Fetal physiology is an evolving area of study. You might not get a sense of that when you go to a CTG study day, as what is taught as the physiological control of the fetal heart rate in labour is typically presented as though the facts were written on stone and handed down from a sage on a mountain top! If changes in fetal heart rate patterns are taught to mean one thing, but actually mean something else, then applying this knowledge in clinical practice won’t improve outcomes – regardless of the method being used.
I aim to keep up with the latest in fetal physiology, and my go-to source of information is the work of Christopher Lear and his team from the Fetal Physiology and Neuroscience Group in Auckland, New Zealand. Lear is an ACTUAL physiologist, now a junior doctor, so I value his insights. His team include obstetricians and paediatricians, so they don’t lose sight of the clinical relevance and importance of their research.
What produces decelerations?
There are two main mechanisms that produce decelerations (slowing of the heart rate) in response to hypoxia (low oxygen levels):
- The peripheral chemoreceptor reflex – sensors in the carotid arteries (in the neck) and the aorta (the main vessel leading out of the heart) detect falling oxygen levels. They transmit messages back to the brain. The brain responds by increasing parasympathetic activity via the vagus nerve, reducing heart rate. This reduces the oxygen requirement of the heart and protects it from cellular damage. The sympathetic nervous system is also activated, causing blood flow to be redirected to the central part of the body. This maintains blood pressure and oxygen supply to vital organs such as the heart, brain, and kidneys. The effect of activation of the chemoreceptor reflex is compensation – it helps the fetus to stay healthy when oxygen levels fall.
- Myocardial hypoxia – when compensatory mechanisms of the peripheral chemoreceptor reflex fail, oxygen levels in the heart fail to the point where heart cells are no longer able to work effectively. Heart rate falls, and so does blood pressure. With ongoing time and increased severity of oxygen deficit, permanent damage occurs and eventually leads to death.
Clearly, one of these things is a good thing and the other a bad thing to happen. The degree to which each mechanism is in action and how that changes over time with ongoing hypoxia has never been studied. Better understanding each mechanism so we might be able to tell when myocardial hypoxia, and not just the peripheral chemoreceptor reflex, is in action would be handy.
What have Lear and his team been up to this time?
Lear and his team have recently published (April 2023) research looking at the physiological response to labour-like reductions in oxygen supply in fetal sheep. They took a group of 19 pregnant sheep, close to term. Some were randomly assigned to vagotomy (a surgical procedure to damage the vagus nerve and thereby block the reflex parasympathetic response when the peripheral chemoreceptor sensors are activated). Others did not have this procedure and therefore had an intact reflex.
Catheters were placed in the arterial and venous system of the fetal sheep and ECG sensors on their chest, so oxygen levels, heart rate, and blood pressure could be measured. EEG monitoring of brain activity was also performed. An inflatable compression device was placed around the umbilical cord, so it could be intermittently occluded and then released, to mimic the reduction in placental blood flow that occurs during labour contractions, resulting in a fall in oxygen levels. The cord was occluded for 60 seconds, released for 90 seconds, then occluded again, relating this cycle over a four hour period, or until significant falls in blood pressure were induced during cord occlusion.
What did they find?
The heart rate dropped quickly with the onset of cord occlusion and recovered promptly when it was released, and decelerations became deeper over time, in both groups of fetal sheep. Over time, it took longer after occlusion for the heart rate to reach its lowest point. Fetal heart rates were higher during occlusion, and between them, in the vagotomy group.
Blood pressure rose initially in both groups of sheep, then settled into a pattern where at the onset of cord conclusion blood pressure rose, then fell, and rapidly returned to baseline once cord flow was re-established. Over time, the point of the lowest blood pressure in this cycle dropped. EEG changes showed reduced brain activity during cord occlusion, with the suppression of EEG activity progressively falling over the time of the study. This was the same in both groups of animals.
Fetuses who had the vagotomy procedure dropped their pH and increased their lactate levels faster than those who did not.
What does all this mean?
The peripheral chemoreceptor reflex appears to be the dominant mechanism in initiating and maintaining decelerations during labour-like hypoxia. Even when blood pressure fell progressively in the later parts of the study, the reflex remained intact – heart rates fell faster in sheep who had an intact vagus nerve. Myocardial hypoxia increasingly contributed to the shape of the second half of the deceleration – the lowest point reached and the timing of when this happened in relation to contractions. Deeper decelerations that reach the bottom later are therefore likely to indicate that myocardial hypoxia is present. This is consistent with accepted clinical wisdom that late decelerations are more predictive of fetal harm.
What differs from accepted clinical wisdom, is what is referred to as baseline tachycardia and is also considered a marker of fetal hypoxia. In Lear and colleagues study, heart rate rises in the periods between cord occlusions were lower and fell over time in the fetuses who had the vagotomy procedure. As myocardial (and overall) hypoxia increased, the baseline heart rate fell, rather than rose.
One of the key messages from the paper was this:
These data support the concept that intrapartum decelerations do indeed represent a physiological adaptation to reduce myocardial work, conserving limited oxygen and substrate supplies, particularly myocardial glycogen reserves, and thus helping to protect the fetus from cardiovascular compromise and hypoxia–ischaemia.
p. 18
When clinicians refer to particular patterns in the fetal heart rate as “fetal distress” they largely miss the point. Rather than reflecting impending or evolving harm, what is being seen is evidence of coping. “Fetal coping” doesn’t have the emotional pull as “fetal distress” – imagine booking an emergency caesarean section for “fetal coping”!
The changed heart rate patterns seen clinically during human labour represent only a tiny proportion of the many physiological protective responses happening with other bodily functions. As Lear and colleagues point out, the EEG changes they observed reflected a shift to a less metabolically demanding state, reducing oxygen demand and protecting the brain. Other physiological events happening in response to hypoxic challenge also remain invisible when the only channel of data available is the heart rate, such as increased peripheral vascular resistance and myocardial contractility.
While the study showed that over time there was a switch to myocardial hypoxia becoming the thing that controlled heart rate, it does not offer us any clues about how to tell when that switch occurs. We need measures other than heart rate to be able to tell when that occurs. Developing a biomarker that can reliably detect this transition could provide the missing link for intrapartum fetal monitoring and help us achieve what CTG monitoring has not.
This study also reinforces previous research from this group showing that the baroreceptor reflex plays no meaningful role in the control of heart rate. So that graph that appears often in teaching materials, illustrating first a rise, then a fall in heart rate, then a rise over the course of a contraction, due to cord compression of first the vein and then the artery – has no basis in actual physiology. The figure in the abstract of the paper (free to access) provides an excellent summary of what actually happens physiologically.
Reference
Lear, C. A., Beacom, M. J., Dhillon, S. K., Lear, B. A., Mills, O. J., Gunning, M. I., Westgate, J. A., Bennet, L., & Gunn, A. J. (2023, Apr 5). Dissecting the contributions of the peripheral chemoreflex and myocardial hypoxia to fetal heart rate decelerations in near-term fetal sheep. Journal of Physiology, in press. https://doi.org/10.1113/JP284286
- Brain changes and accelerations
- The relationship between maternal anaemia and fetal heart rate patterns
Categories: CTG, EFM, New research
Tags: Baroreceptor reflex, Chemoreceptor reflex, Decelerations, fetal sheep, Physiology
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Bravo! Very clear.
C
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Very intrestin reading. I am sorry for those sheeps though 😦
From what I see there may be a typo/missing word in one place:
“In Lear and colleagues study, heart rate rises in the periods between cord occlusions were lower and fell over time in the fetuses who the vagotomy procedure.”
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Thank you – I’ve fixed it!
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