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CLINICAL OBSTETRICS AND GYNECOLOGY

Volume 63, Number 3, 625–634


Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.

Interpretation of Fetal
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Heart Rate
Monitoring in the
Clinical Context
CALLA HOLMGREN, MD
Department of Obstetrics and Gynecology, University of Utah, Salt
Lake City, Utah

Abstract: Use of intrapartum fetal heart rate (FHR) were indicated to decrease intrapartum hy-
monitoring has had limited success in preventing hypoxic poxic-ischemic injury. Unfortunately, this
injury to neonates. One of the most common limitations
of FHR interpretation is the failure to consider chronic goal has not been achieved. Multiple studies
and acute clinical factors that may increase the risk of suggest that intrapartum FHR monitoring
evolving acidemia. This manuscript reviews common has, instead, been associated with increased
clinical factors that may affect the FHR and should be rates of surgical delivery and increased cost to
considered when determining the need for early inter- the medical system, without a recognizable
vention based on changes in the FHR.
Key words: fetal heart rate monitoring, clinical con- effect on fetal outcome.2–4
text, fetal academia Attempts to better utilize the available
technology to improve outcomes has led to
the development of a classification system for
Background FHR interpretation.5 Published in 2008, the
Since the introduction of intrapartum Eunice Kennedy Shriver National Institutes
fetal heart rate monitoring (FHR) in the of Child Health and Human Development
1950s, it has been established as the most (NICHD) instituted a system that classified
common way to evaluate fetal well-being FHR patterns in intrapartum patients into 3
during labor in the United States.1 With the categories. The assignment of a category, 1, 2,
notion that FHR patterns could predict fetal or 3, was solely determined by the character-
acid-base status, and, indirectly fetal oxygen- istics of the FHR tracing. The goal of these
ation, the intent was to accurately assess the definitions was to “allow the predictive value
fetal condition and to determine whether of monitoring to be assessed more meaning-
changes in management or expedited delivery fully and to allow evidence-based clinical
management of intrapartum fetal compro-
Correspondence: Calla Holmgren, MD, Suite 100, Salt mise.” It also allowed standardization of a
Lake City, UT. E-mail: cholmgren73@yahoo.com system that, to that point, had not been orga-
The author declares that there is nothing to disclose. nized in an expanded comprehensive way.5

CLINICAL OBSTETRICS AND GYNECOLOGY / VOLUME 63 / NUMBER 3 / SEPTEMBER 2020

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626 Holmgren

Although this standardization was an gestational age, may alter the individual
improvement for more accurate evaluation characteristics of the FHR that are used
of the fetus in labor, it is limited to use of the to identify evolving acidemia. An under-
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FHR and the differences and changes seen standing of these physiological changes is
during labor and does not account for specific important to avoid misinterpretation.
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antepartum and intrapartum risk factors Pre-existing chronic medical conditions


present that, when used in conjunction with may alter placental function resulting in
the specific patterns of the FHR, can lead to a chronic state of fetal hypoxia and a
improved interpretation. Perhaps because more rapid fetal decline during times of
placental function and maternal-fetal oxygen stress. Presence of these conditions in-
transport are assumed to be a final step in the crease the pretest probability of finding
association between most antepartum factors metabolic acidemia and changes suggest-
and fetal-neonatal compromise, using clinical ing fetal compromise in these pregnancies
findings to consider a pregnancy’s a priori risk must be considered within this context.
for placental insufficiency and neonatal hy- Acute clinical conditions such as infection
poxia and acidosis may allow for FHR or abruption also convey an increased
patterns to be interpreted with consideration rate of fetal deterioration and must be
of the overall picture. considered as part of the interpretation of
fetal status suing the FHR.

Adequate Interpretation EFFECT OF CLINICAL FACTORS ON


Adequate interpretation of the FHR pattern SPECIFIC FHR CHARACTERISTICS
during labor requires an interplay of several
critical steps. First, one must consider the Baseline
clinical context for which the FHR testing Without question, the FHR baseline is of
has been instituted. Clinical factors such as critical importance in the clinical interpreta-
gestational age, the presence of labor, or tion of the FHR tracing. Normal tracings are
infection may result in physiological changes characterized by a stable baseline FHR of
that affect the characteristics of the FHR 110 to 160 beats per minute (BPM), for a
in the absence of acidemia and thus may 10-minute segment and duration ≥ 2 minutes.
alter interpretation. Next, there must be an It excludes periodic and episodic changes,
acceptable technical recording and documen- marked variability, and segments differing
tation of the FHR to allow for any kind of by ≥ 25 BPM.5 Any evaluation of the FHR
interpretation. Last, the providers reviewing tracing demands an initial assessment of the
the documented FHR need to correctly FHR baseline. First, it allows the provider to
evaluate the different components involved; determine if this baseline is in a normal range
specifically, the FHR baseline, presence and and second, it is the measure by which the
degree of variability, the presence of accel- other components of interpretation are eval-
erations, and the presence, type, frequency, uated. For example, if the baseline is not
severity, and recurrent nature of decelera- accurately assigned, then a deceleration may
tions. The providers also must be able to be inaccurately interpreted as an acceleration
evaluate these components as they change and vise-versa.
over time.6 A change in FHR baseline is present when
the change persists for 10 minutes or longer.
A baseline of <110 BPM is defined as
Clinical Context bradycardia.5 Mild bradycardia (100 to 110
An understanding of the clinical context is BPM) can be normal and has been associated
important in the interpretation of the with postterm infants and occipitoposterior
FHR tracing. Clinical factors, such as position.6 Although uncommon, abnormal

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FHR and Clinical Context 627

rates of <100 BPM may be seen in fetuses Variable Decelerations


with congenital heart disease or myocardial Establishing the type of deceleration is
conduction defects such as fetal heart block.7 critical, as these “drops” in the baseline
A baseline > 160 BPM is defined as fetal
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FHR are caused by different conditions.


tachycardia and this finding has been asso- The definitions of various deceleration
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ciated with certain maternal and fetal con- types including early, late and variable
ditions, such as chorioamnionitis, maternal have previously been described.5 Variable
fever and dehydration, as well as tachyar- decelerations vary in terms of shape,
rhythmias. Any drastic change in the FHR depth, and timing in relationship to ute-
baseline outside of the “normal” parameters rine contractions. Overall, variable decel-
of 110 to 160 BPM necessitates evaluation by erations are usually benign changes
a clinician, as this may not be indicative of an caused by cord compression, with subse-
abnormal fetal acid-base status, but is, again, quent changes in peripheral vascular re-
not within the normal range. sistance or oxygenation14 and they are
The gestational age of the pregnancy is very common in the second stage of labor.
important, as FHR patterns are different However, the presence of vaginal bleed-
in the preterm compared with the term ing or intractable pain may suggest the
gestation. Physiological control of FHR possibility of uterine rupture or abruption
and the features observed in the preterm which may not be amenable to normal
fetus can make interpretation difficult.7 interventions and may result in rapid fetal
The preterm fetus often has a FHR with a deterioration. Variable decelerations in
higher baseline and there is a normal, patients with a previous cesarean section
incremental decline in the FHR baseline or risk factors for abruption must be
as the fetal parasympathetic nervous sys- interpreted with caution.
tem matures with advancing gestational
age.8 Thus, relative FHR tachycardia Late Deceleration
may be normal in a less mature fetus. Since recurrent late FHR decelerations
are indications of utero-placental insuffi-
Variability ciency and possible fetal hypoxia, at-
Baseline variability, defined as fluctua- tempts by the clinician to improve
tions in the FHR of > 2 cycles per minute, circulation to the placental unit and the
with grades of fluctuation based on am- fetus is imperative. This is seen in the
plitude range (peak to trough), is crucial, case of maternal hypotension, which may
as it reflects a normal fetal nervous be the result of regional anesthesia, ma-
system, chemoreceptors, baroreceptors ternal factors, such as dehydration or
and cardiac responsiveness. Persistently shock or with medication use. Attempts
minimal or absent FHR variability appears to improve the maternal blood pressure
to be the most significant intrapartum sign of with medication, such as ephedrine or
fetal compromise.9 Fetal metabolic acidosis volume expansion can improve maternal
is one concerning cause for decreased varia- circulation and perfusion of the uterus
bility but other etiologies include central and improve the FHR tracing.15 Admin-
nervous system depressants such as maternal istration of a tocolytic agent, such as
narcotic use, fetal sleep cycles, congenital terbutaline is often employed to transi-
anomalies, prematurity, fetal tachycardia, ently stop contractions, with the under-
administration of betamethasone and pre- standing that in studies evaluating this
existing fetal neurologic abnormality.10–13 administration, improvement in FHR
Interpretation of decreased baseline variabil- tracings in treated groups compared with
ity should consider the presence of benign control groups did not translate into an
causes for this change. improvement in neonatal outcomes

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628 Holmgren

(administration of a tocolytic agent im- respectively, while the relative risks were 1.62
proved FHR tracings compared with un- and 1.67 among women aged 40 to 44 years.
treated control groups, but there were no Performing a population-based cohort study,
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improvements in neonatal outcomes.16 Kenny et al20 compared pregnancy outcomes


in women aged 30 to 34, 35 to 39 and 40 years
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REVIEW OF CHRONIC CLINICAL and above with women aged 20 to 29 years


FACTORS AFFECTING FHR using log-linear binomial regression and
It has long been recognized that maternal found that women greater than 40 years of
antepartum factors play an important age were at increased risk for stillbirth,
role in fetal-placental development and, preterm and very preterm birth, and macro-
therefore, in maternal and newborn out- somia. The risk for pre-eclampsia also in-
comes. Conditions commonly associated creases with AMA. Women aged 40 or older
with nonreassuring fetal status and ab- have a 2-fold higher rate of pre-eclampsia
normal FHR tracings include maternal compared with the general population.21
cardiovascular disease, anemia, diabetes, Collectively, these increased risks from
hypertension, infection, placental abrupt- AMA can likely be linked to placental
ion, abnormal presentation of the fetus, dysfunction. In fact, Lean et al22 suggested
intrauterine growth restriction and um- that placental dysfunction underlies the in-
bilical cord compression, among other creased risk for fetal growth restriction and
obstetric, maternal or fetal conditions. stillbirth in AMA patients.
These elements need to be considered with It is not surprising that AMA has been
interpretation of the FHR tracing in the associated with and increased risk for
clinical setting. abnormal FHR tracings and fetal acid-
emia. In 2013, maternal age above 35 was
Maternal Age 1 of 10 antepartum factors found to be
Advanced maternal age (AMA) is increas- significantly associated with poor neo-
ingly prevalent in developed countries17 and natal outcome when found in association
maternal age has been established as a risk with category II FHR tracings among
factor for specific adverse pregnancy out- > 51,000 patients evaluated.23 In addi-
comes and should be considered as a chronic tion, a prospective cohort study of 8580
condition that may alter the interpretation women with specific electronic fetal mon-
of the FHR, both antepartum and while itoring patterns associated with and pre-
in labor. dictive of acidemia found that these
A retrospective evaluation of the patients patterns were more common in women
from a large, multicenter trial demonstrated designated as AMA.24
that increasing maternal age was significantly In short, there is evidence to suggest that
associated with multiple pregnancy compli- AMA is a known risk factor for adverse
cations including miscarriage, chromosomal obstetric outcome, likely related in part to
abnormalities, congenital anomalies, gesta- placental dysfunction, and demonstrated by
tional diabetes, placenta previa, and cesarean abnormal FHR patterns in labor. AMA
delivery.18 Increased risk for abruption, pre- should be considered a risk factor for adverse
term delivery, low birth weight, and perinatal neonatal outcome in the clinical context of
mortality was noted in women aged 40 years FHR interpretation.
and older. Canterino et al19 demonstrated
increasing rates of fetal death at > 24 and at Obesity
> 32 weeks in patients with increasing mater- Obesity is an important consideration in
nal age. In their cohort, the relative risk for the clinical evaluation of the FHR as it has
fetal death at > 24 and at > 32 weeks among been identified as a risk factor for adverse
women 35 to 39 years were 1.21 and 1.31, pregnancy outcome.25 Obesity often makes

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FHR and Clinical Context 629

it difficult to obtain a readable, and thus oxidative metabolism, placing the fetus at
interpretable, FHR tracing. In fact, the risk for hypoxemia in situations of in-
inferiority of external Doppler ultrasound creased oxygen demand such as labor.
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and toco to internal modalities is well estab-


lished and is more notable in the obese Intrauterine Growth Restriction and
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patient.26 FHR monitoring is of particular Oligohydramnios


importance in the obese patient because high Fetal growth restriction and oligohy-
body mass index is associated with a number dramnios are well established risk factors
of comorbidities, such as diabetes mellitus for abnormal FHR patterns and adverse
and hypertensive disorders. These comorbid- obstetric outcome. Intrauterine fetal
ities are associated with abnormal FHR growth restriction (IUGR) refers to a
tracings and adverse pregnancy outcomes, fetus that has failed to achieve its genet-
such as stillbirth.27 ically determined growth potential and
affects up to 5% to 10% of pregnancies.30
Insulin Dependent Diabetes It is associated with an increase in peri-
Insulin dependent diabetes can have a natal mortality and morbidity, with a
significant impact on the FHR tracing, resultant high risk for intrauterine fetal
both from an acute standpoint and as a demise, and intrapartum fetal morbidity.
more chronic influence. This is to be At delivery, growth restricted infants
expected given the convincing evidence (< 3rd percentile) have nearly twice the
of the diabetes and the effects on the incidence of low Apgar scores and um-
structure and function of both the fetal bilical pH <7.0. Since normal placental
heart and the maternal/fetal placenta. development is required for adequate
Acutely, maternal hyperglycemia has been fetal growth, many of the cases of IUGR
associated with an elevated FHR. Costa and are the result of placental dysfunction and
colleagues prospectively evaluated pregnant this may predispose the fetus to abnormal
women with pregestational diabetes mellitus FHR patterns in labor. Epplin et al31
in the third trimester and found a significant performed a 5-year retrospective cohort
positive correlation (Pearson test, P = 0.0001, study of singleton term laboring patients
r = 0.57) between basal FHR and mean comparing IUGR infants with non-
glycemia. A significant negative correlation IUGR infants and found that IUGR at
was observed between short-term variation term confers an increased risk of late
and mean glycemia (Pearson test, P = 0.003, decelerations and that the patterns in
r = −0.47).28 Tincello and colleagues also these patients may require different inter-
found significant differences between the pretations based on a priori risk and
FHR tracings of those patients with type I clinical factors.
diabetes and control patients including re- Late decelerations would be expected
duced FHR variability and frequency of in the patient with an IUGR fetus given
accelerations observed in third trimester fe- the relationship of those findings to the
tuses of diabetic mothers. These differences etiology of uteroplacental insufficiency.
were felt to represent a more immature form However, the IUGR fetus is also at risk
of FHR than that which would be expected for variable decelerations. Pregnancies
based on gestational age.29 affected by IUGR often have attendant
Chronically, maternal diabetes and hy- oligohydramnios32 and are thus at risk for
perglycemia influences placental develop- intermittent umbilical cord compression.
ment during the embryonic phase Despite this, understanding of the acid/
resulting in changes to fetal metabolic base responses rates of IUGR fetuses to
status. It has been shown that with ma- variable FHR decelerations as might
ternal diabetes, the fetus likely increases occur during human labor, is somewhat

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630 Holmgren

limited. Amaya and colleagues evaluated DFM in a pregnancy with previously normal
the increase in base deficit among chronically fetal movement may be a sign of evolving
hypoxic as compared with normoxic ovine fetal hypoxia. Any pregnancy with a good
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fetuses in response to different simulated clinical history for DFM should be evaluated.
variable FHR decelerations. The researchers In a nonrandomized Norwegian study of
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found that repetitive umbilical cord occlusion > 3000 women presenting with DFM, 97.5%
resulted in the development of acidosis of the women were assessed using a FHR
(pH < 7.0) in both groups, but that in monitoring and 3.2% of the presentations
comparison to the normoxic fetuses, hypoxic were abnormal.36 This demonstrates the
fetuses progressed more rapidly to significant importance of fetal monitoring as a valid
metabolic acidosis in response to moderate screening tool in the setting of DFM, an
FHR variable decelerations. These hypoxic abnormal FHR pattern may be associated
fetuses were also slower to recover with in with poor outcomes. This especially true
utero resuscitation, likely due to impaired when the initial FHR tracing of a patient
placental function and fetal physiological with DFM is remarkably abnormal with
responses.33 The presence of IUGR or oligo- findings suggesting evolving acidemia (ie,
hydramnios in the setting of abnormal FHR tachycardia, minimal or absent variability
may indicate a need to expedite delivery more and repetitive decelerations). Expedited inter-
quickly that identifying the same findings in vention should be considered if reassuring
a normally grown fetus with normal fluid findings cannot be elicited after a short period
volumes. of intrauterine resuscitation.

Previous Cesarean
The assessment of the FHR tracing in the Maternal Infection
clinical context of a prior cesarean delivery is Chronic maternal infection can influence
of particular importance because the FHR the FHR tracing interpretation. Kaneko
tracing is often the initial sign that there and colleagues compared the incidence
may be a concern for uterine rupture. In one of abnormal FHR pattern and umbilical
study published in 2012, among cases of blood gases between 20 pregnancies af-
uterine rupture identified in 9 hospitals, fected by cytomegalovirus (CMV) infection
> 80% of cases of uterine rupture were identi- and normal controls. They found nonreas-
fied secondary to concerning FHR tracing suring FHR patterns (prolonged decelera-
findings, specifically the presence of severe tion and recurrent late deceleration) in 8
repetitive decelerations or fetal bradycardia. of 20 fetuses in the CMV group and in 3 of
Even more importantly, identification of 41 fetuses in the control group (P < 0.05,
these FHR abnormalities was crucial in Fisher test). The most common abnormal-
accomplishing delivery in <18 minutes to ities in the CMV group included prolonged
avoid adverse neonatal outcomes associated decelerations, recurrent late decelerations
with those ruptures.34 and minimal variability and the authors
concluded that CMV-infected fetuses were
ACUTE CHANGES ASSOCIATED WITH more likely to show abnormal intrapartum
POOR CLINICAL OUTCOME FHR patterns.37 Parvovirus B19 is a wide-
spread infection that may affects 1% to 5%
Decreased Fetal Movement (DFM) of pregnant women, mainly with normal
Maternal perception of fetal movement pregnancy outcome, but will occasionally
often begins in the second trimester and result in fetal anemia and resultant FHR
can vary somewhat, depending on the abnormalities, including decreased vari-
time of day and gestational age.35 Although ability, decelerations and occasionally, a
it is a common occurrence, the presence of sinusodal pattern.38

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FHR and Clinical Context 631

INTRAPARTUM CLINICAL MARKERS findings confirm that abnormalities in the


ASSOCIATED WITH POOR OUTCOME FHR in the presence of meconium are
associated with an increased risk for
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Meconium adverse outcome. Thus, the clinician eval-


Meconium, a dark green fecal material uating the abnormal FHR tracing, should
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produced in the intestines of a fetus before assess the situation for the presence of
birth, is a relatively common finding in meconium and consider this finding as an
the amniotic fluid during labor, present in important clinical indicator for decision
10% to 15% of pregnancies, but is more making.
often seen in pregnancies that are post-
dates, in specific maternal conditions such Intrapartum Bleeding
as diabetes and hypertension and in pro- Intrapartum vaginal bleeding should
longed labors. The relationship between prompt immediate evaluation from the
the presence of meconium and abnormal clinical team given the possibility that
FHR patterns was established > 2 deca- the hemorrhage may be originating from
des ago. A study in 1990 concluded that the fetal or placental unit. Placental
meconium in amniotic fluid was associ- abruption, uterine rupture and placenta
ated with placental insufficiency.39 In previa often present with vaginal bleed-
2001, Hadar and colleagues evaluated ing and have demonstrable changes in
perinatal outcomes of infants who had the FHR secondary to interrupted flow
pathologic FHR tracings during the first to the placenta and sometimes, maternal
stage of labor, in comparison with preg- instability.23 These FHR changes include
nancies with normal tracings. In this tachycardia, bradycardia, repetitive varia-
study, the presence of meconium-stained ble decelerations, late decelerations and
amniotic fluid was an independent factor prolonged decelerations. Vasa previa repre-
associated with pathologic FHR monitor- sents direct hemorrhage from the fetal um-
ing during the first stage of labor in a bilical cord blood vessels and although rare,
multivariable analysis [odds ratio (OR), when this occurs, it almost always results in
1.91; 95% confidence interval (CI), an abrupt fetal bradycardia.42
1.03%-3.3%].40 In 2009, a retrospective
cohort of 1638 patients with labors com- Intrapartum Infection
plicated by thick meconium-stained amni- In 2008, Buhimschi and colleagues hy-
otic fluid evaluated the association pothesized that abnormal FHR monitor-
between specific FHR patterns and ad- ing may occur more often in pregnancies
verse perinatal outcomes. In patients with complicated by intra-amniotic inflamma-
thick meconium, the presence of FHR tion which disrupts placental transfer to
tracing abnormalities was associated with the fetus. The researchers evaluated 87
an increased risk of perinatal mortality singleton pregnancies delivered within
and/or neonatal morbidity (moderately 48 hours of amniocentesis and found that
abnormal: adjusted OR, 1.67; 95% CI, the fetuses of women with severe intra-
1.18-2.37; markedly abnormal: adjusted amniotic inflammation had a higher FHR
OR, 2.97; 95% CI, 1.88-4.67). The specific baseline and increased frequency of non-
FHR abnormalities that were associated reactive FHR tracing.43 However, it is not
with this risk included prolonged deceler- clear if abnormal FHR tracings associ-
ations (OR, 1.22; 95% CI, 1.02-1.48), ated with infection and inflammation can
severe variable decelerations (OR, 1.08; be accurately translated into fetal acidosis
95% CI, 1.00-1.16), bradycardia (OR, in labor. In 1983, Duff et al44 evaluated 65
2.49; 95% CI, 1.02-6.11), and tachycardia patients with chorioamnionitis in labor
(OR, 2.43; 95% CI, 1.49-3.94).41 These and found that the most common FHR

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632 Holmgren

abnormalities were diminished or absent risk model consisting of a combination of


variability (77%) and tachycardia (67%); antepartum risk factors and intrapartum
however, despite the high prevalence of FHR characteristics. Using these factors,
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abnormal FHR tracings, only 1 infant the goal was to reliably identify those infants
had a 5-minute Apgar score <7. A more at risk for adverse neonatal outcome in labor.
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recent study evaluated 86 infants diag- Using a nested case-control study of term
nosed with cerebral palsy postdelivery. singleton deliveries at the 9 hospitals, an
These infants all had abnormal FHR initial risk score was determined using data
tracings and were further subdivided into available at 1 hour after admission. Data
1 of 2 groups depending on the presence from > 50,000 patients was used and of
of absence of clinical chorioamnionitis. 31 antepartum variables evaluated, 10 were
The frequency of severe fetal acidemia in associated with an adverse outcome
the group without chorioamnionitis was including maternal age above 35 years, in-
26.3%, compared with 74.6% in the group creasing body mass index, increasing gesta-
with an infection. The authors concluded tional age, nulliparity, maternal diabetes,
that the observation of clinical intrapar- maternal hypertension, pre-eclampsia, pla-
tum infection should be included as a risk cental abruption and induction of labor.
factor for acidemia in the standardized Quite importantly, a major risk factor in this
clinical interpretation of FHR patterns.45 calculation was the presence of a category II
FHR in the first hour of monitoring. Addi-
PUTTING IT ALL TOGETHER tional evaluation of intrapartum charac-
Several studies have attempted to use the teristics in these patients, including
contribution of clinical risk factors with chorioamnionitis, minimal FHR variabil-
the interpretation of FHR patterns, par- ity, recurrent FHR variable decelerations,
ticularly those in category II. Parer and FHR tachycardia and prolonged FHR
Ikeda.46 identified 134 FHR patterns, decelerations, further predicted adverse out-
classified by baseline rate, baseline varia- come. The women with a high initial risk
bility, and type of deceleration, and used score and high intrapartum risk score had an
to assign a risk of newborn infant acid- 11.3% risk of adverse neonatal outcome and
emia or low 5-minute Apgar score They a cesarean delivery rate of 40%.
also evaluated each pattern for the risk The Advanced Life Support in Obstet-
that it would evolve into a pattern with a rics (ALSO) curriculum has developed the
higher risk of acidemia. Each FHR pattern mnemonic “Dr C. Bravado” to teach a
was color-coded, from no threat of fetal systematic, structured approach to con-
acidemia (green, no intervention required) tinuous EFM interpretation that incorpo-
to severe threat of acidemia (red, rapid rates the NICHD definitions. Using this
delivery recommended). The authors es- system, a clinical risk status (low, me-
tablished 3 intermediate categories (blue, dium, or high) of each fetus is assessed in
yellow, and orange) that would require conjunction with the interpretation of the
escalation for intervention and resuscita- continuous EFM tracing. A term, low-
tion, and possibly, preparation for urgent risk baby may have higher reserves than a
delivery. Although this was very helpful in fetus that is preterm, growth restricted, or
establishing the concerning patterns and exposed to uteroplacental insufficiency
standardizing a uniform response, it did because of pre-eclampsia. An increase in
not consider the antepartum or intrapar- risk status during labor, such as the
tum clinical setting for the patient present- diagnosis of chorioamnionitis, may necessit-
ing in labor. ate a change in monitoring from structured
In 2012, Holmgren et al23 published the intermittent auscultation to continuous
development and evaluation of a labor EFM.47

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FHR and Clinical Context 633

Conclusions 11. Babaknia A, Niebyl JR. The effect of magnesium


Unfortunately, the original goal of FHR sulfate on fetal heart rate baseline variability.
Obstet Gynecol. 1978;51(suppl):2S–4S.
monitoring, reduction of intrapartum hy- 12. Ville Y, Vincent Y, Tordjman N, et al. Effect of
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poxic-ischemic injury, has not yet been betamethasone on the fetal heart rate pattern assessed
achieved and instead, there have been
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by computerized cardiotocography in normal twin


increased rates of surgical delivery and pregnancies. Fetal Diagn Ther. 1995;10:301–306.
increased cost associated with FHR mon- 13. Kopecky EA, Ryan ML, Barrett JF, et al. Fetal
response to maternally administered morphine.
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FHR monitoring to detect evolving fetal 14. Hinshaw K, Simpson S, Cummings S, et al. A
acidemia may be the failure to interpret randomised controlled trial of early versus de-
the FHR within the clinical context. layed oxytocin augmentation to treat primary
Chronic and acute clinical factors may dysfunctional labour in nulliparous women.
BJOG. 2008;115:1289–1295.
indicate an increased a priori risk for the 15. Intrapartum Fetal Heart Rate Monitoring: No-
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improve the predictive value of this com- ment Principles. ACOG Practice Bulletin 106;
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