18. Neonatal Development Flashcards
Is the placenta efficient or inefficient compared to the lung at gas exchange?
inefficient
fetal blood distribution max’s what?
02 delivery to vital tissues (heart, brain)
what % of cardiac output do cardiac lungs receive? why?
5-8%. because of high pulm vascular resistance.
in the fetus, the umbilical vein is ox or deox?
ox from placenta
regulation of pulm vascular resistance: what causes vasoconstriction?
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
regulation of pulm vascular resistance: what causes vasodilation?
mostly endothelial-derived.
- NO
- incr 02, high pH
- PGI2 prostacyclin
what structures does the ductus arteriosus connect?
connects pulm artery and aorta. allows oxygenated blood from the placenta to pass directly into systemic circ.
what keeps the ductus open?
prostaglandin E2 keeeeeeeps the ductus open!
what makes the ductus close? think about where it is produced.
the absence of PGE2 allows the ductus to close… PGE2 is made in the placenta, cleared by the fetal lung
what is ET1? what does it do?
endothelin 1, major constrictor of the ductus arteriosus.
for term infants, how does the ductus close?
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
what are the molecules responsible for closing the ductus?
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
what are some physiological changes that cause changes in pulmonary vasc at birth?
- rapid decr in pulm vasc resistance with lung inflation
- additional vasodilator effects of oxygen
- adaptive changes in the heart (closure of shunts)
fetal circulation pattern turns into what? which turns into what?
fetal –> transitional –> neonatal
what are characteristics of the transition from fetal to transitional circ?
- 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.
what forces characterize the transition from transitional to neonatal circulation?
- with neonatal circ, both the FO and the DA are closed
- PVR is lowered further
- LA pressure is consistently higher than RA pressure
what are 2 categories of failure to transition?
persistence of fetal circulation, and a patent ductus arteriosus
what can cause a delay in the decrease in pulm vascular resistance?
- 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
definition of asphyxia?
failure of gas exchange: low Pa02, high PaC02
what happens during perinatal asphyxia (leading to persistence of fetal circ?)?
- 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
clinical presentation of a neonate with hypoxia due to a decr in pulm blood flow?
cyanosis, low 02 sat, incomplete correction in Pa02 when breathing 100% 02. (basically due to a shunt)
describe the hyperoxia test
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.
why might a pulm vasc bed not develop properly?
congenital pulm hypoplasia, secondary pulm hypoplasia (diaphragmatic hernia, neuro causes of decr fetal breathing)
why might there be functional obstruction to neonate lungs?
polycythemia with incr viscosity decr pulm blood flow.
polycythemia is high levels of RBCs in blood, seen w mothers with gestational diabetes
why might there be pulm vascular constriction with a neonate?
perinatal asphyxia, pulm parenchymal disease (RDS, pneumonia), PFC
what might cause neonatal pulm venous hypertension?
pulm venous obstruction, LA, or mitral obstruction
a word about pulm venous outflow obstruction: what does it resemble, what is the treatment?
looks like severe non responsive hypoxia. CXR looks like severe pneumonia.
only chance for survival is urgent surgery.
a very low Pa02 from birth that does not increase with 100% 02 and pos pressure ventilation is what?
cardiac disease until proven otherwise.
most infants with pulm causes of PFC respond to 100% 02 or not?
yes
treatment for a diaphragmatic hernia?
gentle ventilation, surgery after delay if low risk. if high risk, ECMO and then surgical repair.
treatment for left atrial obstruction?
create shunt across atria.
how do we treat PFC?
disease is hyperoxia, hypercapnia, acidosis.
so give 02, hypocapnia, alkalosis.
sedation, ventilation, iNO
how does iNO help in the setting of PFC?
decr pulm vascular resistance
why does the ductus remain patent in premature infants?
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.
treatment of a PDA?
- steroids to mom before birth
- give porstaglandin synthetase inhibitors (indomethacin, ibuprofen)
- surgery
