Chapter 17

Antepartum Cardiotography

Susana Santo and Diogo Ayres-De-Campos

Introduction

Cardiotocography (CTG), derived from the Greek terms “cardio” (heart) and
“tokos” (uterine activity) [1], was introduced into clinical practice during the 1960s
and is nowadays widely used in high-resource countries as a method of assessing
fetal oxygenation during late pregnancy and labor. The physiological principles
behind antepartum CTG are the same as those of intrapartum CTG, as are the main
objectives of both, i.e., evaluation of ongoing fetal oxygenation. For these reasons,
CTG interpretation is similar in both settings.
Fetal heart rate (FHR) is modulated by several stimuli. The central nervous sys-
tem has a major influence on the FHR, mediated via the cardioregulatory center
located in the brainstem. The efferent component of the autonomic nervous system
has a major influence on FHR signals, with sympathetic impulses increasing their
frequency and parasympathetic impulses having the opposite effect [2]. The input of
sympathetic and parasympathetic systems creates a constant fluctuation of the FHR
signal, known as variability [3]. These two components of the autonomic nervous
system mature at different rates during intrauterine life. The sympathetic system
matures faster and therefore preterm fetuses have a higher baseline. Later matura-
tion of the parasympathetic system leads to a constant decrease in FHR baseline
throughout gestation and post-term fetuses may present a baseline between 100 and
110 bpm [4].
The central nervous system is also responsible for the appearance of FHR
accelerations, which are coincident with fetal movements and with the

S. Santo (*) · D. Ayres-De-Campos

Departamento de Obstetrícia, Ginecologia e Medicina da Reprodução, Faculdade de
Medicina da Universidade de Lisboa, Centro Hospitalar Universitário Lisboa Norte –
Hospital de Santa Maria, Lisbon, Portugal

© Springer Nature Switzerland AG 2022 303

R. A. Moreira de Sá, E. B. d. Fonseca (eds.), Perinatology,
[Link]
304 S. Santo and D. Ayres-De-Campos

occurrence of sleep-activity cycles. Fetal behavioral states refer to periods of

deep sleep (no eye movements), alternating with periods of active sleep (rapid
eye movements), and active wakefulness [5]. Constant transitions between dif-
ferent behavioral states are a sign of neurological responsiveness and of the
absence of fetal hypoxia. These transitions usually become clearer after
32–34 weeks of gestation, as a consequence of central nervous system matura-
tion [5]. Deep sleep can last up to 50 min [6] and is associated with borderline
variability and very rare accelerations. Active sleep is the most frequent behav-
ioral state and is represented by normal variability and a moderate number of
accelerations. Active wakefulness is represented by normal variability and a high
number of accelerations. Accelerations may be so frequent as to make baseline
estimation difficult [4].
Uterine contractions are a hallmark of labor but may also occur irregularly before
this period starts. Fetal head compression can stimulate intracranial baroreceptors
and trigger a nervous reflex via the brainstem and parasympathetic pathways, lead-
ing to the appearance of early decelerations [2, 4]. These are not associated with
fetal hypoxia [4].
Contractions can also cause umbilical cord compression, leading to the
appearance of variable decelerations [7]. The pathophysiology behind these
events is the occurrence of a temporary increase in blood pressure, stimulating
baroreceptors located in central fetal vessels, and thus triggering a nervous reflex
via the brainstem and parasympathetic pathways that lead to a drop in FHR. The
response is very rapid, and a quick recovery of the baseline FHR is also
observed [7, 4].
A sudden decrease in blood oxygen concentration activates chemoreceptors
located in central fetal vessels, which stimulates a nervous reflex via the brainstem
and parasympathetic pathways causing late decelerations of the FHR [3]. In com-
parison with baroreceptors, activation of chemoreceptors is associated with a slower
response and time to recover the baseline FHR [4].
Reduced FRH variability is caused, among others, by central nervous system
hypoxia, reducing both sympathetic and parasympathetic activity in the brainstem,
and the resulting oscillations in FHR [4, 8].
As most CTG events occur in response to uterine contractions, efforts were
made in the 1970s and 1980s to artificially stimulate uterine contractions during
antepartum CTGs. Nipple stimulation and exogenous oxytocin were used for this
purpose, in a technique that became known as the “contraction stress test” [9–11].
The time-­consuming nature of the method, and the impossibility of standardizing
the intensity and duration of contractions, led to its progressive abandonment. In
contrast to the previous nomenclature, in some parts of the world, antepartum CTG
without artificial stimulation of contractions became known as the “nonstress test,”
but this terminology has nowadays mostly been abandoned.
The aim of this chapter is to address the basic principles of antepartum CTG
interpretation and to outline the management of normal and abnormal tracings.
17 Antepartum Cardiotography 305

Indications

Antepartum CTG is usually performed in clinical situations associated with an

increased risk of fetal hypoxia. These conditions include prepregnancy diseases
(e.g., systemic lupus erythematosus, antiphospholipid syndrome, diabetes mellitus,
etc.), pregnancy-related diseases (preeclampsia, placental abruption, etc.), and fetal
diseases (fetal growth restriction, congenital malformations, etc.), all of which are
associated with an increased risk of adverse perinatal outcome [10].
Although it is more commonly performed during the third trimester, CTG can be
acquired from around 25 weeks onward. The frequency of exams depends on the
clinical situation, gestational age, interpretation of previous tracings, etc. The inter-
vals of testing usually vary between three times a day and every week.

CTG Tracing Acquisition

All CTG monitors record FHR and uterine contraction signals. An audible FHR
signal is available to help identify the ideal placement of the FHR sensor. The trac-
ing itself may be printed on paper or displayed on a computer monitor. The horizon-
tal scale for CTG registration is commonly called “paper speed,” and the available
options are 1, 2, or 3 cm/min. Paper speed has some impact on the detail of the
information displayed but also on paper length, especially in settings where elec-
tronically storage is not available. In most countries, 1 cm/min is selected, but 3 cm/
min is popular in countries like the USA and Japan. The vertical scale may also
differ, varying from 20 to 30 bpm/cm. Paper scales used in each center should be the
ones with which health care professionals are most familiar because patterns can
look very distinct at different paper speeds. For example, variability may appear
reduced at 3 cm/min for a health care professional familiar with the 1 cm/min
scale [4].
A tracing should be identified from the start of acquisition, including mother’s
name, hospital identification number, date, and time. Modern machines automati-
cally show the last two, but it is important to check that these parameters are cor-
rectly configured.
For antepartum CTGs, both FHR and uterine contraction signals must be acquired
using noninvasive methods, i.e., external transducers placed on the maternal abdo-
men and fixed with elastic bands. External FHR monitoring uses a Doppler-­
ultrasound transducer that detects movement of fetal heart structures such as heart
valves and interchamber septae. The acquired signal is processed using autocorrela-
tion to guarantee an adequate tracing quality, and the result is an approximation to
the real heart cycle [12]. Signal loss due to fetal movements, inadvertent recording
of the maternal heart rate, inaccurate recording of fetal arrhythmias, and signal arti-
facts such as double and half-counting may all occur with this method [13].
306 S. Santo and D. Ayres-De-Campos

Uterine contractility is recorded with an external tocodynameter placed on the

uterine fundus, measuring the tensile strength of the uterine wall during contrac-
tions. The tocodynameter only allows an evaluation of the frequency of contractions
[4]. Resting tone, duration, and intensity of the contractions can only be accurately
assessed with invasive methods that are not applicable before labor. The uterine
contraction signal may also be affected by incorrect placement of the transducer,
inadequate tension applied to the elastic band, and maternal obesity.
Fetal movements are frequently integrated into the antepartum CTG. These can
be recorded by the mother and signaled by pressing an event marker button or auto-
matically extracted from the Doppler signal, using an algorithm that separates the
low-frequency signals that correspond to fetal motor activity.
Some CTG monitors also acquire and record the maternal heart rate. This can be
obtained by electrocardiography, pletismography, or a Doppler sensor placed within
the tocodynamometer. Simultaneous recording of the FHR and maternal heart rate
may be important to distinguish fetal from maternal signals.
Antepartum CTG should be performed in the lateral recumbent or half-sitting
positions, thus avoiding aortocaval compression, which can reduce uterine blood
flow and placental perfusion.

CTG Interpretation

The International Federation of Obstetrics and Gynecology (FIGO) recently updated

their CTG interpretation guidelines, through a large consensus panel including 50
experts [1, 4, 14–16]. As referred before, the pathophysiology behind CTG features
is the same, whether they occur in the antepartum or intrapartum periods, so the
same concepts of CTG interpretation can be used in both periods.

Basic FHR Features

CTG interpretation requires the evaluation of four basic FHR features: baseline,
variability, accelerations, and decelerations [4]. The combined evaluation of these
features allows the classification of the CTG tracing into one of three categories:
normal, suspicious, or pathological.
Baseline is the mean level of the most horizontal and less oscillatory FHR
segments. It is estimated in 10-minute periods and expressed in beats per minute
(bpm). Baseline values may vary between two periods of 10 min, but in antepar-
tum CTGs, it is usually very stable. The baseline may be difficult to evaluate
during the fetal behavioral state of active wakefulness, and review of previous
segments or continued monitoring for longer time periods may be necessary in
these situations. Normal baseline is defined as a value between 110 and 160 bpm
(Fig. 17.1). It is important to consider gestational age in this equation, as preterm
17 Antepartum Cardiotography 307

Fig. 17.1 Normal baseline (130 bpm); accelerations are identified with arrows

fetuses tend to have values toward the upper end of this range and post-term
fetuses toward the lower end [4]. Tachycardia is defined as a baseline value above
160 bpm lasting more than 10 min. Maternal pyrexia is the most frequent cause,
but it can also occur in the initial stages of a nonacute fetal hypoxemia, with the
administration of beta-agonist drugs, parasympathetic blockers, and with fetal
arrhythmias such as supraventricular tachycardia and atrial flutter [4]. Bradycardia
is a baseline value below 110 bpm lasting more than 10 min. However, values
between 100 and 110 bpm may occur in normal fetuses, especially in postdate
pregnancies. Maternal hypothermia, administration of beta-blockers, and fetal
arrhythmias such as atrial-ventricular block are other possible causes of brady-
cardia [4].
Variability refers to the fine oscillations in the FHR signal and is visually esti-
mated as the average signal bandwidth amplitude in 1-minute segments. Normal
variability is defined as a bandwidth amplitude between 5 and 25 bpm [4] (Fig. 17.2).
Reduced variability is a bandwidth amplitude below 5 bpm for more than 50 min in
baseline segments, or for more than 3 min during decelerations [4] (Fig. 17.3).
There is a high degree of subjectivity in the visual evaluation of this parameter, and
therefore careful re-evaluation or computer analysis is recommended in borderline
situations. Reduced variability can occur in situations associated with central ner-
vous system hypoxia that result in decreased autonomic system activity. It may also
occur in fetuses with cerebral injury, infection, and administration of central ner-
vous system depressants or parasympathetic blockers. During deep fetal sleep, vari-
ability is usually in the lower range of normality, but the bandwidth amplitude is
seldom under 5 bpm. Increased variability, also known as the saltatory pattern, cor-
responds to a bandwidth exceeding 25 bpm for more than 30 min [4] (Fig. 17.4).
The pathophysiology of this pattern is incompletely understood, but it has been
described in the initial stages of subacute hypoxia and may be caused by fetal auto-
nomic instability [17].
308 S. Santo and D. Ayres-De-Campos

Fig. 17.2 Normal variability (5–25 bpm)

Fig. 17.3 Reduced variability (<5 bpm). To be clinically meaningful, the pattern needs to last for
at least 50 min, and medication depressing the central nervous system needs to be ruled out

Accelerations are abrupt increases in FHR above the baseline, of more than
15 bpm in amplitude, and lasting more than 15 s but less than 10 min [4] (Fig. 17.1).
Before 32 weeks of gestation, accelerations may be of slightly lower amplitude and
duration. Accelerations usually coincide with fetal movements and are a sign of a
neurologically responsive fetus that is not suffering from hypoxia.
Decelerations are abrupt decreases in FHR below the baseline with an amplitude
of more than 15 bpm and a duration of more than 15 s. Decelerations may be clas-
sified as early, variable, late, or prolonged, mainly according to their shape and
duration. They are usually associated with uterine contractions, and therefore are
much less frequent in antepartum CTGs. Early decelerations are shallow, short-­
lasting, with normal variability within the deceleration, and coincident with
17 Antepartum Cardiotography 309

Fig. 17.4 Increased variability (>5 bpm). To be clinically meaningful, this pattern needs to last for
at least 30 min

Fig. 17.5 Early decelerations (identified with arrows)

contractions (Fig. 17.5). It is believed that they are caused by fetal head compres-
sion and therefore do not indicate fetal hypoxia. Variable decelerations (V-shaped)
exhibit a rapid drop (onset to nadir in less than 30 s), good variability within the
deceleration, and rapid recovery to the baseline. They vary in size, shape, and rela-
tionship to uterine contractions (Fig. 17.6). They translate a baroreceptor-mediated
response to increased arterial pressure, as occurs with umbilical cord compression,
and are seldom associated with an important degree of hypoxia. Late decelerations
(U-shaped or with reduced variability) have a gradual onset or a gradual return to
the baseline (>30 s), or reduced variability within the deceleration. In the presence
of a tracing with reduced variability and no accelerations, the definition of late
decelerations also includes those with an amplitude of 10–15 bpm (Fig. 17.7). Late
310 S. Santo and D. Ayres-De-Campos

Fig. 17.6 Repetitive variable decelerations (identified with arrows)

Fig. 17.7 Repetitive late decelerations (identified with arrows). In the context of a tracing with
reduced variability and no accelerations, late decelerations only need to have 10 bpm of amplitude

decelerations start more than 20 s after the onset of a contraction, have a nadir after
the acme, and return to the baseline after the end of the contraction. They are indica-
tive of a chemoreceptor-mediated response to sudden fetal hypoxemia. Prolonged
decelerations last more than 3 min and are very likely to include a chemoreceptor-­
mediated component, and thus to indicate some degree of hypoxemia (Fig. 17.8).
When they exceed 5 min, FHR is maintained <80 bpm, and there is reduced vari-
ability within the deceleration, they are usually indicative of an episode of acute
fetal hypoxemia and therefore require emergent intervention [4].
The sinusoidal pattern is regular, smooth, undulating signal, resembling a sine
wave that lasts more than 30 min. The amplitude of this undulation is 5–15 bpm, and
the frequency is 3–5 cycles per minute (Fig. 17.9). The pathophysiological basis for
17 Antepartum Cardiotography 311

Fig. 17.8 A prolonged deceleration lasting around 4.5 min

Fig. 17.9 A sinusoidal pattern. To be clinically meaningful, this pattern needs to last at least 30 min

the sinusoidal pattern is incompletely understood, but it is known to occur in asso-

ciation with severe fetal anemia (fetal-maternal hemorrhage, twin-to-twin transfu-
sion syndrome, and ruptured vasa previa). Less frequently, it has been described in
cases of acute fetal hypoxia, infection, or fetal malformations [4]. The pseudosinu-
soidal pattern resembles the sinusoidal pattern but has a more jagged “saw-tooth”
appearance, rather than a smooth undulating form (Fig. 17.10). The duration seldom
exceeds 30 min, and it is characterized by normal patterns before and after. This
pattern has been described after analgesic administration to the mother and during
periods of fetal sucking and other mouth movements. It is sometimes difficult to
distinguish the pseudosinusoidal pattern from the true sinusoidal pattern, and the
short duration of the former is the most important aspect that discriminates between
the two [4].
312 S. Santo and D. Ayres-De-Campos

Fig. 17.10 A pseudosinusoidal pattern

Contractions are bell-shaped gradual increases in the uterine activity signal fol-
lowed by roughly symmetric decreases, with 45–120 s in total duration [4].

Tracing Classification

Classification of CTG tracings requires a systematic evaluation of the basic FHR

features described above (Table 17.1).
A normal CTG tracing has a normal baseline (110–160 bpm), normal variability
(5–25 bpm), and no repetitive decelerations. In the antepartum period, accelerations
also need to be present. It is important to emphasize that sporadic decelerations may
occur in normal tracings and are usually early or variable in nature. A suspicious
tracing lacks at least one characteristic of normality but has no pathological fea-
tures. Pathological tracings have one or more of the flowing criteria: bradycardia
(<100 bpm), reduced variability (<5 bpm for more than 50 min or for more than
3 min in decelerations), increased variability (>25 bpm for more than 30 min),
repetitive late or prolonged decelerations (for more than 30 min; or for >20 min if
variability is <5 bpm), prolonged deceleration with more than 5 min, or a sinusoidal
pattern [4].
Antepartum CTGs have also been classified as reactive or nonreactive, according
to the presence of accelerations within a given period [6, 18, 19]. Causes of nonre-
active tracings include fetal sleep, hypoxia, prematurity, maternal smoking, fetal
neurologic or cardiac abnormalities, or maternal ingestion of drugs. Vibroacoustic
stimulation, using an artificial larynx placed on the maternal abdomen, has been
used to distinguish between the state of deep sleep and fetal hypoxia, but this prac-
tice has largely been abandoned.
17 Antepartum Cardiotography 313

Table 17.1 CTG classification adapted from the 2015 FIGO guidelines [4]

Normal Suspicious Pathological

Baseline 110–160bpm <100 bpm
Reduced variability
Variability 5–25bpm Increased variability
Lacking at least one
Sinusoidal pattern
characteristic of
Repetitive* late or
normality, but with no
prolonged decelerations
No repetitive* pathological features
Decelerations for >30 min (or >20 min if
decelerations
reduced variability)
Deceleration >5 min
Low probability of High probability of
Interpretation No hypoxia/acidosis
hypoxia/acidosis hypoxia/acidosis
*Decelerations are repetitive when associated with > 50% contractions.
Decelerations are repetitive when associated with >50% contractions
*

Clinical Management of Antepartum CTG

Because antepartum CTGs are easy to perform, noninvasive, have no contraindica-

tions, and are usually well-liked by women, they rapidly became part of routine care
in high-resource countries. Although only few skills are needed for signal acquisi-
tion, extensive experience is required for interpretation. Gestational age, maternal
medication, and other accompanying clinical information need to be taken into
account for the interpretation of antepartum CTGs and for subsequent management.
Fetal ultrasound and multivessel Doppler evaluation may add essential elements for
the decision process.
A normal CTG excludes ongoing fetal hypoxia in the central organs, but the
method cannot reliably determine whether this will occur in the near or long-term
future. A suspicious tracing is unlikely to be associated with ongoing hypoxia in the
central organs, but additional tests may be necessary to clarify the cause. Pathological
tracings are frequently associated with ongoing fetal hypoxia in central organs and
it is essential to clarify the underlying cause [4]. Reversible causes of fetal hypoxia
(i.e., excessive uterine contractility, maternal supine position, hypotension) are fre-
quently seen during labor but are rare events in the antepartum period. Irreversible
conditions such as placental insufficiency or placental abruption are the most fre-
quent causes of pathological CTGs in these settings. CTG changes appear late in the
context of chronic placental insufficiency, as they translate hypoxia of central fetal
organs, which are protected until late by the brain-sparing phenomenon.
Antepartum CTG provides valuable information on the oxygenation of the fetal
brain and heart at a given moment in time, but the initial expectations that it can
predict fetal “reserve” or what will occur in the next hours, days, or weeks are unre-
alistic. Fetal oxygenation may be quickly affected by acute and subacute events
(placental abruption, uterine rupture, cord prolapse) that can follow a normal
CTG. On the other hand, abnormal tracings may reflect different degrees of central
hypoxia, and thus have a limited capacity to predict adverse outcomes, such as
metabolic acidosis, low Apgar score, and neonatal intensive care unit admissions. A
314 S. Santo and D. Ayres-De-Campos

meta-analysis of six randomized controlled trials carried out in the 1980s and 1990s,
comparing the use of antepartum CTGs with no use, showed no differences in peri-
natal mortality (RR 2.05, 95% confidence interval (CI) 0.95–4.42) or potentially
preventable deaths (RR 2.46, 95% CI 0.96–6.30) [20]. Studies were clearly under-
powered to evaluate these rare outcomes. Despite the limited scientific evidence,
antepartum CTG continues to be extensively used in high-resource countries and is
recommended by several international scientific societies for the surveillance of
high-risk pregnancies [10, 11].
The complex nature of the FHR signal conditions a limited intra- and interob-
server agreement in the evaluation of basic CTG features and in CTG classification
[21–23]. Several human factors have also been appointed as important limitations of
CTG analysis [24]. They are mainly related to the experience of health care profes-
sionals using the technology, and to the guidelines used for interpretation [25].
In modern days, antepartum CTG relies heavily on the evaluation of variability,
and aspect that, on its own, may swerve the classification from normal to pathologi-
cal. This is a difficult parameter to assess with the naked eye because constant
changes in bandwidth are observed and there is much subjectivity in the evaluation
of their amplitude. This limitation may be overcome by computer analysis of CTGs,
which emerged in the 1080s and 1990s. The Dawes/Redman and SisPorto systems
were the first to be developed for this purpose [26–28]. These systems incorporate
complex mathematical algorithms that estimate the FHR baseline, quantify vari-
ability, and identify accelerations and decelerations. Using computer analysis, vari-
ability can be separated into short-term (oscillations between adjacent or near
adjacent signals) and long-term variability (bandwidth values evaluated over the
course of 1 min), providing additional information on the pathophysiological mech-
anisms of the central nervous system oxygenation.

Conclusions

CTG is one of the most adopted tools for antenatal fetal surveillance in high-­
resource countries. Antepartum and intrapartum CTG share the same pathophysio-
logical mechanisms, so the same CTG interpretation guidelines can be used for both
periods. Antepartum CTG should be used in conditions that carry a high-risk of fetal
hypoxia. A normal CTG tracing excludes the occurrence of ongoing fetal hypoxia
in central organs, but cannot evaluate the “fetal reserve” or predict hypoxic events
occurring at a later time. Chronic placental insufficiency and placental abruption are
the most frequent causes of pathological CTGs. These occur with ongoing hypoxia
in central fetal organs, but may also be mimicked by deep sleep and by medication
given to the mother. CTG changes appear late in the course of chronic placental
insufficiency, as central organs are protected by the brain-sparing effect. Computer
analysis of antepartum CTGs can provide a more reliable quantification of FHR
variability, thus overcoming eyeball limitations in visual analysis and detecting
changes that occur over the course of time. Tracing interpretation and subsequent
17 Antepartum Cardiotography 315

clinical management requires expertise, needing to take into account other aspects
of the clinical situation.

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