in the pulmonary veins & pulmonary vascular congestion

Narrowing of aorta

Pathophysiology:

Clinical Features:


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infants with sever defects demonstrate decreased cardiac output with

faint pulses

Hypotension

Tachycardia & poor feeding

Child ren 's show s s igns of exe rcise intolerance

Chest pain

Dizziness when standing for long time

Characteristic murmur

Endocarditis

Coronary insufficiency

Ventricular dysfunction


1. History collection

2. Physical examination

3. Echocardiogram

4. X-ray (chest x-ray detects dilated ascending aorta & varying degree of

left ventricular enlargement)

5. ECG reveals normal or left ventr icular hypertrophy

6. Echocardiography & Doppler measurement determine peak flow

velocity & can accurately identify the level of obstruction

Management:

Digoxin (lanoxin)

Captopril

Enalapril

Surgical management:


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Balloon dilatation

Aortic valvulotomy or aortic valve replacement

Nursing management:

Reliving respiratory distress

Observe the regularity of respiratory pattern for retraction

Observe for nasal flaring !listen for grunting

Observe color change , irritability or anxiety

Raise the head end -

I. Position the child at a 45degree angle to decrease pressure of the viscera on

diaphragm to increase lungs volume

II. Place an infant in seat or prone position

III. Elevate head of the bed & support arms with pillows

Feed slowly allowing frequent rest periods.

Child may require ga.vage feeding

Observe for abdominal distention which may increase respiratory

difficulty. If present, insert a feeding tube to achieve it.

Tilt the infant's or child's back slightly so as to keep the airways

Straight

Suction the nose and throat if the child is unable to cough up

Secretions adequately

Provide 02 therapy as indicated

Administer diuretics as ordered to help to reduce lung congestion.

Improving cardiac output by avoiding unnecessary activities such

as Frequent, complete bath and clothing changes.


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7). Tetralogy of Fallot

Tetralogy of fallot is the most common type of cyanotic congenital

heart disease. The common cause of cyanotic congenital heart disease is a

communication between the pulmonary and systemic circulation through

which various blood (deoxygenated) enters the systemic circulatory system.

Tetralogy of faliot is an association of 4 anomalies

i. Obstruction to right ventricular outflow (or) pulmonary stenosis.

ii. Ventricular septal defect

iii. Dextraposition or over riding of aorta.

iv. Right ventricular hypertrophy

Pulmonary Stenosis:

Pulmonary stenosis is an obstructive lesion that interferes with blood

flow of the right ventricle. It may occurs an single abnormality or it may

associate with other defects such as those in the atrial or ventricular septal

defect. It may occur also with patent ductus arteries.

Types:

There are 2 types of pulmonary stenosis on the basis of their anatomical

presentation.

1. Valvular stenosis

2. Infundibular stenosis

1. Valvular stenosis:

1 This type of cases occurs in more. The stenoses of the pulmonary valve

are fined in 90% cases. Beyond this is dome like stenotic valve, the

space is often enlarged and right ventricular hypertrophies.

2 Infundibular stenosis


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2. This is less common in the pulmonary valve is often normal but

the outflow tract of the right ventricle is narrow converting the

narrowed region an infundibular channel.

Pathophysiology:

Due to pulmonary stenosis

There is an obstruction of blood flow from the right ventricle to pulmonary

artery

Pressure thus rises in the right ventricle resulting in its hypertrophy

The pressure in the right ventricle rises so as to become equal or slightly

more than the left ventricle

Deoxygenated blood is shunted from the right ventricle through the VSD


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directly in to aorta (right -to- left shunt) essenmenger syndrome

Clinical Features:

A loud pulmonary systolic ejection murmur caused by blood flow through

the stenotic site can be heard over the pulmonic area

in severe cases cyanosis will occur

Cardiac failure can occur

Poor exercise tolerance with exertional dyspneoa due to insufficient

blood flow to the lungs to meet the need for increased cardiac output during


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exertion.

Palpitation and peripheral cyanosis

Growth retardation

Hypertrophy of right ventricles and right atrium due to increased

pressure.

The tachycardia and Tachypnea due to increased cardiac work load.

Cardiomegaly

Clubbing of fingers and toes occur by one to two years of age

Unconsciousness, convulsion, hemiparesis

Mental showers


Physical examination:

Abnormal chest movements cardiac murmurs, tachycardia, tachypnea,

cyanosis.Electrocardiogram:

Indicates the presence of right ventricular hypertrophy with perked 'P'

wave in case of patients with mild pulmonary stenos's. The ECG is often

normal.

Radiography:

It shows the enlargement of heart with hypertrophy of right ventricle

and atrium.

Angiocardiography :

It helps to determine the severe malformation

Boot shape or wooden shoe shape heart in x-ray

Blood test:

To identify the Polycythemia


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Cardiac catheterization:

It shows pulmonary arterial pressure to be normal or low and the right

ventricular systolic pressure, in severe cases, to be higher than the systemic

systolic pressure. It also shows decreased oxygenation on the left side of the

heart.

Complications:

Congestive cardiac failure

Bacterial endocarditis

Pulmonary tuberculosis

Anoxic spells

Treatment

I. Palliative procedure:

1.Water stone Shunt:

Side to s ide anastomosis of the ascending aorta and right

pulmonary artery.

1 . B la lo ck P ro ced ure : Formation of artificial ductus

Anastomosis of the subclavian artery and pulmonary artery.

3. Potts Procedure:

Anastomosis of the upper descending aorta and left pulmonary artery.

3. Brock Procedure:

Pulmonary valvotomy this operation only for pulmonic stenosis

It does not correct the ventricular septal defect

There is no need for surgery in mild cases Antibiotic therapy against

bacterial endocarditis is important.


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Reasonably medication therapy:

Prostaglandin E showed be administered intravenously. It will help to

maintain the ductus arteriosis

Surgical Treatment:

The indications for surgery are

1 Signs of congestive cardiac failure

2 Right ventricular pressure even 75-100 mm/Hg

3 ECG evidence of right ventricular hypertrophy

4 Cyanosis

5 Presence of anomie spells in early life

6 Pulmonary vulvotomy is most successful. This may be performed

either by incision of the fined leaflets under direct vision with

interruption of venous return for the short period of 2-3 unit or by a

vulvotomy through the right ventricle of a beating heart.

Surgery:

1 Cardiopulmonary Bypass

This surgery for young children

2 Heart lung bypass

This surgery for older children

Steps of Surgery:

Closure of ventricular septa' defect

Resection of muscle tissue in pulmonary artery

Improve the pulmonary circulation


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Non Surgical Treatment:

Balloon angioplasty

Post operative management

Administor iv fluids

Monitor vital signs every 15 minutes

Administer antibiotics

Monitor intake and out put chart

Administer diuretics

Eg: Lasix 1-3 mg/kg

Administer cardiac drugs

Digoxin 0.35 mg/kg

8) Transposition of the Great Vessels

In transposition of great arteries, there are two parallel circulations. The

systemic venous return passes from the right atrium to right ventricle and then

into aorta;

And there is a separate circulation of pulmonary venous blood returning to the

left atrium via the left ventricle and back into the pulmonary arteries.

Incidence:

- Males are mostly affected than female.

Pathophysiology:

Aorta carries deoxygenated blood to the systemic circulation.

Pulmonary artery carries oxygenated blood back to lungs.

Can exist to separate blood circulation.


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Systemic Circulation:

1. Deoxygenated blood from body organs

Blood enter into the Right atrium

Blood enter into the Right ventricle

Enter into the Aorta [No purification]

Deoxygenated blood enter in systemic circulation


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Pulmonary Circulation:

2. Lungs (oxygenated blood) (pulmonary veins)

Enter in to the left atrium

Enter in to the left ventricle

Enter the pulmonary artery

Again oxygenated blood goes to lungs.


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Clinical Features:

Symptoms:

Cyanosis; It may be profound and life threatening

Physical Signs:

Cyanosis

Clubbing Fingers

Second heart sound is often closely split or single

Systolic murmur due to increased flow or stenosis

Heart size enlarges after 2 weeks of birth of baby

Congestive heart failure develop shortly after birth

Normal first sound

The electro cardiogram shows right axis deviation and right ventricular

hypertrophy

The cardiac silhoaette has an "egg on side" appearance

Difficulty in feeding


History collection about occurrence of disease

Physical examination

ABGs

Reveal hypoxemia & acidosis


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Chest x-ray:

This may reveal the classic findings of a narrow upper mediastinum

with an "egg on side" appearance of the cardiac shadow.

ECG:

This is rarely helpful in establishing the diagnosis as it is usually normal

Echocardiography:

This is essential to demonstrate the abnormal arterial connections and

associated abnormalities.

Complications:

Arrhythmias

Pulmonary vascular obstructive disease

Residual shunting

Death

Management:

Medical management:

It consist of control of congestive heart failure

Since patient may be very hypoxemic, means digoxin should be administered

Administrations of oxygen by oxygen tent

The balloon atrial septostomy following confirmation of the diagnosis by

cardiac catheterization and angiocardiography

Jatene's switch operation:

The pulmonary artery and aorta are transected. The distal aorta is

anastomosed to the proximal pulmonary stump and the pulmonary artery to the

proximal aortic stump. The coronary arteries are shifted to the aorta.

Mustard or Senning:


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The inferior and superior venacave directly connected in to left atrium .

The pulmonary vein is connected in to right atrium.

Rashkind Procedure (Ballon Septostomy):

Catheter contain balloon, and it inserted through catheterization

Enlarging the foramen ovale by pulling a balloon. To increase the mixing of

blood

Blalock Procedure:

Anastomosis of subclavian artery and pulmonary artery.

Nursing management:

Assess the condition of child

Check the vital signs

Assess for any complication

The child must be carefully followed because of possible complications

of atrial arrhythmias due to injury to the conduction system and

recurrence of cyanosis

Assess the child for any infections

Administer oxygen to the patient

Provide good position

Monitor cardiac functioning (vital signs ECG, resp iratory effort s,

skin colour and temperature

Be alert for signs indicating potential complications.

Health Education:

Ass ess f ami ly a nd chi ld' s l eve l o f understanding

Instruct the parents in feeding techniques to minimize fatigue

Teach parents signs and symptoms for which to be alert.


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Rheumatic Heart Disease:

Rheumatic heart disease was formerly one of the most serious forms

of heart disease of childhood and adolescence. Rheumatic heart disease

involves damage to the entire heart and its membranes.

Rheumatic heart disease is a complication of rheumatic fever and

usually occurs after attacks of rheumatic fever. The incidence of rheumatic

heart disease has been greatly reduced by widespread use of antibiotics

effective against the streptococcal bacterium that causes rheumatic

fever.

Causes Rheumatic Heart Disease

Rheumatic fever causes rheumatic heart disease. Rheumatic fever

results from an untreated strep throat. Rheumatic fever can damage the

heart valves. If the heart valves are damaged, they will fail to open and

close properly. When this damage is permanent, the condition is called

rheumatic heart disease.

Risk for Rheumatic Fever

Rheumatic fever is uncommon in the United States. However,

rheumatic fever can occur in children who have had strepc, , infections that

were untreated or inadequately treated.

Symptoms of Rheumatic Heart Disease

Some of the most common symptoms of rheumatic heart disease are:

breathlessness, fatigue, palpitations, chest pain, and fainting attacks.

Treatment options for Rheumatic Heart Disease


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Treatment of rheumatic heart disease may include medication and

surgery. Medication will aim to avoid overexertion. Surgery may be

needed to replace the damaged valve(s).

Prevention of Rheumatic Heart Disease

The best way to prevent rheumatic heart disease is to seek

immediate medical attention to a strep throat and not let it progress to

rheumatic fever.

Acute Rheumatic Fever (ARF)

Acute rheumatic fever is an autoimmune disease (acquired heart

disease). It occurs as hyper sensitivity reaction to group-A beta hemolytic

streptococcal infection. It is affected in connective and endothelial tissues of

heart, joint, blood vessels and other tissues,

Incidence:

Rheumatic fever is commonly affected school age children in between 5 to

15 years of children:

The school age children are affected in this disease through genetic,

climate, winter and early spring, unhygienic, overcrowding (class room,

family) poor nutritional status.The adole scen ts affec ted throu gh

streptococcal infection.


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Chorea

School age child (between 5-15 Yrs)

O r

Early adolescents

Streptococcal pharyngitis(Group-A beta hemolytic streptococci)

Auto immune reaction to the organism

Acute systemic inflammatory disease

(Rheumatic fever)

Antibiotic therapy

Resolution

Heart

Joint

Skin


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Brain

Inflammatory Hemorrhagic Bullous lesions in any layers of the heart (Aschoffs

bodies)

Fibrous or Serofibrous

Exudates

Resolution

Proneness to Rheumatic fever

Inflammation of synovial membrane of knees, ankles, wrists, elbows

Edema, effusion heart pain

Polyarthritis

Involvement of endo cardium and valves

Vegetative lesions on the valves leaflet (mitral and aortic

valves)

Muscular rash on trunk, extremities, sebaceous on feet, hands, scalp, elbows

Pathophysiology:


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Long term

Prophylaxis

Fibrous scar tissue of valve

Contraction and deformity of the valve

Leaflets shortening of the chorde


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Tendineae fusing of leaflets while healing

Chronic valvular defect in the heart

Clinical Features:

1, Major Manifestation:

Limited range of motion

Extreme tenderness, swelling and redness.

Inflammation

First 1-2 weeks Febrile period

After few days affected joints, it may transmit to other joints.

2. Carditis:

Signs of carditis

Congestive heart failure Increased work load

Cardiomegaly Pericardial pain present


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Pericarditis Muffled heart sound present

Fever especially during sleep and have more pulse(tachycardia)

Presence of significant murmur sound and pre existing murmurs.

Muffled heart sound caused by pericardial effusion.

Pre diastolic gallop

Pericardial friction or rub Chorea (sydenhams chorea)

Children have neurological manifestation of rheumatic fever have. Muscular weakness

Facial grimaces.

Emotional rabiality

Speech disturbance

Restless

Behavioral problem Anxiety

Erythema Marginatum:

Colour change (pink muscle) s Rash without itching

Lesions present on trunk and extremities

The lesions an appear with through heat and transmit one place to

another place.

Subcutaneous Nodules:

A Who had frequently in painless nodules (0.5cm to lcm) and without

tenderness On such a place elbows, knuckles, knees, joint ankles and

scalp,


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Minor Manifestation:

Low grade fever to high fever in afternoon rarefy it goes above 39.5C

Scarlet fever

Tachycardia

Weakness

Fatigue

Weight loss

Epistaxis (unknown causes)

Abdominal pain

Some times had appendicitis

Sore throat

Others:

Pericardial pain

Headache, malaise, sweating.

Vomiting, skin rash, anemia.

Pleuritis (etc).


1. History taking from parents and childespecially for environmental factors

and streptococcal infection

2) Blood Test:

1. ASO titer (antistreptolysin)-increased (normal value 200 1V/ml

2. ESR (erythrocyte sedimentation rate)

3. WBC counts (leucocYtes)

4. CRP (C-reactive protein)

5. Throat culture


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3) Radiology (x-ray)-Cardiomegaly

4) Electrocardiogram-Cardiomegaly

5) Echocardiogram-Cardiomegaiy

6) Serological Test:

1. Antideoxyribonuclease B test

2. Antinicotinamide-adenine -Dinucleotidase test

3. Now a day's streptozyme agglutination test was used to deduct

streptococcal infection.

7) Examination through inspection, palpation percussion and auscultation to

find out any abnormalities in the body (Nodules,Cardiomegaly

etc.)

8) Endomyocardial biopsy to show in a scoffs nodules.

Complications:

Permanent cardiac damage to valve.

Death

Management:

1. To provide bed rest and sleep. It helps to disappear of rheumatic fever

with in 6-8 weeks.

2. Nutrition diet to be providing protein, vitamins and micronutrients.

3. Avoid rich spicy food.

4. Those who are having CCF to avoid salt, otherwise no need of restriction.

Pharmacological Treatment Antibiotic Therapy:

1. Penicillin:

- To control streptococcal infection


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2. Procaine penicillin:

- 4 lack deep IM-deep, 10 to 14 days.

3. Long-acting (Benzedrine penicillin):

- 1.2 mega unit

(Or)

0.6 mega unit every 15 days for IM

4. Oral penicillin:

- 4 lack units every 6 hours for 10 to 14 days

5. Erythromycin:

- Used in penicillin sensitive patients.

6. aspirin:

90 to 120mg/kg/day divided dose To control pain and inflammation -

Duration 12 weeks needed.

- Dose may be changed according to the patient.

7. Antacid:

- Aspirin should not take alone because it leads to pepticuler.

8. Steroid therapy:

It is suppressive therapy along with aspirin.

- Prednisolone 40 to 60mg/day 2mg/kg/day in 4 divided dose for 7 to

10 days

9.Diazepam (or) phenoborbitone: - To treat chorea

9.Symptomatic treatment:

To be provided for other complication of rheumatic fever.

Nursing Management

1.Good nursing care and emotional support to be provided for parents, child,

care givers.

2.Nurse should explain about importance of medication and disease condition


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of the child.

3.Nurse should maintain vital signs (TPR).

4. Nurse should maintain cardiac monitoring (ECG< heart sound).

5.Nurse should assess the level of pain

Nursing diagnosis Nursing intervention

1 Pain related to

disease Condition

(Polyarthritis)

1 Assess the condition of the child

2 Assess the level of pain and characters of

pain.

3 Provide comfortable position, rest and

sleep.

4 Provide hot application (big joints) cold

application for (serial' joints)

5 Provide psychological support to the parentsand Children.

6 Divertidnal therapy (provide music, provide play

materials)

7 Administer, anti inflarnmatwy, analgesics as per

doctors order. (DiclOtinac sodium), (assess the

aspirin toxicity)

2 Decreased cardiac

output related to

carditis

Providing rest and less activities

Provide indoor activity (rnifaaseS)

Providing the balanced diet with adequate

nutrition


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Maintain intake and out put chart

Maintain cardiac function

Salt restriction in case of CCF

Administer medication as doctor's order

Kawasaki Disease (or)Mucocutaneous Lymph Node Syndrome

It is an acute inflammatory disorder

Causes:

Idiopathic

Incidence:

It involves many systems, mostly affected in cardiac system

80% of the cases are seen in children under 4 years of age with a slightly

higher male do min ance .

Clinical Features:

The following criteria are required for the diagnosis:

1 Fever: More than 5 days is present, it is not responsive to antibiotic

2 Mucous membrane involvement: Cracked, erythematous, fissured lips

and a "strawberry tongue," oropharyngeal reddening.

3 Non purulent conjunctivitis: Bilateral inflammation without exudates.

4 Polymorphous rash: Typically involves trunk and extremities5 Lymphadenopathy

6 Digital swelling and desquamation

Peripheral edema, erythema of the palms and soles with desquamation of the

hands and feet.


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1 1, Blood investigation which are WBC, ESR, CRP, Platelet count will

be elevated.

2 Sterile pyuria and anemia may also occur.

3 ECG also shows prolonged P-R interval

4 Echocardiography may show pericardial effusion and is diagnosis

for identifying coronary artery, aneurysms (or) dilatation.

Complications:

Coronary artery aneurysm

Myocardial infarction

Aspirin toxicity

Allergic reaction to the gamma globulin A death

Medical Management:

Salycilate therapy and intravenous gamma globulin (NIG):

Anticoagulation therapy for children for with large aneurysms.

ECGs and echocardiograms to monitor coronary abnormalities

Surgery-unnecessary

Congestive Heart Failure:

A congestive heart failure occurs when the heart is unable to pump out

adequate amount of blood to meet the need of the metabolic demands of the

body this leads to an accumulation of excessive blood volume in the

pulmonary and systemic venous system.

Congestive heart disease is the most common cause of congestive heart

failure in infants and children.


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Incidence:

It is usually occurs with in the first few months to 1 year after birth.

Time of Onset of Congestive Failure in Congenital Lesions:

Age Lesions

Birth to 72 hours

d-lweek

Pulmonary mitrul and aortic atresias hypo

plastic left and right heart syndrome

transposition and malposition of great artories

1 to 4 weeks EndocEtraidal fibroelastosis Coarctation of the

area.

1-2 months E n d o c a r d i a c u s t o m d e f e c t s , V S D

P D A , p u l m o n a r y

2 to 6 months Transposition and malposition complex VSD,

PDA, pulmonary venous connection, aortic

steriosis, coarctation of the aorta.

Causes:

Infant:

1 Congenital heart disease

2 Carditis and primary myocardial disease

3 Paroxysmal tachycardia

4 Anemia

5 Other causes

a) Infection


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b) Upper respiratory obstruction

c) Hypoglycemia

d) Hypocalcernia

e) Neonatal asphxia

f) Persistent fetal circulation

Children:

1 Large VSD, PDA

2 Supraventricular tachycardia

3 A malformation

4 Metabolic car& myopathy

5 Acute hypertension

6 Anomaly origin of left coronary artery

7 Myocarditis

8 Rheumatic carditis

9 Infective endocarditis


Sympathetic nervous system

Stimulation of cholinergic fibers

Sweating Especially on scalp

Increase rate and force of contraction

Tachycardia


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Increased blood volume

Increase vascular tone vasoconstriction

Increased venous return

Increased pulmonary Vascular resistance

Increased systemic Vascular resistance

Increases after load

Decreased blood flow to limbs

Decreased blood flow to kidneys

Production of renin, aldostoerone and ADL

Na and H20 retention

(preload)

Systemic and pulmonary

venous engorgement

PATHOPHYSIOLOGY:


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Clinical features Pulmonary congestion Systemic venous congestion

1 Tachycardia 1 tachypnea 1 weight gains

2 Sweating(in appropriate) 2 Dyspnea 2 Hepatomegaly

3 Decreased Urine Output 3 Retractions (infants) 3 peripheral edema

4 Fatigue 4 Flaring rares 4 Ascites and depended

edema

5 Weakness 5 Exercise intolerance 5 neck vein distention

(children)


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remove the accumulated fluid and sodium

Oxygenation of the tissue is improved by supplying moist oxygen and

by reducing oxygen demands

Sedatives may be prescribed for irritable children.

Management:

Assessment of the patients condition must be done, especially the heart

rate and respiration, temperature and electrocardiograph

Digitals should be administered according to doctor's prescription.

Digitalis help to improve the cardiac activity.

The early sign of toxicity such as arrhythmia, vomiting slow pulse

should be observed

Rest is essential to conserve energy

Nursing care should be organized to prevent unnecessary disturbance

Improving cardiac efficiency or the contractile force of the heart.

Removing accumulated fluid and sodium from the body

Improving oxygenation of the blood and tissue

Reducing the work load of the heart by reducing energy

requirement

Supporting and educating the parents before discharging of child from

hospital

Common nurs ing d iagnoses & intervention of cardiac system:

Nursing diagnoses for AcyanotIc heart defects:

1. Fluid volume excess related to pulmonary vasculature overload.

2. Decreased cardiac output related to an obstructed out flow tract

3. Ineffective breathing pattern related to pulmonary vasculature

overload.


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4. lmbalanced nutritional status less then the body requirements

related to ineffective feeding pattern.

5. Ineffective infant feeding pattern related to shortness of breath and

fatigue

6. Risk for infection related to impaired immune function, surgery.

7. Risk for activity intolerance related to chronic pulmonary vasculature

overload.

8. Impaired family processes related to guilt & grieving over lack of

perfect infant.

9. Risk for caregiver role strain related to child with chronic health

condition.

10. Knowledge deficit (parents) related to special care for chronic

condition.

Nursing diagnoses for cyanotic heart disease:

1. Impaired tissue perfusion related to reduced pulmonary blood flow.

2. Decreased cardiac output related to development of congestive heart

failure.

3. Risk for infection related to unfiltered bacteria in the blood.

4. Impaired nutritional status less then body requirement related to dyspnea

& fatigue with feeding.

5. Risk for caregiver role strain related to care of a child with chronic

illness.

6. Activity intolerance related to cyanosis dyspnea on exertion.

7. Impaired growth & development related to hypoxemia.

8. Risk for ineffective management of therapeutic regimen related to

prophylactic antibiotics for dental care procedures

9. Knowledge deficit (parents) related to assessments & management of


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cyanotic spells, which are unpredictable events.

Nursing intervent ions of cyanot ic & Acyanotic heart defects

Organize nursing care to provide periods of uninterrupted rest

Avoid temperature excess.

Prevent excessive crying

1. Anticipate needs

2. Hold the infant

3. Feed when hungry

4. Keep the infant comfortable

Maintain intake and output chart

Monitor urinary output and laboratory values for evidence of over

hydration

Check vital signs regularly

Regulate parenteral fluids closely to avoid over hydration

Assess for blood pressure, edema, and weight. mucous membranes

electrolytes fontanel.

Administer cardiac support medication as ordered

1. Digoxin (lanoxin)

Check heart rate for one full minute before dose

Don't give with meals; in case of vomiting do not repeat the dose.

Monitor serum drug level and serum electrolyte.

Observe regularity of the respiratory pattern. Observe nasal flaring, listen

the grunting

Raise the head end: position the child at a 45 angle to decrease

pressure of the viscera on the diaphragm and increase lung volume feed

slowly allowing frequent rest periods.


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Provide oxygen therapy as indicated.

Suction the nose and throat if the bhild is unable to cough up secretion

adequately.

Administer diuretics as order to reduce lung congestion.

Feed slowly in a semi erect position; burp infant af te r each ounce

to de cr ea se compression of stomach on heart and. lungs.

Provide small, frequent feeding, provide easy to chew and digest.

Provide foods that have high nutritional value

a) Add needed calories for healing to promote maximal growth.

b) Provide foods high in iron and potassium levels if needed.

Determine the Child likes and dislikes and plan the meals with the

dietician.

Maintain ordered low sodium or fluids restriction in children with

CHF.

Prevent exposure to communicable disease.


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