Abstract
Fetuses are physiologically adapted to cope with labour. However, some fetuses are at risk of hypoxic injury. Whether fetuses are monitored using intermittent auscultation (IA) or continuous cardiotocography (CTG), knowledge of the fetal physiological responses to labour and the various mechanisms of hypoxia is vital to provision of appropriate interventions. Hypoxia in labour can be caused by umbilical cord compression and/or utero-placental insufficiency, sometimes potentiated through infection and inflammation. Recognition of intrapartum risks such as meconium stained liquor, bleeding or maternal pyrexia aid in determining the individual risk of fetal hypoxia but a holistic view needs to be maintained. Detection is only the first step, then requiring appropriate escalation, communication and timely action which are reinforced by initiatives including the Avoiding Brain injury in Childbirth (ABC) programme and the Each Baby Counts (EBC) project. This paper aims to provide an overview of intrapartum fetal monitoring founded in physiological interpretation and insights into new recommendations by the ABC programme.
Introduction
Fetuses are physiologically adapted to cope with the intermittent hypoxia associated with contractions in labour. However, some fetuses are unable to endure these hypoxic insults and are therefore at risk of injury with potential lifelong sequelae. Intrapartum fetal monitoring aims to detect developing fetal hypoxia and instigate action to avoid hypoxic injury without performing unnecessary interventions on the woman or birthing person. Intrapartum monitoring includes both intermittent auscultation (IA) and continuous cardiotocography (CTG). The type of monitoring recommended depends on the background risk of fetal hypoxia which is assessed antenatally and continually intrapartum. Intrapartum interventions such as the use of synthetic oxytocin or prostaglandins can potentiate the risk of hypoxic injury and subsequent risk of perinatal death.
Intrapartum fetal monitoring involves the interpretation of the fetal heartbeat, using IA or the CTG, utilizing knowledge of the fetal physiological response to hypoxic and mechanical stress during labour. Alongside this, the wider clinical context such as maternal pyrexia, meconium stained amniotic fluid or fetal growth restriction and the progress of labour are considered, to formulate individualized care plans for birth. CTG was introduced for fetal monitoring in the 1970’s with the hope it would reduce perinatal morbidity and mortality. Unfortunately, no study to date has shown CTG to reduce mortality, only a reduction in neonatal seizures. Conversely, the rates of clinical intervention have increased significantly. Fetal physiological interpretation has been advocated to improve identification of fetal hypoxia requiring intervention and to reduce unnecessary intervention, and associated costs and complications. However, there are no clinical trials to assess whether physiological interpretation is superior in predicting outcomes.
This review will consider the normal fetal response to labour, how fetal physiology can explain the features of the CTG trace, the mechanisms of intrapartum fetal compromise in labour and the patterns of fetal hypoxia. Furthermore, consideration will be given to the elements surrounding CTG interpretation beyond education including escalation and the vital importance of multi-disciplinary working to achieving the best possible outcomes for mother and baby.
How should the fetus be monitored in labour?
A low risk pregnancy and labour means a gestation greater than 37 weeks with cephalic presentation, spontaneous onset and adequate progress of labour (or minimal intervention such as artificial rupture of membranes (ARM)), and no antenatal risk factors. With maternal consent, monitoring in labour can be via intermittent auscultation (IA). This method of monitoring, when used in the appropriate population, provides monitoring of the fetal condition sensitive enough to result in no change in the proportion of fetuses requiring resuscitation or neonatal care at birth whilst acting as a screening tool for assessment of fetal wellbeing in labour. Continuous risk assessment through labour including assessment of the fetal heart rate is vital to ensure a safe birth. Development of complications during labour such as, but not limited to, antepartum haemorrhage, pyrexia, hyperstimulation or meconium stained liquor should prompt continuous fetal monitoring.
IA monitoring involves listening to the fetal heart every 15 minutes in the 1 st stage of labour and every 5 minutes in the 2 nd stage, both after a contraction and for at least 1 minute. Intelligent intermittent auscultation (IIA) uses 15 second intervals for counting the fetal heart rate. The baseline rate is calculated by adding the counts together and being aware of significant differences in the scores obtained from the different time periods. Only when similar counts for each 15 second interval are obtained can the baseline rate be determined. For example, counts of 34, 32, 30, 32 give a fetal heart of 128 with similar scores in each 15 second count indicating a stable baseline which could be compared to previous from this labour. Where the counts are dissimilar, such as 22, 26, 39, 41, this may suggest a deceleration and further 15 second counts would be required to determine if a baseline can be ascertained. If a deceleration is heard or there is an increase in fetal heart rate baseline by more than 20 beats, this should prompt escalation to continuous monitoring if it persists over 3 consecutive contractions. The rest of this article will consider continuous fetal monitoring by way of CTG.
Normal fetal physiology and associated features of fetal heart rate on the CTG
Baseline heart rate
A stable baseline rate is reflective of the integrity of the fetal myocardium and the fetal autonomic nervous system. The range of normal baseline of fetal heart rate is accepted as 110–160 beats per minute (bpm) but maturation of the fetal parasympathetic nervous system as gestation advances means a lower baseline line rate is expected at term compared with pre-term gestations. A baseline rate of 160 bpm would be acceptable and expected at 28 weeks but should not be accepted as normal at 40 weeks for example. A sudden fall in the fetal baseline heart rate should be termed a prolonged deceleration when occurring for more than 3 minutes and a fetal bradycardia when occurring for more than 10 minutes. A fetal heart rate of more than 160 bpm may be normal in some preterm fetuses but is generally termed a fetal tachycardia. However, a rise in the baseline rate by more than 10% from a previous baseline is suggestive of a fetal catecholamine release due to infection or hypoxia and would be considered abnormal in a fetus of any gestation.
Fetal heartbeat variability
Beat to beat variation of between 5 and 25 bpm is considered normal and reflects integrity of the fetal autonomic nervous system. Reduced variability is when this variation is less than 5 bpm. The commonest reason for reduced variability is fetal sleep and so one would expect a normal CTG to demonstrate periods of normal, and periods of reduced, variability. Fetal sleep periods do not normally exceed 50 minutes and so periods of reduced variability exceeding this duration should be considered abnormal. The observed change from normal to reduced and back again is called cycling and is a marker of fetal wellbeing. Absence of cycling can occur in fetal hypoxia and in neuroinflammation in infection or chorioamnionitis and therefore is viewed as a worrying feature if not present on a CTG. Lack of cycling may represent the inability of the fetus to experience deep sleep which can be seen in chorioamnionitis. Prolonged periods of reduced variability can also be due to other causes such as in-utero fetal stroke.
Accelerations
Accelerations are upward deviations from the baseline by more than 15 bpm and lasting more than 15 seconds. In pre-term infants, an acceleration can be defined as more than 10 bpm. The presence of accelerations is a positive sign of fetal wellbeing and a sign of fetal activity suggesting normal oxygenation of the somatic nervous system responsible for voluntary movements of muscles. During labour, accelerations are not always seen but they should always be present on an antenatal CTG, and their absence would render the antenatal CTG abnormal even if the other features are reassuring. In labour, presence of accelerations, especially during contractions, is not expected and attention to the other features of the CTG should occur to ensure fetal oxygenation is adequate. In addition, monitoring of the maternal pulse should occur to ensure the CTG is not mistakenly monitoring the maternal heart rate. Accelerations may also be seen during fetal stimulation, for example during a vaginal examination. This can be a useful adjunct to assessing fetal wellbeing during labour because a sustained acceleration seen following stimulation suggests a well oxygenated fetus. A normal CTG demonstrating normal baseline rate, variability and accelerations is shown in Figure 1 .
Decelerations
These are downward deflections from the baseline rate by more than 15 beats for more than 15 seconds. Decelerations are fetal cardioprotective reflexes to reduce myocardial oxygen demand during periods of hypoxic stress, mediated by the parasympathetic nervous system. The different types of decelerations will be further discussed in the next section but it is important to realize that the presence of decelerations alone does not equate to a fetus in danger of immediate hypoxic injury. In fact, decelerations during contractions are a normal part of the fetal reflexes to deal with hypoxic stress during labour and interrogation of the baseline rate and variability in between contractions enables the assessment of oxygenation of the fetal nervous system and brain. Even very deep decelerations could be viewed as a sign that the fetal protective reflexes are intact, as long as the baseline rate and normal variability are maintained. In severe hypoxia or acidosis in the fetal brain, the reflexes to generate decelerations may not be present, in which case reduced variability with no or shallow, unprovoked decelerations may be seen. This pattern is typical of chronic hypoxia and shown in Figure 2 . Where prolonged decelerations lasting more than 3 minutes are present, urgent attention should be paid to identify and reverse the provoking event to optimize the fetal cardiovascular system as a prolonged reduction in fetal heart rate reduces cardiac output leading to reduction in blood supply and oxygen to fetal tissues and further hypoxic injury.
Mechanisms of intrapartum fetal compromise
The fetus has autonomous physiology, the components being the cardiovascular, neurological, endocrine and metabolic systems. However, these can also be influenced by maternal pathology such as pyrexia, hypotension and hypoxia. Understanding how the fetal and maternal physiology and pathology interact and influence the CTG is important to enable understanding of how and when to instigate management prior to the fetus sustaining an injury.
Umbilical cord compression
The umbilical cord is designed in such a way as to reduce the risk of compression leading to hypoxia in the fetus. However, factors such as the amount of Wharton’s jelly, the cord position and the intensity of the uterine contractions affect compression and therefore the degree of reduction in blood flow through the cord. Cord compression, and the resultant decelerations on the CTG are very common in labour. Decelerations caused by cord compression have a quick onset, a peak with the contraction and quick offset, often with ‘shouldering’ before and/or after the deceleration as shown in Figure 3 . The size and shape of the deceleration is variable, often altering from one contraction to the next and may be affected by maternal positioning. These ‘variable’ decelerations result from initial partial compression, reduced fetal venous return and a baroreceptor mediated acceleration followed by complete compression of the uterine arteries, leading to fetal hypertension, stimulation of baroreceptors and subsequent reduction in the fetal heart rate via the Vagal nerve. The fetus does not have the ability to increase supply of oxygen and therefore decelerations enable a reduced demand, to maintain aerobic metabolism in the myocardium during a contraction. These types of decelerations are part of the fetal ability to cope with the stress of labour and therefore are not themselves associated with a risk of fetal hypoxia and acidosis. However, cord compression can contribute towards a picture of evolving hypoxia, especially in circumstances of injudicious use of synthetic oxytocin and uterine hyperstimulation. Management therefore may involve reduction in contraction frequency or changes in maternal position to alleviate compression prior to noting fetal compensation through catecholamine release leading to a rising baseline rate or decompensation once reduced variability is noted.
