5 Applying Fetal Physiology to Interpret CTG Traces. Handbook CTG

 5

Applying Fetal Physiology to Interpret

CTG Traces

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Predicting the NEXT Change

Edwin Chandraharan

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

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

Adult Physiological Response to Hypoxic Stress

All living beings are exposed to hypoxic stress in their day-to-day life and have inbuilt

physiological mechanisms to compensate for short-lasting and long-lasting hypoxic

stresses so as to protect the myocardium – the only organ that is protected at all cost.

This is because, if the ‘pump’ (i.e. the myocardium) fails, every other organ in the body

would also fail due to lack of tissue perfusion.

The inherent desire to protect the myocardium is exemplified in the anatomical

arrangement of blood vessels supplying the vital organs. Coronary artery is the first

branch that is given off, from the root of the aorta (where oxygenation is maximum) to

supply the pump (i.e. myocardium). This is followed by the carotid arteries given off

from the arch of the aorta to supply the brain. Therefore, these two organs have been

prioritized from conception: the heart first and the brain next.

Adults are exposed to hypoxic stress during everyday activities, which include

running, exercising, climbing stairs, sexual intercourse as well as brisk walking, all of

which require increased distribution of oxygen and nutrients to muscles or sexual organs(i.e. whichever organ is active at the given time). However, if the heart muscle

(myocardium) is forced to pump blood faster and with greater force (increased rate and

force of contraction of the myocardium) without first ensuring adequate oxygenation of

the myocardium itself, it would lead to myocardial hypoxia and acidosis due to

increased oxygen demand.

Therefore, all living beings are inherently programmed to protect the myocardium

first by maintaining a positive energy balance with the onset of hypoxic stress. This is to

enable the myocardium to be well oxygenated (to maintain aerobic metabolism) prior to

increasing the heart rate to supply the brain and other essential organs during hypoxic

stress.

In adults, increased respiratory rate is seen as the first physiological response to

any hypoxic stress to protect the myocardium from hypoxic injury. With the progression

of intensity of hypoxia, both rate and depth of respiration increase to supply the

myocardium, so that it could start pumping oxygen and nutrients to other essential

organs, after ensuring a positive energy balance in the ‘pump’. This is clearly evident

during physical exercise, such as going on an exercise bike or treadmill, whereby the

rate and depth of respiration progressively increases as the hypoxic stress worsens, and

this is associated with tachycardia due to the release of catecholamines (adrenaline and

noradrenaline).

Catecholamines have three important functions: they increase the heart rate and the

force of contraction of the myocardium to pump blood faster; they cause intense

peripheral vasoconstriction to divert blood from nonessential organs (skin, scalp, gut) to

supply oxygenated blood to central organs as well as a consequent increase in

peripheral resistance thereby increasing systemic blood pressure to maximize the force

with which blood could be supplied to central organs. Finally, they help in the

breakdown of stored glycogen within the myocardium and other cells into glucose to

generate additional energy substrate. All these physiological responses are aimed at

ensuring compensation to ongoing hypoxic stress so as to maintain a positive energy

balance within the myocardium, even at the expense of transient hypoxia to nonessential

organs.Fetal Physiological Response to Hypoxic Stress

A fetus has similar mechanisms to mount a physiological compensatory response to

intrauterine hypoxic stress. In fact, its capacity to respond to hypoxic stress is greater

than that of adults because of the presence of fetal haemoglobin (which has a greater

affinity for oxygen) and the increased amount of haemoglobin (18–22 g/dL), which not

only carries more oxygen but also acts as an effective buffer when there is respiratory or

metabolic acidosis.

Unlike the adult, a fetus does not have the capacity to significantly increase the

stroke volume (i.e. force of contraction of the myocardium) to the same extent and,

therefore, increases the cardiac output predominantly through increase in its heart rate.

In addition, a fetus is able to effectively and rapidly redistribute oxygenated blood to the

central organs (brain, heart and adrenal glands) by shutting off blood supply to all the

organs as the placenta performs the functions of the kidneys, liver and the lungs during

intrauterine life.

However, despite all the additional protective mechanisms to deal with intrauterine

hypoxic stresses, a fetus, unlike the adult, has a huge disadvantage because it is

immersed in a pool of amniotic fluid. Therefore, a fetus is not exposed to the external

environment and has no access to atmospheric oxygen. This means that a fetus, unlike

adults, is unable to rapidly increase the rate and depth of respiration to protect its

myocardium from hypoxic injury (and resultant myocardial acidosis) as its primary

response to hypoxia. It is plainly obvious that increasing the heart rate to increase the

cardiac output to supply central organs to avoid hypoxic ischaemic injury without first

oxygenating the myocardium to maintain a positive energy balance would lead to a rapid

myocardial hypoxia and acidosis, resulting in terminal bradycardia.

Therefore, the only mechanism available for a fetus to maintain a positive

myocardial energy balance during periods of hypoxic stress that occur in utero is to

reduce the demand of myocardial fibres because a rapid increase in the supply of

oxygen by increasing the rate and depth of respiration, as in adults, is not at all possible.

It is for this reason that the fetus slows down the heart rate (decelerations) during

hypoxic stress in order to maintain a positive energy balance in the myocardium during

episodes of hypoxic stress (Figure 5.1). This mechanism of reflex slowing down ofheart rate in response to any hypoxic stress not only reduces myocardial workload and

conserves energy but also improves time available for diastolic filling and coronary

circulation. When oxygenation is restored (i.e. relief of umbilical cord compression or

re-establishment of placental oxygenation as uterine contraction ceases), a fetus is able

to recover its heart rate immediately to its baseline or even can increase it to a higher

rate (due to catecholamine surge) to supply oxygen to the brain and other vital organs

during hypoxic stress.

Figure 5.1 At the onset of hypoxic stress, a fetus may show decelerations to protect its

myocardium in response to strong uterine contractions, while showing accelerations in

between contractions. If hypoxia progresses, these decelerations would become wider and

deeper, and accelerations may disappear as the fetus attempts to conserve oxygen and

energy.

Deceleration, therefore, should be considered as a reflex fetal response to any

mechanical or hypoxic stress to protect its myocardium. It is a useless exercise if one

attempts to ‘name and shame the decelerations’ by using several terminologies such as

‘type I’, ‘type II’, ‘early’, ‘variable’, ‘late’, ‘severe variable’, as one does not do so for

increased rate and depth of respiration that is observed during hypoxic stresses in

adults. The morphology of the decelerations, similar to the rate and depth of adult

respiration, would depend on the intensity and duration of the hypoxic stress. There

needs to a paradigm shift in the reaction to decelerations, as there are not associated

with fetal compromise but rather a fetal response to ongoing stress via a baroreceptor or

chemoreceptor reflex mechanism. Some clinicians panic when they observe

decelerations on the CTG trace, and this is similar to adults in a playground panickingwhen they observe athletes increasing the rate and depth of their respiration during

hypoxic stress (e.g. sprinting).

Decelerations would be progressively wider and deeper as the hypoxic stress

progresses during labour (similar to increase in the rate and depth of respiration in

adults as the exercise becomes more strenuous). Similarly, decelerations would get

shallower and narrower when the hypoxic stress is reversed (similar to a reduction in

the rate and depth of respiration in adults that is seen when the treadmill is slowed

down).

Instead of morphological classification of decelerations into ‘early’, ‘variable’ and

‘late’ and several ‘unknown’ decelerations, clinicians should classify decelerations

according to three main underlying mechanisms:

Baroreceptor decelerations occur secondary to an increase in fetal systemic

blood pressure (occlusion of umbilical arteries during compression of the

umbilical cord) and are characterized by a rapid fall in heart rate without any

delay and a rapid recovery to the original baseline FHR (Figure 5.2).

Chemoreceptor decelerations occur secondary to the accumulation of carbon

dioxide and metabolic acids during hypoxia (utero-placental insufficiency,

repeated and sustained uterine contractions or a prolonged umbilical cord

compression) and are characterized by a gradual and slow recovery to the

original baseline fetal heart rate even after cessation of uterine contractions

(Figure 5.3).

Prolonged decelerations occur as a reflex response to acute hypoxia (placental

abruption, umbilical cord prolapse, uterine rupture or uterine hyperstimulation)

or hypotension (epidural analgesia) to protect the myocardium from hypoxic

ischaemic injury by reducing myocardial workload and to improve coronary

blood flow (Figure 5.4).Figure 5.2 ‘Baroreceptor’ decelerations with a rapid drop and a rapid return to baseline

FHR.

Figure 5.3 ‘Chemoreceptor decelerations’ with a gradual recovery to original baseline

FHR. The depth of deceleration is not marked as a baroreceptor deceleration and the heart

rate continues to recover even after contractions cease.Figure 5.4 A prolonged deceleration. In acute hypoxic stress, a fetus rapidly drops the

heart rate to protect the myocardium until the hypoxic stress disappears. However, in

intr

apartum accidents (e.g. placental abruption), irreversible myocardial damage may occur

due to a combination of hypoxia and fetal hypovolemia.

Physiological Approach to CTG Interpretation:

‘8Cs’ Approach to Management

Clinical picture: One should consider the presence of meconium staining of amniotic

fluid, intrapartum bleeding, evidence of clinical chorioamnionitis, rate of progress of

labour, presence of uterine scar, administration of medications to the mother or fetus,

fetal cardiac malformations, ongoing uterine hyperstimulation and fetal reserve while

interpreting a CTG trace.

Cumulative uterine activity: This refers to the frequency, duration and strength of

uterine contractions over a 10-minute period. Unfortunately, the tocograph does not

provide information regarding the strength of uterine contractions. Calculating the total

duration of cumulative uterine activity (sum of frequency and duration of contractions in

a 10-minute period) would give clinicians a better indication of ongoing uterine activity

rather than solely concentrating on the ‘frequency’ of contractions alone, especially

when oxytocin is used to augment labour. It is important to recognize that fetal hypoxiamay rapidly ensue even if there are only four uterine contractions in 10 minutes but if

these contractions last for 90 seconds each (cumulative uterine activity of 6 minutes).

This is similar to having six uterine contractions lasting for a minute each in 10 minutes.

Similarly, if the strength (tone) of contractions increases, rapid fetal compromise may

ensue.

Cycling of FHR: Cycling refers to alternating periods of activity and quiescence

characterized by normal and reduced baseline FHR variability. The presence of

accelerations signifies a healthy ‘somatic’ nervous system. Although the absence of

accelerations is of uncertain significance during labour, the evidence of cycling should

always be sought while interpreting CTG traces. The absence of cycling may occur in

hypoxia, fetal infections including encephalitis and intrauterine fetal stroke.

Central organ oxygenation: This is determined by a careful assessment of baseline

FHR and baseline variability. Baseline FHR is a function of the myocardium (heart

muscle) due to electrical activity of the sinoatrial node and is modified by the autonomic

nervous system, various medications (e.g. salbutamol) as well as catecholamines.

Baseline variability reflects the function of the autonomic nervous system centres, which

are situated within the brain and, therefore, indicates the optimum functioning of these

centres. An unstable baseline and loss of baseline variability would reflect hypoxia to

the central organs (myocardium and brain) that would require urgent action to improve

utero-placental circulation through intrauterine resuscitation (stopping oxytocin infusion,

intravenous fluids, administration of terbutaline and changing maternal position) and to

ensure immediate delivery if intrauterine resuscitation is not possible or appropriate

(e.g. in uterine rupture) or if the measures to improve fetal oxygenation were not

effective.

Catecholamine surge: A fetus exposed to a gradually evolving hypoxia would

release catecholamines, and this will be reflected on the CTG trace by a slow and

progressive increase in baseline FHR usually over several hours. It is vital to recognize

this attempted fetal compensation to ongoing hypoxic or mechanical stress so as to take

measures to correct any avoidable factors (stopping or reducing oxytocin or changing

maternal position) to improve fetal oxygenation. If corrective measures are effective, the

FHR should come back to its previous baseline rate. Continuing catecholamine surge is

energy-intensive to the myocardium, and if timely intervention is not instituted, this maylead to a loss of baseline variability (decompensation of brain centres) culminating in a

terminal fetal bradycardia secondary to myocardial hypoxia and acidosis.

Chemo- or baroreceptor decelerations: The presence of decelerations would

indicate ongoing mechanical (head compression or umbilical cord compression) or

hypoxic (utero-placental insufficiency) stress. It is important to determine whether the

underlying pathophysiology is through a baroreceptor or a chemoreceptor mechanism. A

slow recovery to baseline FHR reflects a chemoreceptor-mediated response. In

contrast, baroreceptor decelerations are characterized by a rapid fall and an

instantaneous recovery to the original baseline. It is vital to appreciate that the fetal

response is determined in-between the decelerations (i.e. a stable baseline and a

reassuring variability indicative of good oxygenation to the central nervous system as

well as a rise in baseline suggestive of ongoing catecholamine surge).

Cascade: It is important to understand the wider clinical picture and type of

intrapartum hypoxia (acute, subacute or a gradually evolving), and the need for

additional tests of fetal well-being to confirm or exclude intrapartum hypoxia would

become less if fetal response to hypoxic stress (a stable baseline and a reassuring

variability) is determined prior to making management plans. Clinicians should refrain

from merely classifying the CTG trace into ‘normal’, ‘suspicious’ or ‘pathological’ (or

category I, II or III/normal, intermediary or abnormal) based on the patterns observed on

the CTG trace without incorporating the overall clinical picture and fetal response to

stress. A pathological CTG with a stable baseline FHR and a reassuring variability

often needs no intervention as opposed to a ‘suspicious’ CTG with total loss of baseline

variability or with ‘shallow decelerations’.

Consider the NEXT change on the CTG trace if intrapartum hypoxia progresses

(Figure 5.5). If a fetus presents in early labour with a stable baseline FHR, reassuring

variability, presence of accelerations and cycling and is exposed to an evolving

intrapartum hypoxia, it will show decelerations first. These decelerations will become

wider and deeper as hypoxia progresses.

As the fetus attempts to conserve energy (i.e. stops movements of nonessential

muscles), accelerations will disappear from the CTG trace. This will be followed by a

‘catecholamine surge’ to compensate for ongoing hypoxic stress leading to a gradual

increase in baseline FHR. Depending on the individual physiological reserve and therapidity and intensity of hypoxic stress, some fetuses may remain in this compensated

state (i.e. ongoing decelerations with an increased baseline FHR with reassuring

variability). The onset of cerebral decompensation will be heralded by a reduction and

subsequent loss of baseline variability, and finally, if no corrective action is taken,

myocardial decompensation will ensue leading to a ‘stepladder’ pattern to death

culminating on a terminal bradycardia.

Figure 5.5 ‘ABCDE’ approach to predicting the NEXT change in the CTG trace due to

an evolving hypoxia.

Key Messages on Physiology-Based CTG

Interpretation

A fetus would attempt to protect its myocardium in response to a hypoxic or

mechanical stress by slowing its heart rate to conserve energy and to preserve a

positive myocardial energy balance. This reflex slowing of the heart is termed

deceleration.

A stable baseline FHR and a reassuring variability denote good oxygenation of

central organs (myocardium and brain) despite ongoing late or variableExercises

CTG Exercise A

1. A 32-year-old primigravida was admitted with spontaneous onset of labour at 39

weeks plus 3 days of gestation. On vaginal examination, her cervix was 6 cm dilated

with evidence of spontaneous rupture of membranes. Clear amniotic fluid was draining

and the presenting part was at the level of ischial spines. FHR was 128 bpm on

intermittent auscultation. Four hours later, she was still found to be 6 cm dilated and,

therefore, oxytocin infusion was commenced.

Time to predict the NEXT change on the CTG trace:

decelerations that may result in a ‘pathological’ CTG.

Clinicians should anticipate a progressive increase in baseline FHR following

ongoing decelerations due to catecholamine surge. This indicates a

progressively increasing hypoxic stress and fetal compensatory response to

redistribute oxygen to central organs. Immediate action should be taken to

improve intrauterine environment.

If no action is taken, a loss of baseline variability or saltatory pattern (indicative

of hypoxia to autonomic centres of the brain resulting in decompensation) or

terminal bradycardia (myocardial decompensation leading to hypoxia and

acidosis) may ensure.

Deep decelerations which are short-lasting indicate intact fetal reflex responses

to ongoing hypoxic or mechanical stress, while shallow decelerations in

combination of a loss of baseline variability may indicate a depression of brain

centres, and this requires urgent action to improve fetal oxygenation or

immediate delivery, if the CTG is classified as ‘preterminal’.

The ‘8Cs’ approach to CTG interpretation may help understand the wider

clinical picture and fetal response to ongoing hypoxia, type of intrapartum

hypoxia as well as evidence of decompensation.a. What changes would you expect to see on the CTG trace after commencement of

oxytocin infusion if the fetus is exposed to an evolving hypoxic stress?

b. If hypoxia worsens, what would you expect to see happening to the decelerations?

c. If oxytocin infusion is further increased and hypoxia worsens, what would be

expected to be seen on the CTG trace?

d. What would you expect to see on the CTG trace?

e. After the onset of cerebral decompensation (loss of baseline FHR variability), if

oxytocin infusion was further increased, what is the next (i.e. last) organ to fail and what

would you observe on the CTG trace?

CTG Exercise B

1. A primigravida was admitted with spontaneous onset of labour at 40 weeks plus 6

days of gestation. Oxytocin was commenced for failure to progress at 5 cm dilatation, 2

hours after artificial rupture of membranes. Clear amniotic fluid was noted and CTG

trace was commenced. Apply ‘8Cs’ on the CTG trace (Figure 5.11).

Figure 5.11

2. What features would you expect to see on the CTG trace if this fetus is exposed to a

gradually evolving hypoxic stress?

3. After protecting the myocardium, how will the fetus redistribute oxygen to central

organs? What would you expect to see on the CTG trace?

4. What would happen to ongoing decelerations as hypoxia progresses?

5. What would you expect to see if there is onset of fetal decompensation?