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Pediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

causes of increased pulm. blood flow

A 
VSD
large patent ductus arteriosus
transposition of the great arteries
truncus arteriosus 
tital anomalous pulmonary venous connect
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2
Q

CHD causes that result in obstructive lesions

A

severe aortic/pulm/mitral valve stenosis
coarcation of the aorta
interrupted aortic arch
hypoplastic left heart

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3
Q

causes of aq. heart disease - that lead to CHF

A

viral myocarditis

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4
Q

how does anemia cause CHF

A

increase to a high-output state

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5
Q

management of CHF in children

A

cardiac glycosides
loop diuretics
inotropic agent

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6
Q

digoxin - mechanism

A

increase efficency of Myocardial contraction and relieves tachycardia

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7
Q

furosemide - mechanism

A

reduce intravascular volume by maximizing sodium loss – leads to diminished ventricular dilation and improved function

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8
Q

dobutamine- mechanism

A

inotropic medication - given IV

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9
Q

when to use balloon valvuloplasty?

A

critical aortic and pulmonary valve stenosis

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10
Q

common innocent murmur at 2-7yrs

A

stills murmur

mid-left sternal border

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11
Q

sound of stills murmur

A

vibratory/twanging or buzzing

louder supine and when exercising

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12
Q

common innocent murmur at any age

A

pulmonic systolic murmur

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13
Q

pulmonic systolic murmur

A

upper left sternal border
blowing- high-pitched- loudes supine
louder with exercise

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14
Q

common innocent murmur at any age- but mainly school age

A

venous hum

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15
Q

venous hum

A

neck and below the clavicles
continous murmur
heard when sitting or standing
disappears if supine

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16
Q

ASD- classification

A

ostium primum
secundum
sinus venous

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17
Q

asd- ostium primum

A

lower portion

anterior mitral valve leaflet might cause mitral regurg

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18
Q

most common congenital hear lesion in Downs

A

ostium primum

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19
Q

ostium secundum

A

most common type of ASD

middle portion

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20
Q

sinus vinosus

A

high in the septum near the junction of the right atrium and superior vena cava

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21
Q

what are clinical features of ASD

A

minimal - only see them in osteum primeum

bc might develop mitral regurgitation and lead to CHF

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22
Q

PE for an ASD

A

increase ventricular impulse
systolic ejection murmur – best heard in the mid and upper left sternal borders
fixed split second heart sound

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23
Q

how to manage an ASD

A

closure by open heart surgery

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24
Q

vsd PE finding

A

holosystolic murmur LLSB

diastolic rumble at apex if pulmonary blood flow is high

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25
Q

EKG for VSD

A

if small: normal or LVH
if mod: LVH
RVH if pulm. hypertension

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26
Q

chest xray of VSD

A

if mod or large - cariomegaly and increased PVM

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27
Q

EKG of ASD

A

RAxis Deviation ,RVH, R atrial enlargement

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28
Q

xray of ASD

A

r atrial and ventricular enlargmenet

increased pul. vascular marking

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29
Q

patent ductus arteriosus PE

A

continous murmur at ULSB
machine like
brisk pulse

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30
Q

EKG of PDA

A

lvh

rvh if pulm. hypertension present

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31
Q

xray of PDA

A

cariomegaly with increased PVM

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32
Q

coarctation of the aorta pe

A

increased BP in right arm
reduced BP in legs
dampened and delayed femoral pulse
bruit left upper back

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33
Q

coarctation and EKG

A

normal or LVH

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34
Q

coarctation xray

A

rib notching

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35
Q

aortic stenosis PE

A

ejection clic

systolic ejection murmur at the base with radiation to the URSB and carotids

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36
Q

aortic stenosis EKG

A

normal or LVH

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37
Q

aortic stenosis xray

A

normal or mild cardiomegaly

prominent ascending aorta

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38
Q

pulm stenosis PE

A

ejection click

systolic ejection murmur at the ULSB

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39
Q

pulm stenosis EKG

A

RVH

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40
Q

pulm stenosis xray

A

normal

prominent main pulm artery

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41
Q

murmur intensity in VSD

A

as the sound increases the VSD is decreasing in size- as the blood is more forcefully traveling across

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42
Q

what happens when PVR becomes elevated in VSD

A

the second heart sound may be single and loud and noticible now

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43
Q

eisenmenger syndrome

A

condition in which the PVR becomes so high - that there is now a shift of R to L shunting

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44
Q

management of VSD

A

surgical closure if:
- hear dailure refractory to medical management
large VSDs with pulm. hypertension - close btw - 3-6 months
small to mod VSD - close btw 2-6 yrs

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45
Q

PDA

A

L to R shunt
– should have been closed after birth as the PaO2 rises - the ductus normally fibroses
high incidence in premis

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46
Q

clinical present of PDA

A

small - no symptoms
mod-large - CHF
wide pulse pressure >30mmHg
brisk ppulses

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47
Q

management of PDA

A

INDOMETHACIN

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48
Q

coarctation of the aorta

A

usually will be stenosis just below the left subclavian or just proximal to the ductus arteriosus

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49
Q

how do neonates survive the coarctation?

A

need to maintain a PDA to have some R to L shunting

these infants will be mild symptomatic but might develop CHF and worsen if the pDA closes

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50
Q

older kids with coarctation presentation

A

hypertension on R arm - and hypotension in the Lower extremities
femoral pulse is dampened and delayed
might lead to collateral formation - with the intercostal arteries

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51
Q

management of the coarcatation

A

IV PGE open the ductus
low dose dopa is given to maximize renal perfusion
might do surgery- but 50% might recurr

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52
Q

what to do if coarctation returns

A

balloon angioplasty

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53
Q

aortic stenosis and mI risk - why

A

increase O2 demand - and decrease perfusion - and increase demand since pumping so hard to feed the body

54
Q

neonates with severe aortic stenosis - clinical

A

normal and then CHF at 12-14 hours of age

once PDA closes - all systemic flow must pass thru the stenosis -

55
Q

aortic stenosis management

A

balloon valvuloplasty -
surgery - 5-10 yrs after valvuloplasty bc or recurrent stenosis or progressive insuffieciency
replace valve with either pulm valve(ross procedure) or prosthetic

56
Q

pulm stenosis

A

might have some cyanosis - R to L shunt

57
Q

management of pulm stenosis

A

balloon valvuloplasty if pressure gradient >35-40

58
Q

non cardiac causes of central cyanosis

A 
pulm. disease
sepsis 
hypoglycemia
polycythemia
neuromuscular disease
59
Q

cardiac causes of central cyanosis

A 
tetrology of fallot
transposition of great vessels
tricuspid atresia
truncus arteriosus 
total anomalous pulm. venous congestion
60
Q

100% oxygen challenge test

A

if O2 doesnt raise despite 100% o2 then you know it is cyanotic CHD

61
Q

tetralogy of fallot

A 
most common cause of central cyanosis 
VSD
Overriding aorta
pulm stenosis 
RVH
62
Q

tetralogy of fallot PE

A

systolic ejection murmur of pulm. stensosi

63
Q

ekg of tetralogy

A

RVH

64
Q

xray of tetralogy

A

boot shapped

65
Q

transposition of the great arteries PE

A

no murmur

single S2

66
Q

ekg of transposiion

A

normal or RVH

67
Q

chest xray of transposition

A

small hear with narrow mediastinum - egg on a string

increase PVM

68
Q

tricuspid atresia PE

A

no murmur -
single S2
if VSD systolic murmur of VSD

69
Q

ekg of tricuspid

A

LAD, RAE, LVH

70
Q

truncus arteriosus PE

A

single S2

systolic ejection murmur along left sternal border

71
Q

truncus EKG

A

CVH - combined ventricular hypertrophy

72
Q

xray truncus

A

enlarged heart
increased PVM
R aortic arch

73
Q

total anomalous pulm venous connection PE

A

pulm ejection murmur along left sternal border

74
Q

total anomalous pulm venous connection - EKG

A

RVH and RAE

75
Q

total anomalous pulm xray

A

enlarged heart in older unrepaired childrean with supracardiac drainage
increased PVM a

76
Q

how to increase SVR and decrease RVOT

A

volume infusion
systemic hypertension
valsalva
bradycardia

77
Q

tet spells - what are they

A

sudden cyanosis and decreased murmur intensity

78
Q

management of tetralogy

A

complete surgical repair at 4-8months
if really bad when born then might have initial procedure to improve systemic saturation and encourage pulm growth – blalock-taussig shunt
can give IV Na bicarb - to correct acidosis from prolonged hypoxia

79
Q

transposition of great arteries -

A

they systems are parallel and need a VSD/AS/PDA

80
Q

management of transposition

A

PGE
emergent balloon atrial septostomy
arterial switch operation

81
Q

tricuspid atresia

A

ASD or PFO is always present

82
Q

tricuspid atresia and no VSD

A

ventricular septum intact pulmonary atresia is also present –> therefore need PDA to be present

83
Q

tricuspid atresia and VSD

A

L ventricle–> VSD –> pulm artery

84
Q

tricuspid atresia is the only one with EKG findings remarkable for:

A

LAD and LVH

85
Q

management of tricuspid atresia

A

fontan procedure - flow from the inferior vena cava is directed into the pulm arteries and means of extracardiac conduit or intra-arterial baffle or tunnel

86
Q

glenn shunt

A

superior vena cava connected to pulm. artery

87
Q

truncus arteriosum

A

VSD is almost always present

88
Q

clinical of truncus arteriosum

A

CHF signs

diastolic murmur - across the mitral valve at the apex - from pulmonary blood flow that returns to the left atrium

89
Q

management of truncus

A

CHF meds

surgery - close VSD and place homograft btween the rightventricle and pulm. artery

90
Q

total anomalous pul. venous connection

A

there will be the return of pulm blood to the Superior vena cava - and they can only oxygenate through PDA

91
Q

management of total anomalous

A

surgical - after diagnosis -

92
Q

infective endocarditis - who gets it? what bug?

A

80% will be in kids w/ structural abnormalities
gram positive cocci - most common
gram negative - rare
fungal - rare unless chronically ill child

93
Q

signs of infective endocarditis

A 
murmur change/new
splenomegaly
hematuria
splinter hemorrhage
retinal hemorhage
osler's node - 
janeway lesions 
roths spots - spots in retina
94
Q

diagnsosis of infective endocarditis

A

blood culture -
ESR
rheumatoid factor will be elevated in 50%
echo- but transesophageal echo is best -

95
Q

management of infective endocarditis

A

IV antimicrobial therapy

96
Q

pericarditis - causes

A

infection, collagen vascular disease, uremia, inflammatory response after cardiac surgery

97
Q

what is the most common cause of pericarditis

A

viral infection

Cozaski, echo, adeno, influenza, para, EBV

98
Q

causes of purulent pericarditis

A

bacterial infection

staph and step. pneumoniae

99
Q

symptoms of pericarditis

A

chest pain, intense while supine and relieved when sitting upright
friction rub
distant heart sounds
pulsus paradoxus >10mmhg reduction on systolic bP during inpiration
hepatosplenomegaly

100
Q

diagnosis of pericarditis

A

think of it if underwent cardiac surgery and now dyspnea and fever
pericardiocentesis
ESR - elevated

101
Q

management of pericarditis

A

antibiotics - anti-inflammatory agenet - asprin or steroid

drainage

102
Q

myocarditis

A

common cause of sudden death in young athletes

follows URI

103
Q

etiology of myocarditis

A 
enterovirus - coxaskie
bacteria (strep. pyogenes, diphtheria, staph TB)
fungi - crypto/candida
protozoa (typanosma cruzi (chagas ))
autoimmune - SLE/rheumatic fever/sarcoid
kawasaki
104
Q

myocarditis PE

A

muffles heart sounds - resting tachy, hepatomegaly

105
Q

diagnosis of myocarditis

A

elevated ESR
HIGH Cr
CRP
endomyocardial biopsy

106
Q

ekg of myocarditis

A

T wave and ST changes

107
Q

mangament of myocarditis

A

supportive

inotropic agents - diuretics - IVIG might help

108
Q

dilated cardiomyopathy

A

ventricular dilation - and decrease cardiac function

109
Q

dilated cardiomyopathy etiology

A

viral
mitochondrial abnormalities
carnitine defiency
nutritional deficiency – selenium and thiamine def.

110
Q

management of dilated cardiomyopathy

A

medical management
treat underlying metab/nutrional issue
fix ALCAPA
cardiac transplant

111
Q

hypertrophic cardiomyopathy

A

most typical: asymmetric septal hypertrophy

AD

112
Q

hypertrophic cardiomyopathy pathophys

A

poor left ventricular filling –> LVOT obstruction – bc the mitral leaflet gets swept up into the subaortic region during systole

113
Q

diagnosis of hypertrophic cardiomyopathy

A

LVH on EKG

echo

114
Q

management of hypertrophic cardiomyopathy

A

calcium channel blocker- reduce LVOT
surgical myomectomy
antiarrhythmic meds
dual-chamber pacing

115
Q

restrictive cardiomyopathy - etiology

A

amyloidosis

inherited infiltrative disorder (gauchers, fabry disease, hemosiderosis hemochromatosis

116
Q

SVT- supraventricular tachy

A

most common dysrhythmia in childhood
AVRT
AVNRT

117
Q

AVRT

A

retrograde conduction through an accessory pathway

118
Q

AVNRT

A

the abnormality occurs in the different pathways within the AV node

119
Q

WPW on EKG

A

delta waves

short P wave and then a slow rise on the QRS complex

120
Q

WPW

A

when there is anterograde reentry

121
Q

management of supraventricular tachy

A 
vagal maneuvers or ice pack to the face
iv adenosine 
synchronized cardioversion 
chronic medical management - digoxin or propanalol
radiofrequency cather ablation
122
Q

supraventricular tachy

rate; HR variation; P wave on EKG; predisposing factor; response to intervention

A 
rate - >250
HR variation - none
P wave- absent or abnormal axis
predispose - none
response - rapid
123
Q

sinus tachy

rate; HR variation; P wave on EKG; predisposing factor; response to intervention

A

rate-

124
Q

hear block or AV block

A

delayed or interrupted conduction of sinus or atrial impulses
ratio of atrial to ventricular impulses

125
Q

1st degree av block

A

prolonged of the PR interval

126
Q

2nd degree av block

A

type 1 - wenckebach – prolonged pR interval leading to failed AV conduction
type 2- abrupt failure of AV conduction without progressive prolongation of the PR interval

127
Q

3rd degree av block

A

complete block - no conduction of atrial impulses to ventricles

128
Q

etiology of av block

A

congenital third degree - children of moms with SLE
postsurgical av block - (especially VSD repair)
bacterial endocarditis

129
Q

long qt syndrome etiology

A

50% AR jervell-lange-nielsen syndrome - associated with congenital deafness -
romano ward syndrome AD- not associated with deafness

130
Q

drugs that prolong qt interval

A

TCA, erythromycin, terfenadine

131
Q

diagnosis of prolonged qt

A

> .44sec

132
Q

manage qt prolongation

A

b-blocker

Pediatrics (10 decks)

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