Obstetric Evaluation of Fetal Acid Base Balance

Critical Reviews in Clinical Laboratory Sciences, 36(5):407–451 (1999)
Obstetric Evaluation of Fetal

Acid-Base Balance
Critical Reviews in Clinical Laboratory Sciences Downloaded from informahealthcare.com by McMaster University on 11/04/14
Jeffrey L. Ecker and Julian T. Parer*

Vincent Memorial Obstetrics and Gynecology Service, Massachusetts General
Hospital, Harvard Medical School, Boston, Massachusetts and Department of
Obstetrics, Gynecology and Reproductive Sciences, and the Cardiovascular
Research Institute, University of California, San Francisco
Referee: R. Depp, Thomas Jefferson University, Philadelphia, PA
* Author to whom all correspondence should be addressed.
ABSTRACT: Several techniques may be used to evaluate fetal acid-base status during
the ante- and intrapartum periods. Percutaneous blood sampling (cordocentesis) may be
For personal use only.
used to measure standard blood-gas parameters while the fetus is still in utero, but because
of the risks associated with such procedures and the limited clinical utility of the results,
this procedure is recommended for blood gas analysis only as part of a research protocol.
Intrapartum blood specimens may be safely obtained via fetal scalp sampling, but the
need for such sampling has been dramatically reduced by the use of other noninvasive
tests such as fetal scalp stimulation or vibroacoustic stimulation. Finally, assay of blood
obtained from a segment of umbilical cord collected at delivery indicates acid-base status
at birth, but the range of normal values is wide, and only the most abnormal results have
any prognostic significance.
KEY WORDS: obstetric evaluation, fetal acid-base, antepartum, intrapartum,

cordocentesis.
I. INTRODUCTION
As in newborns, children, and adults, the balance of oxidative metabo-

lism in fetuses is reflected in blood pH, carbon dioxide (CO2), oxygen (O2),
and bicarbonate (HCO3). An appropriate balance is needed to provide the
fuel and metabolic environment conducive to fetal enzyme activity and
growth. Obtaining a blood gas in the fetus, however, is not always as straight-
forward as in the adult, where radial or femoral arteries provide easy vascular
Copyright© 1999, CRC Press LLC — Files may be downloaded for personal use only.
Reproduction of this material without the consent of the publisher is prohibited.
407
access. Nonetheless, by sampling blood from the fetal scalp or umbilical cord
segments, fetal acid-base balance may be evaluated and the information
obtained used by clinicians either to make ante- and intrapartum manage-
ment decisions or to counsel parents regarding neonatal prognosis.
The American College of Obstetricians and Gynecologists (ACOG)
stated in 1995 that “umbilical cord blood acid-base analysis provides an
objective method of assessing a newborn’s condition.”1 In this review, we

critically examine the usefulness of such assessment and compare how such
measures perform against traditional tools like Apgar scores or fetal heart
rate tracings. Specifically, we examine fetal blood sampling during three
periods, using three different techniques: antepartum via cordocentesis
(also known as percutaneous umbilical blood sampling, or PUBS), intrapar-
tum via fetal scalp sampling (FBS), and postpartum by sampling a segment
of umbilical cord clamped at the time of birth. We define those settings in
which we believe the risk and/or expense of fetal blood gas evaluation is
warranted.
Much of the writing and research concerning the use (and misuse) of
umbilical blood sampling, includes terms such as “asphyxia,” “birth as-
phyxia,” and “fetal distress.” In individual studies these conditions are often
poorly defined and, between studies, there is considerable variability as to
their definitions. Rather than use such terms, we will endeavor to describe
and define specific blood gas abnormalities (acidemia, hypercarbia, etc.), but
when we review specific studies, we may of necessity be forced to use the
authors’ stated outcomes, however poorly named. Similarly, we will employ
the commonly used terms “reassuring” or “nonreassuring heart rate pattern”
in recognition of the extraordinary false-positive rate such tracings have
when labeled as demonstrative of “fetal distress.” At the conclusion of our
survey, we review the criteria recently proposed by the American College
of Obstetricians and Gynecologists for making the diagnosis of birth as-
phyxia. As we shall see, blood gas analysis is an integral part of this new
definition and the criteria they have developed are considerably more restric-
tive than the general use of the term.
II. MATERNAL-FETAL ACID-BASE RELATIONSHIPS
Before examining the usefulness of fetal blood gas sampling and analy-
sis, it is essential to understand the anatomy and physiology of normal fetal
gas exchange. Such an understanding in turn requires familiarity with both
the anatomy and biochemistry of the fetal-maternal interface.
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A. Anatomy of Maternal-Fetal Placental Exchange
The fetus relies on the mother’s circulatory system both to provide the
nutrients necessary for growth (e.g., O2 and glucose as fuel for aerobic
respiration) and to remove metabolic wastes (e.g., CO2, the end-product of
aerobic respiration, and urea). The placenta serves as the organ of exchange
between fetal and maternal circulations. Modifications of the fetal circu-

latory system ensure that the most highly oxygenated fetal blood is deliv-
ered to those tissues with the greatest metabolic demand and that most fetal
blood avoids the pulmonary circulation as the lungs are not yet organs of
oxygenation (Figure 1).2
FIGURE 1. The fetal circulation. Numbers represent approximate values of the

percentage saturation of the blood hemoglobin with oxygen in utero.
409
The mother’s uterine arteries supply oxygenated blood to the uterus
and placenta contained within its cavity. At term, uterine blood flow is about
700 ml/min and accounts for 10% of maternal cardiac output in contrast to
the 3% the uterus receives in the nonpregnant state. Approximately 20%
of this flow perfuses the myometrium: the majority moves from the uterine
arteries to smaller arterioles that perfuse the intervillous space, which in turn
bathes the syncytiotrophoblast of the individual placental villi (Figure 2a).

Surrounded by cyto- and syncytiotrophoblast, a fetal capillary is within
each villus (Figure 2b). As pregnancy progresses and the placenta matures,
these layers thin and merge so that by the second and third trimester, the
fetal capillary is close to maternal blood, the mean distance of separation
being 3.5 µ.
Exchange across villi may occur by simple diffusion (e.g., O2 and CO2),
facilitated transport (e.g., glucose), or active transport (e.g., amino acids).
Because dissolved gases and small ions (O2, CO2, bicarbonate, and many
acids and bases) move by simple diffusion, their flux is regulated by the
relevant concentration gradients between maternal and fetal circulations.
As a result, maximum fetal oxygen tension (in the umbilical vein), for exam-
ple, cannot be greater than that in blood returning to the mother’s system
(in the uterine vein).
Fetal capillaries join to form a single umbilical vein that returns from
the placenta to the fetus through the umbilical cord. After entering the ab-
dominal wall, the umbilical vein enters the fetal liver where it joins with
the left portal vein. Much of this blood is shunted past the portal microcir-
culation by passing through the ductus venousus to the inferior vena cava
(IVC). Upon entering the heart, much of the IVC flow—which represents
the most highly oxygenated fetal blood—is diverted to the systemic circula-
tion by passage through the foramen ovale, an aperture in the fetal interatrial
septum. The majority of the blood that the right ventricle pumps through
the pulmonary artery (that portion of the IVC return not diverted across the
foramen ovale and the blood returned to the atrium through the superior
vena cava) is in turn shunted to the systemic circulation by passage through
the ductous arteriosus, which connects the pulmonary artery to the descend-
ing aorta. Indeed, the system is designed to minimize circulation through
the pulmonary system which, in utero, can provide no gas exchange. The
left side of the heart receives a small amount of blood from the pulmonary
veins and a larger volume of well-oxygenated blood shunted through the
foramen ovale and pumps the mixture out through the aorta. Blood leaving
the left ventricle—in contrast to that which passes through the ductus
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411
A
FIGURE 2. (A) The circulation of blood in the primate placenta. Fetal circulation is shown in the two panels at the left and in
the umbilical cord above. The panels at the right show the maternal blood spurting from spiral arteries in the basal area through

the intervillous space. The blood passes fetal villi, exchanges substances with fetal blood within the villi, and ultimately drains into veins
in the basal area. (Drawing by Ranice W. Crosby for the late Dr. Elizabeth Ramsey. Reprinted by courtesy of the Carnegie Institution
of Washington, D.C.) (B) Drawing from an electron micrograph of a cross-section through part of two fetal villi, showing tissue
layers that separate fetal and maternal blood in the human placenta. The cytotrophoblastic layer is much less distinct in the third
trimester than is depicted here.
FIGURE 2B
arteriosus directly to the descending aorta—may circulate through the

large vessels that arise along the aortic arch and supply the head and upper
extremities, and the coronary circulation.
The circuit of maternal-fetal exchange is completed as blood returns
from the fetus to the placenta via the two umbilical arteries. Each arises
from the internal iliac artery and exits the fetus at the umbilicus. Because
blood in the umbilical artery represents blood returning from the fetus, it
more accurately reflects the fetal metabolic state than blood in the umbili-
cal vein, which largely reflects the efficiency of placental exchange.
Accordingly, research examining predictors of fetal well being has focused
on umbilical artery cord gas values in preference to umbilical vein values.
There are limitations to even umbilical artery values, however. Such
values may not reflect central oxygenation when, under hypoxic stress, the
fetus preferentially shunts oxygen-rich umbilical venous blood to the brain.
Arterial sample values, in such cases, may more accurately reflect the
hypoxic state of nonvital tissues (muscle, fat, and nonessential organs).
412
Additionally, concentrations of those metabolites (e.g., organic acids) inef-
ficiently cleared by the placenta may be accurately measured in both arterial
and venous samples.
B. Biochemistry of Maternal-Fetal Placental Exchange

The body has mechanisms that attempt to maintain the hydrogen ion
concentration ([H+]) within narrow limits so that cellular biochemical re-
actions are optimized. In the fetus, H+ may be liberated by two types of
acids—carbonic and noncarbonic.
Carbonic acid (H2CO3) is formed by the hydration of CO2, the main by-
product of oxidative respiration. In the adult, PCO2 is primarily regulated
by alveolar ventilation, which normally is set to maintain a CO2 pressure
of 40 mmHg in the alveoli (and thus also in arterial blood). In pregnant
women, this set-point is lower—34 mmHg. In the human fetus, CO2 dif-
fuses rapidly across the placenta and, as a result, concentrations of H2CO3
in fetal plasma are actually quite low because elimination is limited only
by fetal and maternal placental blood flow.

Noncarbonic acids, which include lactic acid and beta-hydroxybutyric
acid—products of anaerobic respiration and fat metabolism, respectively—
are more slowly eliminated. In the adult these so-called “fixed” or meta-
bolic acids are regulated by renal excretion. As with carbonic acids in the
fetus, the placenta is the organ of elimination, but diffusion of noncarbonic
acids across the placenta occurs more slowly than the diffusion of CO2.
Metabolic acids may also be cleared through the fetal kidneys, but this too
is a slow route of elimination. Oxidative metabolism provides an alternate
means of disposal for lactate if oxygenation becomes adequate, but this
process is also relatively slow compared with CO2 diffusion. It is this differ-
ential rate of elimination of carbonic and noncarbonic acids that explains
why metabolic acidoses resolve more slowly than respiratory acidoses in
the fetus.
Both types of acids are buffered in the blood by plasma bicarbonate
and fetal hemoglobin. Together these two systems account for 70% of fetal
buffering capacity; the other 30% is accounted for by erythrocyte bicarbon-
ate, inorganic phosphate, and plasma proteins.
The equilibrium of acid and base is described by the Henderson-
Hasselbalch equation: pH = pK + log [base]/[acid].3 K is the equilibrium
413
constant for the dissociation of H+ for the relevant acid. The pK for the
acid-base pair of carbonic acid and bicarbonate is 6.1; [HCO3] in blood is
normally 24 mm/l; [H2CO3] in blood is normally 1.2 mm/l (calculated as
the product of CO2 pressure—normally 40 mmHg—and the solubility con-
stant for CO2—0.03). Using these figures, “normal” pH is calculated as 7.4.
As predicted by the Henderson-Hasselbalch equation, a change in either
PCO2 or bicarbonate concentration will alter pH. Increasing PCO2 pressure

(e.g., by hypoventilation in the adult, or, as a result of fetal umbilical cord
compression, a decrease in placental flow in the fetus) will cause the pH
to fall, resulting in a respiratory acidosis.4 Similarly, decreasing bicarbon-
ate concentration (by buffering of noncarbonic acids, for example) will also
cause the pH to fall, resulting in a metabolic acidosis. In making distinc-
tions between respiratory and metabolic acidoses, it is important to consid-
er that marked elevations of PCO2 may produce a compensatory increase
of HCO3– (1 mEq/l HCO3– for each 10 mm Hg rise in PCO2); if such com-
pensation were not recognized and corrected for, a mixed acidemia might
be mistakenly classified as a pure respiratory acidemia.5
If two of the three factors in the Henderson-Hasselbalch relationship
are known, clinicians may use the equation to calculate the third factor. In
clinical practice, pH and CO2 pressure are measured, and bicarbonate con-
centration is determined using either a nomogram drawn using the Henderson-
Hasselbalch relationship or the microprocessor, which is part of the auto-
mated blood gas analyzer.
Values for pH, PCO2, and bicarbonate do not tell the whole story, how-
ever, for bicarbonate concentration can change in two ways: it may react
with fixed (noncarbonic) acids and may vary with changes in [CO2] that
occur as the gas is buffered by hemoglobin. As a result of these alternate
possibilities, [HCO3] is of value only for determining the degree of de-
rangement of metabolic activity when CO2 pressure is normal (i.e., 40 mm
Hg). The concept of base excess (BE) was introduced as a measure of the
magnitude of the metabolic acid-base component in the presence of con-
comitant respiratory change and refers to the amount of buffer above or
below normal levels. When depletion of a buffer base (e.g., H2CO3) occurs,
for example, a base deficit exists.
BE is reported along with the other values as part of an umbilical cord
gas result, but it is not measured directly. Instead, BE is calculated from
measured values of pH and CO2 tension by means of a nomogram or
microprocessor. In such calculations, a small correction may be made for
variations in hemoglobin concentration, but by convention, the value is
usually read assuming a concentration of 5 g/dl. This convention is felt to
be a better approximation of whole-body equilibrium.
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C. Normal Fetal and Neonatal Blood Gas Values
The pregnant woman’s pH is the same as that of a nonpregnant woman—

7.4. Pregnant women hyperventilate to such a degree, however, that their
alveolar [CO2] (and arterial [CO2] in parallel) is reduced to approximately
34 mm Hg. It is hypothesized that progesterone stimulates this hyperventi-
lation of pregnancy; administration of progesterone to male subjects pro-

duces similar changes. To offset the fall in PCO2, renal excretion of bi-
carbonate increases, in effect producing a compensated respiratory alkalosis.
Approximations of normal values of acid-base equilibrium and blood
gas variables in human fetuses have been obtained from fetal scalp blood
samples drawn prior to the onset of labor. From these values and those obtained
in chronically catheterized fetal animals (mainly sheep), it was suspected
that acid-base balance in the fetus was very close to that of the mother. The
major difference between mother and fetus is that CO2 tension is higher in
the fetus, reflecting the gradient of CO2 diffusion across the placenta. More
recently, the advent of fetoscopy and ultrasonographically guided umbilical
cord blood sampling have allowed investigators to obtain blood gas samples
from undisturbed third-trimester human fetuses (see techniques described

below). Mean values in these fetuses are close to those of the adult mother
but with a greater range of normal (Table 1).6
TABLE 1
Acid-Base and Blood Gas Values in Umbilical Cord
Vessels in the In Utero Human Fetus at Approximately
35 Weeks’ Gestation
Umbilical artery Umbilical vein
ph 7.33 ± 0.07a 7.38 ± 0.06

Carbon dioxide pressure (mmHg) 45 ± 10 38 ± 8
Bicarbonate (mEq ⋅ l –1) 23 ± 5 23 ± 5
Base excess (mEq ⋅ l –1) –3 ± 3 +0.5 ± 4
Oxygen content (mM ⋅ l –1) — 6.7 ± 0.6
Oxygen pressure (mmHg) 35 ± 15 41 ± 20
Hemoglobin (g ⋅ dl –1) 13 13
Note: n = ≥50.
a Mean ± 2 SD.
Modified from Nicolaides KH, Kypros HN, Rodeck, CH, et al. Effect of
gestational age on fetal and intervillous blood gas and acid-base values
in human pregnancy. Fetal Therapy 1986; 1: 168–175.
415
As described below, intrapartum fetal scalp sampling has permitted in-
vestigators to assess what blood gas parameters are to be expected during
labor. Such work demonstrates that fetuses often develop a mild respira-
tory and metabolic acidosis by the second stage of labor. (The second stage
of labor is the point at which dilatation is complete and pushing begins.)
It has, of course, been considerably easier to study acid-base balance at
delivery by assaying blood collected from umbilical cord samples at birth

(technique also described below). All studies of such cord blood suggest
that, as noted above in studies of blood obtained intrapartum, a mild mixed
respiratory and metabolic acidosis develops during labor. This acidosis is
so common and so minor, however, that it is considered to be a normal
physiologic event of no consequence to the fetus. To discriminate those
acidoses of adverse consequence, it is important to define an appropriate
range of normal, and several large series of blood gas analyses from “nor-
mal” births provide this definition (Table 2).7,8,9 Because umbilical artery
pHs are more reflective of fetal status, we focus on these values in our review.
Yeomans7 described normal values for umbilical arterial and venous
pH, PCO2, PO2, and bicarbonate in 146 infants born after uncomplicated
labor and vaginal deliveries at 37 to 42 weeks’ gestation. All infants in their

analysis had a normal fetal heart rate pattern during the 10 min preceding
delivery. Mean umbilical arterial values +/– 1 SD for the parameters studied
were: pH, 7.28 +/– 0.05; PCO2, 49.2 +/– 8.4 mm Hg; PO2, 18.0 +/– 6.2 mm
Hg; bicarbonate, 22.3 +/– 2.5 m Eq/l. Umbilical venous values were: pH,
7.35 +/– 0.05; PCO2, 38.2 +/– 5.6 mm Hg; PO2, 29.2 +/– 5.9 mm Hg;
bicarbonate, 20.4 +/– 4.1 mEq/l. As part of a study comparing blood gas
values of term and preterm infants, Ramin10 examined cord blood gas
results in 1292 pregnancies that were term and “uncomplicated” and found
values nearly identical to those in Yeoman’s smaller series (Table 2).
Initially, some argued that Yeomans’s7 and Ramin’s10 studies skewed
their “normal” results by excluding all complicated deliveries. In an effort
to address such concerns, Riley and Johnson analyzed results from a popula-
tion of 3522 consecutive term vaginal deliveries.8 Interestingly, these inves-
tigators found that mean arterial pH (7.27) matched the means from earlier
work as did the means for other biochemical measures in both arterial and
venous samples.
More recently, in the largest series to date, Helwig and colleagues ex-
amined a dataset containing blood gas values from 15,073 newborns.9 This
analysis excluded only those infants potentially at risk for intrapartum
asphyxia as defined by a 5 min Apgar of less than 7. By including all
vigorous neonates, the authors sought to better define a normal distribution
416
TABLE 2
Mean and Median Values of Acid-Base and Blood Gas Values in Umbilical Arterial (UA) and Venous (UV)
Cord Blood in Fetuses with Apgar Scores ≥7 at 5 Minutes
Mean Std dev 2.5 percentile 5th percentile Median 95 percentile 97.5 percentile
UA pH 7.26 0.07 7.10 7.13 7.27 7.36 7.38

UA pCO2 (mmHg) 53 10 35 37 52 69 74
UA pO2 (mmHg) 17 6 6 8 17 27 30
UA base excess (mEq ⋅ l –1) –4 3 –11 –10 –4 1 1
UV pH 7.34 0.06 7.20 7.23 7.35 7.44 7.46
UV pCO2 (mmHg) 41 7 28 30 41 53 57
UV pO2 (mmHg) 29 7 16 18 29 40 43
UV base excess (mEq ⋅ l –1) –3 3 –8 –8 –3 1 2
Note: pCO2, carbon dioxide pressure; pO2, oxygen pressure; n = 15,073.
417
From Helwig IT, Parer JT, Kilpatrick SJ, et al. Umbilical cord blood acid base state: what is normal? Am J Obstet Gynecol 1996:
174: 1807–1814. Used by permission.

of values rather than an ideal distribution derived in smaller studies with
many more exclusions, and focused in particular on establishing 2.5 per-
centile cutoffs. The median umbilical arterial values, with 2.5th percentile
values in parenthesis, were: pH 7.26 (7.10), PCO2 52 (74) mm Hg, base
excess –4 (–11) mEq/l, and PO2 17 (6) mm Hg. (Venous data are shown
in Table 2). Although the distributions of these values were skewed
(Figure 3), the mean +/– 2 SDs were similar to these values (Table 2). The
authors separately analyzed these babies by method of delivery, gesta-
tional age, presentation, and presence of thick meconium and found that
although the means were significantly different in all groups, the differ-
ences between groups were relatively small (e.g., mean umbilical artery
pH 7.24 ± 0.07 vs. 7.26 ± 0.07 for babies with and without meconium,
respectively). The results of this study will be central to our later consid-
eration of what should be defined as an abnormal blood gas value.
Many measures of neonatal well being are affected by the neonate’s
gestational age. Because of immaturity of neurologic development and the
frequent need for assistance with ventilation, prematurity, for example, is
associated with lower Apgar scores even after controlling for potential
confounding conditions.11 In an effort to determine if umbilical cord blood

gases are similarly affected by gestational age, several groups have com-
pared analyses of term and preterm cohorts. Such comparisons have dem-
onstrated that cord blood gas values are not affected by gestational age and
this independence has been advanced as an important benefit of the test as
a marker of fetal well being or compromise. In their previously detailed
1993 series, for example, Riley and Johnson compared gases of 3522 term
neonates with those drawn from 1015 preterm newborns.8 Both groups
were delivered vaginally and had similar blood gas values. In an analysis
of infants delivered at Hermann Hospital in Houston, Texas between 1986
and 1989, Dickinson and co-workers12 found no significant difference in
arterial cord gas values between 1872 preterm and 1924 term infants.
Fetuses with congenital anomalies or abnormal fetal heart rate tracings
were eliminated from each cohort in this study. These authors suggested
that “because umbilical cord gas indices are an objective means of assess-
ing the immediate status of the newborn, they may be of more value in
excluding asphyxia than is the Apgar score for preterm infants.” (As is
often the case, in their paper, Dickinson et al. do not define what they mean
by “asphyxia”; the definition and diagnosis of asphyxia is discussed
in detail below.) Echoing the findings in these two studies, Ramin
and colleagues found that pH of <7.20 occurred with equal frequency in
cohorts of term and preterm infants (preterm [n = 77] = 8% vs. term
418
419
FIGURE 3. Frequency distribution of umbilical arterial blood pH in 15,073 preterm and term babies born vaginally or by

Cesarean section with Apgar scores ≥7 at 5 min. The skewness is toward acidosis. The shape of the curve and skewness remain
the same if the values are expressed as hydrogen ion concentration. (From Helwig JT, Parer JT, Kilpatrick SJ, Laros RK Jr.
Umbilical cord blood acid base state: what is normal? Am J Obstet Gynecol 1996, 174: 1807–14. Used with permission.)
[n = 1228] = 10%) even though low one min Apgar scores were found
more commonly in the preterm group (1 min Apgar ≤ 6: preterm = 36% vs.
term = 2.4%).10
III. ABNORMAL UMBILICAL BLOOD GAS VALUES:

DEFINITIONS AND ANTECEDENTS
A. What is an Abnormal or Nonreassuring Umbilical Cord pH?
Although there is impressive concordance among those studies that have

sought to define normal umbilical cord gas values, there is less agreement
about what constitutes an abnormal cord pH. Ideally, the pH value used to
separate out abnormal gases would be preceded by or associated with some
clinically relevant event or outcome, yet, as we shall see, this rational ap-
proach has not always been used. Because clinicians, parents, and/or law-
yers may each value umbilical artery measurements as predictors of future
well being or past mishap, it is worth reexamining existing thresholds for
defining a low cord pH in an effort to establish cutoffs that truly merit
concern or intervention.
Traditionally, a cutoff of 7.20 has been used to distinguish normal from
abnormal umbilical artery pHs,1 but such a cutoff seems unreasonably high.
For many laboratory measures, a value 2 SDs below the mean is used to
establish the “lower limit of normal”, but 7.20 is not 2 SDs below the mean
umbilical artery pH. Recognizing this discrepancy, Thorpe et al. 13 argued
from their own analyses that a value of pH = 7.10 was a more appropriate
cutoff. More recently, Helwig and colleagues determined that in their large
population the 2.5th percentile was 7.10.9 According to their analysis, using
a definition of 7.20 would include neonates up to approximately the 20th
percentile.
Perhaps more relevant, using a value of pH = 7.20 has little prognostic
significance, for the overwhelming majority of neonates with umbilical
artery pHs < 7.20 will be normal at birth and beyond. Specifically, the
majority of newborns with pH < 7.20 are vigorous, have Apgar scores >7,
and later manifest no neurologic deficits.5,14 As clinicians have evaluated
cord pH as a predictor of later pathology, they have recognized that not
until a threshold pH of 7.00 is reached, does the test carry the sensitivity,
specificity, and positive predictive value needed for clinical utility.5,14,15 In-
deed, some investigators have argued that a cutoff of pH = 6.80 is more ap-
propriate for making clinical decisions.16,17 (These and other studies of cord
420
gases as predictors of later outcome are discussed in detail below.) These
new, lower threshold criteria have been incorporated into contemporary
definitions of birth asphyxia, but it is again important to recognize that
even at these more extreme thresholds, the majority of neonates will have
normal outcomes.18 Hence, there is little statistical or clinical support for
the most traditional dictum that defines all pHs below 7.20 as abnormal.
B. What is Asphyxia and What are its Causes?
Although etymologically derived from the Greek meaning pulseless,

asphyxia may be defined as insufficient exchange of respiratory gases. The
discrepancy between the term’s origin and more contemporary definition
is the source of some confusion: in referring to adults, it is the more
extreme circumstance that is commonly construed (e.g., asphyxia by drown-
ing or fire is equated with death) whereas in referring to fetuses, many
describe varying degrees of asphyxia. There is in fact no consensus defi-
nition for much of what is commonly referred to as “fetal asphyxia” and
such states are probably better described by detailing the specific blood gas
abnormalities present (e.g., acidemia) or circumstances leading up to such

abnormalities.
In the fetus, abnormal gas exchange eventually gives rise to physi-
ologic compensatory mechanisms, the most important of which is redistri-
bution of fetal blood flow: blood flow to the heart, brain, and adrenals
increases; flow to the placenta is maintained; and blood flow to virtually
all other areas decreases. Where blood flow is reduced, oxygen delivery
may become inadequate to maintain aerobic respiration. As a result, there
is a shift to anaerobic metabolism that leads initially to local lactate
production and later to systemic lactic acidemia. If the oxygen supply
continues to drop, these compensatory mechanisms themselves fail with
consequent loss of myocardial performance and reduced cardiac output:
umbilical blood flow decreases and the asphyxia worsens. Eventually, the
fetus’s hypoxia results in cellular damage with long-term physiologic
consequences and morbidity.
Following this scheme, it is apparent that pH may be an important—
but not unique or definitive—indicator of asphyxia; the severity of asphyxia
is described in terms of acidosis, hypoxemia, and hypercarbia, all compo-
nents of blood gas analyses. Although fetal asphyxia is commonly ascribed
to insufficient umbilical or insufficient uterine blood flow, such definitions
beg the question of just what is “insufficient.” In fact, the amount of
421
metabolic fuels sufficient at any time depends greatly on maternal and fetal
demands, which are a reflection of and vary with underlying conditions,
pathologies and stresses. Clearly, either maternal or fetal pathophysiology
may disrupt maternal-fetal gas exchange. Specifically, maternal hypoxia
or acidemia, uterine or placental hypoperfusion, placental dysfunction,
compression of the umbilical cord, or inherent fetal conditions may lead
both to asphyxia and abnormal cord blood gas values:
1. Maternal conditions: Maternal conditions resulting in fetal hypoxia

include diseases which, in their most severe forms, may limit alveolar
exchange—asthma or cystic fibrosis—and others that limit oxygen
transport—anemia.19 Because of fetal buffering systems, maternal
acidemia unassociated with hypoxia is unlikely to be directly re-
flected in fetal umbilical gas values, but severe acidemia—alcoholic
or diabetic ketoacidosis—may cause fetal acidemia, often without
concomitant hypoxia.
2. Insufficient uterine blood flow: In general, circulation to the mater-
nal uterine arteries is preserved during pregnancy. There is little
autoregulation of uterine artery caliber during gestation, and the

arteries are most often maximally dilated.20 However, in the event of
marked hypotension—perhaps the consequence of sepsis, severe blood
loss, cardiac collapse, or anesthetic related vasodilatation—flow to
the uterus may be reduced enough to compromise placental perfu-
sion.21
3. Disruption of utero-placental exchange: Placental dysfunction may
also limit maternal-fetal gas exchange. Dysfunction may be the result
of pathology, such as placental abruption, that limits the placental
surface available for exchange. Alternately, there are some diseases
that are thought to affect utero-placental exchange at least in part by
causing changes in placental tissue; hypertensive complications of
pregnancy as well as post-datism (gestations >41 to 42 weeks) are
associated with calcification and thinning of cotyledons, sonographic
changes that some have linked to an altered structure of placental
microvasculature. Finally, some feel that increased placental edema,
like that seen with hydrops fetalis, may limit maternal-fetal gas
exchange.
4. Insufficiency of umbilical blood flow: Compression of the umbili-
cal cord by the fetus or its prolapse through the cervix may result in
partial or total occlusion of umbilical vessels with reduction in blood
flow and oxygen delivery through the cord.22 In cases in which the
422
fetus compresses its own cord, occlusion is almost always transient,
but, occlusion resulting from cord prolapse is generally not self-
limiting and may require urgent Cesarean delivery to minimize fetal
metabolic or mixed acidosis.
5. Fetal complications: Stresses on the fetus’s metabolism may result
in acidosis and an increased demand for oxygen, a demand that may
not match oxygen available through the placenta. Intrauterine infec-

tion is associated with neonatal acidemia, for example. Passage and
aspiration of meconium is similarly associated with acidemia, but is
more likely a marker of other pathology than a primary cause of
in utero asphyxia and acidemia.
The timing and duration of any insult or perturbation is important in

determining the end effect on fetal physiology. Unfortunately, there is little
information on the rate of change of acid-base factors during stress from
cord compression or utero-placental insufficiency. Data from a single mon-
key fetus subjected to total oxygen deprivation by cord clamping at Cesar-
ean birth has been presented by Myers and colleagues.23 In this experi-
ment, the investigators used a femoral artery catheter to sample arterial

blood in the 13 min preceding air breathing but after cord clamping. The
pH fell at a rate of 0.04 units/min, the CO2 tension increased 6 mm Hg/min,
and the base excess fell slightly more than 1 mEq/l/min. The oxygen tension
fell to about 6 mm Hg in 2 min and then stabilized at this level. Sudden
cessation of oxygen delivery to the fetus such as that simulated in this
experiment is probably rare—cord prolapse may be the most clinically
analogous situation—and most cases of fetal acidosis occur by a reduction
of gas exchange for a variable period of time. Obviously, the rate of change
of blood gas parameters will differ in each individual fetus as the duration
and extent of hypoperfusion vary. This continuum begins as a “physiologic
asphyxia” or acidemia reflected in the mild mixed metabolic and respira-
tory acidosis described above in essentially all fetuses at delivery. (Recall
that typical values in umbilical arterial blood at birth are pH = 7.27,
CO2 = 52 mm Hg, and base excess = –4 mEq/l.) The other end of the
spectrum is the extremely severe metabolic and respiratory acidosis seen
in babies suffering asphyxial brain damage following a catastrophic event
such as a compressed prolapsed cord or complete abruption. In the latter
case, values may be of the order of pH = 6.80, CO2 = 90 mmHg, and BE =
–20 mEq/l.
In view of the fact that the state of asphyxia spans a continuum from
“physiologic” to “terminal,” and that pathologic results such as brain dam-
423
age or death are not rigidly predicted by a fetus’s acid-base state, it is not
yet possible to assign any particular value or set of values to the diagnosis
term “asphyxia.” The duration and extent of metabolic acidosis and hy-
poxia that will result in neurologic damage to the human fetus are not
known, and in fact it appears that an extremely wide variation of severity
and duration of asphyxia ultimately result in such damage. In any individ-
ual fetus, a number of other factors—stage of fetal development, metabolic

state, repetitiveness of asphyxic insult—impact on eventual outcome.
In the following sections we consider the techniques involved in ob-
taining fetal or neonatal blood sample for analysis and discuss how such
samples predict or reflect asphyxia and other relevant outcomes.
IV. TECHNIQUES FOR FETAL AND UMBILICAL CORD

BLOOD SAMPLING
Umbilical artery samples may be obtained in utero before labor, during

the intrapartum period, or from the umbilical cord after delivery. Although
different techniques are used for sampling at each stage, the goal of sam-
pling is the same: to predict those babies at risk for morbidity and therefore
likely to benefit from intervention.
A. Cordocentesis
1. Technique
When initially developed, in utero blood sampling was accomplished

under direct visualization with the aid of a fetoscope.24 More recently,
clinicians have used PUBS under ultrasonographic guidance as first de-
scribed by Daffos in 1983 to access the umbilical cord vessels.25
In this technique,26 ultrasound imaging is used to locate an accessible
portion of the cord. The cord insertion at either the placenta or fetus is
preferred, because the cord is less mobile at these sites and therefore easier
to puncture with the sampling needle. When fetal movement prevents
successful sampling, the fetus may be paralyzed prior to sampling with a
sonographic guided, intramuscular or intravenous injection of vecuronium
(1 to 2 mg/kg estimated weight) or other paralyzing agent. Following
localization and identification of an angle of approach, the patient’s skin
424
is cleaned with an antiseptic solution. Local anesthesia is usually all that
is required to comfortably complete the procedure, but if the anticipated
procedure is lengthy or the patient’s tolerance of discomfort low, systemic
analgesia or regional anesthesia may be required. A 20- to 22-gauge spinal
needle is introduced through the anesthetized skin and directed with
sonographic guidance toward the cord. A sharp stab is then used to
puncture the vessel. Because it is of larger caliber, it is almost always

easier to access the umbilical vein, and because pressures in this vessel are
lower, some have argued that sampling the vein in preference to either
artery reduces bleeding complications. Intravascular placement of the
needle is easily confirmed by the ready withdrawal of blood. Specimens
for blood gas analysis may be drawn directly into appropriate heparinized
blood gas syringes. If there is any question as to whether placenta or cord
has been sampled, a small amount of sterile saline may be injected and the
cord examined with ultrasound for subsequent flow of saline microbubbles
to confirm appropriate sampling. Later analysis of the sample for red blood
cell size, nucleation, and/or acid elution will confirm that a fetal rather than
a maternal sample has been obtained. When clinicians plan to intervene
with Cesarean delivery in the event of fetal intolerance of sampling, the

procedure should be performed in an operating room with ready access to
the equipment necessary for Cesarean delivery.
2. Indications
Cordocentesis is indicated when perinatal management requires direct

evaluation of fetal hematologic parameters (e.g., measurement of red
blood cell and/or platelet counts in pregnancies with alloimmune disease)
or serologic markers (e.g., detection of fetal IgM antibody in the face of
possible in utero infection). Also, when rapid genetic diagnosis is required,
fetal lymphocytes can be obtained via cordocentesis and karyotyped in 24
to 48 h, a turn-around significantly shorter than the 10 to 14 d required for
the culture and karyotyping of amniocytes. Finally, cordocentesis permits
the infusion of blood products or other therapeutics to treat life-threatening
in utero conditions remote from term (e.g., severe alloimmune anemia). As
discussed below, cordocentesis is not warranted solely for the evaluation
of in utero fetal acid-base status, unless this evaluation is undertaken as
part of a research protocol in which the patient has given informed consent
to participate.
425
3. Contraindications
There are few contraindications to cordocentesis, although the amount

of amniotic fluid, cord location, and cord size (dependent on gestational age)
may affect success. In fetuses in which there are clearly significant fetal heart
rate changes compatible with rapidly evolving fetal acidemia, intervention
and/or delivery should not be delayed to permit sampling. Ongoing bleed-

ing or preterm contractions are relative contraindications to cordocentesis
because sampling may aggravate such conditions. When the possibility of
a fetal bleeding disorder exists, practitioners may choose to avoid sampling
or, if sampling is deemed necessary (usually for diagnosis of the underly-
ing condition itself), they should be ready to transfuse the appropriate factors
or blood components as soon as vascular access has been obtained. Exces-
sive bleeding and fetal exsanguination has been described in cases of fetal
hemophilia or thrombocytopenia. Because of the risk of vertical transmis-
sion of infection, sampling is avoided in mothers with known intramniotic
infection that may predispose to fetal infection in utero (e.g., HIV).
4. Complications
In 1993, Ghidini and associates reviewed the available literature in an

effort to assess complications related to fetal blood sampling.27 These re-
searchers pooled data from all case series in which greater than 100 cases
were reported. They found that overall there was a 1.4% risk of fetal loss
or perinatal death.
Other complications are more common than fatality, and the same authors
estimated that, conservatively, there was a 2.7% morbidity and mortality
related to cordocentesis. Bleeding is the most common nonmortal complica-
tion and occurs in as many as 50% of samplings but is usually self-limited.
Similarly, cord hematomas are the second most common complication of
cordocentesis. In one series in which cords were examined within 48 h of
the procedure, 17% had evidence of hematoma.28 Hematomas most often
are of little clinical consequence and may be resorbed over time, but in rare
instances the mass may occlude cord flow, and hematomas have been linked
to subsequent fetal bradycardia.
Fetal bradycardia, most often transient, occurs in 3 to 12% of blood
samplings. In only the minority of cases is the bradycardia associated with
a recognizable hematoma. In most cases it is assumed that a vasospastic
426
reflex results in cord occlusion and subsequent fetal bradycardia. Pro-
longed fetal bradycardia may lead to emergent Cesarean delivery.
Although the precise amount of fetal-maternal hemorrhage resulting
from PUBS is difficult to quantify, it has been estimated that some exchange
occurs in nearly half of the cases. Fetomaternal hemorrhage appears to be
reduced when the placenta is not traversed by the sampling needle, and
alternate approaches may merit special consideration in patients at risk for

alloimmunization.29 Certainly, all women who are Rh negative and un-
dergo cordocentesis should receive Rh immune globulin (Rhogam).
Many women experience contractions during or immediately after cor-
docentesis and some have used tocolytics to prevent uterine activity during
this time. Outside of emergent deliveries for fetal intolerance of the pro-
cedure, sampling does not, however, appear to increase the risk of preterm
labor and delivery.
Finally, cases of infection and placental abruption have been reported
following cordocentesis but these appear to occur only rarely.
Because both the rate of success and complications are linked to indi-
vidual operators’ and centers’ experience, some have suggested that sam-
pling be limited to a few sites. It also appears that morbidity and mortality
is increased when blood samples are obtained by puncturing the fetal heart
or hepatic vessels in cases in which the cord circulation is inaccessible.29
Such approaches should therefore be used only as a last resort, for example
to permit intrauterine transfusion in an hydropic fetus whose cord cannot
be punctured.
5. Utility of Acid-Base Cord Blood Analysis

from Cordocentesis
Associated morbidity and mortality aside, there is no sound evidence

to recommend cordocentesis solely for assessing the in utero acid-base
status or oxygenation. Although cordocentesis may be an important tool
for investigation of fetal genetic or infectious disease and may be impor-
tant in the treatment of erythroblastosis fetalis, no study to date has dem-
onstrated a benefit to obtaining cord gas values in utero. Nicolaides et al.
determined that there was significantly more relative hypoxemia, acidemia,
and hypercarbia in the gases obtained by cordocentesis from 196 growth-
restricted fetuses as compared to values obtained from 208 normally
grown subjects (umbilical vein: pH = 7.35, O2 = 31.5, CO2 = 41.0 vs.
427
pH = 7.41, O2 = 42.7, CO2 = 34.9, SGA vs. AGA, respectively; umbilical
artery: pH = 7.32, O2 = 20.8, CO2 = 47.3 vs. pH = 7.37, O2 = 28.0, CO2 =
35.0 , SGA vs. AGA, respectively).30 This initial study raised the hope that
blood gas values might be of clinical use in fetuses in which other testing
of fetal well being was otherwise equivocal. Nicolini et al., however, found
that similar differences in blood gas values did not predict fetal outcome
in a series of 46 samplings.31 Until a well-designed study demonstrates a

clinical benefit to obtaining cord gases in utero, umbilical blood sampling
intended solely for this purpose must be considered experimental.
B. Fetal Blood Sampling (FBS)
1. Technique32
Intrapartum evaluation of fetal acid-base status is accomplished by

obtaining a blood specimen from the scalp (or buttock) of the fetus through
the dilated cervix. Fetal blood is sampled by stabbing the fetal presenting
part with a small blade, approximately 2 mm wide and 1.5 mm long. The
resulting droplet of blood is collected in a glass capillary approximately

20 cm long, which has been pretreated with heparin. Access to the fetus is
facilitated by means of a cone-shaped endoscope with a light source, placed
through the vagina against the fetus. The endoscope also permits cleansing
of the sampling site with a sponge and exclusion of amniotic fluid and blood
(Figure 4).
Reactive hyperemia of the fetal skin may be produced by spraying with
ethyl chloride. Containment of the blood droplet can be aided by use of a
smear of silicone cream on the fetal skin. This technique is similar to that
of the adult “fingerstick” for obtaining small quantities of blood, but it is
important in the fetus to obtain free-flowing blood and to collect it from
the center of the droplet, protecting it from air as much as possible. Speci-
mens in which bubbles of air interrupt the column of blood should be
discarded, as air contamination represents a potential source of error; if
samples were run with air bubbles, values for O2 and pH would be artifac-
tually raised and the value for CO2 artifactually lowered. Generally, a single
stab will suffice, but on occasion an x-shaped incision is necessary. If fetal
hair is copious, it can be brushed aside or trimmed. Sampling should be
done over the scalp or buttock and not on the brow, face, or genitals.
It has been shown that fetal pH tends to be lowest at the end of a variable
heart rate deceleration and recovers between contractions. This situation
428
429
FIGURE 4. Technique of obtaining fetal blood from the scalp during labor. (From Creasy RK, Parer JT. Prenatal care and
diagnosis. In: Rudolph AM, ed. Pediatrics, 16th ed. p 121. New York: Appleton-Century-Crofts, 1977. Used with permission.)
probably results from respiratory acidosis, but it can depress pH profound-
ly. Furthermore, it has been shown that the fetal oxygen tension falls during
slowing of the heart rate by more than 15 beats/min with contractions. Hence,
some have recommended that FBS be performed just before the next expect-
ed contraction, because sampling then will best reflect the baseline state of
the fetus.
The capillary tube contains approximately 0.25 ml of blood, which is

sufficient for measurement of pH and carbon dioxide tension in current
microblood gas analysis machines. It is our practice to obtain two or three
specimens from the same puncture so that duplicate or triplicate analyses
can be made. After collection of the blood, a sponge is pressed against the
sampling site until hemostasis is evident during contractions.
The equipment used for collecting fetal blood is sold in kit form, but
the machinery for determining pH and CO2 tension is more complex. A
number of blood gas analyzers are available commercially, most of which
are automated, and all work on the same general principle. The machines
measure the pH of a sample by transferring blood from the collecting cap-
illary to a suitably calibrated glass electrode kept at 37°C. The reproduc-
ibility of measurements and the variation among well-calibrated machines

are on the order of 0.03 pH units.32 CO2 is measured on the same machine
but with a separately calibrated CO2 tension electrode. In current blood gas
machines, O2 tension is simultaneously measured on the same blood sample.
Warm-up and calibration time on this equipment takes a minimum of
30 min, so to be practical the machine must be left on continuously if it is
to be used in obstetric management. Few labor and delivery services have
the volume to support a dedicated blood gas machine and technician, but
such devices are generally available in neonatal intensive care units (NICUs)
24 h a day, where technicians expert in the maintenance and calibration of
this equipment are present. For hospitals without NICUs, the chance of
being able to obtain accurate, rapid microblood gas analysis is unpredict-
able, because central clinical laboratories may be unfamiliar with micro-
samples, and the turn-around time may be unacceptably long.
2. Contraindications to FBS
Obvious threats to the mother (e.g., profuse hemorrhage) or to the fetus

(e.g., prolonged deceleration or repetitive nonremediable late decelera-
tions) are indications for immediate delivery, delivery which should not be
430
delayed by scalp sampling. Other contraindications to FBS are concern for
vertical transmission of maternal infection (e.g., HIV) or for fetal bleeding
disorders (e.g., hemophilia). Because FBS may be performed only after
rupture of membranes, any contraindication to membrane rupture is also
a contraindication to FBS. Minimal cervical dilatation or excessive fetal
caput (edema) may limit one’s ability to successfully obtain a scalp sample
but are not in and of themselves contraindications to attempting sampling.
3. Complications of FBS
The possibility of hemorrhagic or infectious complications has been

alluded too, but in appropriately chosen patients, such morbidities are
unusual. The incidence of scalp infections has been cited at <1%, and the
majority of these require only local treatment (e.g., hair trimming, disin-
fection). With today’s more common use of spiral electrodes for fetal heart
rate monitoring, the incidence of infectious complications attributable to
scalp sampling is unclear; heart rate monitoring always precedes FBS. The
neonate may have a small scar at the site of sampling but this will be
hidden by the baby’s hair. Finally, although there is no theoretical limit to
the number of samples that can be taken, as a practical matter, numerous
samples (e.g., greater than 10) can result in soft tissue trauma to the fetus.
Use of a vacuum extractor for delivery is not contraindicated after FBS,
but one should be wary of it use in the fetus who has already had several
samplings.
In summary, if mortality resulting from coagulopathies is excluded,
the complications of FBS are quantitatively minor and are of less impor-
tance than is the potentially irreversible problem of asphyxial brain injury
or maternal morbidity of Cesarean delivery, both of which FBS may assist
in avoiding.
4. Utility of FBS
In most centers, fetuses are followed in labor with either intermittent

or continuous monitoring of the fetal heart rate as first described by both
Hon33 and Caldeyro-Barcia.34 Unfortunately, heart rate monitoring has a
high false-positive rate; many of those fetuses with so-called “nonreassuring”
monitor strips do not have biologically significant acidosis and will have
431
normal cord blood gases if delivered immediately (e.g., by Cesarean). Fetal
scalp blood sampling, introduced by Erich Saling of Berlin in the early
1960s,35 has been used by many as a second test to highlight those fetuses
truly in need of delivery or in utero resuscitation. FBS, for example, ap-
peared to be an important preliminary step in the Dublin description of the
active management of labor, a protocol that produced remarkably low rates
of Cesarean deliveries in part, presumably, by eliminating operative deliv-

ery for falsely positive heart rate interpretations.36 Haverkamp et al. 37 found
a significantly reduced rate of Cesarean delivery when FBS was used in
conjunction with electronic fetal monitoring.
In such two-step schemes, certain FHR patterns considered to be omi-
nous are evaluated with a scalp blood sample. If the pH in this sample is
greater than 7.26, labor is allowed to continue with resampling should the
tracing deteriorate further. Those fetuses with pHs <7.20 are delivered as
soon as possible either by Cesarean or operative vaginal delivery. Fetuses
with intermediate pH values are followed closely and resampled in 20 to
30 min if the FHR tracing does not spontaneously improve or deteriorate
to the point at which the need for urgent delivery is obvious. Because the
presence of contractions and variable decelerations of the fetal heart rate

may transiently effect scalp pH, it is important to consider when in relation
to the woman’s heart rate changes and contraction pattern a sample was
obtained; the transient depression of pH associated with such phenomena
are unlikely to result in neonatal morbidity. Similarly, in interpreting fetal
blood gas results, it is important to consider the whole clinical picture:
poor results in the presence of other predictors of morbidity (infection,
meconium, preeclampsia, etc.) are more likely to represent true positives.
Underlying this approach is the assumption that FBS results are valid
approximations of fetal acid-base status, and indeed, the correlation be-
tween the two measures has been demonstrated through several approaches.
In fetal monkeys, the values obtained for the scalp are closely related to
simultaneously sampled blood for the carotid artery and the jugular vein.
In fact, the pH generally falls between the values from these vessels. In
only 5% of cases was the pH of capillary blood found to be more than 0.1
unit lower than that of carotid arterial blood. In human newborns, a good
correlation has been demonstrated between scalp blood pH taken shortly
before delivery and umbilical cord samples.38
Further validation of the technique is seen in correlation between scalp
blood pH and newborn outcomes.39 This is illustrated in Figure 5, in which
the Apgar score at 2 min is related to scalp blood pH collected shortly
before delivery. In this investigation, a blood pH above 7.25 was associ-
432
FIGURE 5. Relationship between fetal blood pH and Apgar score at 2 min. All
samples were taken shortly before delivery. The arbitrary lines separate fetuses
regarded as vigorous (Apgar score 7 or above) and those with normal pH (above
7.2). Note that there is a general relationship between the two variables (seg-
ments A and X) and also approximately 30% spillover into the false-normal and
false-abnormal groups (B and Y). (From Beard RW, Morris ED, Clayton SG, pH
of foetal capillary blood as an indicator of the condition of the foetus. J Obstet
Gynaecol Br Commonw 1967; 74: 812-22. Used with permission.)
ated with a 2-min Apgar of >7 in 92% of infants. A pH of less than 7.15
was associated with a score of less than 6 in 80% of cases. A pH of 7.15
to 7.25 in the second stage of labor was unreliable for predicting the
condition of the baby at birth as judged by the 2-min Apgar score. Other
433
investigators have found a similar correlation between blood pH and
Apgar score.40
Another approach to validation has been to relate fetal blood pH to
“nonreassuring” FHR patterns. Unfortunately, such an approach is not
strictly valid itself, because the former observation is often used to sub-
stantiate the latter. Nevertheless, some impressive correlations have been
noted (Table 3).41 Kubli et al.’s 41 landmark report was felt by many to
confirm the ominousness of certain FHR patterns. Of great importance,
however, is a reanalysis of these data in a study published some years after
the initial publication.42 Instead of a continuum of acidosis in the various
groups of FHR patterns, these later investigators showed that they could
separate patients with late decelerations into two distinct groups based on
the degree of fetal heart rate variability (Figure 6). Those with average or
higher variability were significantly less acidotic than those with de-
creased variability. In fact, in the presence of mild or moderate late
decelerations with average variability (a pattern previously felt to be
ominous), the average baby was not acidotic. This surprising finding is
explained by the presence of two distinct classes of late decelerations:
those resulting from neurogenic (vagal) reflexes and those caused by

hypoxic myocardial depression or failure.17 Only the latter is immediately
worrisome, and FBS can help to distinguish the two, but the presence of
FHR variability and use of other tests (discussed below) are a more
convenient means of accomplishing the same objective.
TABLE 3
Relationship Between Fetal Blood pH
and Fetal Heart Rate Patterns
in Preceding 20 Minutes
FHR deceleration pattern Fetal blood pHa
Early, mild variable, or absent 7.30 ± 0.04

Moderate variable 7.26 ± 0.04
Mild or moderate late 7.22 ± 0.06
Severe late or variable 7.14 ± 0.07
a Approximate mean ± standard deviation.
Modified from Kubli et al. Observations on heart

rate and pH in the human fetus during labor. Am J
Obstet Gynecol 1969; 104: 1190–1206.
434
FIGURE 6. Relationship between fetal blood pH and severity of late decelera-

tions at time of blood sampling. Each FHR classification is further divided into
average (greater than 5 beats/min) or decreased (less than 5 beats/min) FHR
variability. (From Paul RH, Suidan AK, Yeh SY, et al. Clinical fetal monitoring. VII.
The evaluation and significance of intrapartum baseline FHR variability. Am J
Obstet Gynecol 1975; 123: 206–10. Used with permission.)
5. Alternatives to FBS
Because not every facility has the equipment necessary for fetal scalp
blood sampling and analysis available and because FBS entails additional
time, expense, and potential discomfort, clinicians have sought alternative
tests to use when the heart rate tracing argues that the fetus may be at risk
435
for significant metabolic acidemia. Practitioners had often observed, for
example, that some fetuses respond to the stimulation of scalp sampling
with heart rate accelerations and that such accelerations were associated
with reassuring sample pH’s.43 Such observations led investigators to
examine whether fetal scalp stimulation alone might be a useful test of
fetal well being when the heart rate tracing was otherwise “abnormal”.
Clark, Gimovsky and Miller44 studied 100 fetuses whose intrapartum

tracings were suggestive of asphyxia. In their series, a response to scalp
stimulation—noted as an increase in heart rate of 15 beats per min lasting
at least 15 sec—was found in 51 fetuses, all of whom had scalp pHs of
>7.19 (in fact 50 of 51 had pHs >7.23). Nineteen of 49 without a response
had pH <7.19, arguing again that when used alone, the heart rate tracing
has a poor positive predictive value for fetal acidemia. To stimulate the
scalp, these investigators first applied firm digital pressure to the fetal head
during a vaginal exam and then, if there was no response, pinched the fetal
head with an Alllis clamp closed to the first ratchet, leaving the clamp in
place for 15 sec. Although use of such a clamp might seem traumatic, it
is no more traumatic than using a lance to obtain a scalp blood sample, and,
in fact, the investigators found no evidence of scalp trauma on postnatal

exam. As well, we have found that a firm scratch with a gloved finger will
almost always elicit the desired response without resorting to clamps.
Clark et al.44 argued that response to fetal scalp stimulation is evidence
of an intact autonomic system and a nonacidotic fetus. They further
suggested that using scalp stimulation as a step before FBS would reduce
the need for FBS by 50%. More recently, Elimian et al.45 found nearly
identical results when they used scalp stimulation in a series of 108 women
with heart rate tracings suggestive of acidemia.45 These researchers further
argued that lowering the definition of reactivity to stimulation to an
acceleration of 10 beats for 10 sec could safely reduce the need for scalp
sampling by an additional 7% . Additionally, the work found that assess-
ment of heart rate variability before stimulation would reduce the need for
sampling by 74%.
Others have noted fetal response to auditory stimuli.46 Acoustic stimula-
tion with an artificial larynx has been used in several studies to reduce the
incidence of nonreactive nonstress tests without increasing the rate of false
negatives (falsely reassuring exams).47 Such work led Smith et al. to exam-
ine whether a response to auditory stimulation in labor was as reassuring
as a response to scalp stimulation.48 In 64 patients with nonreassuring heart
rate tracings in labor, these investigators applied an artificial electronic larynx
(80 Hz, 80 db) to the maternal abdomen over the fetal vertex and stimulat-
ed the fetus for ≤3 sec. If no initial response was seen, they restimulated the
436
fetus at 1-min intervals for a maximum of three times. If after three stimula-
tions there was still no response, fetal scalp sampling was then performed,
or if this was not technically possible, a Cesarean delivery was undertaken.
Thirty of 64 responded with an acceleration of 15 bpm for >15 sec, and no
such fetus had a pH <7.25. Of 34 who did not respond, 18 (53%) had a pH
<7.25. These investigators predicted that the use of acoustic stimulation
could reduce the need for scalp sampling by 50%.

Based in part on results described above, some clinicians have long
argued that FBS sampling was unnecessary. Perkins49 demonstrated in his
experience of 7100 deliveries on a “high-risk” service that acceptably low
rates of Cesarean and neonatal morbidity could be obtained without using
FBS. Writing in 1985, Clark and Paul50 suggested that “the properly trained
clinician may pursue an approach for the detection of fetal distress that
does not include scalp blood sampling without either compromising his
ability to detect fetal distress or significantly increasing the Cesarean rate.”
More recently, the group at Los Angeles County/University of Southern
California Medical Center has described their experience using alternatives
to FBS and found that between 1986 and 1992 the rate of scalp sampling
at their institution fell from 1.76% to 0.03% without an increase in neona-

tal morbidity or Cesarean delivery.51
Indeed, with the use of fetal scalp stimulation and acoustic stimulation,
and the growing recognition that the presence of fetal heart rate variability
even in the presence of late decelerations (reflex late decelerations) is
predictive of a nonacidemic, vigorous neonate, there is little need for fetal
scalp sampling. Although no randomized controlled trials have demonstrated
the utility of these tests in reducing the need for Cesarean section, most
practitioners assume that like FBS, they are important in preventing overzeal-
ous interpretation of fetal heart rate results. Importantly, these alternate
tests, in addition to requiring less equipment, time, money, and trauma, may
be used in patients whose cervical dilatation will not permit FBS. In those
few patients who do not demonstrate a response to such stimulation and
lack fetal heart rate variability but are close to delivery, FBS values in the
normal range may allow some portion to continue in labor until delivery
may be accomplished vaginally. A reassuring pH from the fetus of a woman
pushing during the second stage of labor, may, for example, allow her to
continue pushing until the baby’s head is low enough to effect a forceps
or vacuum delivery. When immediate delivery is delayed in the presence
of an absent response to scalp or acoustic stimulation, however, clinicians
need to be vigilant for signs of further deterioration requiring urgent deliv-
ery even if scalp pHs are reassuring. No fetal ancillary test has been shown
to be useful in the presence of a normal heart rate tracing, despite poten-
437
tially hazardous clinical situations such as maternal diabetes or fetal pas-
sage of thick meconium because the negative predictive value of a normal
fetal heart rate tracing is so high.
C. Cord Blood Gases Drawn from a Segment Obtained

at Delivery
1. Technique
Although umbilical blood gas values drawn from a segment of cord

clamped and obtained at delivery reflect the in utero environment, for obvi-
ous reasons, the results are not available until after delivery. The technique
is simple.8 At the time of birth the cord is double clamped in two places
about 25 cm apart. The cord is cut between each set of clamps, and blood
is aspirated anaerobically from the umbilical artery and vein using heparin-
ized syringes (Figure 7). The bloods are then analyzed for pH, CO2, and
O2 tension in a blood gas machine of the type described above. Base excess
may also be calculated to assess the presence and degree of metabolic acido-
sis. The greatest accuracy is achieved with careful anaerobic collection and
collection of sufficient volume (more than 0.5 ml) to minimize dilution and
the inevitable exposure to air. Clinicians should also take care to distin-
guish which sample is arterial (usually the smaller caliber vessel) and which
venous, although the results of the individual analyses will usually make
this clear. If there is not enough blood in the artery for an adequate sample,
blood may be drawn from vessels on the placenta’s surface, where arteries
cross over veins.
It has been stated that the cord should be clamped as soon after birth
as feasible, ideally before the baby’s first breath, for the samples to be most
representative of the in utero environment. Although this is usually done
if the baby is depressed or at the time of Cesarean section, there are some
good reasons to delay clamping in the apparently normal, vigorous baby.
In patient-oriented and natural childbirth practices, for example, the new-
born is usually given immediately to the mother and father, and not infre-
quently placed on the mother’s abdomen. Immediate clamping may be
intrusive if such a delivery is planned, and getting the clamp on before the
vigorous child’s first breath may be a challenge regardless of the delivery
plan. Fortunately, vigorous babies are the ones in whom assessing cord
gases are least necessary.
In fact, considerations of blood gas sampling aside, the ideal time to
clamp the cord is still controversial, with some advocating that the atten-
438
439
FIGURE 7. A double clamped segment of umbilical cord immediately after birth. Blood has been aspirated form the umbilical artery,

and blood is now being apsirated anaerobically from the larger umbilical vein.
dant clamp immediately to prevent the transfusion of blood from the pla-
centa, and others recommending the practitioners wait for the cord to stop
pulsating so that the newborn can obtain “the right amount” of blood. There
is no good evidence for either position, and we recommend an approach
of moderation with an intermediate time of clamping (about half a min)
unless, of course, there are other considerations such as resuscitation. If a
short delay has any effect on cord gases, it is more likely to alter the res-
piratory components of the analysis (i.e., CO2 and O2) than the metabolic
components.52
Once the cord is clamped, the time at which the samples are drawn
from the cord53,54 and the interval preceding analysis in the laboratory55–57
appear to be much less critical. Neither is it important that either the cord
or filled syringes remain on ice. Duerbeck et al.54 sampled clamped seg-
ments from 25 patients for 1 h and found that there were no statistically
significant changes in pH, PCO2, or PO2 of umbilical arterial blood.
Strickland et al.55 drew 105 specimens from 33 cords immediately after
vaginal delivery and analyzed the blood at intervals over the next 2 h.55
These investigators found that after an hour’s delay, the pH in only 2 of 84
specimens had fallen by more than 0.04 units, and pCO2 in only 5 of 84
specimens varied by more than 7 torr from the initial reading. In fact, there
was little variation even when samples were run 2 h after collection.
Neither did the investigators find a difference between iced samples and
those stored at room temperature. Together these studies argue that after
the cord is clamped, specimens may be drawn and analyzed at the clinician’s
and laboratory’s convenience. When gases are run only on select newborns
(see discussion below), the interval allows evaluation of the neonate to de-
termine those cases to be selected for blood gas analysis.
2. Contraindications and Complications
Because cord gases are drawn after delivery from a specimen that is
otherwise discarded, there are no contraindications to obtaining gases and
no complications from their sampling.
3. What Do Umbilical Cord Gases Predict? What Do They

Reflect?
Because cord gas values obtained after delivery reflect the in utero
acid-base status, many have hoped that these analyses might predict future
440
neonatal morbidity. But few antepartum events are strong predictors of
acidemia, and only the most marked acidemia even weakly predicts later
morbidity. Therefore, the potential clinical use of cord blood gas analysis
remains limited.
Gilstrap and Cunningham4 recently summarized the work of many
investigators who have linked differences in cord gas values to known
predictors of neonatal morbidity and mortality. Researchers have demon-

strated that the presence of heart rate abnormalities in the second stage of
labor,58 meconium-stained amniotic fluid,59,60 nuchal cords,61 and anesthe-
sia for labor and/or delivery62 are all associated with a statistically increased
risk of umbilical cord pH <7.20. The clinical significance of such associa-
tions, particularly when a pH of 7.20 is used to define the threshold for
acidemia, remains undefined, for most infants in these studies were vigor-
ous and there were few long-term morbidities of consequence in any group.
Almost as interesting as these statistical associations are the purported
risks not associated with a demonstrable difference in cord pH: operative
vaginal delivery, use of high- or low-dose pitocin, infection, and whether
a baby is a first or second twin.4
Although blood gases may retrospectively point to some risks that

practitioners might identify and thereby avoid in future patients, ultimately
blood gas analysis is only useful if it also predicts neonatal morbidity.
Avoiding such morbidity, not acidemia, is, after all, the goal of effective
labor management. Clinicians have long sought a predictor of later morbidity
both to offer parents a more accurate prognosis for their child’s develop-
ment and, potentially, to target resources and interventions to those at
highest risk. The Apgar score, a measure of a neonate’s immediate re-
sponse to the extrauterine environment as well as its need for and response
to resuscitation, is a poor predictor of later neurologic function or other
long-term outcomes.63 Although many have hoped that evaluation of um-
bilical cord acid-base variables might be the tool needed for more accurate
prediction, clinical practice demonstrates that this marker also falls short
of expectations.
Put differently, we expect the great majority of newborns who are
acidemic at birth to develop normally.58,60,61 Winkler and colleagues14 used
the traditional definition of acidemia of pH <7.20 and compared 358 aci-
demic to 358 nonacidemic newborns. They found that only 2 of 358 with
pH <7.20 had seizures, persistent hypotonia, and/or signs of end-organ
damage, and these two neonates were part of a subgroup of 23 with
pH <7.00.
Reflecting Winkler et al.’s 14 finding, others have analyzed the associa-
tion between umbilical artery pH and outcome in an effort to define a lower
441
pH cutoff with an acceptably low false-positive rate for predicting poor
neonatal outcome. Goldaber et al.5 reviewed the outcomes of 3506 neo-
nates with cord umbilical artery pH < 7.20 (Table 4). They found that
infants with pH < 7.00 had a higher risk of unexplained seizures and neonatal
death. These same infants were also more likely to have had low Apgar
scores (<3 at 1 or 5 min). Although these investigators recognized that the
majority of neonates (72/87) with pH < 7.00 had a normal outcome, they
suggested that compared with the traditional cut off of pH < 7.20, pH <
7.00 was a more realistic cutoff for defining pathologic fetal acidemia.
Goodwin et al.16 suggested an even more extreme cutoff in their evaluation
of 129 term neonates with pHs < 7.00; in their analysis a pH <6.8 with
marked hypercarbia (PCO2 > 100 mm Hg) and metabolic acidemia (BE <
–15 mEq/l) was most predictive of later death or neurological dysfunction,
but in practice only the rarest newborn will be so markedly acidemic.
Emphasizing the difficulty of using pH as a predictor of subsequent
neurologic dysfunction, Fee et al.18 studied outcomes among 15,528
neonates. Among 110 term neonates with pH < 7.05 and base excess
< –10 mEq, 101 had normal outcomes. Further, follow-up was available
in 7 of the 9 affected newborns and none of these 7 exhibited major motor

or cognitive abnormality at 12 to 24 months of age. In the hope that by
examining a population at increased risk for poor outcome, the positive
predictive value would be usefully improved, Fee and colleagues18 also
examined the utility of the test among preterm infants in their population.
Seventeen of 32 infants who met their definition of acidemia had normal
outcomes. None of the eight preterm infants in this preterm group with
available outcomes had identifiable deficits. Dickinson et al.12 too found
that even among preterm newborns, the majority with low pH were vigor-
ous at birth.
Summarizing their review of the available literature, Nelson and Emery65
concluded that “(t)he relationship of pH to neurologic syptomatology in
the neonatal period is … weak. The association of pH with long-term neu-
rologic outcome is even weaker … (O)nly extreme and rare values (pre-
dict) even short-term … outcomes.” Even if one could reliably identify a
population at high risk for hypoxic birth injury, because few interventions
are available for those at risk for but not yet manifesting signs of such
injury, the benefit of early identification is uncertain.
A review of the morbidities associated with delivery reveals the limi-
tations of using cord pH as a predictor of neurologic injury.64 The preva-
lence of cord pH < 7.00—a cutoff for acidemia far lower than traditional
442
TABLE 4
Neonatal Morbidity in a Population of 3506 Neonates with Umbilical Artery
Cord pH < 7.20 at Birth
<7.00 7.00–7.04 7.05–7.09 7.10–7.14 7.15–7.19

(n = 87) (n = 95) (n = 290) (n = 798) (n = 2236)
Neonatal deaths 7 (8%) 1 (1.1%) 0 3 (0.4%) 3 (0.1%)

All seizures 11 (12.6%) 4 (4.2%) 0 2 (0.3%) 4 (0.2%)
Unexplained seizures 8 (9.2%) 1 (1.1%) 0 1 (0.1%) 2 (0.1%)
Neonatal death
and seizures 2 (2.3%) 1 (1.1%) 0 0 1 (0.05%)
From Goldabar KG, Gilstrap LC, Leveno KJ, et al. Pathologic fetal acidemia. Obstet Gynecol
1991: 78: 1103–7.
443
definitions of pH < 7.20—is 3 to 4/1000 births, whereas the prevalence of
cerebral palsy (CP) due to intrapartum asphyxia is only 0.25/1000 births
(10% of an overall incidence of 2.5/1000 births). Therefore, even if a pH
< 7.00 were 100% sensitive as a predictor of CP, the positive predictive
value of the test for cerebral palsy would be only 0.073.17
4. Neonatal Acidemia as a Component of the Definition

of Asphyxia
Efforts to link ante- and intrapartum obstetric management with later

neonatal and pediatric outcome have been the focus of much research. Much
of this work has attempted to more accurately identify those newborns who
receive insufficient oxygen before or during delivery. That such neonates
are at increased risk for later morbidity is well known, but because such poor
outcomes are rare, crafting a clinically useful diagnosis of “asphyxia” has
proven difficult.
Older definitions of asphyxia that relied on Apgar scores identified
infants who were depressed at birth, but failed to isolate those at significant
risk for later deficits. Later definitions incorporated an assessment of acid-

base status at delivery, but, as discussed above, by using a pH < 7.20
included many newborns who were in fact at low risk for later morbidity.
More recent definitions have incorporated the conclusions of many studies
discussed above, and set the required pH threshold at a lower, and more
statistically appropriate, value. Contemporary definitions also reflect the
growing realization that “in the absence of moderate or severe encephal-
opathy in the neonatal period, with evidence of multiorgan failure, birth
asphyxia is unlikely to be the cause of a later-discovered disability.”65 For
asphyxia to be invoked as a cause of subsequent neurologic injury, the
American Academy of Pediatrics and the American College of Obstetri-
cians and Gynecologists66 have proposed that at a minimum the following
factors be present:
1. Prolonged metabolic or mixed acidemia (pH < 7.00) in an umbilical

cord arterial blood sample
2. Persistence of Apgar score of 0 to 3 for >5 min
3. Clinical neurologic sequelae in the immediate neonatal period (includ-
ing seizures, hypotonia, coma, or hypoxic-ischemic encephalopathy)
4. Evidence of multiorgan system dysfunction in the immediate neona-
tal period (e.g., pulmonary failure, pulmonary hypertension, oliguria
or renal failure, shock, hepatic dysfunction)
444
Others have added to this list an umbilical arterial base excess of at least
–16 mEq/l and absent fetal heart rate variability on the heart rate tracing
at the time of delivery.17
An umbilical artery pH of >7.00 thereby serves as important evidence
of the absence of clinically relevant asphyxia. This negative predictive
value may be of use to pediatric neurologists or other clinicians struggling
to identify a cause for a newborn’s deficit. Because, on occasion, cases

with transient or lasting deficits will be the center of malpractice action,
appropriate cord gases may also serve as important evidence supporting or
refuting the contribution of obstetric management to such injuries. Indeed,
many have suggested that umbilical artery blood gases are useful more in
excluding asphyxia than in identifying a group at particular risk. In one
analysis, 78% of depressed newborns (1 or 5 min Apgar < 7) had normal
umbilical artery pHs (defined in this study as a pH < 7.1, 2 SD below the
mean for this population of 1924 term, cephalic, nulliparous deliveries).67
In preterm infants, who are more likely to have neonatal depression
reflected in low Apgar scores, cord pH will effectively serve to rule out
asphyxia in most cases.1
5. In Which Patients Should Umbilical Blood Gases Be

Obtained?
As suggested above, an umbilical artery pH >7.00 may be important in

excluding birth asphyxia, but because a vigorous infant also excludes such
injury, few vigorous infants require umbilical blood gas sampling. Univer-
sal sampling may identify pH < 7.1 in as many as 2.5% of vigorous term
neonates,9,66 a finding of no obvious significance. Instead we recommend
setting a segment of cord aside in those infants who are not immediately
vigorous or whose labor and delivery were associated with specific risks
for neonatal depression and/or later morbidity (e.g., meconium, nonreas-
suring fetal heart rate tracing). If such infants remain depressed at 5 min
(Apgar < 7) or demonstrate other signs of injury (e.g., seizure), we then
obtain cord gases from the reserved segment. Additionally, as a matter of
quality control, there may be occasion to obtain gases to evaluate the time-
liness of obstetric interventions or particular interpretations of ancillary
fetal testing such as fetal heart rate strips. Only those involved in research
will want or need to obtain umbilical cord gases from every newborn.
If logistics or finances dictate that only one specimen may be obtained,
then the umbilical artery is preferable because it represents blood coming
445
from the fetus, and there can be wide discrepancies between the values in
the umbilical vein and artery under conditions of poor umbilical blood
flow (e.g., cord prolapse).
V. CONCLUSION
Evaluation of fetal blood samples can provide an accurate assessment

of ante- and intrapartum acid-base balance. Although cordocentesis and fetal
scalp sampling allow such sampling before delivery, the lack of demonstra-
ble clinical benefit as well as the development of other ancillary tests has
largely eliminated the indications for such evaluation. Although obtaining
gases from a section of cord following delivery is simple and nonmorbid,
this test also lacks persuasive predictive utility. Evaluating umbilical cord
gases from the clamped cord may, however, be an important tool in quality
improvement and risk management.
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451

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Critical Reviews in Clinical Laboratory Sciences, 36(5):407–451 (1999)

Obstetric Evaluation of Fetal

Jeffrey L. Ecker and Julian T. Parer*

* Author to whom all correspondence should be addressed.

KEY WORDS: obstetric evaluation, fetal acid-base, antepartum, intrapartum,

As in newborns, children, and adults, the balance of oxidative metabo-

objective method of assessing a newborn’s condition.”1 In this review, we

II. MATERNAL-FETAL ACID-BASE RELATIONSHIPS

between fetal and maternal circulations. Modifications of the fetal circu-

FIGURE 1. The fetal circulation. Numbers represent approximate values of the

bathes the syncytiotrophoblast of the individual placental villi (Figure 2a).

Reproduction of this material without the consent of the publisher is prohibited.

arteriosus directly to the descending aorta—may circulate through the

B. Biochemistry of Maternal-Fetal Placental Exchange

by fetal and maternal placental blood flow.

PCO2 or bicarbonate concentration will alter pH. Increasing PCO2 pressure

The pregnant woman’s pH is the same as that of a nonpregnant woman—

lation of pregnancy; administration of progesterone to male subjects pro-

from undisturbed third-trimester human fetuses (see techniques described

Umbilical artery Umbilical vein

ph 7.33 ± 0.07a 7.38 ± 0.06

delivery by assaying blood collected from umbilical cord samples at birth

labor and vaginal deliveries at 37 to 42 weeks’ gestation. All infants in their

UA pH 7.26 0.07 7.10 7.13 7.27 7.36 7.38

Note: pCO2, carbon dioxide pressure; pO2, oxygen pressure; n = 15,073.

Reproduction of this material without the consent of the publisher is prohibited.

confounding conditions.11 In an effort to determine if umbilical cord blood

Reproduction of this material without the consent of the publisher is prohibited.

III. ABNORMAL UMBILICAL BLOOD GAS VALUES:

DEFINITIONS AND ANTECEDENTS

A. What is an Abnormal or Nonreassuring Umbilical Cord pH?

Although there is impressive concordance among those studies that have

B. What is Asphyxia and What are its Causes?

Although etymologically derived from the Greek meaning pulseless,

abnormalities present (e.g., acidemia) or circumstances leading up to such

both to asphyxia and abnormal cord blood gas values:

1. Maternal conditions: Maternal conditions resulting in fetal hypoxia

autoregulation of uterine artery caliber during gestation, and the

not match oxygen available through the placenta. Intrauterine infec-

The timing and duration of any insult or perturbation is important in

ment, the investigators used a femoral artery catheter to sample arterial

ual fetus, a number of other factors—stage of fetal development, metabolic

IV. TECHNIQUES FOR FETAL AND UMBILICAL CORD

Umbilical artery samples may be obtained in utero before labor, during

When initially developed, in utero blood sampling was accomplished

puncture the vessel. Because it is of larger caliber, it is almost always

with Cesarean delivery in the event of fetal intolerance of sampling, the

Cordocentesis is indicated when perinatal management requires direct

There are few contraindications to cordocentesis, although the amount

and/or delivery should not be delayed to permit sampling. Ongoing bleed-

In 1993, Ghidini and associates reviewed the available literature in an

alternate approaches may merit special consideration in patients at risk for

5. Utility of Acid-Base Cord Blood Analysis

Associated morbidity and mortality aside, there is no sound evidence

in a series of 46 samplings.31 Until a well-designed study demonstrates a

B. Fetal Blood Sampling (FBS)

Intrapartum evaluation of fetal acid-base status is accomplished by

resulting droplet of blood is collected in a glass capillary approximately

The capillary tube contains approximately 0.25 ml of blood, which is

ibility of measurements and the variation among well-calibrated machines

Obvious threats to the mother (e.g., profuse hemorrhage) or to the fetus

but are not in and of themselves contraindications to attempting sampling.

The possibility of hemorrhagic or infectious complications has been