3 Physiology of Fetal Heart Rate Control and Types of Intrapartum Hypoxia. Handbook CTG

3

Physiology of Fetal Heart Rate Control

and Types of Intrapartum Hypoxia

◈

Anna Gracia-Perez-Bonfils and Edwin Chandraharan

Handbook of CTG Interpretation: From Patterns to Physiology, ed. Edwin Chandraharan.

Published by Cambridge University Press. © Cambridge University Press 2017.

Based on the rapidity of evolution, intrapartum hypoxia may be acute (i.e. sudden

cessation of fetal circulation), subacute (developing over 30–60 minutes) or gradually

evolving (developing over several hours). Pre-existing long-standing or chronic hypoxia

may occur in patients with preeclampsia or placental disorders, where the damaging

insult takes place in the antenatal period. However, continuation of labour may

potentiate ongoing ‘chronic’ hypoxic insult. It is essential to understand the features

observed on the cardiotocograph (CTG) trace during different types of intrapartum

hypoxia so as to institute timely and appropriate intervention to improve perinatal

outcomes.

Physiology of Fetal Heart Rate Control

The fetal heart rate (FHR), just like in adults, is controlled by both autonomic and

somatic components of the central nervous system. The former controls visceral

functions and is composed of sympathetic and parasympathetic systems, which are

constantly interacting with each other to increase and decrease the heart rate,

respectively. The ‘agreement’ reached following this interaction is indicated by thebaseline FHR. In addition, the constant fluctuation between sympathetic and

parasympathetic nervous systems creates the ‘bandwidth’ of this baseline, which is

observed on the CTG trace as the baseline variability. Somatic nervous system is

responsible for voluntary control of body movements via skeletal muscles and it

accounts for the occurrence of accelerations on the CTG trace. However, accelerations

may also be seen in anaesthetized fetuses indicating that somatic nervous system activity

may also be centrally mediated.

During labour, a fetus undergoes the most stressful journey of his/her entire life and

will have to use all his/her available resources to adapt to the constantly evolving and

rapidly changing intrauterine environment. Every fetus will have his/her own unique

physiological reserve, which may be modified by a combination of both antenatal (e.g.

pre- or postmaturity intrauterine growth restriction) and intrapartum risk factors (e.g.

infection or meconium and use of oxytocin to augment labour).

Parasympathetic Nervous System

The parasympathetic nervous system is responsible for activities that occur when the

body is at rest (such as listening to calm music, performing yoga). In contrast, the

sympathetic nervous system is responsible for the ‘fight or flight’ response, which is

essential for survival. The parasympathetic system will attempt to reduce the FHR in

order to maintain a positive energy balance in the fetal heart in response to any hypoxic

stress. This is because, unlike adults, a fetus cannot instantly increase the oxygenation to

its myocardium by increasing the respiratory rate as it is immersed in a pool of amniotic

fluid.

Parasympathetic activity is mediated by two kinds of receptors: baroreceptors and

chemoreceptors.

Baroreceptors

These are stretch receptors found in the carotid sinus and arch of the aorta. During

labour with the onset and progression of uterine contractions, both fetal head and

umbilical cord may undergo repeated compression.Chemoreceptors

Increased peripheral resistance secondary to the occlusion of the umbilical

artery leads to an increase in fetal systemic blood pressure and resultant

stimulation of these baroreceptors located in the carotid sinus and aortic arch.

Once stimulated, the baroreceptors would send impulses to the cardiac

inhibitory (parasympathetic) centre in the brain stem. This in turn inhibits the

atrioventricular node situated within the heart via the vagus nerve to slow down

the heart rate.

In addition, stimulation of the baroreceptors also decreases the sympathetic

stimulation of the heart. Such ‘baroreceptor-mediated’ decelerations will be

seen on the CTG trace as variable decelerations secondary to umbilical cord

compression. As these are generally short-lasting episodes related to uterine

contractions, the fetal heart returns to the baseline quickly, and they do not

expose the fetus to any hypoxic injury.

Therefore, in the absence of other abnormalities on the CTG trace (unstable

baseline or changes in baseline variability), the presence of early (head

compression leading to stimulation of the dura mater, which is richly supplied by

the parasympathetic nerves) or typical variable decelerations should be viewed

as pure ‘mechanical stresses’ during labour. Hence, they do not require any

interventions other than continued observation.

These are found peripherally on the aortic and carotid bodies and centrally

within the brain. Chemoreceptors are stimulated by changes in the biochemical

composition of the blood, responding to increased hydrogen ion and carbon

dioxide accumulation and low partial pressure of oxygen.

During labour, the activation of these receptors causes stimulation of the

parasympathetic nervous system, which decreases the FHR. Nonetheless, unlike

the short-lasting decelerations mediated by baroreceptors, when chemoreceptors

are stimulated, it takes longer to recover back to the original baseline heart rate.Therefore, decelerations secondary to the stimulation of baroreceptors will be in

relation to compression of the umbilical cord and will have a sharp drop and a quick

recovery. The duration between the onset and nadir of a variable deceleration is often

shorter than 30 seconds and the total duration of the entire ´typical´ variable

deceleration should be <60 seconds.

Role of Sympathetic System and the Fetal

Adrenal Glands

In response to persistent and ongoing hypoxic stress, fetal adrenal glands secrete

catecholamines (adrenaline and noradrenaline) that have sympathomimetic activity.

Catecholamines not only progressively increase the FHR, but they also cause peripheral

vasoconstriction in order to achieve effective redistribution of blood to selectively

perfuse vital organs at the expense of peripheral tissues and other nonessential organs

(‘centralization’).

This is because fresh oxygenated blood needs to reach the maternal venous

sinuses to remove the stimulus to chemoreceptors.

Due to delayed onset and recovery, they are termed ‘late decelerations’ and are

often associated with fetal metabolic acidosis.

On the other hand, decelerations secondary to chemoreceptor stimulation due to

metabolic acidosis have a more gradual fall from the baseline and take longer to

recover to the original baseline FHR (at least a 15–20-second lag time to reach

the original baseline). Therefore, due to their delayed recovery to the original

baseline, they are called late decelerations.

Therefore, when interpreting a CTG trace, an attempt should be made to

scrutinize for slowly increasing baseline FHR over a period of time to recognize

fetal catecholamine response to a gradually evolving hypoxic stress.

A baseline FHR of 110–160 bpm should not be considered normal during labour

for all fetuses, and the baseline heart rate of each fetus should be used as his/her

own control. For example, a fetus may increase the heart rate from 110 to 150The Somatic Nervous System

Fetal movements cause a transient increase in FHR, which is seen on the CTG trace as

‘accelerations’. However, some studies have shown the presence of accelerations even

after inducing fetal paralysis, and therefore, they are not always associated with fetal

movements and appear to reflect the integrity of the somatic nervous system.

During labour, as a fetus is exposed to uterine contractions, a progressive

intrapartum hypoxia may develop, which would trigger fetal compensatory mechanisms.

Fetus will experience decelerations secondary to umbilical cord (baroreceptors) or

head compression (parasympathetic stimulation secondary to compression of dura mater

of the brain).

bpm due to catecholamine release secondary to ongoing, gradually evolving

hypoxic stress but still be within the ‘normal’ range of 110–160 bpm.

Therefore, the presence of accelerations suggests the integrity of the somatic

nervous system, and a ‘healthy’ fetus not only has sufficient reserve to supply to

central organs but also has sufficient glucose and oxygen to expend on

nonessential somatic activity. Hence, the presence of accelerations is a hallmark

of a healthy, nonhypoxic fetus.

A fetus attempts to compensate for ongoing intrapartum hypoxia initially by the

onset of decelerations to protect the myocardium; the next step in the evolving

hypoxic process is to conserve energy by reducing the movements of skeletal

muscles. This will lead to the disappearance of accelerations on the CTG trace.

In normal conditions, a fetus will have sympathetic and parasympathetic nervous

systems constantly interacting with each other, which will define the baseline

and variability in the CTG trace.

Decelerations resulting from hypoxic stress will progressively become deeper

and wider with continuation of labour.

Moreover, a fetus will reduce its movements, and therefore, accelerations may

disappear from the CTG trace.Features of a Normal CTG

Baseline FHR

This refers to resting heart rate excluding accelerations and decelerations. It is

determined over a 5- to 10-minute period and expressed in beats per minute (bpm). A

normal baseline FHR between 110 and 160 bpm is considered normal for a term fetus

and if it is >160 bpm and persists for >10 minutes, it is called baseline tachycardia.

This could be physiological in a preterm fetus (immaturity of the parasympathetic

system) or be secondary to maternal pyrexia, dehydration, infection or rarely due to

drugs such as betamimetics. Temperature can augment the effect of hypoxia on fetal brain

and may predispose to fetal neurological injury.

In addition, a rise in baseline FHR can be seen as a fetus attempts to respond to

hypoxia, resulting in fetal adrenal glands producing catecholamines. Therefore, as well

as an absolute value, it is important to consider the trend over time; for example,

although a baseline FHR of 150 bpm may be within a normal range according to the

guidelines of CTG interpretation, an increase from a baseline rate of 110 bpm from the

beginning of the CTG to 150 bpm needs to be taken seriously to exclude gradually

evolving hypoxia (increase in baseline FHR is preceded by decelerations) or ongoing

chorioamnionitis (usually increase in baseline FHR without any preceding

decelerations). ‘Complicated tachycardias’, which are often seen alongside a reduction

in baseline variability or decelerations, should be considered ominous. It is vital to

compare current baseline FHR with previously recorded baseline during the last

If hypoxia continues to increase, a fetus will secrete catecholamines that will

progressively increase the baseline FHR to compensate for ongoing hypoxic

stress by obtaining oxygenated blood from the placenta and redistributing this

blood to essential organs at a higher baseline heart rate.

If decompensation sets in, loss of baseline variability may be observed

indicating hypoxia to central nervous system centres followed by myocardial

hypoxia and acidosis leading to a progressive fall in baseline FHR (‘stepladder

pattern to death’) culminating in terminal fetal bradycardia.antenatal clinical visit or from a previous CTG trace to determine a rise in baseline

secondary to a long-standing utero-placental insufficiency.

Similarly, a baseline FHR <110 bpm lasting >10 minutes is called a baseline

bradycardia. Postterm fetuses may have baseline bradycardia due to the predominance

of the parasympathetic nervous system with advancing gestation. Cardiac conduction

defects (congenital heart blocks) can also result in baseline bradycardia. Terminal

bradycardia may occur secondary to acute hypoxic events such as umbilical cord

prolapse, placental abruption or uterine rupture.

Variability

This is a variation in the FHR above and below the baseline (i.e. the ‘bandwidth’) and

reflects the continuous interactions of sympathetic and parasympathetic nervous systems.

Normal variability of 5–25 implies that both components of the autonomic nervous

system are functioning well, and therefore, fetal hypoxia is unlikely. Reduced baseline

variability of <5 bpm may represent a quiet sleep phase or may indicate hypoxia to the

central nervous system (together with an increase in baseline FHR and preceding

decelerations). It may also be secondary to drugs (CNS depressants such as pethidine),

infection or cerebral haemorrhage. Increased variability >25 bpm is called ‘saltatory

pattern’ and needs further consideration as it may occur in a rapidly evolving hypoxia,

especially in the second stage of labour with active maternal pushing. Therefore, an

urgent action is mandatory to improve fetal oxygenation (stopping oxytocin infusion,

stopping maternal pushing) if a saltatory pattern is encountered in association with

decelerations to avoid hypoxic-ischaemic injury. If no interventions are possible, an

urgent delivery should be considered.

Accelerations

These refer to a transient increase in FHR of 15 beats or more for more than 15 seconds.

As discussed previously, accelerations appear to reflect the integrity of the somatic

nervous system as they are usually associated with fetal movements. The significance of

the absence of accelerations in the presence of a normal baseline and variability and the

absence of decelerations has yet to be determined. The presence of accelerations,especially with cycling of FHR, is a hallmark of fetal well-being. Figure 3.1 illustrates

a normal CTG trace with a reassuring, stable baseline fetal heart rate, a reassuring

variability, presence of accelerations and absence of decelerations. However, the

disappearance of accelerations following the onset of decelerations is a feature of

gradually evolving hypoxia.

Figure 3.1 Normal CTG indicating the integrity of the autonomic nervous system (stable

baseline FHR and reassuring variability) and the integrity of the somatic nervous system

(presence of accelerations). In addition, there is no evidence of any hypoxic or mechanical

stress (absence of decelerations) and presence of active and quiet epochs (‘cycling’).

Decelerations

These refer to transient episodes of slowing of the FHR below the baseline rate, >15

beats and lasting more than 15 seconds. The decelerations have been traditionally

classified as early (fetal head compression), late (utero-placental insufficiency) and

variable (umbilical cord compression) in relation to uterine contractions. Nevertheless,

during labour, more than one pathophysiological process (fetal head compression,

umbilical cord compression or utero-placental insufficiency) may arise simultaneously,

and therefore, decelerations may have different characteristics from the three standard

types described below:

Early decelerations: True early decelerations are relatively uncommon in

practice. They are a mirror image of uterine contraction, starting with the onset of

contraction, reaching the nadir with the peak of the contraction and returning to baseline

FHR at the end of contraction. They occur secondary to head compression often late inthe first stage and in the second stage of labour. Compression of the head causes

parasympathetic stimulation through the vagus nerve and a resultant deceleration of the

FHR. It is believed that the fetus attempts to reduce its blood pressure by slowing down

its heart rate so as to compensate for increased intracranial pressure secondary to head

compassion. The presence of decelerations, which resemble early decelerations in early

labour, should be viewed with caution especially if they are associated with a reduced

baseline FHR variability, as head compression is unlikely in early labour and may be

due to atypical variable or late deceleration that has been misclassified.

Late decelerations: Late decelerations are so termed because, in relation to

uterine contractions, they occur ‘late’: both the onset of decelerations as well as the

subsequent recovery to the baseline occurs after the beginning and after the end of a

uterine contraction, respectively. The nadir of these decelerations is seen around 20

seconds after the peak of contraction, with the return to baseline occurring

approximately 20 seconds after the end of contraction.

Late decelerations are usually due to utero-placental insufficiency associated

with fetal hypoxaemia and resultant hypercarbia and developing acidosis. This

results in the stimulation of chemoreceptors leading to a drop in FHR. As uterine

contraction ceases, the placental venous sinuses refill with fresh oxygenated

blood leading to a gradual removal of the stimulus for chemoreceptors. This

results in the delayed recovery of the FHR to its original baseline.

In the presence of late decelerations and based on other features of the CTG

trace and the clinical situation, an intervention aiming to increase the uteroplacental circulation should be instituted.

These interventions may include changing maternal position, administering

intravenous fluids, stopping or reducing oxytocin infusions and use of tocolytics

in cases of uterine hyperstimulation. If there is no improvement in fetal

condition, an additional test of fetal well-being (i.e. digital scalp stimulation or

fetal ECG) may be considered if it is intended to continue with the labour. In the

presence of features suggestive of fetal decompensation (e.g. loss of baseline

FHR variability) or further deterioration of the CTG trace despite intrauterine

resuscitation, immediate delivery should be accomplished.Variable decelerations: These are the most common type of decelerations, and

approximately 80–90 per cent of all decelerations are variable decelerations.

They are so named because they vary in shape, form and timing in relation to

uterine contraction. They are due to umbilical cord compression. Considering the shape

and duration of decelerations, there are two types of variable decelerations, with

different characteristics.

Typical or uncomplicated variable decelerations are characterized by a drop of

<60 bpm, duration of <60 seconds and presence of ‘shouldering’, which consists in a

slight increase in FHR both before and after deceleration. Typical variable

decelerations are secondary to mechanical compression of the umbilical cord, and in the

presence of normal baseline and variability, they may continue for a considerable length

of time before fetal hypoxia develops.

Atypical or complicated variable decelerations have lost the ‘typical’ features

such as shouldering. They can drop more than 60 bpm and last longer than 60 seconds.

They can present with an ‘overshoot’ (an increase of FHR above the baseline following

the recovery of deceleration and returning to baseline) or have loss of variability within

the deceleration or may have a biphasic pattern. (Table 3.1 shows the features of

complicated variable decelerations.)

Table 3.1 Features of complicated (‘atypical’) variable decelerations

Unlike typical variable decelerations, atypical variable decelerations are not due

to transient umbilical cord compression alone.

Duration more than 60 seconds

Drop of more than 60 bpm

Loss of shouldering

Overshoot

Loss of variability within the deceleration

Slow recovery

Biphasic decelerationsThey may be due to sustained and prolonged umbilical cord compression and may

signify coexisting utero-placental insufficiency. If associated with adverse changes in

baseline FHR with loss of baseline variability, it may indicate that the fetus is losing its

ability to compensate for ongoing hypoxic or mechanical stress. It is therefore essential

that the CTG trace is re-evaluated over time.

The importance of reviewing the entire CTG trace and considering the clinical

scenario rather than just a segment of CTG trace in isolation cannot be overemphasized.

Types of Intrapartum Hypoxia

Based on the rapidity of onset, intrapartum hypoxia is classified into the following four

types:

Acute Hypoxia

A single prolonged deceleration with a sudden drop in baseline FHR <80 bpm,

persisting for >3 minutes (Figure 3.2). Such a sharp and long deceleration causes a

rapid onset of metabolic acidosis if it occurs secondary to an intrapartum accident

(placental abruption, umbilical cord prolapse and uterine rupture) and pH decreases at a

rate of >0.01 per minute.

Figure 3.2 Acute hypoxia. Note the sudden fall in FHR due to an acute interruption in fetal

circulation.Recommended management includes:

1. Immediate assessment to exclude the three major ‘accidents’ during labour (cord

prolapse, placental abruption or caesarean scar rupture).

2. Correct iatrogenic causes such as uterine hyperstimulation secondary to an

excess of oxytocin infusion or maternal hypotension due to anaesthesia. Stopping

oxytocin and considering administration of tocolysis (such as terbutaline 250 mcg

subcutaneously) will help resolve uterine hyperstimulation, and the administration

of intravenous saline bolus will help correct maternal hypotension.

3. Change maternal position.

4. Assess the CTG trace seeking for reassuring features:

a. Normality in the CTG trace prior to deceleration.

b. Variability is maintained within prolonged deceleration.

c. Signs of recovery within the first 6 minutes of deceleration.

If these reassuring features are present, in the absence of acute intrapartum

accidents, the likelihood of recovery is up to 90 per cent within the first 6 minutes

and up to 95 per cent within 9 minutes.

The ‘3-6-9-12’-minute rule – which recommends measures to correct iatrogenic

causes by 6 minutes and to transfer the woman to the operating theatre by 9 minutes

if there are no attempts of recovery, so as to commence an operative delivery

within 12 minutes of the beginning of deceleration and to deliver the fetus within

15 minutes – is based on this principle.

Considering the drop of pH of 0.01 per minute, a baby subjected to acute hypoxia

after 15 minutes will have a decrease in pH of 0.15, which could mean, for example, a

drop in pH from 7.20 to 7.05. In case of a fetus exposed to gradually evolving hypoxia

throughout labour, its reserve may be already compromised at the onset of prolonged

deceleration. Therefore, the resultant fetal pH will be even lower.

Subacute HypoxiaIt occurs when the fetus spends <30 seconds on stable baseline and decelerates for >90

seconds (Figure 3.3). Therefore, the fetus spends more time decelerating to protect its

heart with only one-third of the time at the baseline to exchange gases and to protect its

brain. The shortage of sufficient time for oxygenation leads to the development of fetal

acidosis with a drop in fetal pH at a rate of 0.01 per 2–3 minutes. Therefore, the fetal

pH may drop from 7.25 to 7.15 in 20 minutes. When subacute hypoxia is diagnosed,

hyperstimulation with oxytocin should be excluded, and in case of active maternal

pushing, suggesting the mother to stop pushing for a while may allow the fetus to

recuperate.

Figure 3.3 Subacute hypoxia: a fetus spends progressively less time at its normal baseline

as compared to time spent during declarations. Also note the compensatory

‘catecholamine surge’.

Gradually Evolving Hypoxia

When a fetus is exposed to a gradually evolving hypoxic stress, it has sufficient time to

mobilize its resources to compensate (decelerations → loss of accelerations →

secretion of catecholamines leading to an increase in baseline heart rate (Figure 3.4) to

redistribute blood to vital organs as well as to get fresh oxygenated blood from the

placenta). If this compensation fails, then the onset of decompensation sets in, resulting

in a decrease in perfusion to fetal brain. This will be seen on the CTG trace as a loss ofbaseline FHR variability. If no remedial action is taken, the myocardium will suffer a

reduction in oxygenation with consequent acidosis that will be shown in the CTG trace

as instability of the FHR baseline culminating in a ‘stepladder pattern’ to death and

terminal bradycardia.

Figure 3.4 Gradually evolving hypoxia. Note the presence of decelerations, absence of

accelerations and a rise in baseline FHR (catecholamine surge).

Long-Standing (Chronic) Hypoxia

Chronic utero-placental insufficiency and antenatal insults may result in hypoxia

persisting for days and weeks leading to attempts of compensation (increase in baseline

FHR), chemoreceptor-mediated decelerations (‘shallow’ decelerations with late

recovery) and evidence of decompensation (loss of baseline variability).

These fetuses would have reduced physiological reserves to compensate for any

further hypoxic insults and, therefore, may rapidly decompensate with the onset of

uterine contractions leading to a progressive decrease in FHR (myocardial

decompensation). Immediate delivery is indicated if features of chronic hypoxia are

noted on the CTG trace (Figure 3.5), and if uterine contractions have commenced and

immediate delivery is not possible (i.e. operating theatre is busy), tocolytics (e.g.

terbutaline) should be administered to reduce further hypoxic stress until delivery is

accomplished.Figure 3.5 Long-standing hypoxia. The baseline FHR is in the upper limit of normal with a

total loss of baseline variability and ongoing shallow decelerations, which are hallmarks of

chronic hypoxia. Also note the total absence of ‘cycling’.

If baseline FHR is >150 bpm after 40 weeks of gestation, features of chronic

hypoxia should be excluded.

Preterminal CTG

Once the fetus has exhausted all its compensatory mechanisms, a total loss of baseline

variability and shallow decelerations would be observed on the CTG trace. Due to

progressive myocardial decompensation, the baseline heart rate will progressively

decrease (Figure 3.6) and terminal bradycardia may ensue, if delivery is not

accomplished in time.Figure 3.6 Preterminal CTG trace. Note the total loss of baseline variability with ongoing

‘chemoreceptor-mediated’ late decelerations suggestive of fetal acidosis. Unlike chronic

hypoxia, this fetus is unable to maintain a higher baseline FHR to perfuse its vital organs,

and due to myocardial acidosis, a ‘wavy’ baseline may be noted.

Exercises

1. How would you classify decelerations in Figure 3.7, 3.8 and 3.9? Why?

Figure 3.7

Figure 3.8Figure 3.9

Further Reading

1. Chandraharan E, Arulkumaran S. Prevention of birth asphyxia: responding appropriately to

cardiotocograph (CTG) traces. Best Pract Res Clin Obstet Gynaecol. 2007; 21(4): 609–24.

2. Williams KP, Hofmeyr GJ. Fetal heart rate parameters predictive of neonatal outcome in

the presence of prolonged decelerations. Obstetr Gynecol. 2002; 100: 951–4.

3. Pinas A, Chandraharan E. Continuous cardiotocography during labour: Analysis,

classification and management. Best Pract Res Clin Obstet Gynaecol. 2015;

S1521–6934(15)00100-5.