Birth Small Talk

Talking about birth

Changing the woman’s position when the CTG is abnormal

Photo by Ashley Bean on Unsplash

When the fetal heart rate pattern seen on CTG monitoring during labour is considered abnormal, clinicians typically use measures that aim at restoring the pattern to normal. This is often called intrauterine resuscitation. Some of the commonly used approaches are to change the birthing woman’s position, give intravenous fluids, or to administer oxygen. This post is part four of a five-part series looking at the evidence for intrauterine resuscitation. You can read about recent research looking at how often various approaches to intrauterine resuscitation are used here, about oxygen therapy here, and the use of intravenous fluids here.  

It is important to set out expectations for the kind of evidence I am looking for in this series. I don’t believe that it is enough for intrauterine resuscitation attempts to simply restore the wiggles on the CTG to a pattern considered to be normal. Recalling that the aim of intrapartum fetal monitoring is to prevent fetal damage from hypoxia, we should be looking for evidence that these practices improve perinatal outcomes. Or at the very least, resuscitation efforts should reduce the use of other interventions, such as fetal blood sampling, instrumental birth, and caesarean section. 

For each of these posts, I start by setting out the assumptions about how the therapy is proposed to work, and how that lines up with what we know about physiology. I will then share the existing research and summarise key findings. There’s heavy science content in here for those who (like me) delight in such things. You are also welcome to skip to the “too long, didn’t read” (TL;DR) summary at the end of this post (and each of the ones to come) for an answer to the question – does intrauterine resuscitation (in this case changing the woman’s position) when the CTG is abnormal make things better for the fetus and the birthing woman?

Understanding the rationale

I want to begin by separating changing maternal position to ensure that the CTG pattern can be interpreted (eliminating or limiting periods of loss of contact or interference in the signal), from steps taken to manage an interpretable and abnormal pattern. The focus here is to examine the management of an interpretable, abnormal fetal heart rate pattern. There are two main lines of argument for why it might be beneficial to change a woman’s position: the resolution of supine hypotension syndrome (or lesser degrees of alteration in uterine blood flow related to supine positioning) and reducing compression of the umbilical cord. 

Understanding the physiology

Supine hypotension syndrome is a phenomenon that occurs during the later stages of pregnancy when women assume a supine (lying flat on their back) position. In this position the weight of the uterus, with the fetus, placenta, and amniotic fluid inside, rests on the aorta and vena cava. The muscular walls of the aorta resist compression, but this is not the case for the thinner walls of the vena cava, which becomes compressed between the spinal column and the uterus. This leads to a reduction in blood flow from the lower body into the right atrium. The volume of blood being pumped to the lungs for oxygenation falls, as does the volume of blood entering the left atrium. The volume of blood pumped out of the left side of the heart falls with an associated reduction in blood pressure. A rise in heart rate may occur to compensate. Blood flow to the uterus and therefore the placenta is reduced, resulting in reduced oxygen supply for the fetus.

During an episode of supine hypotension, women experience shortness of breath and dizziness, which may progress to feinting. Symptoms, and the alterations to physiology, are rapidly reversed by changing the woman’s position from supine. Lesser degrees of physiological change might also occur in the supine position, such that the woman experiences no symptoms but there is a reduction in uterine blood flow and therefore placental oxygenation. This is supported by research which documents lower blood pressure and stroke volume (the amount of blood shifted per heartbeat), and higher maternal heart rate, in the supine position (Ibrahim, Elgzar, & Saied, 2021; Tamás, et al., 2007). 

Compression of the umbilical cord during uterine contractions has been proposed as a cause of decelerations in the fetal heart rate, specifically variable decelerations. Variable decelerations are the most common form of deceleration seen during labour. Changing maternal position might reduce compression on the cord by shifting the transmission of pressure within the uterus. However, research examining the physiology of decelerations casts doubt on the theory that cord compression activates baroreceptors leading to a fall in heart rate which appears as a variable deceleration.

Baroreceptors are sensory structures within the cardiovascular system that detect changes in blood pressure. Compression of the umbilical cord is proposed to lead to periods of increased fetal blood pressure as more force must be applied to continue the movement of blood towards the placenta. High blood pressure activates baroreceptors, triggering a reflex that increases the activity of the vagus nerve (parasympathetic tone) and decreases activity in the sympathetic nervous system, leading to a reduction in heart rate.

The narrative that cord compression is the cause of variable decelerations was introduced into obstetric practice very early in the history of CTG monitoring (Hon, 1958). Lee and Hon’s later research showed that a rise in fetal blood pressure in response to cord compression was not universal and did not always precede a fall in fetal heart rate (Lee & Hon, 1963), but despite this, the widespread belief about the relationship between variable decelerations and cord compression has continued to this day. 

[As an aside – I have concerns about the ethics of their research. The paper does not record whether consent was sought. The fetuses of eleven women who were having a caesarean section had their cord exposed once the uterus was opened. The cord was deliberately and repeatedly compressed to examine the fetal response to this action. The baby remained in utero while the experiment was conducted, then delivered. Having human data is useful but informed consent is a requirement!] 

Lear and colleagues (2016) have more recently examined the physiology of fetal heart rate changes using sheep rather than human fetuses. They found that once there was a greater than 50% reduction in cord blood flow, heart rate fell but with no change in blood pressure. It is only when complete obstruction of the cord was achieved that an immediate but small rise in blood pressure occurred. The authors summarised:

There is strikingly little evidence to support this concept [that cord compression causes variable decelerations by activating baroreceptors]. Umbilical cord compression can occur in labour, for example, during entanglements of the cord or cord prolapse, albeit there is no empirical evidence that it is the predominant cause of fetal heart rate decelerations in the majority of labours.

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Lee and his team demonstrated that decelerations (regardless of form – early, variable, or late) are instead mediated by chemoreceptors in response to low levels of oxygen. The belief that cord compression causes variable decelerations is so strong that the opportunity to whether this is true has been ignored by obstetric researchers. For example, Utsu in 2006 published research examining the role of the umbilical cord in fetal circulation. They reported a single case where variable decelerations were present in an antenatal CTG and ascribed the cause of this to cord compression. This was done despite not having performed imaging to examine the location of the cord nor Doppler flow assessment to confirm whether there was restriction in flow, even though the remainder of the paper was about using ultrasound for this purpose. 

What would good research look like?

To address the question of whether changing positions is a useful management approach for an abnormal CTG pattern occurring during labour, a randomised controlled trial would be ideal. Designing the trial in a way that would generate clinically useful findings would be challenging. Understanding the exact question is key. Is the goal to identify a particular position associated with the lowest rate of CTG abnormalities, or is it to examine whether changing from one position to another is effective? Researchers would need to consider the impact of epidural use as this limits the range of options for positions the woman might adopt (she is unlikely to be standing for instance), and to control for the use of oxytocin given the higher rate of CTG abnormalities associated with its use.

It would be pragmatic (but not very popular) to restrict women enrolled in the trial to labouring in one position, preferably the supine position as this would be most likely to promote CTG abnormalities. Once the CTG became abnormal (but not so abnormal as to require immediate steps to achieve birth), women would be randomly selected to remain in this position or to change to one, or perhaps a series of different, positions. You would need all women to use a form of CTG monitoring that itself does not limit mobility options. The impact of changing maternal position on the CTG pattern, perinatal outcome, and mode of birth would be examined. Blinding would be impossible as women and carers will know what positions have been used. To minimise the impact of this you could use retrospective reanalysis of the CTG pattern by people blinded to the positions used and the other outcome measures to determine whether the CTG improved or not. 

Recruiting to such a trial would likely be a challenge. I doubt that women would volunteer to have someone dictate the position they can adopt in labour and to change to another position only when the trial protocol dictated. It will come as no surprise that research like this has never been done. 

What do we know from research?

There are two clusters of research activity that offer insights into the impact of maternal positions on the fetus. Most of the data comes from research that sought to identify the ideal position for women to adopt during antenatal CTG monitoring in the third trimester. There are also two studies that have looked at the impact of maternal position in labour on fetal oxygen saturations using a fetal oximetry device.

The first thing that struck me as I read through the research was the attachment to a bed. The positions considered were dominated by those that require a bed: supine (not always defined but when it was this related to lying flat on the back with only one pillow), left or right lateral position (side lying with either the left or right side lowermost), semi-recumbent (typically described as lying on the back with the head of the bed titled up to an angle of thirty degrees), and semi-Fowler position (similar to semi-recumbent but with support under the knees so they were bent to a ninety degree angle). Only one study examined positions that could be achieved without the use of the bed (sitting and walking). Other positions women might adopt in labour (standing, squatting, on hands and knees, or positions that might be achieved while immersed in water) were not considered. 

Antenatal monitoring and maternal position

Findings were consistent across the research. Supine positioning was associated with higher baseline fetal heart rates, lower heart rate variability, fewer accelerations, and a longer time to meet criteria for the CTG to be considered reactive (Alus, et al., 2007; Ibrahim, et al., 2021; Nathan, et al., 2000; Samuel, et al., 2015; Tamás, et al., 2007). The one study examining positions off the bed found that variable decelerations were more common when women were in a reclined position (not defined) compared with women who were walking, and the duration required to achieve a reactive trace was shortest when women were sitting (Cito, et al., 2005). These findings imply that fetal oxygenation was better in non-supine positions but don’t identify one alternate position that was better than others. 

One particularly interesting study also examined antenatal CTG patterns (Stone, et al., 2016). Rather than seeking to identify the best position for performing antenatal CTG testing, this study set out to better understand the known association between supine sleep positions and stillbirth. 29 women in late pregnancy were monitored by abdominal fetal ECG and electrohysterography (the Monica AN24 CTG device). They were randomised to a different sequence of positions consisting of supine, semi-recumbent, left and right lateral. Both the CTG pattern and the fetal behavioural state were assessed in each position. Fetuses typically shift from active awake or active sleep patterns to quiet sleep when oxygen levels fall as this reduces oxygen demand. Quiet sleep was ten times more likely when women were supine rather than in left lateral or semi-recumbent positions. In quiet sleep, the fetal heart rate was reduced (but only by 6 bpm), as was fetal heart rate variability. The authors concluded that supine positioning acted as a fetal stressor, but this appeared to occur within the range of normal oxygenation. The shift to quiet sleep was a compensatory mechanism to adjust for this. 

Fetal oxygen levels in labour

Two papers have addressed the effect of women’s position during labour on fetal oxygen levels. In 1996, Carbonne and colleagues assessed 12 women in labour who were monitored with fetal oximetry. All had epidurals. Oxytocin use was not documented. All had normal fetal oxygenation and heart rate patterns initially. Women were randomised to a different order of position change, cycling through a combination of left and right lateral and supine positioning. Fetal oxygenation was lowest in supine positions but remained in the normal range. The exception was one woman who developed supine hypotension. As she moved from left lateral to supine, her blood pressure dropped from 120/77 to 65/39, and fetal oxygen saturation fell from 42 to 22%, with variable decelerations appearing. The CTG changes reversed with position change back to left lateral and oxygen saturation returned to the previous level. At least in this one example, we have documented evidence that when supine hypotension occurs in labour, it is associated with lower fetal oxygen saturation that improved when the woman’s position was changed.

Simpson and James (2005) studied fetal oxygen saturation in 51 women whose labour was induced and who were planning to use an epidural for analgesia. The CTG was normal. Following the administration of a fluid bolus (randomly chosen to be either 500 or 1000 mL), and approximately one hour after epidural analgesia was commenced, women were randomised to one of six position change sequences. Each position was used for 15 minutes. The positions were semi-recumbent, left lateral, and right lateral. Oxygen saturation was higher in either lateral position (right 47.7%, left 48.3%) than the semi-recumbent position (37.5%), with no significant difference between right and left lateral. Oxygen saturation levels were within the normal range in all positions. Fetal heart rate patterns, perinatal outcomes, or mode of birth were not examined in either this study or the previous one. 


These are the key points:

  • Lying flat during pregnancy and labour changes maternal and fetal circulation in a way that might lead to reduced oxygen levels in the fetus and should be avoided.
  • The belief that cord compression causes variable decelerations via a baroreceptor mediated pathway isn’t supported by research.
  • There’s no direct research evidence to support position changes as management tool for improving abnormal CTGs.

I have two recommendations. First, someone please do research to address the unanswered questions that surround maternal positions and fetal heart rate patterns. Second, if a woman is lying on her back and her CTG is abnormal, advise her to move from this position (and assist if required). But don’t spend ages pfaffing about with this position, and that one, and another, and let’s try that first one again, in response to an abnormal CTG, particularly if the woman wasn’t supine to start with. There is probably another cause for the change in the CTG that is contributing to the abnormal pattern and you need to move on and address that or to expedite birth.


Alus, M., Okumus, H., Mete, S., & Guclu, S. (2007). The effects of different maternal positions on non-stress test: an experimental study. Journal of Clinical Nursing, 16(3), 562-568.

Carbonne, B., Benachi, A., Leveque, M., Cabrol, D., & Papiernik, E. (1996). Maternal position during labor: effects on fetal oxygen saturation measured by pulse oximetry. Obstetrics & Gynecology, 88, 797– 800.

Cito, G., Luisi, S., Mezzesimi, A., Cavicchioli, C., Calonaci, G., & Petraglia, F. (2005). Maternal position during non-stress test and fetal heart rate patterns. Acta Obstetricia et Gynecologica Scandinavica84(4), 335–338.

Hon, E. (1958). The electronic evaluation of the fetal heart rate. American Journal of Obstetrics & Gynecology, 75(6), 1215-1230.

Ibrahim, H., Elgzar, W., & Saied, E. (2021). The effect of different positions during non-stress test on maternal hemodynamic parameters, satisfaction, and fetal cardiotocographic patterns. African Journal of Reproductive Health, 25(1), 81-89.

Lear, C., Galinsky, R., Wassink, G., Yamaguchi, K., Davidson, J., Westgate, J., Bennet, L., & Gunn, A. (2016). The myths and physiology surrounding intrapartum decelerations: the critical role of the peripheral chemoreflex. Journal of Physiology, 594(17), 4711-4725.

Lee, S., & Hon, E. (1963). Fetal hemodynamic response to umbilical cord compression. Obstetrics & Gynecology, 22(5), 553-562. 

Nathan, E., Haberman, S., Burgess, T., & Minkoff, H. (2000). The relationship of maternal position to the results of brief nonstress tests: a randomized clinical trial. American Journal of Obstetrics & Gynecology, 182(5), 1070-1072.

Samuel, R., Karkada, S., Fernandes, S., & Bhat, P. (2015). Materno foetal physiological parameters in sitting and left lateral position during non – stress test (NST) monitoring in pregnancy: A cross over study. Manipal Journal of Nursing & Health Sciences, 1(2), 83-86. 

Stone, P., Burgess, W., McIntyre, J., Gunn, A., Lear, C., Bennet, L., Mitchell, E., Thompson, J., & the Maternal Sleep in Pregnancy Group. (2016). Effect of maternal position of fetal behavioural state and heart rate variability in health late gestation pregnancy. Journal of Physiology, 595(4), 1213-1221.

Tamás, P., Szilágyi, A., Jeges, S., Vizer, M., Csermely, T., Ifi, Z., Bálint, A., & Szabó, I. (2007). Effects of maternal central hemodynamics on fetal heart rate patterns. Acta Obstetricia et Gynecologica Scandinavica, 86(6), 711-714.

Utsu, M. (2006). Ultrasonic assessment of abnormal umbilical cord and its circulation. Ultrasound Review of Obstetrics & Gynecology, 6(3-4), 150-156. 

Categories: antenatal CTG, Basics, CTG, EFM, Obstetrics, Stillbirth

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7 replies

  1. Pure gold, thank you very much. Do you know of any research about ‘faffing around trying to get a better trace’? I think women are ‘tethered to the bed’ far too often (in the UK) for this reason with detrimental effects on their labour and their fetus.

    Liked by 1 person

  2. You should be brave and remove all CTGs from delivery rooms as they are today. A poorly understood physiology that causes almost all problems. Too much use of Oxytocin, which is an evil, too much recurrence of inductions and as a consequence the completion of difficult deliveries with an unprecedented increase in caesarean sections, all in detriment of women themselves and the human species in general. It is incredible how the Obstetrics business introduced more than 70 years ago such artifices without the knowledge that they would have in the long term.
    By the way, the CTG’s neither get better nor worse, they just record and write.



  1. Stopping the oxytocin infusion when the CTG is abnormal – Birth Small Talk
  2. Going backwards with fetal monitoring guidelines – Birth Small Talk

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