MB4 peds cardiac Forsythe

Card Set Information

Author:
mthompson17
ID:
214806
Filename:
MB4 peds cardiac Forsythe
Updated:
2013-04-21 20:19:58
Tags:
Cardiovascular nursing pediatrics
Folders:

Description:
Pediatric CV test 4
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user mthompson17 on FreezingBlue Flashcards. What would you like to do?


  1. Which arm gets arterial blood first?

    Consideration?
    right arm

    most accurate ABG will come from a R radial stick
  2. How many arteries and veins are in the umbilical cord?

    What is their function?
    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
  3. Where does oxygenation take place in the fetus?

    What is oxygenation?
    placenta

    gas exchange
  4. How does oxygenated/nutrient rich blood get from the placenta to the fetus?
    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
  5. Why is blood shunted away from the liver and lungs?
    the baby isn't breathing or metabolizing stuff with the liver so they don't need much blood
  6. What are the 3 shunts that direct O2 rich blood in the fetus? (in order)
    • 1. ductus venosus
    • 2. foramen ovale
    • 3. ductus arteriosus
  7. What is the function of the ductus venosus?

    Where does the blood go?
    routes the blood from the liver into inferior vena cava then the blood enters the R atrium
  8. What happens to O2 rich blood from the placenta once it reaches 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
  9. What occurs in the L atrium of the fetal heart?
    mixing of blood from the R atrium & blood returning from the lungs
  10. 2 most O2 needy organ systems of the fetus?
    brain & coronary arteries (heart)
  11. Flow of blood returning from the upper body?
    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
  12. What can congenital anomalies cause?
    openings b/t the chambers of the heart
  13. What will occur with L to R shunting?

    4 types of defects that can cause this?
    increased pulmonary blood flow

    ASD, VSD, AVSD, PDA
  14. ASD?
    atrial septal defect
  15. VSD?

    Prognosis?
    ventricular septal defect

    close spontaneouly 30 to 40% of the time
  16. AVSD?

    Ass with what?
    atrioventricular septal defect

    Ass. with genetic syndromes - down syndrome
  17. Common occurance with CH with congenital defects?
    resp infections
  18. Consideration if a child is born with down syndrome?
    will need heart checked well for AVSD
  19. PDA?

    What babies are most at risk for this?
    patent ductus arteriosus

    premature <28 weeks
  20. Patho effects of L to R shunting?
    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
  21. 3 complications that can occur with L to R shunting?
    • congestive heart failure CHF
    • pulmonary hypertension
    • frequent resp infections
  22. What do obstructuive or stenotic probs cause?

    3 congenital probs that can cause this?
    decreased cardiac outflow

    • 1. coarctation of the aorta
    • 2. aortic stenosis
    • 3. pulmonary stenosis
  23. 3 complications r/t obstructive/stenotic defects?
    • CHF
    • heart failure
    • stroke
  24. 4 congenital probs that cause cyanotic defects r/t decreased pulmonary blood flow?
    decreased pulmonary blood flow

    • 1. tetralogy of Fallot
    • 2. tricuspid atresia
    • 3. total anomalous pulmonary venous return
    • 4. pulmanary atresia with intact ventricular septum
  25. 3 complications ass. with cyanotic defects r/t decreased pulmonary blood flow?
    • emboli
    • seizures
    • sudden death
  26. 3 congenital defects ass. with cyanotic defects r/t increased pulmonary blood flow?
    • 1. truncus arteriosus
    • 2. transposition of the great arteries
    • 3. hypoplastic L heart syndrome
  27. 3 complications r/t cyanotic defects due to increased pulm blood flow?
    • CHF
    • heart failure
    • death
  28. Why does it take years-decades for an ASD person to become symptomatic?
    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
  29. What occurs in ASD?
    the foramen ovale remains open
  30. What happens to blood in a L to R shunt defect?
    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
  31. Why is blood shunted from the L side of the heart to the R in L to R shunt defects?
    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
  32. Patho of L to R shunt?
    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
  33. What is the site of the abnormal opening in ASD?
    atrium - foramen ovale remains open
  34. When will a person with ASD become symptomatic?
    years to decades when heart failure begins to occur
  35. Clinical manifestations of ASD?
    • 1. palpitations or atrial arrhythmias
    • 2. systolic murmur
    • 3. CHF later in life (rare in CH)
  36. What causes palpitations/atrial arrhythmias in ASD?
    atrial enlargement
  37. What causes systolic murmur in ASD?
    increased BF across the pulmonary valve
  38. Site of abnormal opening in VSD?
    ventricle
  39. 3 S/S of VSD?
    • 1. murmur (systolic/from book)
    • 2. thrill
    • 3. gallop rhythm
  40. Tx of VSD?
    usually spontaneously closes
  41. AVSD?

    S/S?

    TX?
    atrioventricular septal defect - hole in atrium and ventricle

    S/S of CHF

    usually spontaneously closes
  42. Main concern with PDA?
    patent ductus arteriosus - increased workload on the L side of the heart
  43. Which heart defect is ass. with a heart murmur that is continuous and sounds like a machine?
    PDA
  44. Which heart defect is ass. with palpitations, atrial arrhythmias, systolic murmur, and CHF in late childhood?
    ASD
  45. Which heart defect is ass. with murmur, thrill, and gallop rhythm of the heart?
    VSD
  46. Main hormone that causes vasodilation and brings in WBC to site of inflammation?

    What drug can be used to inhibit this hormone and constrict the ductus arteriosus in PDA?
    prostaglandin

    indocin/indomethacin
  47. 2 L to R shunt heart defects that may resolve spontaneously?
    VSD & AVSD
  48. Site of the abnormal opening in PDA?

    What effect does this have on the heart?
    aorta and pulmonary artery

    increases the workload on the L side of the heart
  49. 9 S/S of PDA?
    • 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
  50. Why does pulse pressure widen with PDA?
    continuous "runoff" of the aortic blood flow to the pulmonary arteries
  51. 4 L to R shunting defects?

    4 Tx that may be used for all of the L to R shunting defects?
    • 1. ASD
    • 2. VSD
    • 3. AVSD
    • 4. PDA

    • 1. CHF Tx
    • 2. interventional cardiac catheterization
    • 3. surgery
    • 4 increased caloric density of formula
  52. What cardiac defects increase pulmonary blood flow?
    L to R shunting defects:  ASD, VSD, AVSD, PDA
  53. Blood flow in L to R shunting?
    O2 blood from the left is forced through abnormal opening into the R side -> pulmonary artery -> lungs -> L atrium
  54. L to R shunting involves _____ blood flowing into ______ blood.
    oxygenated into deoxygenated
  55. Which cardiac defects involve decreased cardiac outflow?
    obstructive or stenotic defects
  56. Which side of the heart is most effected by obstructive/stenotic defects?
    L side
  57. CAP?
    • obstructive or stenotic defects: 
    • Coarctation of the aorta
    • Aortic stenosis
    • Pulmonary stenosis
  58. What heart defect is ass. with a disparity in BP and pulses b/t the upper and lower body? 

    Describe the dispartiy.
    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
  59. What pulse is checked in infants?
    brachial not radial
  60. Where can the most accurate BP be obtained?

    Why?
    from the R arm b/c blood flow there slightly fast than to L
  61. Patho of coarctation of the aorta?
    constriction of the aorta (descending) near the ductus arteriosus -> increases workload on L ventricle
  62. What is the end result of coarctation of the aorta?

    3 s/s of this?
    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
  63. What is the major s/s of coarctation of the aorta?
    disparity in pulses and BP b/t upper and lower body
  64. Tx of coarctation of the aorta?

    Action?
    PGE1 - prostaglandin to vasodilate -> causes ductus arteriosus patency -> increases blood flow to the lower body
  65. What will BP be like before and after the point of the coarctation of the aorta?
    before = high BP

    after = low BP
  66. Aortic stenosis?

    3 places it may occur?
    obstruction to blood flow leaving L ventricle that occurs near the aortic valve

    May be supravalvular, subvalvular, or at the level of the valve
  67. Patho of aortic stenosis?
    stenosis of the aortic valve -> increased workload on the L ventricle r/t small opening -> L ventricular hypertrophy
  68. Key indicator of heart probs in an infant?
    feeding difficulties and/or inadequate weight gain r/t dyspnea
  69. Pulmonary stenosis ass. with ____ sided heart failure?
    right
  70. Pulmonary stenosis?

    3 places may occur?
    obstruction to blood flow leaving the R ventricle

    • 1. level with pulm valve
    • 2 supvalvular
    • 3. supravalvular
  71. What is the end result of aortic stenosis?
    L ventricular hypertrophy
  72. S/S of aortic stenosis?
    may be asymptomatic

    • 1. faint peripheral pulses
    • 2. severe CHF
    • 3. feeding difficulties
  73. Why may CHF develop with aortic stenosis?
    blood backs up into pulmonary circulation
  74. End result of pulmonary stenosis?
    R ventricle hypertrophy
  75. S/S of pulmonary stenosis?
    asymptomatic to s/s of CHF
  76. 3 common Tx for obstructive/stenotic defects?
    • 1. CHF tx
    • 2. interventional cardiac catheterization
    • 3. surgery
  77. 4 heart defects involving cyanotic defects with decreased pulmonary blood flow?
    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
  78. Complication that may occur with aortic stenosis?

    Tx?
    endocarditis

    Tx with prophylactic ABX long term
  79. What lesions/defects of the heart are considered non-cyanotic? (7)
    • 1. ASD
    • 2. VSD
    • 3. AVSD
    • 4. PDA
    • 5. coarctation of the aorta
    • 6. aortic stenosis
    • 7. pulmonic stenosis
  80. 7 lesions/defects that are considered cyanotic lesions?
    • 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
  81. When will cyanosis occur in cyanotic heart lesions?
    soon after birth
  82. Tetralogy of Fallot?
    malalignment of ventricular septum resulting in 4 deformities
  83. 4 deformities of tetrology of Fallot?
    • 1. VSD
    • 2. pulmonary stenosis
    • 3. overriding of aorta into the R ventricular side instead of L (opens into both)
    • 4. R ventricular hypertrophy
  84. What is the purpose of PGE1 in cardiac deformities?
    maintiain patency of the ductus arteriosus

    prostaglandin= vasodilation
  85. Hemodynamic alteration in tetralogy of Fallot?
    varies widely due to degree of each defect - can be left to right or right to left shunting
  86. Cyanosis in tetrology of Fallot?
    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
  87. 2 names for hypercyanotic episodes?
    1. tet spells

    2. blue spells
  88. S/S of tetralogy of Fallot?
    • 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
  89. Tx for tetralogy of Fallot?
    • 1. PGE1 infusion to maintain ductal patency
    • 2. positioning during cyanotic episodes
    • 3. elective surgery in the first year of life
  90. Where does the thrill occur in tetralogy of Fallot?
    over the pericordium
  91. Positioning for infants and children during a hypercyanotic episode?
    infants - knee to chest

    children - squatting
  92. Tricuspid atresia?
    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
  93. What happens to the blood in tricuspid atresia?

    Result of this?
    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
  94. S/S of tricuspid atresia?
    1. cyanosis dev from birth to few hours of life

    2. single first heart sound
  95. Why is there only one heart sound in tricuspid atresia?
    there is no closure of the tricuspid valve
  96. Tx of tricuspid atresia?
    PGE1 infusion

    interventional cardiac catheterization

    surgery
  97. Total anomalous pulmonary venous return?
    pulmonary veins don't empty O2 blood into L atrium but will empty somewhere else in heart
  98. 2 places where the pulmonary veins might dump O2 blood in total anomalous pulmonary venous return?
    • 1. R atrium
    • 2. superior vena cava via an innominate vein
  99. What occurs in the R atrium with total anomalous pulmonary venous return?
    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
  100. End result of tatal anomalous pulm venous return?
    R sided hypertrophy
  101. 3 s/s of total anomalous pulmonary venous return?
    • 1. severe cyanosis
    • 2. resp distress
    • 3. progressive clinical deterioration
  102. What is the function of the pulmonary veins?
    carry O2 blood from lungs to the L atrium
  103. What heart defect is associated with cyanosis, tet spells, tiring easily, difficulty feeding, difficulty gaining weight, and a harsh systolic murmur accompanied by thrill
    tetralogy of Fallot
  104. Tx of total anomalous pulmonary venous return?
    surgery soon after birth

    not viable without it
  105. What heart defect requires patent ductus arteriosus for survival?

    Why?
    pulmonary atresia with intact ventricular septum

    blood cannot get to lungs otherwise b/c pulm valve is missing
  106. Pulmonary atresia with intact ventricular septum?
    pulmonary valve doesnt develop and hypoplastic development of the pulonary artery and right ventricle occurs
  107. Hypoplastic?
    under-developed
  108. s/s of pulmonary atresia with intact ventricular septum?

    Tx?    Why?
    profound cyanosis

    continuous PGE1 infusion - must have presence of PDA for survival

    surgery
  109. Truncus arteriosus?
    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
  110. What is the common great artery that occurs in truncus arteriosus called?

    What occurs here?

    What are the 2 end results?
    truncus arteriosus

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

    hypoxemia and desaturation of blood
  111. S/S of truncus arteriosus?
    • 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
  112. 2 heart defects that may cause widened pulse pressures?
    ductus arteriosus & PDA
  113. 2 Tx for truncus arteriosus?
    • 1. CHF tx
    • 2. surgery
  114. Which heart defect involves malalignment of ventricular septum resulting in 4 deformities?
    tetralogy of Fallot
  115. What heart defect involves pulmonary veins not emptying into the L atrium but emptying into R atrium instead?
    total anomalous pulmonary venous return
  116. Which heart defect involves obstruction to blood flow leaving R ventricle?
    pulmonary stenosis
  117. Which heart defect involves pulmonary valve not developing?
    pulmonary atresia with intact ventricular septum
  118. Which heart defect involves constriction of aorta?
    coarctation of the aorta
  119. Which heart defect involves obstruction to blood flow leaving the L ventricle?
    aortic stenosis
  120. Which heart defect involves the tricuspid valve not developing?
    tricuspid atresia
  121. Which heart defect involves failure of normal separation and division of the aorta and the pulmonary artery?
    truncus arteriosus
  122. Transportation of the great arteries?
    pulmonary artery leaves L ventricle and the aorta exits from R ventricle with no communication b/t the systemic and pulmonary circulations
  123. What must occur in transposition of the great arteries in order to have blood entering systemic and pulmonary circulation?
    must be ass. defects such as septal or patent ductus arteriosus
  124. 3 s/s of transposition of the great arteries?
    • 1. cyanotic
    • 2. heart sounds vary according to type of defect
    • 3. cardiomegaly within few weeks after birth
  125. 2 Tx for transposition of the great arteries?
    PGE1

    surgery
  126. 5 anomalies ass. with transposition of the great arteries?
    • 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
  127. 4 consequences of cyanotic lesions with increased pulmonary blood flow?
    • 1. CHF
    • 2. pulmonary hypertension
    • 3. cyanosis
    • 4. hypercyanotic episodes
  128. Hypoplastic left heart syndrome?
    inadequate dev of L side of heart results in only one effective ventricle

    may include other congenital defects
  129. S/S of hypoplastic L heart syndrome?
    • tachypnea
    • early CHF
    • systemic hypoperfusion
    • shock
  130. Tx of hypoplasic L heart syndrome?
    • PGE1 infusion
    • surgical staged repair
    • cardiac transplantation
  131. What type of heart defect involves pulmonary artery leaving L ventricle and aorta leaving R ventricle?
    transposition of the great arteries
  132. Patho of CHF?
    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
  133. Etiologies of CHF?
    1. anemia r/t altered nutrition secondary to VSD

    2. resp infection r/t VSD
  134. S/S of CHF r/t etiologies of CHF?
    • 1. feedings take too long
    • 2. tachypnea with feeding
    • 3. cold-like s/s
  135. s/s of CHF r/t stim of SNS?
    diaphoresis  & tachycardia
  136. S/S of CHF r/t peripheral vasoconstriction and increased pulm vascular resitance?
    • 1. < CRT
    • 2. mottling
    • 3. pallor
    • 4. cyanosis
    • 5. pale cool extremeties
    • 6. weak peripheral pulses
  137. s/s of CHF r/tdecreased blood flow to the body system?
    decreased UO
  138. s/s of CHF r/t Na and H2O retention and increased blood volume?
    • 1. weight gain
    • 2. peripheral edema
    • 3. periorbital and facial edema
    • 4. neck vein distention
  139. S/S of CHF r/t systemic and pulm venous engorgement and cardiomegaly & hepatosplenomegaly?
    • 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
  140. Tx for increased afterload occuring in CHF?
    • digoxin to increase contractility
    • ACE inhibitors to decrease absorption of water and Na
  141. Nursing intervention for decreased UO in CHF?
    monitor I & O
  142. 3 types of clinical manifestations that occur in CHF?
    • 1. impaired myocardial function
    • 2. pulmonary congestion
    • 3. systemic venous congestion
  143. 12 cardiac s/s of CHF?
    • 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
  144. 14 pulmonary congestion s/s of CHF?
    • 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
  145. 6 s/s of venous congestion r/t CHF?
    • 1. weight gain
    • 2. periorbital and facial edema - most common
    • 3. peripheral edema
    • 4. ascites
    • 5. neck vein distention in ch
    • 6. hepatosplenomegaly
  146. Tx for edema in CHF?
    • 1. diuretics
    • 2. weigh daily
    • 3. I & O
    • 4. skin care
    • 5. position frequently
    • 6. monitor electrolytes:  Na, K, and MG esp. K
  147. Increased blood volume = increased _____.

    How can preload be decreased?
    preload

    elevate HOB 30 - 45 degress
  148. 4 Tx for increased blood volume in CHF?
    • 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
  149. Effect of stimulation of the SNS on vascular system?
    peripheral vasoconstriction
  150. Which cardiac defect is associated with endocarditis?
    aortic stenosis
  151. 3 main effects of CHF?
    • 1. impaired myocardial function
    • 2. pulmonary congestion
    • 3. systemic venous congestion
  152. 7 early S/S of CHF?
    • 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
  153. Appearance of baby with CHF?
    will look wasted and have no booty
  154. If heart is not pumping well what will occur?

    Tx?
    decreased blood pressure and flow to the kidneys and decreased UO

    digoxin
  155. Why does the body retain Na and water in CHF?

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

    give lasix - loop diuretic
  156. 3 digoxin effects?
    • 1. decreases heart rate
    • 2. increases heart contractility
    • 3. increases O2 to tissues
  157. Digoxin?

    Other one?
    cardiac glycoside

    lanoxin
  158. Lasix?
    loop diuretic

    furosemide
  159. ACE inhibitor for CHF?
    captopril/capoten
  160. Nursing interventions for echocardiography?
    • 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
  161. Tx goals for CHF?
    • 1. improve cardiac function to increase contractility
    • 2. remove accumulated fluid and Na
    • 3. decrease cardiac demands
    • 4. improve tissue perfusion/oxygenation
  162. Meds for CHF?
    • 1. digoxin/lanoxin
    • 2. furosemide/lasix
    • 3. captopril/capoten
  163. Digoxin name brand, function, classification?
    lanoxin

    increases cardiac contractility, decreases pulse, and increases tissue perfusion

    cardiac glycoside
  164. Furosemide name brand, function, and classification?
    lasix

    loop diuretic - decreases Na and water
  165. Captopril name brand, function, and classification?
    capoten

    decreases water and Na retention

    ACE inhibitor
  166. Positive ionotropic effect?
    increased force of ventricular contraction
  167. Negative chronotropic effect?
    slows heart rate and allows the ventricles to have more time to fill with blood
  168. Action of digoxin?

    3 ways this is accomplished?
    increased cardiac output

    • 1. positive ionotropic effect
    • 2. negative chronotropic effect
    • 3. decreases preload and afterload
  169. Advantage of slowing of heart rate with digoxin?
    decreases cardiac demands
  170. Digoxin effect on kidneys?
    will increase kidney perfusion and have a small diuretic effect
  171. 2 end results of digoxin used in CHF?
    • 1. improves tissue perfusion
    • 2. removes accumulated fluid and Na by perfusion kidneys (mild diuresis)
  172. Therapeutic range of digoxin?
    0.8-2 mg/mL
  173. Electrolyte imbalances that potentiate digoxin toxicity?
    • 1. hypo and hyperkalemia
    • 2. hypercalcemia
    • 3. hypomagnesemia
  174. Digoxin forms and availability?
    IV injection

    PO elixir or tabs
  175. Digoxin dosage?
    digitalizing dose:  oral or IV in divided doses over 24 h

    maintenance dose:  oral bid:  am and pm to maintain blood levels
  176. Giving your child digoxin elixir things to tell pt?
    • 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
  177. Common s/s of digoxin toxicity in children?
    • 1. GI:  NV & anorexia
    • 2. Cardiac:  bradycardia and dysrhythmia
  178. EX of a loop diuretic used in CHF?
    furosemide/lasix
  179. 6 things wasted by loop diuretics?
    • 1. water
    • 2. Na
    • 3. Cl
    • 4. Mg
    • 5. Ca
    • 6. K
  180. Most important electroyte to monitor if pt is on loop diuretics?

    What is the intervention?
    • K
    • supplements
  181. How do we monitor the effectiveness of furosemide in CHF?
    monitor daily weight- weight gain means not working
  182. Call MD if there is a weight gain of _____ g/day in infants or _____ g/day in children.
    50g

    200g
  183. What type of drug is captopril?
    ACE inhibitor
  184. Physiological consequence of CHF involving pulm?
    pulmonary hypertension r/t elevated pulm pressure
  185. What ACE inhibitor is given to young children with CHF?

    Why?

    Effect on Na and K?
    captopril/capoten b/c it can be given in smaller doses

    decreases serum Na and increases K

    no K supplement will be needed
  186. Which heart defect causes increased pulmonary blood flow?
    left to right shunting heart defects:  ASD, VSD, AVSD, and PDA
  187. Patho of pulmonary hypertension?
    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
  188. 3 complications of pulmaonary hypertension?
    • 1. cyanosis or hypoxemia
    • 2. R ventricle hypertrophy
    • 3. R sided heart failure
  189. Tx of pulmonary hypertension?
    • 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)
  190. Eisenmenger syndrome?
    change from acyanotic shunting of blood from L to R to cyanotic shunting of blood from R to L
  191. Therapeutic effects of nitrous oxide in pulm hypertension Tx?
    1. vasodilation of the pulm arteries
  192. When is hypoxemia/cyanosis seen?
    when O2 sat is < 85%
  193. Cyanosis?
    blue discoloration of MM, skin, and nail beds
  194. Assessment of cyanosis?
    • 1. assess in natural light
    • 2. assess skin of centra MM of mouth and conjunctiva and nail beds
    • 3. assess general skin color also
  195. HgB effects on cyanosis?
    • 1. low HgB level - s/s of cyanosis will take longer to show
    • 2. high HgB level - s/s of cyanosis will show faster
  196. Low HgB?
    6-11
  197. O2 sat of 84% with low HgB what will color be?

    If have high HgB what will color do?
    low HgB will go from pink to pale

    high will go from pink to blue
  198. Another name for high HgB?
    polycythemia
  199. 5 complications of hypoxemia?
    • 1. anemia
    • 2. pulmonary hypertension
    • 3. endocarditis
    • 4. polycythemia
    • 5. hypercyanotic episodes or tet spells
  200. Polycythemia?

    Why does it occur?
    compensatory response of body in an attempt to improve tissue oxygenation in response to hypoxemia
  201. Complications of polycythemia?

    Why does these occur?
    • 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
  202. 4 reasons to seek medical care immediately if a child has pulmonary hypertension?

    Why are these things important?
    • 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)
  203. What should temp of room be for child with pulmonary hypertension?
    should be kept cool
  204. 4 char. of hypercyanotic episodes and tets spells?
    • 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
  205. S/S of hypercyanosis and Tets spells?
    • 1. rapid and depp resp
    • 2. irritabilty and crying
    • 3. peripheral vasodilation
    • 4. increased systemic enous return - increased preload
    • 5. increased cyanosis
  206. Is incidence of hypercyanotic spells related to degree of baseline desaturation and cyanosis?
    no
  207. Tx of hypercyanotic episodes in order of priority?
    • 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
  208. What is the effect of morphine sulfate given for Tets spells or hypercyanotic reactions?
    suppresses resp center -> decreases preload

    (increased resp increase blood flow to the heart )
  209. Interventions for risk for infection in pulmonary hypertension?
    • 1. hand washing
    • 2. avoid crowded areas - esp ppl with resp infections
    • 3. ABX prophylaxis
  210. Why is it imp to prevent resp infections in cardiac pt?
    resp infections increase cardiac workload and lead to increased cyanosis and desaturation
  211. 4 interventions to prevent resp infections in cardiac pt?
    • 1. pulmonary hygiene
    • 2. chest physiotherapy
    • 3. prophylactic ABX
    • 4. oxygen
  212. Nutrition goal and intervention for cardiac pt?
    goal:  increase caloric density

    intervention:  increase calories with smaller intake of formula
  213. Nursing interventions for nutrition in cardiac pt?
    • 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)
  214. How often should a cardiac pt be fed?
    q 3 h
  215. Cardiac catheterization purposes?
    interventional procedure or therapeutic procedure
  216. Routes of cardiac cath?
    femoral vein or artery into venous or arterial system and then into heart
  217. Cardiac cath purposes?
    • 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
  218. 3 corrective/palliative interventional heart caths?
    • 1. pulm artery or value and aortic  vavle balloon angioplasty
    • 2. stent placement to maintain patency of vessels
    • 3. repair to cardiac defects
  219. 7 complications ass. with cardiac cath?
    • 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
  220. 4 effects of vasospasms of the cath vessel in heart cath?
    • 1. poor perfusion to affected leg
    • 2. weak or absent peripheral pulses
    • 3. cool, mottled, pallor, and/or cyanosis to extremity
    • 4. <3sec CRT
  221. 2 systems effected by thrombus/embolus formation during heart cath and their s/s?
    1. lung:  dyspnea, tachypnea, and chest pain

    2. brain:  altered LOC, and stroke like s/s
  222. 4 s/s of reaction to heart cath dye?
    • 1. rash
    • 2. pruritis
    • 3. mild vomiting
    • 4. severe anaphylaxis (rare)
  223. 2 things that may occur with heart cath perforation?
    • 1. cardiac tamponade due to fluid accumulation withing the pericardium
    • 2. cardiac arrest
  224. Nursing care for heart cath?
    • 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
  225. Why do you need to mark pulses before heart cath?

    What pulses are marked?
    to facilitate ease of assessment post procedure

    distal pulses
  226. VS post-op heart cath?
    • 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
  227. 4 things to asses for bleeding post op heart cath?
    • 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
  228. Interventions for active bleeding post heart cath?
    • 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
  229. 3 acquired heart diseases?
    • 1. infective endocarditis
    • 2. rheumatic fever
    • 3. kawasaki disease
  230. Infective endocarditis?
    inflammation of cardiac valves and endocardium with vegetative growth on valve
  231. Endocardium?
    inner lining of heart
  232. 3 infective agents that can cause infective endocarditis?
    bacteria, virus, and fungus
  233. 6 etiologies of infective endocarditis?
    • 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
  234. Greatest risk factor for infective endocarditis?
    poor oral hygiene -> bacteria to heart
  235. Patho of infective endocarditis?
    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
  236. 10 Clinical manifestations of infective endocarditis?
    • 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
  237. 4 clinical manifestations of extracardiac emboli formation r/t infective endocarditis vegetation breaking loose?
    • 1. spliter hemorrhages (thin black lines) under nails
    • 2. Osler nodes
    • 3. Janeway lesions
    • 4. petechiae on oral MM
  238. Osler nodes?
    red, painful intradermal nodes found on pads of phalanges
  239. Janeway lesions?
    painless hemorrhagic areas on palms and soles
  240. Dx eval of infective endocarditis?
    • 1. blood cultures:  anaerobic first then aerobic
    • 2. echocardiography
    • 3. erythrocyte sedimentation rate - increased
    • 4. c-reactive protein- increased
    • 5. ECG changes
  241. Most important therapeutic management of infective endocarditis?

    How is this done?
    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
  242. Important consideration when doing blood cultures?
    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
  243. What to teach parents about infective endocarditis?
    • 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
  244. Rationale for early Tx of infective endocarditis?
    prevent further cardiac damage, embolic complications and growth of resistant organisms
  245. Interventions for infective endocarditis?
    • 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
  246. Priority care for child with infective endocarditis
    give ABX on time
  247. Rheumatic fever?
    diffuse inflammatory condition that occurs after infection with group A beta-hemalytic strep infection of upper respiratory tract
  248. When will rheumatic fever occur?
    2 to 6 wks after strep infection
  249. What areas of the body are affected RF?
    joints, skin, brain, serous surfaces, heart esp. valves
  250. Carditis effects r/t rheumatic fever?
    • 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
  251. Polyarthritis s/s in RF?
    • 1. involvement of more than 4 joints
    • 2. swollen, warm, erythmatous
    • 3. painful
    • 4. usually in larger joints:  elbow, knee, ankle, wrist
  252. S/S Chorea or Sydenham's Chorea ass. with RF?
    • 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
  253. Chorea?
    sudden aimless, irregular movements
  254. Erythema marginatum ass. with RF?

    4 char?
    rash

    • 1. annular (circular or ring)
    • 2. wavy, well-demarcated border
    • 3. erythematous macules
    • 4. clear center
  255. Subcutaneous nodules that occur in RF?
    • 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
  256. 5 major s/s of RF?
    • 1. carditis
    • 2. polyarthritis
    • 3. chorea or sydenham's chorea
    • 4. erythema marginatum
    • 5. subcutaneous nodules
  257. Minor clinical manifestations of RF?
    • 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
  258. Dx of RF?
    must have presence of 2 major manifestations OR 1 major and 2 minor manifestations
  259. 5 major clinica manifestations of RF?
    • 1. carditis
    • 2. polyarthritis
    • 3. chorea
    • 4. erythema marginatum
    • 5. subcutaneous nodules
  260. Echocardiogram for RF?
    to eval damage to valves myocardium, and pericardium
  261. 3 goals of medical management of RF?
    • 1. eradication hemolytic streptococci
    • 2. prevention of permenant cardiac damage
    • 3. palliation of other symptoms
  262. Drug therapy for RF?
    • 1. PVK is drug of choice
    • 2. antiinflammatory agents
    •     salicylates
    •     corticosteroids
  263. What drug will be given in RF if the pt is allergic to penVK?
    erythromycin
  264. Intervention with RF to prevent/catch complcations that may occur later in life?
    will follow them medically for at least 5 years
  265. How long is a RF pt susceptible to complications?
    for the rest of their lives
  266. Intervention for RF pt if there is risk for infection after RF recovery?
    ABX prophylaxis for:  dental work, infection, and any invasive procedure
  267. 3 char of prophylactic Tx with RF?
    • 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
  268. Nursing interventions for RF?
    • 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
  269. What is included in a CV assessment of RF pt? (3)
    • 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
  270. 3 non-pharm therapies for pain relief in RF pt?
    • 1. alternating heat and cold to joints for comfort
    • 2. massage
    • 3. distraction or diversional activities:  play therapy, guided imagery, relaxation exercises
  271. Teaching for parents of a child with RF and chorea s/s?
    • 1. Ch sleep on floor
    • 2. no rugs
    • 3. no oral temps
    • 4. spoon only no forks
    • 5. symptoms are temporary
  272. Kawasaki disease AKA?
    mucocutaneous lymph node syndrome
  273. 4 char of Kawasaki disease?
    • 1. acute
    • 2. not communicable
    • 3. idiopathic etiology
    • 4. antecedent upper resp illness
  274. Incidence of kawasaki disease?
    most in children less than 5 with peak 18 to 24 mo

    more in boys than girls and more in Asians
  275. Patho of kawasaki disease?
    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 ->
  276. S/S of kawasaki disease?
    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
  277. Priority problems with kawasaki?
    at risk for aneurysm and MI
  278. 6 s/s of acute phase of kawasaki disease?

    When does it occur?
    • 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
  279. 4 changes that occur in MM with acute phase of kawasaki disease?
    • 1. erythema
    • 2. fissures of tongue
    • 3. cracking of lips
    • 4. strawberry tongue
  280. When does the subacute phase of kawasaki disease occur?

    6 things that occur during this phase?
    day 15 to 25

    • 1. irritability
    • 2. anorexia
    • 3. desquamation (peeling) of fingers and toes
    • 4. arthritis
    • 5. arthralgia
    • 6. CV s/s
  281. CV S/S that may occur in the subacute phase of kawasaki disease?
    • 1. CHF
    • 2. arrhythmias
    • 3. coronary aneurysms
  282. 2 char of the convalescent stage of kawasaki disease?
    • 1. normal sedimentation rate
    • 2. no s/s of illness
  283. Dx eval of kawasaki?
    • 1. fever of 5 days duration in conjunction with at least 4 of the 5 primary clinical findings
    • 2. Dx tests
  284. 5 primary clinical findings with kawasaki disease?
    • 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
  285. Dx tests used for kawasaki disease?
    • 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
  286. Prevention of aneurysm in kawasaki?
    prophylactic aspirin or coumadin
  287. 2 complications that may occur with kawasaki disease?
    • 1. aneurysm
    • 2. MI
  288. S/S of MI?
    • 1. abd pain
    • 2. vomiting
    • 3. restless
    • 4. inconsolable crying
    • 5. pallor
    • 6. shock
  289. Drug therapy for kawasaki?
    • 1. IV gamma globulin
    • 2. salicylate therapy
    • 3. tx of coronary abnormalities with salicylates for life and may get coumadin for large aneurysms
  290. Salicylate therapy in kawasaki?
    • 1. high dose until fever subsides
    • 2. maintenacne - low dose until platelet count returns to normal and no coronary abnormalities
  291. Nursing interventions for kawasaki?
    • 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)
  292. Nursing interventions for symptomatic relief in kawasaki?
    • 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
  293. IVGG?

    Nursing considerations?
    IV gamma globulin

    no live viruses for 11 mo after admin

What would you like to do?

Home > Flashcards > Print Preview