ctg interpretation paeds knowledge

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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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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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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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• 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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REFERENCES

1. Steer PJ, Danielian P. Fetal distress in labor. In: James DK,Steer PJ, Weiner CP, Gonik B, eds. High risk pregnancy— management options, 2nd edn. London: W.B. Saunders, 1999:1121–1149.

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.

5. Vintzileos AM, Antsaklis A, Varvarigis I et al. A randomisedtrial of intrapartum electronic fetal heart rate monitoringversus intermittent auscultation. Obstet Gynecol 1993; 81:899–907

6. Neilson JP. The usefulness of antepartum and intrapartumfetal monitoring. Contemp Rev Obstet Gynaecol 1994; 6:72–78.

7. Thacker SB, Stroup DF. Continuous electronic heart ratemonitoring versus intermittent auscultation for assessment

during labour (Cochrane review). Cochrane Library, Issue 4,Oxford: Update Software, 1999.

8. Thacker SB, Stroup DF, Peterson HB. Efficacy and safety of intrapartum electronic fetal monitoring: an update. ObstetGynecol 1995; 86: 613–620.

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.

10. Donker DK, van Geijn HP, Hasman A. Interobservervariation in the assessment of fetal heart rate recordings. Eur JObstet Gynecol Repro Biol 1993; 52: 21–28.

11. Arulkumaran S, Ingemarsson I, Montan S, et al. Guidelinesfor interpretation of antepartum and intrapartumcardiotocography. Bracknell, Berks: Hewlett Packard 1992.

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.

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