Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5

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Seminars in Fetal & Neonatal Medicine

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Fetal heart rate monitoring

Michael P. Nageotte*
Miller Children's and Women's Hospital, Long Beach, 2801 Atlantic Avenue, Long Beach, CA 90801, USA

s u m m a r y
Keywords:
Electronic fetal monitoring
Category I, II and III fetal tracings
Late decelerations
Variable decelerations
Sinusoidal

Electronic fetal heart rate monitoring is a widely utilized means of assessment of fetal status during labor.
Whereas little evidence exists regarding efcacy, this modality continues to be used extensively in every
modern labor and delivery unit in developed countries. It is of importance that all providers of health
care to the woman in labor and her newborn have a clear understanding of the basic pathophysiology of
fetal heart rate monitoring and an appreciation for labor course and concerns as they arise in order to
optimize outcomes and patient safety.
2015 Elsevier Ltd. All rights reserved.

1. Introduction
Electronic fetal heart rate monitoring (EFM) is widely used in
nearly every modern labor and delivery unit in the developed
world, and was initially introduced for clinical use in the late 1960s
as an alternative to the very labor-intensive auscultation of the fetal
heart. EFM uses either the direct electrical signal of the fetal heart
rate captured through a fetal electrode (direct) or more usually
employs ultrasound technology and Doppler physics to interpret
the changes in frequency of sound waves reected from pulsations
within fetal vessels (indirect). The aim of such monitoring, which is
generally continuous, is to enable clinicians to accurately identify
hypoxic fetuses at risk for deterioration and who might benet
from expedited or immediate delivery either vaginally or by Cesarean section. Whereas EFM remains an accepted component of
labor management and fetal assessment, the true positive predictive value for metabolic acidosis is low. Unfortunately, this often
results in unnecessary interventions and a signicant increase in
the Cesarean section rate for concerns regarding fetal intolerance of
labor. Such an observation may be the result of appropriate early
intervention before worsening of metabolic condition occurs or
inappropriate early intervention from a misreading of the information generated from the fetal monitor. Whereas the negative
predictive value is exceptionally high (a normal fetal heart rate is
associated with a normally oxygenated and non-acidotic fetus) and
the rate of unexpected intrapartum stillbirth approaches zero,
nonetheless, despite the wide usage of EFM, unfortunately there

* Tel.: 1 562 933 2738; fax: 1 562 933 2740.

E-mail address: mnageotte@memorialcare.org.

has been no signicant decrease in the incidence of long-term

neurologic morbidity (including cerebral palsy) or several other
measures of neonatal wellbeing for the term newborn [1]. Despite
these factors, EFM will continue to be utilized and needs to be
understood with clinical concerns clearly communicated to provide
the best care to all patients during pregnancy and in labor. Every
member of the health care team needs to have an understanding of
the suspected fetal status, which is often directly related to ndings
of changes in the fetal heart monitor so care can be best coordinated and effectively rendered in both non-emergency and emergency situations.
2. Physiologic basis of fetal monitoring
Fetal heart rate monitoring is essentially an observation of
ongoing human fetal physiology, most often during labor or prior to
labor, in the assessment of patients with certain high-risk conditions for which antepartum fetal surveillance is indicated. The
question asked in all situations is: what is the adequacy of fetal
oxygenation at this point? Since there are certain characteristic
changes in the fetal heart rate pattern resulting from various hypoxic and non-hypoxic inuences, one needs to appreciate the basic
physiology of fetal respiratory exchange and resultant control of the
fetal heart rate.
The placenta functions as an extracorporeal support system for
the human fetus, serving as the fetal lung (respiratory exchange),
kidney (excretion), gastrointestinal tract (nutrition) and skin surface (heat exchange). In addition, it plays a critical role in protecting
the fetus against certain substances in the maternal circulation,
which may be harmful particularly during early gestation. Further,
the placenta actively produces several steroid and protein

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1744-165X/ 2015 Elsevier Ltd. All rights reserved.

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M.P. Nageotte / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5

hormones critical to successful maintenance of the gestation and

initiation of parturition. The human placenta is termed a hemochorial type, since maternal blood is extravascular when it comes
into contact with the fetal chorionic villus. Exchange of oxygen,
carbon dioxide, nutrients, water, heat, and waste products occurs
within the placenta and must cross two layers of fetal trophoblast,
the fetal connective tissue within the villus and the fetal capillary
wall. Maternal blood ow to the uterus, and in turn to the placenta,
results principally from the uterine arteries as well as from the
internal iliac and ovarian arteries, and it markedly increases over
the course of pregnancy. The arteries feeding the intervillous space
where fetalematernal exchange occurs are termed spiral arteries,
and they must traverse the maternal myometrium. Flow through
these spiral arteries is directly affected by anything that inuences
maternal cardiac output (e.g., hypotension, hemorrhage, sepsis)
with immediate changes noted in the fetal heart rate in response to
the decrease in uterine blood ow. Further and most importantly,
as the uterus contracts, the pressure generated within the myometrium may exceed the intra-arterial pressure of the spiral arteries, resulting in intermittent cessation of maternal blood ow
into the intervillous space. If such stasis is prolonged or associated
with a signicantly compromised placenta (small, infarcted,
inamed or senescent), either acute or chronic episodes of hypoxia
and potentially acidosis in the fetus may result. Such changes are
reected in specic pattern changes in the fetal heart rate. Further,
these conditions may be mitigated by position change of the
mother to a lateral position or by directly addressing and correcting
the causes of the compromised maternal cardiac output. The fetus
also responds to such challenges by redistributing blood ow to
certain vital organs e such as the brain, the heart, and the adrenal
glands e while diminishing blood ow to less vital organs including
the lungs, liver, kidneys, intestine, and periphery. However, if such
changes persist, there may be a loss of cerebral autoregulation as
well as an eventual decrease in fetal cardiac output. Cerebral blood
ow is maintained initially by a fall in fetal cerebral vascular
resistance by as much as 50%. However, if the physiologic condition
continues to be compromised or worsens, then a reduction of cerebral blood ow may result, leading to potential fetal neuronal
injury or death.
3. Essentials of fetal heart rate regulation
Just as in the adult, the fetal heart rate results from the inuences of various intrinsic and extrinsic factors that modify the
rate. The heart rate is actually the reciprocal of the interval between
successive heart contractions. EFM uses the peak of the fetal electrocardiogram (ECG) R-wave to signify the time of the beat. The rate
is then calculated by the interval between consecutive fetal ECG Rwaves when using direct fetal electrodes, while it is calculated
between consecutive pulse waves generated by myocardial contractions when using external monitoring employing ultrasound
technology. It is the change in the fetal heart rate that is observed in
various conditions that constitutes the basis of EFM, and one must
appreciate the various factors that inuence or modify the fetal
heart rate to be able to correctly interpret the patterns generated by
the fetal monitor.
The baseline heart rate of the fetus must be established to
correctly interpret fetal tracings. Baseline heart rate decreases with
advancing gestational age, being higher in early pregnancy than
later. Further, the normal rate for the baseline is between 110 and
160 beats per minute (bpm). Such a rate results normally from the
atrial pacemaker with modulation by parasympathetic and sympathetic factors. Rarely seen are cases of complete fetal heart block
(with the rate usually about 60 bpm) resulting from the intrinsic
ventricular or nodal rate.

In addition to baseline heart rate, key to interpreting EFM is the

variability of the baseline heart rate. Variability is the true variance
in time between consecutive heart beats, and it is normally present in a healthy fetus. Variability results from direct sympathetic
and parasympathetic effects on the heart, which originate either
in the brain stem and are conducted to the heart via the vagus
nerve, or may arise from direct humoral stimulation of cardiac
receptors responding to the release of epinephrine from the fetal
adrenal glands. It is thought that higher brain centers also play a
role in variability of the heart rate. Factors that inuence the
central nervous system such as drugs, hypoxia, metabolic acidosis,
or brain injury affect the baseline variability of the heart rate. The
presence of moderate variability of the heart rate is one of the
most reliable markers of normal oxygenation and absence of
acidosis, and its presence or absence is key to the correct interpretation of EFM.
A normally oxygenated fetus has certain characteristics of its
heart rate. After 32 weeks of gestation, it is well established that
normal fetuses have episodes of acceleration of their heart rate
associated with fetal movements. This is termed reactivity, and,
when present, has a very high association with a normal fetal state
of oxygenation. Whereas there is not necessarily an acceleration of
the heart rate every time a fetus moves, the converse is true. A
normally oxygenated fetus generally demonstrates accelerations at
least every 60e80 min. Certain drugs that affect the central nervous
system can suppress accelerations, as can certain types of primary
central nervous system abnormalities. A basic tenet that has been
demonstrated experimentally is that in a fetus undergoing progressive hypoxia, there will be the appearance of decelerations
before the absence of accelerations.
Fetal monitoring is assessed both in the absence and in the
presence of uterine contractions. As discussed, a uterine contraction may cause intermittent decreases in maternal blood ow into
the intervillous space. This may result in stasis of blood with
inadequate exchange between the mother and fetus of oxygen,
carbon dioxide, and other products. If signicant hypoxia of the
fetus occurs, there may be a decrease in fetal cerebral blood ow,
resulting in a change of the sympathetic and parasympathetic
control of the fetal heart. This may lead to a slowing of the fetal
heart rate or a deceleration. Another frequently occurring mechanism explaining the occurrence of the deceleration is intermittent
occlusion of blood ow through the umbilical cord due to cord
compression or stretching. Such changes, particularly when associated with uterine activity, are considered contraction-related or
periodic changes in the fetal heart rate. Again, key to interpretation of these changes in the fetal heart rate is the understanding
of their physiologic bases.

4. Early decelerations
An early deceleration is a uniformly shaped deceleration of
gradual onset and gradual return to baseline associated with a
uterine contraction. The degree of slowing generally is proportional
to the strength of the associated uterine contraction, and the timing
of the deceleration accompanying the uterine contraction generally
mirrors the contraction with the early deceleration nadir at the
peak of the contraction. Early decelerations are thought to result
from fetal head compression altering cerebral blood ow and
leading to cardiac slowing through a vagal reex. This is supported
by the experimental nding that early decelerations can be abolished or altered by the administration of atropine. Early decelerations are generally seen in active labor and are a pattern not
associated with fetal hypoxia, acidosis, or subsequent depressed
Apgar scores.

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M.P. Nageotte / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5

5. Variable decelerations
The most common deceleration of the fetal heart rate is the
variable deceleration. Variable decelerations frequently occur in
both the rst and second stages of labor and are usually indicative
of some degree of obstruction to fetal blood ow through the
umbilical cord or compression of the vessels within the cord. Again,
the mechanism of such deceleration is thought to be mediated
through the vagus nerve and often bears no temporal relationship
to uterine contractions. Hypoxia is clearly not required to produce
variable decelerations, as changes in fetal blood pressure associated
with umbilical cord compression alone can produce such patterns.
Data from studies using continuous fetal pulse oximetry also have
demonstrated that deep and relatively prolonged variable decelerations occur often without any change in fetal oxygen saturation. Pregnancies complicated with decreased amniotic uid
(oligohydramnios) are associated with more frequent patterns of
variable decelerations, and this is thought to be related to the loss of
the protective effect of the amniotic uid on the fetal umbilical
cord. Such a relationship is further supported by the fact that, in
cases with diminished amniotic uid in labor treated with saline
amnio-infusion via a transcervical catheter, there is a reduction in
the frequency of variable decelerations in both preterm and term
fetuses compared to controls [2].
Variable decelerations characteristically are very abrupt in onset
and return to baseline. They may be associated with fetal movement or uterine contractions and are most commonly seen in the
second stage of labor associated with maternal Valsalva and
pushing efforts. Variable decelerations have different degrees of
decrease of heart rate, time below baseline, and rate of return to
baseline. The vast majority of variable decelerations are not associated with signicant hypoxia or acidosis. Because of their frequency and unpredictability, variable decelerations must be
evaluated and managed closely. With cord compression that is
prolonged and repetitive, there may be the development of progressive fetal hypoxia and respiratory acidosis. Thus, variable decelerations have been graded as mild, moderate, and severe. Mild
variable decelerations last for <30 s regardless of level or a deceleration not <70e80 bpm of any duration. Moderate variable decelerations have a nadir of <80 bpm regardless of duration. Severe
variable decelerations are both <70 bpm and have a duration of
>60 s. More recently, variable decelerations are no longer subclassied as mild, moderate, or severe, but must be a decrease of
15 bpm lasting 15 s and <2 min in individual duration. Variable
decelerations that are recurrent (occurring with >50% of contractions) and that progress to greater depth and longer duration are
moderate variability of the baseline heart rate, or the occurrence of
spontaneous or induced accelerations strongly support the fact that
the fetus is not acidotic. Management should be directed at
attempting to relieve umbilical cord compression with repositioning of the patient or consideration of amnio-infusion.

described a slowing of the fetal heart rate related to uterine contractions with gradual onset usually following the peak of the
uterine contraction and delayed return of the deceleration to the
baseline, usually following the contraction. The gradual decrease in
fetal heart rate is symmetrical and dened from the onset to the
nadir of 30 s in duration. The fetal heart rate rarely falls
>30e40 bpm below baseline and usually not >10e20 bpm. In most
cases, the onset, nadir, and recovery occur following contraction
beginning, peak, and ending. This late deceleration is thought to
have both a fetal reex and hypoxic component. In most instances,
late deceleration is primarily a reex change associated with nonacidotic hypoxia. However, when hypoxia is associated with
acidosis, the mechanism of late deceleration is more concerning,
because of direct myocardial depression, and is not reex.
Late decelerations are signicant and concerning when they are
persistent and not amenable to corrective measures. Variability
often increases during the contraction and is not a reassuring sign.
Most ususally, late decelerations appear before the loss of variability and are reex in nature from transient fetal hypoxia most
often related to uterine activity, frequency and strength, or
maternal hypotension. The presence of persistent late decelerations
with the loss of variability and elevation of the fetal baseline heart
rate is far more signicant than the presence of the decelerations
alone and strongly suggest fetal intolerance to the hypoxic stress of
uterine contractions. Such associations strongly correlate with
neonatal depression.
7. Prolonged decelerations
Prolonged decelerations are generally isolated decelerations
lasting >2 min. Such a decrease must be 15 bpm below baseline
and last <10 min. If a deceleration lasts 10 min, it is termed a
baseline change and considered a bradycardia. Such decelerations
are difcult to classify by pathophysiologic cause, as they appear in
any number of clinical situations. Cord compression is a frequent
etiology for prolonged decelerations. Profound placental insufciency, hypertonic uterine contractions, or severe maternal
compromise (such as seizures, profound hypoxia, cardiac decompensation, trauma) and certain types of drug overdosage may be
associated with prolonged fetal heart rate decelerations. In most
instances, as long as the original insult thought to be responsible for
the prolonged deceleration is corrected, the placenta is a very
effective organ to adequately resuscitate the fetus. Clinical decisions regarding recurrent prolonged decelerations must be individualized and are the most difcult of all patterns to manage.
Gestational age, presumed etiology, course of labor, and other
factors must be considered. Although generally isolated and unpredictable, prolonged decelerations represent a clinical challenge
in both the antepartum and intrapartum management of certain
pregnancies.
8. Sinusoidal pattern

6. Late decelerations
When the blood ow through the intervillous space is decreased
to a degree that causes fetal hypoxia, uteroplacental insufciency
is said to exist. This may be the result of fetal or maternal factors
and can manifest itself in the chronic form with intrauterine
growth restriction, antepartum fetal compromise, or stillbirth. In
the acute form, with the presence of prolonged and deteriorating
fetal intolerance to labor, intrapartum asphyxia or e in the extreme
e intrapartum fetal death, may occur. Associations between certain
characteristic changes in the fetal heart rate associated with uteroplacental insufciency have been established through the early
work of Hon, Caldeyro-Barcia, and many others [3,4]. They

The sinusoidal fetal heart rate pattern is a rare but distinct

baseline pattern. Observed in antepartum, intrapartum, and with
neonatal monitoring, the pattern is strongly associated with profound fetal hypoxia, often resulting from severe fetal anemia. This
pattern has also been reported following the usage of various
intrapartum analgesics, and in this setting does not suggest such an
ominous concern for the fetus. The correct recognition and management of this pattern is critical, and confusion over its correct
interpretation continues to be a challenge. It is dened as a visually
apparent, smooth sine-wave-like undulating pattern in the fetal
heart rate baseline with a cycle frequency of 3e5/min and persisting for 20 min. Although the exact mechanism of such a

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pattern is not clearly understood, an association between sinusoidal heart rate and fetal plasma arginine vasopressin concentration
in response to the anemia has been reported [5].
9. Uterine contractions
A key component of electronic fetal monitoring is the assessment of uterine activity. Generally, uterine activity is deemed
adequate if there is progress in labor with cervical dilation and
descent of the fetal presenting part. Failure of such progress may
result from inadequate uterine activity, and augmentation of labor
is often necessary. However, excessive uterine activity resulting
from pathology such as abruptio placenta or overstimulation of the
uterus with various medications may result in fetal compromise in
the form of hypoxia and acidosis. In labor, uterine contraction frequency is the number of contractions in a 10 min window averaged
over 30 consecutive minutes. Uterine contraction intensity, duration, and relaxation time are also clinically important assessments.
Normal uterine activity is ve or fewer contractions in 10 min
averaged over a 30 min window of time. Tachysystole or increased
uterine activity is greater than ve contractions in 10 min averaged
over a 30 min window. When present, tachysystole should always
be assessed for the presence or absence of decelerations of the fetal
heart rate. When associated with decelerations, tachysystole requires evaluation and treatment. In active labor, patients with
tachysystole thought secondary to the supplemental usage of
oxytocin should be considered as candidates to have the oxytocin
reduced or discontinued to reduce the uterine activity and minimize the risk of suspected evolving fetal hypoxia and potentially
acidosis. Rarely, if efforts to reduce uterine activity are unsuccessful
and the decelerations of the fetal heart rate are concerning (e.g.,
prolonged or recurrent late decelerations), tocolytic agents such as
terbutaline may be indicated to attempt in-utero resuscitation of
the fetus.
10. Three-tier fetal heart rate interpretation system
In 2008, a Eunice Kennedy Shriver National Institute of Child
Health and Human Development (NICHD) consensus panel developed a uniform system of denitions and terminology in the
interpretation of fetal heart rate patterns [6]. This resulted from
concerns relating to lack of consistency in the management and
interpretation of intrapartum fetal heart rate patterns. The goal of
such denitions was to allow the meaningful assessment of the
predictive value of, and to develop evidence-based clinical management protocols for, the clinical management of fetal compromise during labor. This report emphasized that fetal heart rate
tracings need to be evaluated in the context of several different
clinical conditions, which include gestational age, medications,
maternal health status, prior fetal assessments, and suspected
concerning fetal conditions including anemia, arrhythmias, and
growth restriction. Complete assessment of the fetal heart tracing
requires both a qualitative and quantitative description of the
uterine activity, baseline fetal heart rate and variability, presence of
accelerations, periodic or episodic decelerations, and changes or
trends of the pattern over time. Decelerations are dened as
recurrent if they occur with more than half of the uterine contractions in any 20 min window. When decelerations occur with
less frequency they are dened as intermittent. The fetal heart rate
tracing needs to be interpreted in the context of the clinical situation, which is often very dynamic. Consequently, the interpretation
and assignment of certain patterns to certain categories is also
dynamic and likely to change during labor. The presence of either
spontaneous or stimulated accelerations of the fetal heart rate
predicts the absence of fetal metabolic acidosis. However, the

absence of accelerations does not reliably predict fetal acidosis.

Importantly, moderate variability of the fetal heart rate reliably
predicts the absence of fetal metabolic acidosis at the time of
assessment. However, minimal or absent variability does not predict the presence of either hypoxia or acidosis of the fetus.
A three-tier system for the categorization of fetal patterns was
recommended and accepted. Category I tracings are normal and
strongly predictive of normal fetal acidebase status at the time of
observation. They include all of the following features: baseline rate
of 110e160 bpm; moderate baseline variability; absence of late or
variable decelerations; early decelerations and accelerations may
be present or absent. Category III tracings are abnormal and include
either absent baseline variability with recurrent late and/or variable decelerations or bradycardia, or the presence of a sinusoidal
pattern. Category II tracings are essentially every other type of
tracing. While suggested management of both Category I and
Category III tracings have been promulgated by the American
Congress of Obstetrics and Gynecology and are useful, they are
insufcient, since >80% of fetuses in labor demonstrate at times
Category II patterns [7]. Recently, specic management proposals
for Category II tracings have been recommended and generally
utilized [8]. These include the use of various algorithms for management depending upon the presence or absence of variability or
accelerations of the fetal heart rate, the presence or absence of
signicant decelerations, the stage of labor, and evidence of normal
progress in labor.
11. Conclusion
The use of EFM continues to be ubiquitous in modern labor and
delivery units. Whereas there is no clear consensus regarding strict
guidelines for the clinical management of all patients using specic
fetal heart rate patterns, there is little variation in opinion about the
denition of distinctly normal and abnormal patterns. Most fetuses
demonstrate patterns of heart rate during labor that are intermediate between these extremes. In such a setting, the specic clinical
management and presumed fetal status are controversial and there
is not one accepted standard of care for management. With such a
background, it is imperative that clinical concerns regarding fetal or
maternal status must be clearly documented and shared among all
members of the health care team. This includes clear communication among the physicians and nurses managing the patient, as well
as with the neonatal team tasked with caring for and at times
emergently resuscitating the newborn. Whereas strides have been
clearly made toward eliminating the cases of unexpected intrapartum stillbirth, the use of continuous EFM remains a challenge in
the appropriate interpretation, application, and credentialing of
those who utilize it in an effort to safeguard the mother and her
fetus during the process of parturition.

Practice points
 EFM is a highly reliable assessment of normal fetal
oxygenation when it is Category I.
 Over the course of labor, the fetal heart rate will often
change between Categories I and II and does not necessarily suggest any significant worsening of fetal status.
 Category III fetal heart rate patterns are most concerning,
correlate highly with need for neonatal resuscitation, and
need to be acted upon with either improvement or delivery of the fetus.

Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/
10.1016/j.siny.2015.02.002

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References
Research directions
 There needs to be ongoing research into new technologies
that may serve as adjuncts to EFM for fetal assessment.
 Studies utilizing proposed management strategies for
Category II tracing must be done to provide evidence that
such strategies are appropriate.
 Use of a common language and intrapartum management
approach must be stressed for each institution providing
labor and delivery services, as well as monitoring to insure
patient safety and improved perinatal outcomes.

Conict of interest statement

None declared.
Funding sources

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None.

Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/
10.1016/j.siny.2015.02.002