2013-09-09 Neonatal Physio; SIDS Flashcards
Discuss the basic concepts of fetal respiration.
Deoxygenated blood from the fetus —umbilical arteries—>placenta—>fingers of the chorion—>dip into the intervillous space (blood bath) of the placenta—>umbilical veins—>DV—>IVC—>RA—>PFO—>LA—>LV—>Aorta
Descrive the anatomical and physio development of the pulm vasc
- -pre-acinar (pre-resp) branching pattern complete by 16 weeks
- -Airways develop alongside arteries
- -at first, arteries have small lumens and relatively thick SMM layer in media
- *chronic fetal stress can further increase the thickness of the SMM
What is mechanism behind ∆s in PVR?
Morphological Changes Occur in three stages: 1) Rapid Adaptation, 2) Structural Stabilization, 3) Growth
1) Rapid Adaptation
- -endothelial cells in both alveolar (w/in 30 mins) and resp unit arteries (w/in 24 hrs) thin out, making a wider lumen w/ decr PVR
2) Structural Adaptaption
- -Wall thickness of arterial walls —> adult by 3 mos
- -SMM cells deposit stabilizing c.t. around themselves
3) Growth
- -blah over it
Describe some of the problems assoc’d w/ a failure to go thru a nl transition.
PFC - persistence of the fetal circulation
PDA - patent ductus arteriosus
Describe some of the problems assoc’d w/ PFC.
.
Describe some of the problems assoc’d w/ PDA.
.
What is the double Bohr effect?
The Bohr effect describes the effect that pH and pCO2 have on the binding affinity of Hb. Since there are two systems of circulation coming together in the placenta, the Bohr effect is happening twice. Thus the name.
What is 2,3-DPG and what is its effect on Hb?
2,3-diphosphoglycerate
Decreases the affinity of dHbA for O2. (Does not bind with high affinity to HbF.)
How is fetal CaO2 different from pregnant woman different from non-pregnant person.
Fetal CaO2: incr, and is >mom at term because 1) incr [Hgb] and has HbF > HbA.
Mom CaO2: decreased carrying capacity compared w/ non-pregnant b/c decr [Hgb], incr plasma vol
How does fetal SaO2 compare to mom?
Fetal: ~75%
Mom: ~98%
Draw out fetal circulation.
See page 3 of notes.
What are the fetal shunts and where are they?
DV - ductus venosus: allows oxygenated blood in umbilical vein to bypass the liver
FO - foramen ovale: allows oxy’d blood in the RA to shunt over to the LA bypassing the lungs
DA - ductus arteriosus: allows blood that made it through the RA —> RV —> pulm art to shunt into the aorta
What factors ∆ PVR in fetus?
PVR = pulmonary vascular resistance
Vasoconstrict caused by: a) physical (fluid in lung) b) decr O2 and pH c) leukotrienes d) TxA2 (? Endotholin A, PDGF, PAF, AA metabolites)
Vasodilation caused by: a) incr O2 and pH b) NO c) PGI2 (prostacyclin) (?ET_B activation)
How does fetus regulate DA?
PGE2 (prostaglandin E2) = major dilator
- -Made in placenta, cleared in fetal lung
- *THEREFORE NO NSAIDS IN PREGNANCY
ET-1 (endotholin 1) = major constrictor
How does NEOnate regulate DA?
O2 major factor for closing DA after birth
- -Ca2+ mediated
- -also incr ET-1 which overwhelms, PGE2 and NO
- -PGE2 is also lost when placenta is gone and there’s decr in PGE2 receptors in DA wall @ term
–decr flow and later reversed flow thru DA also may responsible
Draw transitions Fetal—>Transitional—>Neonatal circulation
See diagram on notes pg. 6
Describe some of the causes of perinatal asphyxia
MATERNAL: utero-placental insufficiency
- -chronic HTN
- -preg-induced HTN (PIH) = pre-eclampsia 50% decr in intervillous perfusion =(
- -maternal renal, CV dzs
- -uterine anomalies
- -maternal fever (no hot tubs)
- -placental abruption
FETAL
- -CV (e.g. SVT)
- -hydrops fetalis (fetal edema of any cause)
- -polyhydramnios
- -infection
IATROGENIC
- -regional anesthetic hypoperfusion
- -uncorrected supine positioning
- -β-blockade
What is the course of perinatal asphyxia?
- -circ to brain myocardium and adrenal maintained or incr’d
- -causes vasoconstriction in lungs which is good for fetus but BAD for neonate
(also constricts skin, liver, kidney, GI tract)
What is a term infant?
40 weeks
(now avg is 39 wks b/c of elective c-sections and inductions)
GROSSSSSS