Current Development

The role of blood gas and acid-base assessment in the

diagnosis of intrapartum fetal asphyxia
James A. Low, MD
Kingston, Ontario, Canada

The diagnosis of fetal asphyxia requires a blood gas and acid-base assessment demonstrating a
significant metabolic acidosis. However, the fetus may tolerate an asphyxia! insult without central nervous
system injury because of the fetal cardiovascular adaptation to hypoxemia. Prediction of the significance of
an asphyxia! insult to the fetus requires a measure of both the duration and degree of the asphyxia as well
as an expression of the fetal compensatory response to the asphyxia. (AM J OssrEr GvNECOL
1988;159:1235-40.)

Key words: Fetus, asphyxia, blood gas

Intrapartum fetal asphyxia is an important compli-
cation in reproductive health care. However, there are
differences of opinion as to the magnitude of the prob-
lem. 1 A number of intrapartum deaths due to asphyxia
are reported in most perinatal mortality studies. Al-
though questioned by some, there is evidence to in-
dicate an association between intrapartum fetal as-
phyxia and motor and cognitive deficits in surviving
children. 2
This continuing confusion is due, in part, to the lack
of a precise diagnosis of fetal asphyxia. The diagnosis
of asphyxia requires a blood gas and acid-base assess-
ment. This fact, widely accepted in the research labo-
ratory and in adult clinical medicine, has been slowly
acknowledged in fetal medicine. This has been due, in
part, to the relative inaccessibility of the fetus in utero
and the risks of blood sampling of the apparently com-
promised fetus.
Fetal blood gas and acid-base assessment has been
available for 20 years. The objective of this review is to
demonstrate the importance of blood gas and acid-base
assessment in the diagnosis of fetal asphyxia during
labor and delivery and to examine the factors that affect
the significance of this diagnosis to the fetus.
Fetal blood gas and acid-base characteristics
Tlw tmique characteristics of fetal blood gas and
acid-lia,e measures in relation to adult blood gas and
From the Department of Obstetrics and Gynaecology, Queen's Uni-
versity.
Reprint requests: James A. Lqw, MD, Department of Obstetrics and
Gynaecology, Queen's University, Kingston, Ontario K7L 3N6,
Canada.
acid-base measures must be recognized. This is most
striking in regard to oxygen. Fetal oxygen tension is
much lower than corresponding maternal levels, re-
sulting in the maternal-fetal oxygen gradient essential
for the transfer of oxygen across the placenta to the
fetus. Oxygen content of fetal blood is adequate despite
the low oxygen tension, because there is increased oxy-
gen affinity in fetal blood, with displacement of the fetal
oxygen dissociation curve to the left and increased oxy-
gen capacity.
Fetal carbon dioxide tension closely parallels carbon
dioxide tension in the normal adult. This is achieved
because of the fetal-maternal carbon dioxide gradient,
which is due to the hypocapnia with decreased carbon
dioxide tension that occurs in the normal obstetric
patient.
Maternal arterial and venous pH is slightly alkaline
as a result of this modest respiratory alkalosis. The fetal
pH in the umbilical vein and artery is lower than the
maternal pH, with a uterine vein-umbilical vein pH
gradient of 0.06 pH units.
Normal labor with a "clinically normal" fetus may
affect fetal blood gas and acid-base characteristics.
Bretscher and Saling' first described a small decrease
of pH late in the first stage and in the second stage of
labor. This decrease of pH includes a mild metabolic
acidosis as indicated by an increase of the base deficit.
However, there is a spectrum of tissue oxygen debt in
the "clinically normal fetus" during labor. Some infants
demonstrate no increase of lactate and pyruvate levels,
whereas others exhibit a moderate increase in these
levels.
Blood gas and acid-base measures of umbilical vein

1235
1236 Low
Table I. Mean (SD) fetal blood gas and
acid-base measures in umbilical vein and
artery blood in 4500 pregnancies
Umbilical vein Umbilical artery
pH 7.340 0.065 7.262 0.070
Pco 2 41.6 8.0 54.9 9.9
Po2 27.0 6.0 15.l 4.9
Buffer base 43.7 2.8 42.0 3.4
Pco2 , Carbon dioxide partial pressure; Po 2 , oxygen partial
pressure.
and artery blood at delivery represent a valuable ref-
erence point that can be obtained in all pregnancies
without risk to the fetus or newborn. Such values have
been measured in "clinically normal" fetuses after nor-
mal labor and elective cesarean section. Such data have
been useful and have provided the preliminary nor-
mative data in most centers. However, recognizing the
variable effects of labor and delivery, an alternative is
to obtain fetal blood gas and acid-base measures for a
total population. Table I summarizes the measures ob-
tained at delivery from 4500 pregnancies in our center
between May 1984 and June 1987. This closely ap-
proximates a total population with a slight bias toward
so-called high-risk pregnancies.
Measures of fetal asphyxia
Measures of a significant degree of fetal asphyxia
have not yet been established. Fetal hypoxia leads to a
metabolic acidosis. Thus, metabolic acidosis is the best
indicator of the degree of tissue oxygen debt experi-
enced by the fetus.
We have established for our own center an umbilical
artery buffer base of <34 mmol/L as a criterion of
significant fetal asphyxia. This was based on two ob-
servations. An umbilical artery buffer base of 36
mmol/L represented two standard deviations below the
mean in a study of "clinically normal" fetuses at deliv-
ery.4 Lactate represents the principal fixed acid con-
tributing to this metabolic acidosis, with a close corre-
lation between increasing lactate concentrations and
decreasing buffer base. 5 However, an increase in lactate
may be due to an increase of pyruvate as well as hy-
poxia. Observations in the human fetus during labor
have demonstrated that one third of fetal lactate was
due to increased pyruvate and two thirds was due to
hypoxia. 6 Therefore, the umbilical artery buffer base
was adjusted down to 34 mmol/L to serve as a measure
of metabolic acidosis due to hypoxia.
The results in the total population (Table I) with
regard to metabolic acidosis closely approximate the
results from these earlier studies. The incidence of a
metabolic acidosis with an umbilical artery buffer base
<34 mmol/L is about 2%.
November 1988
Am J Obstet Gynecol
Some confirmation of the significance of this degree
of metabolic acidosis has been obtained from recent
follow-up studies. The incidence of neurodevelopmen-
tal deficits at 1 year of age increases as the umbilical
artery buffer base decreases below 34 mmol/ L and par-
ticularly below 20 mmol/L. 7 Examination of the nature
of the deficits indicates that beyond this critical thresh-
old of metabolic acidosis, there is an increased incidence
of both major and minor motor and cognitive deficits,
suggesting a continuum of casualty in such surviving
newborn infants. 8 The assessment of the significance
of this degree of asphyxia with metabolic acidosis will
be strengthened as measures of less severe deficits are
developed.
Clinical proxies for fetal asphyxia
Clinical criteria have been used for the diagnosis of
fetal asphyxia in much of the literature, in the absence
of blood gas and acid-base measures. The commonly
used criteria have been meconium in the amniotic fluid,
low Apgar scores with delayed onset of respiration, and
newborn encephalopathy.
The relationship between fetal asphyxia, as ex-
pressed by umbilical artery blood gas and acid-base
measures, with meconium in the amniotic fluid and
Apgar scores has been examined in 1773 pregnancies. 9
Fetal asphyxia, as expressed by an umbilical artery
. buffer base <34 mmol/L, was observed in 39 fetuses
(2.2%).
Moderate or severe meconium was observed in the
amniotic fluid of 262 patients (15%). Meconium was
present in 12 of the patients with significant metabolic
acidosis, a sensitivity of 32%. However, there were 250
patients with meconium in whom the fetus had normal
blood gas and acid-base values, a false positive rate of
95%.
An Apgar score of 0 to 3 at 1 minute was recorded
in 115 newborns (6%). An Apgar score of 0 to 3 at 1
minute was recorded in 18 of the newborns with sig-
nificant metabolic acidosis, a sensitivity of 46%. How-
ever, an Apgar score ofO to 3 at 1 minute was recorded
in 97 newborns with normal blood gas and acid-base
values, a false positive rate of 84%.
An Apgar score of 0 to 3 at 5 minutes was recorded
in 11 newborns (l %). An Apgar score of 0 to 3 at 5
minutes was recorded in three newborns with signifi-
cant metabolic acidosis at delivery, a sensitivity of 8%.
However, the same was recorded in eight newborns
with blood gas and acid-base values in the normal
range, a false positive rate of 73%.
There is an association between meconium and low
Apgar scores and fetal asphyxia. However, these mark-
ers are not sensitive indicators of intrapartum fetal as-
phyxia. The large number of patients with meconium
and/ or newborns with low Apgar scores, in the absence
 Volume 159
Number 5
of evidence of fetal asphyxia, emphasizes that a number
of mechanisms account for these clinical markers. This
experience is in keeping with the literature. 10 13
Newborn encephalopathy, including abnormalities
of behavior and tone and seizures reflecting abnormal
central nervous system function, is a valuable predictor
of subsequent deficits. The relationship of fetal as-
phyxia, as expressed by blood gas and acid-base mea-
sures, to newborn encephalopathy has been examined
in 303 high-risk newborn infants. 14 Fetal asphyxia with
a significant metabolic acidosis was observed in 25 in-
fants (8.2~).
Severe newborn encephalopathy, characterized by
abnormal tone, seizures, and/or recurrent apnea, was
observed in 27 newborn infants (8.9%). Fetal asphyxia
with metabolic acidosis was present in six newborns with
severe encephalopathy (22%). However, blood gas and
acid-base values were within the normal range at de-
livery in 21 newborns with severe encephalopathy
(78%).
Thus again there is evidence of an association be-
tween fetal asphyxia and newborn encephalopathy.
However, the large number of newborns with severe
encephalopathy and with normal blood gas character-
istics emphasizes that asphyxia is only one of a number
of mechanisms contributing to this complication. The
other mechanisms have as yet to be determined. How-
ever, the significant relationship between severe new-
born respiratory complications and severe newborn en-
cephalopathy suggests that asphyxia in the newborn
period may be an important factor.
Fetal response to asphyxia
There are thos~ who question the value of a measure
of fetal metabolic acidosis because of the apparently
unpredictable association with early outcome measures,
such as Apgar scores, or late outcome measures, such
as motor and cognitive deficits, in surviving children.
Such conclusions fail to recognize the complexity of the
fetal response to asphyxia or to acknowledge the
range of mechanisms that account for these outcome
measures.
The severity of the metabolic acidosis reflects the
degree of the fetal hypoxic insult. However, the effect
of asphyxia on the fetus is influenced by a number of
additional factors, including the pattern of develop-
ment and the duration of the asphyxia and the nature
of the fetal response to the asphyxia.
The degree of the asphyxia is relevant in regard to
outcome. Neuropathologic findings in the fetal monkey
in response to total anoxia are different from those
after partial hypoxia." The human fetus in the clinical
setting may develop ~ significant degree of metabolic
acidosis because of severe hypoxemia acting over a
short period or a milder degree of asphyxia acting over
Diagnosis of intrapartum fetal asphyxia 1237
a longer period. Severe hypoxemia may occur due to
maternal shock, placental separation, or cord prolapse.
However, in general in labor, hypoxemia is relative in
degree and intermittent in occurrence, with a gradual
development of tissue oxygen debt.
The duration of the fetal asphyxia is equally impor-
tant. Studies in the fetal monkey have demonstrated
that total anoxia in excess of 10 to 12 minutes will result
in a neuropathologic state. 16 However, partial hypoxia
with metabolic acidosis must be present for at least 2
hours before neuropathologic damage can be antici-
pated.17 A precise measure of the duration of fetal as-
phyxia in the human fetus is, generally, not available
because of the periodic nature of fetal blood gas and
acid-base assessment and the intervention that abnor-
mal blood gas and acid-base measurements now re-
quire. However, the importance of the duration of fetal
asphyxia was implied in a study of 60 children with
biochemical evidence of intrapartum fetal asphyxia at
delivery. 7 Children with deficits had an episode of as-
phyxia that was more severe and prolonged than the
children with normal motor and cognitive develop-
ment. The findings suggested that the duration of the
episode of hypoxia was usually in excess of 1 hour
before the neuropathologic damage responsible for
motor and cognitive deficits developed.
The fetal response to hypoxemia is the key to the
effect of the degree and duration of fetal asphyxia.
Fetal hypoxemia results in an increase in arterial pres-
sure due to increased vascular resistance. This is as-
sociated with a redistribution of cardiac output char-
acterized by reduced blood flow to the pulmonary, re-
nal, and gastrointestinal circulations and the body, with
increased blood flow to the brain, heart, and adrenal
glands. 18 20 Umbilical placental blood flow is maintained
when fetal hypoxia is a result of maternal hypoxemia
or reduced maternal uteroplacental blood flow. 21 Fetal
hypoxia due to cord oclusion is associated with de-
creased umbilical-placental blood flow. However, blood
flow to the central circulation is maintained through
the ductus venosus, with a marked reduction of blood
flow through the liver. 22
The autonomic nervous system is principally respon-
sible for this increased vascular resistance and redis-
tribution of cardiac output. There is evidence to indi-
cate that this response is initiated through arterial
chemoreceptors23 and may be influenced by circulating
endogenous opiates. 24 Other factors may include in-
creased angiotensin activity 2' and the release of vaso-
pressins. 26
Thus increased cerebral blood flow maintains the in-
tegrity of the central nervous system. Variation of ar-
terial pressures in the normoxic fetal lamb does not
affect cerebral blood flow. 27 However, in hypoxic fetal
lambs, cerebral blood flow is pressure dependent due
1238 Low
to the loss of cerebrovascular autoregulation.2 8 This
evidence of impaired autoregulation and pressure-
dependent flow complements earlier observations in
sick human newborns.2 9 Recent studies in the fetal lamb
indicate that normal cerebral oxygen consumption will
continue for some time in the presence of relative de-
grees of fetal hypoxemia. 30
This compensatory mechanism provides a "period of
protection" so that the fetus may experience an as-
phyxia! insult without manifesting central nervous sys-
tem injury. Such compensation is time limited. Sus-
tained hypoxemia will ultimately lead to cerebral tissue
oxygen debt. This combined with hypertension and loss
of cerebral autoregulation, particularly in the preterm
fetus, may lead to a germinal matrix hemorrhage. Per-
sistence of the asphyxia with cardiovascular decom-
pensation and hypotension results in reduced cerebral
blood flow. The resulting ischemia with hypoxia leads
to brain injury.
Fetal blood gas and acid-base assessment
during labor
The introduction of microelectrode blood gas sys-
tems with appropriate laboratory services dedicated to
the labor and delivery room has provided the oppor-
tunity for fetal blood gas and acid-base assessment dur-
ing labor and delivery.
The first step was blood gas and acid-base assessment
of umbilical vein and artery blood at delivery. This
assessment can be obtained in all patients without risk
to the fetus and newborn. A blood gas and acid-base
assessment at this time can establish, in the presence of
a significant degree of metabolic acidosis, that an epi-
sode of asphyxia has occurred during labor and deliv-
ery. It confirms the diagnosis in the same manner that
an elevated blood sugar estimation confirms the diag-
nosis of diabetes.
However, there are limitations of fetal assessment
during labor. The relative inaccessibility of the fetus in
early labor and the risks of sampling in certain circum-
stances are relevent constraints to caput sampling dur-
ing labor. This can be circumvented, in part, by con-
tinuous electronic fetal heart rate monitoring. There is
a substantial body of knowledge from animal stud-
ies31-3 and studies of the human fetus 35-38 indicating a
relationship between fetal hypoxemia and fetal heart
rate behavior. This has led to a widely accepted con-
sensus of the predictive value of electronic fetal heart
rate monitoring. 39 The recent Dublin randomized con-
trol trial demonstrated an increased incidence of di-
agnosis of fetal asphyxia with the complementary use
of electronic fetal heart rate monitoring and fetal blood
gas and acid-base assessment. 40 Thus fetal heart rate
monitoring can provide an indication of when the risk
November 1988
Am J Obstet Gynecol
of fetal ca put sampling is justified. Such assessment can
exclude or confirm the diagnosis of fetal asphyxia at
the time of sampling during labor.
A single blood gas and acid-base assessment during
labor or at delivery can confirm the diagnosis of as-
phyxia. However, with the exception of an occasional
case of very severe asphyxia (e.g., umbilical a~tery
buffer base <20 mmol/L), it does not establish the sig-
nificance of the asphyxia! episode to the fetus. A single
measure does not indicate the pattern of development,
the duration of the asphyxia, or the nature of the fetal
response to the asphyxia.
Criteria to complement single or periodic blood gas
and acid-base assessments are required to establish the
significance of an asphyxia! episode to the fetus. Such
criteria cif fetal assessment in utero have not been de-
veloped for routine clinical use. However, a number
of int,eresting possibilities have been or are being ex-
amined.
The oxygen tension electrode 41 and pH electrode 42 43
can provide an accurate indication of the duration of
the hypoxemia and the pattern of developing metabolic
acidosis. Although interesting observations have been
obtained, the limitations of current technology are such
that these options are not available for routine clinical
practice. Pulsed Doppler ultrasound can now assess fe-
tal cerebral blood flow velocity in utero. 44 The value of
such observations to assess the fetal response to as-
phyxia has yet to be determined. Assessment of the
metabolic effects of asphyxia is another option. Studies
in animals have demonstrated that central nervous sys-
tem lactate levels can be a useful predictor of central
nervous system injury. 45 The further development of
such complementary observations in the clinical setting
should permit a better prediction of the significance of
an intrapartum episode of asphyxia.
Prediction of significance of fetal asphyxia can be
augmented by newborn behavior. For example, a fetus
with evidence of asphyxia and significant metabolic ac-
idosis at delivery who has a low Apgar score at 5 minutes
and subesquently demonstrates evidence of severe new-
born encephalopathy is at high risk for motor and cog-
nitive deficits. On the other hand, a fetus with a cor-
responding degree of asphyxia with metabolic acidosis
at delivery but with an Apgar score in the normal range
at 5 minutes and no evidence of newborn encephalop-
athy is at much lower risk of such deficits.
Finally, prediction can be enhanced by the growing
number of imaging techniques that will identify new-
born neuropathologic signs. Ultrasound and comput-
erized tomography are well established. Radionucleo-
tide brain scanning can be of value.4 6 Nuclear magnetic
resonance imaging may represent the next important
addition to this diagnostic armamentarium. 47
Volume 159
Number 5
Comment
The diagnosis of fetal asphyxia can be confirmed with
a blood gas and acid-base assessment demonstrating a
significant degree of metabolic acidosis. Clinical mark-
ers cannot be used as proxies for this diagnosis. A con-
sensus to define a significant degree of metabolic aci-
dosis has not yet been established. Presumably, the cri-
terion should represent that degree of metabolic
acidosis at which fetal injury begins. Our current cri-
terion of a significant degree of metabolic acidosis is an
umbilical artery buffer base <34 mmol/L. The inci-
dence of asphyxia during labor in our center, based on
this criterion, is about 2%.
The fetus has a "period of protection" from a partial
asphyxia! insult because there are cardiovascular com-
pensatory mechanisms leading to increased cerebral
blood flow. This "window of diagnostic opportunity"
may, in relation to partial asphyxia, extend for several
hours. Thus a diagnosis of intrapartum fetal asphyxia
can be made and appropriate intervention carried out
without compromise to the fetus or newborn.
The significance of asphyxia to the fetus requires not
only a measure of degree but also of duration of the
asphyxia, as well as an expression of the response of
the fetus to the asphyxia! insult. The current challenge
is to develop such complementary measures as can be
used in the clinical setting.
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