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Pediatrics > Cardiovascular PowerPoint > Flashcards

Cardiovascular PowerPoint Flashcards

1
Q

in utero what heart side is dominant

A

right

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2
Q

in utero why does the blood bypass the lungs

A

because it gets O2 from the placenta

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3
Q

what utero structures help shunt blood away from lungs

A

patent ductus arterosis
patent foramen ovale

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4
Q

normal blood flow

A

vena cava
right atrium
right ventricles
pulmonary artery
lungs
pulmonary veins
left atria
left ventricle
aorta

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5
Q

in children how is the heart compared to the body

A

larger compared to rest of body

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6
Q

heart muscle develops until

A

5years

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7
Q

under 5 years how does the child increase CO

A

increase HR

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8
Q

stroke volume

A

the volume of blood ejected by the ventricle with each contraction

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9
Q

3 factors affecting stroke volume

A

preload
afterload
contractility

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10
Q

preload

A

the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions

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11
Q

afterload

A

the amount of resistance the heart must overcome to open toe aortic value and push the blood volume out into the systemic ciculation

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12
Q

some things to assess

A

skin color
cap refil
heart rate
blood pressure
JVD

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13
Q

thrills

A

murmur you can feel

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14
Q

S1

A

beginning of systole, AV valves close

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15
Q

S2

A

end od systole, closure of semilunar values

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16
Q

S3

A

normal in children
related to rapid filling of ventricle

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17
Q

S4

A

abnormal
heard late in diastole or early systole, heard in CHF and with decreased ventricular compliance

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18
Q

CCHD

A

pulse ox on pre ductal and post ducatal
pre: right hand
normal is >98% with less than 2-3% change

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19
Q

most defects occur during the first __ week of gestaion

A

8

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20
Q

congenital heart defects are categorized by their underlying path into 4 categroesi

A

increased pulmonary blood flow (acyanoitci)
decreased pulmonary flow (cyanotic)
obtructive
mixed

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21
Q

what is the first indication of congenital heart defect

A

murmur

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22
Q

a murmur indicates

A

turbulent blood flow with high pressure to get through a narrowed valve or through a shunt

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23
Q

increased pulmonary blood flow clinical manifestations

A

tachypnea, tachycardia, murmur, CHF, poor weight gain, diaphoresis, edema

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24
Q

decreased pulmonary blood flow clinical manifestations

A

cyanosis, hypoxic spells, poor weight gain, polycythemia

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25
Q

obstruction clinical manifestations

A

diminished pulses, poor color, delayed capillary refill, decreased urine output, CHF with pulmonary edema

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26
Q

mixed defects clinical manifestations

A

cyanosis, poor weight gain, pulmonary congestion

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27
Q

increased pulmonary blood flow

A

PDA
ASD
VSD

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28
Q

PDA
ASD
VSD
class

A

increased pulmonary blood flow
(acynanotic)

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29
Q

increased pulmonary blood flow cause the blood to flow to the

A

lungs instead of the body

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30
Q

PDA
- what is it

A

communication between left pulmonary artery and descending arota

pulmonary artery is a lower pressure system so oxygenated blood flows into the pulmonary artery

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31
Q

when does the PDA close functionally

A

12-24 hours

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32
Q

when does the PDA close structurally

A

2 weeks then turns into a ligament

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33
Q

PDA accounts for what percent of all infants with congenital heart disease

A

5-10%

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34
Q

PDA clinical manifesations

A

may be asymptomatic
dyspena
tachypnea
tachycardia
full bounding pulses
intercostal retractions
poor growth
murmur (KNOW THE TYPE)

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35
Q

PDA murmur claissifcation

A

machinery murmur during systole and diastole and a thrill in the pulmonary area

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36
Q

PDA have high risk for

A

frequent respiratory infections and pneumonia

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37
Q

PDA how will the left ventricle look

A

hypertrophic

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38
Q

clinical therapy of PDA
how to close

A

cardiac Cath by obstruction device

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39
Q

medication for PDA closure

A

IV Ibuprofen or indomethacin
- cannot be used if CHF is present

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40
Q

PDA prognosis

A

no long term sequelae if treated before pulmonary vascular disease

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41
Q

ASD what is it

A

opening in the atrial septum which permits left to right shunting of blood

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42
Q

ASD clinical manifestation s
- small to mod

A

asymtomatic

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43
Q

ASD clinical manifestations
- large

A

CHF, easy tiring, poor growth, mumur

44
Q

large ASD murmur

A

soft systolic ejection murmur with fixed wide splitting of S2 may be heard

45
Q

ASD what will the right ventricle look like

A

dilated

46
Q

what is the most common cardiac defect

A

VSD

47
Q

VSD what is it

A

opening in the ventricular septum results in left to right flow and then increased pulmonary flow

48
Q

VSD small clinical manifestations

A

no symptoms

49
Q

VSD mod to large

A

CHF, poor growth, decreased exercise tolerance, increased number of pulmonary infections

50
Q

VSD murmur

A

systolic 3-4 left intercostal space

51
Q

large vsd echo appearance

A

enlarged heart and pulmonary vascular margins on chest radiograph

52
Q

post op Cath lab what to assess

A

vital signs, bleeding, infection, pressure dressing

53
Q

decreased pulmonary blood flow

A

let of fallot

54
Q

tet of fallot

A

dercreased pulmonary blood flow
(cyanotic)

55
Q

4 defects of tet of fallot

A

stenosis of the pulmonary outflow tract or valve
right ventricular hypertrophy
ventricular septal defect
overriding aorta

56
Q

let of allot how will the chest radiography show

A

BOOT SHAPTED HEARt

57
Q

can metrology of fallout be dented by fetal echo

A

yes

58
Q

TOF the child becomes hypoxic and cyanic as the

A

ductus artetosis closes

59
Q

TOF s/s

A

polycytothemia
hypoxic spells
metabolic acidosis
poor growth
clubbing
exercise intolerance
systolic murmur
won’t eat well
delayed cap refil
right hand is different than left hand

60
Q

what position do TOF toddlers go into

A

squat (knee to chest) to decreased the return of systemic venous blood to the heart = tetspells

61
Q

how does squating help the TOF

A

increases peripheral vascular resistance and thus decreases magnitude of the right to left shunt across the VSD

62
Q

what is the management for tetspells

A

place child in knee to chest
maintain calm enviornment
give O2
morphine or verssed
IV fluids

63
Q

in obstructive lesions what type of blood flow is impared

A

systemic

64
Q

examples of obstructive

A

COA
HLHS

65
Q

COA
HLHS
type

A

obstructive

66
Q

COA

A

narrowing of the descending aorta near the ductus arterioles or left subclavian artery

67
Q

COA manifestations

A

many are asymptomatic
lower blood pressure in legs and higher in arms, neck and head
brachial and radial is bounding
femoral and leg pulses are weak

68
Q

newborn with COA and severe constriction may have

A

cyanosis of lower extremities, heart failure, and shock as the PDA closes

69
Q

chest radiography of COA will be

A

cardiomegaly, pulmonary venous congestion, indentation of the descending aorta

70
Q

what med is given to newborns with COA

A

prostaglandin E to reopen the ductus arterosis

71
Q

what might be a complication of COA

A

HTN and aneurysms

72
Q

what is HLHS

A

mitral and aortic valves are either absent or stenosed along with a small left ventricle and aorta

73
Q

where doe HLHS need to be born

A

level 4 NICU

74
Q

s/s of HLHS

A

progressive cyanosis and signs of CHF
diminished pulses
pale color
delayed cap refill
decreased UO
no murmur

75
Q

CXR HLHS

A

cardiomegaly and increased pulmonary vascular congestion

76
Q

what med will you give for HLHS

A

PGE to keep PDA

77
Q

tx for HLHS

A

transplant

78
Q

mixed issues

A

TGA

79
Q

TGA

A

mixed

80
Q

TGA what is happening

A

pulmonary artery is the outflow tract for the left ventricle and the aorta is the outflow tract for the right ventricle
- pulmonary artery and aorta are switched

81
Q

what do we need for survival of TGA

A

PDA
- so give PGE

82
Q

in TGA does cyanosis improve with oxygen

A

no

83
Q

CXR with TGA

A

egg shaped

84
Q

tx of TGA

A

arterial switch

85
Q

what is a complication of surgery

A

infective cardidis or endocarditis

86
Q

what is Kawasaki syndrome

A

acute febrile systemic vascular inflammatory disorder that affects the small and midsize arteries including the coronary arteries

87
Q

what is the leading cause of acquired heart. disease in children

A

Kawasaki

88
Q

cause of Kawasaki

A

unknown but is thought to be an infectious trigger than leads to an autoimmune response

89
Q

3 stages of kawaksai

A

acute
subacute
convalescent

90
Q

acute Kawasaki

A

fever (5 days) >39
conjunctival hyperemia
cervical lymph node enlargement
strawberry tongue
cracked lips
rash on hands and face and trunk

91
Q

subacute Kawasaki

A

no fever
cracking skin (lips, fingers, toes)
coronary artery aneurisms

92
Q

treatment of Kawasaki

A

IVIG
- 2g/kg start slow
aspirin

93
Q

what should we monitor for in Kawasaki

A

coronary artery answeusms

94
Q

4 main cardio drugs

A

lasix
o2
dig
ACEI

95
Q

s/s of dig tox in children

A

N/V
will still have blurry vision but may not report

96
Q

what is cardiomyopathy affecting

A

the hearts muscle

97
Q

what is the most common cardiomyopathy

A

dilated

98
Q

dilated cardiomyopathy

A

enlargement of all cardiac chambers
systolic dysfunction

99
Q

complication of dilated cardiomyopathy

A

blood clots
increase risk for embolism

100
Q

treatment of dilated cardiomyopathy

A

CHF
- diuretics
- ACEI
- dig

101
Q

hypertrophic cardiomyopathy

A

diastole dysfunction
risk of sudden death in young athletes
thickened left ventricular wall

102
Q

tx for hypertrophic cardiomyopathy

A

beta blockers
calcium channel blockers
cardioverter

103
Q

hypovolemic shock

A

clinical state of inadequate tissue and organ perfusion resulting from inadequate blood or plasma volume in the vascular space

104
Q

s/s of hypovolemic shock

A

pale
cold
diaphoretic
increase hr
thready pulse
no blanching

105
Q

what antibiotic class is dangerous to kidney

A

mycin

106
Q

what tells us there is perfusion

A

UO

107
Q
A

Pediatrics (51 decks)

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