Get in Touch -

Maternity Clinical Network Contact Details

Sharon Head of Maternity [email protected]

Fetal Physiology
Verne Clinical Network
0113 8255344
07900 607507
in relation to
Lindsey
Ryan
Senior Quality
Improvement
[email protected] Electronic Fetal
Manager 07714 773332
Monitoring (EFM)
Jenny Senior Quality [email protected]
Brown Improvement
Manager 0113 8253545
07702 412335

Lana-Lee Quality [email protected]

Jackson Improvement
Manager 07769 361331

Sarah Administrator [email protected]

Pinchbeck
0113 8249294

Produced by the East Midlands Maternity Clinical Network & Senate

Last Updated: February 2019

36
Guidance vs Physiology References
 Z Alfirevic, D Devane, GML Gyte (2013) Continuous cardiotocography as a
form of electronic fetal monitoring for fetal assessment during labour.
Guidance is readily available (NICE, FIGO, Local) Cochraine Database of Systematic Reviews 2013;5:CD006066
correlating different FHR patterns to the percentage likely to  D Gibb and S Arulkumaran (2017) Fetal Monitoring in Practice. 4th Edition.
Elsevier
be acidotic.
 E Chandrahan, S Evans, D Krueger, S Pereira, S Skivens, A Zaima -
Physiological CTG Interpretation (2018) Intrapartum Fetal Monitoring
The problem is two fold – fetuses do not conveniently Guideline. https://physiological-ctg.com/guideline/guideline.html
provide a trace that easily falls into one category and these
guidance tables are generic, not bespoke to the individual  National Institute for Clinical Excellence (2017) CG190 Intrapartum Care
for healthy women and babies. Clinical Guidelines. London: NICE
fetal reserve. https://www.nice.org.uk/guidance/cg190

In addition to this is the complexity of time continuum,  International Federation of Obstetrics and Gynaecology. FIGO Consensus
human interpretation and interaction. Guidelines on Intrapartum Fetal Monitoring. International Journal of
Gynaecology and Obstetrics October 2015, Volume 131, Issue 1, 13-24
https://www.figo.org/news/available-view-figo-intrapartum-fetal-monitoring-
guidelines-0015088

 International Federation of Obstetrics and Gynaecology. FIGO Consensus

Guidelines on Intrapartum Fetal Monitoring: Intermittent Ausculta-
tion. International Journal of Gynaecology and Obstetrics October 2015,
Volume 131, 9-12

 Royal College of Obstetrics and Gynaecologists, Each Baby Counts

https://www.rcog.org.uk/eachbabycounts

 NHS England (2016) Saving Babies’ Lives – a care bundle for reducing
stillbirth. https://www.england.nhs.uk/wp-content/uploads/2016/03/saving-
babies-lives-car-bundl.pdf

 JT Parer (1982) In defense of FHR monitoring's specificity . Consultant

Obstetric Gynaecology 1982;19:228-34

 E Chandrahan (Editor) (2017) Handbook of CTG Interpretation – From

Patterns to Physiology. Cambridge University Press
 Norfolk and Norwich University Hospitals (2016) Clinical Guideline for the
Use of Intrapartum Fetal Monitoring and Fetal Blood Sampling

2 35
Summary

 Changes in CTG cause anxiety and require close

observation and interpretation within the clinical
context unique to that fetus and mother
 Labour is a stressful event for the fetus and most
mount a successful compensatory mechanism to
mechanical or hypoxic stress without sustaining any
lasting HIE (Hypoxic Ischemic Encephalopathy)
 Timely interventions and judicious use of oxytocin to
ensure the uterine environment is optimal for fetal
oxygenation
 When properly interpreted (physiology), assessment of
the FHR changes in most case proves of equal value
to pH measurement (FBS) in predicting fetal outcome
(Parer 1982)
 Accelerations are the hallmark of fetal health
 Baseline variability is a good indicator of fetal well
being
 Fetal acidosis is more common where there is a loss of
baseline variability with tachycardia or late
decelerations

Ask Yourself

 Does this fetus have good reserve?

 Is the fetus compensating to intra-uterine stress?
 Is there evidence of decompensating?

Remember – each baby is different, each cord is different,

each contraction is different – so read the physiology

34 3
The Fetal Reserve Recognising and Managing Sub-Acute Hypoxia

 Defined as when the FHR is spending <30 seconds on a

 Early placentation (first 4 weeks since implantation) stable baseline and >90 seconds in deceleration
utero-placental sinuses are developed for subsequent
supply of nutrients and oxygen to the fetus and  Hence more time protecting its myocardium then at the
removal of waste products baseline exchanges gases and protects its brain

 If placental reserve is low (smaller sinuses) the fetus Common causes of subacute hypoxia –
may have restricted growth antenatally. This is seen in hyperstimulation with oxytocin and second stage
hypertension and pre-eclampsia

 In labour , as the myometrial fibres contract, this low

fetal reserve is likely to develop hypoxia more rapid
than a fetus with a larger reserve

 In diabetic pregnancies there are fewer placental

pools for gaseous exchange – hence more rapid fetal
hypoxia

Hyperstimulation

4 33
  The fetus lives in a relatively hypoxic environment
(arterial oxygen sats at the start of labour are 70%)

 This can drop to 30% with uterine activity

 The placenta is the respiratory organ for the fetus

 Unlike adults, a fetus has 18-22g of fetal haemoglobin

(HbF) which help increase the oxygen carrying
Understanding Decelerations as a sign of Hypoxia

capability of fetal blood

 HbF binds with oxygen molecules at higher partial

pressures and releases oxygen at very lox tensions-
allowing the fetus to maintain adequate oxygenation of
its organs

 In metabolic acidosis the increased HbF also acts as a

buffering system to help avoid fetal neurological
damage

 The fetal circulatory system consists of the ductus

venosus and foramen ovale – both preferentially shunt
oxygenated blood from the umbilical vein to the heart
and brain (the most vital organs)

 The ductus arteriosus diverts blood from the pulmonary

artery to the descending aorta – bypassing the
non-functioning lungs

 Through this arrangement of its vascular system, the

fetus is able to supply its central organs with relatively
well-oxygenated blood as compared to its peripheries

 The fetal heart has to beat faster to rapidly distribute

blood to its organs (110-160bpm)

32 5
Fetal Response to Hypoxia

 In response to hypoxic stress, the fetus attempts to

protect its heart (myocardium) above everything else

 A fetus cannot rapidly increase its oxygen levels

through increasing its respiratory rate like we do as
adults

 It can decrease the myocardium workload by a reflex

slowing of the FHR. This is a deceleration
Concerning Chemical Induced Decelerations
 If this reflex response is insufficient at oxygenating the Suggest Compensation
vital organs, the fetus also conserves non-essential
activity by stopping movements Loss of the features that reassure us
 Loss of shouldering
This is seen as a loss of accelerations on the CTG  Drop below 60 bpm
 Delayed return to baseline
 If the hypoxia continues, stress hormones  Overshoot present
(catecholamines) are released (adrenaline and  Not ‘V’ shaped – may be ‘U’ shaped or ‘W’ shaped
noradrenaline) which increases the heart rate to  If these decelerations continue, there may be a
increase oxygenation. This requires energy – glycogen component of acidosis within time delivery
is broken down to glucose which also maintains
positive energy balance in the heart (further protection)

6 31
What are “variable” Decelerations? Glycogenolysis
 ALL decelerations are technically variable!
 The release of adrenaline stimulate glycogenolysis
Because they vary in shape, length, size and timing to
contractions. Most commonly seen in labour
 When fetal oxygen supply is no longer sufficient to
maintain energy requirements, glucose is released
 Caused by cord compression – baroreceptor
from glycogen stores and metabolised anaerobically
mechanism
(without oxygen)
 Features that reassure us – shouldering, sharp fall
 During anaerobic metabolism, stores of glycogen in the
<60bpm, quick rise, second shouldering and final
heart, muscle and liver are broken down to provide
recovery to baseline. They are V-shaped
energy

 Lactate is the by-product of anaerobic metabolism,

which eventually causes the pH of the fetal blood to fall
further (metabolic acidosis)

“Late” Decelerations

 Occurs late in relation to contraction

 Related to fetal hypoxemia, hypercarbia and fetal

acidosis – which stimulate chemoreceptors

Any change in the baseline FHR (rise) and/or

variability, with preceding late decelerations
requires immediate delivery

30 7
Gas Exchange at the Placenta 8. Baroreceptors to protect the Myocardium

 Gas exchange is impaired during contractions (blood

flow into the intervillous space is interrupted) causing
retention of CO2 and lowering the pH of the fetal blood
 The frequency, duration and strength of uterine
contractions must be considered when interpreting the
CTG
 This should be resolved when placental perfusion is
restored in between contractions, provided there is:
 Sufficient time between contractions
 A healthy placenta
9. These are still baroreceptors – why?
 The cord isn't occluded
 The mother isn't hypotensive
 The onset of active second stage decreases maternal
oxygenation even further.
 Aim for a 90 second inter-contraction period (3-4 con-
tractions in 10 min)

Uterine hyper-contractility is the most frequent cause of

a pathological CTG

Think!
What can you do to improve the fetus uterine environment?

8 29
Remember... A Compensated Response
 Baseline and variability are the most important
features on a CTG – they are indicative of hypoxia  Following these physiological changes
 Remember a fetus will protect its heart muscle as a (reflex response, stopping un-necessary movements
priority…….the other organs and the brain will suffer and releasing stress hormones) , the fetus is showing
the hypoxia first compensation:
 It is during relaxation of the heart muscle (not
contraction ) that the muscle gets its own supply of
oxygen and nutrients - that’s why the rising baseline is Seen as a stable baseline, reassuring varia-
so significant
 Also interpret the CTG in the full clinical context and
bility, albeit with continuing decelerations (non-
understanding of the fetal reserve reassuring) and a rise in baseline

 Recognition and subsequent changes to the uterine

Decelerations environment at this crucial time can reverse this
hypoxia. Remember that chemoreceptor-mediated
 Transient decrease in FHR >15bpm lasting longer than decelerations (the non-reassuring ones) take longer to
15 seconds recover as fresh oxygenated blood from the mother is
 We need to rethink decelerations not as “fetal required to wash out the stress hormones – hence why
compromise / distress” but as fetal response to ongoing they are slower to recover to the baseline
stress
 Reflex response of the fetus to the on-going hypoxia or
mechanical stresses – the team must decide!  Continuing hypoxia causes decompensation in the
central nervous system (inadequate oxygen reaching
Baroreceptor Decelerations – occur secondary to an the fetal brain):
increase in fetal systemic blood pressure (occlusion of
umbilical arteries during compression of the cord)
 Rapid fall then rapid recovery to baseline Seen as a loss of baseline, variability and
ultimately myocardial hypoxia – unstable baseline
Chemoreceptor Decelerations –occur secondary to build and progressive reduction in FHR (bradycardia)
up of carbon dioxide and metabolic acids during hypoxia
(caused by utero-placental insufficiency, repeated and
sustained contractions or prolonged cord compression

28 9
Recognition and Management of Recognising and Managing Sinusoidal Patterns

Evolving Hypoxia
6. Sinusoidal (Saw-tooth)

 Fetal physiology is so very different to that of an Adult In the antenatal CTG – an abnormal pattern distinguishable
from variability as the fluctuations from baseline are regular in
 If you can’t increase your supply -you decrease amplitude and in frequency
your demand!

EFM is the art of reading the physiology within

the clinical context to observe for signs of
hypoxia, whilst improving the uterine
environment to allow for adequate oxygenation
of the vital organs

7. “Pseudo” Sinusoidal CTG

Note normal variability and accelerations prior and after.
Does not normally exceed 30 minutes.

Taken from Hypoxia Classification Table – Physiological CTG.com

10 27
4. Saltatory Variability Observe, Classify, Predict & Act

We must observe and classify the physiology, predict how

it might get worse and act

5. Cycling

26 11
Lactate and FBS 1. Accelerations

 Peripheral testing should not be used in isolation but as

an adjunct to the CTG and clinical picture
 FBS estimates the capillary blood pH from
peripheral scalp surface, hence might not truly reflect
the acid-base status of the fetus
 There is no evidence that FBS reduces caesarean
section rates or improves long-term neurological
outcomes for neonates (Alfirevic et al 2013)
 NICE acknowledge that FBS increases LSCS rates and
instrumental vaginal deliveries
 FBS can in fact cause delay in delivery of the fetus 2. Normal Variability
that warrants it the most
 FBS does not distinguish between respiratory and
metabolic acidemia
 It is metabolic acidosis that is damaging to the fetal
tissues , where as respiratory acidosis is transitory (not
permanent) , and not uncommon in low-risk labours
(Gibb and Arulkumaran 2017)
 When the fetus is in compensatory mode
glycogenolysis will create a rise in lactate and a
further shift of the pH into metabolic acidosis

More comprehensive blood gas analysis – one that

includes PCO2, base excess and lactic acid is more
desirable and predictive 3. Reduced Variability

Think!

Have you experienced the phenomenon of a baby born with

cord pH below 7.00 but Apgar at 1 minute >7?

This would have been respiratory acidosis, not metabolic

12 25
Accelerations  FBS in gradually evolving hypoxia – in the absence
of an acute accident (cord prolapse, abruption, scar
 Transient increase in baseline of >15bpm dehiscence), it is unusual for a fetus who has shown
accelerations and normal baseline variability to become
 Presence of 2 or more in 20 minute period is reassuring hypoxic in labour

 Absent when fetus is sleeping, in chronic hypoxia, drugs  The presence of decelerations – which would classify
and infection the CTG as suspicious, either indicate the presence of
stress – either hypoxic or mechanical. If the baseline
 Erroneous monitoring of maternal pulse may show hasn’t started to rise and the variability remains within
“accelerations” of greater magnitude and coinciding with normal range and hence normal – there is little to be
uterine contractions gained from FBS

 Clinicians must identify the stress-to-distress period,

Variability that will be a unique period of time for each fetus,
depending on the fetal reserve
 Bandwidth variation of the baseline – excluding
accelerations and decelerations NICE advocate that fetal scalp stimulation can also be
deployed to test for hypoxia
 Normal 5-25bpm – a reassuring feature
 Reduced <5bpm – non-reassuring Indeed if the FHR reacts to the VE and start of FBS process
 Saltatory >25bpm – non-reassuring then the FBS should be abandoned.

 Normal variability is unlikely to be associated with

cerebral hypoxia
Interpreting FBS Results
 Cycling – refers to alternating patterns of activity and
Scalp pH Scalp lactate Interpretation
then quiescence – seen as normal and reduced
variability. Accelerations present on a CTG signify a
healthy functioning of the somatic nervous system. ≥ 7.25 ≤ 4.1 Normal
Although the absence of accelerations is of uncertain
significance, evidence of cycling should always be ≥ 7.21-7.24 4.2-4.8 Borderline
sought.
≤7.20 ≥ 4.9 Abnormal
 Absence of cycling may occur with hypoxia, infection
and fetal stroke

24 13
When Not FBS

 The fetal reserve is LOW in HIGH risk situations of:

 Postmaturity

 UGR

 Suspected or confirmed intrauterine infection

Think! MEWS

 Significant Meconium

 Scanty amniotic fluid Recognising and Managing Acute Hypoxia

 Identify if the cause is reversible?

 The challenge to clinicians is the timing of an FBS –
when used as an adjunct to interpreting the physiology  Acute “accidents” – cord prolapse, scar dehiscence,
and the clinical picture abruption require immediate delivery

14 23
Bradycardia or Prolonged Deceleration? Suspected or Confirmed Sepsis
CTG parameters that predict recovery of prolonged
decelerations  Chorioamnionitis is a significant cause of non-
hypoxic fetal compromise
 Most prolonged decelerations with a reversible cause
will respond to conservative measures to improve the  Warning – in cases of intrauterine infection, the high
utero-placental circulation, so the approach to the metabolic rate presents a greater oxygen demand to
woman and her family should be reassuring the fetus
 The CTG features prior to the prolonged deceleration – metabolic acidosis (that can do harm to fetal tissue/
provide information on the oxygenation of the fetus organs) might develop with minimal interruption of placental
prior to the onset on current insult (prolonged perfusion (seen on the CTG as decelerations)
deceleration)
 Coexistence of intrauterine infection and hypoxia
 The variability on the CTG corresponds to the integrity further increase the risk of cerebral palsy
of the fetal autonomic nervous system – If there is
normal variability in the 3 minutes before the  Do not rely on pattern recognition of the
deceleration and in the first 3 minutes of the “pathological” CTG to prompt actions in cases of
deceleration then it is highly likely the FHR will recover suspected or confirmed intrauterine infection
– 90% in 6 minutes and 95% in 9 minutes
 Screen the Mother – history, clinical exam, MEWS,
 If there is reduced variability before the prolonged bloods, involve the senior MDT
deceleration, then even after recovery is seen there is
a high probability of hypoxia and consideration should  Clinical Features of Chorioamnionitis
be given to delivery after consideration of the wider  Maternal pyrexia
clinical picture  Persistent fetal tachycardia (exclude dehydration and
other features of hypoxia)
 Maternal tachycardia
 Uterine tenderness
 Offensive liquor
 Purulent discharge
 Meconium stained liquor may also be a possible sign

22 15
CTG Key Features: Chorioamnionitis Try This Exercise!

Squeeze your fist 130 times in a minute

 Features can include- but none have been seen – this is sustainable.
consistently
Then increase this to 150 times in a minute
– what do you notice?
 Fetal tachycardia
 Reduced variability Take this up to 170 squeezes and your hand starts to hurt
and cramp up.
 Lack of accelerations
 Presence of decelerations Keeping this going is difficult and eventually your had starts to
slow down and become “bradycardic”
 Lack of cycling

 FBS is contraindicated in suspected or diagnosed

intrauterine infection – the test result is unreliable in the
Bradycardia
metabolic context of infection

 Ensure paired cord gasses are taken and the placental

swab for histology

 The placenta should be sent for histopathological

examination

16 21
Tachycardia CTG Key Features:
Applying an understanding of Physiology

Antenatal CTG (no uterine stress)

– what generates CTG features?

Rising baseline in Gradually Evolving Hypoxia

 A fetus exposed to gradually evolving hypoxia will

release stress hormones (catecholamines) – this is
reflected on the CTG as a slow and gradual rise in the
baseline
 Importance of comparing baseline over series of hours
and “fresh eyes” to notice these subtle changes
 It is vital that we notice this attempt by the fetus to
compensate and take actions to improve the uterine
environment (changing maternal position, stopping or
reducing oxytocin)
 This continuing catecholamine surge is energy
intensive and produces lactate within the myocardium
 If the environment is not improved and hypoxia
continues, loss of baseline variability is seen and then
terminal bradycardia.

20 17
Recognition and Management of Chronic
Hypoxia in the antenatal CTG
Baseline Fetal Heart Rate

 Chronic utero-placental insufficiency and antenatal

 The mean level of the FHR when this is stable
insults may lead to a hypoxia that has existed for days
and weeks possibly
 Analysed over 10 minutes
 Compensation attempts (increase in baseline FHR)
stress hormones (shallow decelerations) and evidence
 Normal range 110 – 160bpm
of decompensation (loss of baseline variability) will be
present on the CTG
 Gestational appropriateness – baseline lowers as
 This fetus would have reduced reserve to cope with
gestational age advances and the autonomic nervous
hypoxia in labour
system matures

 Baseline tachycardia (>160bpm) for longer than 10 min

– associated with maternal tachycardia, dehydration
and pyrexia- always suspect intrauterine infection

 Maternal temp rise of 1 degree = 10% increase in

baseline

 Look back at previous CTG’s for an understanding of

Intrapartum CTG – With Stress! baseline

 Bradycardia is a change to the baseline (FHR

<110bpm) that lasts longer than 10 minutes

18 19