UW Peds Cards Flashcards

1
Q

EKG showing left-axis deviation; tall, peaked P waves (d/t RAH) from ASD; small or absent R waves in precordial leads; plus CXR showing normal-sized heart

A

Tricuspid atresia

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2
Q

CXR of tricuspid atresia

A

decreased pulmonary vascular markings and a normal sized heart

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3
Q

Murmur of tricuspid atresia

A

Holosystolic murmur loudest at LLSB (VSD)

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4
Q

increased pulmonary markings and cardiomegaly from excessive pulmonary blood flow and biventricular volume overload

A

CXR of CAVCD

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5
Q

displacement of a malformed tricuspid valve into the RV –> severe TR and RAH

A

Ebstein’s anomaly

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6
Q

Tall P waves and RAD on EKG plus extreme cardiomegaly from heart failure

A

Ebstein’s anomaly

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7
Q

Increased or decreased pulmonary vascular markings on CXR with TOF?

A

Decreased

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8
Q

Defect in which all 4 pulmonary veins fail to make their normal connection to the LA, so the RA receives blood from pulmonary and systemic circumlation

A

TAPVR

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9
Q

EKG of TAPVR

A

RVH and RAD

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10
Q

CXR of truncus arteriosus

A

cardiomegaly and increased pulmonary vascular markings

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11
Q

truncus arteriosus is strongly a/w

A

DiGeorge

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12
Q

benign murmur increases or decreases with standing

A

Decreases

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13
Q

pathologic murmur increases with

A

standing or valsalva

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14
Q

Pathologic murmurs may be a/w loud, fixed split or single S2 or decreases or absent

A

femoral pulses

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15
Q

HOCM murmur increases with standing because

A

standing decreases venous return and preload, which increases the obstruction

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16
Q

3 cardiac anomalies a/w Turner

A

bicuspid aortic valve, coarctation, aortic root dilation (w/ inc risk of aortic dissection)

17
Q

MVP is a/w

A

Marfan, Ehlers-Danlos, OI_

18
Q

PDA is a/w

A

congenital rubella, Char syndrome

19
Q

TOF is a/w

A

Down, DiGeorge

20
Q

VSD is occ a/w

A

trisomies 13, 18, 21

21
Q

carotid pulse has a dual upstroke, + strong apical impulse, + systolic ejection murmur along LSB

22
Q

Maneuvers that increase either preload or after load, such as squatting, leg raise, or sustained hand grip, increase LV cavity size in HOCM and thereby

A

decrease outflow obstruction –> decreased intensity of murmur

23
Q

Maneuvers that decrease preload, such as Valsalva, abrupt standing, or amyl nitrate administration, decrease LV size in HOCM and thereby

A

increase intensity of murmur

24
Q

loud S2 due to pulmonary HTN, systolic ejection murmur from increase flow across P from L to R shunt across AD, holosystolic murmur of VSD

A

findings on auscultation in CAVSD

25
pansystolic murmur that is loudest at LLSB plus diastolic rumble at apex due to increase flow across the mitral valve
VSD
26
stridor at age 6 mos - 6 yrs with barky cough
croup
27
strido most severe at age 4-8 months that worsens in supine position and improves in prone position
Laryngomalacia
28
stridor that presents before age 1 year, improves with neck extension, and is a/w cardiac abnormalities; does NOT improve with steroids, rac epi, or albuterol
vascular ring
29
w/u harsh holosystolic murmur best heard at LLSB
echo to determine location and size of VSD and r/o other defects
30
accentuated peripheral pulses with continuous flow murmur last LSB
PDA
31
mid systolic click with late systolic murmur
MVP
32
Syndrome a/w several cardiac abnormalities including AS, PS, or septal defects
Williams syndrome
33
tx PDA
indomethacin to close; prostaglandin E1 to keep open