Fetal & Neonatal Respiration/SIDs Flashcards
What are 2 fetal adaptations to hypoxia?
1) fetal Hb has a higher affinity for O2 than maternal O2
2) higher Hb concentration
Why do the fetal lungs only receive only 5-8% of the CO? (2)
1) the fetal lungs have high pulmonary vascular resistance in utero
2) blood flow through fetal lungs is NOT needed only for gas exchange, only for the development of the lungs itself.
What causes the high pulmonary vascular resistance observed in the fetal lungs? (multiple factors that cause vasoconstriction in utero)
vasoconstriction is maintained via PEP-TOLL
1) thromboxanes (platelet-derived) stimulate platelet aggregation
2) low O2/low pH - hypoxia induces redistribution of blood flow away from the accessory organs to the heart, brain, and adrenal glands.
1) lung fluid - mechanical compression of small arteries
3) leukotrienes
5) endothelin-1 (ET-1), PAF, PDGF
Factors that cause vasodilation in utero:
1) NO
2) increased O2 (low CO2, high pH)
3) PGI2
Patency of the ductus arteriosus is maintained by:
Which brings us to the following questions:
Why must a pregnant mom refrain from taking NSAIDS during the third trimester?
What is used to maintain patency in the fetus?
PGE2
Pregnant moms should not take NSAIDS because it will promote premature closure of the ductus arteriosus, which lead to pulmonary vasculature abnormalities and pulmonary HTN.
Prostaglandin Es are used to maintain patency of the DA until surgical ligation is performed.
How does the closure of the ductus arteriosus occur after a baby is born? (3 mechanisms)
1) baby take its first breath –> increase in O2 leads to 3 things:
a) decrease pulmonary vascular resistance (remember low O2 causes vasoconstriction), which reduces the BP in the DA lumen
b) Ca influx –> muscle contraction
c) ET2 production
2) removal of placenta reduces PGE2 levels
3) reduce PGE2 receptors in DA wall
all lead to vasoconstriction of the musculature at the ductus arteriosus, and ultimately leading to its closure.
Whats the difference between fetal circulation and neonatal circulation in terms of:
1) placenta
2) FO + DA
3) PVR
4) pulmonary blood flow
5) RAP and LAP
Fetal circulation:
1) placenta - present
2) FO + DA - open
3) PVR - high
4) pulmonary blood flow - low
5) RAP > LAP
Neonatal circulation:
1) placenta - absent
2) FO + DA - closed
3) PVR - low
4) pulmonary blood flow - high
5) RAP < LAP
During the transition from fetal circulation –> neonatal circulation, PVR goes from HIGH –> LOW. What would delay a decrease in PVR?
normally, as soon as the baby takes a breath, there is a decrease pulmonary vascular resistance (remember low O2 causes vasoconstriction), which reduces the BP in the DA lumen.
Oxygen deprivation at the time of birth due to inadequate circulation/perfusion, impaired respiratory effort, inadequate ventilation, etc. This results in low blood flow to the lungs, which results in low O2, which promotes vasoconstriction and ultimately decrease in PVR is delayed.
What causes PFC?
In general, a well formed, “normal” fetus at term would revert back to fetal circulation in the face of stress or lung pathology (pneumonia, RDS, retained fetal lung fluid, amniotic fluid aspiration, blood aspiration, meconium aspiration syndrome, etc).
What is the clinical presentation of a neonate who has PFC (persistence of fetal circulation)?
cyanosis/pallor low PaO2/O2 sat variable PaO2 when breathing 100% O2 tachypnea scaphoid abdomen heart murmur abnormal CXR
What is the hyperoxia test?
What does a low PaO2 value mean? high value?
test that is performed–usually on an infant– to determine whether the patient’s cyanosis is due to lung disease or a problem with blood circulation (shunt).
It is performed by measuring the arterial blood gases of the patient while he breathes room air, then re-measuring the blood gases after the patient has breathed 100% oxygen for 10 minutes.
IF PaO2=HIGH (>150mmHg) = cyanosis is due to poor oxygen saturation by the lungs. By allowing the patient to breath 100% O2 will augment the lungs’ ability to saturate the blood with oxygen, and the partial pressure of oxygen in the arterial blood will rise.
IF PaO2 = LOW (<100mmHg) = cyanosis is most likely due to blood that moves from the systemic veins to the systemic arteries via a right-to-left shunt without ever going through the lungs (the lungs are healthy and already fully saturating the blood that is delivered to them)
What are some causes of pulmonary hypoplasia?
congenital or secondary
secondary causes:
- diaphragmatic hernia
- def. of amniotic fluid (oligohydraminos or anhydraminos)
- absent fetal breathing (neurological deficits)
- pleural effusions (chylo-/hydro-thorax)
What are some causes of pulmonary functional obstruction?
polycythemia - increased viscosity of blood, which leads to decreased pulmonary blood flow; common in diabetic moms.
L atrial obstruction - mitral atresia, hypoplastic
What are some causes of pulmonary venous HTN?
any defect with components downstream of the pulmonary vasculature:
pulmonary veins, L atrium, mitral valve, L ventricle
What causes a baby to be hypoxemic? (general summary)
Babies are hypoxemic because they:
1) have surfactant deficiency and have micro and macroatelectasis and have decreased oxygenation and ventilation
2) have pulmonary edema / retained fetal lung fluid which decreases their ability to oxygenate/ventilate (decreased A-A gradient)
3) have pulmonary fluid from “pus” from pneumonia that decreases ability to oxygenate/ventilate.
Rare causes would be babies whose lungs didn’t grow (like the baby with diaphragmatic hernia or the baby with low amniotic fluid and has underdeveloped lungs—these babies cannot oxygenate bc they don’t have the anatomic structure to support adequate oxygenation/ventilation.
How would you assess whether a baby has PFC?
1) presence of RDS (respiratory distress syndrome) or in utero stress - look for meconium stain
2) hx of oligo-hydraminos
3) sepsis (measure CBC)
4) Hyperoxia test to differentiate between lung disease or a presence of a shunt.
What is ECMO?
extracoporeal membrane oxygenation (ECMO) - basically a lung bypass that takes over the work of the lungs; used in severe cases of neonatal RDS
How is PFC treated? (4)
1) mechanical ventilation
2) sedation to minimize agitation and allow for ventilation
3) iNO or adenosine to decrease PVR
4) keep QUIET to avoid distress
Why is PDA more likely to occur in a premature baby and rarely in a pre-term baby?
In a premature baby, the DA is more sensitive to the vasodilating effects of PGE2 and NO, and the DA musculature has a weaker contractile capability.
In a pre-term baby (40wks), the DA is more sensitive to the vasoconstricting effects of O2, and the musculature of the DA has greater contractile capability, thereby promoting its closure.
