MB4 peds cardiac Forsythe

right arm

most accurate ABG will come from a R radial stick

2 arteries and a vein

artery- wastes and CO2 from the baby to the mother

vein- O2, nutrients, and hormones to the baby from the L ventricle

placenta

gas exchange

umbilical vein -> 1/2 blood to liver & 1/2 to heart -> 3 shunts by pass liver and lungs to direct blood where it needs to go

the baby isn't breathing or metabolizing stuff with the liver so they don't need much blood

• 1. ductus venosus
• 2. foramen ovale
• 3. ductus arteriosus

routes the blood from the liver into inferior vena cava then the blood enters the R atrium

most of the blood enters L atrium through the second shunt - foramen ovale -> L ventricle (mixes with sm amnt of blood returning from the lungs) -> ascending aorta -> upper body - coronary arteries and brain

blood left in R atrium -> R ventricle -> lungs to nourish

mixing of blood from the R atrium & blood returning from the lungs

brain & coronary arteries (heart)

blood that is still O2 and nutrient rich -> superior vena cava -> R atrium -> most goes through tricuspid valve -> R ventricle -> pulmonary artery -> bypasses lungs via ductus arteriosus -> descending aorta -> lower portion of the body -> umbilical arteries -> placenta for gas exchange

openings b/t the chambers of the heart

increased pulmonary blood flow

ASD, VSD, AVSD, PDA

atrial septal defect

ventricular septal defect

close spontaneouly 30 to 40% of the time

atrioventricular septal defect

Ass. with genetic syndromes - down syndrome

resp infections

will need heart checked well for AVSD

patent ductus arteriosus

premature <28 weeks

blood shunted from L to R -> increased BF to the pulmonary circulation -> extra blood from pulm artery -> L side of heart increases work load on L side of heart

L side of the heart and lungs are recieving blood from 2 sources:  R side of heart & patent ductus arteriosus

• congestive heart failure CHF
• pulmonary hypertension
• frequent resp infections

decreased cardiac outflow

• 1. coarctation of the aorta
• 2. aortic stenosis
• 3. pulmonary stenosis

• CHF
• heart failure
• stroke

decreased pulmonary blood flow

• 1. tetralogy of Fallot
• 2. tricuspid atresia
• 3. total anomalous pulmonary venous return
• 4. pulmanary atresia with intact ventricular septum

• emboli
• seizures
• sudden death

• 1. truncus arteriosus
• 2. transposition of the great arteries
• 3. hypoplastic L heart syndrome

• CHF
• heart failure
• death

not symptomatic at first b/c they will be getting plenty of O2 but there is increased workload on the right side of heart which will eventually start to fail

the foramen ovale remains open

oxygenated blood flows from the L side of the heart back into the R side and mixes with deoxygenated blood and is sent to the lungs for re-oxygenation

the L side of the heart has a higher pressure than the R - any abnormal opening will causes pressurized blood to escape into the R side

abnormal opening or connection (atrium, septum, aortic/pulmonary artery) -> reversal of blood flow from L to R side of heart -> volume overload in R side and pulmonary artery -> CHF, pulm hypertension, frequent resp infection

atrium - foramen ovale remains open

years to decades when heart failure begins to occur

• 1. palpitations or atrial arrhythmias
• 2. systolic murmur
• 3. CHF later in life (rare in CH)

atrial enlargement

increased BF across the pulmonary valve

ventricle

• 1. murmur (systolic/from book)
• 2. thrill
• 3. gallop rhythm

usually spontaneously closes

atrioventricular septal defect - hole in atrium and ventricle

S/S of CHF

usually spontaneously closes

patent ductus arteriosus - increased workload on the L side of the heart

PDA

ASD

VSD

prostaglandin

indocin/indomethacin

VSD & AVSD

aorta and pulmonary artery

increases the workload on the L side of the heart

• 1. CHF s/s
• 2. cont./machine sounding murmur
• 3. widened pulse pressure (increased diff b/t systolic and diastolic pressures)
• 4. cardiomegaly
• 5. poor feeding
• 6. poor weight gain
• 7. fatigue
• 8. tachypnea
• 9. diaphoresis

continuous "runoff" of the aortic blood flow to the pulmonary arteries

• 1. ASD
• 2. VSD
• 3. AVSD
• 4. PDA

• 1. CHF Tx
• 2. interventional cardiac catheterization
• 3. surgery
• 4 increased caloric density of formula

L to R shunting defects:  ASD, VSD, AVSD, PDA

O2 blood from the left is forced through abnormal opening into the R side -> pulmonary artery -> lungs -> L atrium

oxygenated into deoxygenated

obstructive or stenotic defects

L side

• obstructive or stenotic defects: 
• Coarctation of the aorta
• Aortic stenosis
• Pulmonary stenosis

coarctation of the aorta

the BP will be high in upper and low in lower body

the pulse will be bounding in the upper body and thready/weak or absent in the lower body

brachial not radial

from the R arm b/c blood flow there slightly fast than to L

constriction of the aorta (descending) near the ductus arteriosus -> increases workload on L ventricle

increased blood supply to the upper body and decreased blood supply to the lower body

1. increased BP in the upper body & decreased BP in the lower body

2. bounding pulse in the upper body and weak/thready/absent pulse in the lower body

3. weak/tingling lower extremities

disparity in pulses and BP b/t upper and lower body

PGE1 - prostaglandin to vasodilate -> causes ductus arteriosus patency -> increases blood flow to the lower body

before = high BP

after = low BP

obstruction to blood flow leaving L ventricle that occurs near the aortic valve

May be supravalvular, subvalvular, or at the level of the valve

stenosis of the aortic valve -> increased workload on the L ventricle r/t small opening -> L ventricular hypertrophy

feeding difficulties and/or inadequate weight gain r/t dyspnea

right

obstruction to blood flow leaving the R ventricle

• 1. level with pulm valve
• 2 supvalvular
• 3. supravalvular

L ventricular hypertrophy

may be asymptomatic

• 1. faint peripheral pulses
• 2. severe CHF
• 3. feeding difficulties

blood backs up into pulmonary circulation

R ventricle hypertrophy

asymptomatic to s/s of CHF

• 1. CHF tx
• 2. interventional cardiac catheterization
• 3. surgery

3T's and a P

• 1. Tetralogy of Fallot
• 2. Tricuspid atresia
• 3. Total anomalous pulmonary venous return
• 4. pulmonary atresia with intact ventricular septum

endocarditis

Tx with prophylactic ABX long term

• 1. ASD
• 2. VSD
• 3. AVSD
• 4. PDA
• 5. coarctation of the aorta
• 6. aortic stenosis
• 7. pulmonic stenosis

• 1. tetralogy of Fallot
• 2. Tricuspid atreasia
• 3. total anomalous pulm venous return
• 4. pulm atresia with intact ventricular septum
• 5. truncus arteriosus
• 6. transposition of the great arteries
• 7. hypoplastic L heart syndrome

soon after birth

malalignment of ventricular septum resulting in 4 deformities

• 1. VSD
• 2. pulmonary stenosis
• 3. overriding of aorta into the R ventricular side instead of L (opens into both)
• 4. R ventricular hypertrophy

maintiain patency of the ductus arteriosus

prostaglandin= vasodilation

varies widely due to degree of each defect - can be left to right or right to left shunting

may be acute or mild cyanosis

usually circumoral or acrocyanosis but may have hypercyanotic episodes where they are all blue esp during crying or after feeding

1. tet spells

2. blue spells

• 1. mild-acute cyanosis
• 2. pink Tet-O2 sat normal or low normal
• 3. tet spells
• 4. tire easily
• 5. difficulty feeding
• 6. difficulty gaining weight
• 7. harsh systolic murmur accompanied by thrill

• 1. PGE1 infusion to maintain ductal patency
• 2. positioning during cyanotic episodes
• 3. elective surgery in the first year of life

over the pericordium

infants - knee to chest

children - squatting

tricuspid valve does not dev so there is no blood flow from right atrium to R ventricle

blood flows thru shunt or patent foramen ovale to L side of heart and through a VSD to the R ventricle and out to lungs

there is a complete mixing of unoxygenated and oxygenated blood in L side of the heart -> systemic desaturation and varying amnt of pulmonary obstruction and decreased pulmonary blood flow

1. cyanosis dev from birth to few hours of life

2. single first heart sound

there is no closure of the tricuspid valve

PGE1 infusion

interventional cardiac catheterization

surgery

pulmonary veins don't empty O2 blood into L atrium but will empty somewhere else in heart

• 1. R atrium
• 2. superior vena cava via an innominate vein

oxygenated and deoxygenated blood is all dumped into R atrium -> mixed blood is pumped to lungs and some goes through ASD to L atrium to be pumped through system

R sided hypertrophy

• 1. severe cyanosis
• 2. resp distress
• 3. progressive clinical deterioration

carry O2 blood from lungs to the L atrium

tetralogy of Fallot

surgery soon after birth

not viable without it

pulmonary atresia with intact ventricular septum

blood cannot get to lungs otherwise b/c pulm valve is missing

pulmonary valve doesnt develop and hypoplastic development of the pulonary artery and right ventricle occurs

under-developed

profound cyanosis

continuous PGE1 infusion - must have presence of PDA for survival

surgery

failure of normal separation of the pulm artery and aorta during dev. that results in dev of a single vessel that recieves blood from both ventricles

truncus arteriosus

blood from R and L ventricles mixes and is circulated to lungs and system

hypoxemia and desaturation of blood

• 1. symptomatic during neonatal period
• 2. volume of pulmonary blood flow determines severity of symptoms
• 3. harsh murmur, thrill, and click
• 4. bounding pulses
• 5. widened pulse pressure

ductus arteriosus & PDA

• 1. CHF tx
• 2. surgery

tetralogy of Fallot

total anomalous pulmonary venous return

pulmonary stenosis

pulmonary atresia with intact ventricular septum

coarctation of the aorta

aortic stenosis

tricuspid atresia

truncus arteriosus

pulmonary artery leaves L ventricle and the aorta exits from R ventricle with no communication b/t the systemic and pulmonary circulations

must be ass. defects such as septal or patent ductus arteriosus

• 1. cyanotic
• 2. heart sounds vary according to type of defect
• 3. cardiomegaly within few weeks after birth

PGE1

surgery

• 1. aorta comes from R ventricle
• 2. pulmonary artery comes from L ventricle
• 3. hole or defect in the ventricular septum
• 4. hole or defect in the atrial septum
• 5. patent ductus arteriosus

• 1. CHF
• 2. pulmonary hypertension
• 3. cyanosis
• 4. hypercyanotic episodes

inadequate dev of L side of heart results in only one effective ventricle

may include other congenital defects

• tachypnea
• early CHF
• systemic hypoperfusion
• shock

• PGE1 infusion
• surgical staged repair
• cardiac transplantation

transposition of the great arteries

etiologies -> stim of SNS -> peripheral vasoconstriction -> increased pulm vascular resistance -> increased systemic vascular resistance -> increased afterload -> decreased blood flow to body system esp kidneys -> increases production of renin, aldosterone, and ADH -> Na and H2O retention -> increased blood volume (increased preload) -> systemic and pulmonary venous engorgement -> cardiomegaly hepatosplenomegaly -> heart failure

1. anemia r/t altered nutrition secondary to VSD

2. resp infection r/t VSD

• 1. feedings take too long
• 2. tachypnea with feeding
• 3. cold-like s/s

diaphoresis  & tachycardia

• 1. < CRT
• 2. mottling
• 3. pallor
• 4. cyanosis
• 5. pale cool extremeties
• 6. weak peripheral pulses

decreased UO

• 1. weight gain
• 2. peripheral edema
• 3. periorbital and facial edema
• 4. neck vein distention

• 1. tachypnea
• 2. dyspnea
• 3. retractions
• 4. flaring nares
• 5. wheezing
• 6. grunting
• 7. cough
• 8. horseness
• 9. exercise intolerance & fatigue
• 10. lethargic an/or irritable

• digoxin to increase contractility
• ACE inhibitors to decrease absorption of water and Na

monitor I & O

• 1. impaired myocardial function
• 2. pulmonary congestion
• 3. systemic venous congestion

• 1. tachycardia
• 2. gallop rhythm
• 3. decreased BP
• 4. weak peripheral pulses
• 5. pale, cool extremities
• 6. sweating
• 7. decreased UO
• 8. fatigue & weakness
• 9. restlessness
• 10. anorexia
• 11. cardiomegaly

• 1. tachypnea
• 2. dyspnea
• 3. grunting
• 4. flaring nares
• 5. retractions in infants
• 6. inter and sub costal
• 7. rales
• 8. wheezing - rare
• 9. orthopnea
• 10. cough, hoarseness
• 11. exercise intolerance
• 12. pallor
• 13. mottling
• 14. cyanosis

• 1. weight gain
• 2. periorbital and facial edema - most common
• 3. peripheral edema
• 4. ascites
• 5. neck vein distention in ch
• 6. hepatosplenomegaly

• 1. diuretics
• 2. weigh daily
• 3. I & O
• 4. skin care
• 5. position frequently
• 6. monitor electrolytes:  Na, K, and MG esp. K

preload

elevate HOB 30 - 45 degress

• 1. HOB elevate 30 to 45 degress r/t pulmonary s/s
• 2. admin O2 prn
• 3. cluster nsg intervention
• 4. small frequent high calorie meals and snacks

peripheral vasoconstriction

aortic stenosis

• 1. impaired myocardial function
• 2. pulmonary congestion
• 3. systemic venous congestion

• 1. often subtle
• 2. mild resting tachypnea
• 3. increased difficulty or poor feeding
• 4. feedings take longer & require frequent rest periods
• 5. diaphoresis during feeding
• 6. increased irritability because feedings are not providing satisfaction
• 7. over time infant fails to gain weight - failure to thrive

will look wasted and have no booty

decreased blood pressure and flow to the kidneys and decreased UO

digoxin

body is trying to compensate for decreased BF to the kidney ->  renin, aldosterone, and ADH

give lasix - loop diuretic

• 1. decreases heart rate
• 2. increases heart contractility
• 3. increases O2 to tissues

cardiac glycoside

lanoxin

loop diuretic

furosemide

captopril/capoten

• 1. quiet and cooperative;  mild sedative or distraction
• 2. skin free of lotions and oils
• 3. noninvasive, relatively painless and no side effects
• 4. gelfoam electrodes

• 1. improve cardiac function to increase contractility
• 2. remove accumulated fluid and Na
• 3. decrease cardiac demands
• 4. improve tissue perfusion/oxygenation

• 1. digoxin/lanoxin
• 2. furosemide/lasix
• 3. captopril/capoten

lanoxin

increases cardiac contractility, decreases pulse, and increases tissue perfusion

cardiac glycoside

lasix

loop diuretic - decreases Na and water

capoten

decreases water and Na retention

ACE inhibitor

increased force of ventricular contraction

slows heart rate and allows the ventricles to have more time to fill with blood

increased cardiac output

• 1. positive ionotropic effect
• 2. negative chronotropic effect
• 3. decreases preload and afterload

decreases cardiac demands

will increase kidney perfusion and have a small diuretic effect

• 1. improves tissue perfusion
• 2. removes accumulated fluid and Na by perfusion kidneys (mild diuresis)

0.8-2 mg/mL

• 1. hypo and hyperkalemia
• 2. hypercalcemia
• 3. hypomagnesemia

IV injection

PO elixir or tabs

digitalizing dose:  oral or IV in divided doses over 24 h

maintenance dose:  oral bid:  am and pm to maintain blood levels

• 1. morning and evening SAME time qd (bid)
• 2. Admin 20 to 30 minutes before a feeding
• 3. measure with an oral syringe not a dropper
• 4. Admin slowly allowing child time to swallow small amnt at a time
• 5. forget a single dose, give when you remember
• 6. Count apical pulse for 1 full minute:  withhold and notify physician if apical pulse is:
•    < 100bpm in infant
•    < 70bpm in child
• 7. Withhold and call MD if:  apical pulse rate is progressively decreasing or apical pulse rate is markedly lower than previous rate
• 8. if vomits dose, do not repeat.  Resume digoxin at next dosage time
• 9. if miss or vomit 2 doses in a row call MD immediately

• 1. GI:  NV & anorexia
• 2. Cardiac:  bradycardia and dysrhythmia

furosemide/lasix

• 1. water
• 2. Na
• 3. Cl
• 4. Mg
• 5. Ca
• 6. K

• K
• supplements

monitor daily weight- weight gain means not working

50g

200g

ACE inhibitor

pulmonary hypertension r/t elevated pulm pressure

captopril/capoten b/c it can be given in smaller doses

decreases serum Na and increases K

no K supplement will be needed

left to right shunting heart defects:  ASD, VSD, AVSD, and PDA

1. increased pulmonary blood flow r/t L to R shunting heart defects (usually VSD or PDA) -> loss of elasticity in pulm artery vessels -> increased pulmonary vascular resistance to blood flow -> blood flow shunting changes to R to L (Eisenmenger syndrome) -> went from being noncyanotic to cyanotic

• 1. cyanosis or hypoxemia
• 2. R ventricle hypertrophy
• 3. R sided heart failure

• 1. surgical repair of congenital defects in first 3 to 6 mo of life before the dev of pulm hypertension and Eismenger syndrome
• 2. Tx of CHF s/s
• 3. avoid strenuous exercise
• 4. avoid high altitudes
• 5. admin of inhaled NO (nitrous oxide)

change from acyanotic shunting of blood from L to R to cyanotic shunting of blood from R to L

1. vasodilation of the pulm arteries

when O2 sat is < 85%

blue discoloration of MM, skin, and nail beds

• 1. assess in natural light
• 2. assess skin of centra MM of mouth and conjunctiva and nail beds
• 3. assess general skin color also

• 1. low HgB level - s/s of cyanosis will take longer to show
• 2. high HgB level - s/s of cyanosis will show faster

6-11

low HgB will go from pink to pale

high will go from pink to blue

polycythemia

• 1. anemia
• 2. pulmonary hypertension
• 3. endocarditis
• 4. polycythemia
• 5. hypercyanotic episodes or tet spells

compensatory response of body in an attempt to improve tissue oxygenation in response to hypoxemia

• 1. increased bruising
• 2. prolonged bleeding

increase in RBC in vascular space crowds out plasma and clotting factors

3. CNS injury r/t abscess or CVA events r/t increased blood viscosity

• 1. poor oral intake
• 2. NV
• 3. diarrhea
• 4. elevated temp (fever or environment)

all can lead to dehydration -> hemoconcentration of blood & increased viscosity (already viscious r/t polycythemia compensatory reaction to hypoxemia)

should be kept cool

• 1. seen most frequently in first 2 years of life
• 2. occur mainly in morning
• 3. often preceded by crying feeding, or defcation
• 4. usually self-limiting but can progress to vicious cycle that can be fatal if not recognized and treated - diminished cerebral oxygenation and ischemic brain injury

• 1. rapid and depp resp
• 2. irritabilty and crying
• 3. peripheral vasodilation
• 4. increased systemic enous return - increased preload
• 5. increased cyanosis

no

• 1. place in cardiac position
•     infant in knee-chest
•     child in squatting position
• 2. calm the child
• 3. morphine sulfate
• 4. drugs that cause vasoconstriction to increase systemic vascular resistance which will decrease the degree of R to L shunting and force blood into the pulm system

suppresses resp center -> decreases preload

(increased resp increase blood flow to the heart )

• 1. hand washing
• 2. avoid crowded areas - esp ppl with resp infections
• 3. ABX prophylaxis

resp infections increase cardiac workload and lead to increased cyanosis and desaturation

• 1. pulmonary hygiene
• 2. chest physiotherapy
• 3. prophylactic ABX
• 4. oxygen

goal:  increase caloric density

intervention:  increase calories with smaller intake of formula

• 1. addition of supplement to infant's formula
• 2. feed soon after awakening
• 3. feed q 3 h
• 4. soft preemie nipple or slit a regular nipple
• 5. position in semi-upright position
• 6. rest periods during feeding
• 7. stroke jaw and cheek to encourage sucking
• 8. limit feedings to no longer than 1/2
• 9. Enteral or gavage feedings, NG tube, gastrostomy tube and/or percutaneous gastrostomy tube (PEG)

q 3 h

interventional procedure or therapeutic procedure

femoral vein or artery into venous or arterial system and then into heart

• 1. Measure O2 sat and pressure in cardiac chambers and arteries
• 2. eval cardiac output
• 3. ID images of structures and blood flow patterns
• 4. map cardicac conduction
• 5. ID locus of arrhythmia-producing cells
• 6. corrective or palliative interventional procedures

• 1. pulm artery or value and aortic  vavle balloon angioplasty
• 2. stent placement to maintain patency of vessels
• 3. repair to cardiac defects

• 1. arrhythmia
• 2. hemorrhage
• 3. vascular damage
• 4. vasospasms of catheterized vessel
• 5. thrombus formation and then leads to embolus
• 6. infection
• 7. reaction to dye
• 8. catheter perforation

• 1. poor perfusion to affected leg
• 2. weak or absent peripheral pulses
• 3. cool, mottled, pallor, and/or cyanosis to extremity
• 4. <3sec CRT

1. lung:  dyspnea, tachypnea, and chest pain

2. brain:  altered LOC, and stroke like s/s

• 1. rash
• 2. pruritis
• 3. mild vomiting
• 4. severe anaphylaxis (rare)

• 1. cardiac tamponade due to fluid accumulation withing the pericardium
• 2. cardiac arrest

• 1. locate and mark distal pulses before the procedure (femoral - popliteal / pedal)
• 2. position affected leg straight for 4 to 6 h after procedure
• 3. HOB raised at only a 20 degree incline - older children (flat is best)
• 4. maintain IV fluids until taking and retaining po fluid

to facilitate ease of assessment post procedure

distal pulses

• 1. obtain q 5 to 15 min for first hour
• 2. continuous initial monitoring of heart rate and BP
• 3. resp rate
• 4. O2 sat
• 5. temp

• 1. dressing
• 2. on sheets
• 3. under child to check for pooled blood
• 4. remove infant's diaper to check perineal area for bleeding under the skin

• 1. place gloved heel of the hand firmly on insertion site
• 2. apply pressure for at least 10 to 15 minutes
• 3. assess the distal perfusion of extremeity
• 4. imm notify cardiologist

• 1. infective endocarditis
• 2. rheumatic fever
• 3. kawasaki disease

inflammation of cardiac valves and endocardium with vegetative growth on valve

inner lining of heart

bacteria, virus, and fungus

• 1. poor oral hygiene
• 2. oral peircings
• 3. dental work
• 4. invasive surgery to resp tract
• 5. UTI
• 6. org. can enter BF from any site of localized infection

poor oral hygiene -> bacteria to heart

infective agent -> vegetational growth (verrucae) on endocardium -> formation of fibrin and platelet thrombi-> invasion of aortic and mitral values-> breaking off of vegetation (emboli)-> spleen, kidney, and CNS ischemia

• 1. low-grade intermittent fever
• 2. anorexia
• 3. nausea
• 4. fatigue
• 5. malaise
• 6. arthralgias
• 7. chest pain
• 8. heart failure
• 9. new murmur
• 10. change in quality of old murmur

• 1. spliter hemorrhages (thin black lines) under nails
• 2. Osler nodes
• 3. Janeway lesions
• 4. petechiae on oral MM

red, painful intradermal nodes found on pads of phalanges

painless hemorrhagic areas on palms and soles

• 1. blood cultures:  anaerobic first then aerobic
• 2. echocardiography
• 3. erythrocyte sedimentation rate - increased
• 4. c-reactive protein- increased
• 5. ECG changes

PREVENTION:

• 1. good oral hygiene:  brushing and flossing; start in infancy
• 2. antibiotic therapy before:  dental procedures, resp, GU, GI, and musculoskeletal, any invasive procedure an/or surgery
• 3. teach parents

put blood in anaerobic bottle first to prevent air from getting in there then put in with aerobic and air will go in with it

• Notify pediatrician if experiencing any of the following s/s: (don't think just cold or flu)
• 1. unexplained fever
• 2. weight loss
• 3. change in behavior
• 4. lethargy
• 5. malaise
• 6. anorexia

prevent further cardiac damage, embolic complications and growth of resistant organisms

• 1. vital signs q 2 to 4 h
• 2. thorough CV and neurologic assessment q
• 3. Admin IV ABX ON TIME
• 4. provide age app. activities that allow for conservation of energy
• 5. videos, drawing, puzzles, reading

give ABX on time

diffuse inflammatory condition that occurs after infection with group A beta-hemalytic strep infection of upper respiratory tract

2 to 6 wks after strep infection

joints, skin, brain, serous surfaces, heart esp. valves

• 1. tachycardia out of proportion to degree of fever
• 2. cardiomegaly
• 3. new murmurs or change in preexisting murmurs
• 4. muffled heart sounds
• 5. pericardial friction rub
• 6. chest pain

• 1. involvement of more than 4 joints
• 2. swollen, warm, erythmatous
• 3. painful
• 4. usually in larger joints:  elbow, knee, ankle, wrist

• 1. sudden aimless, irregular movements of extremeities
• 2. involutary facial grimaces
• 3. emotional lability (instability)
• 4. muscle weakness (can be profound)
• 5. muscle movements exaggerated by anxiety and attempts at fine more activity; relieved by rest
• 6. latency period:  s/s may occur up to 5 mo. after strep pharyngitis

sudden aimless, irregular movements

rash

• 1. annular (circular or ring)
• 2. wavy, well-demarcated border
• 3. erythematous macules
• 4. clear center

• 1. nontender swelling
• 2. located over bony prominences
• 3. may persit for some time, then gradually resolve
• 4. rarely occur & usually as. with severe carditis

• 1. carditis
• 2. polyarthritis
• 3. chorea or sydenham's chorea
• 4. erythema marginatum
• 5. subcutaneous nodules

• 1. fever
• 2. arthralgia
• 3. elevated erythrocyte sedimentation rate
• 4. positive C-reactive protein
• 5. supporting eveidence of antcedent group A strep infection:  postivie throat culture
• 6. increase in ASO titer

must have presence of 2 major manifestations OR 1 major and 2 minor manifestations

• 1. carditis
• 2. polyarthritis
• 3. chorea
• 4. erythema marginatum
• 5. subcutaneous nodules

to eval damage to valves myocardium, and pericardium

• 1. eradication hemolytic streptococci
• 2. prevention of permenant cardiac damage
• 3. palliation of other symptoms

• 1. PVK is drug of choice
• 2. antiinflammatory agents
•     salicylates
•     corticosteroids

erythromycin

will follow them medically for at least 5 years

for the rest of their lives

ABX prophylaxis for:  dental work, infection, and any invasive procedure

• 1. IM PVK q month or qd po antibiotic
• 2. without cardiac complications - 5 years or thourgh age 21 to 25 years whichever is longer
• 3. with rheumatic heart disease - for at least 10 years and at least until age 40

• 1. Bed rest during acute febrile stage
• 2. limit visitors
• 3. encourage contact: phone, letters, cards
• 4. quiet activities to minimize cardiac demands
• 5. place back on bedrest if heart rate increases by more than 20bpm over resting rate
• 6. perform thoroug CV assessment
• 7. provide non-pharm therapies for pin relief
• 8. chorea interventions

• 1. monitor apical pulse 1 full minute for changes in rate, rhythm, mumurs and pericardial friction rub
• 2. assess for edema on face bad, and ankles
• 3. assess for SOB- esp bad if occurs under minimal exertion

• 1. alternating heat and cold to joints for comfort
• 2. massage
• 3. distraction or diversional activities:  play therapy, guided imagery, relaxation exercises

• 1. Ch sleep on floor
• 2. no rugs
• 3. no oral temps
• 4. spoon only no forks
• 5. symptoms are temporary

mucocutaneous lymph node syndrome

• 1. acute
• 2. not communicable
• 3. idiopathic etiology
• 4. antecedent upper resp illness

most in children less than 5 with peak 18 to 24 mo

more in boys than girls and more in Asians

trigger (infection/toxin) -> immune response -> edema and inflammation of vascular walls -> weakens vascular walls & fibrous connective tissue forms

weakened vascular walls -> can cause aneurysm

fibrous conn. tissue forming -> thickening, scarring, & increased platelets -> thrombus formation ->

STRAWBERRY

• S -swollen lymph nodes
• T-tongue red & swollen
• R- rash
• A -arthritis like pain
• W- whites of eyes are red (conjunctivitis)
• B- burning (fever 102-106F) unresp to ABX
• E- edema of hands and feet
• R- red hands and feet
• R- red, chapped, cracked lips
• Y- young child <5

at risk for aneurysm and MI

• 1. high fever - 102 to 106 that is unresponsive to ABX
• 2. bilateral, nonpurulent conjunctivitis
• 3. changes in MM
• 4. swelling and redness of hands & feet
• 5. generalized erythematous rash
• 6. enlared cervical lymph nodes

• 1. erythema
• 2. fissures of tongue
• 3. cracking of lips
• 4. strawberry tongue

day 15 to 25

• 1. irritability
• 2. anorexia
• 3. desquamation (peeling) of fingers and toes
• 4. arthritis
• 5. arthralgia
• 6. CV s/s

• 1. CHF
• 2. arrhythmias
• 3. coronary aneurysms

• 1. normal sedimentation rate
• 2. no s/s of illness

• 1. fever of 5 days duration in conjunction with at least 4 of the 5 primary clinical findings
• 2. Dx tests

• 1. bilateral nonpurulent conjuctivitis
• 2. oral mucosal alterations
• 3. redness of hands & feet followed by desquamation
• 4. rash on trunk
• 5. cervical lymphadenopathy and no other known disease to explain s/s

• 1. lab data nonspecific
• 2. WBC elevated
• 3. elevated erythrocyte sedimentation rate
• 4. elevated C-reactive protein
• 5. sterile pyuria
• 6. elevated platelet count
• 7. echocardiography to detect aneurysm

prophylactic aspirin or coumadin

• 1. aneurysm
• 2. MI

• 1. abd pain
• 2. vomiting
• 3. restless
• 4. inconsolable crying
• 5. pallor
• 6. shock

• 1. IV gamma globulin
• 2. salicylate therapy
• 3. tx of coronary abnormalities with salicylates for life and may get coumadin for large aneurysms

• 1. high dose until fever subsides
• 2. maintenacne - low dose until platelet count returns to normal and no coronary abnormalities

• 1. assess CV status carefully
• 2. assess fluid status
• 3. monitor for S/S of complications:  CHF, thromboembolism, and MI
• 4. symptomatic relief
• 5. delay live-virus vaccines for 11 months after receiving IVIG (MMR & varicella)

• 1. sponge baths with tepid water
• 2. cool cloths to skin
• 3. soft, loose clothing
• 4. mouth care
• 5. clear liquids and soft bland foods
• 6. high in calories and low in acid
• 7. use straw
• 8. salve to lips
• 9. irritability
• 10. talk in gentle tones, play soft music, avoid bright overhead lights, bring soft blankets from home and provide parents time away fro child due to child's irritabiltiy

IV gamma globulin

no live viruses for 11 mo after admin