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Intrapartum fetal heart rate assessment

Author Bruce K Young, MD Section Editor Charles J Lockwood, MD Deputy Editor Vanessa A Barss, MD Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2012. | This topic last updated: jun 15, 2012.
INTRODUCTION Assessment of the fetus during labor is a challenging task. The rationale for monitoring the fetal heart
rate (FHR) is that FHR patterns are indirect markers of the fetal cardiac and medullary responses to blood volume
changes, acidemia, and hypoxemia, since the brain modulates heart rate. Virtually all obstetrical organizations advise
monitoring the FHR during labor. This position is largely based upon the experience of experts and medicolegal
precedent; no trials comparing electronic fetal monitoring versus no monitoring have been performed [1]. A trial comparing
auscultation with no monitoring found that auscultation was associated with an increased risk of operative delivery without
any reduction in perinatal mortality [2]. Furthermore, no reliable auscultatory indicator of fetal distress has been
determined, other than extreme changes in FHR [3]. Thus, neither electronic fetal monitoring nor auscultation has been
proven to reduce mortality, despite large clinical trials [4].
Intrapartum fetal monitoring will be discussed here. Fetal cardiac physiology, FHR patterns, and antepartum FHR
monitoring (nonstress test, contraction stress test) are reviewed separately. (See "Antepartum fetal heart rate
assessment".)
EFFECTIVENESS OF INTRAPARTUM FHR MONITORING The primary goal of FHR monitoring is to identify
hypoxemic and acidotic fetuses in whom timely intervention will prevent death. A secondary goal is to avoid fetal
neurologic injury, if possible. The two commonly used modalities for intrapartum FHR monitoring, continuous electronic
FHR monitoring and intermittent auscultation, have been extensively reviewed; there is no high quality evidence that
these techniques achieve either of these goals or that one performs better than the other in low risk pregnancies [4-10]. A
systematic review of 12 randomized trials including >37,000 women (both low and high risk) comparing these two
techniques showed [6]:

The intrapartum fetal death rate was approximately 0.5 per 1000 births with either approach
Apgar scores and neonatal intensive care unit admission rates were similar for both modalities
Neither approach reduced the risk of long-term neurologic impairment or cerebral palsy.
Use of electronic FHR monitoring instead of intermittent auscultation has not led to a significant reduction in the
overall risk of perinatal death (RR 0.85, 95% CI 0.59-1.23).

A significant decrease in the perinatal death rate would be difficult to demonstrate since death is a rare outcome; even
pooling results from multiple randomized trials lacked sufficient power to provide a definitive conclusion. Analysis of
national data from birth and death certificates provides some insight about these relationships. A retrospective cohort
study of birth and infant data from almost two million singleton births in the United States found that 89 percent of the
labors utilized electronic FHR monitoring and these pregnancies had a significantly lower rate of early neonatal death than
those without electronic FHR monitoring (0.8 versus 1.7 per 1000 births); the magnitude of the reduction in early death
increased as gestational age decreased [11]. However, these data are limited by ascertainment bias inherent in
observational data; unmonitored patients likely had different baseline risk for neonatal death than monitored patients.
Use of electronic FHR monitoring instead of intermittent auscultation has also not led to a reduction in the prevalence of
cerebral palsy (RR 1.74, 95% CI 0.97-3.11) [6]. The absence of a reduction in cerebral palsy is not surprising since most
cases of cerebral palsy are due to a remote antepartum event, rather than intrapartum asphyxia [12]. The lack of a strong
correlation between use of intrapartum monitoring and neurologic outcome is likely related to the observation that most
FHR abnormalities are not associated with fetal acidosis or hypoxemia and most fetal acidosis and hypoxemia does not
result in neurologic disability. Indeed, 99.8 percent of nonreassuring FHR tracings are NOT associated with development
of cerebral palsy [12]. Furthermore, a fetal neurologic disorder may be the cause (rather than the result) of FHR
abnormalities [13]. Lastly, the degree of asphyxia that leads to long-term neurologic damage is close to that causing fetal
death, thus most asphyxiated term fetuses either survive intact or die, rather than survive disabled [7].

The systematic review demonstrated that the major benefits of continuous electronic FHR monitoring were a reduction in
the frequency of neonatal seizures (RR 0.50, 95% CI 0.31-0.80) [6] and, in one trial, better prediction of fetal acidemia at
birth [9]. However, the seizures prevented by electronic FHR monitoring did not appear to be associated with long-term
consequences [14].
The major disadvantage of continuous electronic FHR monitoring was that it led to higher operative delivery rates
(cesarean delivery RR 1.66, 95% CI 1.30-2.13; instrumental vaginal delivery RR 1.16, 95% CI 1.01-1.32) without an
associated neonatal benefit [6]. In particular, compared to intermittent auscultation, continuous electronic FHR monitoring
was associated with a two-fold increase in risk of cesarean delivery performed because of a nonreassuring FHR (RR
2.37, 95% CI 1.88-3.00).
The increased risk of operative delivery persisted in subgroup analysis of low and high risk pregnancies; however, data
were more limited. In any case, any monitoring, even by auscultation, results in more operative deliveries [2].
INDICATIONS The United States Preventive Services Task Force and the Canadian Task Force on Preventive Health
Care have made the following statements [15,16]:

Routine electronic FHR monitoring for low-risk women in labor is not recommended
There is insufficient evidence to recommend for or against intrapartum electronic FHR monitoring for high-risk
pregnant women.

The Royal College of Obstetricians and Gynaecologists recommends [17]:

Continuous electronic FHR monitoring for high risk women


Intermittent auscultation for low risk women

The American College of Obstetricians and Gynecologists stated [5]:

High risk pregnancies (eg, preeclampsia, suspected growth restriction, type 1 diabetes mellitus) should be
monitored continuously during labor.
Either electronic FHR monitoring or intermittent auscultation is acceptable in uncomplicated patients.

Nevertheless, some type of FHR monitoring during labor has become routine for all women in the United States and will
not be abandoned because patients and clinicians are reassured by normal results and believe there is some value in
detecting nonreassuring patterns.
EQUIPMENT AND TECHNIQUES
Doppler ultrasound The FHR is determined noninvasively using a Doppler ultrasound device belted to the maternal
abdomen throughout labor. The device is typically connected to an electronic monitor, which continuously plots the FHR
on a paper strip, while a pressure transducer simultaneously monitors the frequency, timing, and duration of uterine
contractions (this process is called continuous cardiotocography or continuous electronic FHR monitoring) (waveform 1).
In uncomplicated patients, it is common practice for the FHR tracing to be reviewed at least every 30 minutes in the first
stage of labor and every 15 minutes in the second stage, and the interpretation should be documented [5].
Occasionally, the electronic fetal monitor is applied intermittently rather than continuously (called intermittent
cardiotocography or intermittent electronic FHR monitoring), to allow the parturient more mobility. Wireless monitors are
available which enable FHR monitoring while the women is ambulating. Because of the inherent variation in the Doppler
ultrasound signal, auto correlation processing by computer is used. This results in a highly processed record which
smooths out the signal variation and produces a processed sound, which is not the actual fetal heart beat.
Intermittent auscultation is an alternative to continuous electronic FHR monitoring. Using a Doppler device, the FHR is
determined over one to two minutes at intervals of 5 to 30 minutes, depending upon the stage of labor. Ideally, the FHR is
checked both during and immediately after a contraction and the lowest rate is manually recorded. There are no data on
which to base a recommendation for the frequency of intermittent auscultation, but a 1979 National Institutes of Health
consensus conference recommended every 15 minutes in the active phase of the first stage and every 5 minutes in the

second stage, an impractical standard for most Obstetrical Services [18]. In contrast to continuous cardiotocography,
intermittent auscultation does not provide any information about FHR variability, the shape of FHR decelerations, or
uterine contractions. Auscultation of the FHR using a fetal stethoscope is also possible, but more cumbersome.
(See "Antepartum fetal heart rate assessment", section on 'Antepartum FHR monitoring' and "Antepartum fetal heart rate
assessment", section on 'Equipment for FHR monitoring'.)
There is more baseline variability inherent with the external or Doppler technique compared with internal fetal monitoring
(see below). Since a computer calculates the FHR by averaging several consecutive beat-to-beat frequencies to minimize
artifact (called "autocorrelation"), the FHR pattern produced closely resembles that derived from a fetal electrocardiogram
(ECG), but there is more baseline variability inherent with the Doppler technique.
Fetal electrocardiogram Internal measurement of FHR is an invasive procedure; thus, its use is restricted to the
intrapartum period. A bipolar spiral electrode is inserted transcervically to penetrate the fetal scalp and a second reference
electrode is placed upon the maternal thigh to eliminate electrical interference. The internal electrode detects the fetal
electrocardiogram (ECG) and calculates the FHR based upon the interval between R waves. This signal is very clear and
provides accurate measurement of beat-to-beat variability. Artifact is kept to a minimum, and there is little need for
autocorrelation.
External monitoring is usually as reliable as internal monitoring and is the preferred approach since it is noninvasive.
Internal monitoring should be used, however, when the externally derived tracing is difficult to interpret because of poor
technical quality. This occurs in various situations, such as when the fetus or mother is frequently changing position and
sometimes in multiple fetus gestations.
With both internal and external methods, the credence correlation circuitry of the monitor represents signals interpreted as
artifactual with a pen lift, which results in non-recording areas. The accompanying sound should be regarded as an
unreliable signal, since it is generated by the same electronic mechanisms. Nevertheless, certain arrhythmias may
present in this way, and confirmation by sonography may be helpful. (See "Overview of the general approach to diagnosis
and treatment of fetal cardiac arrhythmias".)
Artificial intelligence computer programs Fetal ECG has been the gold standard for signal acquisition during
intrapartum FHR monitoring. Computer analysis of these signals is the standard methodology for recording the signal,
analysis of variability, and more recently, interpretation of fetal status. Application of "artificial intelligence" computer
programs to fetal ECG signal processing has led to clinical devices for overcoming the limitations of FHR pattern
interpretation by an human observer, expert or not. This has been made possible by technical improvements in signal
acquisition and processing, and by algorithms for pattern interpretation based on standardization of visual pattern analysis
and correlation with fetal scalp blood and umbilical artery pH determinations, with improving success as the models have
improved [19-23]. (See 'STAN fetal heart monitor (ST analysis)' below.)
EVALUATION OF THE FETAL HEART RATE
Standards for interpretation Interpretation of FHR tracings is subjective and not very reproducible. Studies have
consistently shown that there is large inter- and intraobserver variability in interpretation of electronic FHR monitoring
tracings [24-26]. For this reason, the National Institutes of Child Health and Human Development convened a workshop to
try to reach consensus, for research purposes, on definitions of FHR patterns (table 1) [27]. This approach to evaluation
has been endorsed by the American College of Obstetricians and Gynecologists [5]. Inter- and intraobserver agreement,
however, remain a problem because of disagreement about absent versus minimal variability in the most concerning
tracings [28].
Of note, these definitions do not apply to computer generated FHR interpretations, and European standards differ from
those in the United States.
Reassuring patterns The FHR pattern recorded by an electronic FHR monitor is typically interpreted as reassuring or
nonreassuring. The presence of a reassuring pattern indicates that there is minimal likelihood of acidemia at that point in
time; it is not predictive of future status, as tracing patterns can change. A reassuring fetal heart rate pattern (category I)
has all of the following components [29]:

A baseline fetal heart rate of 110 to 160 bpm

Absence of late or variable FHR decelerations


Moderate FHR variability (6 to 25 bpm) (waveform 2A-B)
Age appropriate FHR accelerations (waveform 3)

Early decelerations may or may not be present. FHR accelerations are an important finding because their presence,
especially in the presence of moderate variability, almost always indicates that the fetus is not acidotic [29-32]. However,
less than moderate variability does not reliably mean the fetus is acidotic. In the absence of accelerations despite scalp
stimulation, fetal acidemia is present in about 50 percent of patients [29,30].
Slight deviations from the normal baseline and some periodic changes (ie, changes associated with contractions) are
innocuous in the continuum of the FHR pattern. As an example, early decelerations (table 1 and waveform 4) are believed
to be vagally mediated and due to fetal head compression. They are generally not associated with fetal acidosis or poor
neonatal outcome. A baseline FHR of 100 to 110 follows the same physiology; if it persists for more than an hour,
cephalopelvic disproportion may be present [33].
Many cardiac arrhythmias also pose no immediate threat to the fetus, irrespective of a FHR pattern that deviates from
what is considered reassuring. In fact, the majority of fetal arrhythmias are benign and spontaneously convert to normal
sinus rhythm by 24 hours after birth [34]. Persistent tachyarrhythmias may cause fetal hydrops if present for many hours
to days. Persistent bradyarrhythmias are often associated with fetal heart disease (eg, cardiac conduction defects due to
anatomic derangements or autoantibody (SSA, anti-Ro) induced-cardiomyopathy related to lupus), but seldom result in
hypoxemia or acidosis in fetal life. (See "Overview of the general approach to diagnosis and treatment of fetal cardiac
arrhythmias".)
Nonreassuring patterns Nonreassuring tracings (category III) are associated with abnormal fetal acid-base status at
the time of observation. Prompt evaluation of these patients is indicated and expeditious intervention (provision of
supplemental oxygen therapy, change in position, treatment of hypotension, discontinuation of any uterotonic drugs) may
be necessary because fetal or neonatal death or damage may occur if the pattern does not resolve and persists for an
hour or more. Fetal oxygen deprivation can lead to significant fetal acidosis (umbilical artery pH <7.0, base deficit 12
mmol/L), which is the precursor of intrapartum hypoxic neurologic injury. The goal of intervention is to improve fetal
oxygenation by improving uteroplacental perfusion.
Nonreassuring patterns include:
Absent or minimal variability with decelerations or bradycardia Absent variability (table 1) is concerning. The
absence of FHR variability is thought to be a result of cerebral hypoxemia and acidosis, and signifies failure of fetal
compensatory mechanisms to maintain adequate oxygenation of the brain. Thus, absence of variability is often
accompanied by abnormalities in FHR baseline or periodic late decelerations when the fetus is distressed. Nonhypoxiarelated causes of diminished variability include anencephaly and other central nervous system defects, use of some
centrally acting drugs (eg, opiates, magnesium sulfate, atropine), sepsis, defective cardiac conduction (eg, complete heart
block), and quiet fetal sleep.
Absent variability with any of the following FHR changes is predictive of abnormal fetal acid-base status [29].
Recurrent late decelerations Late decelerations (table 1 and waveform 5) are caused by the reflex central nervous
system response to hypoxia and acidemia, as well as direct myocardial depression and humoral factors [35]. They can be
associated with a falling fetal pH and perinatal morbidity and mortality [36]. Recurrent late decelerations (ie, occurring with
50 percent of contractions in a 20-minute segment) with absent variability are especially predictive of current or
impending fetal acidosis due to progressively falling pH [27]. (See "Umbilical cord blood acid-base analysis".)
Recurrent variable decelerations Variable decelerations (table 1 and waveform 6) occur when the umbilical cord is
compressed, such as in the setting of low amniotic fluid volume or a nuchal cord. The thin walled umbilical vein is more
sensitive to compression than the umbilical artery. This results in variable effects on fetal preload and afterload, which
lead to changes in FHR mediated by baroreceptors, and chemoreceptors when there is sufficient hypoxemia. Intermittent
variable decelerations are frequently observed in labor tracings and are not usually associated with adverse
consequences, presumably because transient cord compression is well tolerated by the fetus. Fetal metabolic acidosis or
mixed metabolic and respiratory acidosis can develop, however, with increasing duration and frequency of variable

decelerations

[37].

There are many atypical variations, particularly with this type of deceleration, which is inherently variable [38].
Nevertheless, the data do not support attaching clinical significance to atypical features: variable decelerations with
lambda or W pattern (biphasic deceleration), slow return to baseline, loss of primary or secondary acceleration
(shoulders), persistent secondary acceleration (overshoot), or reduction in post-deceleration baseline. The current
NICHHD classification does not include atypical variable decelerations as a category of FHR pattern. However, it does
consider variable decelerations with absent baseline variability as predictive of an abnormal pH.
Bradycardia Bradycardia with absent variability appears as a smooth FHR below 110 bpm. It is ominous when it
occurs for a prolonged period of time (ie, at least 10 minutes) in the absence of hypothermia, complete heart block, or use
of certain drugs (eg, beta-adrenergic blockers, paracervical block). When the FHR falls below 100, tissue perfusion may
not be adequate; this degree of bradycardia is nonreassuring even when variability is present.
Sinusoidal heart rate pattern A sinusoidal heart rate is defined as a pattern of regular variability resembling a sine
wave, with a fixed periodicity of three to five cycles per minute, an amplitude of 5 to 40 bpm, and lasting for at least 10
minutes (waveform 7) [29]. Decelerations and accelerations in response to movement are absent. The mechanism for the
sinusoidal pattern is believed to be a response to moderate fetal hypoxemia, often secondary to fetal anemia. Beat to beat
changes are often small, but in the same direction, creating the wave pattern.
This pattern was initially thought to be preterminal in all cases, but is no longer considered preterminal or due to acidosis
[39,40]. A sinusoidal-like pattern has been associated with physiological changes in fetal peripheral arterial resistance,
fetal sucking movements, and maternal narcotic administration [41-43].
If a sinusoidal pattern is observed, we try to determine the reason for the pattern, while continuing to monitor the fetal
heart rate. Fetal anemia can be due to bleeding or a chronic process; causes include fetomaternal hemorrhage, iatrogenic
fetal bleeding, fetal bleeding secondary to vasa previa or placental abruption, alloimmunization, and parvovirus infection.
Sonographic evaluation may suggest one of these etiologies. Severe fetal anemia can be diagnosed via Doppler
assessment of the fetal middle cerebral artery peak systolic velocity and fetal bleeding can be determined by a rosette test
(qualitative) or a Kleihauer-Betke test (quantitative) or flow cytometry (semi-quantitative) on maternal venous and/or
vaginal blood (if vaginal bleeding is present). However, rapid results from these tests are seldom available on the labor
floor. We do not consider sinusoidal patterns to be predictive of fetal acidosis [39-41].
Fetal scalp stimulation or fetal blood sampling may provide some reassurance that the fetus is not acidotic [39]. In the
absence of evidence of acidosis or other concerns, fetuses with a sinusoidal FHR pattern do not need to be delivered
immediately. The sinusoidal pattern sometimes resolves; however, if acidosis or a worsening FHR pattern develops, we
suggest urgent delivery.
Indeterminate patterns FHR patterns that are category II are not reassuring and are considered indeterminate. The
fetus may not be acidotic; however, continuation or worsening of the clinical situation may result in fetal acidosis.
Therefore, continued surveillance and evaluation of these patients is indicated. Intervention (provision of supplemental
oxygen, change in position, treatment of hypotension, discontinuation of any uterotonic drugs) may be needed if additional
assessment suggests a progressively worse situation.
Some examples of indeterminate patterns include tachycardia, minimal or marked variability, absent variability without
recurrent decelerations, absence of accelerations without absent variability, recurrent late or variable decelerations
without absent variability, and prolonged decelerations [29].
Pre-existing fetal neurological injury Whether there are FHR patterns that may indicate fetal brain damage before
labor is controversial. Since the first report of fetal intracranial hemorrhage 25 years ago suggesting that cerebral palsy
could be due to antepartum events [44], a consensus has developed that 50 to 90 percent of neurologically impaired
infants are suffering from a problem present before the onset of labor. Specific abnormal FHR patterns associated with
neurological injury have been described and can be observed from the initiation of monitoring. The most common FHR
abnormality is a persistent nonreactive heart rate and a persistent fixed baseline with minimal or absent variability
[13,45,46]. However, these patterns are not uniform and not always present. As an example, a study of 300 neurologically

impaired term singletons in whom 54 percent had a probable injury before labor reported one-half had a normal FHR
pattern until birth [47].
Studies of infants with congenital brain lesions suggest that damage to the medulla oblongata and mid brain may be
responsible for the loss of FHR variability [48].
Differential diagnosis Nonreassuring and indeterminate tracings can be due to:

Fetal arrhythmias (see "Overview of the general approach to diagnosis and treatment of fetal cardiac
arrhythmias").
Technical factors including a faulty leg plate, electrode, or monitor; setting the recording rate at 1 cm/min instead
of the standard 3 cm/min; and the fact that very slow FH rates may be doubled and very fast rates (>240 bpm)
may be halved by the machine.
The fetal and maternal heart beats are typically distinguished by the faster rate of the fetus (110 to 160 versus
<100 bpm). However, they can beat at a similar rate. The fetal heart rate may be the same or slower than the
maternal rate if there is a fetal heart rate deceleration or prolonged bradycardia or in the presence of maternal
tachycardia
due
to
fever
or
stress.
A maternal pulse rate approximating the FHR displayed on the monitor should prompt a reevaluation of the fetal
tracing and the use of another method to distinguish between maternal and fetal patterns. It is important to
confirm that the external fetal monitor is actually recording the FHR and not the maternal heart rate transmitted
from a maternal vessel, such as the aorta or uterine artery. An internal fetal electrode is not definitive, as a fetus
that is recently dead can conduct the maternal cardiac signals though its body to the electrode [49]. The simplest
way to confirm that the FHR is being recorded is to confirm that the sound is not synchronous with the maternal
pulse. Alternatively, the rate on the fetal monitor can be compared with that on a maternal pulse oximeter. If
uncertainty remains, ultrasound examination of the fetal heart can be performed.

LABOR ADMISSION TEST The "labor admission test" refers to an electronic FHR monitoring tracing performed for 20
to 30 minutes upon admission to the labor and delivery unit. It is widely used for initial assessment of the fetus. The goal
is to identify fetuses who may be at increased risk of having nonreassuring FHR patterns during labor and thus might
benefit from continuous FHR monitoring rather than intermittent auscultation [50].
Two randomized trials involving over 12,000 low risk patients compared use of the labor admission test to intermittent
auscultation for initial assessment of the parturient [51,52]. In each trial women admitted to a labor unit were randomly
assigned to receive usual care (Doppler FHR auscultation) or a labor admission test. Women with reassuring results were
followed by intermittent auscultation during labor and those with nonreassuring results were followed by continuous
electronic FHR monitoring. The rates of neonatal morbidity and operative intervention were similar in both groups;
however, women who had a labor admission test were more likely to be continuously monitored and undergo fetal scalp
blood sampling during the remainder of their labors. They also trended toward a higher rate of operative delivery (OR
1.15, 95% CI 1.00-1.32) [52].
The above trials did not assess the effect of normal and abnormal initial testing results on fetal outcomes. This issue was
addressed in an observational study of 845 labor admission tests on high and low risk Norwegian women: 5.9 percent of
these patients developed fetal distress in labor (defined as operative delivery indicated by interpretation of the FHR
pattern or Apgar less than 7 at five minutes) [53]. However, the rate of fetal distress (5 percent) was not significantly lower
in those who had a normal test on admission.
A systematic review of both randomized and quasi-randomized trials of the prognostic value of the labor admission test
also concluded that there was no evidence that the labor admission test resulted in less neonatal morbidity in low risk
women than intermittent auscultation [54].
Based on the above data, the labor admission test does not appear to reliably predict fetal ability to tolerate labor over
time in low risk pregnancies and has not been associated with a reduction in any parameter of neonatal morbidity at birth.
Its use offers no advantage over auscultation of the FHR and may lead to more obstetrical interventions. It has a

theoretical value in detecting cases of immediate fetal jeopardy, but that benefit remains intuitive and unproven. There are
insufficient data to draw any conclusions about its value in women with high risk pregnancies.
MANAGEMENT OF FETAL HEART RATE PATTERNS To be useful, FHR monitoring requires that the clinician
correctly recognize nonreassuring and reassuring FHR patterns, communicate with the patient's other labor and delivery
providers (eg, nursing, obstetrics, anesthesia, pediatrics) when the pattern is nonreassuring, and initiate appropriate and
timely intervention [23]. No randomized trials have evaluated an operative versus a conservative approach to suspected
fetal distress on intrapartum electronic fetal monitoring [55].
Three tier approach In 2008, the National Institutes of Child Health and Human Development creating a three tier
FHR interpretation system (table 2), in which category I represents a normal tracing (predictive of normal fetal acid-base
balance at the time of observation), category II represents an indeterminate tracing, and category III represents an
abnormal tracing (predictive of a significant incidence of abnormal fetal acid-base status at the time of observation) [29].
They recommended prompt evaluation of category III tracings; most patients with these tracings require expeditious
intervention, such as provision of maternal oxygen, change in maternal position, treatment of maternal hypotension, and
discontinuation of any uterotonic drugs being administered [29]. The goal of these interventions is to improve fetal
oxygenation by improving uteroplacental perfusion. Preparations for delivery are made while these interventions are
initiated so that delivery can be performed promptly if the fetal heart rate pattern does not improve. While the fetal impact
of the timing-of-decision to delivery interval is controversial, we try to make the decision to deliver within 15 to 20 minutes
of the start of severe bradycardia (FHR below 100 bpm [33]) and deliver the infant within 20 to 30 minutes of the start of
the bradycardia when there is no improvement despite therapeutic intervention.
Category II tracings are not predictive of abnormal fetal acid-base status, but require continued surveillance, evaluation,
initiation of appropriate corrective measures as indicated, and reevaluation. The guidelines do not offer specific
recommendations for evaluation of these fetuses, but it seems reasonable to employ other diagnostic measures, such as
sonography, scalp stimulation, and scalp blood sampling (see below).
Category I tracings are normal, thus these fetuses are monitored either intermittently or continuously, depending on
underlying risk factors.
This approach to management of FHR tracings has been endorsed by the American College of Obstetricians and
Gynecologists [5,56].
The management of category I, II, and III tracing is discussed in detail separately. (See "Management of intrapartum
category I, II, and III fetal heart rate tracings".)
Further evaluation of nonreassuring patterns Transient episodes of hypoxemia, such as during a contraction or
temporary cord occlusion, are generally well-tolerated by the fetus. Repeated or prolonged episodes, especially if severe,
may lead to fetal acidosis, sometimes with subsequent hypoxic-ischemic encephalopathy (defined as metabolic acidosis
pH <7, base deficit 12 mmol/L and Apgar score 0 to 3 for >5 minutes, and evidence of neurologic sequelae [57]).
(See "Umbilical cord blood acid-base analysis" and "Fetal acid-base physiology".)
One goal of intrapartum fetal surveillance is to distinguish the fetus with a nonreassuring FHR tracing who is hypoxemic,
but well compensated, from one who is acidotic and at risk for neurologic impairment or death. Further evaluation using
ancillary tests are useful for this purpose. After adequate cervical dilation and rupture of the membranes, direct access to
the fetus is readily available and permits measurement of its physiologic status.
One group has attempted to formulate a framework for standardizing management of intrapartum FHR patterns [58]. They
identified 134 FHR patterns (combinations of variability, rate, and various types of decelerations), and determined the risk
of newborn acidemia associated with each pattern. A grid was created to relate the FHR patterns and risk of fetal
acidemia (five gradations from none to severe). Obstetrical interventions were proposed based on the degree of risk. This
algorithm has not been validated clinically.
Since FHR patterns are at best only a screening tool, this approach is a valuable beginning to evaluation and
management of FHR patterns in laboring patients. However, some important variables, such as rate of change of pH
under different circumstances, acidosis despite a vigorous fetus, pre-existing fetal acidemia with a normal FHR pattern,
response to specific therapies, and stage of labor, were not considered. Furthermore, the algorithm does not lend itself to

use of clinical judgment in the setting of complex and rapidly changing conditions. The individual patient needs to
participate in the decision as to whether an immediate cesarean or continued monitoring and evaluation is the best
approach for her. The algorithm is also not useful when there is a 10 percent risk of a depressed infant, and possibly
when the risk of neurological injury or stillbirth is increased, but less than 10 percent.
FHR response to stimulation The fetal scalp stimulation maneuver is easy to perform, inexpensive, readily available,
and not uncomfortable. The examiner stimulates the fetal vertex by prodding it with the examining finger or an instrument,
such as an Allis clamp, during a vaginal examination [30]. If a FHR acceleration is elicited (rise of 15 bpm above baseline
lasting for 15 seconds), absence of acidosis (ie, fetal pH greater than 7.20) is likely. Vibroacoustic stimulation is a less
invasive alternative technique. In general, when accelerations are induced by scalp stimulation, acidosis is present in less
than 10 percent of fetuses, and when no accelerations occur, acidosis is present in about 50 percent of fetuses [30,59,60].
One study, however, reported five fetuses with pH <7.20 out of 70 fetal blood samples; three of these five fetuses had
FHR accelerations and two did not [61]. (See "Antepartum fetal heart rate assessment", section on 'Vibroacoustic
stimulation'.)
Scalp stimulation should be performed when the FHR is at its baseline rate. Performance during a deceleration is not
likely to terminate the deceleration, is not predictive of fetal acid-base status, and might exacerbate fetal compromise if
parasympathetic tone increases in response to the stimulus.
A meta-analysis that assessed performance of various stimulation tests (vibroacoustic stimulation, digital scalp
stimulation, fetal scalp puncture, Allis clamp scalp stimulation) for the prediction of intrapartum fetal acidemia found them
to be similarly effective and more useful for predicting the absence, rather than the presence, of acidemia [59]. Less
traumatic techniques (vibroacoustic stimulation, digital scalp stimulation) are preferable to more traumatic techniques
(fetal scalp puncture, Allis clamp scalp stimulation). For digital stimulation, the pooled likelihood ratio (LR) for acidosis with
a negative test (ie, acceleration elicited) was 0.06, 95% CI 0.01-0.31. Failure to elicit an acceleration was not a definitive
sign of acidosis. For digital stimulation, the pooled LR of acidosis with a positive test (ie, no acceleration) was 15, 95% CI
3-76.
Continued monitoring and repeat testing is advised if the suspicious FHR pattern persists since test results reflect acute
fetal status at the time of the test, and may worsen over time. Rarely, acidemia is present despite FHR accelerations and
a prenatal insult associated with fetal neurological injury may not show FHR abnormalities in the intrapartum period [62].
STAN fetal heart monitor (ST analysis) A technical system, the STAN S31 fetal heart monitor, monitors the fetal
electrocardiogram (ECG) during labor. Use of this device is based on the principle that fetal hypoxemia can result in
elevation or depression of the ST segment. The monitor's software automatically identifies and analyzes changes in the T
wave and the ST segment of the fetal ECG, which is obtained via a spiral electrode attached to the fetal scalp. The
analysis is displayed in the lower section of the monitor's screen as a series of data points ('T/QRS crosses') and event
markers. Studies have reported the STAN computerized interpretation of FHR monitoring system has sensitivity of 38 to
90 percent and specificity of 83 to 100 percent for detecting fetal acidosis [63-65].
The major benefit of this technique appears to be a reduced need for fetal blood sampling [66]. A meta-analysis of five
randomized trials involving a total of 15,352 pregnant women assessed the use of the fetal ECG as an adjunct to
continuous electronic FHR monitoring during labor [67]. In comparison to continuous electronic fetal heart rate monitoring
alone, the use of adjunctive ST waveform analysis was associated with significant reductions in fetal scalp sampling
during labor (RR 0.59, 95% CI 0.44-0.79; number needed to treat 11) and operative vaginal delivery (RR 0.88, 95% CI
0.80-0.97; number needed to treat 64). There were no statistically significant differences in the number of babies with
metabolic acidosis at birth (50/7689 [ST analysis group] versus 73/7641 [usual care group], RR 0.72, 95% CI 0.43-1.19),
cord artery pH <7.05, or rate of cesarean delivery, Apgar score less than 7, NICU admission, neonatal encephalopathy, or
perinatal death.
The STAN S31 fetal heart monitor has been approved by the United States Food and Drug Administration as an adjunct
to assessment of nonreassuring FHR tracings in pregnancies over 36 weeks of gestation, in labor, with vertex
presentation and ruptured fetal membranes. The device should not be used if there is a contraindication to placement of a
fetal scalp electrode. It is also not indicated for monitoring initiated in the second stage of labor or for precipitous labor,
since there may not be enough time to establish the baseline fetal ECG data required for automatic ST event signals.

Transcutaneous Electrical Nerve Stimulation (TENS) for analgesia during labor is another contraindication because TENS
may interfere with acquisition of the fetal ECG signal.
Clinicians using this device should be trained and credentialed in its use and interpretation. This technique is promising,
but at this time, there are inadequate clinical and cost data from a variety of hospital settings to allow a recommendation
for routine use.
Fetal scalp blood sampling Fetal blood sampling is typically performed using a kit. An amnioscope with a light source
is used to expose the fetal scalp, which is cleansed of blood, mucous, and amniotic fluid. The scalp is smeared with
silicone gel so that a droplet of blood forms when the scalp is punctured with a 2-mm blade. The blood is collected in long,
heparinized capillary tubes. The test requires that the cervix be dilated at least 2 to 3 cm, can be difficult to perform, and
can be uncomfortable for the parturient.
Both pH and lactate measurements (see below) require the same laboratory facilities for microsample analysis. Quality
control and laboratory standards must be in place to utilize these tests, and most obstetrical services in the United States
cannot support them, even when shared with neonatology. Most hospitals have centralized laboratories for these tests
and cannot function in a logistically efficient way for patients in labor. The degree of technical skill required, cost, need for
continuous availability of standardized equipment and trained personnel, and parturient discomfort have precluded use of
these tests in many labor and delivery units, despite their proven benefit in diagnosing fetal acidosis.

pH Capillary blood collected from the fetal scalp usually has a pH lower than umbilical venous blood, and
correlates well with fetal arterial values. However, scalp edema can result in erroneous results. A scalp pH value
of <7.20 has traditionally been used to represent the critical value for identifying fetal acidosis [68-70]. However, a
scalp pH below 7.15 is more representative of the 10th percentile and is closer to the threshold currently used in
umbilical cord blood analysis to define fetal acidemia associated with neurological deficits [71]. (See "Umbilical
cord
blood
acid-base
analysis".)
The accuracy of intermittent fetal scalp pH assessment for predicting neonatal acidosis with subsequent
neurologic sequelae has been questioned [71]. It is no longer used in many institutions [72], although its use can
result in fewer cesarean deliveries performed for the indication of nonreassuring fetal status [68,73].

The test has poor sensitivity and positive predictive value (PPV) for predicting umbilical arterial pH <7.0
(sensitivity 35 percent, PPV 9 percent) [71]. The test also has poor sensitivity and PPV for identifying newborns
with hypoxic-ischemic encephalopathy (sensitivity 50 percent, PPV 3 percent). However, logistics and skill in
sampling, as well as laboratory capability, may affect results.
Fetal lactate concentration Fetal lactate concentration is determined by collecting a sample of capillary blood
from the fetal scalp, similar to the method used for assessing scalp pH; however, much less fetal blood is needed
(5 microL versus 35 microL) [74]. A large multicenter randomized trial compared the performance of pH
measurement in fetal scalp blood with the performance of lactate measurement for predicting fetal acidemia and
obstetrical and neonatal outcome [75]. There were no significant differences between the groups in any outcome,
although sampling failure rates were lower in the lactate group (1 versus 10 percent for pH measurement). A
smaller study reported similar results (1.3 versus 20.6 percent for pH measurement) [76].
Lactate has been proposed as the major determinant of fetal pH and it has been known for many years that
lactate measurements are as valid as pH measurement, but, as discussed above, measurement of lactate levels
was problematic [77-79]. We do not measure fetal lactate concentrations routinely because of the practical
difficulties of obtaining results, which are similar to the difficulties of getting results of fetal pH measurements (see
above). Since rapid enzymatic assays for lactate are now available, it may become a more useful test in the
evaluation of possible acidosis.

Fetal pulse oximetry Data from human and animal studies suggest that fetal arterial oxygen saturation (SaO2 by blood
gas co-oximetry) >30 percent is usually associated with pH >7.13 [80]. In humans, the mean fetal oxygen saturation
(SpO2 by fetal pulse oximetry) during the first and second stages of labor is 5910 percent and 5310 percent,

respectively [81]. In the setting of a nonreassuring FHR pattern, fetal SpO2 <30 percent for greater than 10 minutes has
been associated with an increased risk of fetal acidosis [82-84].
There is no evidence that assessment of fetal oxygen saturation by fetal pulse oximetry (FPO) as an adjunct to electronic
FHR monitoring improves neonatal outcome. Four randomized trials have compared the outcome of pregnancies in which
FPO results were available for intrapartum clinical management to the outcome of controls in which this information was
not available [85-88]. All four trials found that use of FPO had no significant effect on the overall rate of cesarean delivery
or on the rate of any maternal or infant outcome evaluated; the rates were similar in both groups. In two of the four trials (n
= 1010, n = 601 subjects), the rate of cesarean delivery performed because of nonreassuring FHR tracings was lower
when FPO was used, but the difference was more cesareans for other indications [85,87]. However, these findings were
not supported by the largest trial (n = 5341 subjects) [88], which also found that low oxygen saturation was present almost
as often in fetuses with reassuring FHR patterns as in fetuses with nonreassuring FHR patterns: 25 and 35 percent of
fetuses, respectively.
We do not recommend use of this device because there is insufficient evidence of any benefit.
Management of nonreassuring FHR patterns

Determine the likely cause of the abnormality, if possible (eg, abruptio placenta, cord prolapse, maternal
medication (table 3), rapid descent of fetal head).
Attempt to correct the problem or initiate general measures to improve fetal oxygenation [89-98]. The approach
for specific FHR patterns is summarized in the table (table 4) [99] and discussed in detail separately.
(See"Management of intrapartum category I, II, and III fetal heart rate tracings".)
If the nonreassuring pattern does not improve within a few minutes, perform ancillary tests to determine the fetal
condition. (See 'Further evaluation of nonreassuring patterns' above.)
Determine whether operative intervention (cesarean or instrumental vaginal delivery) is needed, and the urgency
of this intervention. Prepare for rapid intervention, if needed.

The presence of accelerations almost always assures the absence of fetal acidosis [31,32]. If such accelerations are not
observed, they should be elicited by manual or vibroacoustic stimulation. If accelerations cannot be elicited, further
evaluation by fetal scalp sampling for pH, lactate concentration, or fetal ECG is indicated to help clarify the fetal acid-base
status. Combined results from two series showed that 37 of 87 fetuses (45 percent) in whom accelerations could not be
elicited were acidotic [30,100]. (See 'FHR response to stimulation' above.)
If accelerations cannot be elicited, then variability should be evaluated. Good FHR variability is strongly associated (98
percent) with an umbilical pH >7.15 [101]. If variability is decreased in the setting of repetitive decelerations and absent
accelerations, we suggest delivery. The combination of undetectable or minimal FHR variability and late or variable
decelerations is the FHR pattern most predictive of acidemia, although only one in four to five fetuses with these findings
will be acidotic [101].
Serial evaluation every 20 to 30 minutes is necessary if the FHR pattern remains nonreassuring [99]. Expeditious delivery
is indicated for persistent nonreassuring FHR patterns associated with acidosis or if the presence of acidosis cannot be
excluded (ie, category III tracings (table 2)).
SUMMARY AND RECOMMENDATIONS

The rationale for monitoring the FHR during labor is that the fetal response to blood volume changes, acidemia,
and hypoxemia may be reflected indirectly by FHR patterns since the fetal medullary cardiorespiratory center
modulates the fetal heart rate. (See 'Introduction' above.)
Two commonly used modalities for intrapartum FHR monitoring are continuous electronic FHR monitoring and
intermittent auscultation. In uncomplicated pregnancies, there is no evidence that one of these techniques is
better than the other or that use of these techniques reduces the incidence of stillbirth, low Apgar scores, neonatal
intensive care unit admission, neurological injury, or cerebral palsy. There is evidence that continuous electronic
FHR monitoring leads to higher operative delivery rates than auscultation. (See 'Effectiveness of intrapartum FHR
monitoring' above.)

Medicolegal precedent in the United States mandates some form of intrapartum FHR monitoring. For high-risk
pregnant women, we suggest continuous rather than intermittent intrapartum FHR monitoring (Grade 2C). For low
risk women, we suggest either intermittent or continuous electronic FHR monitoring (Grade 2C). Frequent
intermittent auscultation is cumbersome and difficult for most nursing services to achieve. (See 'Effectiveness of
intrapartum FHR monitoring' above and 'Indications' above.)
The three tier approach (table 2) is a useful method for evaluation and management of FHR patterns. (See 'Three
tier approach' above.)
Transient episodes of hypoxemia, such as during a contraction or temporary cord compression, are generally
well-tolerated by the fetus. Repeated or prolonged episodes, especially if severe, may lead to fetal acidosis.
Further evaluation of a nonreassuring FHR tracing is indicated to distinguish the fetus who is not hypoxemic, or
hypoxemic but well compensated, from one who is acidotic. We recommend assessing the FHR response to
stimulation. In contrast to other modalities, this test is readily available, easy to perform, inexpensive, and
comfortable for the patient. (See 'Further evaluation of nonreassuring patterns' above.)
Normal FHR variability is strongly associated (98 percent) with an umbilical pH >7.15. The combination of
undetectable or minimal FHR variability and late or variable decelerations with late recovery are the FHR patterns
most predictive of acidemia, although only about 23 percent of fetuses with these findings will be acidotic.
(See 'Management of nonreassuring FHR patterns' above.)
If possible, determine the cause of the nonreassuring FHR and initiate potentially corrective interventions (eg,
discontinuing uterotonic drugs, maternal position change, IV fluids, oxygen). We recommend expeditious delivery
for persistent nonreassuring FHR patterns associated with acidosis or if the presence of acidosis cannot be
excluded (Grade 1C). (See 'Management of nonreassuring FHR patterns' above.)

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REFERENCES
1. Freeman RK. Problems with intrapartum fetal heart rate monitoring interpretation and patient management. Obstet
Gynecol 2002; 100:813.
2. WALKER N. The case for conservatism in management of foetal distress. Br Med J 1959; 2:1221.
3. Benson RC, Shubeck F, Deutschberger J, et al. Fetal heart rate as a predictor of fetal distress. A report from the
collaborative project. Obstet Gynecol 1968; 32:259.
4. Young BK. Monitoring the fetal heart: a continuing controversy. Obstet Gynecol Surv 1995; 50:699.
5. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 106: Intrapartum fetal heart rate
monitoring: nomenclature, interpretation, and general management principles. Obstet Gynecol 2009; 114:192.
6. Alfirevic Z, Devane D, Gyte GM. Continuous cardiotocography (CTG) as a form of electronic fetal monitoring (EFM) for
fetal assessment during labour. Cochrane Database Syst Rev 2006; :CD006066.
7. Graham EM, Petersen SM, Christo DK, Fox HE. Intrapartum electronic fetal heart rate monitoring and the prevention of
perinatal brain injury. Obstet Gynecol 2006; 108:656.
8. Thacker SB, Stroup DF, Peterson HB. Efficacy and safety of intrapartum electronic fetal monitoring: an update. Obstet
Gynecol 1995; 86:613.
9. Vintzileos AM, Nochimson DJ, Antsaklis A, et al. Comparison of intrapartum electronic fetal heart rate monitoring versus
intermittent auscultation in detecting fetal acidemia at birth. Am J Obstet Gynecol 1995; 173:1021.
10. Larma JD, Silva AM, Holcroft CJ, et al. Intrapartum electronic fetal heart rate monitoring and the identification of metabolic
acidosis and hypoxic-ischemic encephalopathy. Am J Obstet Gynecol 2007; 197:301.e1.
11. Chen HY, Chauhan SP, Ananth CV, et al. Electronic fetal heart rate monitoring and its relationship to neonatal and infant
mortality in the United States. Am J Obstet Gynecol 2011; 204:491.e1.
12. Nelson KB, Dambrosia JM, Ting TY, Grether JK. Uncertain value of electronic fetal monitoring in predicting cerebral palsy.
N Engl J Med 1996; 334:613.
13. Phelan JP, Kim JO. Fetal heart rate observations in the brain-damaged infant. Semin Perinatol 2000; 24:221.
14. MacDonald D, Grant A, Sheridan-Pereira M, et al. The Dublin randomized controlled trial of intrapartum fetal heart rate
monitoring. Am J Obstet Gynecol 1985; 152:524.
15. U.S. Preventive Services Task Force. Intrapartum Electronic Fetal Monitoring. www.ahcpr.gov/clinic/uspstf/uspsiefm.htm.
(Accessed 3/7/05).
16. Canadian Task Force on Preventive Health Care. www.ctfphc.org/. (Accessed 3/7/05).
17. National Institute for Health and Clinical Excellence (NICE). Intrapartum Care: management and delivery of care to
women in labour. London, NICE, 2007.
18. Antenatal Diagnosis III. NIH publ. #79-1973, Wash DC. 1979.
19. McCartney PR. Computer analysis of the fetal heart rate. J Obstet Gynecol Neonatal Nurs 2000; 29:527.

20. Agrawal SK, Doucette F, Gratton R, et al. Intrapartum computerized fetal heart rate parameters and metabolic acidosis at
birth. Obstet Gynecol 2003; 102:731.
21. Li X, Zheng D, Zhou S, et al. Approximate entropy of fetal heart rate variability as a predictor of fetal distress in women at
term pregnancy. Acta Obstet Gynecol Scand 2005; 84:837.
22. Van Laar JO, Porath MM, Peters CH, Oei SG. Spectral analysis of fetal heart rate variability for fetal surveillance: review
of the literature. Acta Obstet Gynecol Scand 2008; 87:300.
23. Costa A, Ayres-de-Campos D, Costa F, et al. Prediction of neonatal acidemia by computer analysis of fetal heart rate and
ST event signals. Am J Obstet Gynecol 2009; 201:464.e1.
24. Nielsen PV, Stigsby B, Nickelsen C, Nim J. Intra- and inter-observer variability in the assessment of intrapartum
cardiotocograms. Acta Obstet Gynecol Scand 1987; 66:421.
25. Beaulieu MD, Fabia J, Leduc B, et al. The reproducibility of intrapartum cardiotocogram assessments. Can Med Assoc J
1982; 127:214.
26. Chauhan SP, Klauser CK, Woodring TC, et al. Intrapartum nonreassuring fetal heart rate tracing and prediction of adverse
outcomes: interobserver variability. Am J Obstet Gynecol 2008; 199:623.e1.
27. Electronic fetal heart rate monitoring: research guidelines for interpretation. National Institute of Child Health and Human
Development Research Planning Workshop. Am J Obstet Gynecol 1997; 177:1385.
28. Blackwell SC, Grobman WA, Antoniewicz L, et al. Interobserver and intraobserver reliability of the NICHD 3-Tier Fetal
Heart Rate Interpretation System. Am J Obstet Gynecol 2011; 205:378.e1.
29. Macones GA, Hankins GD, Spong CY, et al. The 2008 National Institute of Child Health and Human Development
workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines. Obstet
Gynecol 2008; 112:661.
30. Clark SL, Gimovsky ML, Miller FC. The scalp stimulation test: a clinical alternative to fetal scalp blood sampling. Am J
Obstet Gynecol 1984; 148:274.
31. Krebs HB, Petres RE, Dunn LJ, Smith PJ. Intrapartum fetal heart rate monitoring. VI. Prognostic significance of
accelerations. Am J Obstet Gynecol 1982; 142:297.
32. Powell OH, Melville A, MacKenna J. Fetal heart rate acceleration in labor: excellent prognostic indicator. Am J Obstet
Gynecol 1979; 134:36.
33. Young BK, Weinstein HM. Moderate fetal bradycardia. Am J Obstet Gynecol 1976; 126:271.
34. Young BK, Katz M, Klein SA. Intrapartum fetal cardiac arrhythmias. Obstet Gynecol 1979; 54:427.
35. Westgate JA, Wibbens B, Bennet L, et al. The intrapartum deceleration in center stage: a physiologic approach to the
interpretation of fetal heart rate changes in labor. Am J Obstet Gynecol 2007; 197:236.e1.
36. Myers RE, Mueller-Heubach E, Adamsons K. Predictability of the state of fetal oxygenation from a quantitative analysis of
the components of late deceleration. Am J Obstet Gynecol 1973; 115:1083.
37. Frasch MG, Grasch MG, Frasch MG, et al. Measures of acidosis with repetitive umbilical cord occlusions leading to fetal
asphyxia in the near-term ovine fetus. Am J Obstet Gynecol 2009; 200:200.e1.
38. Krebs HB, Petres RE, Dunn LJ. Intrapartum fetal heart rate monitoring. VIII. Atypical variable decelerations. Am J Obstet
Gynecol 1983; 145:297.
39. Katz M, Wilson SJ, Young BK. Sinusoidal fetal heart rate. II. Continuous tissue pH studies. Am J Obstet Gynecol 1980;
136:594.
40. Young BK, Katz M, Wilson SJ. Sinusoidal fetal heart rate. I. Clinical significance. Am J Obstet Gynecol 1980; 136:587.
41. Johnson TR Jr, Compton AA, Rotmensch J, et al. Significance of the sinusoidal fetal heart rate pattern. Am J Obstet
Gynecol 1981; 139:446.
42. Murotsuki J, Kimura Y, Iwamoto M, et al. [Power spectral analysis of spontaneous rhythm in peripheral blood flow in fetal
lamb]. Nihon Sanka Fujinka Gakkai Zasshi 1993; 45:1394.
43. van Woerden EE, van Geijn HP, Swartjes JM, et al. Fetal heart rhythms during behavioural state 1F. Eur J Obstet
Gynecol Reprod Biol 1988; 28:29.
44. Lustig-Gillman I, Young BK, Silverman F, et al. Fetal intraventricular hemorrhage: sonographic diagnosis and clinical
implications. J Clin Ultrasound 1983; 11:277.
45. Schifrin BS, Hamilton-Rubinstein T, Shields JR. Fetal heart rate patterns and the timing of fetal injury. J Perinatol 1994;
14:174.
46. Phelan JP, Ahn MO. Perinatal observations in forty-eight neurologically impaired term infants. Am J Obstet Gynecol 1994;
171:424.
47. Ahn MO, Korst LM, Phelan JP. Normal Fetal Heart Rate Pattern in the Brain-damaged Infant: A Failure of Intrapartum
Fetal Monitoring? J Matern Fetal Investig 1998; 8:58.
48. Terao T, Kawashima Y, Noto H, et al. Neurological control of fetal heart rate in 20 cases of anencephalic fetuses. Am J
Obstet Gynecol 1984; 149:201.
49. McWhinney NA, Knowles S, Green HL, Gordon H. Transmission of the maternal electrocardiograph via a fetal scalp
electrode in the presence of intrauterine death. Case report. Br J Obstet Gynaecol 1984; 91:1046.
50. Phelan JP. Labor admission test. Clin Perinatol 1994; 21:879.
51. Mires G, Williams F, Howie P. Randomised controlled trial of cardiotocography versus Doppler auscultation of fetal heart
at admission in labour in low risk obstetric population. BMJ 2001; 322:1457.

52. Impey L, Reynolds M, MacQuillan K, et al. Admission cardiotocography: a randomised controlled trial. Lancet 2003;
361:465.
53. Blix E, Sviggum O, Koss KS, ian P. Inter-observer variation in assessment of 845 labour admission tests: comparison
between midwives and obstetricians in the clinical setting and two experts. BJOG 2003; 110:1.
54. Devane D, Lalor JG, Daly S, et al. Cardiotography versus intermittent auscultation of fetal heart on admission to labour
ward for assessment of fetal wellbeing. Cochrane Database Syst Rev 2012; :CD005122.
55. Hofmeyr GJ, Kulier R. Operative versus conservative management for 'fetal distress' in labour. Cochrane Database Syst
Rev 2012; :CD001065.
56. American College of Obstetricians and Gynecologists. Practice bulletin no. 116: Management of intrapartum fetal heart
rate tracings. Obstet Gynecol 2010; 116:1232.
57. Committee on Obstetric Practice, American College of Obstetricians and Gynecologists. ACOG Committee Opinion.
Number 326, December 2005. Inappropriate use of the terms fetal distress and birth asphyxia. Obstet Gynecol 2005;
106:1469.
58. Parer JT, Ikeda T. A framework for standardized management of intrapartum fetal heart rate patterns. Am J Obstet
Gynecol 2007; 197:26.e1.
59. Skupski DW, Rosenberg CR, Eglinton GS. Intrapartum fetal stimulation tests: a meta-analysis. Obstet Gynecol 2002;
99:129.
60. Edersheim TG, Hutson JM, Druzin ML, Kogut EA. Fetal heart rate response to vibratory acoustic stimulation predicts fetal
pH in labor. Am J Obstet Gynecol 1987; 157:1557.
61. Trochez RD, Sibanda T, Sharma R, Draycott T. Fetal monitoring in labor: are accelerations good enough? J Matern Fetal
Neonatal Med 2005; 18:349.
62. Nicolaides KH, Economides DL, Soothill PW. Blood gases, pH, and lactate in appropriate- and small-for-gestational-age
fetuses. Am J Obstet Gynecol 1989; 161:996.
63. Mansano RZ, Beall MH, Ross MG. Fetal ST segment heart rate analysis in labor: improvement of intervention criteria
using interpolated base deficit. J Matern Fetal Neonatal Med 2007; 20:47.
64. Vayssiere C, Haberstich R, Sebahoun V, et al. Fetal electrocardiogram ST-segment analysis and prediction of neonatal
acidosis. Int J Gynaecol Obstet 2007; 97:110.
65. Norn H, Luttkus AK, Stupin JH, et al. Fetal scalp pH and ST analysis of the fetal ECG as an adjunct to cardiotocography
to predict fetal acidosis in labor--a multi-center, case controlled study. J Perinat Med 2007; 35:408.
66. Neilson JP. Fetal electrocardiogram (ECG) for fetal monitoring during labour. Cochrane Database Syst Rev 2012;
4:CD000116.
67. Becker JH, Bax L, Amer-Whlin I, et al. ST analysis of the fetal electrocardiogram in intrapartum fetal monitoring: a metaanalysis. Obstet Gynecol 2012; 119:145.
68. Zalar RW Jr, Quilligan EJ. The influence of scalp sampling on the cesarean section rate for fetal distress. Am J Obstet
Gynecol 1979; 135:239.
69. SALING E. [BLOOD GAS RELATIONS AND THE ACID-BASE EQUILIBRIUM OF THE FETUS IN AN UNCOMPLICATED
COURSE OF DELIVERY]. Z Geburtshilfe Gynakol 1964; 161:262.
70. Banta HD, Thacker SB. Assessing the costs and benefits of electronic fetal monitoring. Obstet Gynecol Surv 1979;
34:627.
71. Kruger K, Hallberg B, Blennow M, et al. Predictive value of fetal scalp blood lactate concentration and pH as markers of
neurologic disability. Am J Obstet Gynecol 1999; 181:1072.
72. Perkins RP. Requiem for a heavyweight: the demise of scalp blood pH sampling. J Matern Fetal Med 1997; 6:298.
73. Young DC, Gray JH, Luther ER, Peddle LJ. Fetal scalp blood pH sampling: its value in an active obstetric unit. Am J
Obstet Gynecol 1980; 136:276.
74. Westgren M, Kruger K, Ek S, et al. Lactate compared with pH analysis at fetal scalp blood sampling: a prospective
randomised study. Br J Obstet Gynaecol 1998; 105:29.
75. Wiberg-Itzel E, Lipponer C, Norman M, et al. Determination of pH or lactate in fetal scalp blood in management of
intrapartum fetal distress: randomised controlled multicentre trial. BMJ 2008; 336:1284.
76. Westgren M, Kublickas M, Kruger K. Role of lactate measurements during labor. Obstet Gynecol Surv 1999; 54:43.
77. Suidan JS, Wasserman JF, Young BK. Placental contribution to lactate production by the human fetoplacental unit. Am J
Perinatol 1984; 1:306.
78. Suidan JS, Antoine C, Silverman F, et al. Human maternal-fetal lactate relationships. J Perinat Med 1984; 12:211.
79. Suidan JS, Young BK. Outcome of fetuses with lactic acidemia. Am J Obstet Gynecol 1984; 150:33.
80. Dildy GA. Fetal pulse oximetry. Clin Obstet Gynecol 2011; 54:66.
81. Dildy GA, van den Berg PP, Katz M, et al. Intrapartum fetal pulse oximetry: fetal oxygen saturation trends during labor and
relation to delivery outcome. Am J Obstet Gynecol 1994; 171:679.
82. Nonnenmacher A, Hopp H, Dudenhausen J. Predictive value of pulse oximetry for the development of fetal acidosis. J
Perinat Med 2010; 38:83.
83. Khnert M, Seelbach-Gebel B, Butterwegge M. Predictive agreement between the fetal arterial oxygen saturation and
fetal scalp pH: results of the German multicenter study. Am J Obstet Gynecol 1998; 178:330.
84. Seelbach-Gbel B, Heupel M, Khnert M, Butterwegge M. The prediction of fetal acidosis by means of intrapartum fetal
pulse oximetry. Am J Obstet Gynecol 1999; 180:73.

85. Garite TJ, Dildy GA, McNamara H, et al. A multicenter controlled trial of fetal pulse oximetry in the intrapartum
management of nonreassuring fetal heart rate patterns. Am J Obstet Gynecol 2000; 183:1049.
86. Klauser CK, Christensen EE, Chauhan SP, et al. Use of fetal pulse oximetry among high-risk women in labor: a
randomized clinical trial. Am J Obstet Gynecol 2005; 192:1810.
87. East CE, Brennecke SP, King JF, et al. The effect of intrapartum fetal pulse oximetry, in the presence of a nonreassuring
fetal heart rate pattern, on operative delivery rates: a multicenter, randomized, controlled trial (the FOREMOST trial). Am J
Obstet Gynecol 2006; 194:606.e1.
88. Bloom SL, Spong CY, Thom E, et al. Fetal pulse oximetry and cesarean delivery. N Engl J Med 2006; 355:2195.
89. Kulier R, Hofmeyr GJ. Tocolytics for suspected intrapartum fetal distress. Cochrane Database Syst Rev 2000;
:CD000035.
90. Simpson KR, James DC. Efficacy of intrauterine resuscitation techniques in improving fetal oxygen status during labor.
Obstet Gynecol 2005; 105:1362.
91. Clark SL, Cotton DB, Pivarnik JM, et al. Position change and central hemodynamic profile during normal third-trimester
pregnancy and post partum. Am J Obstet Gynecol 1991; 164:883.
92. Althabe O Jr, Schwarcz RL, Pose SV, et al. Effects on fetal heart rate and fetal pO2 of oxygen administration to the
mother. Am J Obstet Gynecol 1967; 98:858.
93. Tomimatsu T, Pereyra Pena J, Hatran DP, Longo LD. Maternal oxygen administration and fetal cerebral oxygenation:
studies on near-term fetal lambs at both low and high altitude. Am J Obstet Gynecol 2006; 195:535.
94. Haydon ML, Gorenberg DM, Nageotte MP, et al. The effect of maternal oxygen administration on fetal pulse oximetry
during labor in fetuses with nonreassuring fetal heart rate patterns. Am J Obstet Gynecol 2006; 195:735.
95. Fawole B, Hofmeyr GJ. Maternal oxygen administration for fetal distress. Cochrane Database Syst Rev 2003; :CD000136.
96. Royal College of Obstetricians and Gynaecologists. The use of electronic fetal monitoring. The use and interpretation of
cardiotocography in intrapartum fetal surveillance. London: RCOG Press; 2001. p.136 (Evidence-based clinical
guidelines; no. 8).
97. Pullen KM, Riley ET, Waller SA, et al. Randomized comparison of intravenous terbutaline vs nitroglycerin for acute
intrapartum fetal resuscitation. Am J Obstet Gynecol 2007; 197:414.e1.
98. Egarter CH, Husslein PW, Rayburn WF. Uterine hyperstimulation after low-dose prostaglandin E2 therapy: tocolytic
treatment in 181 cases. Am J Obstet Gynecol 1990; 163:794.
99. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin. Clinical Management Guidelines for
Obstetrician-Gynecologists, Number 70, December 2005 (Replaces Practice Bulletin Number 62, May 2005). Intrapartum
fetal heart rate monitoring. Obstet Gynecol 2005; 106:1453.
100.
Smith CV, Nguyen HN, Phelan JP, Paul RH. Intrapartum assessment of fetal well-being: a comparison of fetal
acoustic stimulation with acid-base determinations. Am J Obstet Gynecol 1986; 155:726.
101.
Parer JT, King T, Flanders S, et al. Fetal acidemia and electronic fetal heart rate patterns: is there evidence of an
association? J Matern Fetal Neonatal Med 2006; 19:289.

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