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Peds Exam 1 > Peds Exam 1 > Flashcards

Peds Exam 1 Flashcards

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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
What CHDs are included in the mixed defects?
transposition of the great vessels hypoplastic left heart syndrome truncus arteriosus
26
What happens in left to right shunting?
there is communication between the pulmonary and systemic circulation which causes increased blood flow to the lungs and causes signs of heart failure
27
What is a pressure gradient?
a change in pressure, normally resulting in a change from an area of high concentration to an area of low concentration
28
What happens in an atrial septal defect?
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
29
What are the manifestations of an ASD?
is asymptomatic in a young child/baby will show fatigue, delayed growth, congestive heart failure SOFT, SYSTOLIC MURMUR
30
How do you diagnose an ASD?
echocardiogram | chest x-ray
31
How do you treat an ASD?
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
32
What is a patent ductus arteriosus?
``` 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 ```
33
What are the clinical manifestations of patent ductus arteriosus?
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
How do you diagnose a patent ductus arteriosus?
chest xray will show LA/LV enlargement ECG will show LV hypertrophy echocardiogram will determine severity
35
How do you treat patent ductus arteriosus?
control CHF administer indomethacin or NSAID (inhibits prostoglandin) interventional cardiac cath to occlude surgical ligation
36
What is a ventricular septal defect?
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
What are the manifestations of a ventricular septal defect?
``` may be asymptomatic is small enough dyspnea, tachypnea delayed growth patterns, reduced fluid intake, fatigue CHF pulmonary dx SYSTOLIC MURMUR ```
38
How do you diagnose a ventricular septal defect?
chest xray, ecg, echocardiogram
39
How do you treat a ventricular septal defect?
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
What are the four features of tetralogy of fallot?
``` PROV pulmonary stenosis right ventricular hypertrophy overriding aorta ventricular defect ```
41
What is a key feature of tetralogy of fallot?
They have tet spells (hypercyanotic spells) and are chronically hypoxemic
42
What is the pathophysiology of tetralogy of fallot?
``` increased R to L shunting = decreased O2 = increased CO2 = decreased PH = hyperapnea = increased systemic venous return ```
43
What are the key characteristics of tetralogy of fallot?
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
How do you treat tetralogy of fallot?
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
What is a tet spell and how does it manifest?
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
What are the manifestations of tetralogy of fallot?
``` cyanosis hypoxia delayed growth polycythemia metabolic acidosis exercise intolerance clubbing of fingers SYSTOLIC MURMUR ```
47
How do you diagnose tetralogy of fallot?
chest x ray, ECG, and echocardiogram | cardiac catheterization
48
How do you treat tetralogy of fallot?
perform surgical correction of all defects palliative surgery including central shunt (aorta to pulmonary artery) blalock-taussig shunt - subclavian to PA
49
What is tricuspid atresia?
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
How do you treat tricuspid atresia?
shunt or PA banding or modified fontan procedure | often multiple surgeries
51
What is pulmonary stenosis?
pulmonic valve becomes stenosed | can be mild, moderate, severe, or life-threatening
52
What is coarctation of the aorta?
``` 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
How does coarctation of the aorta manifest?
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
How do you diagnosis coarctation of the aorta?
the chest x ray will show enlarged LV and dilated ascending aorta ECG will show LV hypertrophy new screening of O2 sats
55
How do you treat coarctation of the aorta?
``` 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
What is transposition of the great arteries?
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
What are the manifestations of transposition of the great arteries?
``` cyanosis with no improvement after oxygen administration hypoxia acidosis tachypnea delayed growth ```
58
How do you diagnose transposition of the great arteries?
chest x ray | echocardiogram
59
How do you treat transposition fo the great arteries?
administer prostoglandins | perform surgical intervention
60
What is hypoplastic left heart syndrome?
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
What is heart failure in pediatrics?
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
What are some key points related to heart failure in pediatrics?
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
What are some generic congestive heart failure clinical manifestations?
tachycardia, poor capillary refill, peripheral edema fatigue, restlessness, cardiomegaly dyspnea, tachypnea, cyanosis, feeding difficulties, crackles and wheezing upon auscultation slow weight gain, perspiration
64
What is kawasaki disease?
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
What are the manifestations of acute kawasaki disease?
``` 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
How do you diagnosis kawasaki disease?
``` 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
What are the manifestations of subacute kawasaki disease?
``` skin on lips hands and feet sloughs off joint pain thrombosis of the heart large aneurysms of coronary arteries MI ```
68
What are the manifestations of convalescent stage of kawasakis disease?
decreased inflammation and permanent heart damage
69
How do you treat kawasaki disease?
admit to the hospital administer IV immunoglobulin therapy administer oral aspirin
70
What are the nursing interventions of kawasaki disease?
``` 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
What is acute rheumatic fever?
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
What are the clinical manifestations of acute rheumatic fever?
``` enlarged, painful, inflamed joints (polyarthritis) fever tachycardia red rash abnormal heart sounds irregular rhythm ```
73
How do you diagnose acute rheumatic fever?
manifestations | antistreptolysin O titer
74
What is the treatment for acute rheumatic fever?
administer antibiotics and anti inflammatory steroids
75
What are the nursing interventions of the acute phase of rheumatic fever?
assess temp q four hours admin IV fluids, prevent overload admin antibiotics and aspirin provide quiet activities and prevent fatigue
76
What are the nursing interventions of the recovery phase of rheumatic fever?
teach patients home care provide limited activites administer long-term antibiotic therapy teach clients prophylactic antibiotics needed for all invasive procedures
77
Explain HTN in children
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
What is important to know about digoxin?
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
What is important to know about antibiotics?
for children with known CHD, give prior to dental work and elective surgery
80
What do you need to know about ace inhibitors?
helps ease stress on heart by lowering BP
81
What does administering potassium do?
it corrects the hypokalemia related to diuretics

Peds Exam 1 (1 decks)

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