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.
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