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 the most common common heart heart diseases, diseases, either either the acyanotic acyanotic or or cyanotic cyanotic heart diseases. 2. State the the nursing nursing assessment assessment of each each congenital congenital heart heart disease. disease. 3. Plan Plan the nursin nursing g managem management ent of each each disea disease. se. 4. List the the methods methods used used in diagn diagnosis osis of of heart dise disease. ase. 5. Plan the the nursing nursing managem management ent of congestive congestive heart heart failure. failure. 6. Identify Identify the the etiolo etiology gy of rheu rheumati matic c fever. fever. 7. Identify the criteria criteria used in diagnosis diagnosis of rheumatic rheumatic fever.
8. Plan Plan the nursing nursing manag manageme ement nt of rheuma rheumatic tic fever. fever. 9. Plan the the nursing nursing care care for for a child undergoin undergoing g heart heart surgery. surgery.
Cardiovascular disorders in children are divided into two major groups: a- Cong Congen enit ital al hea heart rt dis disea ease ses. s. b- Acqu Acquir ired ed hea heart rt dis disor orde ders rs..
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.
Materna Maternall rubell rubella a during during pregnanc pregnancy. y. Maternal alcoholism, alcoholism, age over 40 40 years and insulin insulin dependant dependant diabetes. diabetes. Sever Several al gen geneti etic c facto factors. rs. Expos Exposur ure e to to rad radiat iatio ion. n.
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.
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Heart is completely developed in the first eight weeks of intra-uterine life.
During fetal life, blood carrying oxygen and nutritive materials from the placenta enters the fetal system through the umbilicus via the large umbilical vein. Oxygenated blood enters the heart by the inferior vena cava because of the higher pressure of the blood entering the right atrium and through the foramen ovale to the left atrium.
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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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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.
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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
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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)
Types of Defects: Congenital heart defects have been divided into 2 categories: 1. Traditionally, a physical characteristics, cyanosis has been used as distinguishing feature, dividing the anomalies into:
-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
Pulmonary Blood flow
Cyanotic
Obstruction to blood flow From ventricles
pulmonary blood flow
Mixed Blood flow
-Artial septal defect arteries.
- Coarctation of aorta
-Ventricular septal defect - Aortic stenosis pulmonary venous -Patent ductus arteriosus - Pulmonic stenosis -Atrioventricular canal
-Tetralogy of fallot -Transposition of great
-Tricuspid atresia
-Total anomalous
return. -Tranucus arteriosus - Hypoplastic left heart
syndrome
(Table .1) Comparison of acyanotic-cyantoic and hemodynamic classification system of congenital heart disease.
Acyanotic Defects Most acyanotic defects involve primarily left to right shunting through an abnormal opening. Others result from obstructive lesions that reduce the flow of blood to various areas of the body.
Major Acyanotic Defects:
-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: Patent ductus arteriosus is a vascular connection that during fetal life, short circuits that pulmonary vascular bed and directs blood from the pulmonary artery to the aorta. Functional closure normally occurs soon after birth. If the ductus remains patent flow in the ductus is reversed by the higher
(Fig .2)
Incidence: More common in females (2:1), Higher incidence among premature and commonly associated with maternal rubella.
Hemodynamics:
Blood from aorta
goes to systemic circulation
PDA
poor systemic circulation.
Double flow in pulmonary artery
Double pulm. venous
return
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. Small PDA: asymptomatic and discovered on a routine examination. Large PDA:
•1 •2 •3 •4 •5 •6 •7 •8
Classic machinery murmur, which is continuous from systole into diastole. Dyspnea on exertion and easy fatigability. Under weight thin child. Repeated chest infections. Heart rate over 150 b/m, gallop rhythm due to rapid filling of the ventricle. Bounding pluses due to increased systolic pressure. Left heart failure may develop in infancy in severe cases. Enlarged heart size in large PDA.
Therapeutic Management: 1. Supportive: fluid restriction with diuretics and digitalization for congestive
heart failure CHF. 2. Surgical: surgery can be performed at anytime, although it is preferably done at about 6 months of age, surgery maybe done earlier if the child is in difficulty to prevent complications and growth retardation caused by PDA.
Out come: The child is good with less than 1% mortality.
Complications: 1. Bacterial endocarditis. 2. Congestive heart failure. 3. Pulmonary hypertension.
Atrial Septal Defect (ASD)
Incidence: 7% of all CHD, more common in females. Description and pathology: Abnormal opening between the atrium, allowing blood directed from the higher pressure left atrium to flow to the lower pressure right 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.
(Fig.3)
Hemodynamics:
Blood flow from pulmonary veins
LA
LV
ASD
Increased pulmonary venous return
poor systemic circulation.
double flow in RA
Double flow in RV
Double pulmonary blood flow
Assessment: •1 •2
The clinical manifestations depend on the location and size of the defect. The infant with small defects may be asymptomatic. If there is a large left to right shunt and severe mitral incompetence cardiac enlargement and pericardial bulge are seen. These children are easily fatigued and have recurrent pneumonitis .
•1 •2 •3
In atrial septal defect, pulse and venous pressure are normal and the heart size is normal or slightly enlarged. Systolic murmur is present. The ausculatory finding of a widely split second heart sound is so unusual in complicated atrial septal defects that the diagnosis is not made without it.
Management: 1. Supportive: same as that of the VSD. 2. Surgical: surgery is done on affected children before they enter school
even if no symptoms are present. If surgery is not done during childhood pulmonary hypertension, atrial arrhythmias and cardiac failure make operation more hazardous in adult life.
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 defects vary in size and may occur in either the membranous or muscular portion of the ventricular septum. Due to higher pressure in the right and left ventricles. A shunting of blood from the left to right ventricle occurs during systole. If pulmonary vascular resistance produces pulmonary hypertension, the shunt of the blood is then reversed from the right to the left ventricle, with resulting cyanosis. (Fig 4)
(Fig. 4)
Hemodynamics: to Aorta
Blood from LA (doubled)
LV
VSD
poor systemic circulation
RV
Flow in LA
RV flow
Flow in pulmonary circulation
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 pulmonary infection. Heart failure, cardiac enlargement and mild cyanosis may also occur in large defects.
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.
Pulmonary Stenosis (PS) Description: •
•
It is an obstructive lesion that interferes with blood flow from the right 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)
(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 artery resulting in increased systolic pressure and hypertrophy of the right ventricle. The degree 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 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, 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 to insufficient blood flow to the lungs to meet the need for increased cardiac output during 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.
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: Narrowing or stricture of the aortic valve causing resistance to blood flow in the left ventricle and decreased cardiac output. (Fig 6)
(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 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.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 asymptomatic until increased physical growth requires additional cardiac output. In severe obstruction: fatigue due to exercise intolerance, dizziness, fainting and episodes of pulmonary edema occur, decreased cardiac out put also results in faint peripheral pulses and anginal pain. The most prominent physical manifestation of aortic stenosis is the presence of a coarse systolic ejection murmur, usually accompanied by a thrill over the aortic area, radiating to the neck and apex.
Management and Outcome: • •
If heart failure occurs in infancy, medical management is carried out: like VSD. Surgical: Ballon valvuloplasty or surgical by open aortic volvotomy or aortic valve replacement should be postponed until child has stopped growing.
Coarctation of the Aorta
Description and Pathology: •
•
It is characterized by a narrowed aortic lumen. It exists as a preductal or postductal obstruction, depending on the position of the obstruction in relation to the ductus arteriosus coarctation exist with great variation in anatomical features. The lesion produces an obstruction to the flow of blood through the aorta increased LV pressure and workload. (Fig. 7)
(Fig.7)
Assessment: •
• •
Blood pressure is higher than normal in the upper part of the body, resulting in headache, dizziness fainting, epistaxis, and later cerebrovascular accidents. In the leg, it is relatively low, resulting in absence or diminishing of the femoral pulse. The legs may be cooler than the arms. If the child exercises muscle cramps in the legs may be due to tissue anoxia.
Management and Outcome:
• •
Surgical: repair consists of resection and anastomosis by aortic graft or subclavian flap angioplasty. If blood pressure is not elevated and heart failure is not a problem, it is wise to postpone the operation until the operation descending aorta is at least 50% of adult size (age of child 3-6 years) to avoid re-stenosis.
Out come: Surgery should be done if only a minor defect is present to avoid complication, e.g. hypertension, intracranial hemorrhage and stroke.
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). The classical tetralogy consists of: 1. Pulmonary Cyanosis stenosis. may be seen at first year of life. It increases, as the child grows older. 2. Ventricular septal defect. 3. Overriding of the aorta: aorta receives Major cyanotic defects: blood from both ventricles and this is the of cyanosis. 1. cause Tetralogy of fallot. 4. 2. Right ventricular Transposition hypertrophy. of the great vessels. of fallot, blood normally • In3.tetralogy Tricuspid atresiathe(TA). returns from the systemic circulation to the right atrium and right ventricle. 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. This is a right to left shunt. • Hypertrophy of the right ventricle occurs as a result of the pressure exerted against the pulmonary stenosis, because the blood from the right ventricle is unoxygenated, cyanosis result. • Polycythemia develops because the body attempts to compensate for the unoxygenated blood. The resulting increased viscosity of the blood causes slowing of the circulation and possible thrombophlebitis emboi and vascular disease.
(Fig. 8)
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 closes during 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 knee chest 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 a very low oxygen content, especially after exercise. •
2. Squatting position increase systemic vascular resistance, which diverts right ventricular blood from the aorta into pulmonary artery increasing pulmonary blood flow. This increases the amount of oxygenated blood in the left side of the heart and eventually into systemic circulation. (Fig.10)
(Fig. 10)
• • •
Cyanotic spells. (Hypoxic, blue spells). Apansystolic murmur: it is usually associated with thrill. These children don’t develop congestive heart failure because the overload of the blood in right ventricle flows freely through the septal defect and the overriding aorta into the systemic circulation.
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- chest position.
(Fig.11)
-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:
The clinical manifestation of cyanosis varies in degree depending on the type and size of the associated defects. Children with minimal communication are severely cyanotic at birth. Those with large septal defects or a patent ductus arteriosus may be less severely cyanotic but have symptoms of congestive heart failure usually before 4 months of age. •
•
In these infants the only signs at birth may be cyanosis after crying or feeding and progressive hyperpnea in an attempt to compensate for decreased arterial oxygen saturation. A murmur usually indicates the presence of septal defect or a patent ductus arteriosus cardiomegaly.
(Fig. 12)
•
Management:
Palliative and corrective treatment used for the treatment of transposition of the great vessels. Tricuspid valvular atresia is characterized by a small right ventricle, large left ventricle, and usually diminished pulmonary circulation. Blood from the right atrium passes through an atrial septal into the left atrium, mixes with oxygenated blood returning from the lung, flows into the left ventricle, and is propelled into the systemic circulation. The lungs may 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 the Tricuspid Atresia tricuspid valve resulting in no opening between the right atrium and right ventricle.•It isDescription usually associated withPathology: and other defects that allow some shunting of blood into the left side of the heart, then back to the right ventricle or pulmonary artery.
(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 failure are evident early during infancy if the child survives, systemic consequences of cyanosis and polycythemia may develop.
•
Management: Palliative and corrective treatment can be done.
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 heart muscle. 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 and relationships. 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 cardiac catheterization. 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 circulatory system provides computerized image as vessels and tissue containing dye subtracts all tissue don’t containing dye. •
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. However in many instances symptoms that suggest cardiac anomaly is not present at birth or if manifested is so subtle that they are easily overlooked.
Infants: Cyanosis generalized, especially mucous membranes, lips and tongue. Conjunctiva, cyanosis during exertion such as crying, feeding, straining, or when immersed in water. • Dyspnea, especially following physical effort such as feeding, crying or straining. • Fatigue, paroxysmal hyperpnea, poor growth and development (failure to thrive). • Frequent respiratory tract infection. • Feeding difficulties. • Hypotonia. • Excessive sweating. •
Older Children: • • • • • • • • •
Impaired growth. Fatigue. Orthopnea. Headache. Leg fatigue. Delicate body build. Effort dyspnea. Digital clubbing. Epistaxis.
Nursing Care Plan for Child with Congenital Heart Disease:
1. Decreased cardiac out put related to structural defect. Goal: The patient will: exhibit improved cardiac output.
Intervention: Administer digoxin as ordered. • The child’s apical pulse is always checked before administrating digoxin (as general rule the drug is not given if the pulse is below 90-100 b/m in infants and young children or below 70 b/m in older children). •
Expected Outcome: Heart rate and volume indicate satisfactory cardiac output.
2. Activity intolerance related to imbalance between oxygen supply and demand. Goal: The patient will: Maintain adequate energy levels.
Intervention: • • • •
Allow for frequent of rest. Encourage quite games and activities. Help child to select activities appropriate to age, condition and capabilities. Avoid extremes of environmental temperature.
Expected Outcome: Child determines and engages in activities commensurate with capabilities.
3. Altered growth and development related to inadequate oxygen, nutrients to tissue and social isolation. Goal: The patient will: Achieve normal growth.
Intervention: •
Provide well balanced highly nutritive diet.
Expected Outcome: Child achieves normal growth.
Goal: (2) The patient will: Exhibit adequate iron level.
Intervention: • •
Administer iron preparation as prescribed. Encourage iron rich foods in diet.
Expected Outcome: Child assimilates sufficient iron.
Goal: (3) The patient will: Have opportunity to participate in activities.
Intervention: •
Encourage age appropriate activities.
Expected Outcome: Child engaged in age appropriate activities.
4. High risk for infection related to debilitated physical status. Goal: The patient will: Exhibit no evidence of infection.
Intervention: • • •
Avoid contact with infected persons. Provide for adequate rest. Provide optimum nutrition.
Expected Outcome: Child remains free from infection.
5. Altered family process related to having a child with a heart condition. Goal: The patient will: Experienced reduction of fear and anxieties.
Intervention: •
Discuss with parents their fears regarding child symptoms.
Expected Outcome: Family discusses their fear and anxieties.
Goal: (2) The patient will: Exhibit positive coping behavior.
Intervention: Encourage family to participate in care of child while hospitalized. • Encourage family to include others in child’s care to prevent their own exhaustion. • Assist family in determining appropriate physical activity and disciplining methods for child’s anorexia. •
Expected Outcome: Family copes with child’s symptoms in a positive way.
Goal: (3) The patient will: Demonstrate knowledge of home care.
Intervention: • • • • •
Teach skills for home care. Administration of medications. Feeding techniques. Signs that indicate complications. Where and whom to contact for help and guidance.
Expected Outcome: Family demonstrates ability and motivation for home care.
6. High risk for injury (complications) related to cardiac condition and therapies. Goal: The patient’s family will: Recognize signs of complications early.
Intervention: Teach family to intervene during hypercyanotic spells, place child in knee chest position with head and chest elevated. • Teach family to recognize signs of complications such as: •
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Digoxin toxicity (vomiting, bradycardia, dysrhythmias).
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Hypoxemia (cyanosis, restlessness, tachycardia).
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Cardiovascular collapse (pallor, cyanosis and hypotonia).
Increased respiratory effort (tachypnea, retraction, grunting, cough, cyanosis). Cerebral thrombosis (compensatory polycythemia is particularly hazardous when child is dehydrated).
Expected Outcome: Family recognizes signs of complications and institutes appropriate action.
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. In children CHF most frequently occurs secondary to structural abnormalities that result in increased blood volume and pressure. CHF is a symptom caused by an underlying cardiac defect, not a disease it self, since it is usually the result of an excessive workload imposed on a normal myocardium 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 into the pulmonary artery resulting in increased pressure in the right atrium and systemic venous circulation. Systemic venous hypertension causes Hepatosplenomegaly and occasionally edema. In left sided failure, 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, causing elevated pulmonary pressure and pulmonary 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 cold extremities. •
Causes: Can be classified according to the following changes: 1. Volume overload: especially with left to right shunts that may cause the RV to
hypertrophy 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 the
myocardium, 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 blood exceeds the heart out put (even though the volume may be normal), such as in sepsis, hyperthyroidism and severe anemia.
Therapeutic Management of Congestive Heart Failure: The goals of treatment are to: 1. 2. 3. 4.
Improve cardiac function. Remove accumulated fluid and sodium. Decrease cardiac demands. 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 fowler’s position) and using medication 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.
Nursing care plan of a patient with congestive heart failure: 1. Decreased cardiac out put related to structural defect, myocardial dysfunction. Goal: The patient will: Exhibit improved cardiac output.
Nursing Intervention: •1 •2 •3 •4 •5 •6 •7 •8 •9
Administer digoxin (lanoxin) as ordered. Nursing established precaution to prevent toxicity. Often an E.C.G. rhythm strip is taken to assess cardiac status before administration. Ensure adequate intake of K. Monitor serum potassium levels (decrease enhances digoxin toxicity). Administer medications to decrease over load as ordered. Check blood pressure. Observe for signs of hypotension. Monitor electrolyte levels.
Expected outcome: •1 •2
Heartbeat is strong, regular and within normal limits for age. Peripheral perfusion is adequate.
2. Ineffective breathing pattern related to pulmonary congestion. Goal: (1) The patient will: Exhibit improved respiratory function.
Nursing Intervention:
Place inclined posture of 30 to 45 degree tilt mattress support of incubator, place older infant in sent (fowler’s position). Avoid any constricting clothing or restraints around abdomen and chest. Administer humidified O 2 as prescribed.
•1 •2 •3
Expected outcome: Respirations remain with normal limits; color is good and infant rest quietly.
Goal: (2) The patient will: Experience reduction of anxiety.
Nursing Intervention: Employ flexible feeding schedule. Handle child gently. Hold and comfort the infant. Employ comfort measures found effective in individual cases. Encourage family to provide comfort.
•1 •2 •3 •4 •5
Expected out come: Infant rests quietly and breath easily.
3. Activity intolerance related to imbalance between oxygen supply 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.
Feed small volumes or frequent intervals using soft nipple with moderately large opening. -Implement gavage feeding if infant becomes fatigues before taking an adequate amount. •2
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: •3
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 •2 •3 •4 •5
Administer diuretics as prescribed. Maintain fluid restriction if ordered. Provide skin care for children with edema. Change position frequently. 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 defenses As nursing diagnosis (4) pulmonary congestion. 6. Altered family processes related to child with life threatening illness. As nursing diagnosis (5)
N.B.: feed cyanotic infant in the knee-chest position, head is elevated, he will suck more strongly, ingest more, tire less, and gain weight. Use soft nipple, frequent burping and pauses of rest.
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.
Don’t 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 don’t give a second doses.
If more than 2 consecutive doses have been missed notify the physician.
Don’t increase or double the does for missed doses.
Keep digoxin in a safe place preferably a locked cabinet.
Acquired Cardiovascular
Disorders They occur for a variety of reasons including infection autoimmune responses, environmental factors and familial tendencies.
Acute Rheumatic
Fever
(ARF)
Acute rheumatic fever is a leading cause of acquired heart disease in the pediatric population. In developing nations, the incidence of ARF is still fairly high due to substandard health practices, overcrowded living conditions and poor socioeconomic and educational level.
Definition: R.F. is an inflammatory disease of connective tissue involving mainly the joints and heart and less frequently the CNS, skin and subcutaneous tissues. It has a marked tendency 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 (23years). Boys and girls are equally affected.
Etiology: R .F. is a poorly understood autoimmune reaction to group A –Beta hemolytic streptococcal 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 GABHS pharyngitis 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:
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A genetically predisposed person reacts abnormally to an undefined component of GABHS. This reaction takes 1-3 weeks. The resulting antigen-antibody complexes will cause the immunological damage to the connective tissue of heart and joints.
2. Hypothesis of autoimmunity: Some streptococcal antigens cross-react with human tissue antigens, and crossreactive “ 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 host’s antigens. Thus autoimmunization 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 and here to the specific onset criteria. The ones major and minor criteria are based on clinical findings are essentially objective. The history and laboratory findings determine the minor criteria.
Minor Criteria or Manifestations: • • • • • •
Fever (38-39°C). 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)
Guidelines for the diagnosis of initial attack of Rheumatic fever (Jones criteria, 1992 update) Major
Minor
Manifestations
Manifestations
Carditis
Clinical findings
Polyarthritis
Arthralgia
Chorea
Fever
Erythema marginatum Subcutaneous nodules
Laboratory findings Elevated acute-phase Reactants Erythrocyte Sedimenation rate C- 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- Carditis:
Mitral and aortic valves are most affective valves and they become scarred, fibrous areas 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 can’t completely close, causing a block flower regurgitation (valvular insufficiency) when the valves close so, the following manifestations will be seen. •1 •2 •3 •4 •5 •6 •7
Tachycardia out of proportion to degree of fever. Cardiomegaly. New murmur or change in preexisting murmurs. Muffled heart sound (ventricle gallop exist that is S3). Friction rub (main manifestation of pericarditis). Pericardial pain. Changes in E.C.G.
2-Rheumatic Polyarthritis: •1
•2
•3 •4 •5 •6 •7
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 certain affected joints before moving to other joints. Affected joint is red, warm, swollen, very tender, with limited movements + effusion. Migratory: several joints are commonly involved, either together or one after another. Typically the large joints are affected as knees, wrists, ankles and elbows. It rarely affects fingers, toes or spine. It disappears within 12-24 hours from start of salicylate therapy. If untreated it doesn’t persist in the same joint for more than 1 week. Rheumatic arthritis leaves the joint intact and doesn’t result in chronic disease. N.B.: Rheumatic fever licks the joints but bites the heart.
3- Erythema Marginatum: •1 •2
The lesions are non-pruritic and appear initially as undifferentiated macules on the trunk and inner aspect of the extremities (never on face). Evanescent, and if watched from hour to hour, it will be noted to change gradually.
4- Rheumatic (sydenham’s) Chorea:
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Chorea is characterized by sudden, aimless, involuntary and irregular muscular movements of the extremities. Involuntary facial grimaces. Speech disturbance. Severe muscle weakness (can be profound). Muscle movements exaggerated by anxiety and attempts at fine motor activity are relieved by rest.
5- Subcutaneous Nodules: •1 •2 •3 •4
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. Nodules are generally identified as small (0.5-1Cm) and firm without any tenderness or attachment to the skin. 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. They gradually resolve over a period of time with no residual.
Diagnostic Evaluation: To diagnose R.F. it is necessary to have: •1 •2 •3
•4 •5 •6 •7
Two major criteria +evidence of preceding GABHS or infection or. One major + 2 minor criteria + evidence of preceding GABHS or infection. Children suspected of having A.R.F. are tested for streptococcal antibodies. The most reliable and most standardized test is an elevated or rising antistreptolysino titer (A.S.O.T.). Erythrocyte sedimentation rate (E.S.R.). C- reactive protein. Electrocardiograph. Radiographs.
Therapeutic Management: The aims of medical management are: 1. 2. 3. 4. •1
Eradication of group AB –hemolytic streptococcal infection. Anti-inflammatory agents for Carditis and arthritis. Palliation of the other symptoms. Prevention of recurrents of RF. Penicillin: is the drug of choice to treat GABS infection:
-1 Procaine penicillin 400.000µ /day for 10 days, or -2 Oral penicillin V: 200.000 – 400.000µ (125-250mg)/dose 3 times/ day for 10 days, or
-3 Single IM injection of 600.000-1.200.000µ Benzathine penicillin. •2 •3
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If patient is allergic to penicillin give erythromycin as a substitute in penicillin sensitive children. Salycilates [anti-inflammatory (suppressive) therapy] are used to control the inflammatory process, especially in the joints and reduce the fever and discomfort. Bed rest: is recommended during the acute febrile phase.
Prophylactic Treatment: •1
•2
Against recurrent R.F is started after the acute therapy and involves monthly intramuscular injections of benzathin penicillin (1-2 million Iµ) IM., two daily oral doses of penicillin (400.000µ) or one daily oral dose of sulfadiazine orally or erythromycine orally, twice daily. 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 given Early (within 9 days of GABS infection) for a sufficient period of time (10 days
Complications of Rheumatic Fever:
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Chronic valvular disease Repeated chest infection. Cardiac failure.
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Infective endocarditis.
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Arrhythmias, atrial fibrillation. Thromboemoblism and stroke.
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Nursing Consideration: The objectives of nursing care for child with A.R.F. are to: 1. 2. 3. 4.
Encourage compliance with drug regimens. Facilitate recovery from the illness. Provide emotional support. Prevent the disease.
A. Encourage compliance with drug regimens: •1 •2
Since compliance is a major concern in long term during therapy every effort is made to encourage adherence to the therapeutic plan. When compliance is poor monthly injections may be substituted for daily oral administration of antibiotics.
B. Facilitate recovery from the illness: •1
•2
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 to minimize the effect of the inflammatory process on all body systems, particularly the heart. If the metabolic needs oxygen consumption and expected cardiac response can be very low. The damage to heart muscle and valve tissue may be restricted to what has already occurred. During the febrile phase, 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
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frequent amounts to minimize the exertion of chewing. The diet is gradually increased to meet the child’s nutritional requirements overfeeding is to be avoided. Pain from Carditis or polyarthritis is decreased by administration of antiinflammatory agents (aspirin).
-1 Alternating warm and cold snacks to the affected joints may reduce •2
swelling and inflammation and provide direct and immediate reduction of pain. During chorea the only treatment is prevention of injury during the period when involuntary 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.
C. Provide emotional support: •1
•2 •3 •4
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. Find ways for bed activities, i.e. quiet play and school work while in hospital and home. Allow for parent of normal routine at home. Classmates and sibling can show their concern by card, letters… etc.
D. Prevent the disease: 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 most reliable from the therapy, oral penicillin or erythromycin may be given daily for 10 days, the nurse help the parents to be cooperative. •3 The main nurse’s 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 nursing care plan. •1
Plan of nursing care for a child undergoing heart surgery: Pre-operative care: a-Pre-operative assessment:
It can be done though observation. •2 It will facilitate care planning. Postoperatively, it will include: •1
-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 child’s fluid consumption and which fluids are preferred.
-7 Additional observation (normal activities, rest be noted & reported)- physical and emotional stress should be reported.
-8 Elimination pattern to avoid constipation post-operatively (should be planned in advance).
b. Pre-operative preparation: It should be given throughout the pre-operative period. •1 •2 •3 •4 •5
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Instructing child and parents about tests will be done; operation…. when appropriate. Take child and parents to the operating suite and ICU to be familiar with the physical settings (lights, gown, ….etc). Show them the equipment used gradually. Place child temporarily into oxygen tent to make him accustomed to it and to oxygen mask through play (sometimes fear of suffocation). Introduce them to post-operative procedure, semi fowler’s position, how to turn from side to side. Practice deep inspiration and expiration. Through play, nurse demonstrates deep act of coughing, breathing to the child… let him practice it (tell him that they may cause some discomfort in practice postoperatively). Demonstrate postural drainage and percussion. Prepare them (if old enough) for nasogastric tube catheter for bladder-by telling them about it. During preparation, 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).
c. Physical preparation for surgery: •1 •2 •3
Shaving the child skin the evening before the operation. Cleansing enema may be ordered. Sedation is given for rest (or Dr. order).
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Vital signs are checked.
Postoperative Care: Immediate Admission to ICU: •1 •2 •3 •4 •5
Oxygen immediately. Check each catheter in his chest and attached to the suction machine. Check vital signs. If cardioscopy will be in use, attach it to the patient, then EKG, heart rate and rhythm will observed constantly. 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. 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 period to decrease load on heart, therefore mouth care will also decrease child’s thirsty. Input and output of all fluids must be accurately calculated and recorded. Urine must be analyzed for specific gravity to assess kidney function. Fluids requirement is based on child’s 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 and dyspnea and tachycardia occur. Clamp the chest tube and call Dr. immediately. •1
