DOI: 10.1111/1471-0528.
12900
www.bjog.org
Are we (mis)guided by current guidelines on
intrapartum fetal heart rate monitoring? Case
for a more physiological approach to
interpretation
A Ugwumadu
St George’s Hospital, London, UK
Correspondence: A Ugwumadu, Department of Obstetrics & Gynaecology, St George’s Hospital, Blackshaw Road, London SW17 0QT, UK.
Email augwumad@sgul.ac.uk
Accepted 22 April 2014. Published Online 12 June 2014.
Original interpretations of fetal heart rate (FHR) patterns equated
FHR decelerations with ‘fetal distress’, requiring expeditious
delivery. This simplistic interpretation is still implied in our
clinical guidelines despite 40 years of increasing understanding of
the behaviour and regulation of the fetal cardiovascular system
during labour. The physiological basis of FHR responses and
adaptations to oxygen deprivation is de-emphasised, whilst
generations of obstetricians and midwives are trained to focus on,
and classify, the morphological appearances of decelerations into
Please cite this paper as: Ugwumadu A. Are we (mis)guided by current guidelines on intrapartum fetal heart rate monitoring? Case for a more physiological
approach to interpretation. BJOG 2014;121:1063–1070.
Introduction
Intrapartum electronic fetal heart rate (FHR) monitoring is
widely practiced in the UK, the USA and in many other
developed countries.1,2 It is associated with reduced early
onset neonatal seizures,3 and is credited with the near elim-
ination of unexpected intrapartum fetal mortality;4 how-
ever, its use is associated with the increased costly and not
infrequently harmful operative delivery of nonacidotic
babies.5,6 This results, at least in part, from the training of
obstetricians and midwives to focus on the morphological
appearances of FHR decelerations and their descriptive
labels, rather than understanding how the fetus defends
itself and compensates for intrapartum hypoxic ischaemic
insults. This approach has persisted, in spite of 40 years of
increasing basic science and clinical knowledge of the
behaviour and regulation of the fetal cardiovascular system
during labour. Admittedly, standardised and simplified
clinical guidelines are essential for good-quality clinical care
and patient safety;7,8 however, current guidelines on intra-
partum FHR interpretation may be contributing to the
operative delivery of nonacidotic infants because of their
ª 2014 Royal College of Obstetricians and Gynaecologists
Review article
descriptive categories, with no attempt to understand how the
fetus defends itself and compensates for intrapartum hypoxic
ischaemic insults, or the patterns that suggest progressive loss of
compensation. Consequently, there is a lack of confidence, marked
variation in FHR interpretation, defensive practices, unnecessary
operative interventions, and a failure to recognise abnormal FHR
patterns, resulting in adverse outcomes and expensive litigation.
Keywords CTG practice algorithm, deceleration, fetal
cardiovascular physiology, intrapartum fetal heart rate monitoring.
focus on reference values for baseline FHR, variability, and
classification of FHR decelerations into label categories
without articulating the relationships between these param-
eters, and their collective link with fetal wellbeing, in a way
that is intuitive to a thinking clinician. Many clinicians
apply them in isolation and intervene for fetal compromise
on the basis of isolated FHR tachycardia, reduced variabil-
ity, lack of acceleration, or uncomplicated variable decelera-
tions.
In addition, these guidelines do not provide the clinician
with an unambiguous and comprehensive algorithm for
intrapartum FHR interpretation, with recommendations for
management, and until such an algorithm is developed
there can be no consistent response to FHR patterns. Fur-
thermore, they are silent on scenarios associated with fetal
damage, such as fever, chorioamnionitis, fetal systemic
inflammatory response syndrome (FSIRS) and its noxious
synergistic interaction with hypoxia, fetal strokes, lack of
fetal cycling behaviour, maternal disease, and the recogni-
tion of maternal heart rate (MHR) monitoring, to name a
few. Other pieces of ‘quasi-guidance’ have emerged in
recent years to plug the gaps in the guidelines. For
1063

Ugwumadu
example, many maternity units in the UK require their staff
to apply the mnemonic ‘DR C BRaVADO’ to the interpre-
tation of the cardiotocograph (CTG, a graphical presenta-
tion of the FHR and uterine contractions), where ‘DR’
stands for define risk, C stands for contraction frequency
in 10 minutes, BRa stands for baseline rate, V stands for
variability, A stands for accelerations, D stands for deceler-
ations, and ‘O’ stands for overall classification. The user is
compelled to document their assessment of the CTG fea-
tures by ticking relevant boxes, but no reference is made to
the evolution or progression of the FHR, the success or
failure of fetal compensation, or the potential fetal conse-
quences. Some clinicians regard this ‘tick box’ exercise as
the object of FHR interpretation. The current UK National
Institute for Health and Care Excellence (NICE) guidance
recommends FHR evaluation and documentation every
hour, and by a ‘fresh pair of eyes’ every 2–4 hours. The
evidence for this approach is at best slim, and in the
author’s opinion it makes no difference how many times
the CTG is reviewed and by however many ‘pairs of eyes’ if
they are all ‘programmed’ to provide morphological
description of FHR decelerations. This exercise provides
just a snapshot of the FHR patterns without an under-
standing of their evolution, and cannot possibly permit an
accurate assessment of the fetal condition or a thoughtful
analysis of the urgency or optimum route of delivery. Each
fetus should be used as its own control and greater atten-
tion paid to changes in its FHR characteristics over time.
In 2008 the report of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development
(NICHD), American College of Obstetricians and Gynecol-
ogists, and the Society for Maternal–Fetal Medicine multi-
disciplinary expert workshop on electronic FHR monitoring
recommended a three-tier system for FHR classification:
category 1, normal FHR pattern predictive of normal acid
base status at the time of observation; category II, interme-
diate FHR pattern not classified as category I or III, but not
predictive of abnormal acid base status; and category III,
abnormal FHR pattern associated with abnormal acid base
at the time of observation.9 The three-tier NICHD catego-
ries are similar to the UK NICE classification of ‘normal’
‘suspicious’, and ‘pathological’, but unlike the NICE guid-
ance it avoided the trap of assigning equivalent value to all
CTG features in defining the intermediate category.10 Com-
pared with categories I and III, however, category II is mas-
sively heterogeneous and disproportionately large, including
≥80% of intrapartum FHR patterns.11,12 More importantly,
category II may be interpreted as a cohort of static FHR
patterns with no expectation on the user to: (1) reference
the evolution from an antecedent normal or even a cate-
gory-III pattern; or (2) prospectively predict the likely FHR
trajectory. The inclusion of ‘early decelerations’ amongst the
features of a normal category-I pattern is open to the erro-
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neous interpretation that FHR decelerations synchronous
with uterine contractions are benign. Amongst a panel of
experts, the inter-observer reliability of the three-tier system
of interpretation was found to be moderate only, and poor
for the category-III pattern.13 Parer et al.14 have proposed
the subdivision of category II patterns to create a minimum
of a five-tier system, including a colour-coded example,15
which they suggest would facilitate research in this arena.
An international collaborative revision of the 30-year-old
FHR guidelines from the International Federation of Gyne-
cology and Obstetrics (FIGO) is underway, and one hopes
that a more meaningful and intuitive approach to FHR
interpretation will emerge.
As the FHR is sensitive to hypoxaemia (reduced systemic
pO2) and hypoxia (reduced oxygen in the tissues), but
lacks specificity for the development of acidosis (increased
acid H+ within the tissues), the clinically important end
point of hypoxia, FHR monitoring even with secondary
tests would result in an increase in the operative delivery of
nonacidotic babies. More than 40 years ago, Beard et al.16
showed that most CTG abnormalities were not associated
with fetal acidosis, suggesting that our definition of a ‘path-
ological’ CTG and its relationship with fetal asphyxia must
be flawed. On the other hand, if intrapartum CTG inter-
pretation was based on tracking the evolution of fetal
defensive and compensatory responses to hypoxic ischae-
mic insults, then it should be possible, at least theoretically,
to discriminate from a pool of ‘pathological’ CTGs those
fetuses at genuine risk of acidosis and acidaemia (increased
H+ in the bloodstream) or impaired neonatal adaptation
from the subset that are not. In this commentary the
author will describe the characteristics of the FHR and cur-
rent guidance for their interpretation, the physiological
basis for fetal compensation for types, degrees, and dura-
tions of hypoxic ischaemic insults, and the patterns that
suggest progressive failure of compensation, and propose
an algorithm for intrapartum FHR interpretation based on
what is known about intrapartum fetal adaptation to hyp-
oxic ischaemic insults. The author recently drew from these
principles to describe and explain the CTG patterns associ-
ated with fetal injury.17
The normal CTG and its significance
A normal CTG should have a stable baseline FHR of
110–160 bpm without significant decelerations, normal
variability of 5–25 bpm, and, crucially, periods of reduced
FHR variability, which alternate with periods of increased
variability with or without accelerations: so-called cycling
behaviour. Fetal cycling activity is a key behavioural state
of the normal term or near-term fetus. It suggests neuro-
logical integrity and the absence of significant acidaemia
or acidosis.18,19 Cycling may be absent in hypoxia,
ª 2014 Royal College of Obstetricians and Gynaecologists

chorioamnionitis, fetal infection, severe meconium aspira-
tion syndrome, exposure to drugs, including oxytocin, rec-
reational substances, opiates, major neurological or
chromosomal abnormalities, intracranial haemorrhage or
other forms of brain damage, and in fetuses <28–32 weeks
of gestation. A quantitatively normal FHR variability that
does not exhibit alternating periods of reduced variability
is not normal. Intriguingly, the significance of this key fetal
behaviour is ignored by some regulatory guidelines on in-
trapartum FHR monitoring.
A normal CTG symbolises fetal wellbeing,20 normoxia,21
normal acid base status,22,23 absence of asphyxia,22,23 and a
low probability of developing intrapartum fetal asphyxia,24
barring obstetric catastrophes. It also suggests that the fetal
neurological and cardiovascular systems are intact, and able
to react and defend the fetus against intrapartum insults.
In contrast, the fetus with an abnormal CTG is at risk of
adverse outcome and long-term neurological deficits,24–27
and if exposed to asphyxiating intrapartum insults may dis-
play maladaptive responses instead of the predictable
sequence of compensatory responses.
FHR decelerations
The FHR deceleration induced by cord compression is a
chemoreceptor-mediated parasympathetic reflex, in contrast
to the late decelerations caused by myocardial depression.
It is widely believed that the purpose of these responses is
to reduce myocardial workload and oxygen demand.28 The
appearance of FHR decelerations in response to uterine
contractions suggest that the fetus is either hypoxaemic as
a result of reduced transplacental oxygen transfer, in which
case the decelerations are usually delayed in onset relative
to the contractions, uniform, and slow in downward and
upward trajectories (late decelerations), or that blood flow
through the umbilical cord is interrupted, in which case
the decelerations are immediate and sharp. Therefore, in
my opinion terminologies like ‘unprovoked decelerations’
should be abandoned. There cannot be such a concept sim-
ply because we have not observed or recorded the stimulus
for the FHR deceleration.
Over 80% of the intrapartum FHR decelerations are var-
iable decelerations, yet it is the very CTG abnormality for
which there is the least agreement between observers.29
They are characterised by a sharp fall in FHR from the
baseline to the nadir in ≤30 seconds, and may vary in
depth, shape, duration, and temporal relationship with
uterine contractions. Over the years the emphasis has been
placed on morphological classification, which tells us noth-
ing about fetal wellbeing and the consequences of intermit-
tent cord compression/occlusion, nor does it help us to
predict the FHR behaviour subsequently. Emphasis should
instead be placed on the fetal response and compensation
ª 2014 Royal College of Obstetricians and Gynaecologists
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Current intrapartum fetal heart rate guidelines
to the decelerations. ‘Early decelerations’, as originally
described by Hon and Quilligan, and subsequently as
‘type-1 dips’ by Caldeyro-Barcia (gentle downward and
upward slopes with the nadir synchronous with the con-
tractions) are rare in labour. Because ‘early decelerations’
are not associated with fetal acidosis, many clinicians con-
clude that all decelerations that are synchronous with con-
tractions are ‘early’ and are therefore benign!
The original morphological descriptions of FHR deceler-
ations were derived under controlled animal experimental
conditions based on their presumed mechanisms, which
are not representative of human labour. For example, if
head and cord compressions gave rise to ‘early’ and ‘vari-
able’ decelerations, respectively, what type of hybrid decel-
erations would be observed if both fetal head and cord
were compressed simultaneously, or better still if there was
reduced transplacental oxygen transfer in the same labour?
Therefore, the current obsession with the classification of
the FHR decelerations into categories is unhelpful in assess-
ing the fetal state. The important point is that the fetus is,
or is not, compensating and defending itself adequately,
and this will be evident in the evolving FHR patterns in a
healthy fetus with a previously normal CTG.
Baseline FHR variability
The origin of the FHR variability is complex and its mathe-
matical evaluation is beyond the scope of this commentary.
In practice, it is observed as irregular fluctuations in the
amplitude and frequency of the baseline FHR on a CTG
trace, and is quantified as the amplitude of peak-to-trough
in beats per minute. In order to exhibit a normal FHR var-
iability the fetus requires an intact cerebral cortex, mid-
brain, vagus nerve, and cardiac conductive tissues. Even in
the presence of decelerations or bradycardia a fetus that
exhibits a normal baseline FHR variability has a very low
risk of acidaemia, immediate death, or asphyxial brain
injury.30–32 In contrast, absent or reduced FHR variability
was associated with significant newborn acidaemia in term
and preterm infants.32–34 In a recent systematic review
minimal or undetectable FHR variability was the most con-
sistent predictor of newborn acidaemia.30 In contrast,
increased FHR variation was observed in association with
severe acidosis and hypotension in a hypoxia ischaemia
model using term-equivalent fetal sheep.35 In clinical prac-
tice these increased FHR variations associated with severe
acidosis are often abrupt, erratic, high amplitude, and lack
the natural wavelike characteristic of normal FHR variabil-
ity. Strictly speaking they should not be classified as salta-
tory patterns as this implies exaggerated but normal
wavelike variability. The clinical significance and interpreta-
tion of FHR variability has been reviewed and summarised
as follows.17
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Ugwumadu
1 If the FHR variability is normal there is a limited role
for fetal acid base analysis.36,37
2 Unless fetal asphyxia can be reliably excluded, intermit-
tent or sustained reductions in FHR variability may sig-
nal the onset of decompensation in the presence of
intrapartum FHR decelerations.
3 A fetus with a previously normal FHR variability will
not switch to reduced or absent variability during labour
without the input of asphyxial FHR decelerations.
4 It is not possible to distinguish between asphyxial and
non-asphyxial causes of reduced FHR variability without
determining the fetal acid base status if the FHR vari-
ability is absent at the very outset of the monitoring.
Fetal cardiovascular and metabolic
response to intrapartum hypoxia
As the constant supply of oxygen is essential for cellular
energy production and integrity, the fetal cardiovascular sys-
tem, like its adult counterpart, is programmed to rapidly
detect and redress any form of oxygen deprivation. The main
aim of this program is to centralise the circulation and main-
tain perfusion of the essential organs, the brain, the myocar-
dium, and the adrenals at the expense of the non-essential
organs, such as the fetal lungs, skin, muscles, liver, kidneys,
and the gastrointestinal tract.38,39 This response is qualita-
tively similar but may differ quantitatively across the spec-
trum of insults, and is also finely tuned to match the severity
of the insult and the tolerance of the host. If the hypoxic
insult is slow and persistent the fetus has ample time to make
metabolic adjustments and exhibit different FHR pat-
terns.38,39 In the absence of metabolic acidaemia fetal sheep
at least can sustain these protective cardiovascular adapta-
tions virtually indefinitely,40–42 but they begin to fail with
the development of acidaemia, with substantial falls in fetal
and cerebral oxygen consumption at pH <7.0.
The pathological consequences of acidaemia include loss
of vascular tone, myocardial cell injury/depression, result-
ing in hypotension and ischaemic brain injury; however,
another layer of protection operates within the brain in
which the regional redistribution of flow shunts blood
away from the cortex to the deep nuclei and brainstem
structures.39 In contrast, during acute and total profound
asphyxia (e.g. massive abruption, total cord occlusion, or
uterine rupture) fetal pO2 falls precipitously within min-
utes. Unlike the slow and persistent insult this insult para-
digm produces a rapid and generalised vasospasm mediated
by the chemoreceptors, which is quickly followed by hyp-
oxic decompensation, profound systemic hypotension, and
brain infarction, and the regional brain redistribution of
blood is unsuccessful in protecting the deep nuclei.43,44
In this issue of BJOG, Chandraharan reviewed the tenu-
ous evidence for the use of fetal scalp pH.45 True, the non
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essential fetal tissues may develop acidosis during the
hypoxia-driven centralisation of the circulation, and scalp
pH may not reflect successful fetal cardiovascular compen-
sation; however, it is also true that acidaemia leads to a loss
of vascular tone and hypotensive brain damage. As vasopa-
ralysis results in fetal injury regardless of the pH value, it
follows that successful maintenance of the fetal mean arte-
rial pressure (MAP) during hypoxia is more important
than the pH in ensuring good outcome. Therefore, if the
technology existed fetal MAP would be the ideal parameter
to monitor instead of surrogates like pH or lactate level.
Fetal scalp pH estimation and the CTG may have devel-
oped independently of each other, but they are not inde-
pendent variables in practice. The decision to determine
fetal pH depends on CTG interpretation; therefore, poor
CTG interpretation reduces the value of FBS. As CTG
interpretation has so far been based on features that did
not necessarily predict acidaemia, it is reasonable to suggest
that previous studies of the role of pH included fetuses that
were not at genuine risk of acidaemia, hence the observed
poor correlation between pH and adverse outcomes.
To my mind, the real questions are: (1) what levels and/
or duration of fetal acidaemia (peripheral or otherwise) are
associated with vasoparalysis/fetal hypotension; and (2)
what CTG features, if any, predicted these pH levels? The
precise answers to these questions are currently unknown
and are likely to be host dependent and probably modu-
lated by factors other than hypoxia and acidaemia. Avail-
able data suggest that there is no single pH value at which
damage will occur in all fetuses;46 however, for any individ-
ual fetus, the FHR variability will be reliably depressed
before the pH drops to levels sufficient to induce neurolog-
ical injury.47,48
The role of infection and the
inflammatory response
Fetal SIRS is associated with fetal hypotension, neonatal
encephalopathy, meconium aspiration syndrome, multi-
organ dysfunction,49–51 and cerebral palsy,52 but we know
very little about the FHR changes induced by inflammation
either alone or in combination with hypoxia. Furthermore,
only 10–15% of cases of chorioamnionitis/FSIRS exhibit
maternal signs.53 Although FHR tachycardia, reduced vari-
ability, or lack of cycling may be observed, these are incon-
sistent findings. Current electronic FHR monitoring
technology is not designed to detect FSIRS. In one study,
tachycardic fetuses with infection had an increased risk of
encephalopathy and cerebral palsy, but had no acidaemia
or bradycardia,54 suggesting that infection may exert neuro-
logical injury directly or via a non-hypoxia pathway.
Further still, fetal inflammation and hypoxia appear to act
synergistically to increase the risk of encephalopathy and
ª 2014 Royal College of Obstetricians and Gynaecologists

cerebral palsy exponentially.50,55 Inflammation probably
sensitises the fetal brain to hypoxic damage by lowering the
threshold at which hypoxia triggers neuronal apoptosis.56
Clinicians should exercise caution with uterotonic agents
and traumatic deliveries in these cases.
Intrapartum FHR interpretation—a
step-wise physiologic approach
Step 1—the normal and the abnormal initial CTG
If the CTG is normal the fetus is very likely to be neurolog-
ically intact, normoxic, without acidaemia or acidosis, at
low risk of intrapartum asphyxia, and is able to react and
defend itself against intrapartum hypoxia. Surveillance may
continue depending on the situation or the woman may be
monitored by intermittent auscultation. If the initial base-
line FHR in a term fetus is ≥160 bpm with decelerations
and reduced variability, particularly in association with
meconium-stained amniotic fluid in early labour, the clini-
cian should consider fetoplacental infection, meconium aspi-
ration syndrome, chronic hypoxia, antecedent brain injury,
maternal systemic disease, drugs, or chromosomal abnormal-
ity (Figure 1). Senior staff involvement should be sought
early, with consideration given to delivery by caesarean sec-
tion. The outcome may still be unfavourable because of the
underlying disorder, but the additional challenge of labour
and potential exacerbation of the pre-existing insult will be
avoided. Fetal scalp sampling for pH is often impractical in
early labour, and is an insensitive tool for the assessment of
fetal wellbeing in the presence of FSIRS, fetal stroke, or com-
pensated hypoxic insult. Meconium is strongly associated
with histological chorioamnionitis, and in one study the RR
of fetal infection was ≥50-fold if FHR tachycardia was associ-
ated with meconium in early labour.57
Step 2—recognition of the compensated and the
decompensating fetus
An intact fetus with a previously normal CTG will exhibit
predictable patterns of FHR responses if exposed to hyp-
oxic ischaemic insults during labour, namely: slowly evolv-
ing hypoxia; subacute hypoxia; and acute hypoxia.
Slowly evolving hypoxia
Starting from a normal CTG, the first abnormality to
emerge in response to intermittent episodes of oxygen
deprivation (e.g. cord compression) or hypoxaemia (e.g.
excessive oxytocin infusion) is the appearance of FHR
decelerations. The second is a progressive increase in base-
line FHR if the stressor is persistent and threatening. The
third is reduced variability, which is a marker of
decompensation.22–25 The important point is the order
and temporal relationship between these FHR abnormali-
ties. Recovery follows the same order, and can only be
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Current intrapartum fetal heart rate guidelines
confirmed when the decelerations have disappeared and
the baseline FHR and variability have normalised. The
duration of time that an individual fetus can spend at its
maximum FHR without damage is variable and host
dependent. Fleischer et al.58 showed that 50% of term
well-grown fetuses in spontaneous labour with clear liquor
and ‘reactive’ CTG will develop acidosis in 115 minutes
with late decelerations, 145 minutes with variable deceler-
ation, and 185 minutes with flat and non-variable trace,
but these times will not apply to fetuses with reduced
reserve, such as in the case of intrauterine growth restric-
tion (IUGR) or infection, where acidosis may develop ear-
lier and more rapidly. The following conclusions may be
drawn from the above discussion.
1 If uterine contractions do not provoke FHR decelera-
tions in a previously normal CTG, the fetus is unlikely
to be hypoxaemic, hypoxic, acidaemic, or experiencing
cord compression.
2 In the presence of persistent FHR decelerations a pro-
gressive rise in the FHR suggests additional cardiovascu-
lar adaptation and fetal ‘stress’, but any rise in the FHR
without antecedent decelerations is not attributable to an
evolving intrapartum hypoxia.
3 During labour, reduced FHR variability that was not
preceded by decelerations and a progressive rise or acute
fall in FHR from a previously normal CTG is not associ-
ated with an evolving hypoxia. As the fetal myocardium
fails the FHR may fall slowly towards a terminal brady-
cardia. This should not be mistaken for recovery.
4 The amplitude and duration of the decelerations
depends on the intensity of the stressor. Others may
profoundly disagree, but in my opinion it is irrelevant
whether these decelerations are morphologically ‘early’
or ‘late’ and, provided the baseline FHR and variability
are maintained, the fetus is well compensated (Figure 1).
Subacute hypoxia
This pattern is characterised by complicated variable decel-
erations with amplitude ≥60 bpm, duration ≥90 seconds,
and a recovery phase at the baseline lasting <60 seconds.
This very brief interdeceleration interval is likely to have
two consequences: (1) it is insufficient to rid the fetus of
its carbon dioxide burden accumulated during the decelera-
tions, leading rapidly to respiratory and subsequently meta-
bolic acidosis; (2) the fetus is unable to raise its baseline
FHR and therefore its cardiac output. Provided the FHR
variability is normal and the interdeceleration interval
≥60 seconds the fetus is compensated; however, subacute
hypoxia is associated with a rapid decline in pH of 0.01
every 2–4 minutes.18 Early recognition and remedial action
is essential, as there may be insufficient time for further
assessment, e.g. to obtain, analyse, and react to a fetal scalp
sample result.
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Ugwumadu

Initial intrapartum CTG

Normal
The fetus;
is normoxic, no acidosis
has normal acid base status
is not asphyxiated
has normal CNS & CVS
can react & defend itself
will exhibit predictable and
progressive FHR changes if
exposed to hypoxia ischaemia
has low probability of
intrapartum asphyxia
Abnormal
Baseline FHR ≥160 bpm with
decelerations ± meconium
± reduced FHR variability
Consider
feto-placental infection
meconium aspiration syndrome
chronic hypoxia
antecedent brain injury
maternal systemic disease
drugs,
chromosomal abnormality
FBS not recommended

a
Repeated FHR decelerations
>50% of contractions Consider expeditious delivery
Continue surveillance or
transfer to intermittent b
auscultation Acute prolonged FHR
deceleration >3 min

Compensated fetus Compensated but ‘stressed’ fetus Decompensating fetus

a a a

baseline FHR ≤160 bpm
FHR variability ≥5 bpm
deceleration amplitude ≤60 bpm
interdeceleration interval ≥60 s
± cycling activity
b
FHR 80-100 bpm for >3 min but
≤9 min with normal variability
Recovery to normal or pre
deceleration CTG pattern
- exclude abruption, cord prolapse,
uterne rupture, bolus of oxytocin
- remove cause ±expedite delivery if
decompensation or failure to recover
≥10 min
baseline FHR ≥ or ≤160 bpm
FHR variability ≥5 bpm
deceleration amplitude ≥60 bpm
inter-deceleration interval ≥60 s
± cycling activity
second test of fetal wellbeing
b appropriate
FHR 80-100 bpm for >3 min but
≤9 min with normal variability
Recovery to FHR tachycardia or
baseline FHR higher than pre
deceleration CTG pattern ±
unsuccessful recovery attempts
- exclude abruption, cord prolapse,
uterne rupture, bolus of oxytocin
- remove cause ±expedite delivery if
decompensation or failure to recover
≥10 min
baseline FHR ≥ or ≤160 bpm
FHR variability <3-5 bpm
deceleration amplitude ≥ or ≤60 bpm
inter-deceleration interval <60 s
duration of deceleration >60 s
second test of fetal wellbeing if
b
FHR ≤80-100 bpm for >3 min with;
- reduced FHR variability <5 bpm
- no signs of recovery observed
- previously pathological FHR pattern
- abrupt and erratic ‘saltatory’ pattern
- no obvious cause identified or no
response to remedial action
- consider expeditious delivery

Figure 1. Proposed clinical algorithm for intrapartum FHR interpretation based on fetal defensive and compensatory responses to hypoxic ischaemic
stimuli. Firstly, a starting normal FHR pattern is essential to establish fetal wellbeing and the capability to react and defend itself. Then, using each
fetus as its own control, the behaviour of the FHR is tracked/monitored as it adjusts and adapts to intrapartum insults over time. The emphasis is on
the sequence and temporal relationships between the FHR features that characterise adequate/appropriate adaptation and those that suggest
progressive failure of compensation.

Acute hypoxia (prolonged FHR deceleration and
bradycardia)
The majority of acute onset intrapartum FHR decelerations,
in which the baseline FHR stabilises around 80–100 bpm,
with normal variability, are associated with non-asphyxial
vagal events,59–61 and usually arise from normal or near
normal FHR patterns. In the absence of cord prolapse or
occlusion, major abruption, uterine rupture, maternal col-
lapse, or infusion of a bolus of oxytocin, 90% of these epi-
sodes will recover or show signs of recovery by 6 minutes,
and 95% will recover by 9 minutes.18 They can be managed
expectantly. The mother should be turned to her left side
and rehydrated if she is hypotensive. If, however, the FHR
falls <80 bpm, with a loss of baseline variability, immediate
delivery should be considered, especially if the antecedent
CTG was abnormal as loss of variability signals fetal decom-
pensation and injury. Although some of these patterns do
recover, many do not. Against this background the NICE

1068 ª 2014 Royal College of Obstetricians and Gynaecologists


guidance on prolonged decelerations defined as baseline
FHR < 100 bpm (abnormal) and 100–109 bpm (suspi-
cious) for <3 or 3–10 minutes is open to misinterpretation.
Many of these cases are transferred urgently to the theatre,
during which time the FHR recovers but operative delivery
is undertaken anyway to comply with the guideline and fear
of recurrence if the delivery was deferred.
Conclusion
The continuing focus on the morphological appearances of
FHR decelerations by current guidelines and training mod-
ules denies the clinician an understanding of how the fetus
defends itself, compensates for intrapartum hypoxic ischae-
mic insults, and the ability to recognise the patterns that sug-
gest loss of compensation. This may be adding to the
increased operative delivery of nonacidotic babies. An intact
fetus with a normal CTG will exhibit a predictable set and
sequence of FHR responses if exposed to hypoxic ischaemic
insults during labour. In the presence of an abnormal CTG
using the trends in fetal defensive/compensatory responses
for interpretation allows the clinician to discriminate between
the fetus at risk of acidosis from one that is not at risk.
I make no claim for the superior clinical utility of the
proposed algorithm without a significant shift in our
attitude to intrapartum FHR interpretation, the content of
current training modules, and prospective field evaluation;
however, its basis on available data on the behaviour and
regulation of the fetal cardiovascular system during labour
is undeniable. The author has successfully used and taught
others to use the algorithm to monitor fetuses in labour
and to fine-tune the application of existing guidelines in
his institution and also in training courses for the last 12
years.
Disclosure of interests
AU runs courses on intrapartum CTG and fetal ECG analy-
sis at St George’s Hospital in London, and in other UK
hospitals and overseas. He uses fetal ECG monitoring in
his practice. He accepts instructions from and advises
claimants’ and defendants’ lawyers on matters related to
fetal monitoring, and is also involved in the revision of the
FIGO guidelines on FHR monitoring.
Contribution to authorship
Sole author.
Details of ethics approval
Not applicable.
Funding
None.
ª 2014 Royal College of Obstetricians and Gynaecologists
14710528, 2014, 9, Downloaded from https://obgyn.onlinelibrary.wiley.com/doi/10.1111/1471-0528.12900 by Readcube (Labtiva Inc.), Wiley Online Library on [24/04/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Current intrapartum fetal heart rate guidelines
Acknowledgements
None. &
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ª 2014 Royal College of Obstetricians and Gynaecologists