Peds Exam 1 Flashcards

1
Q

What is the most common type of congenital heart defect in children?

A

Ventricular Septal Defect

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2
Q

When do infant deaths most often occur due to congenital heart defects?

A

During the first 28 days of life

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3
Q

What is there a correlation between with disease severity of congenital heart defect?

A

Correlation between disease severity and developmental delay.

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4
Q

What are some genetic risk factors of CHD?

A
  • Fetal exposure to teratogens
  • Maternal dx or infection
  • Familial risk factor 3-4 fold with 1st degree relative
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5
Q

What are the teratogens the fetus can be exposed to that are a CHD risk factor?

A

lithium, etoh, anticonvulsants

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6
Q

What are some maternal diseases/infections that can increase the risk of getting a CHD?

A

DM - 5x greater risk
Rubella - only viral illness
systemic lupus erythemotosus

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7
Q

What are the acronyms that are group as multifactorial causes of CHD?

A

VACTREL

CHARGE

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8
Q

What does VACTREL stand for?

A
Vertebral anomalies 
anal atresia 
cardiac defects 
tracheo-esophogeal fistula 
radial defects 
limb anomalies
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9
Q

What does CHARGE stand for?

A
coloboma 
heart defects
choanal atresia 
restriction of growth and development 
genital anomalies 
ear anomalies
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10
Q

What can an ear abnormality be associated with?

A

Can be associated with a kidney/renal issue

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11
Q

What happens with the A&P of the infant pediatric cardiovascular system?

A

ductus arteriosis and foramen ovale close
the left side has higher pressure than the right
heart muscle fibers are immature
the ventricles are less compliant to SV
preload and afterload affect cardiac output

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12
Q

What is cardiac output?

A

CO = SV X HR ,

stroke volume is the amount of blood pumped from a ventricle in a single heartbeat

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13
Q

Explain the vascular resistance in fetal circulation

A

There is high pulmonary vascular resistance (only 5-10% of cardiac output goes to lungs and fetal lungs extract oxygen from placental blood)

There is low systemic vascular resistance

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14
Q

What happens in neonatal circulation?

A
  • the three shunts close

- aeration of the lungs

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15
Q

What causes the three shunts to close?

A

foramen ovale is caused by increased pressure in LA

ductus areteriosus is from increased O2 levels and loss of prostaglandins from placenta and increased metabolism in the lungs (takes about 72 hours for it to close)

ductus venosus - umbilical vein is shut off

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16
Q

What does aeration of the lungs cause?

A
  • decreased PVR causes increased LA and RA pressures
  • increased SVR
  • increased pulmonary blood flow
  • thinning of the pulmonary artery walls
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17
Q

What can help close the shunts?

A

A prostoglandin inhibitor such as indomethazine

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18
Q

What is the normal electrical pathway of the heart?

A

SA noe - AV noe - bundle of his - ventricular septum - purkinje fibers

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19
Q

What are the clinical s/s of a CHD?

A

Cyanosis (this may be the only sign in first week of life)
murmur (50% have this during first two days of life)
RR greater and 60
bounding or weak pulses, 4 extrm BP & O2
BP
CHF

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20
Q

What is the difference between central and peripheral cyanosis?

A

Central:
arterial blood desat/abnormal hb seen in R-L shunt, impaired pulmonary function, or abnormal hb
seen in conjunctiva palate tongue, inner side of lips and cheeks, assoc with clubbing and polycythemia

Peripheral:
d/t low CO and from cold air or water or abnormally large extraction of o2 from normally saturated blood seen in ears, nose, cheeks, outer lips, and hands and feet. Clubbing is absent

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21
Q

What are the four classifications of congenital heart defects?

A

increased pul bl flow
decreased pul bl flow
obstruct systemic bl flow
mixed

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22
Q

What CHDs are included in increased pulmonary blood flow ?

A

Atrial septal defect
ventricular septal defect
patent ductus arteriosus

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23
Q

What CHDs are included in decreased pulmonary blood flow?

A

tetralogy of fallot
tricuspid atresia
pulmonary stenosis

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24
Q

What CHDs are included in the obstructive systemic blood flow?

A

Coarctation of the aorta
pulmonary stenosis
aortic stenosis

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25
Q

What CHDs are included in the mixed defects?

A

transposition of the great vessels
hypoplastic left heart syndrome
truncus arteriosus

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26
Q

What happens in left to right shunting?

A

there is communication between the pulmonary and systemic circulation which causes increased blood flow to the lungs and causes signs of heart failure

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27
Q

What is a pressure gradient?

A

a change in pressure, normally resulting in a change from an area of high concentration to an area of low concentration

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28
Q

What happens in an atrial septal defect?

A

there is an opening in the septum between atria and a L TO R shunt causing right atrium dilation and increased pulmonary blood flow

foramen ovale is not closed
results in right ventricular hypertrophy

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29
Q

What are the manifestations of an ASD?

A

is asymptomatic in a young child/baby
will show fatigue, delayed growth, congestive heart failure
SOFT, SYSTOLIC MURMUR

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30
Q

How do you diagnose an ASD?

A

echocardiogram

chest x-ray

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31
Q

How do you treat an ASD?

A

perform a surgical closer or patch
perform a cardiac cath with septal occulder
surgical repair normally done between 3-5 years of age on cardiopulmonary bypass

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32
Q

What is a patent ductus arteriosus?

A
the connecting duct between the pulmonary artery and the aortic arch is still open (normally closes within 24 hours of life)
the ductus arteriosus fails to close
blood flows from aorta to pulmonary vein
increased blood flow to the lungs
causes right ventricular hypertrophy
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33
Q

What are the clinical manifestations of patent ductus arteriosus?

A

full, bounding pulse, dyspnea, tachypnea
delayed growth patterns related to poor feeding and irritability increased HR and RR
CONTINUOUS MACHINE LIKE SYSTOLIC MURMUR
PULMONIC THRILL at LSB, 2ND TO 4TH ICS

34
Q

How do you diagnose a patent ductus arteriosus?

A

chest xray will show LA/LV enlargement
ECG will show LV hypertrophy
echocardiogram will determine severity

35
Q

How do you treat patent ductus arteriosus?

A

control CHF
administer indomethacin or NSAID (inhibits prostoglandin)
interventional cardiac cath to occlude
surgical ligation

36
Q

What is a ventricular septal defect?

A

opening between ventricles
blood flows from left to right
shunting occurs during systole when semilunar valves open
the degree of shunting is determined by the size of the defect
LV vol overloads
increased pulmonary blood flow

37
Q

What are the manifestations of a ventricular septal defect?

A
may be asymptomatic is small enough
dyspnea, tachypnea
delayed growth patterns, reduced fluid intake, fatigue
CHF
pulmonary dx
SYSTOLIC MURMUR
38
Q

How do you diagnose a ventricular septal defect?

A

chest xray, ecg, echocardiogram

39
Q

How do you treat a ventricular septal defect?

A

50% close on their own
must early correct for large VSD, CHF, or poor weight gain
small defects only need a suture close
large defects need a patch graft

40
Q

What are the four features of tetralogy of fallot?

A
PROV
pulmonary stenosis
right ventricular hypertrophy
overriding aorta
ventricular defect
41
Q

What is a key feature of tetralogy of fallot?

A

They have tet spells (hypercyanotic spells) and are chronically hypoxemic

42
Q

What is the pathophysiology of tetralogy of fallot?

A
increased R to L shunting =
decreased O2 =
increased CO2 = 
decreased PH =
hyperapnea =
increased systemic venous return
43
Q

What are the key characteristics of tetralogy of fallot?

A

rapid deep breathing
fainting
increased blueness
increased intensity of heart murmur
child assumes a knee to chest position to relieve cyanotic spell
clubbing of the fingers is a manifestation in an older child

44
Q

How do you treat tetralogy of fallot?

A

initially treat with morphine and fentanyl
you are treating the acidosis
(O2 does not help this problem because pul blood flow is not oxygenated)
hold infant over shoulder knees to chest which puts pressure on the arteries in the legs and increases afterload
beta blockers
fluids to also increase arterial pressure and afterload

45
Q

What is a tet spell and how does it manifest?

A

may be spontaneous or precipitated by events associated with decreased systemic vascular resistance such as
tachycardia
hypotension
exertion during feeding
defecation
crying
can be short 15-30 min that may result in seizure, stroke or lead to death

46
Q

What are the manifestations of tetralogy of fallot?

A
cyanosis
hypoxia
delayed growth 
polycythemia
metabolic acidosis
exercise intolerance
clubbing of fingers
SYSTOLIC MURMUR
47
Q

How do you diagnose tetralogy of fallot?

A

chest x ray, ECG, and echocardiogram

cardiac catheterization

48
Q

How do you treat tetralogy of fallot?

A

perform surgical correction of all defects
palliative surgery including central shunt (aorta to pulmonary artery)
blalock-taussig shunt - subclavian to PA

49
Q

What is tricuspid atresia?

A

triscuspid valve is absent
valve between RA and RV is hypoplastic with decreased blood flow
ASD, VSD or PDA are necessary for survival!
RA hypertrophy
blood instead goes through the atrial septum (FO)
mixing of deoxygenated blood in the LA
must maintain PDA and FO for adequate circulation
and give prostoglandins!

50
Q

How do you treat tricuspid atresia?

A

shunt or PA banding or modified fontan procedure

often multiple surgeries

51
Q

What is pulmonary stenosis?

A

pulmonic valve becomes stenosed

can be mild, moderate, severe, or life-threatening

52
Q

What is coarctation of the aorta?

A
narrowing of the aorta
which obstructs systemic blood flow
most common in the arch
HTN can lead to CHF
collateral circulation develops
HTN can happen later in life
53
Q

How does coarctation of the aorta manifest?

A

may be asymptomatic
BP will be high in the arms than legs
weak pulses in the legs
bounding pulses in the arms, neck, and head
weakness and pain in legs after exercise
congestion might be shown as headaches and the newborn will cry

54
Q

How do you diagnosis coarctation of the aorta?

A

the chest x ray will show enlarged LV and dilated ascending aorta
ECG will show LV hypertrophy
new screening of O2 sats

55
Q

How do you treat coarctation of the aorta?

A
balloon dilation
anastomosis
perform surgical resection b/t 3-10 years of life
(end to end anastomosis)
teach patients the s/s of reoccurrence
HTN can be issue if untreated in life
56
Q

What is transposition of the great arteries?

A

it is a mixed defect
It is where the aorta and pulmonary artery positions are reversed
aorta is connected to RV
pulmonary artery is connected to LV
survival depends on PDA
unoxygenated blood moves in and out of the heart
oxygenated blood moves through the heart and lungs

57
Q

What are the manifestations of transposition of the great arteries?

A
cyanosis with no improvement after oxygen administration 
hypoxia
acidosis
tachypnea
delayed growth
58
Q

How do you diagnose transposition of the great arteries?

A

chest x ray

echocardiogram

59
Q

How do you treat transposition fo the great arteries?

A

administer prostoglandins

perform surgical intervention

60
Q

What is hypoplastic left heart syndrome?

A

called a single ventricle
all structures on left side of the heart are underdeveloped
left side is unable to supply blood to systemic circulation
treatment is surgery
s/s appear as PDA
high morbidity and mortality and would see in the first 72 hours of life

61
Q

What is heart failure in pediatrics?

A

circulatory deficits and the heart’s inability to pump effectively
often in children with CHD
decreased CO
treat with O2, diuretics, and heart transplant

62
Q

What are some key points related to heart failure in pediatrics?

A

infants are sensitive to volume and pressure overload because heart muscle fibers are not fully developed and therefore not as compliant

CHF is characterized by the type of heart defect

Left sided - cyanotic, dyspnea, RESPIRATORY RALES, orthopnea, tachycardia, fatigue, restlessness

Right sided - distended neck veins, tachycardia, liver enlargement, weight gain, and edema

63
Q

What are some generic congestive heart failure clinical manifestations?

A

tachycardia, poor capillary refill, peripheral edema
fatigue, restlessness, cardiomegaly

dyspnea, tachypnea, cyanosis, feeding difficulties, crackles and wheezing upon auscultation

slow weight gain, perspiration

64
Q

What is kawasaki disease?

A

it is an acquired heart disease that is an acute systemic illness
cause unknown
a mucocutaneous lymph node syndrome
it involves the skin, mouth, lymph nodes and effects kids normally from 3-5 years old
if left untreated it can lead to vasculitisis and arrhythmias which can be permanent and cause MIs in children
tends to happen in the winter and spring when strep is most common

65
Q

What are the manifestations of acute kawasaki disease?

A
fever
conjunctival hyperemia (red eyes)
red throat
changes in the lips, tongue, and/or mouth
changes in the fingers and toes such as swelling, discoloration and peeling 
swollen hands and feet
rash in the trunk or genital area 
large swollen lymph nodes in the neck
enlarged cervical lymph nodes
66
Q

How do you diagnosis kawasaki disease?

A
No single test can diagnose
Most will have a fever for over 5 days and have the clinical manifestation s/s 
get an erythrocyte sedimentation rate
platelet count 
CRP
WBC
Echo
67
Q

What are the manifestations of subacute kawasaki disease?

A
skin on lips hands and feet sloughs off 
joint pain
thrombosis of the heart 
large aneurysms of coronary arteries
MI
68
Q

What are the manifestations of convalescent stage of kawasakis disease?

A

decreased inflammation and permanent heart damage

69
Q

How do you treat kawasaki disease?

A

admit to the hospital
administer IV immunoglobulin therapy
administer oral aspirin

70
Q

What are the nursing interventions of kawasaki disease?

A
take temp q four hours
aspirin
assess for bleeding 
monitor conjunctive, oral mucosa, skin
assess for dehydration/malnutrition
auscultate q four hours
provide oral and bath care gently
admin IV fluids and soft foods
maintain bed rest with repositioning
teach parents home care
71
Q

What is acute rheumatic fever?

A

inflammatory disorder
follows beta-hemolytic strep infection
causes autoimmune response which damages heart, CNS, skin
may reoccur with further heart damage
strep through > rheumatic fever > rheumatic HR dx

72
Q

What are the clinical manifestations of acute rheumatic fever?

A
enlarged, painful, inflamed joints (polyarthritis)
fever
tachycardia
red rash
abnormal heart sounds
irregular rhythm
73
Q

How do you diagnose acute rheumatic fever?

A

manifestations

antistreptolysin O titer

74
Q

What is the treatment for acute rheumatic fever?

A

administer antibiotics and anti inflammatory steroids

75
Q

What are the nursing interventions of the acute phase of rheumatic fever?

A

assess temp q four hours
admin IV fluids, prevent overload
admin antibiotics and aspirin
provide quiet activities and prevent fatigue

76
Q

What are the nursing interventions of the recovery phase of rheumatic fever?

A

teach patients home care
provide limited activites
administer long-term antibiotic therapy
teach clients prophylactic antibiotics needed for all invasive procedures

77
Q

Explain HTN in children

A

normally secondary to kidney dx, coarctation of aorta, obesity, and side effects of some meds
need appropriate/accurate BPs with right size cuff
care should include assessing O2 status, promoting oxygenation, energy conservation, and fluid and electrolyte balance

78
Q

What is important to know about digoxin?

A

increases the force of myocardial contraction which increases CO
slows down heart rate and increases contractility
monitor apical pulse for one full min before administering
NEEDS 2 RN TO CHECK
withhold dose and notify HCP if pulse rate less than 70 in child or less than 90 in an infant

79
Q

What is important to know about antibiotics?

A

for children with known CHD, give prior to dental work and elective surgery

80
Q

What do you need to know about ace inhibitors?

A

helps ease stress on heart by lowering BP

81
Q

What does administering potassium do?

A

it corrects the hypokalemia related to diuretics