1. Module 5 – Pediatric Cardiac Disorders
Revised, Summer 2008
Brief overview of Pedi cardiac disorders with quick review of fetal circulation and the changes from fetal to newborn

2. Fetal Circulation
Ductus venosus- structure shunts blood past the portal circulation (vein from umbilical cord)
Foramen Ovale- opening between right and left atria (upper chambers- unnecessary during fetal circulation- why? Blood oxygenated by mother!
Ductus arteriosus- vessel between the aorta and pulmonary artery that shunts blood from the pulmonary artery to the aorta
***shunts should close in several days after delivery!!**

3. Changes in Circulation
Umbilical cord clamped
Pulmonary
Pressure
Pulmonary resistance
Cord clamped- ductus venosus non-functional (no longer supply O2 to NB)
Then decreased pulmonary vascular resistance causes an increased pulmonary blood flow
Pressure changes- increase pressure in the left atrium with decreased pressure in the right atrium causes closure of foramen ovale
Pulmonary resistance is less than systemic resistance so there is left-to-right shunting that results in closure of the ductus arteriosus

4. Critical thinking: When are most cardiac anomalies discovered?
What is included in the initial cardiac assessment of a newborn?
Why?
Ultrasound- during Antepartum
Examination of the umbilical cord for 3 vessels- often first indication of cardiac anomalies

5. Assessment History Physical Diagnostic
History- Family hx- contact with known teratogens – chromosomal abnormalities which one in particular???- Downs Trisomy 21- Poor weight gain- poor feeding **recent streptococcal infections**
Physical assessment- Inspection-
color- what color is a “normal child”? What color might you see with cardiac problems? Why? cyanosis- where first-circumoral in NB and extremities-
the fingers become clubbed why?- decreased O2 and circulation stunts growth
Chest is deformed- enlarged with cardiomegly or pigeon chest from using extra muscles for breathing
Palpation/percussion- protruding sternum- unequal pulses on brachial/femoral and bilaterally
Abd- hepatomegally or splenomegaly- page 1256 & 1257 has chart)
Auscultation***- what do you expect to find- #1 assessment finding- murmur*** may have tachycardia or bradycardia
Diagnostic- ABG- arteria blood gases- chest x-ray- ECG (electro cardiogram)- Pulse ox normal is what ( ) Clinical cyanosis is not visible until sat rate <85%
Echocardiogram- for size, anatomy, & function (would show valve leakage, septal defects and thickness of cardiac muscle)
Cardiac Catheterization (last resort)

6. Importance of the Nurse Knowing Normal Value for O2 Saturations
Children respond to severe hypoxemia with BRADYCARDIA
Cardiac arrest in children generally r/t prolonged hypoxemia
Hypoxemia is r/t to respiratory failure or shock
BRADYCARDIA is a significant warning sign of cardiac arrest
At what O2 sat does cyanosis occur? Mild 90%-95%; moderate 85-90%; Severe: <85%
Need to know this bec. Brain damage occurs at or below 85%

7. Congestive Heart Failure
Pump Failure- cannot meet needs of the body
Fluid accumulation- myocardium cannot circulate enough oxygenated blood. Usually developed slowly- may not have recognizable symptoms early on.
Classic pathophysiology:
Peripheral vasoconstriction is a sympathetic nervous system response to adrenals release of norepinephrine (cuts off blood & O2 to extremities)
Tachycardia- body attempts to maintain cardiac output (O2 starved extremities)
Decreased renal perfusion causes and increase in renin and ADH secretion (anti-diuretic hormone). This results in Na and H2O retention increased fluid to the heart and edema
What does this mean for the child?

8. Clinical Manifestations
Pump Fails – cannot meet the demands of the body = CHF
How do you know when something is wrong?
Tires easily during feeding
Periorbital edema, weight gain
Rales and rhonchi
Dyspnea, orthopnea, tachypnea
Diaphoretic / sweating
Tachycardia
Weight
Earliest signs are tiring with feeding and rapid respirations (why?)
Tachypnea, dyspnea, orthopnea (shortness of breath just like in adults)- may also present with retractions, grunting, nasal flaring
Wheezing, rales, rhonchi
Easily fatigued- tires with play
Restlessness, apprehension, irritable- O2 starvation
Impaired Cardiac Output:
Tachycardia & diminished pulses– extremities are going to have what assessment findings??- cool-pale or cyanosis- what about capillary refill??—slow >2 sec.
Diaphoretic/sweating
Hypotension (what do we normally get with adults and CHF related to BP??)
Systemic venous congestion:
Hepatomegaly
Edema** periorbital and in face first-then peripheral
Weight gain ***weigh daily when hospitalized***
but what about early on? Failure to thrive-FTT slow weight gain in the NB

9. Goal of Treatment: Improve cardiac function
Remove accumulated fluid and Na+
Decrease cardiac demands
Decrease O2 consumption
So how are we going to get there?

10. Medications: Digoxin –what do we assess prior to administration?
Which VS? Weigh diapers for strict I & O
Double check
Digoxin levels
Parent teaching
Digitalis toxicity
ACE inhibitors
Capoten (Captoril)
Vasotec
VS- Heart rate (apical pulse)- hold if: infant <100beats/min; child <80 beats/min; adolescent <60 beats/min
IF PULSE IS > 100 BPM **GIVE**
2 nurses must check dose (like insulin)
Assess digoxin levels - normal is mg./ml
Parent teaching- page 1262 of McKinney (remember to teach them about S&S digoxin toxicity)
S&S of toxicity**Cardiac dysrrhythmia *1st sign in children** bradycardia, anorexia, nausea & vomiting, dizziness, weakness
Therapeutic range for Dig: ng/ml (nanogram per milliliter)
ACE inhibitors- inhibit conversion of angiotension I to II- resulting in vasodilation
Nursing care includes
Promote rest
Maintain o2 therapy and evaluate o2 saturation levels

11. Medications continued…
Furosemide (Lasix)
Chlorothiazide (Diuril)
Zarozolyn (Thiazide type)
Spironolactone (Aldactone)
Remove accumulated Fluid & Na+
Furosemide- Lasix- use for rapid diuresis dose 1mg/kg What lab value do we check?? K+ low-- K+ levels lead to increase chance of toxicity-** monitor electrolytes, weigh daily, monitor what else?? I&O (either weigh diapers or catheterize if necessary)
Diuril- use for maintenance diuresis
Diet therapy-what do we do with our adult patients? Do not always restrict fluids or Na+ with children because of the danger of dehydration. Infants rarely restrict fluids (they are dietarilly dependent on fluids)
Nursing care includes:
Measure I&O
Monitor peripheral circulation
Abdominal measurements daily- note increases in girth for ascites
Skin care (decreased activity and edema lead to breakdown)
Turning schedule WHY???- prevent pneumonia
Thiazide preparations are diuretics and mild vasodilators

12. Nursing care Reduce metabolic needs Diet therapy
Decrease Cardiac Demands
Improve tissue oxygenation
Promote rest-keep calm, quiet play, organize care
Maintain O2 therapy and evaluate O2 saturation levels
Why is maintain body temp important?- chilling increases metabolic rate
Diet therapy-what do we do with our adult patients? Do not always restrict fluids or Na+ with children because of the danger of dehydration. Infants rarely restrict fluids (they are dietaraly dependent on fluids): Small frequent feedings (too tiring to eat more than 30 minutes at a time- what other methods of feeding are there?- NG (gavage, G-tube, IV of TPN)
Nursing care includes:
Measure I&O
Monitor peripheral circulation
Abdominal measurements daily- note increases in girth for ascites
Skin care (decreased activity and edema lead to breakdown)
Turning schedule WHY???- prevent pneumonia
IMPROVE TISSUE OXYGENATION- all previous measures add supplemental cool humidified oxygen

13. Congenital Cardiac Anomalies
Childhood cardiac disorders are divided into 2 major groups: Congenital heart disease and acquired heart disorders
MAIN CLASSIFICATIONS OF CONGENITAL HEART DISEASE- underlying pathophysiology:
Left to right shunting
Abnormal opening between cardiac chambers or greater arteries (how do we usually identify this?? Murmurs) increase volume overload on right side of heart cardiac workload increases to compensate for volume overload  increased pulmonary blood flow  obstruction of blood flow from ventricles causes ventricular hypertrophy, dilation  congestive heart failure
Obstructive or stenotic lesions
Narrowing or constriction of valve or vessel  pressure increases behind obstruction  increase cardiac workload  ventricular strain  decreased perfusion to left side of body **what NB assessment piece clues us in on this defect??- bilateral peripheral pulses
Cyanotic lesions with decreased pulmonary perfusion
Obstruction on right side of heart decreases amount of blood to the lungs  decreased O2 sat to left side of heart  cynaosis
Cyanotic lesions with increased pulmonary blood flow
Heart does not develop separate pulmonary and systemic circulation or a reversal of circulation in the heart  mixing of saturated and desatruated blood  saturated blood goes to pulmonary circulation  desatruated blood goes systemic  cyanosis occurs

14. Classifying congenital heart defects
By defects that increase pulmonary blood flow
Patent ductus arteriosus
Atrial septal defect
Ventricular septal defect
By defects that decrease blood flow and mixed defects
Pulmonic stenosis
Tetralogy of Fallot
Tricuspid atresia
Transposition of the great arteries
Truncus arteriosus
These are on the learning guides, p. 19
**The main complication associated with increased pulmonary blood flow: p. 1472, causes constriction of the pulmonary vascular bed and pulmonary artery hypertension with Right ventricular hypertrophy; hypoxemia results
Defects with decreased blood flow: The bone marrow is stimulated to produce more RBCs to increase hemoglobin available to carry O2. Polycythemia may result and place the child at risk for thromboembolism. Platelet survivial is reduced and clotting factors are impaired, increasing risk of bleeding during surgery. ***cyanosis that does not respond to O2 is a classic sign. Administer prostaglandin E1 (PGE1) to re-open the ductus arteriosus

15. What is most common indication of a congenital heart defect?
Signs & Symptoms
What is most common indication of a congenital heart defect?
Exam question***
Continuous heart murmur (transient are often auscultated for first 2-3 days after birth)

16. Cardiac catheterizations
Used to determine anomalies
Measures O2 sats in cardiac chambers and great arteries
Evaluates cardiac output
Identify detailed images of blood flow patterns
May allow for corrective or palliative measures
Corrective measures: pulmonary artery or valve and aortic valve balloon angioplasty,
stent placement to maintain patency of vessels, septostomy for creating an atrial septal defect and may be useful to close septal defects of coil embolization of a patent ductus arteriosus

17. Nursing interventions pre and post cardiac catheterization
Assessment pre-op for baselines
Assessment post-op:
Vital signs (which ones are priority?)
Extremities
Activity
Hydration
Medications
Comfort measures
Assessment of pulses gives the nurse a baseline and also includes skin temperature, color, and strength for compasison
Vital signs priority: apical pulse and BP
Extremities: popliteal and pedal pulses, temp, color of skin, cap refill, response and sensation
Activity: direct pressure applied to the area for 15 minutes with a pressure dressing for 6 hrs post procedure. The child is kept on bed rest for 6 hrs with an effort to keep the leg straight for several hours. Avoid elevating the head of bed as flexion of the hips is not permitted during this period. Activity is limited for 24 hrs. Provide quiet diversional acitivities to keep the child occupied
Hydration: enc. Fluids to flush dye out of body and prevent thromboembolism. Drink small amts of clear liquids and progress as tolerated. Monitor I & O
Medications: no nsaids, ASSA (due to blood thinning properties). May have antibiotics prophylactacially to prevent endocarditis
Comfort: acetaminophen, ice packs, minimize activity

18. Teaching after cardiac catheterization
Parental teaching
Watch for s/s of bleeding, bruising at site
Foot temp on side of cath cooler
Loss of sensation in foot on side of cath
When to call the physician
If any of above s/s noted within 1st 24 hrs

19. Patent Ductus Arteriosus
Blood shunts from aorta (left) to the pulmonary artery (right)
Returns to the lungs causing increase pressure in the lung
Congestive heart failure
Failure of fetal ductus arteriosus to close completely at birth
Note stimuli for closure:
Increased oxygen levels in blood when NB breaths normally
Decreased prostaglandin levels (removed from maternal supply)
Decreased pulmonary resistance
WHEN DUCTUS FAILS TO CLOSE- oxygenated blood from the aorta backs up through PDA  returns to lungs causes left to right shunting  increase cardiac workload on the left side of heart  increased pulmonary blood  congestive heart failure

20. Treatment Medical Management Medication Indomethacin Surgical
____Ligate the ductus arteriosus
Medical management- IV Indomethacin (Indocin)- a prostaglandin inhibitor, to promote closure of the ductus (60% successful in 1st 14 days)
Surgical- cardiac catheterization/transcatheter closure- coil placed that promotes occlusion of ductus arteriosus- less invasive than surgery**- similar to adult cardiac catheterization
Surgical intervention- open heart with ligation of ductus  thoracotomy incision

21. Nursing Care: Pre-op Patient/parent teaching Assess for infection
Obtain lab values for chart
Post-op
ABCs
Rest
Hydration/nutrition
Prevent complications
Discharge teaching
Pre-op-
demo tubes/bandages, scar, show pictures-dolls- chest tubes are very frightening to children and adults** support group
Teach C&DB and use of IS remember to use age appropriate instructions/pictures, written information for parents- this is a very overwhelming time for them
Tour hospital, ICU, and introduce to staff
Assess for S&S of infection
Post-op
ABCs- patent airway- IPPB (intermittent positive-pressure breathing)- suction as necessary- O2, monitor respirations and lung sounds- monitor chest tubes and chest draingae
circulation- VS- *check I&O every hour-**why is I&O an indicator of cardiac function?- need BP to maintain renal perfusion and function also check for blood clots-cyanosis, pale extremity or cool/cold peripheral pulses
provide for rest
Hydration/nutrition- maintain fluid and electrolyte balance
prevent complications-
Turn q2 hours
Skin care
Passive ROM
Check dressing
Keep comfortable –pain medication
Prepare for discharge- *remind that need regular assessment by physician and prophylaxis of antibiotics prior to dental visits/cleanings

22. Atrial Septal Defect
Oxygenated blood is shunted from left to right side of the heart via defect
A larger volume of blood than normal must be handled by the right side of the heart hypertrophy
Extra blood then passes through the pulmonary artery into the lungs, causing higher pressure than normal in the blood vessels in the lungs  congestive heart failure
Defects that happen during development of atrioventricular canal with an opening between the atrium
Patent foramen ovale happens in 20 % of all births- slit-like opening in the atrial septum. This defect is usually functional and requires no surgical intervention (what is the indication of this condition??- murmur)
Patent foramen ovale  left to right shunting through the defect enlarged right arium increased pulmonary blood flow congestive heart failure
Signs and symptoms- frequently no S&S other than minor murmur. Congestive heart failur develops later in life- May have frequent respiratory infections

23. Treatment Medical Management Surgical repair Medications – digoxin
Suture or simple patch
Medical management- close observation by cardiologist- monitor for spontaneous closure usually by first birthday
If surgery required ay use a suture to close the defect or a patch (next slide)

24. During cardiac catheterization the occluder is placed in the
Treatment
Device Closure – Amplatzer septal occluder
Tissue eventualy covers the device and closes the defect
During cardiac catheterization the occluder is placed in the
Defect

25. Ventricle Septal Defect
Oxygenated blood is shunted from left to right side of the heart via defect
A larger volume of blood than normal must be handled by the right side of the heart hypertrophy
Extra blood then passes through the pulmonary artery into the lungs, causing higher pressure than normal in the blood vessels in the lungs  congestive heart failure
Opening between the ventricles- severity related to size of the defect and amount of pulmonary blood flow that backs up into the lungs
Left to right shunting: blood flows from left ventricle through the defect to the right ventricle and re-circulates to the lungs  causing increased pulmonary congestion
Signs & Symptoms: depends on severity- tachypenic, diaphoretic, fatigue easily (activity intolerance), overweight for age- in infants they tier before feeding completed- *in sever cases they experience congestive heart failure (like adults)

26. Treatment Surgical repair with a patch inserted
Usually no treatment (close in first few years of life)
Treat the complications- congestive heart failure
Surgical intervention- closure with sutures or a patch during cardio pulmonary bypass surgery *nursign interventions are samy for this surgery as for any other cardiac surgery

27. Obstructive or Stenotic Defects

28. Pulmonic or Aortic Stenosis
Narrowing of entrance that
decreases blood flow
Treatment:
Medications – Prostaglandins to keep the PDA open
Cardiac Catheterization
Balloon Valvuloplasty
Surgery
Valvotomy
Pulmonic stenosis- lesion obstructs flow from right ventricle (narrowing of entrance to pulmonary artery) this leads to right ventricular hypertrophy (enlarges the right ventricle)
Aortic- lesion obstructs flow of blood from left ventricle (usually narrow entrance of aorta)  left ventricle hypertrophy
Signs & Symptoms- depend on severity- usually asymptomatic may have murmur and have abnormal EKG with exertion
Treatment:
Medication- prostaglandins to keep patent ductus arteriosus open-so some oxygenation occurs
Cardiac Cath- Balloon valvuloplasty -balloon dilates the valve, may also place stents to keep open
Valvotomy- slit placed in the valve so that it is patent

29. Coarctation of the Aorta
Narrowing of Aorta causing obstruction of left ventricular blood flow
Left ventricular hypertrophy
Signs and Symptoms
 B/P in upper extremities
B/P in lower extremities
Radial pulses full/bounding and femoral or popliteal pulses weak or absent
Leg pains, fatigue
Nose bleeds
Why does this lead to pulmonary edema??– because the blood backs up because it cannot leave the heart efficiently.Signs & symptoms
Increased BP in upper extremities
Decreased BP in lower extremities
Radial pulses strong & bounding- femoral or popliteal weak or absent
Leg pains with exertion, weakness or tingling in lower legs
Fatigue
Headache, nose bleeds

30. Treatment
Goals of management are to improve ventricular function and restore blood flow to the lower body.
Medical management with Medication
A continuous intravenous medication, prostaglandin (PGE-1), is used to open the ductus arteriosus (and maintain it in an open state) allowing blood flow to areas beyond the coarctation.
Balloon dilation
Surgery
Medication to keep PDA open until surgical repair- either balloon dilation (with or without stents) or removal of coarctation area
Resect narrow
area
Anastomosis

31. Cyanotic Disorders
Conditions which allow unozygenated blood into systemic circulation and other conditions that result in obstructive pulmonary blood flow

32. Tetralogy of Fallot Signs and Symptoms 2 1. 3 4
1. Four defects with right to left shunting
Signs and Symptoms
Failure to thrive
Lack of energy
Infections
Polycythemia
Clubbing of fingers
Squatting
Cerebral absess
Cardiomegaly
Cyanosis 2 1.
Hemodynamics- a right to left shunt arises due to the position of the aorta and hypertrophied right ventricle  partially unoxygenated blood is sent back to the systemic circulation through the VSD (ventricular septal defect) very profound murmur!
Frequent infections- What type do we suspect? Respiratory
Polyycythemia-abnormal increase in number of red blood cells
Clubbing of fingers- because of lack of nutrients and O2
Squatting- with fatigue and an attempt to increase circulation to upper part of body
Cerebral abscess- from hypoxic events
Cardiomegaly- enlargement of the heart because of increased/ineffectual stroke
What do you think happens to the BP? 3 4

33. Treatment Surgical interventions
Blalock – Taussig or Potts procedure – increases blood flow to the lungs.
Open heart surgery
Survival depends upon mixing of blood from pulmonic and systemic circulation
Treatment in first few days of life—either Palliative (creatran artificial PDA) until corrective treatment appropriate- Blalck-Taussing or Potts procedure
Open-heart- correction of the VSD and pulmonary stenosis

34. Ask Yourself ?
Laboratory analysis on a child with Tetralogy of Fallot indicates a high RBC count. The polycythemia is a compensatory mechanism for:
a. Tissue oxygen need
b. Low iron level
C. Low blood pressure
d. Cardiomegaly
Tissue oxygen need

35. Mixed blood flow
Survival depends upon mixing of blood from pulmonic and systemic circulation
Cyanotic Disorders:
Truncus arteriosus
Hypoplastic left heart
Transposition of the great arteries

36. Truncus arteriosus
A single arterial trunk arises from both ventricles that supplies the systemic, pulmonary, and coronary circulations. A vsd and a single, defective, valve also exist.
Entire systemic circulation supplied from common trunk.

37. Hypoplastic heart
May have various left-sided defects, including coarctation of the aorta, aortic valve & mitral valve stenosis or artresia

38. Transposition of Great Vessels
Aorta arises from the right ventricle, and the pulmonary artery arises from the left ventricle –
not compatible with survival unless there is a large defect present in ventricular or atrial septum.
aorta

39. Nursing Diagnosis & Goals:
DX: Alteration in cardiac output: decrease R/T heart malformation
Goal: Child will maintain adequate cardiac output AEB:
AEB: Resp rate- within a specific range noted by MD-cardiologist
B/P as set by MD
Clear equal breath sounds (bilat upon auscultation)
O2 saturation as ordered (normal is what?? % significant at what level 85%
Monitor weight- inappropriate weight gain (<30G/day), absence of puffy eye lids
Skin warm to touch
Capillary refill 2-3 seconds
Adequate urinary output (state specific amount-= .5-2ml/kg/hr) or 0>60% of intake
Maintain specific gravity of urine at
Absence of S&S of congestive heart failure

40. Nursing Care: Monitor VS I&O Medications Position Metabolic rest
Assess and document child/family interactions
Parent teaching
VS- maintain temp to avoid increase metabolism and O2 consumption- also monitor for S&S of decreased cardiac outpu- peripheral pulses
Monitor I&O-include specific gravity of urine
Administer cardiac medications as ordered
Position with head of bed elevated to 30%- Why? Facilitate breathing and cardiac function- prevent aspiration
Organize care to allow for rest include small feedings and prevent crying (keep parents at bedside if appropriate)
Family interactions- important to recovery
Teach family how to assist with care for child in hospital and at home- teaching begins prior to surgery and continues until discharge- These children may need repeated surgeries to complete re-construction

41. Acquired Cardiac Diseases

42. Mucocutaneous lymph node syndrome Not contagious
Kawasaki Disease
Mucocutaneous lymph node syndrome
Not contagious
Preceded by upper respiratory tract infection
Cause unknown
Acute systemic inflammatory illness- multisystem vasculitis- inflammation of blood vessels in the body especially the coronary arteries with antigen-antibody complexes.
Usually preceded by an upper respiratory infection- cause unknown
Complications include- CHF, aneurysms, coronary thrombosis

43. Clinical Manifestations:
Acute Phase days
Subacute Phase days
Convalescent Phase days
Acute phase days- classic onset:
Rapid onset of fever lasting for more than 5 days (generally F or C)**does not respond to antibiotics *Bilateral conjunctivitis lasting 3-5 weeks
Rash on day 5 of illness, usually macular spreading from extremities to trunk (very important to note- most viruses go from trunk to extremities) *Cervical lymphadenopathy- swollen glands *Irritability & lethargy “whiney-fussy) * Anorexia,(no appetite), possible diarrhea, hepatic dysfunction (frothy dark urine)
Acute pericarditis- severe pain in the chest and chest wall *Hands and feet edematous and red- classic*Red throat (similar to strept)
Subacute phase days fever disappears and most symptoms resolve:
Continued irritability *Anorexia, diarrhea *Arthritis and arthralgia (aches to joints) *Lip cracking and peeling- classic strawberry tongue *Desquamation of extremities- palms and soles *Cervical lymphadenopathy with large nodes *Possible coronary aneurysms, potential for thrombosis formation
Convalescent Phase days * disease self-limiting, signs of illness decrease and disappear *transverse lines called Beau’s line form on nails * lasts until the erythrocyte sedimentation rate returns to normal and all S&S of illness disappear

44. Diagnosis: ECG CBC, WBC PT ESR SGOT, SGPT IgA, IgG and IgM
ECG- echocardiogram displays abnormal function- first-degree heart block
CBC & WBC- elevated
PT- elevated- platelet levels
ESR- elevated- erythrocyte sedimentation rate
SGOT (serum glutamic-oxaloacetic transaminase) & SGPT (serum glutamic pyruvic transaminase) both elevated RT hepatic dysfunction
IgA, IgG, IgM elevated- immunoglobulin increase to combat the disease

45. Nursing Care: Medication Therapy Nursing Interventions Aspirin
Gamma Globulin
Nursing Interventions
Assess/monitor
Decrease stimulation
Comfort measures
Discharge teaching
Medication- Aspirin- why??*decrease aneurysm (weakening of vessel) formation & fever 100mg/kg/day in four doses until fever resolved, then doses decrease for 6-8 weeks or until aneurysms gone Gamma Globulin- high dose IV- IVGG (strengthen immune system)
Nursing interventions: Monitor/assess VS (including BP)—assess oral mucosa (lubricate lips and provide small frequent feedings of cool, soft, bland foods and liquids)*popsicles are great-why is orange juice not a welcome liquid??- assess rash on extremities and body- provide comfort measures/skin care- antipyretics as ordered- Monitor I&O (particularly look at urine concentration for S&S of hepatic dysfunction)- decrease stimulation- these children are extremely ill and need all their resources to recover, they may have pericarditis and pain with exertion, or increase fever with activity- Comfort measures- cool compresses, tepid sponge baths, passive ROM (facilitate joint movement)Discharge Teaching- ASA for anticoagulation therapy, other interventions for elevated temp- skin care and comfort measures- follow up with cardiologist for ECG, CXR every 3 months for 1 year!!- Call MD if chest pain, SOB, dizziness, change in behavior, not eating or drinking, illness or any other concerns. These children need to see the cardiologist for any illness! Also need to have prophylaxis antibiotics prior to dental cleaning or work.

46. Rheumatic Fever Systemic inflammatory disease
Follows group A beta-hemolytic
streptococcus infection
Causes changes in the entire heart especially the valves
Systemic inflammatory disease of connective tissue (collagen) that usually follows a group A beta-hemolytic streptococcus infection. This disorder causes changes in eh entire heart (especially the valves), joints, brain, and skin tissues.
Children used to die from Scarlet fever and Rheumatic Fever- Dad’s sister Pearl died at 12 with scarlet/Rheumatic fever

47. Clinical Manifestations
Jones Criteria
Major
Minor
Supporting Evidence
Jones criteria- list of – positive for Reumatic fever with 2 major criteria or 2 major and 2 minor
MAJOR: Carditis, valvulitis- polyarthritis (specific to knees, ankles, hips & shoulders- joint stiffness and pain with movement)- Chorea (involuntary purposeless, jeerky movements of legs, arms and face caused by CNS involvement)- Erthyema marginatum (red, painless skin lesions, start on the trunk)- subcutaneous nodules (rare in rheumatic fever but may appear as non-tender lumps on joints or bony prominences.)
MINOR: Fever- arthralgia (large joints, usually knoees, wrists, elbows)- Previous rheumatic fever or reheumatic heart disesase- eleveated erythrocyte sedimentation rate- positive C-reaction protein—P-R interval prolonged –elevated antistreptolysin O titer
Supporting Evidence: recent scarlet fever- positive throat culture for group A streptococci- Increased strept antibodies

48. Therapeutic Intervention
Medication
long term
prophylaxis
Nursing
Prevention
Parent teaching (ANTIBIOTICS)
Medication- antibiotics***for five years after illness*** to prevent residual heart disease- usually use Penicillin or erythromycin
ASA for joint symptoms and relieve pain
Protect with antibiotics prior to dental visits
Nursing interventions:- Teach measures in PREVENTION ***EVERY CHILD WHO HAS A STREP INFECTION MUST COMPLETE ENTIRE COURSE OF ANTIBIOTICS AND DO NOT DISCONTINUE BECAUSE THE CHILD FEELS BETTER***
Assess compliance to medication therapy—encourage bed rest—prevent further infection

49. Subacute Bacterial Endocarditis
Infectious disease involving abnormal cardiac tissue:
Usually rheumatic lesions or congenital defects
Infection may invade adjacent tissues- aortic and mitral valves
May be called “vegetation on the valves”

50. Clinical Manifestations:
Onset insidious
Fever
Lethargy/general malaise
Anorexia
Splenomegaly
Retinal hemorrhages
Heart murmur –90%
Diagnosis- positive blood cultures

51. Nursing Care Medication-large doses antibiotic Bed rest
Teach to notify dentist prior to dental work
Penicillin, Amoxicillin, Clindmycin

52. Principles that apply to all cardiac conditions:
Encourage normal growth and development
Counsel parents to avoid overprotection
Address parents’ concerns and anxieties
Educate parents about conditions, tests, planned treatments, medications
Assist parents in developing ability to assess child’s physical status