ALTERATIONS IN CARDIOVASCULAR FUNCTION

The Flow of Blood Through the Heart

Paediatric Differences
Infants heart are immature muscle fibers are less

developed distension of ventricles is not easily achieved. The heart is fully developed by 5yrs Systemic blood pressure reaches that of an adult by puberty Heart rate is high, due to infants high metabolic rate and oxygen requirements.

1. CONGENITAL HEART DISEASES

Congenital - Of or relating to a condition that is

present at birth, as a result of either heredity or environmental influences

Ususally- defects in the heart or great vessels or

persistence of a fetal structure after birth ductus arteriosus, foramen ovale

More than 35 types of heart defects have been

documented

Etiology
Fetal Exposure to drugs as phenytonin, lithium,

warfarin and alcohol Maternal viral infections as rubella Maternal metabolic disorders as DM Maternal complications of pregnancy as increased age and antepartum bleeding Genetic factors Chromosomal abnormalities as Turner syndrome, Marfan syndrome, Down syndrome

New Developments
Knowledge of genetic mutations associated with

cardiovascular defects are emerging

Deletion of the chromosome 22q11 has been found to be

associated with several congenital heart defects

Incidence will rise as people with defects survive

Classification of Congenital Heart Defects .1

Cyanotic Defects deoxygenated blood shunt from

the right side of the heart to the left side . Mixed blood thus enters the body
Acyanotic defects- oxygenated blood shunts for the

left side of the heart to the right side. Oxygenated blood goes to both right side of the heart and to the body.

Cyanotic Defects

Cyanotic Defects
Transposition of the great arteries

Truncus arteriosus
Tetralogy of Fallot Tricuspid Astresia

Total anomalous pulmonary venous return

Acyanotic Defects

Acyanotic Defects
Atrial Septal Defects(ASDs) Patent Foramen Ovale Secundum defects Sinus Venosus Primum Defects Ventricular Septal Defects (VSDs) Muscular VSD Membranous VSD Coronal Septal Defect AV canal Defect

Classification 2.
Those Increase pulmonary blood flow
Decrease pulmonary blood flow
Mixed defects Obstruct systemic blood flow

1. Defects That Increase Pulmonary Blood Flow (pg 751 handout)

The defect results in a connection between the left and

right side of the heart e.g. a septal or ventricular defect Blood flows between the left and right side of the heart since the pressure on the left side of the heart is greater , blood shunting from the left side to the right side increases the amount to the lungs Increased pulmonary vascular resistance ; increased pulmonary hypertension right ventricular hypertrophy to overcome increased pulmonary vascular resistance; congestive heart failure

Defects That Increase Pulmonary Blood Flow

Patent Ductus arterious

Atrial septal defect

Ventricular septal defect Atrioventricular canal defect

Truncus arteriosus
Total anomalous pulmonary venous return (see

video)

Clinical Manifestations
Tachypnea

Tachycardia
Heart murmur Poor weight gain

Diaphoresis when feeding

Periorbital edema Frequent respiratory infections

Signs of congestive heart failure; dyspnea, tachypnea,

periorbital edema

2. Defects Causing Decreased Pulmonary Blood Flow (758/table 21-4 handout)

These defects obstruct the pulmonary blood flow

resulting in little or no blood reaching the lung to get oxygenated. If an atrial or ventricular septal opening exists between the left and right side of the heart , right sided pressures exceed those on the left , resulting in right to left shunting cyanosis often results Polycythemia risks for thromboembolism Hypercyanotic episodes associated with increased cardiac output as in crying, feeding, exercise, warm baths, straining with defecation

 If a hypercyanotic episode occurs, the infant is placed in a

knee-chest position immediately The knee-chest position improves systemic arterial oxygen saturation by decreasing venous return so that smaller amounts of highly saturated blood reach the heart. Toddlers and children squat to get into this position and relieve chronic hypoxia. Additional interventions include administering 100% oxygen by face mask, morphine sulfate, and intravenous fluids, as prescribed.

Defects Causing Decreased Pulmonary Blood Flow

Pulmonic stenosis

Tetralogy of fallot
Pulmonary atresia Tricuspid atresia

Transposition of the great arteries (see video)

Clinical Manifestations
Cyanosis shortly after birth that does not respond

to oxygen Dyspnea Heart murmur Hypercyanotic episodes Poor weight gain Polycythemia

3. Defects Causing Mixed Defects (table 21-5)

A combination of defects that make the newborn

dependent upon mixing pulmonary and systemic circulations i.e. Oxygen saturated and de-saturated blood

Cyanosis Pulmonary congestion

Defects Causing Mixed Defects

Transposition of The Great Arteries

Total Anomalous pulmonary Venous Connection Truncus Arteriosus Double Outlet Right Ventricle

Clinical Manifestations
Cyanosis

Poor weight gain

Pulmonary congestion Congestive Heart Failure

4. Defects Obstructing Systemic Blood Flow (pg 766)

An anatomic stenosis of the aorta causes obstruction

to blood flow results in Pressure on the left ventricle is increased Decreased cardiac output

Defects Obstructing Systemic Blood Flow

Aortic stenosis

Coarctation of aorta
Hypoplastic left heart syndrome Mitral stenosis

Interrupted aortic arch

Clinical Manifestation
Diminished pulses

Poor colour
Delayed capillary refill time Congestive heart

Decreased urine output

Congestive heart failure Pulmonary oedema

Nursing Management
Nursing Assessment Height and weight. Plot on a growth chart Record vital signs and oxygen saturations Skin color: pink, cyanotic, mottle Mucous membranes: moist, dry, cyanotic. Extremities: check peripheral pulses for quality and symmetry; dependent edema; capillary refill; color and temperature. Assess for clubbing (cyanotic heart disease). Assess chest wall for deformities Auscultate for crackles, wheezing, congestion, stridor Identify murmur Assess and record the child's level of activity- play, feeding, developmental level: age-appropriate behavior, cognitive skills, gross and fine motor skills.

Nursing Management
Impaired Gas Exchange related to altered pulmonary

blood flow or pulmonary congestion Decreased Cardiac Output related to decreased myocardial function Imbalanced Nutrition: Less Than Body Requirements related to excessive energy demands required by increased cardiac workload Excess Fluid Volume r/t heart failure and pulmonary overload Ineffective Infant Feeding pattern r/t shortness of breath and fatigue

Nursing Management
Risk for infection related to pulmonary vascular congestion

and chronic illness Risk for infection related to surgery Interrupted family processes related to crisis of childs serious illness Decreased cardiac output related to ventricular restriction and an obstructed outflow tract Activity intolerance related to cyanosis and dyspnea on exertion Caregiver Role Strain related to care of a child with chronic illness Delayed growth and development related to congenital anomaly and hypoxemia

Interventions
Relieving Respiratory Distress Position the child in a reclining, semi-upright position. Suction oral and nasal secretions as needed. Identify target oxygen saturations and administer oxygen as prescribed. Administer prescribed medications and document response to medications (improved, no change, or worsening respiratory status).

Diuretics. Bronchodilators.

May need to change oral feedings to nasogastric feedings

because of increased risk of aspiration with respiratory distress.

Improving Cardiac Output

Organize nursing care and medication schedule to

provide periods of uninterrupted rest. Provide play or educational activities that can be done in bed with minimal exertion. Maintain normal temperature Administer medications as prescribed.

Diuretics (furosemide, spironolactone):

Give the medication at the same time each day. For older children, do not give a dose right before bedtime. Monitor the effectiveness of the dose: measure and record urine output.

Improving Cardiac Output

Digoxin:
Check heart rate for 1 minute. Withhold the dose and notify the physician for bradycardia (heart rate less than 90 beats/minute [bpm]). Lead II rythm strip may be ordered for PR interval monitoring. Prolonged PR interval indicates first-degree heart block (dose of digoxin may be withheld). Give medication at the same time each day. For infants and children, digoxin is usually divided and given twice per day. Monitor serum electrolytes. Increased incidence of digoxin toxicity associated with hypokalemia.

Afterload-reducing medications (captopril, enalapril):

When initiating medication for the first time: check BP immediately before and 1 hour after dose. Monitor for signs of hypotension: syncope, light-headedness, faint pulses. Withhold medication and notify the physician according to ordered parameters.

Improving Oxygenation and Activity Tolerance

Place pulse oximeter probe (continuous monitoring

or measure with vital signs) on finger, earlobe, or toe. Administer oxygen as needed. Assess response to oxygen therapy: increase in baseline oxygen saturations, improved work of breathing, and change in patient comfort. Explain to the child how oxygen will help. If possible, give the child the choice for face mask oxygen or nasal cannula oxygen.

Providing Adequate Nutrition

For the infant: Small, frequent feedings. Fortified formula or breast milk (up to 30 cal/oz). Limit oral feeding time to 15 to 20 minutes. Supplement oral feeds with nasogastric feedings as needed to provide weight gain (ie, continuous nasogastric feedings at night with ad-lib by-mouth feeds during the day).

Providing Adequate Nutrition

For the child:

Small, frequent meals. High-calorie, nutritional supplements. Determine child's likes and dislikes and plan meals accordingly. Allow the parents to bring the child's favorite foods to the hospital.

Report feeding intolerance: nausea, vomiting, diarrhea. Document daily weight (same time of day, same scale,

same clothing). Record accurate inputs and outputs; assess for fluid retention. Fluid restriction not usually needed for children; manage excess fluid with diuretics.

Preventing Infection
Maintain routine childhood immunization schedule.

Prevent exposure to communicable diseases.

Good hand washing. Report fevers.

Report signs of URI: runny nose, cough, increase in nasal

secretions. Report signs of GI illness: diarrhea, abdominal pain, irritability

Reducing Fear and Anxiety

Educate the patient and family.

Involve in plan of care

Allow to express fears and concerns Provide the family with contact phone numbers: how

to schedule a follow-up visit; how to reach a cardiologist during the work week, evenings, weekends, and holidays

Family Education and Health Maintenance

Instruct the family in necessary measures to

maintain the child's health:

Complete immunization. Adequate diet and rest. Prevention and control of infections. Regular medical and dental checkups. The child should be protected against infective endocarditis when undergoing certain dental procedures. Regular cardiac checkups

Family Education and Health Maintenance

Teach the family about the defect and its treatment. Provide patients and families with written and verbal information regarding the CHD. Offer appropriate Internet resources for information about CHD and medical and surgical treatment options. Signs of hypercyanotic spells associated with cyanotic defects and need to place child in knee-chest position. Need to prevent dehydration, which increases risk of thrombotic complications. Emergency precautions related to hypercyanotic spells, pulmonary edema, cardiac arrest (if appropriate). Special home care equipment, monitors, oxygen

Family Education and Health Maintenance

Encourage the parents and other people (teachers, peers) to

treat the child in as normal a manner as possible.

Avoid overprotection and overindulgence. Avoid rejection. Promote growth and development with modifications. Facilitate performance of the usual developmental tasks within the limits of the child's physiologic state. Prevent adults from projecting their fears and anxieties onto the child. Help family deal with its anger, guilt, and concerns related to the disabled child.

Stress the need for follow-up care. Encourage attendance in support groups for patients and

families

Congestive Heart Failure

A condition in which cardiac output is inadequate to support the bodys circulatory needs
Causes Pulmonary Venous Congestion Clinical Manifestation Tachypnea, wheezing, crackles,retratcions,cough,grunting, nasal flaring,feeding difficulties, irritability, tiring with play

Systemic venous congestion Impaired Cardiac Output

Hepatomegaly, ascites, peripheral edema Tachycardia, diminished pulses, hypotension, capillary refill time greater that 2 seconds, pallor, cold extremities, oliguria
Failure to thrive or slow weight gain

High metabolic rate

Pathophysiology
Blood volume overload due to congenital heart defects When ventricles contract, blood flows from the left to

right side of the heart so extra blood is pumped to the pulmonary system rather that through the aorta Overload can lead to pulmonary hypertension Obstructive conditions restrict flow of blood heart muscle hypertrophies Decreased cardiac output leads to insufficient nutrients and oxygen to body organs compensatory mechanisms E.g. The kidney activates the renin- angiotensin mechanism to retain salt and water Compensatory mechanisms usually lead to more stress on heart

CHF Manifestations

Diagnosis
Manifestations

Chest x-ray shows cardiomegaly

Electrocardiogram shows tachycardia, bradycardia

or ventricular hypertrophy

Medications Used
Drug Digoxin Furosemide Thiazides Action Increases myocardial contractibility Rapid Diuresis Maintenance diuresis, decreases absorption of sodium, water, potassium, chloride and bicarbonate in renal tubules Maintenance diuresis (potassium paring) Promotes vascular relaxation and reduced peripheral vascular resistance Increases contractibility Improves left ventricular function, promotes vasodilation of systemic circulation for chronic heart failure and dilated cardiomyopathy

Spironalactone Angiotensin converting enzyme (ACE) inhibitor Propanolol Carvedilol

 SEE NURSING CARE PLAN FOR CHF HANDOUT

PAGE 771-776

ACQUIRED HEART DISEASES

Rheumatic Fever

Infective Endocarditis
Kawasaki Disease

RHEUMATIC FEVER
Autoimmune consequence of infection with Group A

streptococcal infection

Results in a generalised inflammatory response-

inflammatory lesions of connective tissue and endothelial tissue, primarily affecting the joints and heart also brain, skin, subcutaneous tissues

The clinical presentation can be vague and difficult to

diagnose.

RHEUMATIC HEART DISEASE

Rheumatic Heart Disease is the permanent heart

valve damage resulting from one or more attacks of ARF. It is thought that 40-60% of patients with ARF will go on to developing RHD. The commonest valves affecting are the mitral and aortic, in that order. However all four valves can be affected

Cause/ Pathophysiology
Hypothesis autoimmune response to the M proteins in

the strep organism affects heart, joints etc. In a child that is genetically pre-disposed Autoantibodies attack the myocardium, pericardium, and cardiac valves. Leading to valvular lesions 1-3 weeks after untreated strep infection, Aschoff bodies ( hemorrhagic bullous lesions) develop on the valves, possibly leading to permanent valve dysfunction, especially of the mitral and aortic valves. Inflammation of the large joints causes a painful arthritis that may last 6 to 8 weeks. Involvement of the nervous system causes chorea (sudden involuntary movements

Cause/ Pathophysiology
Acute rheumatic heart disease often produces a pancarditis

characterized by endocarditis, myocarditis, and pericarditis. The mitral valve is most commonly and severely affected (6570% of patients), and the aortic valve is second in frequency (25%). The tricuspid valve is deformed in only 10% of patients and is almost always associated with mitral and aortic lesions. The pulmonary valve is rarely affected. Pericarditis, when present, rarely affects cardiac function or results in constrictive pericarditis

Cause/ Pathophysiology
Fusion of the valve apparatus resulting in stenosis or

a combination of stenosis and insufficiency develops 2-10 years after an episode of acute rheumatic fever, and recurrent episodes may cause progressive damage to the valves.
Rheumatic heart disease is responsible for 99% of

mitral valve stenosis in adults in the United States

Mortality/Morbidity

Variables that correlate with severity of valve disease include

the

number of previous attacks of rheumatic fever, the length of time between the onset of disease and start of therapy sex.

The disease is more severe in females than in males.

Clinical Presentation
A diagnosis of rheumatic heart disease is made after

confirming antecedent rheumatic fever.

The presence of 2 major or 1 major and 2 minor criteria for

the diagnosis of rheumatic fever.

The major diagnostic criteria include carditis, polyarthritis,

chorea, subcutaneous nodules, and erythema marginatum.

Clinical Presentation
The minor diagnostic criteria include fever,

arthralgia, prolonged PR interval on ECG, elevated acute phase reactants (increased erythrocyte sedimentation rate, presence of C-reactive protein, and leukocytosis. One of the following must be present: -Positive throat culture or rapid streptococcal antigen test result -Elevated or rising streptococcal antibody titer -History of previous rheumatic fever or rheumatic heart disease

CARDIAC MANIFESTATIONS
Pancarditis is the most serious and second most

common complication of rheumatic fever (50%). In advanced cases, patients may complain of dyspnea, mild-to-moderate chest discomfort, pleuritic chest pain, edema, cough, or orthopnea. Upon physical examination, carditis is most commonly detected by a new murmur and tachycardia out of proportion to fever (18bpm per degree rise in temp). New or changing murmurs are considered necessary for a diagnosis of rheumatic valvulitis. Other cardiac manifestations include congestive heart failure and pericarditis.

CARDIAC MANIFESTATIONS OF CHRONIC RHD

Valve deformities, thromboembolism, hemolytic

anemia, atrial arrhythmias are the most common Progressive fibrosis (i.e., thickening and calcification of the valve) takes place over time, resulting in enlargement of the left atrium and formation of mural thrombi in that chamber, leads to stenosis The stenotic valve is funnel-shaped, with a "fish mouth" resemblance..

NON CARDIAC MANIFESTATIONS

polyarthritis, chorea, erythema marginatum, and

subcutaneous nodules.
Other clinical, noncardiac manifestations

include abdominal pain, arthralgias, epistaxis, fever, and rheumatic pneumonia.

Lab Studies
Throat culture
Throat

culture findings for group A beta hemolytic Streptococcus are usually negative by the time symptoms of rheumatic fever or rheumatic heart disease appear.
test allows rapid detection of group A streptococcal antigen and allows the diagnosis of streptococcal pharyngitis and the initiation of antibiotic therapy

Rapid antigen detection test

This

Lab Studies
Antistreptococcal antibodies

The clinical features of rheumatic fever begin at the time antistreptococcal antibody levels are at their peak.
The elevated level of antistreptococcal antibodies is useful, particularly in patients that present with chorea as the only diagnostic criterion. Antibody titers should be checked at 2-week intervals in order to detect a rising titer.

Lab Studies
Acute phase reactants

C-reactive protein and erythrocyte sedimentation rate are elevated in rheumatic fever due to the inflammatory nature of the disease. Heart reactive antibodies Tropomyosin is elevated in acute rheumatic fever.

The

IMAGING STUDIES
Chest roentgenography
Cardiomegaly,

pulmonary congestion, and other findings consistent with heart failure may be seen on chest radiography.
the patient has fever and respiratory distress, chest radiography helps differentiate heart failure from rheumatic pneumonia.

When

Imaging Studies
Doppler-echocardiogram Identifies valve insufficiency and ventricular dysfunction. With mild carditis, Doppler evidence of mitral regurgitation may be present during the acute phase of disease but resolves in weeks to months.

Heart catheterization

In acute rheumatic heart disease, this procedure is not indicated. With chronic disease, heart catheterization has been performed to evaluate mitral and aortic valve disease and to balloon stenotic mitral valves.

OTHER TESTS
On ECG, sinus tachycardia most frequently

accompanies acute rheumatic heart disease.. First-degree atrioventricular (AV) block (prolongation of the PR interval) is observed in some patients. - a nonspecific finding and should not be used as a criterion for the diagnosis of rheumatic heart disease
Second-degree (intermittent) and third-degree (complete)

AV block with progression to ventricular standstill have been described

HISTOLOGIC FINDINGS
Pathologic examination of the insufficient valves may

reveal verrucous lesions at the line of closure . Aschoff bodies are found in the pericardium, perivascular regions of the myocardium, and endocardium.

TREATMENT AND MANAGEMENT

Medical therapy in rheumatic heart disease includes

attempts to prevent rheumatic fever (and thus rheumatic heart disease). In patients who develop rheumatic heart disease, therapy is directed toward eliminating the group A streptococcal pharyngitis (if still present), suppressing inflammation from the autoimmune response, and providing supportive treatment for congestive heart failure. Following the resolution of the acute episode, subsequent therapy is directed towards preventing recurrent rheumatic heart disease in children and monitoring for the complications

Prevention of rheumatic fever in patients with group A beta hemolytic streptococci (GABHS) pharyngitis
Oral (PO) penicillin V remains the drug of choice for

treatment of GABHS pharyngitis, but ampicillin and amoxicillin are equally effective. When PO penicillin is not feasible or dependable, a single dose of intramuscular benzathine penicillin G or benzathine/procaine penicillin combination is therapeutic. For patients who are allergic to penicillin, administer erythromycin or a first-generation cephalosporin. Other options include clarithromycin for 10 days, azithromycin for 5 days, or a narrow-spectrum (firstgeneration) cephalosporin for 10 days. As many as 15% of patients who are allergic to penicillin are also allergic to cephalosporins.

Prevention of rheumatic fever in patients with group A beta hemolytic streptococci (GABHS) pharyngitis
For recurrent group A streptococci (GAS) pharyngitis, a second 10-day

course of the same antibiotic may be repeated. Control measures for patients with GABHS pharyngitis are as follows: Hospitalized patients: Place hospitalized patients with GABHS pharyngitis of pneumonia on droplet precautions, as well as standard precautions, until 24 hours after initiation of appropriate antibiotics. Exposed persons: People in contact with patients having documented cases of streptococcal infection first should undergo appropriate laboratory testing if they have clinical evidence of GABHS infection and should undergo antibiotic therapy if infected. School and childcare centers: Children with GABHS infection should not attend school or childcare centers for the first 24 hours after initiating antimicrobial therapy.

Treatment of the acute inflammatory manifestations of acute rheumatic fever

Aspirin in anti-inflammatory doses effectively reduces all

manifestations of the disease except chorea. If rapid improvement is not observed after 24-36 hours of therapy, question the diagnosis of rheumatic fever. Maintain aspirin at anti-inflammatory doses until the signs and symptoms of acute rheumatic fever are resolved or residing (6-8 wk) and the acute phase reactants (APRs) have returned to normal. Anti-inflammatory doses of aspirin may be associated with abnormal liver function tests and GI toxicity, and adjusting the aspirin dosage may be necessary. When discontinuing therapy, withdraw aspirin gradually over weeks while monitoring the APRs for evidence of rebound. Chorea is most frequently self-limited but may be alleviated or partially controlled with phenobarbital or diazepam

Treatment of the acute inflammatory manifestations of acute rheumatic fever

If moderate to severe carditis is present as indicated by

cardiomegaly, third-degree heart block or congestive heart failure, substitute PO prednisone for salicylate therapy.
Continue prednisone for 2-6 weeks depending on the severity of the

carditis, and taper prednisone during the final week(s) of therapy.

Include digoxin and diuretics, supplemental oxygen, bed rest, and

sodium and fluid restriction as additional treatment for patients with acute rheumatic fever and heart failure.
The diuretics most commonly used in conjunction with digoxin for

children with heart failure include furosemide and spironolactone.

Initiate digoxin only after checking electrolytes and correcting

hypokalemia

Treatment for patients following rheumatic heart disease (RHD)

Preventive

and prophylactic therapy is indicated after rheumatic fever and acute rheumatic heart disease to prevent further damage to valves.

Primary

prophylaxis (initial course of antibiotics administered to eradicate the streptococcal infection) also serves as the first course of secondary prophylaxis (prevention of recurrent rheumatic fever and rheumatic heart disease).

Treatment for patients following rheumatic heart disease (RHD)

An injection of 0.6-1.2 million units of benzathine penicillin G intramuscularly every 4 weeks is the recommended regimen for secondary prophylaxis Although PO penicillin prophylaxis is also effective, data from the World Health Organization indicate that the recurrence risk of GABHS pharyngitis is lower when penicillin is administered parentally

The duration of antibiotic prophylaxis is controversial.

Treatment for patients following rheumatic heart disease (RHD

Continue antibiotic prophylaxis indefinitely for patients at high risk (eg, health care workers, teachers, daycare workers) for recurrent GABHS infection. Patients with rheumatic fever with carditis and valve disease should receive antibiotics for at least 10 years or until age 40 years depending on the time of the last episode of ARF and whether they have RHD or not.

Treatment for patients following rheumatic heart disease (RHD)

Patients with rheumatic heart disease and valve damage

require a single dose of antibiotics 1 hour before surgical and dental procedures to help prevent bacterial endocarditis.
Patients who had rheumatic fever without valve damage do not

need endocarditis prophylaxis.

Do not use penicillin, ampicillin, or amoxicillin for

endocarditis prophylaxis in patients already receiving penicillin for secondary rheumatic fever

Surgical Care
When heart failure persists or worsens after aggressive

medical therapy for acute rheumatic heart disease, surgery to decrease valve insufficiency may be lifesaving.
In patients with critical stenosis, mitral valvulotomy,

percutaneous balloon valvuloplasty, or mitral valve replacement may be indicated.

Nursing Management
Nursing Assessment Assess for signs of cardiac involvement by auscultation of the heart for murmur and cardiac monitoring for prolonged PR interval. Monitor pulse for 1 full minute to determine heart rate. Assess temperature for elevation. Observe for involuntary movements: stick out tongue or smile; garbled or hesitant speech when asked to recite numbers or the ABCs; hyperextension of the wrists and fingers when trying to extend arms. Assess child's ability to feed self, dress, and do other activities if chorea or arthritis present. Assess pain level using scale appropriate for child's age. Assess parents' ability to cope with illness and care for child. Assess need for home schooling while patient is on bed rest.

Nursing Diagnoses
Decreased Cardiac Output related to carditis

Acute and Chronic Pain related to arthritis

Risk for Injury related to chorea

Nursing Interventions
Improving Cardiac Output Explain to the child and family the need for bed rest during the acute phase (approximately 2 weeks) and as long as CHF is present. In milder cases, light indoor activity is allowed. In severe cases, organize care so that the child will not have to exert self and will have hours of uninterrupted rest. Maintain cardiac monitoring if indicated. Administer course of antibiotics as directed. Be alert to adverse effects, such as nausea, vomiting, and GI distress. Administer medications for CHF as directed. Monitor BP, intake and output, and heart rate

Relieving Pain
Administer anti-inflammatory medication, analgesics, and

antipyretics as directed. Monitor for signs of aspirin toxicity, such as tinnitus, nausea and vomiting, and headache. Monitor for signs of corticosteroid use- GI distress, acne, weight gain, emotional disturbances or long-term effects, such as rounded face, ulcer formation, and decreased resistance to infection. Administer all anti-inflammatory medications with food to reduce GI injury. Be aware that anti-inflammatories may not alter the course of myocardial injury.

Relieving Pain
Teach family the importance of maintaining dosage

schedule, continuing medication until all signs and symptoms of the ARF have gone, and tapering the dose as directed by health care provider. Assist child with positioning for comfort and protecting inflamed joints. Suggest diversional activities that do not require use of painful joints Cold compresses reduce joint swelling and inflammation, helps ease inflammation and pain. Heat compresses relax your muscles and stimulate blood flow.

Protecting the Child with Chorea

Use padded side rails if chorea is severe. Assist with feeding and other fine-motor activities as needed. Assist with ambulation if weak. Avoid the use of straws and sharp utensils if chorea involves

the face. Make sure that child consumes nutritious diet with recommended vitamins, protein, and calories. Be patient if speech is affected, and offer emotional support. Protect the child from stress. Administer phenobarbital or other medication for chorea as directed. Observe for drowsiness

Family Education and Health Maintenance

Teach the appropriate administration of all

medications, including prophylactic antibiotic. Encourage all family and household members to be screened for streptococcus and receive the appropriate treatment. Instruct on additional prophylaxis for endocarditis with dental procedures and surgery as indicated. Encourage following activity restrictions, resuming activity gradually, and resting whenever tired.

Family Education and Health Maintenance

Encourage keeping appointments for follow-up evaluation

by cardiologist and other health care providers. Advise the parents that child cannot return to school until health care provider assesses that all disease activity is gone. Parents may need to discuss with teachers how the child can catch up with schoolwork. Instruct on follow-up with usual health care provider for immunizations, well-child evaluations, hearing and vision screening, and other health maintenance needs. Provide general health education about early identification and treatment seeking for any possible streptococcal infection (fever, sore throat). Compliance with 10 to 14 days of antibiotics can greatly reduce the risk of ARF and other poststreptococcal sequelae

Infective Endocarditis
Inflammation of the lining , valves and arterial vessels of

the heart Caused bacterial/fungal Risk children with CHD, RHD, artificial valve, central venous catheters Symptoms- fever, fatigue, weakness, joint and muscle pains, weight loss and diaphoresis, Signs- new or changing heart murmur, CHF, dyspnea, hematuria, petechia, conjuctival haemorrhage S&S may be mild and develop slowly or rapid

Diagnosis
Blood culture

Elevated ESR, C-protein, WBC

Anemia Alterations in ECG

Heart murmurs

Treatment
IV Antibiotics- penicillin G or others depending on

C&S 2-8 weeks Serum levels are monitored Valve placement surgery if necessary Treat CHF

Nursing Management
Monitor child's respiratory and cardiovascular

status, oxygen saturation Administer meds as prescribed Monitor effects and side effects of meds Aseptic techniques when performing invasive procedures- keep to minimum Bed rest Age appropriate activities Follow up on discharge

Prevention
Children at risk should

Be encouraged to have continuous dental care

Discouraged from body piercing and tattoos

Kawasaki Disease
Inflammation in the walls of small- and medium-

sized arteries throughout the body, including the coronary arteries Kawasaki disease is also called mucocutaneous lymph node syndrome because it also affects lymph nodes, skin, and the mucous membranes inside the mouth, nose and throat. Cause- unknown Hypothesized genetic pre-disposition

Manifestations
Acute stage- fever, irritability, conjuctival hyperemia,

red throat, swollen hands and feet, rash on trunk, enlarged cervical lymph nodes, diarrhoea Subacute stage cracking lips, fissures, desquamation of the skin on tips of fingers and toes 10 days after fever, joint pain, cardiac disease thrombocytosis Convalescent stage - 6-8 weeks after disease , lingering signs of inflammation but child is normal

Risk factors
Age. Children under 5 years old are most at risk of

Kawasaki disease. Sex. Boys are slightly more likely than girls are to develop Kawasaki disease. Ethnicity. Children of Asian descent, such as Japanese or Korean, have higher rates of Kawasaki disease.

Diagnosis
Fever of 39 degrees Celsius for 5 days or longer along

with 4 of the 5 Changes in extremities as erythema of palms, oedema of feet Changes in lips and oral cavity,dry peeling, cracking lips, strawberry tongue, diffuse erythema of the buccal and pharyngeal mucosa Conjuctival redness without exudates painless Maculopapular rash on trunk and extremities Cervical lymphadenopathy

Treatment
Hospitalisation 3-4 days

IV Immunoglobulin reduces incidence of coronary

artery lesions High doses of aspirin may help treat inflammation. Aspirin can also decrease pain and joint inflammation, as well as reduce the fever. Kawasaki treatment is a rare exception to the rule against aspirin use in children

After the initial treatment

low-dose aspirin for as long as six to eight weeks, and

longer if child develops a coronary artery aneurysm. Aspirin helps prevent clotting.

Complications
Kawasaki disease is a leading cause of acquired heart

disease in children Heart complications include: Inflammation of the heart muscle (myocarditis) Heart valve problems (mitral regurgitation) Abnormal heart rhythm (dysrhythmia) Inflammation of blood vessels (vasculitis), usually the coronary arteries, that supply blood to the heart

Nursing Management
Risk for Imbalanced body temperature

Impaired oral mucous membranes

Impaired skin Integrity Altered comfort

Altered nutrition
Interrupted family processes

Interventions
Administer meds monitor fro bleeding

Promote comfort- keep skin clean and dry, lubricate

lips, tepid sponge, change clothes and linen frequently Small feeding, cool drinks Passive range of motion exercises Plan rest periods Age appropriate activities Encourage visit and participation of care by parents Follow up care

THATS ALL FOLKS

References
Paediatric Nursing . Caring For Children. Ball and Binder 4th edition Lipincott Manual For Nursing Practice 8th Edition