18. Neonatal Development Flashcards

1
Q

Is the placenta efficient or inefficient compared to the lung at gas exchange?

A

inefficient

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2
Q

fetal blood distribution max’s what?

A

02 delivery to vital tissues (heart, brain)

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3
Q

what % of cardiac output do cardiac lungs receive? why?

A

5-8%. because of high pulm vascular resistance.

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4
Q

in the fetus, the umbilical vein is ox or deox?

A

ox from placenta

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5
Q

regulation of pulm vascular resistance: what causes vasoconstriction?

A

generally: mechanical means, 02, hormones from arachodonic acid.
- low 02 and low pH (remember this is pulm so it is backwards in terms of pH)
- leukotrienes
- thromboxane A2

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6
Q

regulation of pulm vascular resistance: what causes vasodilation?

A

mostly endothelial-derived.

  • NO
  • incr 02, high pH
  • PGI2 prostacyclin
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7
Q

what structures does the ductus arteriosus connect?

A

connects pulm artery and aorta. allows oxygenated blood from the placenta to pass directly into systemic circ.

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8
Q

what keeps the ductus open?

A

prostaglandin E2 keeeeeeeps the ductus open!

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9
Q

what makes the ductus close? think about where it is produced.

A

the absence of PGE2 allows the ductus to close… PGE2 is made in the placenta, cleared by the fetal lung

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10
Q

what is ET1? what does it do?

A

endothelin 1, major constrictor of the ductus arteriosus.

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11
Q

for term infants, how does the ductus close?

A

functional closure with smooth muscle vasoconstriction within hours of birth. local action.
anatomic occlusion over days with intimal thickening and loss of smooth muscle cells from inner muscle media

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12
Q

what are the molecules responsible for closing the ductus?

A

02 appears to be ultimately responsible.
incr in P02 increases for formation of ET-1.
ET-1 promotes constriction, overcomes the dilating effects of PGE2/NO
also, removal of the placenta decreases the concentration of PGE2

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13
Q

what are some physiological changes that cause changes in pulmonary vasc at birth?

A
  • rapid decr in pulm vasc resistance with lung inflation
  • additional vasodilator effects of oxygen
  • adaptive changes in the heart (closure of shunts)
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14
Q

fetal circulation pattern turns into what? which turns into what?

A

fetal –> transitional –> neonatal

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15
Q

what are characteristics of the transition from fetal to transitional circ?

A
  • placenta: has been part of circuit, now removed.
  • FO and DA have been open; now FO closes and flow through the DA reverses
  • there has been high PVR; now it decreases
  • RA pressure has been higher than LA pressure; now LA pressure rises and LA pressure falls
  • pulm blood flow overall increases.
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16
Q

what forces characterize the transition from transitional to neonatal circulation?

A
  • with neonatal circ, both the FO and the DA are closed
  • PVR is lowered further
  • LA pressure is consistently higher than RA pressure
17
Q

what are 2 categories of failure to transition?

A

persistence of fetal circulation, and a patent ductus arteriosus

18
Q

what can cause a delay in the decrease in pulm vascular resistance?

A
  • perinatal asphyxia: low 02 during delivery, causes baby to try to maintain fetal breathing style
  • sepsis
  • undergrowth of pulm vasculature
  • idiopathic PFC (persistence of fetal circ): we don’t know
19
Q

definition of asphyxia?

A

failure of gas exchange: low Pa02, high PaC02

20
Q

what happens during perinatal asphyxia (leading to persistence of fetal circ?)?

A
  • blood flow to the lungs remains decr as it was in utero.
  • in the fetus, blood flow to the placenta is maintained unless there is cord obstruction
  • flow to vital organs is maintained
  • blood to liver, kidneys, GI, skin decreases
21
Q

clinical presentation of a neonate with hypoxia due to a decr in pulm blood flow?

A

cyanosis, low 02 sat, incomplete correction in Pa02 when breathing 100% 02. (basically due to a shunt)

22
Q

describe the hyperoxia test

A

allows you to tell is a problem in pa02 is due to a shunt (persistence of fetal circ) or due to a problem with gas exchange in the lung.
if due to PFC, giving 100% 02 won’t help. if due to a problem of incomplete gas exchange in the lung, it will raise Pa02.

23
Q

why might a pulm vasc bed not develop properly?

A

congenital pulm hypoplasia, secondary pulm hypoplasia (diaphragmatic hernia, neuro causes of decr fetal breathing)

24
Q

why might there be functional obstruction to neonate lungs?

A

polycythemia with incr viscosity decr pulm blood flow.

polycythemia is high levels of RBCs in blood, seen w mothers with gestational diabetes

25
Q

why might there be pulm vascular constriction with a neonate?

A

perinatal asphyxia, pulm parenchymal disease (RDS, pneumonia), PFC

26
Q

what might cause neonatal pulm venous hypertension?

A

pulm venous obstruction, LA, or mitral obstruction

27
Q

a word about pulm venous outflow obstruction: what does it resemble, what is the treatment?

A

looks like severe non responsive hypoxia. CXR looks like severe pneumonia.
only chance for survival is urgent surgery.

28
Q

a very low Pa02 from birth that does not increase with 100% 02 and pos pressure ventilation is what?

A

cardiac disease until proven otherwise.

29
Q

most infants with pulm causes of PFC respond to 100% 02 or not?

A

yes

30
Q

treatment for a diaphragmatic hernia?

A

gentle ventilation, surgery after delay if low risk. if high risk, ECMO and then surgical repair.

31
Q

treatment for left atrial obstruction?

A

create shunt across atria.

32
Q

how do we treat PFC?

A

disease is hyperoxia, hypercapnia, acidosis.
so give 02, hypocapnia, alkalosis.
sedation, ventilation, iNO

33
Q

how does iNO help in the setting of PFC?

A

decr pulm vascular resistance

34
Q

why does the ductus remain patent in premature infants?

A

ductus of a preterm infant is less sensitive to 02 constriction.
ductus of a preterm infant is more sensitive to dilating effects of PGE2 and NO than that of a term infant.

35
Q

treatment of a PDA?

A
  • steroids to mom before birth
  • give porstaglandin synthetase inhibitors (indomethacin, ibuprofen)
  • surgery