Keywords

FormalPara Learning Objectives

At the conclusion of this chapter, the learner will be able to:

  • Define electronic fetal monitoring (EFM)

  • Describe the process of fetal oxygenation and intrauterine adaptation

  • Describe the pathophysiology of fetal distress

  • Understand the different fetal heart rate patterns and the underlying control mechanisms

  • Identify the indications for EFM

  • Describe and interpret a CardioTocoGraphy (CTG) trace

  • Determine basic resuscitative measures and interventions following a pathologic CTG trace

  • Differentiate between an antenatal and an intrapartum CTG

  • Enumerate potential challenges and some mitigating factors in EFM in LMIC

  • Describe some basic steps in setting up a CTG unit in a low-resource setting

1 Introduction

Electronic fetal monitoring (EFM) refers to the use of medical equipment that has the ability to detect, record, analyse and present the records of the fetal heart rate changes with time. These recordings can then be used as assessment of the fetal health in utero for the purpose of reassurance/intervention/management in order to prevent fetal injury/death chiefly from hypoxia. EFM is often also called cardiotocographic (CTG) monitoring.

2 History

Electronic fetal monitoring dates back to the 1960s and 1970s. Prior to this time, the standard of care for intrapartum monitoring of the foetus was intermittent auscultation (IA). In one of the earliest published studies, it was observed that abnormal fetal heart patterns, especially prolonged fetal bradycardia, was associated with fetal hypoxia and fetal death [1]. It was already known that the autonomic nervous system controlled the fetal heart rate pattern. It was hypothesised that fetal hypoxia led to changes in the autonomic nervous system outflow, hence leading to abnormalities in the fetal heart rate pattern. This fetal heart rate pattern could be easily documented by the emerging technology of EFM. It was therefore believed that this new technology would be the panacea for avoidable fetal morbidity and mortality, especially the long-term handicap from hypoxia – cerebral palsy.

Numerous studies over the years however, have been unable to detect real statistical benefit of EFM over IA in improving fetal outcome and at best have reported slightly conflicting results [2,3,4,5]. However, it has been recommended that for low-risk pregnancies, EFM increased Caesarean section rate with no improvement in neonatal outcome. Caesarean section rates have been found to increase by about a third following introduction of EFM in many obstetric centres [6]. Therefore, more recent studies have concentrated on high-risk pregnancies and on improving the technology. In addition, there have been reviews of guidelines to further standardise cardiotocographic (CTG) criteria suggestive of fetal compromise [7, 8].

Subjectivity in criteria interpretation was also considered as a limiting factor to achieving the ideal aim of EFM. Attempts to eliminate human bias in CTG trace interpretation led to introduction of computerised interpretation of EFM tracings. Another innovation that was introduced was the computerised interpretation of specific components of the electrocardiographic (ECG) trace such as the ‘ST-segment’ analysis. This ECG trace required the use of fetal scalp electrodes. While these have added more available information and knowledge on fetal monitoring and physiology, they are yet to solve the unequivocal superiority dilemma of the new technologies of EFM over IA in the detection of fetal hypoxia [9].

3 Basic Fetal Physiology Relating to Oxygen Consumption

Oxygen is essential for the production of energy. Energy is necessary for the survival of the foetus. Energy is derived as shown in the following schema:

$$ \mathrm{Glucose}+\mathrm{Oxygen}\to \mathrm{Energy}+\mathrm{Carbon}\ \mathrm{Dioxide}+\mathrm{water} $$

3.1 Delivery of Oxygen to Reach the Foetus

The oxygen supply to the foetus is derived entirely from the mother through the placenta. Essentially, the mother inhales oxygen which is carried in her blood mainly as oxyhaemoglobin eventually getting to the placenta through the uterine arteries and its branches to reach the placenta sinuses. This oxygen in maternal blood diffuses through the placenta sinuses to reach the foetus through the umbilical vein. At the tissue level, the oxygen is utilised for energy production and carbon dioxide is released into the blood. The oxygen-depleted/carbon dioxide-rich blood is transported through the umbilical arteries to reach the placenta where carbon dioxide diffuses freely through the membrane and is carried out of the uterus through the uterine veins.

3.2 Oxygen Saturation Across the Placenta

The placenta acts as a transport organ for exchange of materials between the mother and the baby. Blood on the maternal side of the placenta is usually almost 100% saturated with oxygen. However, the placenta being a living organ requires energy for its activities, hence it also requires oxygen. So the placenta consumes part of the oxygen that is presented to it for transfer to the foetus. The placenta consumes as much as 40% of the oxygen presented to it, hence the oxygen saturation of the blood after it has passed through the placenta and getting to the umbilical vein is drastically reduced. In addition, the placenta membrane is a very thin one allowing easy transport of gases. However, in certain abnormal conditions, chiefly exemplified by preeclampsia, thickening of the membrane could occur resulting in impedance to transfer of substances including oxygen across the placenta membrane, further worsening the level of oxygen saturation getting to the foetus – a prelude to fetal hypoxaemia.

4 Clinical Implications of Hypoxia

  • Fetal distress – Antenatal or intrapartum fetal compromise resulting from fetal hypoxia.

  • Hypoxaemia – This refers to reduced oxygen tension in the fetal blood.

  • Hypoxia – This is more severe and refers to reduced oxygen tension in the fetal blood and tissues. This in turn can lead to acidaemia and acidosis.

  • Acidaemia – The increase in fetal H+ concentration in fetal blood or the reduction in the pH of fetal blood.

  • Acidosis – This is a serious condition and refers to the increased H+ concentration in fetal blood and tissues or the reduction of the pH in fetal blood and tissues.

  • Asphyxia – This refers to the clinical manifestations due to inability of the foetus to respire and take in adequate oxygen at birth. This usually results in brain damage and damage to other tissues.

Hypoxaemia can lead to fetal hypoxia which in turn can lead to birth asphyxia, hypoxic ischaemic encephalopathy and then to cerebral palsy. Fetal hypoxia can also lead to damage of other organs and tissues including:

  • Gastrointestinal tract – Necrotising enterocolitis

  • Renal – Acute renal failure

  • Heart – Myocardial ischaemia, etc.

It is in a bid to reduce or mitigate these effects that it is essential to reduce the incidence of fetal hypoxia through adequate use of electronic fetal monitoring.

5 Determinants of Severity of Fetal Damage From Fetal Hypoxia

  1. 1.

    Severity of the hypoxia

  2. 2.

    Duration of the hypoxia

  3. 3.

    Repetitive nature of the hypoxia

  4. 4.

    Availability and adequacy of fetal reserve

  5. 5.

    Individual capacity of the foetus to cope

6 Fetal Coping Mechanisms to Avoid Fetal Hypoxia

A reduction in oxygen supply to the foetus, whether acute or chronic, does not lead immediately to deleterious effect. This is because the baby has developed various coping mechanisms that enable it deal with the inevitable occasional drop in oxygen tension reaching it. This is even more necessary in labour when the blood flow to the placenta is momentarily shut down during uterine contractions. It is these coping mechanisms that allow most foetuses to remain calm during these upheavals in oxygen supply.

On a basic level, the foetus is ‘oversupplied’ with oxygen in utero despite the reduction in oxygen tension reaching it across the placenta. This may be likened to the mechanisms developed in persons living in high altitude regions of the world. These regions have been known to produce world record holders in the long distance races as exemplified by athletes from Kenya and Ethiopia. Like these, the babies have:

  • A higher hematocrit (compare fetal hematocrit of over 60% to adult hematocrit of less than 50%).

  • The foetuses also have a comparatively faster heart rate, hence a cardiac output for body weight that is far higher than the adult (compare a fetal heart rate of 140/minute to the adult of about 80/minute).

  • Foetuses also have fetal haemoglobin (HBF) that has a higher affinity for oxygen, especially at low oxygen tension than the adult haemoglobin (HBA). This enables the fetal haemoglobin to extract more oxygen from an already oxygen-depleted blood that reaches it.

  • The fetal haemoglobin has a higher level of 1,3-DPG unlike the adult haemoglobin that has a higher level of 2,3-DPG. 1,3-DPG results in a shift of the oxygen dissociation curve to the left, hence a higher affinity for oxygen by fetal haemoglobin.

Once this basic coping mechanism of being oversupplied is overstretched, the baby starts to manifest with certain signs all in a bid to reduce its oxygen usage. These will include features like:

  • Reduction in growth referred to as intrauterine growth restriction (IUGR)

  • Reduction in fetal movement (the mothers often giving the complaints of not feeling the baby’s kicks as previously)

Often too, the foetuses start to use up their glycogen reserves. These reserves are majorly in the liver and the heart. So, there may be:

  • Reduction in fetal abdominal circumference (this can be accurately detected by ultrasonography).

As the hypoxaemia persists/worsens, there is prioritisation of blood flow to the more essential areas of the brain, heart and adrenal glands. Conversely, blood is shunted away from the kidneys (hence oligohydramnios), skin and gastro-intestinal tract [hence increased risk of Necrotising-Entero-Colitis (NEC)]. In these instances, there may be:

  • A reduction in the amniotic fluid index (AFI).

  • A reduction of the pulsatility index (PI) in the middle cerebral artery (MCA). This implies increased flow of blood to the brain. This is referred to as placenta-cerebral redistribution.

  • Reversal of the ratio of the umbilical artery PI to MCA PI. This implies shunting of blood away from the peripheral circulation to supply the brain. This is referred to as centralisation of fetal blood flow. These latter two features can be demonstrated on fetal Doppler studies.

If the hypoxia worsens, then the foetus, in its attempt to survive, starts to use anaerobic respiration to produce energy. This is wasteful as it produces one-nineteenth of the equivalent amount of energy that aerobic respiration will produce for the same amount of glucose. Worse still, this process results in the production of lactic acid which is injurious to the tissues, giving acidaemia and subsequent acidosis.

In anaerobic respiration:

$$ {\displaystyle \begin{array}{c}\mathrm{Glycogen}\to \\ {}\mathrm{Glucose}\to \mathrm{Energy}+\mathrm{lactic}\ \mathrm{acid}\to \mathrm{Lactate}+\mathrm{H}+\end{array}} $$

These mechanisms listed above are called upon in the long term when chronic hypoxaemia/hypoxia occurs. The worse the condition is, the more the manifestations seen. This manifestation of fetal hypoxia is referred to as fetal distress.

In acute or acute-on-chronic fetal distress, the predominant fetal reaction is somewhat different. In dire circumstances of severe oxygen lack, as already stated above, anaerobic respiration is resulted to. Anaerobic respiration, while helping the foetus stay alive, unfortunately leads to the production of the harmful lactic acid and subsequent acidosis. The predominant reaction of the foetus in these acute cases is in abnormality of the fetal heart rate pattern. The type and extent of the fetal heart rate reaction depends on the factors listed above including the prior state of health of the foetus and the severity and the duration of onset of the insult.

7 Regulation of Fetal Heart Rate and Rhythm in Pregnancy

The Sino-Atrial (S.A) node is the pacemaker of the heart. Electrical impulses are generated from the S.A node and are transmitted to the musculature of the heart leading to myocardial contraction. The S.A node is primarily responsible for the determination of the fetal heart rate. However, the S.A node is responsive to influences, both nervous and humoral. The nervous influences are mainly autonomic. The vagus nerve, which is parasympathetic, is the main autonomic nervous supply to the heart. Its influence on the S.A node is the reduction of the fetal heart rate. The myocardium also has a lot of sympathetic fibres supplying it. Sympathetic impulses through its adrenergic influence lead to increase in the fetal heart rate. Humoral influences are mainly adrenergic from the adrenal gland which leads to increase in the fetal heart rate. Fetal movement gives rise to stimulation of the sympathetic nervous system and also release of adrenaline both having positive chronotropic effect on the heart.

Optimal regulation of these influences requires an intact fetal central nervous system (CNS) which is in turn dependent on the gestational age of the foetus. Generally, the CNS is fully developed for this function by 28 to 30 weeks of gestation. In the resting stable fetal state, all the nervous and humoral influences continuously come to play. They result in moment-by-moment change in the duration between consecutive heart beats. The Doppler transducer of the CTG machine (see below) is able to detect these changes which are reflected in the continuous subtle changes in the fetal heart rate referred to variability. The CTG Doppler feature of autocorrelation is majorly responsible for the accuracy of this. Adrenergic response is excited by fetal movement and this results in momentary increase in the fetal heart rate referred to as acceleration (see below).

Acute transient reduction in oxygen tension in the foetus is detected by the chemoreceptors located at the carotid sinus of the carotid arteries and the aortic arch. This leads to stimulation of the brain stem to activate the sympathetic nervous system and the release of adrenergic substances resulting in a positive chronotropic and inotropic effect on the heart. The ensuing increased heart rate attempts to restore fetal perfusion especially to the vital organs of the brain, heart, adrenals and the placenta and the reduction of blood flow to the peripheral organs. This later action is usually due to vasoconstriction of the vessels supplying these peripheral tissues and organs.

If the hypoxia persists, the increased peripheral resistance and consequent increased blood pressure results in the stimulation of the baroreceptors also in the carotid arteries and the aortic arch. This, in turn, leads to stimulation of the vagus nerve leading to the reduction of the fetal heart rate. There is also concurrent hormonal influence from release of adrenergic hormones from the adrenal gland. These complex events give rise to varying changes in the fetal heart rate pattern of the affected foetus. This pattern can be detected by the CTG used in EFM.

8 Factors That Could Affect Fetal Heart Rate Pattern Include

Gestational age: The fetal heart rate reduces with advancing gestational age from an average of 140 to 160 beats per minute at less than 26 weeks gestation to an average of about 120 to 140 beats per minute at term.

Cord compression: This leads to interruption of blood supply to the foetus and can result in varying fetal heart rate pattern changes chief of which is the presence of decelerations.

Drugs: The effect of the drugs will depend on their effect on the autonomic nervous system. Atropine will reduce vagal stimulation, hence leading to increased fetal heart rate. Salbutamol, a sympathomimetic drug, will increase the fetal heart rate.

Hypoxia: This can have profound changes in the fetal heart rate pattern as discussed.

Cerebral activity: Increased activity leads to increased fetal heart rate and presence of accelerations. Fetal sleep can give rise to absence of accelerations and reduction in variability. (Sleep cycles can last up to 50 minutes).

Maternal blood pressure: Maternal hypotension can give rise to fetal heart rate changes as seen in fetal hypoxia. Similar changes can also occur in severe maternal hypertension.

Maternal pyrexia: This can lead to increased baseline fetal heart rate called fetal tachycardia.

Maternal pH: Maternal acidosis could result in fetal acidosis leading to profound fetal heart rate pattern as seen in fetal distress including prolonged and persistent late decelerations and fetal bradycardia.

9 Indications for Electronic Fetal Monitoring

Maternal

  • Previous Caesarean section

  • Preeclampsia

  • Post-term pregnancy

  • Prolonged rupture of membranes

  • Induced labour

  • Diabetes mellitus

  • Antepartum haemorrhage

Other maternal medical conditions:

  • Fetal

    • Intrauterine growth restriction

    • Breech presentation

    • Oligohydramnios

    • Abnormal Dopplers

    • Meconium stained liquor

    • Multiple pregnancy

  • Intrapartum

    • Augmentation of labour

    • Fresh meconium stained liquor

    • Abnormality in intermittent auscultation

    • Antepartum haemorrhage

    • Maternal pyrexia

    • Epidural analgesia

10 Cardiotocography (CTG)

This is electronic fetal monitoring using the CTG machine. The CTG is the continuous measurement of the fetal heart rate and uterine contractions with the aim of preventing death and/or serious morbidity from hypoxia. The CTG machine, otherwise called the cardiotocograph , is a device that monitors and plots on a graph the various changes in the fetal heart rate and also the uterine contractions with time. The graphical plot of the fetal heart rate pattern and uterine contractions is called the cardiotocogram . There are two types of transducers attached to the machine:

  • The Doppler transducer that acquires the fetal heart rate

  • The tocodynamometer that acquires the uterine contractions

A careful look at the trace will easily reveal the fetal heart rate changes which are then analysed to detect the presence and the severity of fetal distress.

10.1 The CTG Procedure

This requires a comfortable room with the CTG machine and a couch. The rested patient lies in the semi-recumbent or right lateral position to avoid the supine hypotension syndrome which could affect the CTG trace. It is more convenient for the patient to have an empty bladder before the procedure but this is not essential. The position of the fetal back is identified and the fetal heart confirmed either with a Pinard stethoscope or a sonicaid. Thereafter, ultrasonic gel is gently applied to the surface of the Doppler probe which is then applied over the region where the fetal heart tone was loudest and confirmed to be picking up the fetal heart tone. This is then strapped in place with the elastic belt tied loosely around the paturient’s abdomen. Thereafter, the tocodynamometer is applied towards the fundus of the uterus without application of the ultrasonic gel. This is also strapped loosely in place with the elastic belt. In the event of twin gestation and having a machine that has double Doppler probe, the procedure is similar. However, it is expedient to use a scan to identify the position where the different fetal heart tones can be assessed. In the absence of an ultrasound scan, clinical means can be used to identify these and then place the probes simultaneously over the areas. The trace can then be obtained continuously as previously described. Occasionally, contact is temporarily lost. The probe position can then be adjusted to re-establish contact and continue the acquisition of the trace.

figure a

Picture of CTG machine (the cardiotocograph) with the Doppler probe, the event marker and the tocodynamometer (from left to right of picture)

figure b

  • Baseline fetal heart rate

  • Variability

  • Uterine contraction

  • A typical normal CTG trace

10.2 Basic Features of the CTG

Baseline fetal heart rate (bFHR)

This refers to the mean level of the most horizontal and less oscillatory FHR segments over a 10-minute period. It is recorded as beats/minute. It is the basic feature from which the other features derive. The normal baseline fetal heart rate is 110–160 beats/minute [10]. A bFHR above 160 beats/minute is referred to as fetal tachycardia while that below 110 beats/minute is referred to as fetal bradycardia. Common causes of fetal tachycardia include:

  • Maternal pyrexia

  • Intrauterine infection like chorioamnionitis

  • Maternal drug ingestion like Beta 1 receptor agonist, e.g. Salbutamol

  • Excessive fetal movement

  • Fetal hypoxia

While causes of fetal bradycardia include:

  • Fetal hypoxia

  • Fetal heart block

  • Administration of Β-blockers like propranolol

Baseline variability

This refers to the oscillations of the fetal heart rate above and below the baseline. It is evaluated as the average bandwidth of this oscillation in a one-minute period (that is the width between the peak and the trough of the oscillation). It is recorded as beats/minute. The normal value is between 5 and 25 beats/minute. The presence of variability is a strong factor favouring fetal health and absence of fetal hypoxia. Reduced baseline variability is variability less than 5 beats/minute. Causes of reduced baseline variability include:

  • Fetal sleep

  • Maternal drugs use including anxiolytics

  • Fetal hypoxia

Increased baseline variability above 25 beats/minutes is uncommon and could be due to excessive fetal movement.

Acceleration

This refers to an increase in the fetal heart rate of at least 15 beats/minute above the baseline lasting at least 15 seconds. In foetuses less than 32 weeks gestation, acceleration occurs at an increase of 10 beats/minute lasting at least 10 seconds. A CTG trace that shows the presence of at least 2 accelerations over a 20-minute period is referred to as being reactive. Reactivity is a sign of an intact central nervous system control of fetal heart rate, hence a sign of fetal health and absence of fetal hypoxia.

It is a reassuring sign in electronic fetal monitoring. Accelerations may be absent in conditions such as:

  • Fetal sleep

  • Maternal use of central nervous system depressants

  • Fetal hypoxia

Deceleration

This refers to a decrease in the fetal heart rate of at least 15 beats/minute below the baseline lasting at least 15 seconds. In routine antenatal CTGs, decelerations are absent. Deceleration most times denotes fetal response to stress and not necessarily to fetal distress. This is commonly encountered in intrapartum CTG. There are different types of deceleration. The type and duration of the deceleration may signify the clinical significance.

Early deceleration – This is one of the common types of decelerations encountered in labour. It is usually short lasting, shallow, a mirror image of the contraction and there is presence of variability throughout the deceleration. It is caused by fetal head compression with consequent fetal vagal nerve stimulation and is considered innocuous. It is a common accompaniment of contractions in labour.

Variable deceleration – This is believed by many to be the commonest type of deceleration. It is characterised by not being in phase with contractions, is ‘V’ shaped and has good variability during the period of deceleration. It is believed to be caused by fetal cord compression during labour and does not signify fetal hypoxia, especially if it is non-repetitive.

figure c

Variable deceleration (which also shows very deep troughs which could be disturbing)

Late deceleration – This type of deceleration is commonly ‘U’ shaped, has absence of variability during the deceleration and is not in phase with the uterine contraction. It commences at least 20 seconds after the onset of the contraction and the nadir occurs after the peak of the contraction with the return to the baseline at least 20 seconds after the end of the contraction. It is a strong indicator of fetal hypoxia. Features that heighten its indication of fetal hypoxia are absence of variability and the duration of more than 3 minutes. This latter feature is referred to as prolonged deceleration.

figure d

Late deceleration (however with good variability)

Sinusoidal CTG pattern – This is an uncommon but peculiar type of CTG trace. It is characterised by the presence of a regular undulating pattern resembling a sine wave. It has amplitude of 5–15 beats/minute, a frequency of 3–5 cycles/minute and has neither variability nor acceleration. The duration is usually more than 30 minutes. It is believed to be indicative of fetal anaemia.

figure e

Sinusoidal CTG pattern

Contractions – This is the trace acquired by the tocodynamometer. These are indicated by bell-shaped tracings at the bottom of the CTG trace. They are, at best, indicators of the presence of contractions and the frequency of these contractions. They cannot reliably indicate strength or duration of a contraction. A contraction frequency of greater than 5 in 10 minutes averaged over 30 minutes is referred to as tachysystole and may be associated with fetal hypoxia. Uterine hypertonus refers to a contraction lasting more than 90 seconds. It is also abnormal and can cause fetal heart rate abnormality. However, this condition cannot be reliably diagnosed using the CTG.

11 Types of CTG Evaluation

Cardiotocography can be either antenatal or intrapartum.

11.1 Antenatal CTG

There are two basic types of antenatal CTG – the non-stress test (NST) which is the conventional CTG and the contraction stress test (CST).

Notable high-risk cases indicating antenatal CTG will include:

  • Previous bad obstetric history

  • Hypertensive disorders of pregnancy

  • Disparity in fetal growth (disparity in symphysiofundal measurement)

  • Poor growth detected by ultrasound scan

  • Oligohydramnios

  • History of reduced fetal movement

  • Abdominal trauma

  • Multiple gestation

  • Antepartum haemorrhage

  • Chronic medical disorders including diabetes mellitus

The NST is carried out during the pregnancy in the absence of contractions. It is recommended that antepartum fetal monitoring with the non-stress test (NST) commences at least after the attainment of gestational age not less than the salvage gestational age for the centre. However, due to the confounding factor of prematurity on the CTG findings, commencing monitoring at least at 28 weeks gestation is advised. Interventions based on the CTG findings will depend on various factors including the severity of the CTG abnormality, the gestational age, the salvage gestational age at the centre, the maternal clinical features and the obstetric history of the parturient.

The fetal gestational age is a strong factor affecting the interpretation and guiding the intervention following a CTG trace. Due to immaturity of the fetal brain including immature development of the vagus nerve and its connections, the fetal heart rate is higher, acceleration is less frequent with less amplitude and duration and the fetal heart variability is also less before 28 weeks gestation. These must be considered in deciding on the intervention to be instituted. However, the presence of repetitive decelerations is a strong factor that can be relied upon for intervention even in the preterm foetus. In deciding on delivery in these cases, apart from the severity of the CTG pattern, worsening maternal clinical state is a useful factor. Deciding on conservative management to improve gestational age is a useful consideration if the gestational age is well below the expected fetal salvage age in the centre.

A bad obstetric history may indicate earlier intervention with a non-reassuring CTG. Historically, fetal monitoring is expected to commence at least 4 weeks before the gestational age at which the last fetal demise occurred with the aim of achieving delivery of the foetus before it gets to the same gestational age, especially if the same complication is seen in the mother that may have led to the previous fetal demise. However, the condition may not be recurrent and a normal CTG is reassuring in such circumstances. The CTG should be repeated at regular intervals to ensure it remains normal in such pregnancies with bad obstetric history in which the event may not have recurred.

Worsening maternal illness or clinical state is an indication for delivery irrespective of the features seen in the CTG. However, if the maternal condition warrants it, then fetal monitoring can continue at reasonable intervals. While there is no specific recommendation to the timing interval for repeating the CTG in high-risk cases, the interval could be from 6 hourly to weekly. The timing interval should be dictated not only by the prevailing circumstances as above but also by the availability of resources for the repeat tests and system infrastructural concerns.

A non-reassuring CTG finding at term or at least after 34 weeks requires a definite action. In the absence of contractions, an NST finding of persistent bradycardia or repetitive decelerations of any kind is worrisome. Delivery by Caesarean section is a recommendation. Other abnormalities of the CTG in similar circumstances may be less worrisome. The finding of absence of accelerations or variability should indicate use of other ancillary testing if available including ultrasound scans to assess growth (if not already done), liquor and fetal Dopplers if available. These could assist in decision making. Reactivity of the NST at this gestational age is reassuring. Repeat of the test will be indicated by the clinical features and may range from a few days to weekly.

The contraction stress test (CST) is a test of utero-placental function and relies on eliciting uterine contractions and assessing the fetal heart rate pattern. The uterus is stimulated to achieve 3 uterine contractions in 10 minutes. This stimulation more commonly is achieved using dilute oxytocin solution or less commonly by nipple stimulation. In the latter, the parturient gently massages one or both nipples until 3 uterine contractions in 10 minutes are elicited. The fetal heart rate pattern is then assessed. The result could either be positive or negative. A positive CST refers to the presence of repetitive late or variable decelerations while a negative result is the absence of this. The test is said to be unsatisfactory when there are fewer than 3 contractions in 10 minutes or in the presence of poor tracing. The test could also be additionally described as reactive or non-reactive (see previous notes). A negative CST precludes fetal hypoxia in over 99% of cases and requires no further action other than repeat tests at regular intervals depending on the risk factor elicited. However, a positive CST indicates fetal hypoxia in about 50% of cases and could indicate further testing or delivery.

The CST is rapidly falling out of favour. This is because it is time consuming, quite cumbersome, more expensive and more invasive. It could also get complicated by preterm labour and delivery. It is contraindicated in conditions that preclude vaginal delivery like placenta praevia, more than one previous Caesarean section and abnormal fetal lie. Furthermore, not many studies have been able to demonstrate any superiority over the simpler and commoner NST.

11.2 Intrapartum CTG

In this instance, the trace is obtained from a parturient in labour, based on indication. The procedure, interpretation and decision-making following intrapartum CTG are more challenging. There is a higher incidence of signal loss, especially in the second stage due to the inherent nature of maternal change of position, fetal descent and pain during labour. EFM is recommended to be reserved for the high-risk intrapartum parturient (see indications above). Intermittent CTG monitoring for the high-risk patient may suffice. However, in the event of a suspicious or abnormal CTG finding, then continuous CTG is recommended. In addition, the finding of abnormal fetal heart rate and/or rhythm on intermittent auscultation indicates confirmation with the CTG. If the abnormal finding is not confirmed after at least 20 to 40 minutes of the CTG, then reversion to the previous monitoring regime is recommended provided it is normal. If it is still abnormal, then CTG monitoring is continued. Persistence of abnormal findings, especially if it is remote from delivery, is an indication for Caesarean section.

11.3 Interpretation of a CTG Trace

In the interpretation of a CTG trace, it is important to appreciate that though the cardiotocogram is similar, the interpretation and implication of findings differ between the antenatal CTG and the intrapartum CTG. Understanding these differences is essential to avoid pitfalls in management decisions based on the CTG trace. Some of the important differentiating features in terms of clinical relevance are as below.

The antenatal CTG

In this, the presence of accelerations is very important in the classification of the CTG and the determination of the health of the foetus, hence the CTG is classed as either reactive or not reactive. The presence of all the other reassuring features further contributes to this diagnosis. These other reassuring features are baseline fetal heart rate of 110–160 beats/minute and variability of 5–25 beats/minute. Decelerations are generally absent in antenatal CTGs and even if present, they are infrequent. The presence of repetitive decelerations could be an ominous sign here as there is generally no uterine contraction.

The intrapartum CTG

In this, the absence of accelerations is of uncertain significance. While the baseline heart rate and the variability give confidence of the fetal health as in the antenatal CTG, there is major focus on the decelerations. Unlike in the antenatal CTG, decelerations are not infrequently seen here and the presence of type 1 decelerations show normal fetal reaction to intermittent labour contractions and are considered innocuous. Emphasis is placed then on the type of deceleration and the frequency. Presence, duration and repetitiveness of variable and type 2 decelerations are associated with presence of fetal hypoxia. The absence of the other non-reassuring features, especially the variability, strengthens this association.

figure f

The above table is a recent (2015) FIGO classification of CTG. Following the interpretation of the CTG features as itemised earlier, the next step is the classification into normal, suspicious and pathologic. It is noteworthy that in many centres, especially in the United States, the terminology used is Category 1, 2 and 3, respectively.

It is important to note that the CTG is a screening tool for fetal hypoxia and NOT a diagnostic tool. There are features seen on CTG that may strongly suggest fetal hypoxia but the diagnosis of fetal hypoxia is by fetal blood pH estimation. It is worth emphasising that a CTG trace that shows acceleration and/or variability denotes a foetus that does not have hypoxia. Put more scientifically, the CTG has a high sensitivity of about 99%. This therefore means that the risk of a foetus having hypoxia following a normal reactive CTG is very slim. However, the contrary is not the case. A foetus that does not have acceleration and/or variability is not equivalent to a foetus with fetal hypoxia. More scientifically, the CTG has a low specificity of about 40 to 60%. This therefore means that for a non-reactive CTG, only about 40% of the foetuses may be hypoxic with the remaining being false positive.

In the interpretation of the CTG, it is important to consider:

  • The clinical condition

  • The features of the trace

  • Other associated features like recent positional change, drug administration, insertion of epidural analgesia.

11.4 Clinical Implication

The CTG is a very useful tool for giving reassurance in the case of a foetus with normal features. In other words, it is very sensitive. However, the specificity is much lower in that it being abnormal does not necessarily imply a foetus with fetal hypoxia. This therefore underscores the need for training and retraining in CTG interpretation to avoid unnecessary maternal morbidities through unwarranted interventions.

In deciding the best approach to management, it is worth considering the following:

  • Maternal background history.

  • The features of the CTG trace preceding the abnormal trace.

  • Any inciting event. If the trace had been previously normal and suddenly showed features of abnormality, there is likely to be an inciting event that should be explored.

  • Progress of labour.

  • Presence of Fetal Scalp Blood Sampling (FBS) facilities or other ancillary tests including ultrasound Dopplers.

  • Stage of labour.

  • Station of the fetal presentation.

Normal CTG trace – This gives reassurance of fetal health. There is no extra intervention. It is important to note that in cases where there is reduced baseline variability and absence of accelerations, this may be due to fetal sleep. Fetal deep sleep could last up to 50 minutes [11], hence there may be need to continue the CTG monitoring for beyond 50 minutes if other parameters are normal.

Suspicious or pathologic CTG trace – This is an indication for action. The actions may include:

  • Reversing any identified cause. This could be abnormal positioning, especially maternal dorsal position causing aorto-caval compression. In this situation, the mother should adjust her position to a lateral position. It could also be as a result of the use of the bed pan or administration of epidural anaesthesia with consequent maternal hypotension. If it follows epidural analgesia, rapid intravenous infusion may reverse the hypotension and its effects. The action taken could also involve putting off any oxytocic agent being used, especially if hyperstimulation is observed.

  • Institution of palliative/resuscitative measures. One of these is the administration of tocolysis if there is uterine tachysystole. The use of bolus dose of intravenous infusion has only been shown to benefit those cases with fluid deficit [12] while the routine administration of oxygen to the mother has not been shown to be beneficial [13].

  • Reassessment to see the impact of the above resuscitative measures.

  • Closer monitoring of foeto-maternal status. This involves maintenance on continuous EFM, especially after the institution of the above measures.

  • Institution of other methods to evaluate fetal oxygenation if available. This includes fetal scalp stimulation which results in FHR acceleration indicating good health. Another measure could be fetal scalp blood sampling (FBS) to assess fetal blood pH if the cervix is dilated.

  • If following these adjunctive tests, the foetus is adjudged not to be hypoxic, labour is allowed to continue with more astute monitoring.

  • If following the above resuscitative measures, there is no improvement in the fetal state or there is deterioration, then plans for delivery should be made.

  • The mode of delivery will depend on the aetiology of the fetal distress, the severity and the stage of labour. If delivery is imminent, then instrumental vaginal delivery is an option if all favourable conditions are met.

  • If the aetiology of the abnormal CTG trace is identified as an acute severe event like abruptio placentae, uterine rupture or cord prolapse, immediate delivery preferably by Caesarean section should immediately be undertaken as the features obviate the need for any other confirmatory test.

12 Controversies Surrounding the Use of EFM

While EFM finds use in most centres in the high-income countries and many low-income countries, there still is no concrete scientific proof of benefit over intermittent auscultation. Presently, there is also no scientific proof of benefit of continuous EFM against intermittent use of EFM, especially in the low-risk patients. In one of the largest studies that involved almost 35,000 patients, there was no reported benefit of continuous over-intermittent EFM in terms of stillbirth rate, Apgar scores, assisted ventilation at birth, NICU admission or seizures [14]. EFM was also not found to confer any significant benefit in parturients with preterm labour in terms of Caesarean section rate, fetal acidosis, neonatal seizures, respiratory distress syndrome and intracranial haemorrhage [15, 16].

There have been criticisms of these reported studies. They were carried out in the earlier days of EFM when a lot of the available information now was still sketchy. Studies have also shown a high degree of inter- and intra-observer variability in CTG interpretation [17]. It is also believed that most of the studies lacked the statistical power to detect differences in the rates sought. These studies were carried out in high income countries where the perinatal mortality rates are quite low, hence it will require very large study population. However, conducting large-scale studies in contemporary obstetric practice is an ethical challenge. In present day practice, it is considered unethical to randomise patients to not having what may be considered as adequate intrapartum monitoring. Based on expert opinion and many medico-legal antecedents, it is imperative to offer EFM to women who qualify for its use.

In a recent review on possible reasons for the finding of absence of statistical benefit of EFM, it was opined that there is a need to always critically review the CTG trace preceding the abnormal trace. This will help in deciding if the foetus is responding to an insult from which it may recover or it is in a downward spiral to acidosis which requires major interventions like Caesarean section. In addition, it was suggested that the strict adherence to the written protocols without the full understanding of fetal behavioural pattern may be responsible for the increased Caesarean section rate following use of EFM [18]. It therefore behoves on individuals using EFM to constantly update their knowledge of fetal physiology and the changing guidelines and interpretations of EFM traces.

13 Relevance of EFM in Low- and Medium-Income Countries (LMIC)

As earlier stated, EFM has become the standard of care in most of the high-income countries exemplified by those in Europe and the United States of America. However, the same cannot be said of the resource-constrained countries mainly in Asia and sub-Saharan Africa. In most instances, fetal monitoring, especially in the intrapartum period, is by the use of intermittent auscultation with the Pinard stethoscope. In some centres, there has been the introduction of IA using the hand-held sonicaids. There have been attempts by some centres to introduce cardiotocography as a form of EFM.

It is estimated that up to 98% of stillbirths occur in low- and medium-income countries [19, 20]. Similar figures are believed to exist for early neonatal deaths in the region. Though there is dearth of reliable data, it is believed that a high percentage of this occurs due to actions and inactions in the intrapartum period. Impaired placental function and growth restriction are believed to account significantly to this. Improved care at birth has been proposed to be essential to prevent 1.3 million intrapartum stillbirths, end preventable maternal and neonatal deaths, and improve child development [20]. This underscores the need for improvement in intrapartum management of the parturient. While unequivocal benefits of EFM are presently unavailable, intuitively, it is believed that improved fetal monitoring is necessary to produce significant decline in perinatal mortality rates.

Antenatal electronic fetal monitoring is believed to be necessary in the management of high-risk pregnancies and in confirming the impact of complications occurring in pregnancy. It is also invaluable in the triaging of pregnancies to various levels of care and in confirmation of some complaints in pregnancy as exemplified by complains of reduced fetal movement by the parturient. It will be a useful tool in the monitoring of foetuses of mothers with bad obstetric history like those with previous intrauterine fetal death and those with previous still birth and also as useful tool in medical audit.

EFM will assist in early detection of fetal heart rate abnormalities, hence indicating adjustment of care in the clients before irreversible damage occurs. In addition, the recognition of the fact that there is an electronic record of the fetal heart rate will encourage greater attention to the care of the foetus in a parturient in labour. The records from EFM can also act as training and teaching tools, even in cases of fetal demise, to help prevent recurrence. While presently not so common in LMIC, records from EFM can assist in the resolution of medico-legal issues. In areas with severe labour ward staff lack, EFM can come to the rescue enabling a limited number of midwives monitor fetal health in such staff-constrained labour wards.

14 Challenges with EFM in Low- and Medium-Income Countries

While EFM is believed to be an important tool in the reduction of perinatal morbidity and mortality in low resource countries, there are major system and implementation challenges that potentially militate against its introduction. One of these is the cost of procurement of the machines. In many of the countries, health budgets are limited and various equipment compete for this lean budget. Based on some other pressing and established demands, such technologies may not be affordable on a large scale. Another important challenge is the supporting infrastructure – mainly electricity. With the lack of adequate electricity in many LMIC, the challenge becomes real that EFM may be a far-fetched technology. There also is lack of experience and training in EFM. Training has been shown to be essential to maximise the beneficial effect of introduction of new technology. EFM is not left out of this assertion. Many healthcare workers will have to be trained in the effective deployment of EFM. The maintenance of these equipment is also a challenge as they are not manufactured locally and service and maintenance services may be unavailable. Many centres in LMIC still lack expedient intervention to salvage cases requiring emergency intervention and also poor salvage rates for prematurity. In the absence of effective intervention when EFM detects a condition requiring such, one doubts the usefulness of its introduction.

15 Recommended Practical Approach for the Deployment and Use of EFM in LMIC

It is recommended that there should be antenatal and intrapartum CTG services in obstetric units in LMIC. These should be for specific indications and for high-risk obstetric patients. Realising that there is an essential learning curve for EFM and its introduction usually results in an increase in Caesarean section rates due to its high false positivity, limiting this technology to high-risk patients will result in reduction of this setback.

16 Setting Up a CTG Unit

This should be in two different sections if the availability of machines permits – the antenatal section should be domiciled in the antenatal clinic while the intrapartum service should be domiciled in the labour ward.

Setting up a new CTG monitoring unit comes with its challenges. Despite the lack of specific guidelines on this subject, it is pertinent to share experiences that have been beneficial in some centres. The first consideration is to have staff that will be dedicated to the care and maintenance of the machine and who will take responsibility for carrying out the test. Experience has shown that the doctors, based on pressure of work, are ill suited to maintain the service. Based on this, the nurses are recommended to supervise the acquisition of the CTG trace and the care of the machine. This is however not exclusive.

17 The Antenatal Unit: Recommendations Here Include

  • A practical training workshop/seminar conducted by a professional experienced in the practice of the CTG. This should precede the commencement of the service in the centre.

  • Provision of a dedicated room for the service. The room should be in the antenatal clinic with a comfortable couch and lighting. Having an air conditioner is desirable.

  • Service should run a minimum of the full working hours. 24-hour service is ideal.

  • There should be a dedicated nurse to run the service. She should have at least basic knowledge of trace acquisition and basic interpretation. Depending on manpower need, the nurse may be a member of the antenatal nursing team who is called upon to carry out the CTG when necessary. However, if the demand is high and manpower is not a challenge, the nurse can be stationed in the CTG monitoring unit.

  • A CTG machine fit with a power surge protector and a UPS system to maintain power to the device in the event of power loss while the machine is already in use.

  • Having a computer in place for record purpose is encouraged.

  • Once a CTG evaluation is requested, the requisite request is made by the managing team and the test carried out by the nurse. It is recommended that there be a continuous 20-minute trace acquired per client. However, if the demand is high, a normal trace with at least two accelerations acquired in at least 10 minutes is sufficient. If however there is absence of accelerations in 20 minutes, the trace could be continued for up to 40 to 50 minutes during which time, at least two accelerations are expected in a normal healthy foetus. The trace is then sent back to the managing team for interpretation and action. However, if the nurse notices the trace to be pathologic or persistently lacks accelerations, it is advised that she takes direct action to alert the managing team for review and immediate action.

  • Practice like this helps to build the system and maintain the equipment over time. Experience gathering also occurs in the process.

18 The Intrapartum Unit: Recommendations Here Include

  • Ideally , every delivery suite should have a CTG machine. In practice, this is impracticable in many centres in LMIC. Each centre should provide the optimum number of machines it can reasonably afford depending on resources and need.

  • Each machine should be equipped with a power surge protector and a UPS system. The unit should be on a movable trolley to prevent damage.

  • If there is more than one machine, there should be some stationed in particular rooms while one could be mobile, again to prevent undue damage.

  • As indicated, high-risk patients could be on intermittent CTG monitoring. If normal, this is continued at regular intervals without disrupting the regular intermittent auscultation using the Pinard stethoscope or the sonicaid. However, in the event of any abnormality in the tracing on intermittent CTG, the patient may then be commenced on continuous CTG monitoring.

  • Depending on the local circumstances, the nurse/midwife carries out the CTG and the trace is reviewed by the attending doctor. This does not preclude the doctor from carrying out the CTG when necessary.

  • Any abnormal trace requires prompt attention for either resuscitation or delivery as indicated.

19 Summary

Electronic fetal monitoring often also referred to as cardiotocography (CTG) is the use of a special Doppler device to monitor the fetal heart rate patterns. Abnormal patterns are associated with fetal hypoxia. The aim is early detection of these patterns and institution of corrective measures and/or delivery in order to prevent fetal damage or death. There is the antenatal and the intrapartum CTG. The non-stress test is a form of antenatal CTG that is recommended after the age of viability in pregnancies complicated by features suggestive of bad fetal outcome from hypoxia. The contraction stress test is a less common form of antenatal CTG that assesses the placenta reserve and relies on the eliciting of 3 contractions in 10 minutes and assessment of the ensuing heart rate changes. The features of a CTG are the baseline fetal heart rate, variability, acceleration and deceleration. A CTG trace (cardiotocogram) with at least 2 accelerations is said to be reactive and is very reassuring of the fetal health. The CTG has a high sensitivity and a less impressive specificity. Therefore, a pathologic CTG is not diagnostic but may be indicative of further evaluation. Though there are obvious challenges to the deployment of the CTG in LMIC, it is a recommended form of care in the management of high-risk pregnancies.