NURSING CARE PLAN FOR ACYANOTIC HEART DISEASE

Nursing Management of cardio vascular Diseases.

General Objectives:
The student will be able to describe the most common cardiovascular diseases among children and their management by the end of this unit.

Specific Objectives:
The student will be able to: 1. Define the most common heart diseases, either the acyanotic or cyanotic heart diseases. 2. State the nursing assessment of each congenital heart disease. 3. Plan the nursing management of each disease. 4. List the methods used in diagnosis of heart disease. 5. Plan the nursing management of congestive heart failure. 6. Identify the etiology of rheumatic fever. 7. Identify the criteria used in diagnosis of rheumatic fever.

8. Plan the nursing management of rheumatic fever. 9. Plan the nursing care for a child undergoing heart surgery.

Cardiovascular disorders in children are divided into two major groups:
a- Congenital heart diseases. b- Acquired heart disorders.

Congenital Heart Disease (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. 2. 3. 4. Maternal rubella during pregnancy. Maternal alcoholism, age over 40 years and insulin dependant diabetes. Several genetic factors. Exposure to radiation.

Fetal Circulation:
The characteristics of fetal circulation ensure that the most vital organs and tissues receive the maximum concentration of oxygenated blood. The fetal brain requires the highest oxygen concentration. The lungs are essentially nonfunctional, and the liver is only partially functional, therefore less blood is needed in these organs in fetal life. During fetal life, blood carrying oxygen and nutritive materials from the placenta enters the fetal system through the umbilicus via the large umbilical vein. Oxygenated blood enters the heart by the inferior vena cava because of the higher pressure of the blood entering the right atrium and through the foramen ovale to the left atrium. In this way, the better-oxygenated blood enters the left atrium and ventricle to be pumped through the aorta to the head and upper extremities.

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Heart is completely developed in the first eight weeks of intra-uterine life.

- Blood from the head and upper extremities entering the right atrium from the superior vena cava is directed downward through the tricuspid valve into the right ventricle. - From the right ventricle, it is pumped through the pulmonary artery, where the major portion is shunted to the descending aorta via the ducts arteriosus to supply

the trunk and lower extremities. Only small amount flows to the non-functioning fetal lungs for the purposes of nutrition.

Circulation Change at Birth:

-1 With cessation of placental blood flow from clamping of the umbilical cord the
expansion of the lungs at birth, the hemodynamis of the fetal vascular system undergo abrupt changes.

-2 With the first breath, the lungs are expanded and oxygen causes pulmonary vasodilatation, pulmonary pressure start to fall, a systemic pressures given the removal of the placenta start to rise. -3 Normally, the foramen ovale closes as the pressure in the left atrium exceeds the pressure in the right atrium and it closes completely at third month of infant life. -4The ducts arteriosus starts to close in the presence of increased oxygen
concentration in the blood and other factors and it closes completely at fourth month of infant life. (Fig. 1)

(Fig . 1)

-2 Acyanotic defects. The defining characteristics is blood flow patterns: -1 Increased pulmonary blood flow. -3 Obstruction of blood flow out of the heart. cyanosis has been used as distinguishing feature. Traditionally. Another classification system based on Hemodynamic characteristics also is used. -2 Decreased pulmonary blood flow. a physical characteristics.Types of Defects: Congenital heart defects have been divided into 2 categories: 1. -4 Mixed blood flow in which saturated and desaturated blood mix within the heart or great arteries. 2. Classification of Congenital Heart Disease: (Table 1) Classification of congenital heart disease Acyanotic Cyanotic Pulmonary Blood flow Obstruction to blood flow From ventricles pulmonary blood flow Mixed Blood flow . dividing the anomalies into: -1 Cyanotic defects.

.Coarctation of aorta -Tetralogy of fallot -Transposition of great -Tricuspid atresia -Total anomalous return.-Artial septal defect arteries. .Hypoplastic left heart -Ventricular septal defect . -Tranucus arteriosus .Aortic stenosis pulmonary venous -Patent ductus arteriosus .Pulmonic stenosis -Atrioventricular canal syndrome (Table .1) Comparison of acyanotic-cyantoic and hemodynamic classification system of congenital heart disease.

-3 Ventricular septal defect (VSD). short circuits that pulmonary vascular bed and directs blood from the pulmonary artery to the aorta. Functional closure normally occurs soon after birth. . Others result from obstructive lesions that reduce the flow of blood to various areas of the body. Patent Ductus Arteriosus (PDA) Description and Pathophysiology: Patent ductus arteriosus is a vascular connection that during fetal life.Acyanotic Defects Most acyanotic defects involve primarily left to right shunting through an abnormal opening. -5 Aortic stenosis (AS). -4 Pulmonic stenosis (PS). -6 Coarctation of aorta (COA). If the ductus remains patent flow in the ductus is reversed by the higher pressure in the aorta. -2 Atrial septal defect (ASD). Major Acyanotic Defects: -1 Patent ductus arteriosus (PDA).

PDA return Double flow in pulmonary artery Double pulm. venous Double flow in aorta proximal to PDA Double flow in LV Doubled flow in LA Assessment: Clinical manifestation will depend on the size of duct and amount of shunting. Large PDA: .2) Incidence: More common in females (2:1). Hemodynamics: Blood from aorta goes to systemic circulation poor systemic circulation. Small PDA: asymptomatic and discovered on a routine examination. Higher incidence among premature and commonly associated with maternal rubella.(Fig .

Bacterial endocarditis. Pulmonary hypertension. Supportive: fluid restriction with diuretics and digitalization for congestive heart failure CHF. Dyspnea on exertion and easy fatigability. Out come: The child is good with less than 1% mortality. Left heart failure may develop in infancy in severe cases. Complications: 1. . Congestive heart failure. Bounding pluses due to increased systolic pressure. Under weight thin child. Repeated chest infections. Surgical: surgery can be performed at anytime. gallop rhythm due to rapid filling of the ventricle. Enlarged heart size in large PDA. Heart rate over 150 b/m. although it is preferably done at about 6 months of age. 2.•1 •2 •3 •4 •5 •6 •7 •8 Classic machinery murmur. surgery maybe done earlier if the child is in difficulty to prevent complications and growth retardation caused by PDA. 2. 3. which is continuous from systole into diastole. Therapeutic Management: 1.

more common in females. allowing blood directed from the higher pressure left atrium to flow to the lower pressure right atrium. .Atrial Septal Defect (ASD) Incidence: 7% of all CHD. Description and pathology: Abnormal opening between the atrium. The resulting left to right shunting of blood places. A blood places a burden on the right side of the heart resulting in an increased pulmonary blood flow.

These children are easily fatigued and have recurrent pneumonitis. .(Fig. •2 If there is a large left to right shunt and severe mitral incompetence cardiac enlargement and pericardial bulge are seen. The infant with small defects may be asymptomatic.3) Hemodynamics: Blood flow from pulmonary veins LV poor systemic circulation. LA ASD double flow in RA Double flow in RV Increased pulmonary venous return Double pulmonary blood flow Assessment: •1 The clinical manifestations depend on the location and size of the defect.

Ventricular Septal Defect (VSD) Incidence: Commonest (30% of all cases of CHD) Description and Pathology: Ventricular septal defect is an abnormal opening between the right and left ventricles. the shunt of the blood is then reversed from the right to the left ventricle. Surgical: surgery is done on affected children before they enter school even if no symptoms are present. Management: 1. The defects vary in size and may occur in either the membranous or muscular portion of the ventricular septum.•1 In atrial septal defect. Supportive: same as that of the VSD. atrial arrhythmias and cardiac failure make operation more hazardous in adult life. •3 The ausculatory finding of a widely split second heart sound is so unusual in complicated atrial septal defects that the diagnosis is not made without it. If surgery is not done during childhood pulmonary hypertension. pulse and venous pressure are normal and the heart size is normal or slightly enlarged. •2 Systolic murmur is present. with resulting cyanosis. Due to higher pressure in the right and left ventricles. If pulmonary vascular resistance produces pulmonary hypertension. 2. (Fig 4) . A shunting of blood from the left to right ventricle occurs during systole.

feeding difficulties and frequent pulmonary infection. 4) Hemodynamics: to Aorta Blood from LA (doubled) LV VSD poor systemic circulation RV RV flow Flow in pulmonary circulation Flow in LA Flow in pulmonary circulation Assessment: • • • The most frequently seen defects are small. cardiac enlargement and mild cyanosis may also occur in large defects. Heart failure. Therapeutic Management: . slow physical development. Medium sized or larger defects during infancy may produce symptoms such as: dyspnea. so these defects are asymptomatic.(Fig.

If the defect is larger. Surgical repair requires open-heart surgery and cardiopulmonary bypass. Pulmonary Stenosis (PS) Description: • • It is an obstructive lesion that interferes with blood flow from the right ventricle.• • • If the defect is small and asymptomatic. It may also occur with patent ductus arteriosus. medical care is given for CHF when it occurs: oral diuretics and digoxin. treatment is conservative because spontaneous closure may occur before 1 or 2 years of age. (Fig 5) . It may occur as a single abnormality or it may be associated with other defects such as those in the atrial or ventricular septa.

discovered on routine examination. poor exercise tolerance with exertional dyspnea due to insufficient blood flow to the lungs to meet the need for increased cardiac output during exertion. Severe PS: may present by right heart failure in infancy: cyanosis and cardiac failure may occur. Management: .5) Pathophysiology: • • • • The pulmonary valve is obstructed by fusion of the cusps of their (ommissures) valve orifice so that their movement is restricted. ECG shows gross right ventricular hypertrophy. partially compensating for the obstruction. If the right ventricle can’t eject the necessary amount of venous blood into the pulmonary circulation systemic cyanosis occurs. If a patent ductus arteriosus is also present. blood is shunted from the aorta to the pulmonary artery and then to the lungs. The murmur and changes in the second heart sound can be analyzed with echocardiography. Another cause of obstruction is a muscular or fibrous that is caused by the failure of involution of an embryonic structure. Radiography shows enlargement of the heart. Assessment: • • • • • Mild PS: asymptomatic. The degree of change depends on the size of the constricted valvular opening. The passage of blood is obstructed from the right ventricle to the pulmonary artery resulting in increased systolic pressure and hypertrophy of the right ventricle.(Fig.

• 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.Children having mild and even moderate pulmonic stenosis may need no treatment. (Fig 6) . Description: Narrowing or stricture of the aortic valve causing resistance to blood flow in the left ventricle and decreased cardiac output.

In severe obstruction: fatigue due to exercise intolerance. medical management is carried out: like VSD. the infant may grow normally to be asymptomatic until increased physical growth requires additional cardiac output.(Fig.B. Management and Outcome: • • If heart failure occurs in infancy. fainting and episodes of pulmonary edema occur. The most prominent physical manifestation of aortic stenosis is the presence of a coarse systolic ejection murmur. Assessment: Depend on the severity of the lesion. decreased cardiac out put also results in faint peripheral pulses and anginal pain. pulse pressure is the difference between systole and diastole). dizziness. Coarctation of the Aorta . radiating to the neck and apex. • • • If there is mild aortic stenosis.6) Pathology: When there is resistance to blood out flow the left ventricle to the aorta left ventricular hypertrophy occurs. causing increased pressure in that chamber resulting in increased pressure in the pulmonary veins and pulmonary vascular congestion when severe obstruction occurs the pulse pressure in the aorta is narrowed (N. Surgical: Ballon valvuloplasty or surgical by open aortic volvotomy or aortic valve replacement should be postponed until child has stopped growing. usually accompanied by a thrill over the aortic area. blood backs up in the left atrium.

epistaxis.7) Assessment: • Blood pressure is higher than normal in the upper part of the body. resulting in absence or diminishing of the femoral pulse. • • Management and Outcome: .Description and Pathology: • It is characterized by a narrowed aortic lumen. The legs may be cooler than the arms. If the child exercises muscle cramps in the legs may be due to tissue anoxia. depending on the position of the obstruction in relation to the ductus arteriosus coarctation exist with great variation in anatomical features. 7) • (Fig. it is relatively low. In the leg. and later cerebrovascular accidents. It exists as a preductal or postductal obstruction. dizziness fainting. The lesion produces an obstruction to the flow of blood through the aorta increased LV pressure and workload. resulting in headache. (Fig.

hypertension. the blood normally 3. Right ventricular of the great • In tetralogy of fallot. • Hypertrophy of the right ventricle occurs as a result of the pressure exerted against the pulmonary stenosis. If blood pressure is not elevated and heart failure is not a problem. cyanosis result. It increases.g. intracranial hemorrhage and stroke. 2. 4. 1. Ventricular septal defect. This is a right to left shunt. 3. Overriding of the defects: Major cyanotic aorta: aorta receives blood from both ventricles and this is the cause of cyanosis. Transposition hypertrophy. • Polycythemia develops because the body attempts to compensate for the unoxygenated blood. The out flow of the blood from the right Tetralogy of Fallot ventricle resisted by the pulmonary stenosis so that the blood flows through the ventricular septal defect into the aorta. Tetralogy of fallot. Cyanosis may be seen at first year of life. . Cyanotic Congenital Heart Disease The common cause of cyanotic congenital heart disease is a communication between the pulmonary and a systemic circulations through which venous (unoxygenated) blood enters the systemic circulatiory system (right to left shunts or obstruction of pulmonary blood flow or obligatory mixing of venous and arterial blood). it is wise to postpone the operation until the operation descending aorta is at least 50% of adult size (age of child 3-6 years) to avoid re-stenosis. Out come: Surgery should be done if only a minor defect is present to avoid complication. The resulting increased viscosity of the blood causes slowing of the circulation and possible thrombophlebitis emboi and vascular disease. because the blood from the right ventricle is unoxygenated.vessels. e. returns from the systemic circulation to the right atrium and right ventricle. as the child grows older. The classical tetralogy consists of: 1.• • Surgical: repair consists of resection and anastomosis by aortic graft or subclavian flap angioplasty. Tricuspid atresia (TA). Pulmonary stenosis. 2.

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cyanosis becomes evident after the ductus closes during the first months of life. 8) Assessment: The neonate who has tetralogy of fallot is not cyanotic because of the presence of the patent ductus arteriosus. • Clubbing of the fingers and toes (in long standing cases ) (Fig.9) .(Fig. 9). • (Fig.

• Stunted growth. especially after exercise. • Intolerance to effort: exercise usually causes severe dyspnea. Older children. but then they mustres infants assure a knee chest position rather than extending their extremities when they lie down. learn that the squatting position relieves dyspnea because: 1. . Flexing the legs decrease venous return from the lower extremities which have a very low oxygen content. Infant and toddlers may be able to play for a short time.

(Fig. 10) .10) (Fig. which diverts right ventricular blood from the aorta into pulmonary artery increasing pulmonary blood flow. This increases the amount of oxygenated blood in the left side of the heart and eventually into systemic circulation. Squatting position increase systemic vascular resistance.2.

Management: • Medical: 1. .11) -Give morphine sulfate. Treatment of cyanotic spells: -Oxygen therapy. -Put the child in knee. Apansystolic murmur: it is usually associated with thrill.chest position. 2. These children don’t develop congestive heart failure because the overload of the blood in right ventricle flows freely through the septal defect and the overriding aorta into the systemic circulation. blue spells). Antibiotic prophylaxis before tooth extraction or GIT and urinary procedures.• • • Cyanotic spells. (Fig. (Hypoxic.

V. Transposition of Great Vessels • Description and Pathology: (Fig. Those with large septal defects or a patent ductus arteriosus may be less severely cyanotic but have symptoms of congestive heart failure usually before 4 months of age. beta. . sodium bicarbonate.-I. -If acidosis is present give I. A murmur usually indicates the presence of septal defect or a patent ductus arteriosus cardiomegaly.adrenergic inhibitor. • Surgical: palliative and total corrective surgery is being done on infants and children of all ages. Children with minimal communication are severely cyanotic at birth.12) The clinical manifestation of cyanosis varies in degree depending on the type and size of the associated defects.V. • Assessment: • • In these infants the only signs at birth may be cyanosis after crying or feeding and progressive hyperpnea in an attempt to compensate for decreased arterial oxygen saturation.

The lungs may receive blood through one of three routes: • A small ventricular septal defect. Tricuspid valvular atresia is characterized by a small right ventricle. flows into the left ventricle.• is usually associated with It Description and Pathology: other defects that allow some shunting of blood into the left side of the heart. then back to the right ventricle or pulmonary artery. • Patent ductus arteriosus. 12) • Management: Palliative and corrective treatment used for the treatment of transposition of the great vessels.(Fig. N. B. Blood from the right atrium passes through an atrial septal into the left atrium. . mixes with oxygenated blood returning from the lung. and usually diminished pulmonary circulation. and • Bronchial vessels. and is propelled into the systemic circulation. large left ventricle.: it means the absence of the Tricuspid Atresia tricuspid valve resulting in no opening between the right atrium and right ventricle.

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Electrocardiography: Measures electrical potential generated from the heart muscle. Ultrasonography: Similar to echocardiography is synchronized with the E.G. Echocardiography: Short pulses of ultrasounds transmitted through heart bounce off heart structure reflex test on a screen. systemic consequences of cyanosis and polycythemia may develop. Severe cyanosis. Diagnostic Evaluation for Heart Diseases: A variety of invasive and noninvasive tests may be used in the diagnosis of heart disease.C. . 2. anoxic spells and signs of right-sided heart failure are evident early during infancy if the child survives.(Fig. 1. to provide a three dimensional recording of heart structure. 4. Roentgenography. 13) • Assessment: The degree of cyanosis depends on the amount of pulmonary blood flow. • Management: Palliative and corrective treatment can be done. 3. dyspnea.

paroxysmal hyperpnea. especially following physical effort such as feeding. pressure managements and blood samples provide additional sources of information. 5. or when immersed in water. straining. feeding. • Angiocardiography: Opaque media injected into circulatory system outlines blood flow through heart and vessels. . position.Fluoscopy: Provides direct observation of heart size. Cardiac Catheterization: Opaque catheter introduced into heart chambers via large peripheral vessels is observed by fluoroscopy or image intensification. • Dyspnea. Digital Subtraction Angiography (D. Conjunctiva. • Fatigue. Infants: • Cyanosis generalized. cyanosis during exertion such as crying. • Hypotonia. poor growth and development (failure to thrive). • Excessive sweating. • Nursing Care of Family and Child with Congenital Heart Disease Assessment: Nursing care of the child with congenital heart disease begins soon as the diagnosis is suspected. lips and tongue.S. especially mucous membranes. contour and relationships. • Frequent respiratory tract infection. • Feeding difficulties. However in many instances symptoms that suggest cardiac anomaly is not present at birth or if manifested is so subtle that they are easily overlooked. • Radiography: Provides permanent record of heart size.A): Opaque media injected into circulatory system provides computerized image as vessels and tissue containing dye subtracts all tissue don’t containing dye. configuration. crying or straining. performed in conjunction with cardiac catheterization. 6.

Epistaxis. Decreased cardiac out put related to structural defect. Goal: The patient will: Maintain adequate energy levels. Headache. Delicate body build. Digital clubbing. The child’s apical pulse is always checked before administrating digoxin (as general rule the drug is not given if the pulse is below 90-100 b/m in infants and young children or below 70 b/m in older children). Fatigue.Older Children: • • • • • • • • • Impaired growth. . Orthopnea. Heart rate and volume indicate satisfactory cardiac output. Effort dyspnea. Expected Outcome: 2. Leg fatigue. Nursing Care Plan for Child with Congenital Heart Disease: 1. Activity intolerance related to imbalance between oxygen supply and demand. Goal: The patient will: exhibit improved cardiac output. Intervention: • • Administer digoxin as ordered.

Goal: The patient will: Achieve normal growth. Encourage iron rich foods in diet. Encourage quite games and activities. Intervention: • • Administer iron preparation as prescribed. Expected Outcome: 3. Goal: (2) The patient will: Exhibit adequate iron level. nutrients to tissue and social isolation.Intervention: • • • • Allow for frequent of rest. • Provide well balanced highly nutritive diet. . Help child to select activities appropriate to age. condition and capabilities. Altered growth and development related to inadequate oxygen. Intervention: Expected Outcome: Child achieves normal growth. Expected Outcome: Goal: (3) The patient will: Have opportunity to participate in activities. Child assimilates sufficient iron. Avoid extremes of environmental temperature. Child determines and engages in activities commensurate with capabilities.

Expected Outcome: 5. Child remains free from infection.Intervention: Expected Outcome: Child engaged in age appropriate activities. Goal: The patient will: Exhibit no evidence of infection. . Intervention: Expected Outcome: Family discusses their fear and anxieties. • Encourage age appropriate activities. High risk for infection related to debilitated physical status. • Discuss with parents their fears regarding child symptoms. Intervention: • • • Avoid contact with infected persons. Altered family process related to having a child with a heart condition. Provide for adequate rest. Provide optimum nutrition. 4. Goal: The patient will: Experienced reduction of fear and anxieties. Goal: (2) The patient will: Exhibit positive coping behavior.

Intervention: • • • • • Teach skills for home care. Goal: The patient’s family will: Recognize signs of complications early. Family demonstrates ability and motivation for home care. Family copes with child’s symptoms in a positive way.Intervention: • • • Encourage family to participate in care of child while hospitalized. • Teach family to recognize signs of complications such as: . Expected Outcome: 6. Where and whom to contact for help and guidance. Encourage family to include others in child’s care to prevent their own exhaustion. Administration of medications. Signs that indicate complications. Assist family in determining appropriate physical activity and disciplining methods for child’s anorexia. place child in knee chest position with head and chest elevated. Feeding techniques. Intervention: • Teach family to intervene during hypercyanotic spells. Expected Outcome: Goal: (3) The patient will: Demonstrate knowledge of home care. High risk for injury (complications) related to cardiac condition and therapies.

retraction. . cough. Cerebral thrombosis (compensatory polycythemia is particularly hazardous when child is dehydrated). Cardiovascular collapse (pallor. restlessness. cyanosis and hypotonia). tachycardia). Expected Outcome: Family recognizes signs of complications and institutes appropriate action. Hypoxemia (cyanosis. cyanosis). dysrhythmias). grunting. bradycardia. - Digoxin toxicity (vomiting.Increased respiratory effort (tachypnea.

2. In left sided failure. Pressure overload: resulting from obstructive lesions such as valvular stenosis or coarctation of the aorta. CHF is a symptom caused by an underlying cardiac defect. since it is usually the result of an excessive workload imposed on a normal myocardium most children who experience CHF are infants. orthopnea or paroxysmal nocturnal dyspnea. cough. causing elevated pulmonary pressure and pulmonary edema. the left ventricle is unable to pump blood into the systemic circulation resulting in increased pressure in the left atrium and pulmonary veins. The lungs become congested with blood. not a disease it self. . dyspnea. right sided and left sided failure. tachycardia and profuse sweating. Systemic venous hypertension causes Hepatosplenomegaly and occasionally edema. the right ventricle is unable to pump blood effectively into the pulmonary artery resulting in increased pressure in the right atrium and systemic venous circulation. • Dyspnea. cyanotic. anorexia. Abdominal pain. In children CHF most frequently occurs secondary to structural abnormalities that result in increased blood volume and pressure. Volume overload: especially with left to right shunts that may cause the RV to hypertrophy in order to compensate for the additional blood volume. • • Causes: Can be classified according to the following changes: 1. fever.Congestive Heart Failure (CHF) CHF is the inability of the heart to pump an adequate amount of blood to the systemic circulation to meet the metabolic demands of the body. Pathophysiology: Heart failure is often separated into two categories. Clinical Manifestation: The child may suddenly become dyspnic. Palpitation. In right sided failure. develop suddenly in a young child. pallor or peripheral cyanosis and cold extremities.

2. High cardiac output demands: in which the body ‘s need for oxygenated blood exceeds the heart out put (even though the volume may be normal). such as in sepsis. possible fluid restriction and possible sodium restriction. 3. Remove accumulated fluid and sodium: Treatment consists of diuretics. low level of potassium. Decrease cardiac demands. Decreased contractility: primarily factors that affect the contractility of the myocardium.3. Therapeutic Management of Congestive Heart Failure: The goals of treatment are to: 1. Remove accumulated fluid and sodium. Decrease cardiac demands: . such as cardiomyopathy or myocardial schema from severe anemia or asphyxia. calcium or magnesium. 1. glucose. 2. 3. Improve cardiac function: Through administration of digitalis glycosides [digoxin (lanoxin)]. 4. Improve cardiac function. Improve tissue oxygenation and decreased oxygen consumption. 4. hyperthyroidism and severe anemia. Diuretics to eliminate excess water and salt to prevent re-accumulation.

Criteria for impaired myocardial function:               Tachycardia. Cyanosis. treating any infection.              Sweating. Neck vein dysfunction. Criteria for systemic venous congestion: . Flaring nares. Tachycardia. Dyspnea. Pale. Fatigue. Assessment: 1. Weight gain. 4. Retraction (infants). Weakness. Decreased urine output. This is accomplished by limiting physical activities( bed rest) preserving body temperature. Cool extremities. Grunting. Restlessness. Decreased blood pressure. Improve tissue oxygenation and decrease oxygen consumption: Supplemental cool humidified oxygen is usually provided to increase the amount of oxygen during inspiration. 2. Exercise intolerance. Wheezing. Hepatomegaly. Ascitis. Cough. reducing the effort of breathing (semi fowler’s position) and using medication to sedate an irritable child. Peripheral edema. Weak peripheral pulses. Criteria for pulmonary congestion: 3. Anorexia.The workload on the heart is reduced when metabolic needs are kept to a minimum. Orthopenea. Cardiomegaly.

Nursing Intervention: . Goal: The patient will: Exhibit improved cardiac output. •3 Often an E. •6 Administer medications to decrease over load as ordered. Nursing Intervention: •1 Administer digoxin (lanoxin) as ordered. •7 Check blood pressure. Decreased cardiac out put related to structural defect. myocardial dysfunction. regular and within normal limits for age. rhythm strip is taken to assess cardiac status before administration. Goal: (1) The patient will: Exhibit improved respiratory function. •8 Observe for signs of hypotension. •2 Peripheral perfusion is adequate. •1 Heartbeat is strong.C. Ineffective breathing pattern related to pulmonary congestion. •2 Nursing established precaution to prevent toxicity.G. •5 Monitor serum potassium levels (decrease enhances digoxin toxicity). •9 Monitor electrolyte levels. Expected outcome: 2. •4 Ensure adequate intake of K.Nursing care plan of a patient with congestive heart failure: 1.

place older infant in sent (fowler’s position). Goal: (2) The patient will: Experience reduction of anxiety. Nursing Intervention: •1 •2 •3 •4 •5 Employ flexible feeding schedule. •2 Avoid any constricting clothing or restraints around abdomen and chest. •3 Administer humidified O2 as prescribed. . Handle child gently. color is good and infant rest quietly. Respirations remain with normal limits. Hold and comfort the infant. Expected out come: 3. Goal: The patient will: Exhibits no additional respiratory or cardiac stress. Nursing Intervention: •1 Maintain neutral thermal environment. Activity intolerance related to imbalance between oxygen supply and demands. Employ comfort measures found effective in individual cases. Encourage family to provide comfort.Expected outcome: •1 Place inclined posture of 30 to 45 degree tilt mattress support of incubator. -Keep infant warm and treat fever promptly. Infant rests quietly and breath easily. -Place newborn in an incubator or under warmer.

Maintain fluid restriction if ordered. . Fluid volume excess related to fluid accumulation (edema). and weight loss. frequent urination. ingest more.•2 Feed small volumes or frequent intervals using soft nipple with moderately large opening. 4. Infant exhibits evidence of fluid loss. Use soft nipple. tire less. Use resilient mattress or mattress cover. Change position frequently. Nursing Intervention: •1 •2 •3 •4 •5 Administer diuretics as prescribed. frequent burping and pauses of rest. As nursing diagnosis (5) N. Expected out come: Infant rest quietly.: feed cyanotic infant in the knee-chest position. -Implement gavage feeding if infant becomes fatigues before taking an adequate amount.B. •4 Implement measures to reduce anxiety. •5 Respond promptly to crying or other expressions of distress. Provide skin care for children with edema. As nursing diagnosis (4) 6. Goal: The patient will: Exhibit no evidence of fluid excess. he will suck more strongly. head is elevated. Expected outcome: 5. Altered family processes related to child with life threatening illness. High risk for infection related to reduce body defenses pulmonary congestion. •3 Time nursing activities to disturb infant as little as possible. and gain weight.

Profuse scalp sweating. Fatigue. vomiting. especially in infants. . Parent guidelines in administrating Digoxin: Give digoxin at regular intervals. Respiratory distress. Early signs of CHF:            Tachycardia. Sudden weight gain.Nurse should be alert for: 1. Irritability. Common signs of Digoxin toxicity: Gastrointestinal: nausea. Cardiac: bradycardia. and anorexia. especially during rest and slight exertion. dysrhythmias.

Don’t increase or double the does for missed doses. Acquired Cardiovascular Disorders They occur for a variety of reasons including infection autoimmune responses. environmental factors and familial tendencies.     If the child vomits don’t give a second doses. if less than 4 hours has elapsed give the next doses. overcrowded living conditions and poor socioeconomic and educational level. the incidence of ARF is still fairly high due to substandard health practices. 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 more than 2 consecutive doses have been missed notify the physician. Keep digoxin in a safe place preferably a locked cabinet. .  Don’t mix it with other foods or fluids (inaccurate intake of the drug). In developing nations. Acute Rheumatic Fever (ARF) Acute rheumatic fever is a leading cause of acquired heart disease in the pediatric population.

The school age children are he most susceptible to contracting this disease.F. Boys and girls are equally affected. develops in 3 steps: Phase I: GABHS infection of the upper respiratory tract. Phase III: the silent period is followed by the onset of acute rheumatic fever. It has a marked tendency to recur. skin and subcutaneous tissues. It may rarely start at earlier age (23years). is a poorly understood autoimmune reaction to group A –Beta hemolytic streptococcal upper respiratory tract infection (GABHS). The attack of GABHS pharyngitis may be extremely mild or moderately severe.F peaks between 5-10 years of age. Pathophysiology: Rheumatic fever is essentially a group of bodily responses to a streptococcal infection following upper respiratory tract infection. The most acceptable current hypotheses for the development of RF are: 1. is an inflammatory disease of connective tissue involving mainly the joints and heart and less frequently the CNS.F. R. Etiology: R . it assumes that: . Hypothesis of abnormal immune response to GABHS: This is the most popular hypothesis.Definition: R.R. 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. Incidence: The incidence of A. F.

loss of appetite. The history and laboratory findings determine the minor criteria. Unexplained epistaxis. The ones major and minor criteria are based on clinical findings are essentially objective. pallor.R. weight loss. and crossreactive “ anti-heart” antibodies have been found in rheumatic fever patients. streptococcal antigens may elicit antibodies capable of reacting not only with the microbial products. CRP). is to strictly and here to the specific onset criteria. problematic environmental factors or recent exposure are the most efficient ways to diagnose A. Minor Criteria or Manifestations: • • • • • • Fever (38-39°C). fatigue. but also with the host’s antigens. •3 The resulting antigen-antibody complexes will cause the immunological damage to the connective tissue of heart and joints. According to this hypothesis. Elevated acute phase reactants (ESR. Hypothesis of autoimmunity: Some streptococcal antigens cross-react with human tissue antigens. •2 This reaction takes 1-3 weeks. Assessment: Accurate history should be taking from parents and child.•1 A genetically predisposed person reacts abnormally to an undefined component of GABHS.F. Abdominal pain. Weakness. Arthralgia (pain in joints) without arthritic changes. 2. See table (2) . Thus autoimmunization maybe the underlying basis for the cardiac lesion.

Carditis: .Guidelines for the diagnosis of initial attack of Rheumatic fever (Jones criteria.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) Major Manifestations: 1. 1992 update) Major Manifestations Carditis Polyarthritis Chorea Erythema marginatum Subcutaneous nodules Minor Manifestations Clinical findings Arthralgia Fever Laboratory findings Elevated acute-phase Reactants Erythrocyte Sedimenation rate C.

•2 Evanescent.: Rheumatic fever licks the joints but bites the heart. it will be noted to change gradually. The valve edges may become so scarred that they can’t completely close. 4. N. swollen. This process causes obstruction to the blood flow into the left ventricle or aorta or both. •2 Affected joint is red. •5 It disappears within 12-24 hours from start of salicylate therapy. toes or spine. 2-Rheumatic Polyarthritis: •1 It is the most common criterion: typical arthritis occurs in 70% of cases. Cardiomegaly. either together or one after another.B. wrists.Rheumatic (sydenham’s) Chorea: . Muffled heart sound (ventricle gallop exist that is S3). the following manifestations will be seen. Changes in E. •1 •2 •3 •4 •5 •6 •7 Tachycardia out of proportion to degree of fever. •4 Typically the large joints are affected as knees. with limited movements + effusion. and if watched from hour to hour. New murmur or change in preexisting murmurs. fibrous areas when healed. It rarely affects fingers. Friction rub (main manifestation of pericarditis). •6 If untreated it doesn’t persist in the same joint for more than 1 week. •7 Rheumatic arthritis leaves the joint intact and doesn’t result in chronic disease.C. stenosis as the leafiers (cusps) of the valves occurs because of their fusing together.G. warm. 3. very tender. It occurs during the first 1-2 weeks the febrile period and lasts for a few days in certain affected joints before moving to other joints. Pericardial pain.Mitral and aortic valves are most affective valves and they become scarred.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). •3 Migratory: several joints are commonly involved. causing a block flower regurgitation (valvular insufficiency) when the valves close so. ankles and elbows.

•4 Erythrocyte sedimentation rate (E.R. •3 Children suspected of having A.F. •3 They can be palpated over the extensor surfaces of joints such as elbows. •5 C. aimless. . •7 Radiographs. •3 Speech disturbance. Diagnostic Evaluation: To diagnose R. are tested for streptococcal antibodies. •6 Electrocardiograph.).F. •2 Involuntary facial grimaces. 5. or over the scalp and spinous processes of the vertebrae. The most reliable and most standardized test is an elevated or rising antistreptolysino titer (A.5-1Cm) and firm without any tenderness or attachment to the skin.R. involuntary and irregular muscular movements of the extremities. it is necessary to have: •1 Two major criteria +evidence of preceding GABHS or infection or. •2 Nodules are generally identified as small (0. ankles.).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.reactive protein.R.O.F.S. •5 Muscle movements exaggerated by anxiety and attempts at fine motor activity are relieved by rest. •4 Severe muscle weakness (can be profound).•1 Chorea is characterized by sudden. •4 They gradually resolve over a period of time with no residual.S. knees.T. •2 One major + 2 minor criteria + evidence of preceding GABHS or infection.

Prevention of recurrents of RF.200.F. or •2 If patient is allergic to penicillin give erythromycin as a substitute in penicillin sensitive children. Eradication of group AB –hemolytic streptococcal infection. •4 Bed rest: is recommended during the acute febrile phase. •4 Infective endocarditis. two daily oral doses of penicillin (400. •3 Salycilates [anti-inflammatory (suppressive) therapy] are used to control the inflammatory process. Anti-inflammatory agents for Carditis and arthritis.000µ (125-250mg)/dose 3 times/ day for -3 Single IM injection of 600.000 – 400. 10 days.F. 3.F. •5 Arrhythmias. for the rest of their lives and should be followed medically for at least 5 years. especially in the joints and reduce the fever and discomfort. Prophylactic Treatment: •1 Against recurrent R.. .000µ Benzathine penicillin. •2 Children who have had acute R. 2. Palliation of the other symptoms. twice daily.000µ /day for 10 days. 4.000-1.: Streptococci can be eradicated and R. are susceptible to recurrent R.000µ) or one daily oral dose of sulfadiazine orally or erythromycine orally. or -2 Oral penicillin V: 200. •6 Thromboemoblism and stroke.Therapeutic Management: The aims of medical management are: 1. atrial fibrillation.F is started after the acute therapy and involves monthly intramuscular injections of benzathin penicillin (1-2 million Iµ) IM. N.B. •1 Penicillin: is the drug of choice to treat GABS infection: -1 Procaine penicillin 400. •3 Cardiac failure. prevented if penicillin is given Early (within 9 days of GABS infection) for a sufficient period of time (10 days Complications of Rheumatic Fever: •1 Chronic valvular disease •2 Repeated chest infection.

B. The diet is gradually increased to meet the child’s nutritional requirements overfeeding is to be avoided. •2 During chorea the only treatment is prevention of injury during the period when involuntary jerking and possibly violent movements occur. Encourage compliance with drug regimens. are to: 1. •1 Pain from Carditis or polyarthritis is decreased by administration of antiinflammatory agents (aspirin). 2. Facilitate recovery from the illness. .Nursing Consideration: The objectives of nursing care for child with A.R. fluids are encouraged to prevent dehydration but overdehydration is avoided because hypervolemia places increased demands on the heart -1 As soon as a child is willing to eat a liquid or soft diet is given in small frequent amounts to minimize the exertion of chewing. -2 Feeding the child to prevent injury.F. •2 When compliance is poor monthly injections may be substituted for daily oral administration of antibiotics. Provide emotional support. •2 During the febrile phase. 4. -4 Restraints to prevent the child from falling from a chair. -1 Assist once during walking. Prevent the disease. padding on the sides of the beds or chair to prevent injury. Encourage compliance with drug regimens: •1 Since compliance is a major concern in long term during therapy every effort is made to encourage adherence to the therapeutic plan. The aim of the bed rest is to minimize the effect of the inflammatory process on all body systems. 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. If the metabolic needs oxygen consumption and expected cardiac response can be very low. -1 Alternating warm and cold snacks to the affected joints may reduce swelling and inflammation and provide direct and immediate reduction of pain. The damage to heart muscle and valve tissue may be restricted to what has already occurred. 3. -3 Bed rails to prevent the child from falling out of bed. A. particularly the heart.

D. . •2 After streptococcal pharyngitis has been diagnosed. letters… etc.F. N. antimicrobial treatment is given to eradicate the infection. classmates. A single injection of benzathine penicillin is the most reliable from the therapy. C. peer group and parents. quiet play and school work while in hospital and home. i.B. •4 Massive screening program with throat cultures and support of patient cooperation in therapy can eradicate the disease. 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. •3 Allow for parent of normal routine at home. •3 The main nurse’s role in prevention is to help educate the public as well as the individual patient and family. •4 Classmates and sibling can show their concern by card.-5 Behavioral changes and learning difficulties are discussed with school. try to develop the appropriate nursing care plan.R.: from the previous discussion about A. oral penicillin or erythromycin may be given daily for 10 days. 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 his feelings.e. the nurse help the parents to be cooperative. •2 Find ways for bed activities.

Plan of nursing care for a child undergoing heart surgery: Pre-operative care: a-Pre-operative assessment: .

•8 During preparation. E. gown.e.C.•1 It can be done though observation. when appropriate. Practice deep inspiration and expiration. Pre-operative preparation: It should be given throughout the pre-operative period. Physical preparation for surgery: •1 Shaving the child skin the evening before the operation. nurse demonstrates deep act of coughing. •7 Prepare them (if old enough) for nasogastric tube catheter for bladder-by telling them about it. •6 Demonstrate postural drainage and percussion. it will include: -1 Admission history and physical examination. -8 Elimination pattern to avoid constipation post-operatively (should be planned in advance). •2 Take child and parents to the operating suite and ICU to be familiar with the physical settings (lights. -5 Sleep/ awake –patterns. •2 Cleansing enema may be ordered. -7 Additional observation (normal activities. . order). •5 Through play. how to turn from side to side. -3 Height and weight measurement for fluid replacement. Show them the equipment used gradually. b. semi fowler’s position. -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.etc). rest be noted & reported). the nurse must be aware of the level of child’s anxiety (so discussion should be ended if she felt the child is very anxious). Lab Tests should be prepared. c. Postoperatively. •1 Instructing child and parents about tests will be done. …. -4 Pre-operative studies. •2 It will facilitate care planning.physical and emotional stress should be reported. breathing to the child… let him practice it (tell him that they may cause some discomfort in practice postoperatively). operation…. •4 Introduce them to post-operative procedure. i. •3 Sedation is given for rest (or Dr. •3 Place child temporarily into oxygen tent to make him accustomed to it and to oxygen mask through play (sometimes fear of suffocation).G. -6 Fluid intake: to estimate the child’s fluid consumption and which fluids are preferred.

5. order. it must be in proper position (no filtration). heart rate and rhythm will observed constantly. 6. •5 I. Check vital signs. . Tell patient that operation is over when he re-awakes. •1 Temperature: if there is fever. color and consistence. •2 Blood pressure: Should be taken and notifying doctor for any change. bleeding. (Warm – cold). Monitor fluids: if cut down is used for I. 2. not be too rapid. Fluids requirement is based on child’s weight and body surface area. catheter may be used. •2 Respiration: . If cyanosis. reduce it by tepid water sponges. Then: 4. attach it to the patient.. Oral fluids are restricted in immediate post-operative period to decrease load on heart. Clamp the chest tube and call Dr.Do suction if respiration becomes noisy and rapid. . Observe: skin color. Check each catheter in his chest and attached to the suction machine. If no voiding within 8-12 hours after operation.•4 Vital signs are checked. If cardioscopy will be in use. immediately. moisture (dry – moist).Check depth and rate of respiration and chest expansion on both sides is equal. therefore mouth care will also decrease child’s thirsty. sudden sharp chest pain around the catheter and dyspnea and tachycardia occur. Postoperative Care: Immediate Admission to ICU: •1 •2 •3 •4 Oxygen immediately.V. fluids must be checked and regulated carefully. Narcotic may be given as Dr. Urine must be analyzed for specific gravity to assess kidney function.V. Vital signs are taken each hour or more often if necessary (temperature – rectally as cool atmosphere in oxygen tent may affect temperature). …Below bed level and observe the amount. •1 Pulse: it should be observed for: regular rhythm and power. ice bags or ice water mattress. be sure that they are patent (free from blood clots) and well tighten to patient. Care for chest tubes (under-water seal)…. 7. Observe the drainage. then EKG. Input and output of all fluids must be accurately calculated and recorded. Important: be sure that the bottles. 1. 3.

To provide rest.C.more demanding) understand his behavior as a nurse –once his condition improves help him to gain control of his situation. Child may regress in his behavior (cry. Before discharge: plan of care must be done with the health team and parents. 13. 9. bleeding or infection at side of operation. to decrease disturbance. Observe: color of legs and its coldness. 14. Change position every hour. . 11.more physical contact. good plan of N. Encourage patient to be out of bed (according to his condition and severity of operation) on wheel chair after chest tubes have been removed. 10.8. 12. Encourage child for deep breathing and coughing exercise and support his chest especially over the incision area and praise him. 15. Support the body with pillows if he can’t maintain his position. Encourage him to move himself.

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