cardio vascular diseases(1)

8/6/2019 Cardio Vascular Diseases(1)

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Cardiovascular disorders in children are divided into two major groups:

a- Congenital heart diseases.b- Acquired heart disorders.

Congenital HeartDisease (C.H.D.)

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 thehighest 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 leftatrium.- 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 rightventricle.- 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 thetrunk and lower extremities. Only small amount flows to the non-functioning fetal lungsfor the purposes of nutrition.

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Types of Defects: Congenital heart defects have been divided into 2 categories:

1. Traditionally, a physical characteristics, cyanosis has been used as distinguishingfeature, dividing the anomalies into:

-1 Cyanotic defects.-2 Acyanotic defects.

2. Another classification system based on Hemodynamic characteristics also is used.The defining characteristics is blood flow patterns:

-1 Increased pulmonary blood flow.-2 Decreased pulmonary blood flow.-3 Obstruction of blood flow out of the heart.-4 Mixed blood flow in which saturated and desaturated blood mix within the heart

or great arteries.

Classification of Congenital Heart Disease:(Table 1)

Classification of congenital heart disease

Acyanotic Cyanotic

Pulmonary Obstruction to pulmonary MixedBlood flow blood flow blood flow Blood flow

From ventricles

-Artial septal defect - Coarctation of aorta -Tetralogy of fallot -Transposition of great arteries.-Ventricular septal defect - Aortic stenosis -Tricuspid atresia -Total anomalous pulmonary venous-Patent ductus arteriosus - Pulmonic stenosis return.-Atrioventricular canal -Tranucus arteriosus

- Hypoplastic left heart syndrome (Table .1) Comparison of acyanotic-cyantoic and hemodynamic classification system of congenital heart disease.

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Patent ductus arteriosus is a vascular connection that during fetal life, shortcircuits that pulmonary vascular bed anddirects blood from the pulmonary artery tothe aorta.Functional closure normally occurs soonafter birth. If the ductus remains patent flowin the ductus is reversed by the higher pressure in the aorta.

Acyanotic Defects

Most acyanotic defects involve primarily left to right shunting through an abnormalopening. Others result from obstructive lesions that reduce the flow of blood to variousareas of the body.

Major Acyanotic Defects:-1 Patent ductus arteriosus (PDA).-2 Atrial septal defect (ASD).-3 Ventricular septal defect (VSD).-4 Pulmonic stenosis (PS).

-5 Aortic stenosis (AS).-6 Coarctation of aorta (COA).

Patent Ductus Arteriosus (PDA)

Description and Pathophysiology:

(Fig .2)Incidence:

More common in females (2:1), Higher incidence among premature and commonlyassociated with maternal rubella.

Hemodynamics: Blood from aorta goes to systemic circulation poor systemic circulation.

PDA Double flow in pulmonary artery Double pulm. venous return

Double flow in aorta proximal to PDA Double flow in LV Doubled flow in LA

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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:1 Classic machinery murmur, which is continuous from systole into diastole.2 Dyspnea on exertion and easy fatigability.3 Under weight thin child.4 Repeated chest infections.5 Heart rate over 150 b/m, gallop rhythm due to rapid filling of the ventricle.6 Bounding pluses due to increased systolic pressure.7 Left heart failure may develop in infancy in severe cases.8 Enlarged heart size in large PDA.

Therapeutic Management:1. Supportive : fluid restriction with diuretics and digitalization for congestiveheart failure CHF.

2. Surgical : surgery can be performed at anytime, although it is preferablydone at about 6 months of age, surgery maybe done earlier if the child is indifficulty to prevent complications and growth retardation caused by PDA.

Out come:The child is good with less than 1% mortality.

Complications:1. Bacterial endocarditis.2. Congestive heart failure.3. Pulmonary hypertension.

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Ventricular septal defect is anabnormal opening between the right andleft ventricles. The defects vary in size andmay occur in either the membranous or muscular portion of the ventricular septum.Due to higher pressure in the right and leftventricles. A shunting of blood from the leftto right ventricle occurs during systole. If pulmonary vascular resistance producespulmonary hypertension, the shunt of theblood is then reversed from the right to theleft ventricle, with resulting cyanosis.(Fig 4)

Ventricular Septal Defect (VSD)

Incidence:Commonest (30% of all cases of CHD)

Description and Pathology:

(Fig. 4)

Hemodynamics:to Aorta poor systemic circulation

Blood from LA LV VSD RV RV flow Flow in pulmonary circulation (doubled)

Flow in LA Flow in pulmonary circulation

Assessment:

The most frequently seen defects are small, so these defects are asymptomatic. Medium sized or larger defects during infancy may produce symptoms such as:

dyspnea, slow physical development, feeding difficulties and frequent pulmonaryinfection.

Heart failure, cardiac enlargement and mild cyanosis may also occur in largedefects.

Therapeutic 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.

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It is an obstructive lesion that

interferes with blood flow from theright ventricle. It may occur as a single abnormality

or it may be associated with other defects such as those in the atrial or ventricular septa. It may also occur with patent ductus arteriosus.(Fig 5)

Pulmonary Stenosis (PS)Description:

(Fig.5)Pathophysiology:

The pulmonary valve is obstructed by fusion of the cusps of their (ommissures)

valve orifice so that their movement is restricted. The passage of blood is obstructed from the right ventricle to the pulmonary arteryresulting in increased systolic pressure and hypertrophy of the right ventricle. Thedegree of change depends on the size of the constricted valvular opening. Another cause of obstruction is a muscular or fibrous that is caused by the failure of involution of an embryonic structure.

If the right ventricle cant eject the necessary amount of venous blood into thepulmonary circulation systemic cyanosis occurs.

If a patent ductus arteriosus is also present, blood is shunted from the aorta to thepulmonary artery and then to the lungs, partially compensating for the obstruction.

Assessment: Mild PS: asymptomatic, discovered on routine examination. Severe PS: may present by right heart failure in infancy: cyanosis and cardiac

failure may occur, poor exercise tolerance with exertional dyspnea due toinsufficient blood flow to the lungs to meet the need for increased cardiac outputduring exertion.

ECG shows gross right ventricular hypertrophy. Radiography shows enlargement of the heart. The murmur and changes in the second heart sound can be analyzed with

echocardiography.

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Narrowing or stricture of the aortic valvecausing resistance to blood flow in the leftventricle and decreased cardiac output. (Fig6)

Management: Children having mild and even moderate pulmonic stenosis may need no treatment. Sever defect: - Medical treatment: like in VSD.

-Surgical : catheter ballon valvuloplasty if pulmonary valve gradient>60 mmHg. This reduces the narrowing by 75% or more.

Aortic Stenosis (AS)

Incidence:It is more common in boys.

Description:

(Fig.6)

Pathology:When there is resistance to blood out flow the left ventricle to the aorta left

ventricular hypertrophy occurs, blood backs up in the left atrium, causing increasedpressure in that chamber resulting in increased pressure in the pulmonary veins andpulmonary vascular congestion when severe obstruction occurs the pulse pressure in theaorta is narrowed (N.B. pulse pressure is the difference between systole and diastole).

Assessment:Depend on the severity of the lesion.

If there is mild aortic stenosis, the infant may grow normally to be asymptomaticuntil increased physical growth requires additional cardiac output.

In severe obstruction: fatigue due to exercise intolerance, dizziness, fainting andepisodes of pulmonary edema occur, decreased cardiac out put also results in faintperipheral pulses and anginal pain.

The most prominent physical manifestation of aortic stenosis is the presence of acoarse systolic ejection murmur, usually accompanied by a thrill over the aorticarea, radiating to the neck and apex.

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The classical tetralogy consists of:

1. Pulmonary stenosis.2. Ventricular septal defect.3. Overriding of the aorta: aorta receives

blood from both ventricles and this isthe cause of cyanosis.

4. Right ventricular hypertrophy. In tetralogy of fallot, the blood normally

returns from the systemic circulation tothe right atrium and right ventricle. Theout flow of the blood from the rightventricle resisted by the pulmonarystenosis so that the blood flows throughthe ventricular septal defect into theaorta. This is a right to left shunt.

Hypertrophy of the right ventricleoccurs as a result of the pressureexerted against the pulmonary stenosis,because the blood from the right ventricleis unoxygenated, cyanosis result.

Polycythemia develops because thebody attempts to compensate for theunoxygenated blood. The resultingincreased viscosity of the blood causesslowing of the circulation and possiblethrombophlebitis emboi and vascular disease.

Cyanotic Congenital Heart Disease

The common cause of cyanotic congenital heart disease is a communicationbetween 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.Major cyanotic defects:

1. Tetralogy of fallot.2. Transposition of the great vessels.3. Tricuspid atresia (TA).

Tetralogy of Fallot

(Fig. 8)

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Assessment: 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 closesduring the first months of life.

Clubbing of the fingers and toes(in long standing cases ) (Fig. 9 ).

(Fig.9)

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 kneechest position rather than extending their extremities when they lie down. Older children, learn that the squatting position relieves dyspnea because:

1. Flexing the legs decrease venous return from the lower extremities which have avery low oxygen content, especially after exercise.

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2. Squatting position increase systemicvascular resistance, which diverts rightventricular blood from the aorta intopulmonary artery increasing pulmonaryblood flow. This increases the amount of oxygenated blood in the left side of theheart and eventually into systemiccirculation. (Fig.10)

(Fig. 10) Cyanotic spells. (Hypoxic, blue spells). Apansystolic murmur: it is usually associated with thrill. These children dont develop congestive heart failure because the overload of the

blood in right ventricle flows freely through the septal defect and the overriding aortainto the systemic circulation.

Management: Medical:

1. Antibiotic prophylaxis before tooth extraction or GIT and urinary procedures.2. Treatment of cyanotic spells:

-Oxygen therapy.

-Put the child in knee- chestposition.

(Fig.11)

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The clinical manifestation of cyanosis

varies in degree depending on thetype and size of the associateddefects. Children with minimalcommunication are severely cyanoticat birth. Those with large septaldefects or a patent ductus arteriosusmay be less severely cyanotic buthave symptoms of congestive heartfailure usually before 4 months of age.

In these infants the only signs at birthmay be cyanosis after crying or feeding and progressive hyperpnea inan attempt to compensate for decreased arterial oxygen saturation.

A murmur usually indicates thepresence of septal defect or a patentductus arteriosus cardiomegaly.

-Give morphine sulfate.-I.V. beta- adrenergic inhibitor.-If acidosis is present give I.V. sodium bicarbonate.

Surgical: palliative and total corrective surgery is being done on infants and

children of all ages.

Transposition of Great Vessels Description and Pathology:

(Fig.12)

Assessment:

(Fig. 12)

Management:Palliative and corrective treatment used for the treatment of transposition of the

great vessels.

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Tricuspid valvular atresia ischaracterized by a small rightventricle, large left ventricle, andusually diminished pulmonarycirculation. Blood from the right atriumpasses through an atrial septal into theleft atrium, mixes with oxygenatedblood returning from the lung, flowsinto the left ventricle, and is propelledinto the systemic circulation. The lungsmay receive blood through one of three routes:

A small ventricular septal defect, Patent ductus arteriosus, and Bronchial vessels.

N. B.: it means the absence of thetricuspid valve resulting in no openingbetween the right atrium and rightventricle. It is usually associated withother defects that allow some shuntingof blood into the left side of the heart,

then back to the right ventricle or pulmonary artery.

Tricuspid Atresia

Description and Pathology:

(Fig. 13) Assessment:

The degree of cyanosis depends on the amount of pulmonary blood flow.

Severe cyanosis, dyspnea, anoxic spells and signs of right-sided heart failureare evident early during infancy if the child survives, systemic consequencesof cyanosis and polycythemia may develop.

Management:Palliative and corrective treatment can be done.

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Diagnostic Evaluation for Heart Diseases: A variety of invasive and noninvasive tests may be used in the diagnosis of heart

disease.1.

Electrocardiography: Measures electrical potential generated from the heartmuscle.2. Echocardiography: Short pulses of ultrasounds transmitted through heart bounce

off heart structure reflex test on a screen.3. Ultrasonography: Similar to echocardiography is synchronized with the E.C.G. to

provide a three dimensional recording of heart structure.4. Roentgenography;

Fluoscopy: Provides direct observation of heart size, position, contour andrelationships.

Radiography: Provides permanent record of heart size, configuration. Angiocardiography: Opaque media injected into circulatory system outlines

blood flow through heart and vessels, performed in conjunction with cardiaccatheterization.5. Cardiac Catheterization: Opaque catheter introduced into heart chambers via

large peripheral vessels is observed by fluoroscopy or image intensification,pressure managements and blood samples provide additional sources of information.

6. Digital Subtraction Angiography (D.S.A): Opaque media injected into circulatorysystem provides computerized image as vessels and tissue containing dyesubtracts all tissue dont containing dye.

Nursing Care of Family and Child with CongenitalHeart 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 notpresent 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 whenimmersed in water.

Dyspnea, especially following physical effort such as feeding, crying or straining.

Fatigue, paroxysmal hyperpnea, poor growth and development (failure tothrive).

Frequent respiratory tract infection. Feeding difficulties. Hypotonia. Excessive sweating.

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Older Children: Impaired growth. Fatigue. Orthopnea. Headache. Leg fatigue. Delicate body build. Effort dyspnea. Digital clubbing. Epistaxis.

Nursing Care Plan for Child with Congenital HeartDisease:

1. Decreased cardiac out put related to structural defect.Goal:

The patient will: exhibit improved cardiac output.Intervention:

Administer digoxin as ordered. The childs 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 youngchildren 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 oxygensupply 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 inadequateoxygen, 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.

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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 heartcondition.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 childs care to prevent their own exhaustion. Assist family in determining appropriate physical activity and disciplining methods for

childs anorexia.Expected Outcome:

Family copes with childs symptoms in a positive way.

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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 cardiaccondition and therapies.Goal:

The patients family will: Recognize signs of complications early.Intervention:

Teach family to intervene during hypercyanotic spells, place child in knee chestposition 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.

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Congestive Heart Failure (CHF)

CHF is the inability of the heart to pump an adequate amount of blood to thesystemic circulation to meet the metabolic demands of the body. In children CHF mostfrequently occurs secondary to structural abnormalities that result in increased bloodvolume and pressure. CHF is a symptom caused by an underlying cardiac defect, not adisease it self, since it is usually the result of an excessive workload imposed on a normalmyocardium most children who experience CHF are infants.

Pathophysiology:Heart failure is often separated into two categories; right sided and left sided

failure. In right sided failure , the right ventricle is unable to pump blood effectively intothe pulmonary artery resulting in increased pressure in the right atrium and systemic

venous circulation. Systemic venous hypertension causes Hepatosplenomegaly andoccasionally edema.

In left sided failure, the left ventricle is unable to pump blood into the systemiccirculation resulting in increased pressure in the left atrium and pulmonary veins. Thelungs become congested with blood, causing elevated pulmonary pressure andpulmonary edema.Clinical Manifestation: The child may suddenly become dyspnic, cyanotic. Abdominal pain, fever, anorexia, dyspnea, cough; develop suddenly in a young

child.

Dyspnea, orthopnea or paroxysmal nocturnal dyspnea.Palpitation, tachycardia and profuse sweating, pallor or peripheral cyanosis and coldextremities.

Causes:Can be classified according to the following changes:

1. Volume overload: especially with left to right shunts that may cause the RV tohypertrophy in order to compensate for the additional blood volume.

2. Pressure overload: resulting from obstructive lesions such as valvular stenosis or coarctation of the aorta.

3. Decreased contractility: primarily factors that affect the contractility of themyocardium, such as cardiomyopathy or myocardial schema from severe anemia or asphyxia, low level of potassium, glucose, calcium or magnesium.

4. High cardiac output demands: in which the body s need for oxygenated bloodexceeds the heart out put (even though the volume may be normal), such as insepsis, hyperthyroidism and severe anemia.

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Therapeutic Management of Congestive Heart Failure:The goals of treatment are to:

1. Improve cardiac function.2. Remove accumulated fluid and sodium.3. Decrease cardiac demands.4. Improve tissue oxygenation and decreased oxygen consumption.

1. Improve cardiac function:Through administration of digitalis glycosides [digoxin (lanoxin)].

2. Remove accumulated fluid and sodium:Treatment consists of diuretics, possible fluid restriction and possible sodium

restriction. Diuretics to eliminate excess water and salt to prevent re-accumulation.3. Decrease cardiac demands:

The workload on the heart is reduced when metabolic needs are kept to a minimum.This is accomplished by limiting physical activities( bed rest) preserving body temperature,treating any infection, reducing the effort of breathing (semi fowlers position) and usingmedication to sedate an irritable child.

4. Improve tissue oxygenation and decrease oxygen consumption:Supplemental cool humidified oxygen is usually provided to increase the amount of

oxygen during inspiration.

Assessment:1. Criteria for impaired myocardial function:

Tachycardia.Decreased urine output.Weakness.Anorexia.Cool extremities.Decreased blood pressure.

Sweating.Fatigue.Restlessness.Pale.Weak peripheral pulses.Cardiomegaly.

2. Criteria for pulmonary congestion:Tachycardia.Retraction (infants).Exercise intolerance.

Cough.Wheezing.

Dyspnea.Flaring nares.Orthopenea.

Cyanosis.Grunting.3. Criteria for systemic venous congestion:

Weight gain.Peripheral edema.Neck vein dysfunction.

Hepatomegaly.Ascitis.

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3. Activity intolerance related to imbalance between oxygensupply and demands.

Goal:The patient will : Exhibits no additional respiratory or cardiac stress.Nursing Intervention:

1 Maintain neutral thermal environment.-Place newborn in an incubator or under warmer.-Keep infant warm and treat fever promptly.

2 Feed small volumes or frequent intervals using soft nipple with moderately largeopening.

-Implement gavage feeding if infant becomes fatigues before taking anadequate amount.

3 Time nursing activities to disturb infant as little as possible.4 Implement measures to reduce anxiety.5 Respond promptly to crying or other expressions of distress.

Expected out come:Infant rest quietly.

4. Fluid volume excess related to fluid accumulation (edema).Goal:

The patient will : Exhibit no evidence of fluid excess.Nursing Intervention:

1 Administer diuretics as prescribed.2 Maintain fluid restriction if ordered.3 Provide skin care for children with edema.4 Change position frequently.5 Use resilient mattress or mattress cover.

Expected outcome:Infant exhibits evidence of fluid loss, frequent urination, and weight loss.

5. High risk for infection related to reduce body defensespulmonary congestion. As nursing diagnosis (4)

6. Altered family processes related to child with life threateningillness. As nursing diagnosis (5)

N.B.: feed cyanotic infant in the knee-chest position, head is elevated, he will suck morestrongly, ingest more, tire less, and gain weight. Use soft nipple, frequent burping andpauses of rest.

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Nurse should be alert for:

1. Early signs of CHF:

Tachycardia, especially during rest and slight exertion.

Profuse scalp sweating, especially in infants.

Irritability.

Respiratory distress.

Fatigue.

Sudden weight gain.

Common signs of Digoxin toxicity:

Gastrointestinal: nausea, vomiting, and anorexia.

Cardiac: bradycardia, dysrhythmias.

Parent guidelines in administrating Digoxin:

Give digoxin at regular intervals.

Dont mix it with other foods or fluids (inaccurate intake of the drug).

If a dose is missed and more than 4 hours has passed withhold the dose and give

the next dose at the regular time, if less than 4 hours has elapsed give the next doses.

If the child vomits dont give a second doses.

If more than 2 consecutive doses have been missed notify the physician.

Dont increase or double the does for missed doses.

Keep digoxin in a safe place preferably a locked cabinet.

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Acquired CardiovascularDisorders

They occur for a variety of reasons including infection autoimmune responses,

environmental factors and familial tendencies.

Acute RheumaticFever (ARF)

Acute rheumatic fever is a leading cause of acquired heart disease in the pediatricpopulation. In developing nations, the incidence of ARF is still fairly high due tosubstandard health practices, overcrowded living conditions and poor socioeconomic andeducational level.

Definition:R.F. is an inflammatory disease of connective tissue involving mainly the joints andheart and less frequently the CNS, skin and subcutaneous tissues. It has a markedtendency to recur.

Incidence:The incidence of A.R.F peaks between 5-10 years of age. The school age children

are he most susceptible to contracting this disease. It may rarely start at earlier age (2-3years). Boys and girls are equally affected.

Etiology:R .F. is a poorly understood autoimmune reaction to group A Beta hemolyticstreptococcal upper respiratory tract infection (GABHS).

Pathophysiology:Rheumatic fever is essentially a group of bodily responses to a streptococcal

infection following upper respiratory tract infection.R. F. develops in 3 steps:

Phase I: GABHS infection of the upper respiratory tract. The attack of GABHSpharyngitis may be extremely mild or moderately severe.

Phase II: the symptoms of URTI subside quickly and are followed by a latent or silent period usually lasting for 1-3 weeks, during which the patient is symptom-free.

Phase III: the silent period is followed by the onset of acute rheumatic fever.

The most acceptable current hypotheses for the development of RF are:1. Hypothesis of abnormal immune response to GABHS:

This is the most popular hypothesis, it assumes that:1 A genetically predisposed person reacts abnormally to an undefined

component of GABHS.2 This reaction takes 1-3 weeks.3

The resulting antigen-antibody complexes will cause the immunologicaldamage to the connective tissue of heart and joints.

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2. Hypothesis of autoimmunity:Some streptococcal antigens cross-react with human tissue antigens, and cross-reactive anti-heart antibodies have been found in rheumatic fever patients.According to this hypothesis, streptococcal antigens may elicit antibodies capable of reacting not only with the microbial products, but also with the hosts antigens. Thusautoimmunization maybe the underlying basis for the cardiac lesion.

Assessment:Accurate history should be taking from parents and child, problematic environmental

factors or recent exposure are the most efficient ways to diagnose A.R.F. is to strictly andhere to the specific onset criteria. The ones major and minor criteria are based on clinicalfindings are essentially objective. The history and laboratory findings determine the minor criteria.Minor Criteria or Manifestations:

Guidelines for the diagnosis of initial attack of Rheumatic fever (Jones

criteria, 1992 update)Major ManifestationsCarditisPolyarthritisChoreaErythema marginatumSubcutaneous nodules

Minor ManifestationsClinical findings

ArthralgiaFever

Laboratory findingsElevated acute-phase

ReactantsErythrocyte

Sedimenation rateC- reactive protein

Supporting Evidence of Antecedent Group A Streptococcal Infection

Positive throat culture or rapid streptococcal antigen test Elevated or rising

streptococcal antibody titer.Table (2)

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Fever (38-39C). Arthralgia (pain in joints) without

arthritic changes. Abdominal pain. Unexplained epistaxis. Weakness, fatigue, pallor, loss of

appetite, weight loss. Elevated acute phase reactants (ESR,

CRP). See table (2)


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Major Manifestations:1- Carditis:

Mitral and aortic valves are most affective valves and they become scarred, fibrousareas when healed, stenosis as the leafiers (cusps) of the valves occurs because of their fusing together. This process causes obstruction to the blood flow into the left ventricle or aorta or both. The valve edges may become so scarred that they cant completely close,causing a block flower regurgitation (valvular insufficiency) when the valves close so, thefollowing manifestations will be seen.

1 Tachycardia out of proportion to degree of fever.2 Cardiomegaly.3 New murmur or change in preexisting murmurs.4 Muffled heart sound (ventricle gallop exist that is S3).5 Friction rub (main manifestation of pericarditis).6 Pericardial pain.7 Changes in E.C.G.

2-Rheumatic Polyarthritis:1 It is the most common criterion: typical arthritis occurs in 70% of cases. It occurs

during the first 1-2 weeks the febrile period and lasts for a few days in certainaffected joints before moving to other joints.

2 Affected joint is red, warm, swollen, very tender, with limited movements + effusion.3 Migratory: several joints are commonly involved, either together or one after

another.4 Typically the large joints are affected as knees, wrists, ankles and elbows. It rarely

affects fingers, toes or spine.5 It disappears within 12-24 hours from start of salicylate therapy.6 If untreated it doesnt persist in the same joint for more than 1 week.7 Rheumatic arthritis leaves the joint intact and doesnt result in chronic disease.

N.B.: Rheumatic fever licks the joints but bites the heart.

3- Erythema Marginatum:1 The lesions are non-pruritic and appear initially as undifferentiated macules on the

trunk and inner aspect of the extremities (never on face).2 Evanescent, and if watched from hour to hour, it will be noted to change gradually.

4- Rheumatic (sydenhams) Chorea:1 Chorea is characterized by sudden, aimless, involuntary and irregular muscular movements of the extremities.

2 Involuntary facial grimaces.3 Speech disturbance.4 Severe muscle weakness (can be profound).5 Muscle movements exaggerated by anxiety and attempts at fine motor activity are

relieved by rest.

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5- Subcutaneous Nodules:1 These occur rarely in the general population but are frequently found in individuals

who have severe Carditis or who have had repeated attack of A.R.F.2 Nodules are generally identified as small (0.5-1Cm) and firm without any

tenderness or attachment to the skin.3 They can be palpated over the extensor surfaces of joints such as elbows, knees,

ankles, or over the scalp and spinous processes of the vertebrae.4 They gradually resolve over a period of time with no residual.

Diagnostic Evaluation:To diagnose R.F. it is necessary to have:

1 Two major criteria +evidence of preceding GABHS or infection or.2 One major + 2 minor criteria + evidence of preceding GABHS or infection.3 Children suspected of having A.R.F. are tested for streptococcal antibodies. The

most reliable and most standardized test is an elevated or rising antistreptolysin-otiter (A.S.O.T.).

4 Erythrocyte sedimentation rate (E.S.R.).5 C- reactive protein.6 Electrocardiograph.7 Radiographs.

Therapeutic Management:The aims of medical management are:

1. Eradication of group AB hemolytic streptococcal infection.2. Anti-inflammatory agents for Carditis and arthritis.3. Palliation of the other symptoms.4. Prevention of recurrents of RF.1 Penicillin: is the drug of choice to treat GABS infection:

-1 Procaine penicillin 400.000 /day for 10 days, or -2 Oral penicillin V: 200.000 400.000 (125-250mg)/dose 3 times/ day for 10

days, or

-3 Single IM injection of 600.000-1.200.000 Benzathine penicillin.2 If patient is allergic to penicillin give erythromycin as a substitute in penicillin

sensitive children.3 Salycilates [anti-inflammatory (suppressive) therapy] are used to control the

inflammatory process, especially in the joints and reduce the fever and discomfort.4 Bed rest: is recommended during the acute febrile phase.

Prophylactic Treatment:1 Against recurrent R.F is started after the acute therapy and involves monthly

intramuscular injections of benzathin penicillin (1-2 million I) IM., two daily oraldoses of penicillin (400.000) or one daily oral dose of sulfadiazine orally or erythromycine orally, twice daily.

2 Children who have had acute R.F. are susceptible to recurrent R.F. for the rest of their lives and should be followed medically for at least 5 years.

N.B.: Streptococci can be eradicated and R.F. prevented if penicillin is givenEarly (within 9 days of GABS infection) for a sufficient period of time(10 days

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Complications of Rheumatic Fever:1 Chronic valvular disease2 Repeated chest infection.3 Cardiac failure.4 Infective endocarditis.5 Arrhythmias, atrial fibrillation.6 Thromboemoblism and stroke.

Nursing Consideration:The objectives of nursing care for child with A.R.F. are to:

1. Encourage compliance with drug regimens.2. Facilitate recovery from the illness.3. Provide emotional support.4. Prevent the disease.

A. Encourage compliance with drug regimens:1 Since compliance is a major concern in long term during therapy every effort ismade to encourage adherence to the therapeutic plan.

2 When compliance is poor monthly injections may be substituted for daily oraladministration of antibiotics.

B. Facilitate recovery from the illness:1 The major role of the nurse is to assist the child and parents to understand the need

for the amount of bed rest ordered by the physician. The aim of the bed rest is tominimize the effect of the inflammatory process on all body systems, particularly theheart. If the metabolic needs oxygen consumption and expected cardiac responsecan be very low. The damage to heart muscle and valve tissue may be restricted towhat has already occurred.

2 During the febrile phase, fluids are encouraged to prevent dehydration butoverdehydration is avoided because hypervolemia places increased demands onthe heart

-1 As soon as a child is willing to eat a liquid or soft diet is given in smallfrequent amounts to minimize the exertion of chewing. The diet is graduallyincreased to meet the childs nutritional requirements overfeeding is to beavoided.

1 Pain from Carditis or polyarthritis is decreased by administration of anti-inflammatory agents (aspirin).

-1 Alternating warm and cold snacks to the affected joints may reduce swellingand inflammation and provide direct and immediate reduction of pain.

2 During chorea the only treatment is prevention of injury during the period wheninvoluntary jerking and possibly violent movements occur.

-1 Assist once during walking.-2 Feeding the child to prevent injury.-3 Bed rails to prevent the child from falling out of bed.-4 Restraints to prevent the child from falling from a chair, padding on the

sides of the beds or chair to prevent injury.-5 Behavioral changes and learning difficulties are discussed with school,

classmates, peer group and parents.

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C. Provide emotional support:1 The parents and child need to know that all the manifestations of rheumatic fever

are temporary expected for the cardiac involvement let the child verbalize hisfeelings.

2 Find ways for bed activities, i.e. quiet play and school work while in hospital andhome.

3 Allow for parent of normal routine at home.4 Classmates and sibling can show their concern by card, letters etc.

D. Prevent the disease:1 The nurse should be alert to any child who has abrupt onset of signs and symptoms

of a streptococcal sore throat.2 After streptococcal pharyngitis has been diagnosed, antimicrobial treatment is given

to eradicate the infection. A single injection of benzathine penicillin is the mostreliable from the therapy, oral penicillin or erythromycin may be given daily for 10days, the nurse help the parents to be cooperative.

3 The main nurses role in prevention is to help educate the public as well as the

individual patient and family.4 Massive screening program with throat cultures and support of patient cooperation

in therapy can eradicate the disease.N.B.: from the previous discussion about A.R.F. try to develop the appropriate nursingcare plan.

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Plan of nursing care for a child undergoing heartsurgery:Pre-operative care:a-Pre-operative assessment:

1 It can be done though observation.2 It will facilitate care planning.

Postoperatively, it will include:

-1 Admission history and physical examination.-2 Baseline vital signs (apical pulse and blood pressure) in all examinations should be

obtained for evaluation at rest and with activity-report any change.

-3 Height and weight measurement for fluid replacement.-4 Pre-operative studies, i.e. E.C.G. Lab Tests should be prepared.

-5 Sleep/ awake patterns.-6 Fluid intake: to estimate the childs fluid consumption and which fluids arepreferred.

-7 Additional observation (normal activities, rest be noted & reported)- physical andemotional stress should be reported.

-8 Elimination pattern to avoid constipation post-operatively (should be planned inadvance).

b. Pre-operative preparation:It should be given throughout the pre-operative period.

1 Instructing child and parents about tests will be done; operation. whenappropriate.

2 Take child and parents to the operating suite and ICU to be familiar with thephysical settings (lights, gown, .etc). Show them the equipment used gradually.

3 Place child temporarily into oxygen tent to make him accustomed to it and tooxygen mask through play (sometimes fear of suffocation).

4 Introduce them to post-operative procedure, semi fowlers position, how to turn fromside to side. Practice deep inspiration and expiration.

5 Through play, nurse demonstrates deep act of coughing, breathing to the childlethim practice it (tell him that they may cause some discomfort in practice post-

operatively).6 Demonstrate postural drainage and percussion.7 Prepare them (if old enough) for nasogastric tube catheter for bladder-by telling

them about it.8 During preparation, the nurse must be aware of the level of childs anxiety (so

discussion should be ended if she felt the child is very anxious).c. Physical preparation for surgery:

1 Shaving the child skin the evening before the operation.2 Cleansing enema may be ordered.3 Sedation is given for rest (or Dr. order).4

Vital signs are checked.

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Postoperative Care:Immediate Admission to ICU:

1 Oxygen immediately.2 Check each catheter in his chest and attached to the suction machine.3 Check vital signs.4 If cardioscopy will be in use, attach it to the patient, then EKG, heart rate and

rhythm will observed constantly.5 I.V. fluids must be checked and regulated carefully.

Then:1. Tell patient that operation is over when he re-awakes.2. Narcotic may be given as Dr. order.3. Vital signs are taken each hour or more often if necessary (temperature rectally

as cool atmosphere in oxygen tent may affect temperature).1 Temperature: if there is fever, reduce it by tepid water sponges, ice bags or

ice water mattress.2 Respiration: - Check depth and rate of respiration and chest expansion on

both sides is equal.- Do suction if respiration becomes noisy and rapid.

1 Pulse: it should be observed for: regular rhythm and power.2 Blood pressure: Should be taken and notifying doctor for any change.

4. Observe: skin color, moisture (dry moist). (Warm cold).5. Monitor fluids : if cut down is used for I.V.; not be too rapid, it must be in proper

position (no filtration). Oral fluids are restricted in immediate post-operative periodto decrease load on heart, therefore mouth care will also decrease childs thirsty.Input and output of all fluids must be accurately calculated and recorded. Urinemust be analyzed for specific gravity to assess kidney function. Fluids requirementis based on childs weight and body surface area.

6. If no voiding within 8-12 hours after operation, catheter may be used.7. Care for chest tubes (under-water seal). Observe the drainage, bleeding, be

sure that they are patent (free from blood clots) and well tighten to patient. Important: be sure that the bottles. Below bed level and observe the amount,color and consistence. If cyanosis, sudden sharp chest pain around the catheter anddyspnea and tachycardia occur. Clamp the chest tube and call Dr. immediately.

8. Encourage child for deep breathing and coughing exercise and support his chestespecially over the incision area and praise him.

9. Change position every hour.10.Support the body with pillows if he cant maintain his position. Encourage him to

move himself.11.Observe: color of legs and its coldness, bleeding or infection at side of operation.12.To provide rest, good plan of N.C. to decrease disturbance.13.Encourage patient to be out of bed (according to his condition and severity of

operation) on wheel chair after chest tubes have been removed.14.Child may regress in his behavior (cry- more physical contact- more demanding)

understand his behavior as a nurse once his condition improves help him to gaincontrol of his situation.

15. Before discharge : plan of care must be done with the health team and parents.

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References:1. Chow MP. Handbook of Pediatric Primary Care. 6 th ed. New York: John Whiley and

sons co., 1984. 729-744.

2. Wong DL. Whaley and Wongs Nursing Care of Infant and Children. 6 th ed. London:

Mosby co., 1999. 1583 1649.

3. Oldham KT. Surgery of Infants and Children: Scientific principles and Practice.

Philadelphia: lippincott-Raven co., 1997. 999-1004.

4. Madkour A. Essential of Pediatrics. Faculty of Medicine: Egypt, 2001. Pp 133-159.

5. Finkelmeier B. Cardio thoracic Surgical Nursing.3 rd ed. Philadelphia: JB Lippincott

co., 2000. 169-180.

6. Woods S. Cardiac Nursing.3 rd ed. Philadelphia B Lippincott co., 1995. 820 830.

cardio vascular diseases(1)

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