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Flashcards in Placental physiology + amniotic fluid Deck (62):

Placental metabolism

not passive
rapid growth in first trimester, size >fetus for 16 weeks
decreased growth rate during later pregnancy but extensive maturation - increased branching, decreased thickness, functionally increased surface area
Blood/energy supply to placenta via maternal uterine artery
Placenta uses more energy than fetus (1/2 O and 2/3 glucose delivered to uterus)
Synthesizes glycogen
Produces proteins/steroids
Active transport of some elements


Concurrent blood flow in placenta

maternal + fetal blood flow in the same direction
Both enter in arteries, both leave in veins (parallel transport)


Hemochorial placentation

fetal blood within chorionic villi
Villi bathed in maternal blood
Maternal blood propelled into intervillous space in jetlike streams travelling towards chorionci plate
Blood then percolates down around villi to maternal venous drainage


Gas exchange at the placenta

placental barrier highly permeable to oxygen and CO2
Rate, volume and pressure of blood flow to placenta is major rate determining factor
Maternal:fetal partial pressure also important
Maternal and fetal hemoglobin O2 affinity also important


Simple diffusion in placenta

common for substances with:
- large gradient between mom and fetus
- minimal electronic charge
- high lipid solubility
generally - O2, CO2, H2O


Facilitated diffusion in placenta

Main fetal nutrient
Placenta doesn't produce glucose until late gestation, so uptake of maternal glucose is essential
favourable gradient from mother to fetus
Facilitated diffusion with glucose receptors on placenta
- non-energy dependent, non-insulin dependent
- even more efficient than simple diffusion alone at ensuring adequate glucose supply to fetus

Pregnancy: relative insulin resistance --> increases glucose availability to fetus


Active transport in placenta

Amino acids:
- work against gradient
- large amounts of lactate produced by placental metabolism are transferred to maternal circulation by active transport


Endocytosis in placenta

IgG transfer
- very large
- no concentration gradient
- picked up by receptors at placental barrier
- IgG can also work against us - Rhesus hemolysis etc

- likely that some viruses transfer to fetus


Leakage at placenta

Disruption in feto-maternal barrier
Occurs in normal pregnancies in small amount due to microtears at syncytiotrophoblastic barrier
Significant disruption/transfer can occur with abruptio placenta --> massive fetomaternal hemorrhage and fetal anemia/death


Ketone transfer at placenta

- used by fetus when glucose is low
- liposoluble, can cross by simple diffusion


Free FA transfer at placenta

- also used by fetus for energy when low glucose supply (starvation)
- some too large to cross
- essential FFA will cross slowly by simple diffusion
- possibly also some endocytosis


Drug transfer across placenta

depends on: size, charge, gradient, degree of drug protein binding, liposolubility
Many drugs cross in some amount, mostly by simple diffusion
Liposoluble drugs rapidly cross placenta - e.g. inhalational anesthetics
Large drug molecules will not cross (heparin, thyroxin replacement, insulin)



glycoprotein very similar to LH (same alpha subunit as LH, FSH, TSH; beta subunit unique but similar to LH)
produced almost exclusively by syncytiotrophoblast
Detectable in blood 8-9 d post-ovulation (blastocyst implantation)

Serum level doubles every 48 h, peak at 10 weeks, declines then plateaus
--> useful in following early pregnancy in patients with risk factors/complications


Actions of hCG

rescue/maintenance of corpus luteum (therefore progesterone production)
6 weeks: placenta takes over progesterone production
stimulates fetal testis production of testosterone



human placental lactogen
Produced by syncytiotrophoblasts (not exclusively)
proportional to placental mass
- production rises steadily until 34-36 weeks
- twins have higher hPL

- supports nutritional needs of fetus
- fail-safe mechanism to ensure adequate nutrient supply to fetus especially in fasting state


hPL - maternal fasting state

lipolysis --> increased FFA (maternal energy) and ketones (fetal nutrition)


hPL - maternal fed state

increased FFA interferes with insulin-directed entry of glucose into cells --> higher circulating glucose --> favours glucose transport to fetus --> gestational diabetes


Gestational diabetes

3-10% of all pregnancies
CH intolerance of variable severity with first onset/recognition during pregnancy
increased in twins due to higher hPL


Progesterone production during pregnancy

From maternal cholesterole
initially by corpus luteum
hCG rescue of CL ensures progesterone production by CL until 6-10 wks
Placental production of progesterone takes over at 6-10 weeks
Also some production by decidua and fetal membranes


Progesterone action during pregnancy

role in endometrial preparation/implantation
Maintain uterine quiescence during pregnancy "pro-gestation"
smooth muscle relaxation of uterus
inhibits uterine PG production (delays cervical ripening)
immunological modulation
Placental progesterone is pool of substrate for production of fetal adrenal corticosteroids


Estrogen production during pregnancy

from maternal androgens (in early pregnancy)
fetal androgens (later pregnancy)
by placenta


Estrogen action during pregnancy

increased uterine blood flow/CO
- peripheral v/d-
- regulates blood volume by stimulation of RAS
Uterine preparation for labour
Uterine contraction in labour
prepares breast for lactation
increase liver production of hormone-binding globulins


Corticosteroid production during pregnancy

by fetal adrenals from placental progesterone


Corticosteroid action during pregnancy

promotes fetal lung maturation
maternal fluid expansion (to fill estrogen-vasodilated vessels)


Amniotic fluid function

vital to fetal survival
cushions from trauma
prevents compression of umbilical cord
allows room for fetus to grow and move
- important for limb development and critical for fetal lugn development
Temperature homeostasis


1st trimester amniotic fluid

initial AF is isotonic with maternal blood
likely derived from transudate of maternal and fetal plasma
- transmembranous: exchange between maternal compartment and fetal compartment
- intramembranous: exchange from one fetal component to another (across unkeratinized fetal skin to amniotic fluid, across fetal surface of placenta to amniotic fluid)
2nd trimester fetal skin keratinized - impermeable

Small volume ~50 ml by 12 wks


2nd/3rd trimester amniotic fluid

balance between production/resorption
Production: fetal urine, lung liquid
Resorption: fetal swallowing, intramembranous pathway


Amniotic fluid production from urine

main component of 2nd/3rd trimester amniotic fluid (>90%)
Fetal kidneys relatively immature in concentrating ability, so fetal urine relatively hypotonic, creating hypotonic amniotic fluid
Urine production is influenced by renal blood flow (dictated by placental blood flow) and hormonal influence (vasopressin, aldosterone)


Amniotic fluid production from fetal lung

produce fluid to expand lungs to facilitate growth
excess fluid leaves lungs during breathing movements - 50% swallowed, 50% into AF
clinical implications for testing fetal lung maturity via amniocentesis (surfactant testing)


Fetal swallowing of AF

main route of fluid resorption
starts in 2nd trimester
500-1000 ml/day


Intramembranous flow of amniotic fluid

flow from fetal compartment to fetal compartment
hypotonic AF resorbed across osmotic gradient to vascular fetal surface of placenta
200-400 ml/day


Amniotic fluid production at term

Fetal urine 800-1200 ml
lung liquid 200 ml


Amniotic fluid resorption at term

fetal swallowing 500-1000 ml
intramembranous pathway 200-400 ml


Assessing amniotic fluid volume

AFI (amniotic fluid index): sum of deepest vertical pocket in 4 quadrants in mm (normal 50-250 )
DVP (Deepest vertical pocket) normal 20-80 mm
Objective measure and subjective assessment have both been proven to be reliable
Clinical assessment by SFH may raise suspicion of abnormal AFV





Oligohydramnios chronic causes

Fetal anomalies:
renal agenesis
multicystic dysplastic kidneys
Bilateral UPJ obstruction
posterior urethral valves

Chronic fetal hypoxia
Growth restriction (uteroplacental insufficiency)
post-term pregnancy
chronic maternal hypoxia

maternal NSAID use
maternal dehydration


Complications due to oligohydramnios

limb contractures
facial deformities
pulmonary hypoplasia
umbilical cord compression
prematurity (iatrogenic)


Oligohydramnios treatment

generally we cannot treat/modify long-term complications
Only successful when we can treat underlying cause (bladder shunts for bladder outlet obstruction)
Others have been tried:
- maternal hydration - only useful if dehydrated
- serial amnioinfusion: limited success, significant risks
- Amnio plugging for ruptured membranes - no benefit



AFI > 250 mm or DVP > 8 cm
excess accumulation of amniotic fluid


Fetal etiology of polyhydramnios

structural: decreased swallowing due to GI obstruction, neurological impairment
Cardiac arrhythmias
genetic syndromes


Maternal etiology of polyhydramnios

isoimmunization (hydrops)
diabetes - ?glucose load


Placental etiology of polyhydramnios

twin-to-twin tarnsfusion syndrome


Complications of polyhydramnios

Premature/preterm rupture of membranes
preterm labour
maternal discomfort
fetal malpresentation in labour
umbilical cord prolapse
antepartum and postpartum hemorrhage


Treatment of polyhydramnios

Serial amniotic fluid dcompression via amniocentesis (up to 3L each time)
NSAIDs: historical - rarely used now; knock out fetal kidneys
Treat underlying condition
- laser for TTTS
- intrauterine fetal transfusion for anemia
- fetal surgery for resection of lung mass


Maternal oxygen capacity

total oxygen content in arterial blood
influenced by:
- Hb concentration/saturation (almost completely saturated)
- Hb oxygen affinity (Temp, acidity, 2,3-DPG levels)
- dissolved oxygen

Optimal maternal oxygenation requires adequate ventilation/pulmonary integrity


Uterine blood flow

Not autoregulated - dependent on maternal BP
Can impact fetal oxygenation
- hypertensive disease with v/c
- hypotension - supine hypotensive syndrome, severe hemorrhage
During labour: contractions reduce blood flow - many short contractions rather than a long one


Oxygen transfer at placenta

not all of O2 from intervillous space gets to fetus
- shunting: diverted to placenta/uterus (10-30% for placenta)
- uneven placental perfusion
- diffusing capacity of placenta for oxygen

Oxygen transfers from mother--> fetus because:
- O2 gradient
Bohr effect
fetal Hb has higher affinity for O2 than maternal Hb (curve shifted to left)


Mean pO2 of mother's blood

arterial - 100 mmHg
intervillous space - 50 mmHg


Mean pO2 of fetus

umbilical vein: 30 mmHg
umbilical artery: 20


Bohr effect in placenta

Intervillous space:
Fetal metabolites/CO2 pass to mother
- IVS becomes more acidic --> facilitates O2 release from mother as maternal curve shifts right

As fetus gives up CO2, fetal pH rises --> shifts curve further left --> facilitates O2 uptake


CO2 exchange at placenta

from fetus to mother
CO2 gradient exists due to physiological hyperventilation of pregnancy


Mean pCO2 of fetus/mother

umbilical artery: 48 mmHg
intervillous space: 43
maternal blood: 30

maternal blood has higher affinity for CO2


fetal oxygen capacity

influenced by:
-fetal Hb concentration/oxygen affinity

Low absolute pO2 but can perfuse efficiently due to:
- higher Hb concentration, higher O2 capacity (HbF), higher CO

Physiologically, low pO2 helpful because it keeps DA open and pulmonary vascular bed constricted


Fetal Hemoglobin

more concentrated/ different structure

Different globin chains


Fetal acid-base exchange

Fetus produces carbonic acids and organic acids (lactate, ketones)


Carbonic acid

produced by fetus during normal oxidative metabolism
dissociates into CO2 and H2O
CO2 rapidly diffuses across placenta


Organic acids

result from anaerobic metabolism, e.g. lactic acid
Produced when fetal oxygenation impaired
- reduced placental oxygen transfer
- umbilical cord collapse

Organic acids cross placenta slowly (hours instead of seconds)
- lactic acids require specific, pH-dependent carrier


Placental acid-base exchange problems

if blood flow interrupted for a brief time period (e.g. placental abruption, cord compression)
--> fetal pH drops and CO2 rises --> respiratory acidosis
If oxygen lack is sustained,
- fetus decreases O2 consumption
- redistributes blood flow to vitals
- relies partly on anaerobic metabolism to meet energy needs --> anaerobic metabolism

Fetus copes with excess organic acids by buffering: Hb and bicarbonate
- if too much lactate, can be overwhelmed --> metabolic acidosis


Umbilical cord gases

drawn at every high risk delivery to determine acid-base status of fetus to reflect metabolic/respiratory demand
1) look at pH: pathologic increased risk of brain injury, seizures, need to CPR/NICU admin
2) pCO2 - respiratory acidosis? HCO3- and BE: metabolic acidosis?


Base excess of fetus

HCO3- excess
buffers depleted in attempt to normalize pH as fetal acidemia worsens
"base" value --> amount of organic acids produced by fetus
larger base excess = worse severity/duration of anaerobic metabolism or impaired fetal oxygenation
Prefer to look at umbilical artery values


Respiratory acidosis in fetus

pH 60 high
HCO3- normal (short duration of respiratory acidosis; buffer not depleted yet)
BE normal


Metabolic acidosis in fetus

fetal oxygenation impaired for sustained time period
buffer used up - subsequent anaerobic metabolism