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Presentation on theme: "NURSING CARE OF THE CHILD WITH A CARDIOVASCULAR DISEASE"— Presentation transcript:


History Physical assessment general appearance pulse, blood pressure, & respirations *Review the normal anatomy of the heart. Figure 41-1. History: Heart disease in the newborn may or may not be recognized before birth (during prenatal testing) or even during the newborn period while the baby is still in the hospital. Because the newborn with cardiac problems will be tachycardic and tachypneic, the baby may first present to the pediatrician’s office due to poor feeding (due to fatigue and difficulty breathing). Questions to ask the parents during the newborn period include those related to the baby’s feeding patterns and those related to the mother’s pregnancy history (maternal infections, medication use during pregnancy, and any radiation exposure). With older children, the main symptom may be complaints of fatigue. Ask the parents how much activity it takes before the child becomes tired and has to rest. Also, what position does the child assume when resting? Infants with congenital heart disease usually prefer a knee-chest position, while older children will assume a squatting position (these positions trap blood in the lower extremities because of the sharp bend at the knee and hip, allowing the child to oxygenate the blood remaining the upper body more effectively). Other questions for the parents include inquiring about the frequency of infections (children with congenital heart disorders are more susceptible to lower respiratory tract infections), amount of perspiration (if any), voiding behaviors & number of wet diapers, the presence of any edema and/or cyanosis, history of nosebleeds and/or headaches, and complaints of “growing pains” (pain in the legs on running). Because some congenital heart disorders are genetic, be sure to ask about any family history of congenital heart disorders. Physical Assessment: The physical assessment begins with measuring height and weight, comparing it to the standard growth chart (looking for signs of failure to thrive). The general appearance assessment then focuses on the body systems that would be affected by a heart disorder. (See picture, pg 1231). Vital signs are assessed. The presence of any heart murmur is also discussed with the parents. “Innocent” murmurs are murmurs of no significance and are sometimes referred to as “functional” murmurs. A murmur associated with a congenital heart defect is termed an “organic” murmur. Children with innocent heart murmurs are not restricted in activity and does not require any further diagnostic testing or treatment (innocent murmurs are not a prelude to heart disease). Organic murmurs will require monitoring by a physician. (See table 41-2: comparison of innocent and organic murmurs).

Diagnostic tests Electrocardiogram Radiography Echocardiography Phonocardiography & magnetic resonance imaging Exercise testing Laboratory tests Read slide. Should be familiar with from BMS.

Defects with increased pulmonary blood flow Ventricular Septal Defect Opening between ventricles S/S 4-8 weeks, fatigue and harsh murmur Therapeutic management Most close spontaneously, those that don’t require open heart surgery Figure 41.8 VSDs are the most common congenital cardiac defect. VSD…with pressure in the LV being greater than that in the RV, blood will shunt from left to right across the septum; resulting in blood that should go into aorta being shunted back in the pulmonary circulation making the heart pump it AGAIN into the lungs and increasing the size of the right ventricle. S/S: Most of the time, VSD is not diagnosed at birth. Usually at about 4-8 weeks of age, the infant begins to demonstrate signs of fatigue and develops a loud harsh murmur (that is evident along the left sternal border at the third or fourth intercostal space. Diagnosis is usually made by echocardiogram or MRI. Therapeutic management: Most of the VSDs close spontaneously (small ones). Other larger VSDs may require open heart surgery before the age of 2 years. Postoperatively, the child may receive prophylactic antibiotics to prevent endocarditis for up to 6 months after surgery.

5 Defects with increased pulmonary blood flow
Atrial Septal Defect Opening between the atria S/S Murmur, second heart sound splitting Management Surgery Figure 41.9 ASD…There is an abnormal opening between the two atria, allowing blood to shift from left to right atrium causing the atrium to hypertrophy and eventually leading to RV enlargement (due to the RV handling twice the amount of blood flow than normal). S/S of ASD include a harsh systolic murmur heard over the pulmonic area (due to the extra amount of blood crossing the pulmonic valve) and splitting of the second heart sound. DX is made by echocardiogram or cardiac catheterization. Treatment centers around open heart surgery or interventional cardiac catheterization to repair the defect.

6 Patent Ductus Arteriosus
Fetal structure that should begin closing with the first breath and should complete by 3 months S/S Wide pulse pressure and continuous murmur Management Administration of indomethacin Cardiac Catheterization Surgery Figure 41.11 PDAs are twice as common in girls as boys. PDA…is an accessory fetal structure that normally closes at birth. When it fails to close blood shunts from the aorta to the pulmonary artery. The shunted blood then returns to the left atrium, passes to the left ventricle, out to the aorta, and again to the pulmonary artery, causing right ventricular hypertrophy. S/S include a wide pulse pressure (the difference between systolic and diastolic pressures) and a continuous murmur that is heard best at the upper left sternal border or under the clavicle in older children. DX is made by echo. Treatment of PDA that has failed to close upon birth consists of administration of PO or IV indomethacin (the medication can be repeated as many as three times 12 to 24 hours apart), interventional cardiac catheterization, and surgery.

Obstructive defects Pulmonic Stenosis Narrowing of the pulmonary valve or artery causing the right ventricle to hypertrophy S/S Mild right sided heart failure Cyanosis SEM Therapeutic Management Balloon angioplasty to relieve the stenosis Figure 41.12 Pulmonic stenosis-narrowing of the pulmonary valve or artery resulting in the inability of the right ventricle to evacuate blood by way of the pulmonary artery (due to the obstruction), thus causing the right ventricle to hypertrophy. S/S include: signs of mild right sided heart failure, (if stenosis is severe) cyanosis may be present, systolic ejection murmur heard loudest at the upper left sternal border radiating to the suprasternal notch, and split second heart sound. DX by echo. Treatment consists of balloon angioplasty of the stenotic valve.

8 -Aortic Stenosis Stenosis of the aortic valve prevents blood from passing from the left ventricle into the aorta, leading to hypertrophy of the left ventricle S/S Usually asymptomatic but with murmur May have chest pain and even sudden death Therapeutic Management Stabilization with a Beta Blocker or Calcium Channel Blocker Balloon valvuloplasty Valve replacement Figure 41.13 Aortic stenosis: Read slide….S/S: most children are asymptomatic. A rough systolic murmur is heard loudest in the aortic space and may radiate to the right shoulder, clavicle, and up the neck. If the stenosis is severe, the child may show signs of decreased cardiac output and develop chest pain during activity. Sudden death may also occur. DX by echo. Treatment with Beta blockers or Calcium channel blockers is used to reduce cardiac hypertrophy before the defect is corrected. Balloon valvuloplasty is the treatment of choice; however, surgery may be indicated in which case a valve replacement may be performed.

9 Coarctation of the Aorta
Narrowing of the lumen of the aorta S/S Absence of palpable femoral &/or brachial pulses; headache, vertigo, nosebleeds, CVA; leg pain Therapeutic Management Surgery or angiography Figure 41.14 Coarctation of the aorta is a narrowing of the lumen of the aorta due to a constricting band. This makes if difficult for blood to pass through the narrowed lumen of the aorta, causing increased blood pressure in the heart and upper portions of the body. The child may have a headache and vertigo due to the increased pressure. With younger children, irritability may be the only sign that there is a problem. Nosebleeds and cerebrovascular accidents (CVAs) may also occur due to the high pressure. Older children may complain of leg pain. Depending upon the degree of coarctation, the child may exhibit absence of palpable brachial and/or femoral pulses. Treatment involves either interventional angiography or surgery.

10 Defects with decreased pulmonary blood flow
Tricuspid Atresia The tricuspid valve is closed, blood flows through the patent foramen ovale into the left atrium, bypassing the lungs. Then it is shunted back through a PDA into the lungs. When these structures close, cyanosis, tachycardia, and dyspnea occur. Surgery must correct. Treatment: IV infusion of PGE until surgery Figure 41-18 With Tricuspid Atresia, the tricuspid valve is completely closed, allowing no blood to flow from the right atrium to the right ventricle. Since blood cannot flow in the normal pattern, blood crosses through the patent foramen ovale into the right atrium, bypassing the lungs and the step of oxygenation. It is then shunted back through the PDA (patent ductus arteriosis) into the lungs. As long as these structures remain open, the child can obtain adequate oxygenation; however, once these structures close, the child will develop severe cyanosis, tachycardia, and dyspnea. Treatment consists of an IV infusion of PGE (prostaglandin) to keep the ductus open until surgery can be performed.

11 Defects with decreased pulmonary blood flow
Tetralogy of Fallot Four anomalies Pulmonary stenosis VSD Dextroposition of the aorta Hypertrophy of right ventricle S/S Cyanosis Polycythemia (increase in number of RBC) Dyspnea, growth restriction, clubbing of fingers Therapeutic Management Surgery Figure 41-19 Tetralogy of Fallot: consists of four anomalies: pulmonary stenosis, dextroposition of the aorta, VSD, and hypertrophy of the right ventricle. Due to the pulmonary stenosis, pressure builds up on the right side of the heart. Blood is then shunted to the left ventricle and aorta. Newborns may not exhibit any S/S immediately after birth. However, as the infant becomes more active, cyanosis develops. Polycythemia occurs in an effort to provide enough oxygenated blood to all parts of the body. This could lead to severe complications (due to increased viscosity of the blood), such as thrombophlebitis, embolism, or CVA. If untreated, the child eventually develops severe dyspnea, growth restriction, and clubbing of the fingers. Children also tend to assume a squatting or knee-chest position when resting (provides relief to heart by trapping blood in the lower extremities). Treatment consists of surgery.

Congestive Heart Failure S/S Tachycardia, tachypnea Right sided: increased venous pressure, hepatomegaly Left sided: dyspnea, crackles (rales), cyanosis, and, eventually, ride sided failure Therapeutic management Reduce workload of the heart using diuretics, inotropics, and vasodilators CHF results from blood pooling in the heart or in the pulmonary or venous systems because the heart can’t pump and circulate enough blood. CHF in children is most commonly going to occur in children less than 1 year old. Assessment: Usually the first sign of CHF in children is tachycardia, which is quickly followed by tachypnea. With right sided heart failure, the child will exhibit signs of increased venous pressure and hepatomegaly (enlarged liver). The enlarged liver may cause the child to experience abdominal pain, irritability, and restlessness. Lower extremity edema is a late sign of CHF in children. With left sided heart failure, the blood accumulates in the pulmonary system, causing the child to show signs of dyspnea (early sign), crackles upon auscultation, possible blood sputum, and cyanosis. Left sided heart failure can eventually lead to right sided heart failure. Treatment of CHF centers around the use of diuretics, inotropics, and vasodilators. Digoxin…apical pulse for one full minute, above 100 for infants, above 70 in older children Review pg “A child with heart failure”

13 Rheumatic fever S/S Therapeutic management Systolic murmur
Chorea (sudden involuntary movement of the limbs) Macular rash on the trunk Swollen and tender joints, SQ nodules on tendon sheaths Positive ASO titer and increased ESR and C-reactive protein Therapeutic management Bedrest Antibiotics to eliminate Group A Beta hemolytic Strept Prognosis depends on how much heart involvement Autoimmune disease that occurs as a reaction to a group A beta hemolytic streptococcal infection. Inflammation from the immune response leads to fibrin deposits on the endocardium and valves especially the mitral valve and major joints. This disorders often follows pharyngitis, tonsillitits, scarlet fever, “strep throat”, or impetigo ( all caused by group A beta-hemolytic strep). If left untreated or not treated with the appropriate antibiotic, mitral valve insufficiency can result and may not be diagnosed until later in life (adulthood). Especially girls may be left with mitral valve insufficiency. S/S of rheumatic fever include: systolic murmur upon auscultation of the heart, chorea (sudden involuntary movement of the limbs), macular rash on the trunk, swollen and tender joints, subcutaneous nodules on tendon sheaths. Important lab findings include a positive ASO titer and increased ESR (sed rate) and C-reactive protein levels. Treatment consists of bedrest during active phase of illness (course of illness usually lasts 6-8 weeks) and antibiotics appropriate for Group A hemolytic strep (penicillin or erythromycin if allergic to penicillin). The prognosis will depend upon how much heart damage has occurred from the illness. Chorea disappears without any residual effects

14 Kawasaki disease S/S (early) S/S (late) Therapeutic management
High fever that doesn’t respond to therapy Swollen hands and feet, enlarged joints Strawberry tongue, red lips, conjunctiva Enlarged cervical lymph nodes S/S (late) Skin desquamation Platelet count increases aneurysms Therapeutic management Administration of Ibuprofen for inflammation and platelet aggregation IV immunoglobulin to decrease immune response Most children recover fully but some will need heart surgery to repair damage Kawasaki disease is a febrile, multisystem disorder that occurs almost exclusively in children before puberty. It most commonly occurs in boys less than 4 years old. Vasculitis (inflammation of blood vessels) is the principal finding and is life-threatening. Vasculitis can lead to the formation of aneurysm and myocardial infarction. The cause is unknown, although there may be some genetic predisposition. After an infection, altered immune function occurs. There has also been an association between having your carpets professionally cleaned and the development of the disorder in young children within the household. S/S include: Acute phase – high fever that does not respond to antipyretics, lethargy and irritability, reddened & swollen hands and feet, conjunctivitis, “strawberry tongue” and red cracked lips, various rashes in the diaper area, enlarged cervical and internal lymph nodes, abdominal pain, diarrhea, and anorexia. Swollen and reddened joints may also occur. Important lab findings during the acute phase include and elevated WBC and ESR. The subacute phase begins about 10 days after onset. During the subacute phase children may exhibit S/S of skin desquamation on the palms and soles, a rise in the platelet count, and possibly the formation of aneurysms. The convalescent phase is between the 25th day until the 40th day post onset of S/S. The symptoms are often confused with JRA. Treatment centers around the administration of ibuprofen for inflammation and platelet aggregation and the administration of IV immunoglobin to decrease the immune response. Most children will recover fully but some will need heart surgery to repair damage.


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