Relias
-
Fetal
Heart
Monitoring
uterine
blood
supply
-
ANS
-
uterine
arteries
deliver
oxygenated
blood
to
spiral
arteries
which
bring
oxygen
rich
blood
to
intervillous
space
of
placenta
that
has
fetal
capillaries
-
fetal
capillaries
carry
the
O2
rich
blood
to
umbilical
VEIN
that
goes
to
fetus
-in
contrast,
the
umbilical
ARTERIES
return
waste
products
to
that
intervillous
space
that
go
into
mother's
venous
system
Potential
issues
that
negatively
affect
fetal
oxygenation
-
ANS
*Maternal
Oxygenation:*
asthma,
hyper-
or
hypo-
ventilation
*Maternal
Circulation:*
decreased
maternal
cardiac
output,
hypotension,
decreased
Hgb
*Placental
O2
and
CO2
Exchange:*
postterm,
abruption,
HTN,
hypotension,
uterine
tachysystole
*Fetal
circulation:*
cord
compression
or
occlusion
Fetal
hypoxia
-
ANS
-
can
occur
d/t
reduced
fetal
O2
reserves,
excessive
uterine
activity,
or
reduced
uteroplacental
blood
flow
-
worsening
fetal
hypoxia
can
lead
to
abnormal
FHR
patterns,
mostly
minimal
or
absent
variability
from
acidemia
(1)
hypoxemia
vs.
(2)
hypoxia
-
ANS
1
-
reduce
O2
in
blood
2
-
reduced
O2
delivery
at
tissue
level
Fetal
anaerobic
metabolism
-
ANS
-
occurs
when
long
term
O2
delivery
is
insufficient
to
meet
cellular
needs
of
tissues
-
results
in
production
of
lactic
acid
and
other
non
carbonic
acids
-
ACIDOSIS
is
the
presence
of
excessive
acids
in
tissues
acidosis
-
ANS
pH
below
7.35
pH
is
low
(acidosis
is
the
process
that
leads
to
low
blood
pH,
or
acidemia)
alkalosis
-
ANS
pH
above
7.45
pH
is
high buffers
-
ANS
-
help
maintain
acid
base
homeostasis
-
2
major
fetal
buffers
are
plasma
bicarbonate
and
hgb
base
excess
and
base
deficit
-
ANS
-
base
deficit
is
expressed
as
a
positive
number
-
base
excess
is
expressed
as
a
negative
number
~
they
are
equivalent
and
terms
are
used
interchangeably
~
fetal
acidosis
-
ANS
-
when
O2
is
decreased
to
fetus,
tissue
hypoxia
results
in
acidosis,
which
then
shows
a
drop
in
pH,
a
loss
of
bicarb,
and
increase
in
base
deficit
acidemia
-
ANS
assoc
w/
widespread,
deleterious
effects
on
vital
organ
and
body
function
fetal
hypoxia
during
birth
-
ANS
assoc
w/
neonatal
depression,
low
apgars,
neonatal
encephalopathy,
and
cerebral
palsy
respiratory
acidosis
-
ANS
*low
pH
(<
7.10),
high
pCO2
(>
60),
normal
base
deficit
(
<
12)*
-
increase
of
pCO2
for
fetus
that
lowers
pH
but
doesn't
affect
base
deficit
factors
that
contribute
to
resp
acidosis
-
ANS
-
sudden
decrease
in
placental
or
cord
perfusion
-
uterine
tachysystole
-
maternal
hypoventilation
metabolic
acidosis
-
ANS
*ph
<
7.10
,
normal
pCO2
(<60),
high
base
deficit
(>12)*
-
a
higher
base
deficit
(such
as
>
12)
has
been
assoc
w/higher
risk
for
severe
neonatal
complications
-
most
common
cause
of
metabolic
acidosis
in
fetus
is
r/t
inadequate
O2
delivery
-
prolonged
hypoxic
insult
to
fetus
results
in
depletion
of
bicarb,
which
is
a
base
buffer
that
normalizes
pH
levels
mixed
acidosis
-
ANS
*pH
<
7.10
,
high
pCO2
>
60,
and
high
base
deficit
>12*
-
may
develop
when
resp
acidosis
persists
for
a
prolonged
period
of
time
-outcome
for
neonates
is
dependent
on
degree
and
severity,
but
typically
the
lower
pH
and
higher
base
deficit
means
worse
neonatal
outcomes
-
most
often
seen
in
prolonged
bradycardia
at
time
of
birth
What
is
used
to
evaluate
fetal
acidosis?
-
ANS
arterial
umbilical
cord
blood
artery
values
(fetus
to
placenta)
-
ANS
Normal
ranges:
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