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86 Cards in this Set

  • Front
  • Back
gas exchange area of human placenta
~ 5 meters squared
oxygenated blood from placenta reaches fetus via what?
umbilical vein
compare efficiency of gas exchange in human placenta vs. lung
10-20x more O2 exchanged in lung per mass

VO2 of placenta is significant (consumes 20-50%)

Placenta is a much larger functional shunt (20-35% shunt, vs. 2% shunt in lung)
Factors that determine placental gas exchange
*PaO2 of the uterine artery and umbilical artery (GRADIENT)
what factors promote O2 transfer from maternal to fetal HGB
1) Difference in relative amounts of HGB
2) difference in relative affinities of HGB
3) Double BOHR effect (co2 exchange accounts for 8% of O2 exchange)
4) Double Haldane Effect (effect of O2 exchange on CO2 exchange)
5)small amt of CO causes big change in fetal O2
fetal PaO2
20-30 mmHg
02 consumption of fetus relative to adult (per unit weight)
O2 consumption of fuetus is 2x that of an adult
oxygen reserve of fetus is enough for how long?
1-2 minutes
Fetal Adaptations to hypoxic environment
1) Fetal Hgb (beta chains vs. alpha, higher affinity Hgb)
2) Fetal and Maternal O2 content (fetal [Hgb] increases while maternal O2 capacity decreases during gestation)

3) Fetal Blood Flow distribution (highest PaO2 goes to vital tissues)
at term what percentage of Hgb is fetal Hgb?
contrast fetal Hgb to adult Hgb
fetal Hgb has >> O2 affinity
-oxyhemoglobin curve shifted left
-P50 for fetal Hgb is lower (20) than for adult Hgb (26)
-fetal Hgb does not bind 2,3, DPG as well as adult Hgb
-for any given sat. PaO2 << that of adult Hgb
what happens to fetal [Hgb] during gestation
increases to ~14 (versus adult 12)
to ~85% of total Hgb

decrease Hgb saturation in fetus
what percentage of combined CO goes to fetal lungs?
why does such a small % of combined caridac output go to fetal lungs?
1) High PVR (pulmonary vascular resistance)
2) flow to lungs not needed for gas exchange, some needed for growth and development
placental blood flow is influenced by what?
pulmonary blood flow
-as Pulmonary BF decreases
-placental BF increases
blood with the highest O2 concentration flows from the placenta to where?
Umbilical vein --->
Ductus Venosus -->
mixing and streaming of blood in the heart is decreased by what structure?
Foramen Ovale

distributes high [O2] blood from RA to LA so that it can go directly to the brain and heart
3 big fetal adaptations to hypoxic enviro
specialized Hgb
increased red cell mass
specialized distribution of Cardiac output
despite a low PaO2 and an Hgb sat 25% lower than the adult, the Oxygen content of fetal blood is great than or equal to that of
the moterh
what accompanies and develops with airways in the fetus?
what type of branching pattern is complete by 16 weeks gestation
pre-acinar (pre-respiratory) branching pattern
when do intra-acinar arteries develop?
later (after 16 weeks) and continue to form after birth
what prevents bloodflow through fetal lungs?
high pulmonary vascular resistance

ductus arteriosus allows circulation to bypass lungs
Placenta --> ??? --> FO --> Left Heart --> ???
Ductus Venosus

Body/ Placenta
what factors affect PVR (pulmonary vascular resistance)
Morphology (vessls themselves)
Relative hypoxia and acidosis
otehr factors
factors promoting vasoconstriction (increasing PVR)
-physical (lung fluid)
-decreased O2 and pH
factors promoting vasodilation (decreasing PVR)
-increasing O2 and pH
Major dilator of the ductus arteriosus
-produced in placental, cleared in fetal lung
Major constrictor of the ductus arteriosus

(formation increased by increasing PO2)
what is responsible for closing the ductus after birth
apparently O2
associated with increase in intracellular Ca2+ and depolarization of SM cell membranes

probably involves changing balance of constrictor and dilator factors

+PO2 leads to + ET-1
ET-1 overcomes dilating effects of PGE2 and NO
May be assisted by decrease in vascular pressure
Stage I of pulmonary vascular changes at birth
rapid adaptation (24 hours)
Stage II of pulmonary vasculature changes following birth
structural stabilization (3 months)
Stage III of pulmonary vasculature changes following birth
transitional circulation
placenta removed
FO and DA still open
PVR decreasing

once FO and DA clos
PVR is low
main changes in Pulmonary vasculature post-birth
decreased PVR (mechanical and O2)
main changes in circulation following birth
closure of foramina
-ductus arteriosus
-foramen ovale
-ductus venosus
what establishes continuous breathing?
the first breath and expulsion of fetal lung fluid
2 clinical problems associated with failure of transition
PFC (persistance of fetal circulation, or delay in normal decrease in PVR)

PDA (patent ductus arteriosus)
what can cause persistance of fetal circulation?
-asphyxia around time of birth
-undergrowth of pulmonary vasculature
-chronic intrauterine hypoxia
-idiopathic PFC
failure of gas exchange (decreased PaO2 and increased PaCO2)

fetus: placental failure
newborn: pulmonary failure
redistribution of blood flow during asphyxia
-BF to lung remains decreaed or decreases
-flow to vital organs is maintained or increased
-in fetus, blood flow to placenta is maintained unless there is cord obstruction
-blood flow to liver, kidneys, GI tract, and skin decreases
PFC causes profound hypoxia caused be a decrease in pulmonary blood flow:
characterized by...
low O2 saturation or PaO2 in room air
variable increases in PaO2 when breathing 100% oxygen (hyperoxia test)
clinical presentation of PFC
tachypnea, scaphoid abdomen, heart murmur, abnormal chest x-ray
clinical classification of PFC
-decreased size of pulmonary vascular bed
-functional obstruction
-pulmonary vascular constriction
-pulmonary venous hypertension
causes of decreased size of pulmonary vascular bed
congenital pulmonary hypoplasia

secondary pulmonary hypoplasia (diaphragmatic hernia, oligohydramnios, absent fetal breathing, congenital chylo or hydro-thorax)
an example of a functional obstruction leading to PFC
POLYCYTHEMIA (too many RBCs) with increased viscosity, decreases pulmonary blood flow (often due to placental transfusion, high altitude birth)
examples of pulmonary vascular constriction (that can result in PFC)
perinatal asphyxia

pulmonary parenchymal disease (RDS, pneumonia)

transient Persistence of Fetal Circulation syndrome (PFC)
Pulmonary Venous hypertension can be caused by:
OBSTRUCTION: pulmonary venous, left atrial or mitral obstruction

LV FAILURE secondary to congential heart disease

Transient LV dysfunction
severe, non-responsive hypoxia and a chest xray that looks like HMD, severe pneumonia or pulmonary venous congestion strongly suggests:

only chance of survival = URGENT SURGERY
how does one differentiate non-cardiac hypoxia from cyanotic congenital heart disease
measure PaO2 in 100% oxygen
if you get PaO2 > 150mmHg probably not congenital heart disease
what does meconium staining reveal about hypoxia?
hypoxia increases peristalsis, meconium can be swallowed by hypoxemic fetus
rule of thumb regarding suspected congenital heart disease
a very low PaO2 from the moment of birth that doesn't increase substantiall with 100% oxygen and positive pressure ventilation is cardiac disease until proven otherwise by echo- TGA, TAVR, Truncus arteriosis, Tricuspid atresia, Tetralogy of Fallot (the 5 Ts)
most infants with pulmonary causes of PFC respond to 100% oxygen +/- positive pressure ventilation early in their course with...
a substantial increase in PaO2 (> ~150 torr)
Conventional Tx for diaphragmatic hernia
-gentle ventilation (to establish risk)
-low risk: surgery after delay
-high risk: early ECMO --> surgical repair
Experimental Tx for Diaphragmatic hernia
fetoscopic temporary tracheal occulsion (effort to expand lungs)
Tx for Left Atrial Obstruction
create shunt ax atria
general Tx for PFC
HYPERVENTILATION (reduces PVR by decreasing PaCO2 and increasing pH)
NO inhalation (reduces PVR by direct effect)
Experimental pulmonary vasodilators
what leads to PDA in premature infants?
-ductus less sensitive to constricting effects of O2
-ductus more sensitive to dilating effects of PGE2 and NO
-incomplete muscle development (less contractile capacity)
clinical presentation of PDA
premature infant
respiratory distress syndrome (increasing compliance)
failure to improve
physical exam findings of PDA
wide pulse pressure (BPs-BPd)
full/bounding peripheral pulses
hyperactive precordium
heart murmur
Tx of PDA
-administration of steroids to mom reduces incidence of PDA
-INDOMETHACIN (prostaglandin synthetase inhibitors, inhibits production of PGE)
complications of INDOMETHACIN (prostaglandin synthetase inhibitor used to treat PDA)
renal failure

GI perforations
formation of proximal airways happens when?
embryonic period
wks 3-8
3 weeks:
26 days:
28 days:
33 days:
41 days:
52 days:
3 weeks: median pharyngeal groove, laryngotracheal sulcus, caudal end of which is the respiratory primordium
26 days: ventral outpouching from foregut: respiratory bud
33 days: LOBAR BUDS
41 days: SEGMENTAL BUDS (completion of proximal airway dvpt)
52 days: pleural cavity separate from peritoneal cavity
pseudoglandular phase
8-16 wks
formation of conducting airways

bronchial tree arborizes (16-25 generations, final = terminal bronchioles)

advancing airways with COLUMNAR EPITHELIUM surrounded by mesenchyme
canalicular phase
16-24 weeks
Formation of Acini
budding and branching of terminal bronchioles to form respiratory bronchioles

differentiation of respiratory epithelium, thinning into Type I pneumocytes and appearance of type II pneumocytes

capillary proliferation and closer proximity to air spaces
respiratory units distal to terminal bronchioles
when do pneumocytes form/appear?
Type I form by thinning of respiratory epi
and Type II appear in

CANALICULAR phase of development

(16-24 weeks)
what is limiting factor of survival in extremely premature infants
at the end of the canalicular phase (24 wks) there are only respiratory bronchioles and no true saccules or air exchange spaces

(even if there is surfactant sufficiency there still is no gas exchange area)
saccular phase
24 weeks to term

formation of gas exchange sites
~3 generations of respiratory bronchioles
1 generation transitional duct
3 generations of saccules (last = terminal saccule)
decreased thickness of interstitial tissue is marked
close spatial relationship bt caps and epithelial layer develops
epithelium differentiates fully into Type I and II pneumocyte
alveolar phase
post natal: birth- 8 years

at birth there are few true alveoli
increase air phase surface area (increase in capillaries)

saccules and transitory ducts become alveolar sacs and ducts
~300 million alveoli
postnatal phase
growth pahse
> 8 years
furthing thinning of interstitium
cells of endodermal origin
those associated with conducting airways

alveolar cells:
- Type I Pneumocyte (simple, covers 96% of surface)
-Type II Pneumocyte (surfactant secreting)
cells of mesodermal origin
SM cells (surround conducting airways, pulmonary arteries and arterioles)
Vascular endothelium
Capillary pericytes
Cells of ECTODERMAL origin
pulmonary innervation
Free cells
lymphocytes, plasma cells, macrophages, mast cells, granulocytes
factors affecting structural development
1) intrauterine environment
2) fetal breathing
3) corticosteroids
Function of Surfactant
Lower surface tension on dynamic compression

re-spread after dynamic compression past monolayer collapse

adsorb well from subphase to interface
composition of surfactant
phospholipid composition ? %

pulmonary surfactant proteins ?
factors affecting development of SURFACTANT
fetal sex, race
fetal stress, asphyxia,
maternal diabetes
beta-adrenergic stimulation
thyroid hormones
composition of extracellular matrix
pulmonary mechanics at the onset of breathing
a) conversion from fluid to air-filled lungs
B) decreased PVR, chnage in circulation
examples of Pulmonary hypoplasia
renal agenesis
diaphragmatic hernia
second trimester prolonged rupture of membranes
RSD (surfactant deficiency)
infants of diabetic mothers
transitional problems
transient tachypnea
bronchopulmonary dysplasia often results
due to iatrogenic disease (ventilation causes more severe damage)