Birth Small Talk

Talking about birth

Stopping the oxytocin infusion when the CTG is abnormal

Photo by Jose Aragones 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 the final post 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, the use of intravenous fluids here, and changing the woman’s position here

I have previously set out my expectations for the kind of evidence I have been looking for in this series. Recalling that the aim of intrapartum fetal monitoring is to prevent fetal damage from hypoxia, we should be looking for evidence 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 have set out the assumptions about how the therapy is proposed to work, and how that lines up with what we know about physiology. I then shared the existing research. 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 for an answer to the question – does intrauterine resuscitation (in this case turning off the oxytocin infusion) when the CTG is abnormal make things better for the fetus and the birthing woman?

Understanding the rationale

Oxytocin is a hormone released from the posterior pituitary. It has many important roles, including social and psychological effects. If you are keen to learn more about oxytocin, I recommend Kerstin Uvnäs Moberg’s comprehensive, well researched, and very readable books about oxytocin . For today’s post, I am focussing on the use of synthetic oxytocin (known as Syntocinon or Pitocin depending on where you are from) administered intravenously to either start labour (induction) or to speed up labour (augmentation). 

Identifying how often oxytocin use leads to CTG abnormalities is challenging. The answer depends on the reason why oxytocin is being used, the dose being used, and how you define CTG abnormalities. Looking at a selection of recent research, the incidence of excessive uterine contractions with abnormalities in the fetal heart rate pattern on CTG ranged from 9 to 21% when oxytocin was in use (Aboshama, et al., 2021; Bostanci, et al., 2020). It seems reasonable to assume that synthetic oxytocin administration is likely to be the cause of most abnormalities in the fetal heart rate pattern when it is in use. If this is the case, then turning off the oxytocin infusion or significantly reducing the rate could reasonably be expected to lead to the heart rate pattern returning to normal.

Exploring the physiology

Blood flow through the uterine arteries is reduced when the uterus contracts during labour (Li, Gudmundsson, & Olofsson, 2003). Each contraction also compresses the spiral arteries (the tiny ones that go from the uterine arteries to the placenta) as they pass through the muscular wall of the uterus. Blood flow to the placental bed is therefore reduced during contractions (Borell, et al., 1965). Oxygen saturation levels in the fetus rise at the start of the contraction, fall to their lowest level about 2 minutes after the start of the contraction, then return to the previous level (Paternoster, et al., 2001). (Or at least they did in the women with epidurals who participated in this research.) The researchers presumed that initial rise in oxygen saturation was due to a bolus of blood returning to the fetus in response to the contraction squeezing the placenta. When the rest period between contractions decreases, it is likely that fetal oxygen saturation levels don’t have time to return to normal before beginning to fall again. 

Each fetus has different, difficult to determine, dynamic, requirements for oxygen supply. These oxygen requirements depend on many factors such as fetal weight and body composition (muscle requires more oxygen at rest than fat does), fetal activity, and fetal body temperature. The level of oxygen one fetus manages to get by perfectly well with may not be adequate for another. This makes it difficult to predict how long any individual fetus needs to recover between contractions to ensure adequate oxygenation is maintained. There is evidence that physiological feedback mechanisms exist to protect the fetus by reducing contractions when fetal hypoxia develops (Wiberg-Itzel, 2021).

When oxytocin is administered intravenously during labour, the dose used is determined principally by the frequency and duration of contractions. For example, the Queensland Health protocol for oxytocin use advises that the dose should be titrated up until three to four contractions occur in a ten-minute period, with the contractions having a duration of 40–60 seconds and a resting period between contractions of not less than 60 seconds. Tachysystole (too many contractions) is typically defined as more than five contractions in a ten-minute period, and hypertonus as a resting period of less than 60 seconds, or contractions that last for more than 120 seconds. When either tachysystole or hypertonus occur along with abnormal fetal heart rate patterns in the CTG, this is called hyperstimulation. 

However, the fetus with high oxygen demand and a less-than-stellar placenta might experience a potentially damaging drop in oxygen levels with three 60-second-long contractions in a ten-minute period. Giving oxytocin prevents physiological feedback mechanisms from reducing the frequency, strength, and duration of contractions when oxygen levels begin to fall. We can’t know precisely what sort of contraction pattern any individual fetus can manage to maintain, so it seems reasonable to assume that any abnormal heart rate pattern in a fetus exposed to synthetic oxytocin, despite the contraction pattern being considered “normal”, is due to the oxytocin. 

Turning the oxytocin off makes physiological sense, both in terms of achieving a diagnosis (if the heart rate pattern improves, it was due to the oxytocin) and as a form of resuscitation (oxygenation returns to normal). Fortunately, the half-life of synthetic oxytocin is very short, having been measured at four minutes (Christensson, et al., 1989). As a rule of thumb, it takes five half-lives to clear a substance from the body. A reduction in contractions is likely within ten minutes and a return to “baseline” within 20 minutes. 

[As an aside – this is why I don’t support the argument that giving an intravenous fluid bolus is an effective way to manage hyperstimulation due to oxytocin use. It takes less time for the oxytocin concentration to fall when the oxytocin infusion is ceased, than it does to start the fluid bolus, deliver it, and wait for fluid redistribution to reduce the oxytocin concentration.]

What would good research look like?

Women whose labour is being induced or augmented would be asked to participate in a randomised controlled trial. It would be important to be able to analyse data from women being induced and those being augmented separately as there may be differences in outcomes. The use of oxytocin would be governed by a protocol. If CTG abnormalities developed, then randomisation would occur to either continuing oxytocin as per the protocol while continuing to monitor the CTG and acting on it appropriately, or stopping oxytocin for a defined period. Blinding might be achieved by having two infusions running, one containing oxytocin and the other saline, but labelled as infusion A and B so clinicians did not know which contained the active hormone. Randomisation would select which of the two infusions was ceased. The outcomes measured would include the CTG pattern, mode of birth, and standard perinatal outcomes.

No such research has ever been conducted. I suspect that it would be impossible to obtain ethics approval for such a randomised controlled trial, as the cessation of oxytocin when CTG abnormalities occur is considered an established and important safety mechanism. 

What do we know from research?

It was quite challenging to find research that helps to shine some light on whether turning oxytocin off when the fetal heart rate pattern is abnormal is a good idea or not. What I found was research confirming that too many contractions can impact fetal wellbeing. I couldn’t find anything that spoke about the impact of turning off, or down, and oxytocin infusion. 

Simpson and James (2008) examined the effect of oxytocin induced hyperstimulation of the uterus. They found that more frequent contractions preceded reductions in fetal oxygen saturation and were associated with abnormal FHR patterns. This research was conducted with 56 women who were given oxytocin for labour induction. Epidural use was not commented on in the paper. 

More recently, Reynolds and team (2020) have undertaken a systematic literature review, questioning the relationship between uterine activity and short- and long-term neonatal outcomes. The research analysed included trials where oxytocin was in use and some where it was not but did not make a distinction between outcomes between these two groups. Excessive uterine contractions were found to be associated with a higher rate of hypoxic-ischaemic encephalopathy but this was assessed in only one study of 726 women. Some studies, but not others, showed higher rates of acidosis in the umbilical artery at birth or soon after when tachysystole (more than five contractions every ten minutes) was present. Three studies looked at the relationship between contraction frequency and abnormal fetal heart rate patterns and all three found that abnormal patterns occurred more often when tachysystole occurred. 

There is evidence about other risks and benefits for labour augmentation and induction of labour where oxytocin use is common. Whether induction of labour can be argued as being evidence-based or not depends to a great extent on the reason for considering induction of labour and the gestational age at which it is planned. I won’t review all that evidence here (it is huge!) but would direct readers to the work of Dr Sara Wickham and Dr Rachel Reed who have both written extensively about this. 

Despite the frequent use of oxytocin for labour augmentation we don’t have particularly robust evidence to support its use. The Cochrane review by Bugg, Siddiqui, and Thornton (2013) used data from eight studies including 1338 women. Only women at low risk were included in the trials. Compared to waiting, immediate oxytocin use when labour progress was slow did not alter the rate of caesarean section, instrumental birth, or non-instrumental vaginal birth. There were no differences in outcomes for the neonate. Uterine hyperstimulation with abnormal fetal heart rate patterns was 2.5 times more common when oxytocin was used. The only benefit from oxytocin augmentation was a reduction in the duration of the first stage of labour, with a difference of 2.2 hours on average. This may or not be an important enough outcome to make it worth the risk to the fetus from low oxygen levels.


The key messages are:

  • Synthetic oxytocin administration for labour induction or augmentation has the potential to cause fetal hypoxia.
  • Abnormal fetal heart rate patterns are common when intravenous oxytocin is in use.
  • We can’t measure fetoplacental reserve accurately, so using contraction frequency and duration is not an effective means to prevent fetal hypoxia when intravenous oxytocin is in use.
  • There is not always robust evidence of benefit for the use of intravenous oxytocin for labour induction or augmentation, despite it being commonly used and even advised in guidelines.
  • While there is no direct research evidence to support stopping oxytocin when the fetal heart rate pattern becomes abnormal, it does make sound physiological sense and has no downsides.

As I finished writing this series, I was aware that there are some other approaches used for intrauterine resuscitation that I haven’t touched on (tocoloysis and amnioinfusion come to mind). I might come back and address these later. Are there other things you do when the CTG is abnormal that you would like to see me provide an evidence summary for?


Aboshama, R., Abdelhakim, A., Shareef, M., AlAmodi, A., Sunoqrot, M., Alborno, N. M., Gadelkarim, M., Abbas, A., & Bakry, M. (2021). High dose vs. low dose oxytocin for labor augmentation: a systematic review and meta-analysis of randomized controlled trials. Journal of Perinatal Medicine, 49(2), 178-190.

Borell, U., Fernström, I., Ohlson, L., & Wiqvist, N. (1965). Influence of uterine contractions on the uteroplacental blood flow at term. American Journal of Obstetrics & Gynecology, 93(1), 44-57.

Bostanci, E., Kilicci, C., Ozkaya, E., Abide Yayla, C., & Eroglu, M. (2020). Continuous oxytocin versus intermittent oxytocin for induction of labor: a randomized study. Journal of Maternal-Fetal & Neonatal Medicine, 33(4), 651-656.

Bugg, G., Siddiqui, F., & Thornton, J. (2013). Oxytocin versus no treatment or delayed treatment for slow progress in the first stage of spontaneous labour. Cochrane Database of Systematic Reviews, 6,CD007123. 10.1002/14651858.CD007123.pub3. 

Christensson, K., Nilsson, B., Stock, S., Matthiesen, A., & Uvnas-Moberg, K. (1989). Effect of nipple stimulation on uterine activity and on plasma levels of oxytocin in full term, healthy, pregnant women. Acta Obstetricia et Gynecologica Scandinavica, 68(3), 205-210.

Li, H., Gudmundsson, S., & Olofsson, P. (2003, Dec). Uterine artery blood flow velocity waveforms during uterine contractions. Ultrasound in Obstetrics & Gynecology, 22(6), 578-585.

Paternoster, D., Micaglio, M., Tambuscio, Bracciante, R., & Chiarenza, A. (2001). The effects of epidural analgesia and uterine contractions on fetal oxygen saturation during the first stage of labour. International Journal of Obstetric Anesthesia, 10(2), 103-107.

Reynolds, A. J., Geary, M. P., & Hayes, B. C. (2020, Sep 12). Intrapartum uterine activity and neonatal outcomes: a systematic review. BMC Pregnancy Childbirth, 20(1), 532.

Simpson, K., & James, D. (2008). Effects of oxytocin-induced uterine hyperstimulation during labor on fetal oxygen status and fetal heart rate patterns. American Journal of Obstetrics & Gynecology, 199(1), 34.e1 – e5.

Wiberg-Itzel, E. (2021). Amniotic fluid lactate (AFL): a new predictor of labor outcome in dystocic deliveries. Journal of Maternal-Fetal & Neonatal Medicinein press, 1-6.

Categories: Basics, CTG, EFM

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