Birth Small Talk

Talking about birth

What’s the deal with early decelerations and head compression?

I have been watching the work of Christopher Lear and his team at the Fetal Physiology and Neuroscience Group in New Zealand for several years. Collectively, they have been working to advance our understandings of the mechanisms behind the changes we see in the fetal heart rate during labour. This work is fundamental. There is no possible way that we can ever get fetal heart rate monitoring (of any type) to prevent fetal damage effectively and safely if we don’t know how the heart rate is controlled and how it changes in response to low oxygen levels. Their research has been highlighting that some of the assumptions that are built into professional guidelines don’t reflect what happens, physiologically speaking. Their most recent paper (Lear et al., 2021) summarises what they and other researchers know about fetal head compression during labour and early decelerations. Most of what is in this post is drawn from their paper.

Does the fetal head get compressed during labour and is this a problem?

Historically speaking, it has been assumed that the fetal brain is at risk of damage as it passes through the birth canal. In 1918, Pomeroy (quoted in Arney, 1982, p 72) described the fetal head as a “battering ram” that must “shatter a resisting outlet”. There is evidence that there is a small increase in pressure inside the fetal head during contractions. The presence of suture lines and fontanelles allows for the process known as moulding to occur. This redistributes pressure and reduces the possibility that levels high enough to do harm might occur during a normal labour.

Does head compression cause changes in the fetal heart rate and if so, how?

Physiology research in fetal sheep, fetal goats, and newborn rabbits have shown no consistent evidence of a fall in heart rate when intracranial pressure is deliberately increased. Compression of the fetal head produces a rise in intracranial pressure, reducing blood flow to the brain and activating both mechanical and chemical receptors. These receptors trigger activation of the sympathetic nervous system with a consequent increase in heart rate and blood pressure, ensuring that blood flow to the brain is preserved during periods of increased pressure. It is only at extremely high (life threatening) levels of intracranial pressure that the parasympathetic nervous system is activated via the Cushing response, with a fall in heart rate. The expected fetal heart rate pattern that would be seen in response to fetal head compression is tachycardia rather than a deceleration. 

Reviewing the human data

Lear and colleagues have done an amazing job of pulling together all the case reports and studies that report on the effect of pressure on the fetal head on heart rate patterns. Some of this I was previously aware of (and have written about) but much of it was new to me. These studies applied pressure via the vagina; either digitally, with a pessary, or by applying forceps and deliberately compressing the skull (not a part of the usual application process when performing forceps assisted birth I might add, and not at all like the forces that apply during normal birth); or by pressing on the woman’s abdomen. In most studies the degree of pressure applied was not measured. The best conducted of the trials (Chung and Hon, way back in 1959) was conducted with only six fetuses, where 18 of 19 episodes of compression with a pessary resulted in brief decelerations of under 10 seconds duration. The human data doesn’t present compelling evidence that pressure on the fetal head that occurs during uterine contractions produces the pattern we recognise now as an early deceleration (most definitions requiring a duration of at last 15 seconds with slow onset and recovery). 

If early decelerations are not due to head compression, what causes them?

As Lear and colleagues point out, it is impossible to separate the occurrence of physiological compression of the fetal head during labour from uterine contractions that also impact blood flow through the placenta simultaneously. The fetus has several mechanisms for tolerating lower levels of oxygen during a contraction. Increased parasympathetic tone, reducing the need for oxygen while also reducing the heart rate temporarily, is one such mechanism. It is far more plausible that the shallow, repetitive, short-lived decelerations coinciding with contractions that we label as early decelerations are signs of adequate fetal compensation to a small reduction in fetal oxygen supply (Lear et al., 2018). 

Rethinking CTG interpretation guidelines in the face of new physiological evidence

Lear and colleagues point out: 

There is a long-standing belief that late first stage and second stage decelerations are benign when they occur simultaneously with a contraction, on the presumption that they are mediated by pressure on the head. In part, this reflects a mistaken application of Hon’s term ‘early deceleration’ (shallow mild decelerations that mirror contraction shape) to mean any deceleraction of any shape or size which occurs within the time-frame of a contraction. As a result, large variable decelerations are sometimes ignored, with disastrous outcomes.

Lear et al., 2021

Professional guidelines that continue to state that early decelerations are due to head compression and are benign, generate the potential that fetal hypoxia will go unnoticed. It is important that all fetal monitoring guidelines used in clinical practice reflect the evidence-base about the physiology responsible for changes in fetal heart rate patterns. Continuing to educate maternity clinicians that “early decelerations are due to head compression” is no longer acceptable.


Arney, W. R. (1982). Power and the profession of obstetrics. University of Chicago Press. 

Lear, C. A., Westgate, J. A., Bennet, L., Ugwumadu, A., Stone, P. R., Tournier, A., & Gunn, A. J. (2021). Fetal defenses against intrapartum head compression – implications for intrapartum decelerations and hypoxic-ischemic injury. American Journal of Obstetrics and Gynecology, in press

Lear, C. A., Westgate, J., Ugwumadu, A., Nijhuis, J. G., Stone, P. R., Georgieva, A., Ikeda, T., Wassink, G., Bennet, L., & Gunn, A. J. (2018, Dec). Understanding fetal heart rate patterns that may predict antenatal and intrapartum neural injury. Seminars in Pediatric Neurology, 28, 3-16.

Categories: CTG, EFM, New research

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12 replies

  1. Fascinating blog post Kirsten, thank you for the thought provoking exploration of the science examining fetal heart rate patterns and what they mean.


  2. Very interesting read as always, thank you.
    I found this point particularly interesting-
    …The expected fetal heart rate pattern that would be seen in response to fetal head compression is tachycardia rather than a deceleration.

    So if I’m thinking along the right line, baseline tachycardia in late first stage and second stage could reflect a physiological fetal response to head compression as opposed the often heard interpretation “rising baseline” which is often followed by “this is a sign your baby is getting tired and we should help” ie instrumental assisted birth.


  3. Kirsten, how should this change our practice?


    • Guidelines and education needs to change to fulfil its promise to be evidence based and grounded in physiology. If you individually change your practice, you will risk professional censure for going against guidelines. In the meantime, don’t assume that all early decelerations are benign. Watch how to trace evolves over the next hour to see if there are other indicators of hypoxia or whether the pattern resolves. As always, look for and address reversible causes (oxytocin use being the main culprit).


  4. So interesting and thought provoking Kirsten, thanks for always keeping us in the present and questioning practice in light of new evidence.


  5. Did my RANZCOG FSEP today. They no longer teach early decel= head compression. Simply uterine activity reducing blood flow.



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