7 Antenatal Cardiotocography. Handbook CTG

 7

Antenatal Cardiotocography

Francesco D’Antonio and Amar Bhide

Handbook of CTG Interpretation: From Patterns to Physiology, ed. Edwin Chandraharan.

Published by Cambridge University Press. © Cambridge University Press 2017.

Key Facts

Indications for Antenatal Fetal Testing

Table 7.1 Common indication for antenatal CTG assessment

Maternal,

pregestational

Maternal, gestational Fetal

The aim of antenatal fetal surveillance is to identify fetuses that are at risk of

suffering intrauterine hypoxia with resultant damage including death. This

includes each and every pregnancy, as no pregnancy is free of this risk.

The goal of antepartum fetal surveillance is, therefore, to prevent fetal death and

to avoid unnecessary intervention.1

Several conditions pose additional risks to the fetus, thus theoretically requiring

additional ways of assessment of fetal well-being. These conditions include

prepregnancy or pregnancy-related maternal diseases and fetal-specific

problems that may have a potential negative impact on fetal survival and

development2 (Table 7.1).Cardiac diseases Preeclampsia IUGR

Pulmonary diseases Gestational diabetes Infections

Renal diseases Prelabour rupture of the membranes Multiple

pregnancies

Thyroid diseases Prolonged pregnancy Fetal anaemia

Autoimmune disease Vaginal bleeding Fetal arrhythmias

Hypertension Reduced fetal movements Oligohydramnios

Diabetes Abdominal trauma

Previous history of adverse obstetric

outcome

Current techniques employed for antepartum fetal surveillance include maternal

perception of fetal movements, CTG, vibroacoustic stimulation and ultrasound

assessment of growth, biophysical profile and fetal Doppler.

Role of Antenatal Cardiotocography

CTG is a continuous electronic record of the fetal heart rate (FHR) obtained via an

ultrasound transducer placed on maternal abdomen and traced on a paper strip. Uterine

activity is assessed using a spring-loaded device, which quantifies the extent of

indentation of the uterine wall and is also traced simultaneously on the same paper. CTG

is the most commonly adopted tool of fetal assessment before labour. It may be used in

isolation or combined with other methods of fetal assessment, such as ultrasound and

Doppler, as a part of fetal biophysical profile.3

Pathophysiology behind CTG Features

The hypothesis behind the use of CTG is that the integrity of autonomic central

nervous system (CNS), which primary regulates FHR, is a prerequisite for a

healthy fetus.Interpretation of a CTG Trace

Correct interpretation of CTG requires a complete understanding of the basic features.

These are represented by baseline heart rate (BHR), variability, accelerations and

decelerations. It is important to remember that the knowledge of these basic features and

the interpretation of CTG in the antenatal period are mainly derived from its use in

labour.

Baseline Heart Rate

All those conditions causing hypoxemia and acidaemia may induce depression of

the CNS of the fetus. This is reflected in abnormal features on the FHR trace.

The mechanism by which hypoxemia and acidaemia induce an alteration on the

CTG trace is not completely understood, but it is likely to be the result of the

depression of the brain stem centres regulating the activity of the pacemaker

cells of the heart.4

Physiological conditions may alter the CTG trace. Fetal sleep cycle is

associated with reduced baseline variability along with absence of fetal

movements. It is a common cause of apparently abnormal CTG trace and may

last for up to 50 minutes. Maternal administration of drugs that depress the CNS

may also result in an abnormal CTG pattern.

Accurate interpretation of a CTG trace should take into account the

pathophysiology behind an abnormal trace. A fetus that is not suffering from a

condition potentially leading to hypoxemia and acidaemia is unlikely to have an

abnormal CTG on the basis of a pathological mechanism. Therefore, alternative

causes should be investigated.

BHR refers to the mean FHR over a period of 5–10 minutes in the absence of

accelerations and/or decelerations and expressed in beats per minute. A BHR

between 110 and 160 is considered normal. A BHR <110 bpm is termed

baseline bradycardia, and >160 bpm is termed baseline tachycardia.Fetal Tachycardia

The main cause inducing fetal tachycardia is represented by maternal fever following

infection, although fever from any source may increase BHR. Other causes of fetal

tachycardia are represented by maternal administration of drugs acting on the

sympathetic (terbutaline) or parasympathetic (atropine) system, fetal cardiac

tachyarrhythmia (supraventricular tachycardia or atrial flutter), fetal hyperthyroidism

and obstetric emergencies such as placental abruption.7

Fetal Bradycardia

Bradycardia may reflect the final stage of fetal compromise and impending fetal

death,9,10 especially in those conditions leading to severe fetal hypoxemia and

acidaemia. It can also be associated with cardiac arrhythmias, especially complete fetal

heart block. Short period of moderate bradycardia (BHR between 100 and 109, in the

absence of other abnormalities on CTG trace) are not considered harmful for the fetus.

Variability

Gestational age is the main determinant of BHR. There is a progressive decrease

in BHR across gestation and should be taken into account especially when

interpreting a CTG trace before 28 weeks.5 The progressive reduction in BHR

across gestation is thought to be likely the result of the maturation of the

parasympathetic system.6

Uncomplicated moderate bradycardia (defined as a BHR between 100 and 109)

and moderate tachycardia (defined as a BHR between 160 and 179), especially

in the absence of other abnormalities of the CTG trace, are not strong indicators

of adverse neonatal outcome and have a poor predictive value for fetal

acidaemia.7,8

Variability refers to the frequency bandwidth through which the basal heart rate

varies in the absence of accelerations or decelerations. It is determined by theAccelerations

Accelerations are defined as abrupt increase in baseline FHR of >15 bpm and lasting

for >15 seconds. They are usually considered a reliable indicator of a healthy fetus. The

amplitude of accelerations may be lower before 30 weeks of gestation.

Decelerations

Decelerations are defined as abrupt decrease in baseline FHR. A deceleration is

defined on the basis of its relation with uterine contraction, shape, depth and duration.

Refer to Chapter 2 for details.

Sinusoidal Pattern

continuous and opposing influences of sympathetic and parasympathetic

autonomic nervous system on the cardiac pacemaker.

FHR variability is known to depend on several factors such as gestational age,

baseline FHR, hypoxia, fetal sleep cycles and maternal administration of

medications. Variability is sometimes further divided in long-term (LTV) and

short-term (STV) variability. This distinction is valid for computerized analysis

of the FHR. Such a distinction is impossible on visual interpretation, and the

variability should be called ‘baseline variability’.

It is important to stress that reduced variability does not always represent an

ominous cause. A careful assessment of physiological and pathological

conditions leading to a reduction in CTG variability should be taken into account

in order to correctly stratify the risk for the fetus.

Reduced variability may represent an ominous sign for the fetus, predicting fetal

compromise and eventually death, even in the absence of other pathological

features on CTG trace.11

A sinusoidal FHR was originally defined according to the criteria by Modanlou

and Freeman.12Types of CTG Examinations

Contraction Stress Test

Stable BHR between 120 and 160 bpm with regular oscillations.

Amplitude between 5 and 15 bpm.

Frequency of oscillations between 2 and 5 cycles per minute.

Absence of accelerations.

Oscillation above and below the baseline.

A transient period of sinusoidal FHR may be present in a normal fetus,

especially when it coexists with periods of normal variability. This is often seen

during labour and is not associated with an adverse outcome.13

A sinusoidal trace may be associated with various pathological conditions such

as fetal anaemia due to red cell alloimmunization, fetomaternal haemorrhage,

intracranial haemorrhage, twin-to-twin transfusion syndrome and ruptured vasa

previa, medications, chorioamnionitis and umbilical cord occlusion.121415

Contraction stress test (CST) is based on the response of FHR to uterine

contractions and, thus, is a test of utero-placental function. The hypothesis

behind the use of CST is that increased myometrial pressure following a uterine

contraction leads to a collapse of the vessels running through the myometrium,

decreasing the blood flow and oxygen exchange in the intervillous space. A

healthy fetus is able to tolerate this relative reduction in oxygen supply. In the

setting of utero-placental insufficiency, a compromised fetus is unable to tolerate

the added stress and exhibits abnormal features on the CTG.

Contractions are induced by incremental intravenous oxytocin infusion until a

contraction pattern of three contractions in 10 minutes is established.16 Nipple

stimulation may also be used to induce uterine contractions1 as an alternative.

Observation of late decelerations following ≥50 per cent of contractions

constitutes an abnormal CST. Relative contraindications of CST are representedNon-Stress Test

by conditions that increase the risk of preterm labour: uterine rupture and

haemorrhage, such as preterm prelabour rupture of the membranes, previous

history of preterm birth, placenta previa and previous classical caesarean

section. CST is largely historical and not used widely in clinical practice.

Non-stress test (NST) is one of the most widely used methods of antenatal fetal

surveillance. The hypothesis behind the use of NST is that the heart of a fetus

with an intact CNS responds to a movement with an acceleration of the heart rate

(reactive or negative NST). NST is usually performed after 28 weeks of

gestation and for a period of 30 minutes. The optimal interval between two

consecutive tests is not clearly established and depends on the underlying

maternal and fetal conditions, gestational age at examination and the results of

the previous test.

The absence of fetal heart acceleration following fetal movement or absence of

fetal movements is interpreted as a nonreactive or positive NST. The longer the

time interval with absence of movements/FHR accelerations, the less likely that

the explanation is physiologic variability.

NST is a visual assessment and subjective interpretation of the FHR pattern.

Several previous publications show that it has substantial inter- and intraobserver variability.17–22 A reactive test is highly predictive of a healthy fetus;

however, a nonreactive test does not necessarily indicate fetal compromise.

False-positive rates up to 90 per cent have been reported in the past,23 and a

careful evaluation of the preexisting maternal and fetal diseases, gestational age

at examination, fetal sleep cycles and maternal administration of medication

acting on fetal CNS should be carried out when interpreting a CTG trace. NST is

primarily a test of fetal function. A fetus that is acidotic is likely to have a CTG

with abnormal features on the basis of a hypoxaemic mechanism. The first issue

is, therefore, to identify those fetuses potentially suffering from conditions that

may lead to hypoxaemia and acidaemia, such as IUGR. Ultrasound and Doppler

assessment may help in this scenario.The following parameters are widely accepted to be normal for the term fetus.24

Figure 7.1 shows a normal antenatal CTG.

Figure 7.1 Normal antenatal CTG.

BHR variability and accelerations may decrease or disappear and decelerations in

the FHR may occur when the fetus is hypoxic.24 Figure 7.2 shows a pathological

antenatal CTG.

Baseline FHR of 110 to 160 bpm.

Baseline variability of at least 5 bpm.

Presence of two or more accelerations of FHR >15 bpm, sustained for at least

15 seconds in a 20-minute period25 – this pattern is termed reactive.

Absence of decelerations.Figure 7.2 Pathological antenatal CTG. Note loss of variability and an unprovoked

deceleration.

Computerized CTG

1. The recording must contain at least one episode of high variation.

2. The STV must be >3.0 ms, but if it is <4.5 ms, the LTV averaged across all

episodes of high variation must be greater than the third percentile for gestational

age.

3. There must be no evidence of a high-frequency sinusoidal rhythm.

4. There must be at least one acceleration or a fetal movement rate ≥20 ms per hour

and a LTV averaged across all episodes of high variation that is greater than the

tenth centile for gestational age.

5. There must be at least one fetal movement or three accelerations.

6. There must be no decelerations >20 lost beats if the duration of the recording is

<30 minutes and no more than one deceleration of 21–100 lost beats if the duration

of the recording is >30 minutes. However, no deceleration with an amplitude of

>100 lost beats should occur at any time.

7. The basal heart rate must be 116–160 bpm if the recording is <30 minutes.

CTG use is limited by problems with interpretation. Many studies have

consistently shown suboptimal inter- and intra-observer reliability, potentially

leading to unnecessary intervention or to lack of intervention when it is

required.17–22

A scoring system reduces the consistency of visual assessment but does not

eliminate it. In order to overcome this limitation, computerized CTG (cCTG) is

often used.4,25,26

The CTG information is analysed by a computer to satisfy the criteria of

normality over a period of 60 minutes, but the analysis can be stopped if the

criteria are met before this time. These are called ‘Dawes–Redman criteria’

after their developers and are reported below.27,288. The LTV must be within 3 SDs of its estimated value, or (a) the STV must be

>5.0 ms, (b) there must be an episode of high variation with ≥0.5 fetal movement

per minute, (c) the basal heart rate must be ≥120 bpm, and (d) the signal loss must

be <30 per cent.

9. The final epoch of recording must not be a part of a deceleration if the recording

is <60 minutes, or a deceleration at 60 minutes must not be >20 lost beats.

10. There must be no suspected artefacts at the end of the recording if the recording

is <60 minutes.

The risk for fetal hypoxia/acidaemia is extremely low if the Dawes–Redman

criteria for normality are met.28 Figure 7.3 shows a typical report of antenatal cCTG.

Note that Dawes–Redman criteria were met at 20 minutes.

Figure 7.3 cCTG trace reporting the evaluation of Redman–Dawson criteria.

Pearls: CTG in Clinical Practice

CTG is the most commonly adopted tool for fetal surveillance before labour.

Indications for antenatal CTG include prepregnancy or pregnancy-specific

maternal medical problems and fetal diseases, all having a negative impact onPitfalls

fetal development,2 and CTG evaluation is recommended in all those situations,

such as IUGR, potentially leading to fetal hypoxaemia and acidaemia that are

mainly responsible for a change in normal FHR.29

The main purpose of CTG as well as all antenatal fetal tests is to identify those

fetuses at risk of suffering hypoxaemia and acidaemia in utero in order to

organize prompt intervention.

Although it is widely used in different clinical conditions, the effectiveness of

antenatal CTG in improving outcome for mother and fetuses during and after

pregnancy is questionable. A recent Cochrane meta-analysis comparing no CTG

with traditional CTG showed no significant difference in perinatal mortality or

potentially preventable deaths, Apgar score or caesarean section rate.

The risk ratio for using antenatal traditional CTG compared to not using one was

2.05 (95% CI 0.95–4.42).30 This means that the use of traditional CTGs may be

associated with a higher risk of stillbirth. Moreover, all the women involved in

the studies assessed in this meta-analysis were at increased risk for

complications. The use of antenatal CTGs is likely to do more harm than good in

low-risk pregnancies, due to the low probability of fetal hypoxia. Computerized

antenatal CTG was associated with significantly lower relative risk for perinatal

mortality (RR 0.2; 95% CI 0.04–0.88) as compared to conventional CTG for

fetal assessment in high-risk pregnancies, without any difference in Caesarean

section rate. However, there was no significant difference identified in

potentially preventable deaths (RR 0.23; 95% CI 0.04–1.29). Current

improvements in ultrasound and Doppler allow reliable recognition of those

fetuses that are at increased risk of complications.31 Antenatal CTG may be of

potential benefit in this group as an additional test on which to base clinical

management. Moreover, cCTG looks promising in reducing perinatal mortality,

and randomized clinical trials are needed to clarify its role.Consequence of Mismanagement

Possible Future Developments

Adult cardiology literature has shown that mathematical assessment of variability of the

heart rate is related to survival.32 These investigators introduced a method called phaserectified signal averaging (PRSA) that measures the variable elements in the signal,

noise and artefacts of the CTG. The PRSA series can be employed to quantify the

‘average acceleration capacity’ (AC) and ‘average deceleration capacity’ (DC) of the

signal. In the fetus, AC and DC are thought to quantify the activities of the sympathetic

and parasympathetic nervous system. AC/DC have been reported to be significantly

lower in IUGR fetuses as compared to normally grown controls matched for the

gestational age.33 PRSA is reported to perform at least as well as the STV on cCTG.34 It

is uncertain if PRSA will prove to be better than cCTG in the identification of

compromised fetuses.

Conclusions

Conventional CTG is widely used for antenatal fetal assessment in the absence of robust

evidence. There is potential for more harm than good with its use. Large inter- and intraobserver variability is one of the possible reasons behind this. cCTG has proven

advantage over conventional CTGs, but the drawback is that it may not be widely

available. The use of antenatal CTG to assess fetal well-being in low-risk pregnancies

is not recommended.

References

Antepartum stillbirth

Hypoxic ischaemic encephalopathy

Unnecessary operative interventions1. American College of Obstetricians and Gynecologists (ACOG). Antepartum fetal

surveillance. 1999. Practice Bulletin No. 9, October, Reaffirmed 2007.

2. National Institute for Health and Clinical Excellence. Antenatal care: routine care for the

healthy pregnant woman. 2008. London: RCOG Press.

3. Lalor JG, Fawole B, Alfirevic Z, Devane D. Biophysical profile for fetal assessment in high

risk pregnancies. 2008. Cochrane Database Syst Rev. 23;CD000038.

4. Dawes GS. The control of fetal heart rate and its variability in counts. In: Fetal heart rate

monitoring. Ed. Kunzel W. 1985. Berlin, Springer-Verlag, p. 188.

5. Pillai M, James D. The development of fetal heart rate patterns during normal pregnancy.

1990. Obstet Gynecol. 76;812–816.

6. Renou P, Newman W, Wood C. Autonomic control of fetal heart rate. 1969. Am J Obstet

Gynecol. 15;949–953.

7. Gilstrap LC, Hauth JC, Toussaint S. Second stage fetal heart rate abnormalities and

neonatal acidosis. 1984. Obstet Gynecol. 63;209–213.

8. Gilstrap LC, Hauth JC, Hankins GD, Beck AW. Second-stage fetal heart rate abnormalities

and type of neonatal acidemia. 1987. Obstet Gynecol. 70;191–195.

9. Jaeggi ET, Friedberg MK. Diagnosis and management of fetal brady-arrhythmias. 2008.

Pacing Clin Electrophysiol. 31;S50–S53.

10. Larma JD, Silva AM, Holcroft CJ, Thompson RE, Donohue PK, Graham EM.

Intrapartum electronic fetal heart rate monitoring and the identification of metabolic acidosis

and hypoxic-ischemic encephalopathy. 2007. Am J Obstet Gynecol. 197;e1–8.

11. Smith JH, Anand KJ, Cotes PM, Dawes GS, Harkness RA, Howlett TA, Rees LH,

Redman CW. Antenatal fetal heart rate variation in relation to the respiratory and metabolic

status of the compromised human fetus. 1988. Br J Obstet Gynaecol. 95;980–989.

12. Modanlou HD, Freeman RK. Sinusoidal fetal heart rate pattern: its definition and clinical

significance. 1982. Am J Obstet Gynecol. 15;1033–1038.

13. Young BK, Katz M, Wilson SJ. Sinusoidal fetal heart rate. I. Clinical significance. 1980.Am J Obstet Gynecol. 1;587–593.

14. Epstein H, Waxman A, Gleicher N, Lauersen NH. Meperidine-induced sinusoidal fetal

heart rate pattern and reversal with naloxone. 1982. Obstet Gynecol. 59;22S–25S.

15. Murphy KW, Russell V, Collins A, Johnson P. The prevalence, aetiology and clinical

significance of pseudo-sinusoidal fetal heart rate patterns in labour. 1991. Br J Obstet

Gynaecol. 98;1093–1101.

16. Freeman RK. The use of the oxytocin challenge test for antepartum clinical evaluation of

uteroplacental respiratory function. 1975. Am J Obstet Gynecol. 15;481–489.

17. Borgatta L, Shrout PE, Divon MY. Reliability and reproducibility of nonstress test

readings. 1988. Am J Obstet Gynecol. 159; 554–558.

18. Donker DK, van Geijn HP, Hasman A. Inter-observer variation in the assessment of fetal

heart rate recordings. 1993. Eur J Obstet Gynecol Reprod Biol. 52;21–28.

19. Flynn AM, Kelly J, Matthews K, O’Conor M, Viegas O. Predictive value of, and

observer variability in, several ways of reporting antepartum cardiotocographs. 1982. Br J

Obstet Gynaecol. 89;434–440.

20. Hage ML. Interpretation of nonstress tests. 1985. Am J Obstet Gynecol. 1;490–495.

21. Lotgering FK, Wallenburg HC, Schouten HJ. Interobserver and intraobserver variation in

the assessment of antepartum cardiotocograms. 1982. Am J Obstet Gynecol. 15;701–705.

22. Trimbos JB, Keirse MJ. Observer variability in assessment of antepartum

cardiotocograms. 1978. Br J Obstet Gynaecol. 85;900–906.

23. Devoe LD, Castillo RA, Sherline DM. The non-stress test as a diagnostic test: a critical

reappraisal. 1986. Am J Obstet Gynecol. 152;1047.

24. Gribbin C, Thornton J. Critical evaluation of fetal assessment methods. In: High risk

pregnancy management options. Eds. James DK, Steer PJ, Weiner CP. 2006. Elsevier.

25. Devoe LD. The nonstress test. 1990. Obstet Gynecol Clin North Am. 17;111–128.

26. Smith JH, Dawes GS, Redman CW. Low human fetal heart rate variation in normalpregnancy. 1987. Br J Obstet Gynaecol. 94;656–664.

27. Dawes GS, Redman CW, Smith JH. Improvements in the registration and analysis of fetal

heart rate records at the bedside. 1985. Br J Obstet Gynaecol. 92;317–325.

28. Pardey J, Moulden M, Redman CW. A computer system for the numerical analysis of

nonstress tests. 2002. Am J Obstet Gynecol. 186;1095–1103.

29. Nijhuis IJ, ten Hof J, Mulder EJ, Nijhuis JG, Narayan H, Taylor DJ, Visser GH. Fetal heart

rate in relation to its variation in normal and growth retarded fetuses. 2000. Eur J Obstet

Gynecol Reprod Biol. 89;27–33.

30. Grivell RM, Alfirevic Z, Gyte GM, Devane D. Antenatal cardiotocography for fetal

assessment. 2012. Cochrane Database Syst Rev. 12;CD007863.

31. Alfirevic Z, Stampalija T, Gyte GM. Fetal and umbilical Doppler ultrasound in high-risk

pregnancies. 2010. Cochrane Database Syst Rev. 20;CD007529.

32. Bauer A, Kantelhardt JW, Barthel P, Schneider R, Mäkikallio T, Ulm K, Hnatkova K,

Schömig A, Huikuri H, Bunde A, Malik M, Schmidt G. Deceleration capacity of heart rate as

a predictor of mortality after myocardial infarction: cohort study. 2006. The Lancet.

367;1674–1681.

33. Stampalija T, Casati D, Montico M, Sassi R, Rivolta MW, Maggi V, Bauer A, Ferrazzi E.

Parameters influence on acceleration and deceleration capacity based on trans-abdominal

ECG in early fetal growth restriction at different gestational age epochs. 2015. Eur J Obstet

Gynecol Reprod Biol. 188;104–112.

34. Huhn EA, Lobmaier S, Fischer T, Schneider R, Bauer A, Schneider KT, Schmidt G.

New computerized fetal heart rate analysis for surveillance of intrauterine growth restriction.

2011. Prenat Diagn. 31;509–514.

35. Modanlou HD, Murata Y. Sinusoidal heart rate pattern: reappraisal of its definition and

clinical significance. 2004. J Obstet Gynaecol Res 30;169–180.

36. National Institute for Health and Clinical Excellence. Intrapartum care: care of the

healthy woman and their babies during childbirth. 2007. London: RCOG Press.

37. Pillai M, James D. The importance of the behavioural state in biophysical assessment ofthe term human fetus. 1990. Br J Obstet Gynaecol. 97;1130–1134.

38. Henson G, Dawes GS, Redman CW. Characterization of the reduced heart rate variation

in

growth-retarded fetuses. 1984. Br J Obstet Gynaecol. 91;751–755.

Nhận xét