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Flashcards in Cardio Developmental Defects Deck (37):
1

what kind of shunt is more common

L to R shunt

2

when do L to R shunts cause cyanosis

later--> "blue kids"

3

What is the most common congenital cardiac anomaly

VSD

4

3 L to R shunts

1. VSD
2. ASD
3. PDA (patent ductus arteriousus)
*this is the order of prevalence

5

loud S1; wide, fixed split S2

ASD

6

continous machine-like murmur

PDA

7

MCC of early cyanosis

Tetralogy of Fallot

8

5 R to L shunts (early cyanosis)

1. Persistant Truncus arteriosus
2. Transposition of great vessels
3. Tricuspid atresia
4. Tetralogy of Fallot
5. Total anomalous venous return

9

defect in persistant truncus arteriosus

failure of TA to divide into pulmonary trunk and aorta--> only one vessel of outflow for the heart and complete mixing of oxy and non-oxy blood

10

2 physical exam findings in persistent truncus arteriosus

1. loud S2
2. systolic ejection murmur at left sternal border
*also bounding arterial pulses (increased volume); biventricular hypetrophy also possible--> boot shaped heart maybe
*most pts have accompanying VSD

11

defect in tricuspid atresia

absence of tricuspid valve and hypoplastic RV

*need both a VSD and ASD for viability

12

why does transposition of great vessels produce profound cyanosis

there are two closed, independent loops

13

tx for transposition of g.v.?

prostaglandins to keep ductus arteriosus patent--> needs a shunt to mix some of the blood

14

defect in total anomalous venous return

pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc)

15

4 defects in tetralogy of Fallot

1. pulmonic stenosis
2. right ventricular hypertrophy (boot-shaped heart)
3. VSD
4. Overriding aorta (overrides VSD)

*caused by anterosuperior displacement of infundibular septum

16

what kind of flow causes cyanosis?

R to L (unoxygneated blood into systemic circulation)

17

why does squatting help during cyanotic episodes (tet spells) in tetralogy

increases peripheral vascular resistance, increasing afterload; increased L ventricular pressure forces blood L to R across the VSD

18

tx for patent ductus arteriosus (PDA)

indomethacin--> NSAID that decreases prostaglandins and allows it to close

19

where does coarctation of aorta occur in infants

proximal to insertion of ductus arteriosus--> this the only place aorta is receiving blood from

20

what congenital anomaly is coarctation of aorta most commonly associated with

bicuspid aortic valve

21

High BP in upper extremities, no pulses in lower extremities; pulsatile intercostal arteries

coarctation of aorta in adults--> occurs distal to ductus arteriosus (is now the ligamentum arteriosum)

*notching of ribs due to collateral flow through the intercostal arteries

22

Truncus arteriosus, tetralogy of fallot associated w/ which genetic disorder

22q11 syndrome--> DiGeorge syndrome

*heart defect + hypocalcemia = Digeorge

23

endocardial cushion defect (ASD, VSD, AV septal defects ass. w/

Down's syndrome

* as is AML, ALL, Alzheimer's

24

heart defects expected if congenital rubella

1. septal defects
2. PDA
3. pulmonary artery stenosis

25

coarctation of aorta associted w/ What other heart defect is commonly seen with this

Turner syndrome

*commonly have bicuspid aortic valve also

26

Aortic insufficiency ass. w/

Marfans

*later, aortic dissection

27

Infants of diabetic mothers have an increased risk of which heart defect

transposition of great vessels

28

Adult coarctation of the aorta can eventually lead to heart failure symptoms because what happens

develop aortic regurgitation--> increased afterload due to obstructions wears the valve out over time

29

what is Eisenmenger's syndrome

reversal of a L to R shunt (VSD, ASD, PDA) to a R to L shunt

30

pathgenesis of Eisenmengers

pulmonary vascular hypertension develops due to the increased left volume due to L to R shunt; eventually R side pressure exceed L side and the blood begins to flow from R to L

31

4 symptoms of cyanotic heart dz

1. cyanosis
2. clubbing
3. SOB
4. polycythemia

* seen later in L to R shunts and in Eisenmenger's syndrome

32

what is Ebstein anomaly ( 2 main features)

1. Tricuspid leaflets are displaced into right ventricle--> tricuspid regurg or stenosis
2. Hypoplastic right ventricle

33

What happens in Ebstein due to the shitty tricuspid valve/ right ventricle

right atrium dilates--> due to poor flow through the malformed tricuspid into the small right ventricle

34

what do 80% of children with Ebstein anomaly have associated (heart defect)

Patent foramen ovale-> R to L shunt (pressures are higher in the dilated right atrium)

35

2 physical exam finding in Ebstein

1. widely split S2
2. Tricuspid regurgitation

36

What causes Ebstein malformation

maternal Li use

37

2 arrythmias kids with Ebstein are at increased risk for

1. WPW
2. supraventricular Tachycardia (SVT)

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