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This article reviews our current understanding of
fetal cardiotocography interpretation, with an
emphasis on the essential knowledge required by
paediatricians.
KEY POINTS
• Interpretation of the fetal heart rate is part of the
essential information required by the paediatrician
when called to the delivery room
• Accelerations and normal baseline variability are
indicative of fetal health
• Hypoxia and acidosis may develop quickly in the
presence of an abnormal trace with scanty thick
meconium, intrauterine growth restriction,
intrauterine infection, prematurity and post-term
gestation
• Consideration of the overall clinical picture and
the cardiotocograph provides necessary
information to ensure optimal management of thelabour.
WHAT IS A CTG?
The cardiotocograph (CTG) records the fetal heart
rate (FHR) and uterine activity in real time. The
beginning of each CTG trace should be annotated
with the maternal pulse rate to show this to be differ-
ent from the recorded FHR.1,2 The mother’s name
and hospital number should also be noted.
Monitoring of FHR uses either an external
Doppler ultrasound probe or an internal screw-type
fetal scalp electrode. An external pressure transducer
attached near the uterine fundus records uterine
activity. The standard paper speed in the United
Kingdom is 1 cm min –1. The vertical scale on the
paper is standardized to display between 50 and
210 beats per minute (bpm).
WHAT IS THE AIM OF CTG
INTERPRETATION?
The central aim of CTG interpretation is to predict
the likelihood that fetal compromise is occurring at
the earliest opportunity. No CTG can be interpreted
without considering the context of the clinical
situation and the presence of any ‘high-risk’ factors
(Table 1). Many fetuses show abnormal ‘stress’ pat-
terns on the CTG, and the challenge is to recognize
when this progresses to hypoxic ‘distress’.
WHY DO PAEDIATRICIANS NEED TO KNOW
ABOUT THE FETAL CTG?
Clear and concise communication between obstetri-
cians and paediatricians is essential in order to safely
manage the perinatal care of distressed fetuses.
Understanding CTG monitoring during labour is of
paramount importance. Appropriate newborn resus-citation requires a good understanding of the state of
the fetus at the time of delivery. This is obtained from:
• An accurate history of pregnancy and labour
• The intrapartum CTG
Serial: Obstetrics
Cardiotocograph interpretation: essentialknowledge for paediatricians
R. Varma, C. Smith, S. Arulkumaran
Rajesh Varma, SHO Obstetrics and Gynaecology, Queen’s Medical
Centre, University Hospital, Nottingham, UK, Craig Smith,Senior Registrar Paediatrics, Queen’s Medical Centre, UniversityHospital, Nottingham, UK, S. Arulkumaran, Professor Obstetricsand Gynaecology, School of Human Development, AcademicDivision of Obstetrics and Gynaecology, University of Nottingham, Derby City Hospital, UK.
Correspondence and request for offprints to: RV.
85
Current Paediatrics (2000) 10, 85–91
© 2000 Harcourt Publishers Ltddoi: 10.1054/ cupe.2000.0083, available online at http://www.idealibrary.com on
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86 Current Paediatrics
• Fetal scalp blood sample (FBS) acid-base result, if
available
• Planned mode of delivery
Fewer than 2% of all deliveries require full resuscita-
tion and intubation. However around 80% of these
can be predicted from observations made on intra-
partum fetal well-being.1 Some of these factors are
recognized as acceptable indications for requesting a
paediatrician to be present at delivery (Table 2).
EVIDENCE FROM CONFIDENTIAL ENQUIRY
INTO STILLBIRTHS AND DEATHS IN
INFANCY (CESDI)
The 4th CESDI report, published in 1997, investi-
gated stillbirths and neonatal deaths of normally
formed babies weighing 1.5 kg or more and dying due
to intrapartum asphyxia in England, Wales and
Northern Ireland from 1994–1995.3 The enquiry
reported suboptimal care in 77% of cases. Suboptimalcare was most often identified during labour with
problems in the use and interpretation of the CTG
cited as the main concern. The standard of resuscita-
tion was criticized in 22% of neonatal deaths.
WHAT ARE THE RISKS AND BENEFITS OF
CTG MONITORING IN HIGH-RISK LABOURS?
A normal CTG pattern is highly predictive that the
fetus is not hypoxic. Fewer than 2% of babies with a
normal CTG will have an intrapartum blood pHbelow 7.25.4 However, the CTG has a poor predictive
value for detecting hypoxic fetuses; a severely abnor-
mal trace is associated with significant fetal acidosis in
only 50% of cases.3
One randomized study has shown that continuous
CTG monitoring, used as the primary and only
method of intrapartum surveillance, is associated
with a decreased perinatal mortality, but also with
higher rates of surgical intervention for suspected
fetal distress.5 Meta-analysis6–8 of studies comparing
the routine use of continuous CTG monitoring withintermittent auscultation (recording CTG every 15–
30 min during a contraction and for 30 s thereafter to
identify a fetal response) showed that continuous
CTG monitoring:
• decreased the risk of having an Apgar score at
1 min less than 4 (Relative Risk=0.82)
• decreased the risk of neonatal seizures (RR=0.5)
• increased the rate of caesarean delivery (RR 1.3)
and total operative delivery (RR 1.23)
• produced no significant differences in the number
of Apgar scores at 1 min less than 7, rates of admission to neonatal intensive care units and
perinatal death.
This apparent increase in operative delivery can be
reduced if decisions based on continuous CTG moni-
toring are supported by FBS. No studies have ever
shown that CTG monitoring actually prevents short-
or long-term neurological impairment arising from
intrapartum asphyxia.9
WHAT ARE THE RULES OF CTG
INTERPRETATION?
A systematic approach to interpreting FHR patterns
is important to limit inter-observer variation.10 Four
principle features of the FHR pattern are considered.
• Baseline rate
• Baseline variability
• Presence or absence of accelerations
• Presence and nature of any decelerations
Baseline rate is the average stable FHR
(BL) between uterine contractions
with accelerations and
decelerations excluded.
Table 1 High-risk pregnancies
Maternal medical illnessHypertensive disease of pregnancyMaternal diabetes mellitusDrug abuse
Obstetric complications
Antepartum or intrapartum vaginal bleedingProlonged rupture of the membranesIntrauterine infectionBreech and multiple pregnancyOligohydramniosThick meconium-stained liquorPrevious caesarean sectionOxytocin augmentation
Fetal factorsPre-term (42 weeks gestation)Poor fetal growth (IUGR, SGA)Congenital malformationsHydrops fetalisReduced fetal movements
IUGR, intra-uterine growth restriction; SGA, small for gestationalage.
Table 2 Indications for calling a paediatrician to be present atdelivery
Prematurity Gestation below 36 weeksFetal distress Thick meconium staining of the liquor
Abnormal CTGFetal scalp blood pH
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Interpreting cardiotocographs 87
Baseline variability corresponds to the amplitude of
(BLV) variation in FHR. Ideally this is
taken from the CTG period
where the fetus is active and
exhibiting FHR accelerations.
Accelerations are transient increases in FHR
of 15 bpm or more and lasting
15 s or more. The recording of
at least two accelerations in a
20-min period is indicative of
optimal fetal health and this
FHR pattern is termed reactive.
Decelerations are transient reductions in FHR
from the baseline by more than
15 bpm and lasting for more
than 15 s. These indicate
episodes of fetal stress.
PHYSIOLOGY OF CTG PARAMETERS
Accelerations on the CTG reflect integrity of the brain
stem mediated pathways. These are more vulnerable to
hypoxia than the autonomic nervous system. As
hypoxia develops, fetal movements decline and FHR
accelerations become infrequent. Further hypoxia
leads to a compensatory increase in the FHR to main-
tain adequate cardiac output and organ perfusion.
Baseline variability reflects the balance between
sympathetic and parasympathetic drives. Reduced
variability may be physiological (e.g. quiet phase) – orsecondary to prolonged hypoxia or pethidine.
Quiet–active patterns of fetal activity may appear as
reduced BLV (
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88 Current Paediatrics
DEFINING ABNORMAL CTG
CHARACTERISTICS
A bradycardia is a baseline FHR150 bpm (Table 4).Other abnormal CTG characteristics are summarized
in Table 5 and are based on the classification produced
by FIGO.12 FIGO has emphasized the need to catego-
rize a CTG as normal, suspicious or abnormal. As the
table descends, the abnormality within the parameter
becomes more severe and suggestive of fetal hypoxia.
The overall combination of parameters is needed for
CTG interpretation and the prediction of likely fetal
compromise.
CLASSIFICATION OF ABNORMAL CTGPATTERNS
Abnormal CTG traces will not always fit a definitive
category, however the majority will fall into one of the
following four groups.2
Fig. 1 Early decelerations
Fig. 2 Late decelerations (L)
Fig. 3 Normal CTG. The CTG has a normal baseline rate(140 bpm) and baseline variability (10–15 bpm), is reactive (morethan two accelerations in 20 min) and shows no decelerations.
Fig. 4 CTG suggestive of gradually developing hypoxia. Thisfetus originally has a normal admission CTG with a baseline at140 bpm. Repetitive variable decelerations have led to a gradualincrease in the baseline (tachycardic at 160–170 bpm), diminishedbaseline variability (5–10 bpm) and absent accelerations. A fetal pHperformed later confirmed acidosis. Fetal outcome was normal.
Table 4 Causes of FHR baseline bradycardia and tachycardia
Fetal tachycardia Fetal bradycardia
160–200 bpm 200bpm usually involves
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Interpreting cardiotocographs 89
1. Gradually developing hypoxia
Repeated decelerations (variable or late) without a rise
in baseline rate or reduction in BLV represent a ‘stress’
pattern CTG. Episodes of transient fetal hypoxia are
depicted as ‘late’ or ‘variable’ type decelerations in this
‘stress’ pattern. As hypoxia develops there are no accel-
erations and the FHR rises to its maximum (usually an
increment of 20–30 bpm from admission trace) and
the BLV decreases (60 bpm) and prolonged
(>60 s) decelerations, with only brief periods of recov-
ery (60 s duration or
late recovery)FHR 170 bpm (>25 bpm with no accelerations) with changes in shape (overshoot,
slow recovery)Transient prolonged bradycardia Reduced BLV—‘silent trace’ Biphasic or combined; variable(FHR 2 min or (40 min) followed by late decelerations3 min)Prolonged bradycardia (>10 min) Reduced BLV Repetitive late decelerations
(90 min)Progressive bradycardia: FHR Shallow decelerations (
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90 Current Paediatrics
• Intracerebral haemorrhage or central nervoussystem malformation
• Ischaemic brain lesions
• Cardiac anomaly or arrhythmia
FETAL STATE AND THE ABNORMAL CTG
In general, the more of the four key parameters of the
CTG that become abnormal, the greater the likeli-
hood that the fetus is acidotic. Decelerations represent
episodes where the fetus is being ‘stressed’, whereas
alterations in baseline heart rate, baseline variabilityand accelerations reflect the overall fetal responsive-
ness and well being. Studies have shown that a well-
grown fetus can cope with hypoxic stress for as long as
90 min before the fetal pH begins to fall.1 However,
decreased BLV in combination with late or variable
deceleration patterns indicate an increased risk of
fetal pre-acidosis (pH 7.20 to 7.25) or acidosis (pH
60 bpm) and prolonged (>60 s)decelerations, with only brief periods of recovery (
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Interpreting cardiotocographs 91
REFERENCES
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2. CESDI Confidential Enquiry into Stillbirths and Deaths inInfancy. 4th Annual Report. Maternal and Child HealthResearch Consortium, London 1997.
3. Gibb DMF, Arulkumaran S. Fetal monitoring in practice,2nd edn. Oxford: Butterworth Heinemann,1997.
4. Beard RW, Filshie GM, Knight CA, Roberts GM. Thesignificance of the changes in continuous foetal heart rate inthe first stage of labour. J Obstet Gynaecol of the BritishCommonwealth, 1997; 78: 865–881.
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6. Neilson JP. The usefulness of antepartum and intrapartumfetal monitoring. Contemp Rev Obstet Gynaecol 1994; 6:72–78.
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9. Shy KK, Luthy DP, Benett FC et al. Effects of electronic fetalheart rate monitoring, as compared with periodicauscultation, on the neurological development of prematureinfants. N Engl J Med 1990; 322: 588–593.
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12. FIGO. Guidelines for the use of fetal monitoring. Int JGynaecol Obstet 1987; 25: 159–167.
13. Ingemarsson I, Arulkumaran S, Ratnam SS. Single injectionof terbutaline in term labour: effect of fetal pH in cases withprolonged bradycardia. Am J Obstet Gynecol 1985; 13:859–865.
14. Krebs HB, Petres RE, Dunn LJ, Jordaan HV, Segreti A.Intrapartum fetal heart rate monitoring. Classification andprognosis of fetal heart rate patterns. Am J Obstet Gynecol1979; 133: 762–772.