‘By applying the ear to the mother’s belly; if the child is alive you hear quite clearly the beats of its heart and easily distinguish them from the mother’s pulse’.
François Mayor
Biblioth Universelle des Sciences et Arts. Geneva: 1818; 9:249
Intermittent Auscultation
Available evidence suggests that intermittent auscultation (IA) is adequate in low-risk pregnancies. Electronic fetal monitoring (EFM) reduces neonatal convulsions and increases operative interventions, but has not been shown to reduce cerebral palsy. Most national organizations accept IA to be adequate and appropriate for low-risk pregnancies and recommend continuous EFM for high-risk pregnancies. Auscultation of the fetal heart rate (FHR) should be for 1 full minute soon after a contraction, every 15 minutes in the first stage and every 5 minutes in the second stage of labour. If IA cannot be provided as recommended or the mother wishes to have EFM, it should be provided. Low risk before labour may become high risk during labour and this should prompt conversion to EFM.
Intermittent auscultation is practised with a fetal stethoscope (Pinard or De Lee) or by using a Doppler device. Increasingly the mother prefers the latter as the family enjoy listening to the FHR. The practice of listening for 15 seconds and multiplying by four to calculate the rate per minute gives rise to erroneous FHR/min because of the possibility of multiplying the error by four. Doppler devices electronically calculate and provide digital display of the FHR and are accurate.
Prior to IA, recording the latest time the woman felt fetal movements reassures that the fetus is healthy. The baseline FHR should be auscultated and recorded on admission. Further reassurance is derived by the attendant and mother palpating for fetal movements (FM) and recording that event and the auscultated acceleration of the FHR > 15 beats above the baseline at the time of FM. As a next step auscultation should be performed immediately after contraction that should identify any FHR deceleration. Such ‘intelligent auscultation’ may reveal the presence of accelerations with FHR and no decelerations and is equivalent to a reactive cardiotocograph (CTG) trace. It is likely that the baseline variability will be normal in a reactive CTG with FHR accelerations and FMs.
‘One day whilst examining a patient near term and trying to follow the movements of the fetus with the stethoscope I was suddenly aware of a sound that I had not noticed before; it was like the ticking of a watch. At first I thought I was mistaken, but I was able to repeat the observation over and over again. On counting the beats I found that these occurred 143–148 times per minute and the patient’s pulse was only 72 per minute’.
Jacques Alexandre Kergaradec
Memoire sur l’auscultation, appliqué a l’etude de la grossesse. Paris: Mequignon-Marvis, 1822
The deceleration that returns to the baseline rate before the contraction abates is unlikely to be harmful to the fetus provided the duration of decelerations is less than the duration of the FHR at the baseline rate so as to generate adequate perfusion. Auscultation with a fetal stethoscope during a contraction is uncomfortable for the mother and there is attenuation of the fetal heart sound with thickening of the contracting myometrium. A Doppler device can be used during and just after a contraction. Most of the ‘harmful’ FHR decelerations are late, atypical variable and prolonged decelerations and should be identified by auscultation immediately after a contraction. Subsequent to the initial ‘intelligent auscultation’ the attendant can listen every 15 minutes in the first stage and every 5 minutes in the second stage of labour for 1 minute just after a contraction. Should there be audible abnormality of the FHR (rise in baseline rate, decelerations), or difficulty in auscultation, or should a high-risk factor become evident in labour (e.g. meconium, bleeding or blood-stained liquor, need for oxytocin augmentation), the process of IA should be converted to continuous EFM.
High-Risk Pregnancy and Continuous EFM
EFM provides a continuous recording of the FHR with the use of a trans-abdominal ultrasound transducer or a fetal scalp electrode after the membranes have ruptured. Those identified as high risk ( Table 6-1 ) during the antenatal period or in labour should be offered continuous EFM. The FHR is recorded on the upper ‘cardio’ channel and the contractions are recorded on the lower ‘toco’ channel of the recording graph paper and this CTG displays the FHR in relation to the contractions.
| Maternal | Fetal |
|---|---|
| Pre-eclampsia | Intrauterine growth restriction (IUGR) |
| Diabetes | Prematurity |
| Prelabour rupture of membranes (> 24 hours) | Prolonged pregnancy (> 42 weeks) |
| Previous caesarean section | Breech presentation |
| Antepartum haemorrhage | Abnormal fetal function tests |
| Maternal medical disorders | Oligohydramnios/meconium-stained liquor |
| Induced labour | Multiple pregnancy |
There are four features in the FHR trace recorded by electronic FHR monitors: baseline rate, baseline variability, accelerations and decelerations. These are described below and are based on the NICE guidelines (National Institute of Clinical Excellence, UK).
Baseline Fetal Heart Rate
Each fetus will exhibit its own baseline rate. It is deduced by drawing a line where the FHR is steady for a period of 2 minutes without the transient changes of accelerations and/or decelerations. The normal baseline rate at term is 110–160 beats per minute (bpm).
Baseline Variability
Baseline variability is the ‘wiggliness’ of the baseline and is a reflection of the integrity of the autonomic nervous system and its influence on the heart rate. The ascending limb is due to the sympathetic and the descending limb is due to the parasympathetic activity of the fetal autonomic nervous system. The baseline variability is assessed by measuring the bandwidth of the ‘wiggliness’ seen at the baseline rate during a 1-minute segment of the FHR trace. The normal baseline variability is 5–25 bpm. When it is < 5 bpm the baseline variability is reduced – which may be due to fetal sleep, drugs that act on the central nervous system, hypoxia, brain haemorrhage, infection, chromosomal or congenital malformation of the brain or heart.
Accelerations
Accelerations are a sudden rise of the FHR from the baseline by > 15 beats for a duration of > 15 seconds. These are usually associated with activity in the brain associated with FM (‘somatic nervous system’). Two such accelerations in a 15-minute CTG trace are termed reactive and this usually indicates a non-hypoxic fetus. It is very unusual for the neonate to be acidotic at birth if the FHR trace was reactive just before delivery.
Decelerations
Decelerations are a sudden fall of the baseline rate of > 15 bpm for > 15 seconds. The shapes of the decelerations and relationship to contractions vary. Decelerations indicate a transient stress to the fetus. Based on the shape and timing of decelerations to the contractions, one can identify the cause of the stress.
Early decelerations are ‘mirror images’ of contractions and are associated with head compression in the late first and second stages of labour ( Fig 6-1 ). There is a slow reduction in FHR as the intensity of contraction increases – the lowest FHR or nadir of the deceleration is at the peak or acme of the contraction. There is slow recovery of the FHR to the baseline rate as the contraction abates and returns to the baseline. Since they are ‘uniform’ decelerations and are reflective of head compression causing vagal stimulation they should be seen only in the late first stage or second stage of labour. Early decelerations are not due to hypoxia and generally they do not decelerate > 40 bpm below the baseline rate.
Variable decelerations are ‘non-uniform’ and have a precipitous fall from the baseline rate and a quick recovery back to the baseline FHR. They vary in shape, size and timing in relation to contractions. They are due to cord compression. They can also be due to head compression, being common with malpresentations and malpositions and when this is the case they do not have the slight increase in the FHR just prior to and at recovery of the FHR known as ‘shouldering’. Those due to cord compression have a transient slight increase in the baseline FHR just before and after the deceleration (‘shouldering’) due to baroreceptor-mediated responses. These pre and post humps that are described as ‘shouldering’ are shown in Fig 6-2 . Variable decelerations due to cord compression may be relieved by change of position of the mother or by amnioinfusion.
Atypical variable decelerations ( Fig 6-3 ). In a pregnancy, more than one mechanism of stress may operate on the fetus. There may be cord compression due to oligohydramnios causing variable decelerations and the same pregnancy may be associated with placental insufficiency, and with contractions the fetus may also exhibit late decelerations. When both mechanisms operate (cord compression and uteroplacental insufficiency at the same time) there may be a variable followed by late deceleration and these are known as ‘combined’ or ‘biphasic’ decelerations. The merger of the two of these can present as variable deceleration with late recovery of the FHR to the baseline rate, i.e. after the contraction has reached the baseline pressure. Variable decelerations with duration > 60 seconds and depth > 60 beats, and those with absence of baseline variability during the deceleration and between variable decelerations at the baseline rate, or an overshoot of the returning heart rate, or the absence of shouldering after being initially present, are classified as atypical variable decelerations. Atypical variable decelerations are considered an abnormal feature in a CTG trace, whilst simple variable decelerations are considered a non-reassuring feature.
Late decelerations start towards the end or soon after the contraction peaks and the rate does not recover until well after the contraction has ceased. There is a lag of greater than 20 seconds before the onset of the contraction and that of the deceleration. When blood flow and oxygen supply to the intervillous space are critically reduced the FHR slows – an effect mediated via chemoreceptors. Typical late decelerations are shown in Figure 6-4 . The combination of late decelerations (however subtle) with persistent tachycardia and reduced baseline variability is the most pathological FHR pattern and is almost invariably associated with fetal hypoxia ( Fig 6-5 ).
Fetal Behavioural State in the CTG – ‘Cycling’
Non-hypoxic fetuses have alternate ‘ active’ and ‘ quiet’ sleep epochs on the CTG and this is referred to as ‘cycling’. During the active sleep epoch there are several accelerations and good baseline variability. During the quiet epoch there are no or occasional accelerations and the baseline variability may be reduced to < 5 bpm. The quiet period can be 15–40 minutes and rarely more than 90 minutes unless influenced by medication. In the late first stage of labour the CTG may show a long quiet epoch when the head is deeply in the pelvis or after a narcotic is given for pain relief. Occasionally, a healthy fetus that has accelerations and good baseline variability may show segments of reduced variability and shallow decelerations during the quiet epoch but this period does not usually last for > 40 minutes, and rarely > 90 minutes, and seems to be associated with fetal breathing episodes.
The absence of cycling indicates the possibility of an insult or injury that may have already happened or it may be that the fetus is hypoxic or has sustained some injury such as infection or prior hypoxic insult. If the trace was reactive and cycling and then becomes pathological one may be able to identify the time of the insult. If the trace is pathological from the time of admission then the insult/injury may have already taken place and the timing of injury may be difficult to ascertain. A reactive heart rate pattern of a fetus that exhibits cycling from early labour to near full dilatation is shown in Figure 6-6 .
Cycling with an ‘active’ followed by a ‘quiet’ sleep pattern suggests that the baby is well oxygenated and likely to be non-hypoxic and ‘neurologically normal’. Absence of cycling may be due to drugs, infection, cerebral haemorrhage, chromosomal or congenital malformation, or previous brain damage. A previously brain damaged fetus may or may not show cycling but the cord pH is likely to be normal if there are accelerations. Such infants may exhibit signs of neurological damage later on in life.
‘The foetal pulsation is much more frequent than the maternal pulse … being about 130 or 140 in the minute; however, it is not necessarily observed to beat always at this rate … This variation may depend upon a variety of inherent vital causes in the foetus … An obvious explanation, however, is muscular action on the part of the foetus; and we shall very generally observe the pulsation of the foetal heart increased in frequency after such. The external cause which we shall find most frequently to operate on the fetal circulation, is uterine action, particularly when long continued, as in labour’.
Evory Kennedy
Observations on Obstetric Auscultation. Dublin: Longman, 1833
Identification of Individual Features of CTG Trace and Their Classification
The NICE guidelines have provided a framework to categorize the CTG as normal, suspicious or pathological. Once the trace is categorized as suspicious or pathological by the attendant he/she has to seek the possible cause and take action. Action may be one or more of the following: observation and continue with labour, hydration, stopping oxytocin, repositioning the mother, tocolysis, fetal scalp blood sampling, or delivery by the most appropriate route. This decision will depend on the parity, cervical dilatation, rate of progress of labour, and risk factors based on the past and current obstetric history. The mother should be told of the issues involved and the possible actions needed, which should be based on informed choice and with her consent.
Classification of the Individual Features of the FHR Trace
See Table 6-2 .
| Baseline Rate (bpm) | Variability (bpm) | Decelerations | Accelerations * | |
|---|---|---|---|---|
| Reassuring | 110–160 | ≥ 5 | None | Present |
| Early | ||||
| Non-reassuring | 100–109 | < 5 for ≥ 40 min but < 90 min | Variable for > 50% over 90 mins | |
| 161–180 | Single prolonged < 3 min | |||
| Abnormal | < 100 | < 5 for > 90 min | Atypical variable &/or late for > 50% of contractions over a 30 min period | |
| > 180 | Sinusoidal pattern for > 10 min | Single prolonged deceleration > 3 min |
* The absence of accelerations with an otherwise normal CTG is of uncertain significance.
Classification of the Cardiotocograph
- •
Normal – all four features are reassuring.
- •
Suspicious – one of the features is non-reassuring.
- •
Pathological – ≥ 2 non-reassuring features; ≥ 1 abnormal feature.
The course of action necessary may vary even within the pathological category. If there is one feature that is abnormal (e.g. only atypical variable decelerations), simple remedial action/s (stopping oxytocin, hydration, repositioning the woman, tocolytics) and observation may be adequate. On the other hand if three features are abnormal (tachycardia, reduced baseline variability and atypical variable or late decelerations) the remedial actions may be those indicated earlier and in addition may include fetal scalp blood sampling (FBS) for pH or delivery, as thought to be most appropriate depending on the clinical situation.
Sinusoidal Pattern
Sinusoidal pattern is a description of the trace where the FHR appears like a sine wave form ( Fig 6-7 ) but has none of the other features of baseline variability, accelerations or decelerations. Sinusoidal pattern was first described in fetuses with severe anaemia – pathological sinusoidal pattern. Fetuses that are healthy and thumb sucking, as observed in an ultrasound examination, can also exhibit a physiological sinusoidal pattern. Doppler velocimetry of the middle cerebral artery shows increased velocity and is currently used to detect fetal anaemia. The following are the known reasons for fetal anaemia that could give rise to a sinusoidal pattern.
Blood Group Antibodies that Cross the Placenta
In Rhesus iso-immunization higher concentration of antibodies can give rise to in utero anaemia. Maternal blood tests will reveal the presence of Rhesus antibodies and the concentration of antibodies can be measured. Presence of anti-Kell and anti-Duff antibodies can cause fetal anaemia. ABO blood group antibodies usually cause neonatal jaundice rather than fetal anaemia. Lewis a and b and M and N blood group antibodies are less likely to cause fetal anaemia.
Haemoglobinopathy
Alpha-thalassaemia in the fetus results in anaemia that may be associated with a sinusoidal pattern. Usually the mother presents in early third trimester with oedema and signs of pre-eclampsia. Ultrasound examination may reveal polyhydramnios, hyperplacentosis and hydrops fetalis (‘Bart’s hydrops’ due to four gene deletions). In these cases the mother may be a known thalassaemia carrier. Termination of pregnancy should be offered, as the fetus with Bart’s hydrops does not survive. Currently, in utero stem cell therapy is being studied to salvage these fetuses.
Fetal Infection
Parvo virus infection is known to cause fetal anaemia. If a mother comes with a history of reduced or no FM after a flu-like infection, an ultrasound examination would be useful in the presence of a sinusoidal pattern. A fetus appropriate for gestational age with reduced movement and with poor tone (open palm), or a hydropic fetus with ascites is suggestive of fetal anaemia. Referral to a fetal medicine unit would be necessary to make a definitive diagnosis and possible therapy by intrauterine blood transfusion.
Feto-Maternal Transfusion
This is a well-known cause of fetal anaemia and may show a pseudo-sinusoidal pattern ( Fig 6-8 ). The Kleihauer–Betke test should identify fetal cells in maternal blood to confirm that the cause of anaemia is feto-maternal haemorrhage.
