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Intrapartum fetal heart rate monitoring: Overview

AUTHOR: David A Miller, MD
SECTION EDITOR: Vincenzo Berghella, MD
DEPUTY EDITOR: Vanessa A Barss, MD, FACOG

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Mar 2024.

This topic last updated: Oct 25, 2022.

INTRODUCTION

Normal human labor is characterized by regular uterine contractions, which cause repeated
intermittent reductions of blood flow to the intervillous spaces resulting in repeated transient
interruptions of fetal oxygenation. Contractions may also compress the umbilical cord and fetal head.
Most fetuses tolerate this process well because of placental reserve and effective compensatory
mechanisms, but some do not because of preexisting uteroplacental insufficiency and/or intrapartum
factors. The fetal heart rate (FHR) pattern helps to distinguish the former from the latter as it is an
indirect marker of fetal cardiac and central nervous system responses to changes in blood pressure,
blood gases, and acid-base status. (See "Nonstress test and contraction stress test", section on
'Physiologic basis of fetal heart rate changes'.)

The rationale for intrapartum FHR monitoring is that identification of FHR changes potentially
associated with inadequate fetal oxygenation, such as changes in baseline rate, frequent decelerations,
and/or absent/minimal variability, may enable timely intervention to reduce the likelihood of hypoxic
injury or death. In addition, accurate identification of appropriately oxygenated fetuses may prevent
unnecessary intervention. Although virtually all obstetric societies advise monitoring the FHR during
labor, the benefit of this intervention has not been conclusively demonstrated, and this position is
largely based upon expert opinion and medicolegal precedent.

The procedure for intrapartum FHR monitoring, physiology behind FHR accelerations and
decelerations, classification of FHR tracings, and use of ancillary tests to evaluate the fetus will be
discussed here. Intrapartum management of category I, II, and III FHR tracing is reviewed separately
(see "Intrapartum category I, II, and III fetal heart rate tracings: Management"). Antepartum FHR
monitoring (nonstress test, contraction stress test) is also reviewed separately. (See "Nonstress test and
contraction stress test".)

DOES INTRAPARTUM FHR MONITORING IMPROVE OUTCOME?

Although some evidence suggests that intrapartum FHR monitoring is associated with a reduction in
intrapartum death [1], a reduction in long-term neurologic impairment has not been proven. All
available data are derived from trials comparing techniques (eg, continuous electronic monitoring with
intermittent auscultation). No randomized trials have compared intrapartum FHR monitoring with no
intrapartum FHR monitoring.

For both low- and high-risk pregnancies, continuous electronic FHR monitoring is not clearly superior to
intermittent auscultation with respect to preventing death or poor long-term neurologic outcome and
has a high false-positive rate [2,3]. The lack of superiority has been attributed, at least in part, to intra-
and interobserver variability in interpretation of continuous electronic FHR tracings [4].

Evidence:

● Meta-analysis – A 2017 meta-analysis that compared continuous electronic FHR monitoring with
intermittent auscultation (13 randomized trials, >37,000 low- and high-risk pregnancies) reported
the following major findings [2]:

• No statistically significant differences between techniques were noted for the following
newborn/childhood outcomes:

- Acidemia (measured in cord blood) (relative risk [RR] 0.92, 95% CI 0.27-3.11)

- Apgar score <4 at five minutes (RR 1.80, 95% CI 0.71-4.59)

- Neonatal intensive care unit admission (RR 1.01, 95% CI 0.86-1.18)

- Hypoxic-ischemic encephalopathy (RR 0.46, 95% CI 0.04-5.03)

- Perinatal mortality (RR 0.86, 95% CI 0.59-1.24)

- Neurodevelopmental impairment at ≥12 months of age (RR 3.88, 95% CI 0.83-18.2)

- Cerebral palsy (RR 1.75, 95% CI 0.84-3.63)

• Although use of continuous electronic FHR monitoring resulted in fewer neonatal seizures (RR
0.50, 95% CI 0.31-0.80), there were no differences in long-term neurologic outcomes [2,5].

• Continuous electronic FHR monitoring resulted in:

- More operative vaginal births for abnormal FHR patterns or acidosis (RR 2.54, 95% CI 1.95-
3.31)

- Fewer spontaneous vaginal births (RR 0.91, 95% CI 0.86-0.96)

- More cesarean births for abnormal FHR patterns or acidosis (RR 2.38, 95% CI 1.89-3.01)

- More operative vaginal and cesarean births overall (RR 1.15 and 1.63, respectively). Data
for low-risk and high-risk subgroups, preterm pregnancies, and high-quality trials were
consistent with these overall results.

It is important to note that all seven trials published after 1980 (including the only trial with
several thousand patients) found no significant increase in the rate of cesarean birth for patients
monitored continuously compared with those monitored by intermittent auscultation, in contrast
 to the four small trials published before 1980, which found significantly higher rates of cesarean
birth with continuous monitoring [2].

It is also important to note that a statistical reduction in the perinatal death rate is difficult to
demonstrate because death is a rare outcome. Even the pooled results from multiple randomized
trials lacked sufficient power to permit a definitive conclusion in the 2017 meta-analysis [2].
However, a previous meta-analysis that specifically evaluated perinatal deaths attributed to fetal
hypoxia in low- and high-risk pregnancies concluded that this outcome was significantly less
common in continuously monitored patients than those monitored with intermittent auscultation
(7/9398 versus 17/9163; 0.7 versus 1.8 per 1000; odds ratio 0.41, 95% CI 0.17-0.98; nine trials) [1].

A statistical reduction in the incidence of cerebral palsy with continuous intrapartum FHR
monitoring is also difficult to prove for several reasons. Many cases of cerebral palsy are due to
antepartum, rather than intrapartum, events. In such cases, intrapartum interventions are
unlikely to change the course of the disease [6]. In addition, most FHR abnormalities are not
associated with fetal acidemia or hypoxemia, and most fetal acidemia and hypoxemia does not
result in neurologic disability. In fact, one study calculated that 99.8 percent of "abnormal" FHR
tracings are not associated with the later development of cerebral palsy, yielding a positive
predictive value that is equal to, or lower than, the prevalence of cerebral palsy in the general
population [6]. Another potentially confounding factor is that a preexisting fetal neurologic
disorder may be the cause, rather than the result, of an intrapartum FHR abnormality [7]. In many
cases, the interventions that are undertaken in the setting of abnormal FHR tracings may alter the
natural history of fetal oxygen deprivation, potentially decoupling FHR abnormalities from hypoxic
neurologic sequelae such as cerebral palsy. Lastly, the degree of fetal oxygen deprivation that
leads to long-term neurologic injury is close to that causing fetal death; thus, many severely
depressed term fetuses may either survive intact or die, rather than survive with disability [8].

● Network meta-analysis – A 2021 network meta-analysis (33 trials, >118,000 participants)

evaluated multiple forms of intrapartum fetal monitoring, including intermittent auscultation and
cardiotocography with and without computer-aided decision support, fetal scalp lactate
assessment, fetal scalp pH analysis, fetal pulse oximetry, and fetal ST segment analysis (STAN) [3].
Major findings were:

• No method of intrapartum fetal monitoring increased or decreased the overall cesarean birth
rate.

• Compared with other forms of intrapartum fetal monitoring, intermittent auscultation neither
reduced nor increased adverse neonatal outcomes, including low Apgar scores, neonatal
acidemia, neonatal intensive care unit admissions, or perinatal deaths. Intermittent
auscultation was associated with fewer emergency cesarean births overall and fewer
emergency cesarean births for fetal distress.

CANDIDATES FOR INTRAPARTUM FETAL MONITORING

Any patient with a pregnancy in which detection of an FHR abnormality would prompt intervention
(maternal maneuvers to improve fetal oxygenation and/or operative delivery) is a candidate for
intrapartum fetal monitoring.

Some degree of FHR monitoring during labor has become routine in the United States, even though the
clinical benefit has not been established conclusively (see 'Does intrapartum FHR monitoring improve
outcome?' above). It is unlikely that this practice will be abandoned in the near future because most
patients and clinicians are reassured by normal FHR monitoring results, and most believe that detection
of an FHR abnormality and prompt intervention is likely to be beneficial.

Intermittent versus continuous monitoring

● Low- or average-risk pregnancies – Some major national organizations endorse monitoring low-
risk pregnancies intermittently using a Doppler device or fetal stethoscope (eg, Pinard or DeLee
stethoscope); however, this is relatively uncommon in the United States because it provides
limited information about FHR variability, accelerations, or decelerations and requires one-to-one
nursing care, which is costly and impractical for most maternity units. The possible increase in
operative birth associated with continuous electronic FHR monitoring usually is considered a
reasonable trade-off for a possible reduction in risk of adverse fetal/neonatal outcome and the
reduction in personnel costs. (See 'Does intrapartum FHR monitoring improve outcome?' above.)

American College of Obstetricians and Gynecologists (ACOG) guidelines state that either
continuous electronic FHR monitoring or intermittent auscultation is acceptable in uncomplicated
patients [9].

● High-risk pregnancies – There is consensus that high-risk pregnancies should be monitored

continuously during labor. A high-risk pregnancy can be defined as one with antepartum or
intrapartum complications that may lead to maternal or fetal compromise (eg, previous cesarean
birth, preeclampsia, growth restriction, diabetes mellitus requiring medication for glucose control,
abruption or unexplained vaginal bleeding, chorioamnionitis or sepsis, meconium-stained
amniotic fluid, postterm pregnancy).

PROCEDURE

Choice of equipment — External FHR monitoring is as reliable as internal FHR monitoring in most
cases [10]. However, internal FHR monitoring is preferable when the externally derived tracing is
difficult to obtain or interpret because of poor technical quality. This may result from a number of
conditions, including early gestational age, maternal habitus, frequent maternal or fetal movement,
uterine myomata, polyhydramnios, or multiple gestation

External electronic monitoring — Noninvasive external FHR monitoring can be performed

continuously or for variable periods of time with a Doppler ultrasound device on the maternal
abdomen. This device detects the motion of the fetal heart and uses this information to create a
complex wave form. The computer then detects the peaks of successive waves to calculate a
mechanical R wave-to-R wave (RR) interval. To minimize artifact caused by the inherent variation in the
Doppler ultrasound signal, the computer calculates the FHR by averaging several consecutive RR
intervals. This technology, called autocorrelation, reduces signal variation. The FHR tracing derived
from Doppler ultrasound using the autocorrelation technique closely resembles that derived from a
fetal electrocardiogram (ECG), although baseline variability may be more apparent with the Doppler
technique. An alternative technology (eg, Monica AN24) uses several electrodes placed on the maternal
abdomen to detect the electrical fetal RR interval. Wireless monitors enable FHR monitoring while the
patient is ambulating [11].

Intermittent auscultation — A Pinard or DeLee fetal stethoscope ( figure 1) (also called a

fetoscope) or a Doppler device may be used for intermittent auscultation. A systematic review
concluded that available evidence is limited and inadequate to make a strong recommendation for
choosing one device versus another [12].

Internal electronic monitoring — A fetal ECG can be obtained by placing a bipolar spiral electrode
into the fetal scalp transcervically; a second reference electrode is placed on the maternal thigh to
eliminate electrical interference from maternal cardiac activity. A computer calculates the FHR based on
the RR interval ( waveform 1). Artifact is minimal so the signal is clear and provides accurate
measurement of the variability between successive heartbeats without the need for autocorrelation.

Application of artificial intelligence computer programs to fetal ECG signal processing has led to
development of devices to overcome the limitations of FHR pattern interpretation by human observers
[13,14]. 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. As an example, the STAN
monitor analyzes the fetal T wave and ST segment. However, this technology has not been widely
adopted in the United States and remains investigational. (See 'ST analysis' below.)

Frequency and duration of monitoring

Electronic FHR monitoring — Upon admission to the labor unit, the standard of care in most
hospitals in the United States is to assess the FHR for a minimum of 20 to 30 minutes, along with
uterine activity and maternal vital signs. The goal is to identify fetuses who have or are at increased risk
for abnormal intrapartum FHR patterns and who might benefit from continuous rather than
intermittent intrapartum FHR monitoring [15]. This initial assessment and additional assessments
during labor may also inform decisions regarding the use of uterine stimulants, such as oxytocin or
prostaglandins. However, a systematic review of randomized trials found that, in low-risk pregnancies,
this "labor admission test" did not reliably predict fetal ability to tolerate labor over time and did not
reduce neonatal morbidity compared with intermittent auscultation of the FHR [16]. There were
insufficient data to draw conclusions about the value of the labor admission test in patients with high-
risk pregnancies.

In the United States, a common practice in low-risk pregnancies with a normal initial FHR pattern is to
monitor the FHR continuously when possible (ie, patient is not ambulating, bathing, moving around,
etc) and review the FHR at least every 30 minutes in the active phase of the first stage of labor and at
least every 15 minutes in the second stage [9]. High-risk pregnancies are monitored continuously, and
the FHR is usually reviewed at least every 15 minutes in the active phase of the first stage of labor and
at least every 5 minutes in the second stage.

The interpretation of the FHR should be documented in the intrapartum record. (See 'NICHD
classification of FHR patterns' below.)
 Intermittent auscultation — As discussed above, intrapartum intermittent auscultation is used
relatively infrequently in the United States. (See 'Candidates for intrapartum fetal monitoring' above.)

No trials have compared protocols for performing intermittent auscultation [12]. If used in low-risk
pregnancies, a common approach is to listen to the FHR for ≥60 seconds and record the rate during and
immediately after a uterine contraction at least every 30 minutes during the active phase of the first
stage of labor and at least every 15 minutes during the second stage [17]. If risk factors for fetal
compromise are present, the FHR is determined, evaluated, and recorded preferably before, during,
and after a uterine contraction at least every 15 minutes during the active phase of the first stage of
labor and at least every 5 minutes during the second stage.

The American College of Nurse-Midwives considers abnormal findings to be any of the following:
irregular rhythm, decrease in FHR below the baseline, tachycardia, or bradycardia [18]. An increase in
the baseline fetal heart rate by ≥20 beats/minute from the start of labor is also concerning [19].

Assessment of uterine activity — Interpretation of intrapartum monitoring should include

assessment of measures of uterine activity in context, and this assessment should be incorporated
routinely into FHR management decisions. In the United States, the National Institute of Child Health
and Human Development (NICHD) has identified several essential components of uterine activity,
including uterine contraction frequency, contraction intensity, contraction duration, resting time
between contractions, and resting tone between contractions [20]. Normal uterine contraction
frequency was defined as five or fewer contractions in 10 minutes, averaged over 30 minutes.
Contraction frequency above this limit was termed tachysystole.

Normal ranges for the other components of uterine activity are addressed elsewhere. (See "Labor:
Overview of normal and abnormal progression".).

PHYSIOLOGIC SIGNIFICANCE OF SELECTED FHR CHARACTERISTICS

Baseline FHR — A normal baseline FHR is 110 to 160 bpm ( table 1) and reflects lack of pathology
related to factors that regulate FHR. These factors include intrinsic cardiac pacemakers (sinoatrial node,
atrioventricular node), cardiac conduction pathways, autonomic innervation (sympathetic,
parasympathetic), intrinsic humoral factors (catecholamines), extrinsic factors (medications), and local
factors (calcium, potassium), which are discussed in detail separately. (See "Nonstress test and
contraction stress test", section on 'Physiologic basis of fetal heart rate changes'.)

Baseline bradycardia may be related to maternal beta blocker therapy, hypothermia, hypoglycemia,
hypothyroidism, or fetal heart block or interruption of fetal oxygenation.

Baseline tachycardia may be related to maternal fever, infection, medications, hyperthyroidism,

elevated catecholamines, fetal anemia, arrhythmia, or interruption of fetal oxygenation.

Variability — FHR variability is the result of integrated activity between the sympathetic and
parasympathetic branches of the autonomic nervous system. Moderate baseline variability reflects
adequate oxygenation of the central nervous system and reliably predicts the absence of damaging
degrees of hypoxia-induced metabolic acidemia at the time it is observed ( table 1) [20-22]. However,
the converse is not true: Minimal or absent variability alone is a poor predictor of fetal metabolic
acidemia or hypoxic injury at the time it is observed [20]. Other conditions potentially associated with
minimal or absent variability include normal cyclic variation, fetal sleep cycle, fetal arrhythmia,
extremely preterm fetus, fetal cardiac anomaly, preexisting fetal neurologic injury, or fetal effects of
maternally administered medications.

Most of the literature regarding decreased variability does not differentiate between absent variability
(amplitude range undetectable) and minimal variability (amplitude range detectable but ≤5 bpm).
Therefore, it is not possible to make definitive conclusions about the clinical significance of absent
versus minimal variability. Variability is generally present at ≥24 weeks of gestation and may increase as
pregnancy progresses, but not to a degree that can be accurately measured by conventional Doppler-
based cardiotocography and applied clinically [23,24]. The National Institute of Child Health and Human
Development (NICHD) guideline for classification of FHR patterns does not provide gestational-age
specific definitions of variability because no clinical data support using different criteria at earlier
versus later gestational ages, in contrast to accelerations where criteria vary before and after 32 weeks
[20,25].

The significance of markedly increased variability is unclear. It may be a normal variant or an

exaggerated autonomic response to transient or sustained interruption of fetal oxygenation. It has
been observed in the early stages of intrapartum fetal hypoxemia and before birth in some acidotic
newborns [26,27].

Accelerations — FHR accelerations are frequently associated with fetal movement, possibly as a result
of stimulation of peripheral proprioceptors, increased catecholamine release, and autonomic
stimulation of the heart. As with moderate baseline variability, FHR accelerations reliably predict the
absence of damaging degrees of fetal hypoxia and fetal metabolic acidemia at the time they are
observed [20,22]. (See 'FHR response to stimulation' below.)

However, the converse is not true. The absence of accelerations is a poor predictor of fetal metabolic
acidemia or hypoxic injury [20]. Other conditions potentially associated with the absence of
accelerations include normal cyclic variation, fetal sleep cycle, arrhythmia, medications, extreme
prematurity, congenital anomalies, fetal anemia, and preexisting neurologic injury.

The definition of an acceleration varies by gestational age ( table 1). Before 32 weeks, accelerations
are defined by a ≥10 bpm rise above baseline lasting for ≥10 seconds and at ≥32 weeks they are defined
by a ≥15 bpm rise above baseline lasting for ≥15 seconds. This distinction was introduced in the 1997
National Institute of Child Health and Human Development (NICHD) guideline for classification of FHR
patterns and has been carried forward since that time [20,25], although the scientific evidence
supporting the gestational age-related distinction is extremely limited [28,29].

Decelerations unrelated to fetal oxygenation

Early deceleration — An early deceleration ( table 1) likely represents an autonomic response to

changes in intracranial pressure and/or cerebral blood flow caused by intrapartum compression of the
fetal head during a uterine contraction and maternal expulsive efforts, although the precise physiologic
mechanism is not known. Early decelerations are clinically benign: They are not associated with an
interruption of fetal oxygenation, metabolic acidemia, or hypoxic-ischemic neurologic injury. (See
"Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Category I
pattern: Normal'.)

Decelerations related to interruption of fetal oxygenation

Late deceleration — In most cases, a late deceleration is a reflex fetal response to transient
hypoxemia during a uterine contraction ( table 1 and waveform 2 and waveform 3 and
waveform 4 and waveform 5 and waveform 6) [30]. When uterine contractions compress
maternal blood vessels traversing the uterine wall, maternal perfusion of the intervillous space is
reduced; myometrial diastolic blood flow may cease temporarily when intrauterine pressure exceeds 35
mmHg [31,32]. Reduced delivery of oxygenated blood to the intervillous space due to strong,
excessively frequent, and/or prolonged contractions can reduce diffusion of oxygen into the fetal
capillary blood in the chorionic villi, leading to a decline in fetal PO2. The fetus can compensate for
reductions in oxygen delivery by the high oxygen affinity of fetal red cells (high hemoglobin F) and the
high oxygen-carrying capacity of fetal blood (high hemoglobin level) [33].

When fetal PO2 falls below the normal range (approximately 15 to 25 mmHg in the umbilical artery),
chemoreceptors initiate an autonomic reflex response. Initially, sympathetic outflow causes peripheral
vasoconstriction, shunting oxygenated blood flow away from non-vital vascular beds and toward vital
organs such as the brain, heart and adrenal glands. The resulting increase in fetal blood pressure is
detected by baroreceptors, which trigger a parasympathetic reflex and slow the heart rate, reduce
cardiac output, and return blood pressure to normal. After the contraction, fetal oxygenation is
restored, autonomic reflexes subside, and the FHR gradually returns to baseline. This combined
sympathetic-parasympathetic reflex response to transient interruption of fetal oxygenation has been
confirmed in animal studies [30,34-42]. Interruption of the oxygen pathway to the fetus can occur at
multiple maternal levels in addition to uterine contractions, such as the lungs (eg, maternal
hypoxemia), heart (eg, poor cardiac output) or vasculature (eg, hypotension).

Rarely, fetal oxygenation is interrupted sufficiently to result in both severe hypoxemia and metabolic
acidemia and, in turn, direct myocardial depression and late decelerations [30]. Late decelerations
related to severe hypoxemia, metabolic acidemia, and myocardial depression increase the risk of
adverse neonatal outcome. Late decelerations resulting from a reflex response to transient hypoxemia
can be distinguished from more concerning late decelerations by the presence of moderate baseline
variability or accelerations, which reliably exclude the presence of damaging degrees of hypoxia-
induced metabolic acidemia [20-22]. Recurrent late decelerations with absent/minimal variability and
no accelerations require prompt attention [20-22,30]. (See "Intrapartum category I, II, and III fetal heart
rate tracings: Management", section on 'Category III pattern: Abnormal' and "Intrapartum category I,
II, and III fetal heart rate tracings: Management", section on 'Late decelerations without loss of
variability'.)

Variable deceleration — A variable deceleration reflects a fetal autonomic reflex response to

transient mechanical compression of the umbilical cord ( table 1 and waveform 7 and
waveform 8) [38,43-51]. Initially, compression of the umbilical cord occludes the thin-walled,
compliant umbilical vein, decreasing fetal venous return and triggering a baroreceptor-mediated reflex
rise in FHR (sometimes referred to as a "shoulder"). Further compression occludes the umbilical
arteries, causing an abrupt increase in fetal peripheral resistance and blood pressure. Baroreceptors
detect the abrupt rise in blood pressure, triggering an increase in parasympathetic outflow and an
abrupt decrease in heart rate. As the cord is decompressed, this sequence of events occurs in reverse.

Cord compression with or without other sources of interrupted fetal oxygenation may result in
recurrent variable decelerations with absent/minimal variability and no accelerations. These
decelerations often become deeper and last longer over time (reaching a nadir >60 bpm below baseline
or <60 bpm and lasting longer than 60 seconds is concerning [21,52]). In such cases, prompt attention
is required because ongoing hypoxic injury cannot be excluded by the tracing alone [20-22]. (See
"Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Category III
pattern: Abnormal' and "Intrapartum category I, II, and III fetal heart rate tracings: Management",
section on 'Variable decelerations without loss of variability or accelerations'.)

Classification of variable decelerations as mild, moderate, or severe does not correlate with outcome
and is not recommended by the National Institute of Child Health and Human Development [20].
Similarly, the clinical significance of "atypical" features of variable decelerations is unclear (atypical
features include a slow return of the FHR to baseline after the end of the contraction [sometimes called
a "variable with a late component"], biphasic decelerations, tachycardia after the variable deceleration
[sometimes referred to as "overshoot"], accelerations preceding and/or following the variable
deceleration [sometimes called "shoulders"], or reduction in post-deceleration baseline) [20]. Terms
such as "variable with a late component," "shoulders," "overshoots," "Hon pattern," and "conversion
pattern" have been used in some descriptive reports to identify FHR patterns that have not been
demonstrated to impact fetal condition or neonatal outcome in appropriately controlled studies. Such
terms are not included in standard fetal monitoring terminology. In the absence of appropriate
scientific confirmation of clinical significance, the use of such terms should be avoided.

Prolonged deceleration — A prolonged deceleration reflects a fall in FHR by ≥15 bpm, lasting ≥2 but
<10 minutes ( table 1) [20,25]. It is caused by the same physiologic mechanisms responsible for late
or variable decelerations, but interruption of fetal oxygenation occurs for a longer period of time. As
discussed above, absent/minimal variability and no accelerations require prompt attention because
ongoing hypoxic injury cannot be excluded by the FHR tracing alone.

If the fall in FHR lasts ≥10 minutes, it is defined as a baseline change [20]. A baseline change with
absent/minimal variability and no accelerations requires prompt attention because ongoing hypoxic
injury cannot be excluded. (See "Intrapartum category I, II, and III fetal heart rate tracings:
Management", section on 'Category III pattern: Abnormal' and "Intrapartum category I, II, and III fetal
heart rate tracings: Management", section on 'Fetal bradycardia/prolonged deceleration without loss of
variability'.)

Sinusoidal pattern — The sinusoidal pattern is rare. It is defined as a smooth, sine wave-like
undulating pattern in FHR baseline with a cycle frequency of three to five cycles per minute of regular
amplitude of 5 to 15 bpm that persists for at least 20 minutes ( table 1 and waveform 9). The
sinusoidal pattern was historically associated with severe fetal anemia, although the pathophysiologic
mechanism has not been definitively proven [53-55]. Variations of the pattern have been described in
association with administration of opioids. (See "Intrapartum category I, II, and III fetal heart rate
tracings: Management", section on 'Management of sinusoidal category III pattern'.)
NICHD CLASSIFICATION OF FHR PATTERNS

Interpretation of an FHR tracing includes several components:

● Qualitative and quantitative descriptions of baseline rate and variability

● Presence/absence of accelerations, decelerations, or sinusoidal pattern
● Changes or trends of the FHR over time
● Assessment of uterine activity

Standard definitions of FHR baseline, variability, accelerations, decelerations, and sinusoidal pattern
( table 1) were proposed by the National Institute of Child Health and Human Development (NICHD)
in 1997 and reaffirmed in 2008 [20,25]. They are used clinically throughout the United States, and have
been endorsed by American College of Obstetricians and Gynecologists (ACOG) [9]. The International
Federation of Gynecology and Obstetrics (FIGO) published a similar consensus guideline in 2015
(FIGO2015) ( table 2), which is used in many countries [56].

In 2008, the NICHD also introduced a three-tier FHR classification system ( table 3), in which category
I represents a normal tracing (predictive of normal fetal acid-base status at the time of observation),
category II represents an indeterminate tracing, and category III represents an abnormal tracing
(associated with an increased risk of abnormal fetal acid-base status at the time of observation) [20].
Some evidence suggests that neonatal outcomes can be improved with use of this standardized
approach to pattern recognition coupled with a standardized package of therapeutic interventions
( table 4) [57]. These patterns are described below briefly and elsewhere in more detail along with
management recommendations. (See "Intrapartum category I, II, and III fetal heart rate tracings:
Management".)

Category I FHR pattern — A category I pattern is normal: it indicates minimal likelihood of significant
metabolic acidemia and ongoing fetal hypoxic injury at that point in time. The fetal status and FHR
pattern may remain stable over time, or the fetal status may change, resulting in a category II or
category III pattern.

A category I pattern has all of the following components ( table 3 and waveform 10) [20]:

● A baseline FHR of 110 to 160 bpm

● Moderate FHR variability (6 to 25 bpm)
● Absence of late, variable, or prolonged FHR decelerations
● Early decelerations may or may not be present ( waveform 11)
● Accelerations may or may not be present

Category I patterns were observed at some point during labor in over 99 percent of tracings in one
large study [58].

Category III FHR pattern — A category III pattern is abnormal: it is associated with an increased
likelihood of severe hypoxia and metabolic acidemia at that point in time.

A category III tracing has at least one of the following components ( table 3) [20]:

● Absent variability with recurrent late decelerations ( waveform 2 and waveform 3)

 ● Absent variability with recurrent variable decelerations ( waveform 7)
● Absent variability with bradycardia
● A sinusoidal pattern ( waveform 9)

Late decelerations and variable decelerations are considered recurrent when they occur with at least 50
percent of uterine contractions in a 20-minute window [20,25].

Category III patterns were observed at some point in 0.1 percent of tracings in one large study [58].

Prompt evaluation, expeditious use of conservative measures to improve fetal oxygenation, and/or
expeditious delivery are indicated when a category III pattern is observed because fetal/neonatal
morbidity or mortality may occur if the pattern persists. (See "Intrapartum category I, II, and III fetal
heart rate tracings: Management", section on 'Category III pattern: Abnormal'.)

However, category III patterns may also be caused by conditions unrelated to hypoxemia. (See 'Pitfalls
in attributing category II and category III patterns to fetal hypoxia' below.)

Category II FHR pattern — Category II FHR patterns include all FHR patterns that are not classified as
category I (normal) or category III (abnormal) ( table 3). Because category II tracings may remain
stable for a prolonged period of time, have variable prognostic significance based on the specific
components, and are common (observed at some point in 84 percent of tracings [58]), pregnancies
with this pattern are the most difficult to evaluate and manage. (See "Intrapartum category I, II, and III
fetal heart rate tracings: Management", section on 'Category II pattern (Indeterminate)'.)

Pitfalls in attributing category II and category III patterns to fetal hypoxia — Category II and
category III patterns can be related to a number of conditions other than hypoxia:

● Normal cyclical variation – FHR tracings in labor can move between category I and category II
with variable frequency. Episodes of moderate variability often alternate with episodes of minimal
variability. Normal cyclic variation should be considered when interpreting the FHR tracing.

● Fetal sleep cycle – Fetal quiet sleep is associated with decreased variability and reduced
frequency of accelerations, as well as decreased fetal movement. Quiet sleep cycles may last up to
40 minutes [59].

● Technical factors – Technical factors include a faulty leg plate, electrode, or monitor; setting the
recording rate at 1 cm/min instead of the standard 3 cm/min; and the computer algorithm used
by the monitor, which may double very slow FHRs and halve fast rates (>240 bpm).

● Maternal heart rate artifact – Maternal artifact refers to an electronic fetal monitor record that
shows the maternal, rather than the fetal, heart rate [60]. It may occur in several scenarios, which
can be detected if the clinician is aware of the phenomenon, and evaluates suspicious tracings.
Evaluation for maternal artifact involves using more reliable methods for documenting the
maternal heart rate (eg, checking the radial pulse, applying a pulse oximetry or
electrocardiographic [ECG] monitor) and FHR (eg, ultrasound of fetal heart, internal scalp
electrode).

• If the fetus is not alive, an internal fetal scalp electrode may detect the maternal ECG and
record the maternal heart rate instead of the FHR [61].
 • The external Doppler device may record the maternal heart rate from a nearby artery (eg,
uterine artery), even if the fetus is alive. When the mother is tachycardic, the maternal heart
rate pattern can appear deceptively similar to a normal FHR pattern, including normal-
appearing baseline rate and variability. In a prospective study, nearly 10 percent of parturients
had a heart rate ≥120 bpm and nearly 20 percent had a heart rate ≥110 bpm in the second
stage of labor [62].

• If the maternal heart rate is recorded, maternal heart rate accelerations during uterine
contractions can be mistaken for FHR accelerations [63-65]. Heart rate accelerations that
coincide with uterine contractions should prompt further evaluation to exclude this
phenomenon, especially during maternal pushing in the second stage.

• The external Doppler device can alternate between recording the fetal and the maternal heart
rate. When switching from one to the other, the tracing will not necessarily show visual
discontinuity; therefore, visual continuity does not reliably exclude this phenomenon. Some
newer electronic monitors will alert the user to "signal coincidence" or "signal ambiguity" when
the monitor's computer logic determines that the maternal heart rate derived from a maternal
ECG or pulse oximetry transducer is the same as the presumed FHR derived from the Doppler
transducer (or scalp electrode).

Suspected signal coincidence or ambiguity should prompt further evaluation to confirm the
source of the heart rate signal, since the maternal heart rate is not informative of fetal
condition. If there is any question, other methods should be employed as needed, including
ultrasound of the fetal heart, palpation of the maternal pulse, fetal scalp electrode, or maternal
pulse oximetry.

● Drug effects – Transplacental passage of maternal medication can affect the FHR. For example,
opioids and magnesium sulfate can decrease variability, butorphanol can cause a sinusoidal
pattern, and beta-blockers and atropine can increase FHR [9].

● Maternal fever – Maternal fever is associated with increased baseline FHR and decreased
variability.

● Fetal cardiac arrhythmias – Electronic FHR monitoring patterns may suggest the presence of a
fetal arrhythmia, which may be benign or may seriously affect cardiac function. Other
sonographic and non-sonographic modalities are needed to make a definitive diagnosis and
treatment plan. (See "Fetal arrhythmias".)

The following are clues that an arrhythmia is present; however, any FHR less than 110 bpm
requires thorough evaluation before it can be attributed to a benign condition.

• Sharp downward spikes that nadir at approximately half of the baseline rate suggest dropped
beats.

• A sharp upward spike followed immediately by a downward spike suggests a premature beat
with a compensatory pause.
 • A persistent or intermittent baseline rate that is approximately half of the normal rate may be
due to 2:1 heart block.

• A baseline rate less than 110 bpm but higher than half of the normal rate suggests sinus
bradycardia. Structural cardiac abnormalities may be associated with bradyarrhythmias, such
as complete heart block.

• An FHR >240 bpm suggests a tachyarrhythmia; however, because the upper limit of the FHR
graph on standard paper is 240 bpm, the monitor may not record any heart rate or it may
record half of the FHR.

● Preexisting fetal neurologic injury – Abnormal FHR patterns observed from the moment
monitoring is initiated have been attributed to antepartum neurologic injury, such as stroke. The
most commonly described pattern is a persistent nonreactive heart rate and a persistent fixed
baseline with minimal or absent variability [7,66].

However, normal intrapartum FHR monitoring does not exclude the possibility of antepartum
neurologic injury since antepartum injury does not always manifest in the intrapartum FHR
tracing [67].

Studies of infants with congenital brain lesions suggest that damage to the medulla oblongata
and midbrain may be responsible for the loss of FHR variability [68].

CLINICAL APPROACH TO FHR MONITORING AND EVALUATION OF ABNORMAL

PATTERNS

To improve neonatal outcome, it is crucial that clinicians correctly define and interpret FHR tracings,
communicate effectively with other labor and delivery providers when the pattern is not normal, and
initiate appropriate and timely interventions [57].

Key principles — Key principles when monitoring the FHR pattern include:

● Confirm that the monitor is recording the FHR and uterine activity adequately to permit
appropriately-informed management decisions. Ensure that the maternal heart rate is not being
recorded. (See 'Pitfalls in attributing category II and category III patterns to fetal hypoxia' above.)

● Assess uterine activity along with baseline FHR, variability, accelerations, decelerations, and
sinusoidal pattern, and place the tracing in a category (I, II, or III).

● If the tracing is category I and the patient is low-risk, initiate routine intrapartum fetal
surveillance.

● If the tracing is not category I, evaluate the integrity of the fetal oxygen pathway (maternal lungs,
heart, and vasculature, as well as the uterus, placenta, and umbilical cord).

Attempt to correct the problem, if possible, by initiating measures to improve fetal oxygenation,
such as maternal position changes, intravenous fluid bolus, correcting hypotension, stopping or
 reducing uterine stimulants, administering a uterine relaxant, amnioinfusion, and/or modifying
maternal pushing efforts. If the mother is hypoxemic, provide supplemental oxygen.

Also employ ancillary tests to further assess the fetal condition. (See 'Useful ancillary tests for
intrapartum fetal evaluation' below.)

The management of category II and III tracings is summarized in the table ( table 4) and
discussed in detail separately. (See "Intrapartum category I, II, and III fetal heart rate tracings:
Management".)

● Assess how the FHR pattern is evolving. Deepening decelerations, increasing frequency and
longer duration of decelerations, decreasing variability to minimal or undetectable, and change in
baseline (usually tachycardia) are signs that acidosis may be developing. In fetuses with initially
normal FHR tracings, newborn acidosis has been observed when decelerations in combination
with decreasing FHR variability develops and persists over approximately one hour [69].

● If the FHR pattern does not improve within a reasonable period of time, begin planning for the
possible need for rapid delivery. This may include availability of an operating room and specialized
equipment, notification of anesthesia and pediatrics, consent forms, and laboratory tests.

● Determine whether operative intervention (cesarean or operative vaginal birth) is needed and the
urgency of this intervention. Consider individual characteristics of the facility, staff, mother, fetus,
and labor, and make an informed estimate of the time needed to accomplish delivery in the event
of a sudden change in maternal or fetal condition.

Useful ancillary tests for intrapartum fetal evaluation

FHR response to stimulation — An FHR acceleration rising ≥15 bpm above baseline lasting for ≥15
seconds almost always assures the absence of fetal acidemia [70,71]. Before 32 weeks of gestation,
accelerations with a rise of ≥10 bpm and a duration of ≥10 seconds almost always assure the absence
of fetal acidemia [20].

In the absence of spontaneous FHR accelerations, the fetal scalp stimulation maneuver is easy to
perform, inexpensive, and readily available. The examiner uses the first and second fingers to rub the
fetal scalp for approximately 15 to 30 seconds during a vaginal examination. As early studies of the
efficacy of scalp stimulation used a gentle pinch with an atraumatic (Allis) clamp as the fetal stimulus,
digital stimulation should be sufficiently firm to approximate this level of stimulation. Fetal
vibroacoustic stimulation to the maternal abdominal wall overlying the uterus is another effective
method of fetal stimulation [72]. If an internal electrode has not been applied, fetal scalp puncture
during application of the electrode is also effective. Regardless of the technique used, stimulation
should be performed when the FHR is at its baseline rate because performance during a deceleration is
unlikely to terminate the deceleration and is not predictive of fetal acid-base status.

When accelerations are induced in this setting, the fetal pH is >7.20 in over 90 percent of cases, and
when no accelerations occur, pH is <7.20 in approximately 50 percent of cases [72-76]. Accelerations
elicited by fetal scalp stimulation have the same ability to exclude on-going hypoxic injury as
spontaneous accelerations [20].
A meta-analysis of observational studies 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 [74]. For digital stimulation, the
pooled likelihood ratio (LR) for acidemia with a negative test (ie, acceleration elicited) was 0.06 (95% CI
0.01-0.31), and the pooled LR of acidemia with a positive test (ie, no acceleration) was 15 (95% CI 3-76).
Data from adequately powered randomized trials are not available. (See "Evaluating diagnostic tests",
section on 'What are the positive and negative likelihood ratios?'.)

In resource-limited and nonobstetric settings where a change in FHR in response to acoustic

stimulation cannot be assessed electronically, maternal perception of sound-provoked fetal movement
appears to be predictive of fetal well-being [77-81].

Less common ancillary tests

ST analysis — Use of ST analysis does not appear to result in meaningful improvements in pregnancy
outcome.

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. A visual alert ("ST event") appears when ST changes occur. Studies have
reported the STAN computerized interpretation of FHR monitoring system has 38 to 90 percent
sensitivity and 83 to 100 percent specificity for detecting fetal acidemia [82-84].

Clinicians who choose to use ST analysis should be trained and credentialed in its use and
interpretation. The STAN S31 fetal heart monitor has been approved by the US Food and Drug
Administration as an adjunct to assessment of abnormal FHR tracings in pregnancies over 36 weeks of
gestation, in labor, with vertex presentation and ruptured fetal membranes. It is not indicated for
monitoring initiated in the second stage of labor, since there may not be sufficient 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.

Three meta-analyses concluded use of ST analysis did not result in meaningful improvements in
pregnancy outcome [85-87]. As an example, in a 2016 meta-analysis including seven randomized trials
with a total of over 27,000 pregnancies, intrapartum fetal ECG analysis (PR to RR interval, ST segment)
did not improve any neonatal outcome or decrease cesarean birth rates compared with continuous
electronic FHR monitoring alone, but fewer fetal scalp sampling procedures were performed [87]. The
largest randomized trial in the review assigned over 11,000 patients to "open" or "masked" monitoring
with fetal ST-segment analysis and reported no significant between-group differences in the rate of
cesarean birth, any operative birth, or the primary composite outcome (stillbirth, neonatal death, 5-
minute Apgar score ≤3, cord artery pH ≤7.05 and base deficit in extracellular fluid ≥12, intubation in the
delivery room, seizures, neonatal encephalopathy) [72,84].
These conclusions have been challenged in an editorial in which the authors asserted that, while the
meta-analyses of ST analysis did not confirm a significant reduction in perinatal death, neonatal
seizures, or neonatal encephalopathy, these outcomes are so uncommon that it is unlikely a study
sufficiently large to prove no benefit statistically will ever be performed [88]. They also argued that
reductions in the rates of fetal blood sampling, operative vaginal birth, and metabolic acidemia are
clinically relevant, despite the lack of reduction in more patient-important neonatal outcomes.

Fetal scalp blood sampling — Fetal scalp blood sampling is an intrapartum procedure intended to
assess the presence and degree of fetal acidemia by analyzing fetal capillary blood. 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 is dilated at least 2 to 3 cm, can be difficult to perform, and can be
uncomfortable for the parturient. It is contraindicated when the mother is known to have a serious
transmissible infection, such as HIV or hepatitis, and in fetuses at increased risk of a bleeding diathesis.
Rare complications described in case reports include infection, hemorrhage, and leakage of
cerebrospinal fluid [89-91].

Both pH and lactate measurements require the same laboratory facilities for microsample analysis.
Less blood is needed for measurement of lactate than pH, otherwise one test does not clearly perform
better than the other [92]. Intrapartum fetal scalp blood sampling to measure pH (and base
excess/deficit) or lactate has not been clearly proven to reduce emergency cesarean deliveries or
operative vaginal births or to improve long-term perinatal outcome [93-95]. For this reason and many
others, including quality control issues, cost, patient discomfort, sample failure rates up to 10 percent,
and unavailability of sampling kits, fetal scalp blood sampling is performed only rarely in the United
States and elsewhere. (See "Umbilical cord blood acid-base analysis at delivery".)

Fetal pulse oximetry — Although intuitively a promising technique for fetal evaluation, fetal pulse
oximetry has not been useful clinically.

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 [82,96]. In humans, the mean fetal oxygen
saturation (SpO2 by fetal pulse oximetry) during the first and second stages of labor is 59±10 percent
and 53±10 percent, respectively [83,97]. In the setting of an abnormal FHR pattern, fetal SpO2 <30
percent for greater than 10 minutes has been associated with an increased risk of fetal acidemia
[84,85,98-101].

However, in a meta-analysis of randomized trials comparing the outcome of pregnancies in which both
fetal pulse oximetry and cardiotocography results were available for intrapartum clinical management
with the outcome of controls in which only cardiotocography results were available (7 trials, 8013
participants), fetal pulse oximetry had no statistical effect on the overall rate of cesarean birth or the
rate of maternal or neonatal outcomes evaluated; the rates were similar in both groups [76,102].

Use of decision/interpretation aids and algorithms — Although recognition and management of

category I and III tracings is relatively straightforward, the potential for development of progressive
fetal hypoxia, metabolic acidosis, and metabolic acidemia varies widely across the different types of
category II tracings. In part for this reason, investigators have proposed various algorithmic
approaches to recognition, interpretation, and management of FHR tracings beyond category I. These
approaches have had some success in achieving earlier recognition of tracings associated with
metabolic acidemia [103]. However, their ability to improve neonatal outcome and/or reduce
unnecessary interventions remains unproven, thus a change in the standard clinical approach
described above is not warranted [104,105].

The following are examples of some decision/interpretation aids:

● A five-tier FHR classification system has been proposed to identify fetuses at risk of developing
acidosis [106-108]. The system focuses on baseline FHR, variability, and decelerations to stratify
the risk of evolution to acidemia. Depending on risk level, the system suggests different
interventions, such as conservative measures or delivery. The five-tier has not been validated in a
large prospective or randomized trial and no data are available to indicate that it improves
neonatal outcome or reduces operative intervention.

● An online risk assessment calculator is available for management of category II tracings [109]. It
takes into account factors such as labor stage (latent or active first stage or second stage), labor
progress (normal or abnormal), assessment of variability (presence/absence of moderate
variability or accelerations), and assessment of decelerations (frequency and duration of recurrent
decelerations). Based on information entered by the clinician, the calculator suggests observation
or delivery. The algorithm on which the calculator is based has been reported to facilitate earlier
recognition of some, but not all, FHR tracings associated with metabolic acidemia without
increasing the rate of operative intervention [21,103]. The performance of the calculator has not
been assessed in a clinical trial.

● Artificial intelligence has also been used for interpretation of FHR tracings, but meta-analyses
have concluded that it did not improve neonatal outcomes compared with usual clinical
assessment of FHR tracings, and inter-rater reliability between experts and computer systems was
moderate at best [110,111]. The analyses were dominated by two randomized trials (FM-ALERT
[104] and INFANT [105]), which evaluated the use of continuous intrapartum FHR monitoring with
computerized interpretation and real-time alerts. Neither trial reported a benefit in any maternal
or neonatal outcome compared with usual care (intrapartum fetal monitoring with clinician
interpretation).

The larger INFANT trial included over 47,000 pregnancies at or near term and followed offspring
to two years of age [105]. Compared with usual care, the intervention did not increase recognition
of abnormal FHR patterns, did not increase the rate of spontaneous vaginal birth, and did not
improve neonatal outcome (composite or individual endpoints such as pH <7.05, metabolic
acidosis, seizures, neonatal encephalopathy, hospital stay). Developmental assessment at age two
years was similar for both groups.

● In 2018, one group described a standardized algorithm for the management of category II FHR
tracings with recurrent "significant" FHR decelerations, defined as late decelerations, prolonged
decelerations, or variable decelerations lasting at least 60 seconds and reaching a nadir of ≤60
bpm or at least 60 bpm below baseline [112]. Six hospitals in a large health system participated in
a cohort study comparing maternal and neonatal outcomes before and after the introduction of
the algorithm. Fetal monitor tracings that demonstrated moderate (or marked) variability and
 significant decelerations with >50 percent of contractions for 30 minutes were managed as
follows:

• If cervical dilation was <4 cm and recurrent decelerations did not resolve with conservative
corrective measures, delivery was accomplished.

• If cervical dilation was ≥4 cm, labor was permitted to continue only if progress was normal
(first stage: cervical dilation ≥1 cm/hour; second stage: descent with pushing, total duration
≤90 minutes).

• Delivery was indicated if criteria for normal labor progress were not met or if the FHR tracing
demonstrated a persistent pattern of minimal-absent variability.

Nearly 98 percent of screened patients were managed according to the algorithm. After its
introduction, the rate of primary cesarean birth fell from 19.8 to 18.3 percent, low 5-minute Apgar
scores fell from 2.3 to 1.7 percent, and a composite of severe newborn complications fell from 1.6
to 1.2 percent (all statistically significant differences).

If the results of this study can be replicated in other clinical settings, the approach may provide
valuable guidance in the management of some of the most difficult category II FHR tracings. In
the meantime, it seems reasonable to consider adopting more conservative expectations for
normal labor progress, such as those described in this study, in a subset of patients with
significant recurrent decelerations or minimal-absent variability that persists despite appropriate
conservative corrective measures.

INVESTIGATIONAL PREVENTIVE THERAPY

Sildenafil citrate has marked vasodilatory effects on the pelvic and pulmonary circulations. It has been
hypothesized that, if given prophylactically in early labor, its favorable effects on uteroplacental and
fetal blood flow [113,114] may reduce the frequency of intrapartum fetal distress and, in turn,
emergency cesarean or operative vaginal birth for this indication.

In a trial that randomly assigned 300 pregnant patients at term in early labor to receive sildenafil (50
mg orally every eight hours to a maximum of three doses) or placebo, sildenafil reduced the frequency
of strictly defined pathologic FHR patterns by 43 percent (25.3 versus 44.7 percent, relative risk [RR]
0.57, 95% CI 0.41-0.79) [115]. Importantly, sildenafil was associated with a 51 percent reduction in
emergency operative births (18 versus 36.7 percent, RR 0.49, 95% CI 0.33-0.73), without an increase in
adverse neonatal outcomes (20.7 versus 21.3 percent, RR 0.97, 95% CI 0.62-1.50). Maternal side effects
were mild and self-limited, and there was no increase in postpartum bleeding. The findings of this trial
are promising; however, larger trials are needed to confirm the safety and efficacy of sildenafil in this
setting before it can be routinely recommended as part of the management of pathologic FHR
patterns.

CONTROVERSIAL THEORIES
There is clear consensus that normal intrapartum FHR monitoring, when accompanied by normal
Apgar scores, normal umbilical artery blood gas results, or both, is inconsistent with an acute
intrapartum hypoxic-ischemic event sufficient to cause hypoxic-ischemic encephalopathy (HIE) and
cerebral palsy (CP) [22,116]. Intrapartum hypoxic injury that is sufficient to cause CP requires significant
interruption of fetal oxygenation, usually manifested by significant neonatal metabolic acidemia
(reflected by low umbilical artery pH and elevated base deficit), immediate newborn depression (usually
reflected by low Apgar scores), and moderate-severe neonatal encephalopathy. (See "Etiology and
pathogenesis of neonatal encephalopathy".)

Contrary to this consensus, one group has proposed that the standard markers of intrapartum fetal
hypoxia described above need not be present to establish that an intrapartum event was the cause of
later neurologic impairment and that impairment can be due to the effects of mechanical forces of
labor on the fetal head [117]. Although mechanical forces of labor cause pressure on the fetal head,
injury by this hypothetical mechanism has no scientific basis: It has never been reported, and a
systematic review concluded that fetal intracranial pressure is well protected from extracranial forces
and available data do not support intrapartum extracranial pressure as a cause of fetal brain injury
[118].

Another group has proposed a risk-scoring system, dubbed the "Fetal Reserve Index (FRI)," for
interpretation and management of FHR patterns [119-121]. The FRI is a weighted calculation of eight
risk categories, including 10 maternal risk factors (eg, chronic debilitating disease, short stature), 9
obstetric risk factors (eg, placental abruption, malpresentation), and 12 fetal risk factors (eg, meconium
passage, chorioamnionitis). Their criteria for abnormal FHR patterns and uterine activity are defined
differently from standard National Institute of Child Health and Human Development and international
definitions. This system has never been validated; furthermore, the authors' lack of standard criteria for
diagnosing cases of HIE, lack of appropriate controls, and multiple obvious sources of potential bias
preclude reasonably founded conclusions regarding safety or utility of the FRI.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions around the
world are provided separately. (See "Society guideline links: Labor".)

SUMMARY AND RECOMMENDATIONS

● Goal – Normal human labor is characterized by regular uterine contractions and repeated
episodes of transient interruption of fetal oxygenation. Most fetuses tolerate this process well, but
some do not. The primary goal of intrapartum fetal heart rate (FHR) monitoring is to assess the
adequacy of fetal oxygenation during labor so that timely intervention can be undertaken when
appropriate to reduce the likelihood of neurologic injury or death. Another important goal is
accurate identification of appropriately oxygenated fetuses so that unnecessary intervention can
be avoided. There is evidence that intrapartum fetal monitoring is associated with a reduction in
intrapartum death. However, conclusive evidence of a reduction in long-term neurologic
 impairment is lacking. (See 'Does intrapartum FHR monitoring improve outcome?' above and
'Clinical approach to FHR monitoring and evaluation of abnormal patterns' above.)

● Candidates

• Medicolegal precedent in the United States mandates some form of intrapartum FHR
monitoring. For most high-risk pregnancies, continuous electronic FHR monitoring is
recommended. For low-risk pregnancies, either intermittent or continuous electronic FHR
monitoring is reasonable, but frequent intermittent monitoring can be cumbersome and
difficult for many institutional nursing services to achieve. (See 'Candidates for intrapartum
fetal monitoring' above.)

• Intrapartum FHR monitoring is usually not performed when detection of an FHR abnormality
would not prompt any intervention (eg, conservative maneuvers to improve fetal oxygenation
and/or cesarean birth). For example, pregnancies at a gestational age below the limit of
viability and pregnancies in which the fetus has an untreatable anomaly lethal in the newborn.
(See 'Candidates for intrapartum fetal monitoring' above.)

● Continuous versus intermittent – Two commonly used modalities for intrapartum FHR
monitoring are continuous electronic FHR monitoring and intermittent auscultation. Neither test
has been proven to be superior, provided that intermittent auscultation is performed as
prescribed in randomized trials. (See 'Does intrapartum FHR monitoring improve outcome?'
above.)

● Definitions and classification

• Standardized FHR definitions proposed by the National Institute of Child Health and Human
Development (NICHD) and endorsed by the American College of Obstetricians and
Gynecologists (ACOG) are summarized in the table ( table 1). (See 'NICHD classification of
FHR patterns' above.)

• The three-tier system of FHR classification proposed by the NICHD is summarized in the table
( table 3). General concepts of intrapartum FHR management are summarized in the table
( table 4). Use of this standardized approach to pattern recognition coupled with a
standardized package of therapeutic interventions may improve neonatal outcome. (See
'NICHD classification of FHR patterns' above and "Intrapartum category I, II, and III fetal heart
rate tracings: Management".)

• Interpretation of intrapartum monitoring should include assessment of measures of uterine

activity in context, and this assessment should be incorporated routinely into FHR
management decisions. In the United States, the NICHD has identified several essential
components of uterine activity, including uterine contraction frequency, contraction intensity,
contraction duration, resting time between contractions, and resting tone between
contractions. Normal uterine contraction frequency was defined as five or fewer contractions
in 10 minutes, averaged over 30 minutes. Contraction frequency above this limit was termed
tachysystole. (See 'Assessment of uterine activity' above.)
 ● Interpretation and evaluation – Key principles for evaluation of the FHR tracing and
management of FHR patterns include (see 'Key principles' above):

• Confirm that the monitor is correctly recording the FHR and uterine activity. Make sure that the
recorded heart rate is not maternal.

• Assess uterine activity and classify the tracing in a category (I, II or III).

• If the tracing is category I and the patient is low-risk, initiate routine intrapartum fetal
surveillance. Moderate baseline variability and/or FHR accelerations reflect the oxygenation of
the central nervous system and reliably predict the absence of ongoing hypoxic injury and
metabolic acidemia at the time it is observed. (See 'Variability' above and 'Accelerations' above.)

• If the tracing is not category I, evaluate the fetal oxygenation pathway. Attempt to correct
oxygenation problems, if appropriate. Remember that the appearance of the FHR tracing can
be affected by factors other than fetal oxygenation (eg, fetal sleep and arrhythmias, maternal
artifact and medications). (See 'Pitfalls in attributing category II and category III patterns to
fetal hypoxia' above.)

• The management of category II and III tracings is summarized in the table ( table 4) and
discussed in detail separately. (See "Intrapartum category I, II, and III fetal heart rate tracings:
Management".) In the absence of spontaneous FHR accelerations, fetal scalp stimulation
resulting in a FHR acceleration rising ≥15 bpm above baseline lasting for ≥15 seconds almost
always assures the absence of fetal acidemia. (See 'Useful ancillary tests for intrapartum fetal
evaluation' above.)

• If the FHR pattern does not improve within a reasonable period of time, begin planning for the
possible need for rapid delivery.

● Predictive value

• Electronic fetal monitoring has a very high false-positive rate for predicting adverse neurologic
outcomes. However, the false-negative rate of electronic fetal monitoring is very low. Fetal
monitoring is not a diagnostic test for fetal injury; it is a screening test for interrupted fetal
oxygenation. A normal FHR tracing identifies a fetus with a very low risk of hypoxic intrapartum
injury. An abnormal FHR tracing signals the need for further evaluation of fetal oxygen status.
(See 'Does intrapartum FHR monitoring improve outcome?' above.)

• Contemporary evidence does not confirm earlier assumptions that electronic FHR monitoring
is associated independently with a significant increase in the rate of cesarean birth. (See 'Does
intrapartum FHR monitoring improve outcome?' above.)

ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges Bruce K Young, MD, who contributed to an earlier version of
this topic review.
 Use of UpToDate is subject to the Terms of Use.

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Topic 418 Version 110.0
GRAPHICS

DeLee and Pinard style fetoscopes

Graphic 127215 Version 1.0

Top portion of figure displays successive R-R intervals

The interval, in fractions of a second, between these beats is used to calculate the instantaneous beat to beat
interval and then a rolling average is taken and recorded of the fetal heart rate tracing.

Graphic 65200 Version 2.0

NICHD definitions of FHR characteristics and patterns

Variability
Fluctuations in baseline that are irregular in amplitude and frequency

Absent = amplitude undetectable

Minimal = amplitude 0 to 5 bpm

Moderate = amplitude 6 to 25 bpm

Marked = amplitude over 25 bpm

Measured in a 10-minute window. The amplitude is measured peak to trough. There is no distinction between
short-term and long-term variability.

Baseline rate

Bradycardia = below 110 bpm

Normal = 110 to 160 bpm

Tachycardia = over 160 bpm

The baseline rate is the mean bpm (rounded to 0 or 5) over a 10-minute interval, excluding periodic changes,
periods of marked variability, and segments that differ by more than 25 bpm. The baseline must be identifiable
for two minutes during the interval (but not necessarily a contiguous two minutes); otherwise, it is considered
indeterminate.

Acceleration

An abrupt* increase in the FHR. Before 32 weeks of gestation, accelerations should last ≥10 sec and peak ≥10
bpm above baseline. As of 32 weeks gestation, accelerations should last ≥15 sec and peak ≥15 bpm above
baseline.

A prolonged acceleration is ≥2 minutes but less than 10 minutes. An acceleration of 10 minutes or more is
considered a change in baseline.

Late deceleration

A gradual* decrease and return to baseline of the FHR associated with a uterine contraction. The deceleration is
delayed in timing, with the nadir of the deceleration occurring after the peak of the contraction. The onset, nadir
and recovery usually occur after the onset, peak, and termination of a contraction.

Early deceleration
A gradual* decrease and return to baseline of the FHR associated with a uterine contraction. The nadir of the
FHR and the peak of the contraction occur at the same time. The deceleration's onset, nadir, and termination are
usually coincident with the onset, peak, and termination of the contraction.

Variable deceleration

An abrupt* decrease in FHR below the baseline. The decrease is ≥15 bpm, lasting ≥15 secs and <2 minutes from
onset to return to baseline. The onset, depth, and duration of variable decelerations commonly vary with
successive uterine contractions.

Prolonged deceleration
A decrease in FHR below the baseline of 15 bpm or more, lasting at least 2 minutes but <10 minutes from onset
to return to baseline. A prolonged deceleration of 10 minutes or more is considered a change in baseline.

NICHD: National Institute of Child Health and Human Development; FHR: fetal heart rate; bpm: beats per minute;
sec: seconds.
* "Gradual" and "abrupt" changes are defined as taking ≥30 seconds or <30 seconds, respectively, from the onset
of the deceleration/acceleration to its nadir/peak.

Adapted from:
1. National Institute of Child Health and Human Development Research Planning Workshop. Am J Obstet Gynecol 1997; 177:1385.
2. 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.

Graphic 65859 Version 10.0

Late decelerations

Late decelerations are characterized by a gradual decrease and return to baseline of the fetal heart rate
associated with uterine contractions. The deceleration is delayed in timing, with the nadir of the deceleration
occurring after the peak of the contraction. The onset, nadir, and recovery usually occur after the onset, peak,
and termination of a contraction. In this example, variability is minimal.

Courtesy of Robert L Barbieri, MD.

Graphic 67464 Version 3.0

Late decelerations 2

Late decelerations are characterized by gradual decrease and return to baseline of the fetal heart rate associated
with a uterine contraction. The deceleration is delayed in timing, with the nadir of the deceleration occurring after
the peak of the contraction. The onset, nadir, and recovery usually occur after the onset, peak, and termination of
a contraction. In this tracing, late decelerations have occurred after the first two contractions.

Graphic 96432 Version 1.0

Late deceleration

Courtesy of Dr. Christina Davidson.

Graphic 96977 Version 1.0

Recurrent late decelerations

Yellow tracing in the upper panel represents the fetal heart rate. Arrow points to the nadir of a late deceleration.

Courtesy of Dr. Christina Davidson.

Graphic 96980 Version 1.0

Deep late deceleration

Yellow tracing in the upper panel represents the fetal heart rate. Arrow points to the nadir of the late
deceleration.

Courtesy of Dr. Christina Davidson.

Graphic 96978 Version 1.0

Variable decelerations

Recurrent variable decelerations with absent to minimal variability.

Courtesy of Bruce K Young, MD.

Graphic 86060 Version 3.0

Variable decelerations with minimal to absent variability

Variability is minimal to absent.

Courtesy of Bruce K Young, MD.

Graphic 86062 Version 3.0

Sinusoidal FHR pattern

Sinusoidal heart rate pattern in a patient presenting with spontaneous fetomaternal hemorrhage near term. The
patient reported decreased fetal movement.

FHR: fetal heart rate.

Graphic 61189 Version 4.0

FIGO cardiotocography classification criteria, interpretation, and recommended
management*

Normal Suspicious Pathological

Baseline 110 to 160 bpm Lacking at least one <100 bpm

characteristic of normality,
but with no pathological
features

Variability 5 to 25 bpm Lacking at least one Reduced variability, increased

characteristic of normality, variability, or sinusoidal
but with no pathological pattern
features

Decelerations No repetitive ¶ decelerations Lacking at least one Repetitive ¶ late or prolonged

characteristic of normality,
but with no pathological
features
decelerations during >30
minutes or 20 minutes if
reduced variability, or one
prolonged deceleration with
>5 minutes

Interpretation Fetus with no Fetus with a low probability of Fetus with a high probability
hypoxia/acidosis having hypoxia/acidosis of having hypoxia/acidosis

Clinical No intervention necessary to Action to correct reversible Immediate action to correct

management improve fetal oxygenation causes if identified, close reversible causes, additional
state monitoring or additional methods to evaluate fetal
methods to evaluate fetal oxygenation [1] , or if this is no
oxygenation [1] possible expedite delivery

In acute situations (cord

prolapse, uterine rupture, or
placental abruption)
immediate delivery should be
accomplished

FIGO: International Federation of Gynaecology and Obstetrics; bpm: beats per minute.

* The presence of accelerations denotes a fetus that does not have hypoxia/acidosis, but their absence during
labor is of uncertain significance.

¶ Decelerations are repetitive in nature when they are associated with more than 50% of uterine contractions [2] .

References:
1. Visser GH, Ayres-de-Campos D, FIGO Intrapartum Fetal Monitoring Expert Consensus Panel. FIGO consensus guidelines on
intrapartum fetal monitoring: Adjunctive technologies. Int J Gynaecol Obstet 2015; 131:25.
2. Cahill AG, Roehl KA, Odibo AO, Macones GA. Association and prediction of neonatal academia. Am J Obstet Gynecol 2012; 207:206.
From: Ayres-de-Campos D, Spong CY, Candaharan E. FIGO consensus guidelines on intrapartum fetal monitoring: Cardiotocography. Int J
Gynaecol Obstet 2015; 131(1):13-24. https://obgyn.onlinelibrary.wiley.com/doi/abs/10.1016/j.ijgo.2015.06.020. Copyright © 2015
International Federation of Gynecology and Obstetrics. Reproduced with permission of John Wiley & Sons Inc. This image has been provided
by or is owned by Wiley. Further permission is needed before it can be downloaded to PowerPoint, printed, shared or emailed. Please contact
Wiley's permissions department either via email: permissions@wiley.com or use the RightsLink service by clicking on the 'Request Permission'
link accompanying this article on Wiley Online Library (http://onlinelibrary.wiley.com).

Graphic 116405 Version 1.0

NICHD criteria for category I, II, and III FHR tracings

Category I

All of the following criteria must be present. Tracings meeting these criteria are predictive of normal fetal
acid-base balance at the time of observation.

Baseline rate: 110 to 160 bpm

Moderate baseline FHR variability

No late or variable decelerations

Early decelerations may be present or absent

Accelerations may be present or absent

Category III

Category III tracings are predictive of abnormal fetal acid-base status at the time of observation. Prompt
evaluation is indicated and most parturients will require expeditious intervention, such as change in
position, treatment of hypotension, and discontinuation of any uterotonic drugs being administered.
Category III tracings include either (1) or (2) below.

(1) Absent baseline FHR variability and any of the following:

Recurrent late decelerations

Recurrent variable decelerations

Bradycardia

(2) Sinusoidal pattern

Category II

FHR tracing does not meet criteria for either category I or III and is considered indeterminate.

NICHD: National Institute of Child Health and Human Development; FHR: fetal heart rate; bpm: beats per minute.

Data from: 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.

Graphic 57583 Version 11.0

Management of intrapartum fetal heart rate tracings

Fetal heart rate Possible etiologies and

Management
tracing interpretation

Category I

Baseline 110 to 160 This is a normal tracing. Intermittent or continuous fetal

beats per minute with monitoring based on clinical status and
moderate variability underlying risk factors. Review every 30
and no late or variable minutes in the first stage and every 15
decelerations. minutes in the second stage of labor.
Accelerations and early
decelerations may be
present or absent.

Category II

Intermittent variable Common finding usually associated with No intervention required.

decelerations (<50% of normal outcome.
contractions)

Recurrent variable Umbilical cord compression. May be
decelerations (>50% of associated with impending acidemia,
contractions) especially if progressive increase in
depth, duration, and frequency.
Moderate variability and/or accelerations
suggest fetus is not currently acidemic.
Reposition mother to left or right lateral.
Amnioinfusion is an option. Adjunctive
measures to promote fetal oxygenation
(intravenous fluid bolus, reduce uterine
contraction frequency) may be useful.
Initiate scalp stimulation to provoke fetal
heart rate acceleration, which is a sign
that the fetus is not acidotic.

Delivery is indicated if tracing does not

improve and acidemia suspected.

Recurrent late Transient or chronic uteroplacental
decelerations insufficiency, such as from hypotension,
tachystole, or maternal hypoxia.
Accelerations and/or moderate variability
suggest fetus is not currently acidemic.
Reposition mother to left or right lateral.
Adjunctive measures to promote fetal
oxygenation include intravenous fluid
bolus, reduce uterine contraction
frequency. Persistent late decelerations
with minimal variability and absent
accelerations suggest fetal acidemia; this
is even more likely if variability is absent
(category III). Initiate scalp stimulation to
provoke fetal heart rate acceleration,
which is a sign that the fetus is not
acidotic.

Delivery is indicated if tracing does not

improve.

Fetal tachycardia Infection, medication, maternal medical
(baseline heart rate disorders, obstetric complications, fetal
greater than 160 beats tachyarrhythmia (typically rate over 200
per minute for at least beats per minute). Fetal acidemic more
10 minutes) likely when associated with minimal or
absent variability, absent accelerations,
and/or recurrent decelerations.
Treat underlying cause, if known. Initiate
scalp stimulation to provoke fetal heart
rate acceleration, which is a sign that the
fetus is not acidotic.
Delivery is indicated if tracing does not
improve and acidemia suspected.
 Bradycardia (baseline Acute onset may be due to hypotension, Treat underlying cause, if known. Initiate
heart rate less than 110 umbilical cord occlusion, rapid fetal scalp stimulation to provoke fetal heart
beats per minute for at descent, tachysystole, abruption, uterine rate acceleration, which is a sign that the
least 10 minutes) rupture. Fetal acidemia more likely when fetus is not acidotic. Delivery is indicated
associated with minimal or absent if tracing does not improve and acidemia
Prolonged
variability and absent accelerations suspected.
decelerations (15 beats
during baseline periods.
per minute drop below
baseline for more than
2 and less than 10
minutes)

Minimal variability Fetal sleep, medication, fetal acidemia. If
due to fetal sleep, should recover in 20 to
60 minutes. If due to maternal
medication, should recover as medication
wears off.
If decreased fetal oxygenation suspected
reposition mother to left or right lateral.
Adjunctive measures to promote fetal
oxygenation include intravenous fluid
bolus, reduce uterine contraction
frequency. Initiate scalp stimulation to
provoke fetal heart rate acceleration,
which is a sign that the fetus is not
acidotic.

If no improvement and no accelerations,

delivery is indicated if acidemia
suspected or confirmed by scalp pH.

Tachysystole (more Spontaneous labor: Tachysystole may be Reposition mother to left or right lateral,
than 5 contractions in associated with fetal acidemia if intravenous fluid bolus. If ineffective,
10 minutes, averaged accompanied by recurrent fetal heart reduce uterine contraction frequency
over 30 minutes) with rate decelerations. with a tocolytic.
fetal heart rate
Initiate scalp stimulation to provoke fetal
changes.
heart rate acceleration, which is a sign
Tachysystole that is that the fetus is not acidotic.
spontaneous and
associated with a Induction or augmentation. Decrease or stop uterotonic medications
normal fetal heart rate Reposition mother to left or right lateral,
pattern does not intravenous fluid bolus. If ineffective,
require treatment, but reduce uterine contraction frequency
the possibility of with a tocolytic. Initiate scalp stimulation
placental abruption as to provoke fetal heart rate acceleration,
the underlying etiology which is a sign that the fetus is not
should be considered. acidotic.

Category III

Absent baseline Increased risk of fetal acidemia. Prepare for delivery and reposition
variability and mother to left or right lateral,
recurrent late intravenous fluid bolus. Initiate scalp
decelerations, stimulation to provoke fetal heart rate
recurrent variable acceleration, which is a sign that the
decelerations, or fetus is not acidotic. If no improvement
bradycardia after conservative measures and scalp
stimulation does not result in
acceleration, delivery is advisable.

Sinusoidal Increased risk of hypoxemia. Risk of Prepare for delivery and reposition
acidemia increased if prolonged or mother to left or right lateral,
intravenous fluid bolus. Initiate scalp
 amplitude of 15 beats per minute or stimulation to provoke fetal heart rate
more. acceleration, which is a sign that the
fetus is not acidotic. If no improvement
after conservative measures and scalp
stimulation does not result in
acceleration, delivery is advisable.

This chart represents a suggested approach to the interpretation and management of fetal heart rate patterns. It
is not intended as a standard of care. Patient-specific factors need to be considered in the evaluation and
management of individual patients.

Modified from: American College of Obstetricians and Gynecologists Practice Bulletin. Management of intrapartum fetal heart rate tracings.
Obstet Gynecol 2010; 116:1232.

Graphic 71679 Version 8.0

Normal variability and accelerations

Normal fetal heart rate pattern: the baseline rate is in the normal range (between 110 to 160 bpm), moderate FHR
variability (ie, amplitude 6 to 25 bpm) is present, and both late and variable decelerations are absent. In the
United States, this tracing would be classified as Category I.

bpm: beats per minute; FHR: fetal heart rate.

Courtesy of Bruce K Young, MD.

Graphic 86064 Version 2.0

Early deceleration

Early decelerations are uniform, mirror the contractions, and decelerate only 10 to 20 beats per minute.

Reproduced with permission from: Freeman RK, Garite TJ, Nageotte MP, Miller LA. Basic Pattern Recognition. In: Fetal Heart Rate Monitoring.
Lippincott, Williams & Wilkins, Philadelphia 2012. Copyright © 2012 Lippincott Williams & Wilkins. www.lww.com.

Graphic 94981 Version 4.0

Contributor Disclosures
David A Miller, MD Consultant/Advisory Boards: CCSI [Fetal monitoring]. Other Financial Interest: GE Healthcare
[Proceeds for learning program – Fetal monitoring]. All of the relevant financial relationships listed have been
mitigated. Vincenzo Berghella, MD Consultant/Advisory Boards: ProtocolNow [Clinical guidelines]. All of the
relevant financial relationships listed have been mitigated. Vanessa A Barss, MD, FACOG No relevant financial
relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
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