Introduction

Electronic fetal heart rate monitoring (EFM) involves the use of a cardiotocograph (CTG) to record the fetal heart rate (FHR) so as to determine the fetal well-being in order to detect signs of intrapartum hypoxia.

EFM was introduced in the late 1960s, and the first equipment used phonocardiography to record the FHR, and this was later substituted by Doppler signals with significant improvement on the quality of the signals . It was initially introduced to prevent brain injury secondary to intrapartum fetal hypoxia. Unfortunately, the rates of cerebral palsy have remained stable over the last 50 years. Moreover, the rates of caesarean section and instrumental deliveries have been continuously increasing over the last 40 years .

CTG not only has a 60% false-positive rate , but also has a high intra-observer variability . The knowledge of neonatal outcomes also influences retrospective classification of the CTG traces . Therefore, a good understanding of fetal physiology is essential to adequately interpret and manage the findings on the CTG, irrespective of the availability of other ‘additional tests’ (fetal scalp blood sampling or FBS, fetal scalp lactate, fetal pulse oximetry and analysis of the fetal electrocardiogram (ECG) using ST-Analyser or STAN). It is paramount to analyse the CTG trace in the context of the existing and evolving clinical picture during labour and not in isolation. Risk factors such as prolonged spontaneous rupture of membranes (SROMs), prematurity, intrauterine growth restriction (IUGR), infection or the presence of meconium-stained liquor, the use of oxytocin for failure to the progress of labour and the presence of a uterine scar need to be considered whilst interpreting the CTG trace. Therefore, the overall management needs to be modified in the presence of an ‘a priori’ reassuring CTG. In addition, a critical analysis of the CTG trace needs to be made to differentiate a fetus that is compensating well with the ongoing hypoxic and/or mechanical stress from a fetus that is unable to compensate or has begun the process of decompensation, based on the features observed on the CTG trace. Failure to understand the fetal physiology during labour and to correlate the CTG patterns with the clinical picture may result in an increase in unnecessary operative interventions and/or an increase in the risk of intrapartum hypoxic injury leading to hypoxic–ischaemic encephalopathy (HIE), severe metabolic acidosis culminating in long-term neurological sequelae (cerebral palsy) or perinatal death.

In modern obstetric practice, in view of the high false-positive rate of CTG, several additional tests of fetal well-being have been developed in an attempt to improve the detection rate of hypoxia. FBS, analysis of the fetal ECG using STAN, fetal pulse oximetry and fetal scalp blood lactate levels have been attempted with variable success rates.

Technical aspects

The FHR is recorded using a transducer placed on the maternal abdomen (external monitoring) or using an electrode placed on the fetal scalp (internal monitoring), and it is printed on a paper in a similar way to an ECG. This is the ‘cardiac’ part of the CTG. The external transducer is an ultrasound device that uses the Doppler principle. There is a second transducer, the ‘toco’ component, which is also placed on the maternal abdomen below the uterine fundus, and it records the contractions. It is important to be aware that this transducer gives us information about the frequency and duration of the uterine contractions, but not about their strength. The amplitude or the ‘height’ of the recording merely reflects a change in the tension of the anterior abdominal wall. Currently, there are intrauterine pressure catheters that can be placed inside the uterus once the membranes are ruptured, and they detect the strength of the contractions as well as the frequency and duration .

Before starting CTG recording, it is mandatory to check the maternal pulse to avoid erroneous recording of maternal heart rate as fetal . External FHR monitoring is less reliable than internal as it is more likely to have signal loss, record maternal heart rate or produce other signal artefacts, especially during the second stage of labour. If there is a suspicion that the maternal heart rate is being monitored at any point in labour, it should be checked immediately, and internal monitoring using a fetal scalp electrode (FSE) should be used, if appropriate. There are contraindications for internal monitoring in the presence of infections such as human immunodeficiency virus (HIV) and hepatitis B due to the risk of vertical transmission or in fetuses with suspected or confirmed bleeding disorders .

When starting the CTG monitoring, it is important to ensure that ‘paper speed’ is set correctly. In most countries, it is set at 1 cm/min; however, in the USA, it is set at 3 cm/min, and some European centres use 2 cm/min. Failure to set the speed correctly will result in errors on the correct interpretation of the FHR variability as well as in identifying the depth and duration of decelerations.

Technical aspects

The FHR is recorded using a transducer placed on the maternal abdomen (external monitoring) or using an electrode placed on the fetal scalp (internal monitoring), and it is printed on a paper in a similar way to an ECG. This is the ‘cardiac’ part of the CTG. The external transducer is an ultrasound device that uses the Doppler principle. There is a second transducer, the ‘toco’ component, which is also placed on the maternal abdomen below the uterine fundus, and it records the contractions. It is important to be aware that this transducer gives us information about the frequency and duration of the uterine contractions, but not about their strength. The amplitude or the ‘height’ of the recording merely reflects a change in the tension of the anterior abdominal wall. Currently, there are intrauterine pressure catheters that can be placed inside the uterus once the membranes are ruptured, and they detect the strength of the contractions as well as the frequency and duration .

Before starting CTG recording, it is mandatory to check the maternal pulse to avoid erroneous recording of maternal heart rate as fetal . External FHR monitoring is less reliable than internal as it is more likely to have signal loss, record maternal heart rate or produce other signal artefacts, especially during the second stage of labour. If there is a suspicion that the maternal heart rate is being monitored at any point in labour, it should be checked immediately, and internal monitoring using a fetal scalp electrode (FSE) should be used, if appropriate. There are contraindications for internal monitoring in the presence of infections such as human immunodeficiency virus (HIV) and hepatitis B due to the risk of vertical transmission or in fetuses with suspected or confirmed bleeding disorders .

When starting the CTG monitoring, it is important to ensure that ‘paper speed’ is set correctly. In most countries, it is set at 1 cm/min; however, in the USA, it is set at 3 cm/min, and some European centres use 2 cm/min. Failure to set the speed correctly will result in errors on the correct interpretation of the FHR variability as well as in identifying the depth and duration of decelerations.

Analysis

There are four features that need to be analysed on a CTG: baseline rate, accelerations, variability and decelerations.

• a)
  

  Baseline heart rate

It is defined as the mean FHR after excluding accelerations and decelerations. It is analysed over 5–10 min and expressed in beats per minute (bpm). The normal range is considered to be 110–160 bpm. It is regulated by the combined action of the sympathetic and parasympathetic nervous systems. Consequently, preterm fetuses with a less developed parasympathetic system will commonly show a higher baseline rate compared with term or post-term fetuses when the parasympathetic system is well developed, and they will usually have baseline rates between 110 and 130 bpm. It is not uncommon for a post-term fetus to have a baseline heart rate between 90 and 110 bpm as a consequence of maturity of the parasympathetic nervous system. This should be considered as normal if other parameters on the CTG trace are reassuring.

An increase in the baseline rate of >160 bpm persisting for >10 min is called baseline tachycardia. It can be a reflection of maternal tachycardia due to dehydration or maternal pyrexia (infection) or more rarely secondary to a fetal arrhythmia. It can also be related to chronic hypoxia when it occurs in combination with reduced baseline FHR variability and shallow decelerations.

A baseline FHR of <100 bpm, which persists for >10 min, is called baseline bradycardia, and in the presence of accelerations, good variability and absence of decelerations, it may reflect postmaturity. However, conduction defects of the heart (heart blocks), sympatholytic drugs and acute hypoxia to the myocardium may also present with a baseline bradycardia.

• b)
  

  Accelerations

It is a transient increase in the baseline of >15 bpm, lasting for 15 s or more and returning to the normal baseline. The presence of two or more accelerations over a 20-min period is a reassuring feature suggestive of fetal well-being as they are caused by the somatic nervous system activity usually associated with fetal movements. They are absent in the presence of fetal sleep, chronic hypoxia, drugs (e.g., pethidine), infection and brain haemorrhage (intrauterine fetal stroke). The erroneous monitoring of maternal heart rate may result in accelerations of greater magnitude and/or duration coinciding with uterine contractions.

• c)
  

  Variability

It is the bandwidth variation of the baseline, which is determined after excluding accelerations and decelerations. It is maintained by the interaction between the sympathetic and the parasympathetic systems. Hence, the presence of good baseline variability gives information about the integrity of the autonomic nervous system. It is classified as reduced (<5 bpm), normal (5–25 bpm) and saltatory (>25 bpm).

A normal variability is unlikely to be associated with cerebral hypoxia. During periods of fetal sleep, it can be reduced, but it will be associated with periods of normal variability. The combination of these two patterns is called ‘cycling’, and it is a reassuring feature of fetal well-being ( Fig. 1 ). Periods of reduced variability can also be associated with drugs (central nervous system (CNS) depressants), or it may be a sign of hypoxia in the CNS. Correlation with the clinical picture is essential to perform a differential diagnosis.

CTG showing ‘cycling’ : alternating periods of quiescence (reduced variability) and periods of activity (accelerations, variability of 5–25 bpm).

The saltatory pattern (baseline variability of >25 bpm) may be associated with a rapidly evolving hypoxia usually with active maternal pushing or with the use of oxytocin infusion to augment labor . Although the exact mechanism is still debated, it is proposed that it reflects attempts by the autonomic nervous system to maintain the stability of the baseline heart rate when there is a rapidly evolving hypoxic stress. It should be considered an abnormal feature in the presence of late or variable decelerations, especially with a ‘subacute pattern’ on the CTG trace ( Fig. 2 ). In this case, immediate action should be taken to relieve hypoxic stress by recommending the cessation of active pushing or by stopping oxytocin as appropriate to improve fetal oxygenation.

• d)
  

  Decelerations

Saltatory pattern suggestive of rapidly evolving hypoxia to the central nervous system, and this is usually seen with injudicious use of oxytocin or during active maternal pushing as was in this case.

They are defined as a transient decrease of the FHR of >15 bpm lasting for >15 s. Traditionally, they have been classified in relation to the uterine contractions as early, late and variable. However, clinicians need to understand that decelerations are a reflex response of a fetus to the ongoing hypoxic or mechanical stresses in labour to protect against fetal stroke (variable decelerations) or to hypoxic injury to fetal myocardium (late decelerations). This is because, unlike an adult, a fetus is not exposed to atmospheric oxygen, and, therefore, it is unable to increase the rate and depth of respiration to oxygenate the myocardium to maintain a positive energy balance when exposed to hypoxic stress. Therefore, the only way a fetus could immediately protect the energy balance within the myocardium is by rapidly slowing its own heart rate to reduce oxygen consumption and to improve its coronary blood flow during intrapartum hypoxic stress.

Clinicians also need to understand that, although guidelines classify decelerations as ‘early’, ‘variable’ and ‘late’, in reality, a combination of decelerations may occur as uterine contractions may compress the fetal head and the umbilical cord at the same time .

• 1.
  

  Early decelerations

They start with the onset of uterine contraction, reach their nadir at the peak of the contraction and return to the normal baseline when the contraction ceases. They are associated with head compression, and they are generally benign. They are present on the late first stage or second stage of labour, but they only represent <2% of the decelerations.

• 2.
  

  Late decelerations

The deceleration occurs ‘late’ in relation to the contraction. The nadir of the deceleration occurs after the peak of the contraction, and the heart rate returns to the baseline after the contraction has finished. Usually, there is a 10–20-s ‘lag time’ for the deceleration to return to the normal baseline, and, therefore, they are termed ‘late decelerations’. They are related to fetal hypoxemia, hypercarbia and acidosis, which stimulate the central and peripheral chemoreceptors. Fetal well-being should be assessed by determining the baseline FHR and variability, which denote the oxygenation of central organs (brain and the heart). Additional tests of fetal well-being may need to be considered if there is a progressive rise in the baseline FHR with reassuring variability, if a decision is made to continue labour. Any change in the baseline variability associated with preceding late decelerations and/or a rise in baseline FHR requires an immediate intervention such as intrauterine resuscitation if appropriate or immediate delivery.

• 3.
  

  Variable decelerations

They are the most common type of deceleration during labour. They vary in shape, length, size and timing in relation to the ongoing uterine contractions. They are related to umbilical cord compression, and they are mediated by a ‘baroreceptor’ mechanism. There are different nomenclatures depending on the classification used.

A ‘typical’ or an ‘uncomplicated’ variable deceleration has four components; initially, there is a slight rise in the FHR (‘shouldering’) followed by a sharp fall from the baseline (<60 bpm) with a quick rise that gives a second ‘shouldering’ and a final recovery to the baseline. They last for <60 s. The pathophysiology behind these decelerations is a compression of the umbilical cord in the absence of acidosis; the first shouldering is caused by the selective compression of the thin-walled umbilical vein (the fetus receives less blood from the placenta, whilst it continues to pump its blood through umbilical arteries and increases the heart rate to compensate for ongoing fetal hypovolaemia and hypotension); the sharp fall is secondary to the compression of the umbilical arteries (the fetus reduces the heart rate as a protective mechanism when systemic hypertension occurs to avoid stroke), and the recovery to the baseline occurs as soon as the compression ends. It is a baroreceptor-mediated response.

An ‘atypical’ variable deceleration does not have the features of the ‘typical’ deceleration described earlier. The initial and final shouldering disappear; drop in the FHR of >60 bpm may denote the complete occlusion of the umbilical cord, and the recovery to the original baseline may be delayed. They may have an ‘overshoot’, which may indicate ongoing fetal hypotension secondary to the intense and prolonged compression of the umbilical cord. The pathophysiology of these decelerations is a combination of baroreceptor- and chemoreceptor-mediated response. If these decelerations are recurrent, there may be a component of acidosis with time.