(Originally posted in October 2020, this post has been revised and updated).
As a medical student in the 1980s I was taught that early decelerations (when the fetal heart rate slows slightly during a contraction and returns to where it started as the contraction ends) in the fetal heart rate are due to head compression, and are a reassuring sign of normal fetal oxygen levels. I have been told this many, many times since. As I started doing background work in the lead up to my PhD, I began to recognise that this sounded more like received wisdom (eat your crusts, they’ll make you hair curly) than scientific evidence (in this particular population, under these specific circumstances, researchers A & B showed that in 79% of the population….). I wanted to get under the surface of the story that “head compression causes early decelerations” and find out when and where the story started, who started it, and whether it is really backed up by evidence.
How the story begins
Tracking down the early deceleration story proved to be fascinating and it reveals a lot about how obstetric knowledge is constructed. The beginning of the story takes place in the late 1950s, in Connecticut in the USA, with obstetrician Edward Hon. (2025 Kirsten adding an editing comment – actually, I have found references about this that go back to the mid 1800’s, so Hon was really just saying what others had been saying for a long time. But for the first timeHon was presenting early decelerations as a research finding rather than an opinion.) Hon was later to go on and become a director of a company called Corometrics, who manufactured CTG monitors for clinical use. In 1958 we find him writing a paper which he offered as a preliminary report about the electronic evaluation of fetal heart rate patterns during labour (Hon, 1958). This paper predated the creation of the CTG machine but was an important step in making them possible.
Hon made electronic recordings of the fetal heart rate using an external ECG monitor that recorded both maternal and fetal ECG patterns, and then subtracted the maternal ECG so the fetal ECG could be recorded. Contractions were recorded manually, presumably by a labour and delivery nurse. His study included 80 women in “normal” labour (his use of quote marks – not mine) without explaining what this meant. No information was provided in the paper about these women, their pregnancy or labour, or medical interventions that might have been used. It is important to bear in mind that the use of heavy sedation (scopolamine and morphine being a common combination) during labour was not uncommon at this point in time.
Hon wrote:
The drop in fetal heart rate noted with contractions was related to the degree of cervical dilatation present. In normal labour this was not noted before 4 cm or after 8 cm of dilatation. Initially this was puzzling…. The possibility that fetal bradycardia might be related to increased intracranial pressure rather than momentary anoxia following compression of the placenta was then explored. …
In an attempt to determine experimentally the effect of increased intracranial pressure, patients who had exhibited no drop in fetal heart rate with contractions were taken to the delivery room after 8 cm of dilatation. Between contractions pressure was applied to the fetal skull with the examining hand and minimal drops in the fetal heart rate noted. Similar results were obtained when a 3 cm ring pessary was placed on the fetal skull and pressure applied. However, when a 6 cm pessary was applied and pressure exerted a marked bradycardia similar to that noted with uterine contractions in other labours was obtained consistently.
p 1219 – 1222
No indication was given about the number of women to which this technique was used. Two illustrative graphs accompany this text (again no clinical information is provided), so we know that at least two women contributed to generating this data. Whether they were the only two can’t be determined from the description provided.
On the basis of this experimentation, Hon went on to say:
from the available data it seems reasonable attribute the “physiologic” drop in fetal heart rate at the height of a contraction to an increase in intracranial pressure. The final mechanism by which this is accomplished is not known, but it may be relation to variation in blood flow to the brain stem as a result of altered intracranial dynamics.
p. 1223
It is clear that he is tossing about ideas here – not proving the thing beyond a shadow of a doubt. But that’s not the way this research, and similar research produced by others over the next decade or so was later put to use by obstetricians. The idea that “early decelerations are due to head compression” settled as an indisputable fact fairly quickly.
Was this ethical?
Let’s stop for a moment and consider this research from the women’s perspective. There is no indication in the paper that their consent was sought to participate in this experiment. It is possible that they were deeply sedated and completely unaware of what was being done. A clinician, possibly Hon, inserted first their hand, then a series of different sized objects into their vagina, and pushed upwards over an extended period of time in order to deliberately place pressure on the fetal skull to see what would happen. This is definitely the sort of thing that women should be asked permission for before it happens!
Obstetric knowledge has often been built on experiments conducted on women without their consent. This misogynist attitude gets baked into the very technology used every day in maternity care settings around the world, and it continues to play a role in how women are treated.
Does the idea hold up to scrutiny?
Skipping forward almost sixty years, let’s meet Christopher Lear, a physiologist who has been working on understanding the fetal response to hypoxia. His work has been experimental in nature, using pregnant sheep and their fetuses, permitting experiments that are simply not possible for human fetuses. In 2016, Lear and his co-authors reviewed the physiology literature and summarised:
Direct fetal head compression inconsistently causes decelerations and so is very unlikely to be a major contributor to intrapartum decelerations during the majority of labours. … If decelerations due to head compression do occur, for example during obstructed labour when the fetal head is engaged in the birth canal, these data suggest that such decelerations reflect severe cerebral hypoperfusion and hypoxia and in contrast with current proposed interpretation (the NICE and FIGO guidelines), should not be considered benign.
p. 4713 – 4714
Lear’s subsequent physiological research has confirmed that all decelerations, regardless of their shape or timing in relation to contractions, are related to lower oxygen levels in the fetus, and represent efforts to actively compensate for the reduction in oxygen in order to prevent tissue damage (Lear et al., 2018). In other words – they are a sign that a fetal coping mechanism has kicked in.
Do current fetal monitoring guidelines accurately describe the evidence on fetal physiology?
Lear’s findings are a significant departure from the simple mantra of “early decelerations are due to head compression and are a reassuring sign of normal fetal oxygenation”. While the message “all decelerations are a sign of fetal compensation to low oxygen levels” is more soundly based in physiology, this evidence has not consistently been taken up by obstetric professional organisations who write guidelines.
Here in Australia, RANZCOG list early decelerations as a sign that is “unlikely to be associate with fetal compromise” (RANZCOG, 2019, p 16). The NICE (2022) guideline puts early decelerations in the “white” or normal category. The Irish fetal monitoring guideline (HSE, 2019, p 17) states that early decelerations are “are believed to be caused by fetal head compression and do not indicate fetal hypoxaemia/acidaemia”. None of these line up with the current understandings of fetal physiology.
As increasing evidence that CTG monitoring doesn’t work the way people think it should has accumulated, the common response has been to argue that people interpreting CTGs didn’t do it correctly. If (and this is far from being a given) CTG monitoring has the potential to actually detect low oxygen levels so that maternity professionals can intervene, then the best hope of achieving this is to acknowledge that our understanding of fetal physiology is deeply flawed and we need a new evidence base. This evidence base should be built on sound research, rather than guesses. And it should never be derived from unconsented experimentation on a handful of women’s bodies.
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References
Health Service Executive National Women and Infants Programme. (2019). National Clinical Guideline for Intrapartum Fetal Heart Rate Monitoring.
Hon, E. H. (1958,). The electronic evaluation of the fetal heart rate. American Journal of Obstetrics and Gynecology, 75(6), 1215-1230.
Lear, C. A., Galinsky, R., Wassink, G., Yamaguchi, K., Davidson, J. O., Westgate, J., Bennet, L., & Gunn, A. J. (2016). The myths and physiology surrounding intrapartum decelerations: the critical role of the peripheral chemoreflex. The Journal of Physiology, 594(17), 4711-4725. https://doi.org/10.1113/JP271205
Lear, C. A., Wassink, G., Westgate, J., Nijhuis, J. G., Ugwumadu, A., Galinsky, R., Bennet, L., & Gunn, A. J. (2018). The peripheral chemoreflex: indefatigable guardian of fetal physiological adaptation to labour. The Journal of Physiology, 596(23), 5611-5623. https://doi.org/10.1113/JP274937
National Institute for Health and Care Excellence. (2022). Fetal monitoring in labour. www.nice.org.uk/guidance/ng229
Royal Australian and New Zealand College of Obstetricians and Gynaecologists. (2019). Intrapartum fetal surveillance clinical guideline. https://ranzcog.edu.au/statements-guidelines
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Tags: Early decelerations, Head compression, Hon, Lear, Physiology
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