ALTERATIONS IN CARDIOVASCULAR FUNCTION

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 5yrsSystemic blood pressure reaches that of an adult by pubertyHeart 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 documentedEtiologyFetal Exposure to drugs as phenytonin, lithium, warfarin and alcoholMaternal viral infections as rubellaMaternal metabolic disorders as DMMaternal complications of pregnancy as increased age and antepartum bleedingGenetic factorsChromosomal abnormalities as Turner syndrome, Marfan syndrome, Down syndromeNew DevelopmentsKnowledge 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 .1Cyanotic 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 DefectsTransposition of the great arteriesTruncus arteriosusTetralogy of Fallot Tricuspid AstresiaTotal anomalous pulmonary venous return

Acyanotic Defects

Acyanotic DefectsAtrial Septal Defects(ASDs)Patent Foramen OvaleSecundum defectsSinus VenosusPrimum DefectsVentricular Septal Defects (VSDs)Muscular VSDMembranous VSDCoronal Septal DefectAV canal DefectClassification 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 defectBlood 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 failureDefects That Increase Pulmonary Blood FlowPatent Ductus arteriousAtrial septal defectVentricular septal defectAtrioventricular canal defect Truncus arteriosusTotal anomalous pulmonary venous return (see video)Clinical ManifestationsTachypneaTachycardiaHeart murmurPoor weight gain Diaphoresis when feedingPeriorbital edemaFrequent respiratory infectionsSigns of congestive heart failure; dyspnea, tachypnea, periorbital edema2. 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 positionimmediatelyThe 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.Additionalinterventions include administering 100% oxygen by face mask, morphine sulfate, and intravenous fluids,as prescribed.Defects Causing Decreased Pulmonary Blood FlowPulmonic stenosisTetralogy of fallot Pulmonary atresiaTricuspid atresiaTransposition of the great arteries (see video) Clinical ManifestationsCyanosis shortly after birth that does not respond to oxygen Dyspnea Heart murmurHypercyanotic episodes Poor weight gainPolycythemia 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 DefectsTransposition of The Great ArteriesTotal Anomalous pulmonary Venous Connection Truncus ArteriosusDouble Outlet Right VentricleClinical ManifestationsCyanosisPoor weight gainPulmonary congestion Congestive Heart Failure4. 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 increasedDecreased cardiac output Defects Obstructing Systemic Blood FlowAortic stenosisCoarctation of aortaHypoplastic left heart syndromeMitral stenosisInterrupted aortic arch

Clinical ManifestationDiminished pulsesPoor colourDelayed capillary refill timeCongestive heart Decreased urine outputCongestive heart failurePulmonary oedemaNursing Management Nursing AssessmentHeight and weight. Plot on a growth chartRecord vital signs and oxygen saturationsSkin color: pink, cyanotic, mottleMucous 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 deformitiesAuscultate for crackles, wheezing, congestion, stridorIdentify 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 congestionDecreased Cardiac Output related to decreased myocardial functionImbalanced Nutrition: Less Than Body Requirements related to excessive energy demands required by increased cardiac workloadExcess Fluid Volume r/t heart failure and pulmonary overloadIneffective Infant Feeding pattern r/t shortness of breath and fatigue Nursing Management Risk for infection related to pulmonary vascular congestion and chronic illnessRisk for infection related to surgery Interrupted family processes related to crisis of childs serious illnessDecreased cardiac output related to ventricular restriction and an obstructed outflow tract Activity intolerance related to cyanosis and dyspnea on exertionCaregiver Role Strain related to care of a child with chronic illnessDelayed growth and development related to congenital anomaly and hypoxemiaInterventionsRelieving Respiratory DistressPosition 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 OutputOrganize 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 temperatureAdminister 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 OutputDigoxin: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 TolerancePlace 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 NutritionFor 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 NutritionFor 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 InfectionMaintain 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 careAllow to express fears and concernsProvide 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

38Family Education and Health MaintenanceInstruct 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 MaintenanceTeach 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 MaintenanceEncourage 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 FailureA condition in which cardiac output is inadequate to support the bodys circulatory needs

CausesClinical ManifestationPulmonary Venous CongestionTachypnea, wheezing, crackles,retratcions,cough,grunting, nasal flaring,feeding difficulties, irritability, tiring with playSystemic venous congestionHepatomegaly, ascites, peripheral edemaImpaired Cardiac OutputTachycardia, diminished pulses, hypotension, capillary refill time greater that 2 seconds, pallor, cold extremities, oliguriaHigh metabolic rateFailure to thrive or slow weight gain PathophysiologyBlood 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 hypertensionObstructive 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 waterCompensatory mechanisms usually lead to more stress on heart

CHFManifestations

Diagnosis ManifestationsChest x-ray shows cardiomegalyElectrocardiogram shows tachycardia, bradycardia or ventricular hypertrophy Medications UsedDrugActionDigoxinIncreases myocardial contractibilityFurosemideRapid DiuresisThiazidesMaintenance diuresis, decreases absorption of sodium, water, potassium, chloride and bicarbonate in renal tubules SpironalactoneMaintenance diuresis (potassium paring)Angiotensin converting enzyme (ACE) inhibitorPromotes vascular relaxation and reduced peripheral vascular resistancePropanololIncreases contractibilityCarvedilolImproves left ventricular function, promotes vasodilation of systemic circulation for chronic heart failure and dilated cardiomyopathy SEE NURSING CARE PLAN FOR CHF HANDOUT PAGE 771-776ACQUIRED HEART DISEASESRheumatic FeverInfective EndocarditisKawasaki Disease

RHEUMATIC FEVERAutoimmune 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 DISEASERheumatic 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 lesions1-3 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 (65-70% 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 MANIFESTATIONSPancarditis 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 RHDValve deformities, thromboembolism, hemolytic anemia, atrial arrhythmias are the most commonProgressive 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 stenosisThe stenotic valve is funnel-shaped, with a "fish mouth" resemblance..

Aortic stenosis from chronic rheumatic heart disease is typically associated with aortic insufficiency. The valve commissures and cusps become adherent and fused, and the valve orifice becomes small with a round or triangular shape.Upon auscultation, S2 may be single because the aortic leaflets are immobile and do not produce an aortic closure sound. The systolic and diastolic murmurs of aortic valve stenosis and insufficiency are heard best at the base of the heart. Thromboembolism occurs as a complication of mitral stenosis. It is more likely to occur when the left atrium is dilated, cardiac output is decreased, and the patient is in atrial fibrillationCardiac hemolytic anemia is related to disruption of the RBCs by a deformed valve. Increased destruction and replacement of platelets also may occur. Atrial arrhythmias are typically related to a chronically enlarged left atrium. Successful cardioversion of atrial fibrillation to sinus rhythm is more likely to be successful if the left atrium is not markedly enlarged, the mitral stenosis is mild, and the patient has been in atrial fibrillation for less than 6 months.

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NON CARDIAC MANIFESTATIONSpolyarthritis, chorea, erythema marginatum, and subcutaneous nodules.

Other clinical, noncardiac manifestations include abdominal pain, arthralgias, epistaxis, fever, and rheumatic pneumonia.

Erythema marginatum, also known as erythema annulare, is a characteristic rash that occurs in 5-13% of patients with acute rheumatic fever.It begins as 1-3 cm in diameter, pink-to-red nonpruritic macules or papules located on the trunk and proximal limbs but never on the face. The lesions spread outward to form a serpiginous ring with erythematous raised margins and central clearing. The rash may fade and reappear within hours and is exacerbated by heat. If the lesions are not well visualized, they can be accentuated by the application of warm towels, a hot bath, or the use of tangential lighting. The rash occurs early in the course of the disease and remains long past the resolution of other symptomsSubcutaneous nodules are currently an infrequent manifestation of rheumatic fever. When present, the nodules appear over the extensor surfaces of the elbows, knees, ankles, knuckles, and on the scalp and spinous processes of the lumbar and thoracic vertebrae where they are attached to the tendon sheath. They are firm, nontender, and free from attachments to the overlying skin and range in size from a few mm to 1-2 cm. They vary in number from one to dozens (mean 3-4). Subcutaneous nodules generally occur several weeks into the disease and resolve within a month. These nodules are strongly associated with severe rheumatic carditis, and, in the absence of carditis, the diagnosis of subcutaneous nodules should be questioned. Abdominal pain usually occurs at the onset of acute rheumatic fever. This pain resembles abdominal pain from other conditions with acute microvascular mesenteric inflammation and may mimic acute appendicitis. Epistaxis may be associated with severe protracted rheumatic carditis.Fevers above 39C with no characteristic pattern are initially present in almost every case of acute rheumatic fever. Patients with rheumatic pneumonia present with the same signs as patients with infectious pneumonia.Rheumatic pneumonia should be differentiated from respiratory distress related to congestive heart failure

61Lab Studies Throat cultureThroat culture findings for group A beta hemolytic Streptococcus are usually negative by the time symptoms of rheumatic fever or rheumatic heart disease appear. Rapid antigen detection testThis test allows rapid detection of group A streptococcal antigen and allows the diagnosis of streptococcal pharyngitis and the initiation of antibiotic therapyLab Studies Antistreptococcal antibodiesThe 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.

The most common extracellular antistreptococcal antibodies tested include antistreptolysin O (ASO), antideoxyribonuclease (DNAse) B, antihyaluronidase, antistreptokinase, antistreptococcal esterase, and anti-DNA.

63Lab Studies Acute phase reactantsThe C-reactive protein and erythrocyte sedimentation rate are elevated in rheumatic fever due to the inflammatory nature of the disease. Heart reactive antibodiesTropomyosin is elevated in acute rheumatic fever.

IMAGING STUDIESChest roentgenographyCardiomegaly, pulmonary congestion, and other findings consistent with heart failure may be seen on chest radiography.

When the patient has fever and respiratory distress, chest radiography helps differentiate heart failure from rheumatic pneumonia.

Imaging StudiesDoppler-echocardiogramIdentifies 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 catheterizationIn 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 TESTSOn 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 diseaseSecond-degree (intermittent) and third-degree (complete) AV block with progression to ventricular standstill have been described

HISTOLOGIC FINDINGSPathologic 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 MANAGEMENTMedical 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 complicationsPrevention of rheumatic fever in patients with group A beta hemolytic streptococci (GABHS) pharyngitisOral (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 (first-generation) 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) pharyngitisFor 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 feverAspirin 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 feverIf 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 (RHDContinue 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 CareWhen heart failure persists or worsens after aggressive medical therapy for acute rheumatic heart disease, surgery to decrease valve insufficiency may be life-saving.

In patients with critical stenosis, mitral valvulotomy, percutaneous balloon valvuloplasty, or mitral valve replacement may be indicated.

Nursing ManagementNursing AssessmentAssess 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 DiagnosesDecreased Cardiac Output related to carditisAcute and Chronic Pain related to arthritisRisk for Injury related to chorea

Nursing InterventionsImproving Cardiac OutputExplain 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 PainAdminister 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 PainTeach 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 jointsCold compresses reduce joint swelling and inflammation, helps ease inflammation and pain.Heat compresses relax your muscles and stimulate blood flow.

Protecting the Child with ChoreaUse 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 MaintenanceTeach 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 MaintenanceEncourage 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 EndocarditisInflammation of the lining , valves and arterial vessels of the heartCaused bacterial/fungalRisk children with CHD, RHD, artificial valve, central venous cathetersSymptoms- fever, fatigue, weakness, joint and muscle pains, weight loss and diaphoresis,Signs- new or changing heart murmur, CHF, dyspnea, hematuria, petechia, conjuctival haemorrhageS&S may be mild and develop slowly or rapid DiagnosisBlood cultureElevated ESR, C-protein, WBCAnemiaAlterations in ECGHeart murmursTreatment IV Antibiotics- penicillin G or others depending on C&S 2-8 weeksSerum levels are monitoredValve placement surgery if necessaryTreat CHF Nursing ManagementMonitor child's respiratory and cardiovascular status, oxygen saturation Administer meds as prescribedMonitor effects and side effects of medsAseptic techniques when performing invasive procedures- keep to minimum Bed restAge appropriate activitiesFollow up on dischargePreventionChildren at risk shouldBe encouraged to have continuous dental careDiscouraged from body piercing and tattoosKawasaki DiseaseInflammation 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- unknownHypothesized genetic pre-dispositionManifestationsAcute stage- fever, irritability, conjuctival hyperemia, red throat, swollen hands and feet, rash on trunk, enlarged cervical lymph nodes, diarrhoeaSubacute stage cracking lips, fissures, desquamation of the skin on tips of fingers and toes 10 days after fever, joint pain, cardiac disease thrombocytosisConvalescent stage - 6-8 weeks after disease , lingering signs of inflammation but child is normal Risk factorsAge. 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.

DiagnosisFever of 39 degrees Celsius for 5 days or longer along with 4 of the 5Changes in extremities as erythema of palms, oedema of feetChanges in lips and oral cavity,dry peeling, cracking lips, strawberry tongue, diffuse erythema of the buccal and pharyngeal mucosaConjuctival redness without exudates painlessMaculopapular rash on trunk and extremitiesCervical lymphadenopathyTreatmentHospitalisation 3-4 daysIV Immunoglobulin reduces incidence of coronary artery lesionsHigh 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. ComplicationsKawasaki disease is a leading cause of acquired heart disease in childrenHeart 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 ManagementRisk for Imbalanced body temperatureImpaired oral mucous membranesImpaired skin IntegrityAltered comfortAltered nutrition Interrupted family processesInterventionsAdminister meds monitor fro bleedingPromote comfort- keep skin clean and dry, lubricate lips, tepid sponge, change clothes and linen frequentlySmall feeding, cool drinks Passive range of motion exercisesPlan rest periodsAge appropriate activitiesEncourage visit and participation of care by parentsFollow up care THATS ALL FOLKS

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