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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 of
heart 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 panicking
when 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).