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
How do you Dx perinatal hypoxia due to decreased pulm blood flow?
- -cyanosis/pallor
- -low SaO2 on room air which improves w/ 100% O2 (Hyperoxia test)
- -tachypnea, scaphoid abd, heart murmur, abnormal CXR
What are four categories of problems that could cause decreased pulm blood flow?
1) decreased size of pulm vasc bed
2) f(X)al obstruction
3) pulm vasc constrict
4) pulm venous HTN
DDx for decreased size of pulm vasc bed?
congenital pulm hypoplasia 2° pulm hypoplasia --diaphragmatic hernia --oligo/an-hydramnios --absent fetal breathing (neurologic) --congen chylo- (accumulation of lymphatic fluid in the pleural space) or hydro-thorax
DDx for f(x)al obstruction?
polycythemia (incr viscosity)
DDx for pulm vasc constriction?
- -perinatal asphyxia
- -pulm parenchymal dz (RDS, pneumonia)
- -persistence of fetal circ syndrome (PFC)
DDx for pulm venous HTN?
- -pulmonary venous, LA or mitral obstruction
- -LV failure 2° to congen heart dz
- -transient LV dysfunction
If very low PaO2 from birth doesn’t improve with 100% O2, assume…
…congenital cardiac dz until proven otherwise
Order a STAT Echo
Tx for PFC?
Persistant Fetal Circ causes:
–hypoxia, hypercarbia and acidosis
TX: sedation, vent, iNO, QUIET
Clinical presentation of baby w/ PDA?
premie w/ RDS that doesn’t respond to mech vent
- -wide pulse pressure (PP = SBP - DBP)
- -bounding periph pulses
- -“hyperactive pericordium”
- -murmur
- -CXR show pulm edema, cardiomegaly
Order Echo
Prevent an tx a PDA
prevent w/ steroids to mom prenatally (betamethasone)
tx: indomethacin or ibuprofen or surgery
What is periodic breathing?
“PB” is that crazy breathing patter babies do that’s very rapid and shows up as a quick oscillating wave on the monitor.
Stupid question: which is worse for a baby: bradycardia or hypoxia?
bradycardia
Compare neonatal and adult ventilatory responses to increased pCO2.
- -How does hypoxia affect them?
- -How about sleep?
ADULT
linear relationship between pACO2 and ventilation increases that is very sensitive to small changes in pO2
–hypoxia makes even more sensitive
NEONATE
linear relationship between pACO2 and ventilation increases that is NOT very sensitive (shallow slope) to small ∆s in pO2.
–even less sensitive when asleep
–hypoxia? (doesn’t say)
Compare and contrast the degree of neuronal connectivity in the respiratory pattern generator between adults and neonates.
–What consequences does this have for neonates.
neonates have far fewer connections when compared to adult’s impressive connectivity and redundancy
–leaves neonate more dependent on external stimuli/CO2/hypoxia to ensure rhythmic stability
Compare neonatal and adult ventilatory responses to hypoxia.
Both have non-linear and not very sensitive responses to hypoxia.
- -even less sensitive to hypoxia if the pACO2 is low.
- -especially week hypoxic drive in preemies
An experiment was performed in which the minute ventilation was measured for 5 minutes in a full-term, healthy infant at 2 days of age breathing room air (21% oxygen) and then measured for an additional 5 minutes while the infant was breathing 15% oxygen.
- After 1 minute of breathing 15% oxygen, would you expect the minute ventilation to be increased, decreased, or unchanged from that observed while breathing room air?
The more mature the baby, the more it will increase.
An experiment was performed in which the minute ventilation was measured for 5 minutes in a full-term, healthy infant at 2 days of age breathing room air (21% oxygen) and then measured for an additional 5 minutes while the infant was breathing 15% oxygen.
- What would you expect the change in minute ventilation to be after 5 minutes of 15% oxygen breathing?
- How would the adult ventilatory response to 15% oxygen breathing differ from that in this full-term 2-day-old newborn?
It will decrease because of biphasic response to hypoxia which says RR will increase in the first few minutes of hypoxia (or plateau in the case of a preemie) and then begin to decrease.
This is true of both kiddos and adults, but neonates will lower their RR to below their original baseline while adult while lower it to a point that is still above the original (i.e. pre-hypoxic) RR.
An experiment was performed in which the minute ventilation was measured for 5 minutes in a full-term, healthy infant at 2 days of age breathing room air (21% oxygen) and then measured for an additional 5 minutes while the infant was breathing 15% oxygen.
- What would you expect to observe if the experiment were repeated at 3 to 4 weeks of age in this same infant?
The decrease in RR during the biphasic response to hypoxia will be less dramatic than with a younger neonate (i.e. more like that of an adult).
An experiment was performed in which the minute ventilation was measured for 5 minutes in a full-term, healthy infant at 2 days of age breathing room air (21% oxygen) and then measured for an additional 5 minutes while the infant was breathing 15% oxygen.
- What would you expect to observe if this experiment were performed in a 24-week-gestation infant at 2 days of age? At 3 to 4 weeks to age? At 6-8 weeks of age?
A 24 wk GA infant’s biphasic response would be of a plateau’d RR (vs. an increased RR as compared with a term infant or an adult) followed by a very dramatic decrease in RR after just 1 minute to a rate less than 1/2 the original RR.
With increasing age the first half of the biphasic response would look more adult (i.e. the RR would increase) and the decrease would be less dramatic.
Random Fact: What is %FIO2 on a transcontinental flight?
~18% O2
How does hypoxia affect the ventilatory response to CO2?
It blunts it
Why does having a smaller FRC make hypoxia in situations of decreased RR worse?
- If one has little lungs/smallFRC,changes in ventilation cause large changes in PAO2 and PACO2 – the small reservoir is easily emptied and filled -not stable.
- If one has big lungs/largeFRC, the FRC acts as a reserve (like thermal inertia) and slows rate of change and reduces amplitude of gas changes.
Sum Up: What factors contribute to oscillatory breathing patterns and apnea in premature infants?
• immature wiring • Decreased responsiveness to CO2 • Biphasic Ventilatory response to hypoxia • LowFRC • Easily collapsible upper airway • Issues with‘loop gain’–unstable system ^^NOT SURE WHAT THAT MEANS
What is the gold standard therapy for PB and apnea in infants?
PB = periodic breathing
- -caffeine
- -CPAP
- -O2 to prevent hypoxia (not too high!)
- -tactile stimulation
- -Time until brain matures
Define asphyxia
Asphyxiaisanysituationinwhichthereisa decrease in oxygen (O2) and an increase in carbon dioxide (CO2) in the body.
– If you stop breathing
– If your mouth, nose, or airway becomes obstructed.
– If you “rebreath” (imagine an infant face down in soft bedding).
Define suffocation
a form of asphyxia
Define entrapment
Entrapment is when an infant is “trapped” in a
situation that produces asphyxia.
Define Strangulation
Strangulation is when bed clothes or other material is wrapped around the neck, blocking the airway causing asphyxia.
What are the A Level Recommendations to parents to prevent PB/apnea/SIDS/SUID?
back to sleep firm sleep surface no soft objects or loose bedding in crib regular prenatal care no smoke exposure during preg or after breastfeed room share w/o bed sharing pacifier at nap time and bedtime avoid overheating do not use at-home cardio-resp monitor avoid EtOH before and after birth
