Prework 3: Fetal Circulation and Congenital Heart Defects Flashcards

1
Q

describe the general fetal circulation

A

blood is oxygenated in the placenta and delivered to the embryo via the umbilical vein
most blood passes through the ductus venosus within the liver and returns to the RA via the IVC
blood returns to the placenta via 2 umbilical arteries

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2
Q

what is the right to left fetal shunt?

A

blood shunted from RA to LA via foramen ovale
shunted from pulm outflow to aortic arch via ductus arteriosus
lung bypasses

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3
Q

what happens with the first breaths at birth

A

bradykinin is released from lungs
vascular resistance is decreased in lungs
increased O2 levels cause smooth muscle to contract, increasing blood flow to lungs

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4
Q

what is the result of increasing blood flow to the lungs?

A

increased blood returning from lungs into the LA

significant increase in LA pressure

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5
Q

why does the pressure in the RA decrease after birth?

A

blood flow to the RA decreased because blood flow from placenta is lost when cord is cut

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6
Q

result of LA pressure > RA pressure

A

septum primum is pushed against septum secundum closing the foramen ovale
anatomically closes within 1 year

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7
Q

normal closure of ductus arteriosus

A

functionally closes within 36 h of birth due to loss of prostaglandin E
anatomically closes within 3 months forming ligamentum arteriosum

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8
Q

symptoms of patent DA

A
rapid breathing
increase in the work of breathing
rapid HR
more frequent respiratory infections
tiring more easily
poor eating/growth
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9
Q

what population is prone to PDA and what is a treatment?

A

premature infants are slower in closing the DA

indomethican, a prostaglandin inhibitor can be given to speed closure

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10
Q

epidemiology of congenital heart defects

A

heart and vascular abnormalities make up largest category of birth defects
1% of liveborn infants
incidence 10x higher in stillborns

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11
Q

inherited defects that affect heart development

A

genes that encode transcription factors
cause partial loss of function
autosomal dominant
6-10% of babies with CHDs have chromosomal abnormalities (associated with genetic syndromes)

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12
Q

environmental stresses and CHDs

A

during 1st trimester, these stresses can alter the same genes and conceivably lead to acquired defects that mimic those produced by heritable mutations

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13
Q

maternal diseases linked to heart defects

A

insulin dependent diabetes

hypertension

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14
Q

shunt

A

abnormal communication between chambers or blood vessels

allows blood to flow down pressure gradients

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15
Q

obstruction

A

abnormal narrowing of chambers, valves, or blood vessels

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16
Q

atresia

A

complete obstruction of chambers, valves blood vessels

17
Q

hypertrophy

A

increase in muscle mass of cardiac chamber (increased size of cells)

18
Q

hypoplasia

A

decrease in muscle mass of cardiac chamber (fewer cells) BEFORE birth

19
Q

atrophy

A

decrease in volume and muscle mass of cardiac chamber (degeneration of cells) AFTER birth

20
Q

left to right shunt examples

A

systemic to pulmonary
ASD
VSD
PDA

21
Q

right to left shunt examples

A

TOF
transposition of great arteries
persistent truncus arteriosus (common arterial trunk)

22
Q

obstruction examples

A

coarctation of the aorta

valvular stenosis or atresia

23
Q

effects of left to right shunt

A

increased pulm blood flow
not initially associated with cyanosis
chronically elevates both V and P in pulm circulation, leading to medial hypertrophy of pulmonary arteries and vasoconstriction
RVH results

24
Q

end stage of left to right shunt

A

Eisenmenger syndrome
pulmonary resistance approaches systemic levels
left to right shunt becomes a right to left shunt

25
Q

effects of right to left shunt

A

pulmonary circulation is bypassed, thus decreasing pulmonary blood flow
poorly oxygenated venous blood enters the systemic arterial system
hypoxia and cyanosis results

26
Q

paradoxical embolism

A

emboli from venous circulation bypass the lungs and enter the systemic circulation
happen in right to left shunts