Answers to Exercises
Chapter 3. Physiology of Fetal Heart Rate
Control and Types of Intrapartum Hypoxia
1. How would you classify the decelerations in Figures 3.7, 3.8 and 3.9? Why?
Figure 3.7Figure 3.8
Figure 3.9
Answer
1. Typical variable decelerations. This is because they vary in size, shape and in
relation to uterine contractions (i.e. variable) and are characterized by a sharp drop
and sharp recovery to the baseline (<60 seconds) due to ‘baroreceptor reflex
response’. Also note the presence of shouldering.Late decelerations. Unlike variable decelerations, a drop in FHR is more gradual,
and more importantly, the recovery to normal baseline occurs late, even after the
contraction has subsided. This is because they are mediated through chemoreceptors,
and fresh oxygenated blood needs to ‘wash out’ all the accumulated carbon dioxide
and metabolic acids during uterine relaxation to remove the stimulus.
Atypical (or complicated) variable decelerations. Note the sharp drop and rapid
recovery (i.e. variable mediated through the baroreceptor reflex), but the duration of
these decelerations last for >60 seconds. In addition, ‘biphasic pattern’ is also seen
with total loss of shouldering.
Chapter 5. Applying Fetal Physiology to
Interpret CTG Traces: Predicting the NEXT
Change
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:
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?Figure 5.6 Note the appearance of variable decelerations secondary to repeated umbilical
cord compression, loss of accelerations and an increase in baseline FHR secondary to
catecholamine surge, 4 hours after commencing oxytocin infusion. Note that the baseline
FHR is stable and the variability is reassuring, which indicates good oxygenation of the
central organs.
b. If hypoxia worsens, what would you expect to see happening to the decelerations?
Figure 5.7 Note that within 40 minutes of continuation of hypoxic stress, decelerations
have become wider and deeper. The baseline FHR is stable and the baseline variability is
reassuring, indicating adequate oxygenation of the central organs.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?
Figure 5.10 Note the onset of myocardial hypoxia and acidosis leading to a ‘stepladder’
pattern to death.
Answers
1.
a. Decelerations will be noted as the first sign of hypoxic stress as the fetus
attempts to protect its myocardium by reducing myocardial workload. If the
hypoxic stress continues, accelerations will disappear to conserve oxygen and
nutrients by reducing nonessential body movements (somatic nervous system
activity). A further increase in hypoxic stress secondary to oxytocin infusion may
result in fetal catecholamine surge to increase the baseline FHR to perfuse vital
organs at a faster rate and also to obtain more oxygen from the placenta (Figure
5.6).b. Decelerations would become wider and deeper (Figure 5.7) as the fetus attempts
to protect its myocardium for prolonged periods of time to maintain a positive
energy balance. This is similar to a progressive increase in the rate and depth of
respiration in adults with prolonged and strenuous exercise to oxygenate the heart.
As long as the baseline FHR and variability are normal and the time spent on the
baseline is more than the time spent during decelerations (Figure 5.7), the central
organs are well perfused and the risk of fetal acidosis is very low.
c. The fetal reserve of a well-grown, term fetus with normal adrenal glands may
release more catecholamines to compensate and, therefore, may further increase its
heart rate (Figure 5.8), whereas a fetus with limited reserves (e.g. intrauterine
growth restriction) may rapidly decompensate, leading to a loss of baseline FHR
variability.
Figure 5.8 Note a further increase in FHR to above 170 bpm, which is significantly
higher than the baseline FHR on admission (128 bpm), which indicates the degree of
catecholamine surge. The fetus is still attempting to maintain a stable baseline FHR
and a reassuring variability (arrow), but rapid decompensation may ensue if oxytocin
in
fusion is further increased.
Unfortunately, clinicians had failed to notice the increase in baseline FHR
secondary to catecholamine surge and, therefore, wrongly classified the CTG trace
as ‘normal’. They had considered ongoing decelerations as ‘typical’ variabledecelerations and,therefore, opined that the CTG would become ‘suspicious’ only
if these decelerations persisted for >90 minutes, according to NICE guidelines.
Therefore, they further increased the rate of oxytocin infusion.
d. Depending on the fetal reserve, either a further increase in FHR due to the
release of catecholamines or a reduction of baseline FHR variability secondary to
the onset of fetal decompensation.
The CTG trace clearly shows a final attempt by the fetus to maintain oxygenation
by increasing the baseline heart rate to 200 bpm (Figure 5.9). However, such
marked tachycardia would result in reduced ventricular filling time leading to
reduced cardiac output and resultant reduction in carotid blood supply. The onset
of cerebral hypoxia and acidosis will result in a reduction in baseline FHR
variability (Figure 5.9).
Figure 5.9 Note the final attempt by a fetus to maintain oxygenation to vital organs
and the onset of reduction in baseline variability suggesting that this attempt was
unsuccessful and that the fetus had moved from compensation to decompensation.
The onset of reduction in baseline variability requires urgent action to improve
utero-placental circulation. These include immediate stopping of oxytocin infusion,
rapid infusion of intravenous fluids to dilute oxytocin concentration in maternal
circulation and changes in position to relieve umbilical cord compression and use
of tocolytics, if variability does not improve with initial measures. Unfortunately,due to a total lack of understanding of fetal physiological response to an evolving
hypoxic stress, clinicians continued to increase oxytocin infusion to achieve
‘progress’ of labour and also commenced maternal active pushing to expedite
delivery.
e. The last organ to fail is the myocardium (i.e. the heart) as persistent baseline
fetal tachycardia increases the workload of the heart and reduces its own blood
supply due to a reduction in cardiac relaxation time. In addition, increasing the rate
of oxytocin infusion during the second stage of labour and maternal active pushing
can result in a rapidly evolving hypoxia leading to fetal decompensation. The onset
of myocardial hypoxia and acidosis will be characterized by the ‘stepladder’
pattern to death (Figure 5.10), culminating in terminal bradycardia.
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?
Answers
1. Clinical picture – Primigravida on oxytocin for augmentation of labour
Cumulative uterine activity – Difficult to determine. However, there are no
ongoing decelerations suggestive of hypoxia
Cycling – Present
Central nervous system oxygenation – Stable baseline FHR and a reassuring
variability suggestive of good oxygenation of fetal myocardium and autonomic nerve
centres in the brain
Catecholamine surge – None
Chemo- or baroreceptor decelerations – None
Cascade – Continue monitoring
Consider the NEXT change on the CTG trace – Onset of decelerations
2. Onset of decelerations (Figure 5.12) to protect fetal myocardium so as to maintain
a positive energy balance.
Figure 5.12
Figure 5.12: Note the appearance of decelerations.
3. The fetus will release catecholamines to redistribute blood from nonessential to
essential organs as well as compensatory tachycardia to supply vital organs and to get
oxygenated blood from the placenta at a faster rate. Note a gradually increasing
baseline from 110 to 130 bpm secondary to catecholamine surge with ongoing
decelerations (Figure 5.13), which could be easily missed.Figure 5.13
As national guidelines give a wide range (110–160 bpm), such an increase in
baseline FHR may be easily missed, if one does not understand fetal physiological
response to hypoxic stress.
4. The decelerations would become wider and deeper (Figure 5.14) with a further
increase in baseline FHR due to catecholamine release to help oxygenate the vital
organs.
Figure 5.14
Figure 5.14: Note the decelerations becoming wider and deeper with progressively
worsening hypoxic stress and an attempt by the fetus to compensate for this by further
increasing the baseline fetal FHR secondary to catecholamine surge.
However, the end of the CTG trace shows loss of baseline FHR variability
illustrating the onset of decompensation. Rapid action is required to improve fetal
oxygenation (i.e. stopping oxytocin and rapid infusion of intravenous fluids, changing
maternal position and use of tocolytics, if variability does not improve with initial
measures).5. Loss of baseline FHR variability due to lack of oxygen to the brain (Figure 5.14). If
no action is taken, myocardial hypoxia and acidosis will ensue leading to a stepwise
pattern to death culminating in terminal bradycardia.
Chapter 8. Intermittent (Intelligent)
Auscultation in the Low-Risk Setting
1. A 30-year-old primigravida presented with spontaneous labour at 39 weeks, having
had a low-risk pregnancy. On vaginal examination, cervix was 6 cm dilated, fully
effaced with the presenting part 2 to the ischial spines. Bulging membranes were felt.
She is requesting entonox for analgesia.
a. Is CTG monitoring indicated? Why?
b. On auscultation of the fetal heart, for 1 minute after the contraction, the heart rate
is heard at an average of 140 bpm. Using the principles of IA, what is your
diagnosis? What other information do you need?
c. What is your action plan following assessment?
d. Before the next vaginal examination was due, decelerations were heard using a
hand-held Doppler following a contraction. What would your actions be?
2. Having had a low-risk pregnancy, with normal scans, a 25-year-old primigravida
presented with spontaneous labour at 41 weeks and 2 days. Spontaneous rupture of
membranes was confirmed on speculum 14 hours ago. On vaginal examination, cervix
was found to be 5 cm dilated, fully effaced, and well applied to the fetal head, with the
presenting part 2 to the ischial spines. Clear liquor is noted.
a. On auscultation of FHR for 1 minute after a contraction, the fetal heart is heard at
a rate of 150 bpm. What other information do you need?
b. What are the possible causes of the findings?
c. Is CTG monitoring indicated? Why?
Answers1.
a. No. The woman is ‘low risk’, and therefore the use of CTG in this situation will
not improve the neonatal outcome, but may increase the likelihood of unnecessary
interventions.
b. Normal baseline rate, but need to listen for an acceleration to exclude chronic
hypoxia. Have the fetal movements been normal? The care provider should listen
following a contraction to ensure that there are no (late) decelerations.
c. If the aforementioned initial assessment is normal, plan for intermittent
auscultation every 15 minutes in first stage, every 5 minutes in second stage.
Mobilize, analgesia as required, reassess progress in 4 hours. If no accelerations
are heard, fetal movements are reported as reduced, or decelerations are heard
during intermittent auscultation, then a CTG is indicated.
d. Assess vaginally to exclude imminent delivery and commence CTG. If normal
for 20 minutes, then discontinue and return to intermittent auscultation.
2.
a. Are fetal movements normal? Has acceleration been heard? Are there any
decelerations? Have there been any previous CTGs or antenatal recording of the
fetal heart for comparison, as 150 bpm is high for this gestation although within
normal limits by national guidelines. What are the maternal observations? Is there
any offensive liquor?
b. Chorioamnionitis; maternal tachycardia (secondary to pyrexia or dehydration);
evolving hypoxia; normal rate for the individual fetus.
c. Yes, as this is a high baseline rate for this gestation (although within national
guidelines), and there is already a risk factor for sepsis (prolonged rupture of
membrane [PROM] 14 hours). If all observations are satisfactory and evidence
shows that this may be a normal rate (e.g. previous CTG with baseline at 150
bpm), then consider discontinuing. Continuous monitoring is indicated if PROM
>24 hours, maternal temperature, suspected chorioamnionitis.Chapter 10. Role of Uterine Contractions and
Intrapartum Reoxygenation Ratio
1. A 25-year-old primigravida at 39 weeks of gestation presented with a history of
spontaneous onset of labour. On vaginal examination, her cervix was 6 cm dilated
with the presence of grade 2 meconium staining of the amniotic fluid.
Four hours later, her labour was augmented with syntocinon (oxytocin) infusion
as there was no progress of labour, and ongoing uterine contractions were deemed
inadequate.
Two hours after commencement of syntocinon infusion, uterine contractions were
occurring 6 in 10 minutes each lasting 60 seconds on the CTG trace (Figure 10.2).
Figure 10.2
a. What is your differential diagnosis?
b. Is CTG monitoring indicated?
c. What abnormalities will be noted on the CTG based on the differential
diagnosis?
d. What is your management?
e. What will be noticed on the CTG trace if treatment is instituted?
Answers
1.
a. Uterine hyperstimulationb. Yes, it is important to monitor the FHR continuously if oxytocin infusion is used
and/or in the presence of meconium.
c. Frequent uterine contractions, less relaxation time in between contractions with a
stable baseline rate of 140 and a reassuring baseline variability. Repeated variable
decelerations with a stable baseline FHR and reassuring variability suggestive of
compensated fetal stress response.
d. Reduce oxytocin infusion in the first instance and observe for reduction in the
depth and duration of variable decelerations and increased relaxation time. If no
such changes are observed within 3–5 minutes (half-life of oxytocin), then oxytocin
infusion should be stopped. Intravenous fluids may be administered to dilute
oxytocin and to improve placental circulation. Terbutaline should be administered
if no improvement is noted with initial measures.
e. Disappearance of decelerations, more time on baseline and reappearance of
accelerations (Figure 10.3)
Figure 10.3
Figure 10.3: CTG trace 40 minutes after stopping oxytocin infusion. Note the
disappearance of decelerations and appearance of accelerations.
Chapter 11. Intrapartum Monitoring of a
Preterm Fetus1. A 24-year-old primigravida presents at 28 weeks with reduced fetal movements.
The CTG trace is shown in the figure.
Figure 11.1
a. Classify the CTG applying the ‘8Cs’ approach.
b. What are the specific features different from those of a term fetus?
c. What changes would you expect to see if you repeat the CTG in 4 weeks’ time?
d. How would you assess fetal well-being at this stage of pregnancy?
Answers
1.
a. Clinical picture: Preterm fetus, 28 weeks. Reduced fetal movements.
Cumulative uterine activity: Not registered in this case.
Cycling of FHR: This is a preterm fetus and FHR cycling may not be evident. The
autonomic nervous system is not fully developed at this stage, and therefore, an
apparent reduction variability may be seen due to unopposed activity of the
sympathetic nervous system without opposing effect of the parasympathetic nervous
system.
Central organ oxygenation: It is difficult to assess in preterm fetuses as this is
shown by the variability which, as mentioned earlier, is expected to be reduced in
preterm fetuses due to immaturity.
Catecholamine surge: The predominant component of the autonomic nervous
system is the sympathetic component, and therefore, an increased baseline rate(150–160 bpm) would be expected.
Chemo- or baroreceptor decelerations: There are some baroreceptor
decelerations which in preterm fetuses can be due to fetal movements.
Cascade: This patient has presented with reduced fetal movements. An ultrasound
scan to assess fetal growth and Doppler and computerized CTG are more appropriate
to assess fetal well-being.
b. Baseline heart rate is increased (150–160 bpm) due to the predominant effect of the
sympathetic nervous system without opposing effect of the parasympathetic nervous
system. Due to immaturity of the somatic nervous system, accelerations may be absent
or may have a low amplitude without any clinical significance.
The variability can be reduced due to immaturity of the autonomic nervous system.
The presence of variable or early decelerations is indeterminate usually secondary to
compression of the umbilical cord during fetal movements due to the absence of the
Wharton jelly and should not trigger delivery on a preterm fetus.
c. Consider the NEXT Change on the CTG if pregnancy is allowed to continue The
baseline rate will decrease to ranges between 140 and 150 bpm, as the
parasympathetic system develops. For the same reason, variability will also increase
as the gestation advances. Accelerations would become more pronounced with the
maturation of the somatic nervous system.
d. In preterm fetuses, fetal well-being is more reliably assessed by Doppler and
short-term variability on computerized CTG as the usual features (baseline FHR,
variability and decelerations) analysed are unreliable in fetuses <32 weeks.
Chapter 12. Role of Chorioamnionitis and
Infection
1. A primigravida was admitted for induction of labour at 41 weeks + 3 days of
gestation. She had no antenatal risk factors. CTG trace was commenced (Figure 12.3).Figure 12.3
a. How would you classify the CTG trace?
b. What is your management plan?
A plan was made for expectant management and the maternal pulse rate was noted
to be 108 bpm.
c. What is the likely diagnosis?
d. What is your management plan?
e. What are the signs and symptoms you would be anticipating in this case?
A plan was made to continue with labour. Three hours later, maternal temperature
was recorded as 38.2°C. Paracetamol and intravenous antibiotics were administered.
Six hours later, cervix was found to be 4 cm dilated and artificial rupture of membranes
was carried out and meconium staining of amniotic fluid was noted.
f.
What is your diagnosis?
g. What is your management plan and why?
Answers
1.
a. According to guidelines, this would be a suspicious CTG as the baseline FHR is
between 160 and 180 bpm. The absence of cycling (alternative periods of activity
and quiescence) has been persisting for >40 minutes.b. The baseline FHR would be expected to be closer to the lower limit of normal
(i.e. 110 bpm) at 41 weeks + 3 days due to parasympathetic dominance. Although
the absence of accelerations during established labour is of uncertain significance,
accelerations should always be observed during the antenatal period or in early
labour. In addition, the absence of cycling reflects depression of the central
nervous system centres (sympathetic and parasympathetic that control the heart
rate). Therefore, in view of an increased baseline FHR and absence of cycling, a
strong index of clinical suspicion of subclinical chorioamnionitis should be made.
In the absence of decelerations, chronic hypoxia is unlikely and maternal
dehydration may cause fetal tachycardia but not absence of cycling or loss of
accelerations.
Therefore, a careful observation of other features of chorioamnionitis (maternal
tachycardia, maternal pyrexia, meconium staining of amniotic fluid) should be
carried out. One needs to remember that hypoxia secondary to the onset of uterine
contractions worsens neurological injury in the presence of fetal infection.
c. Onset of maternal tachycardia strongly suggests ongoing subclinical
chorioamnionitis.
d. If the CTG trace continues to show increased baseline FHR as compared to
expected 110 bpm and loss of accelerations and cycling, delivery should be
recommended. This is because the patient is a primigravida and delivery is not
imminent and continuation of labour would not only result in prolonged exposure of
the fetal brain to inflammatory mediators, but it may also result in additional
hypoxic stress secondary to uterine contractions.
Note uterine irritability and presence of episodes of ‘saltatory pattern’ on the
CTG trace suggestive of possible chorioamnionitis. Saltatory pattern has been
described in cases of fetal infection (autonomic instability due to increased
temperature).
e. Maternal tachycardia, meconium staining of amniotic fluid and offensive vaginal
discharge.f.
Clinical chorioamnionitis – beyond any reasonable doubt.
g. As delivery is not imminent and she is a primigravida, an emergency ‘category
2’ caesarean section (aim to deliver within the next 60 minutes) should be
performed. This is because continuation of labour may lead to neurological damage
and decompensation of the brain. Inflammatory damage to the myocardium may
result in myocardial dysfunction and cardiac membrane damage leading to terminal
bradycardia.
The absence of variability and of cycling are hallmarks of decompensation of the
central nervous system secondary hypoxia, acidosis and inflammatory brain
damage, and continuation of labour when delivery is not imminent may lead to
myocardial decompensation and terminal bradycardia.
Comment: This case illustrates the role of CTG in highlighting ongoing
subclinical chorioamnionitis and the importance of avoiding additional hypoxic
stress (prostaglandins, artificial rupture of membranes and use of oxytocin to
augment labour) unless fetal well-being could be absolutely determined based on
the features observed on the CTG trace. An increase in baseline FHR (albeit within
the normal range of 110–160 bpm) for the given gestation with absence of
accelerations and cycling are ominous features, and delivery should always be
considered if it is not imminent. Continuation of labour may result in additive
detrimental effects of hypoxic stress (uterine contractions and umbilical cord
compression) on a fetus already experiencing inflammatory damage and thereby
may potentiate neurological injury.
Chapter 14. Intrapartum Bleeding
1. A 36-year-old primigravida presented with a history of painless vaginal bleeding
with reduced fetal movements at 40 weeks of gestation. On examination, the abdomen
was soft and nontender and FHR was 160 bpm. On speculum examination, fresh vaginal
bleeding was noted.
a. What is your differential diagnosis?b. Is CTG monitoring indicated?
c. What abnormalities on the CTG would be expected based on your differential
diagnosis?
d. CTG was commenced and the following features were noted (Figure 14.5). What
is your diagnosis?
Figure 14.5
e. What is your management?
Answers
1.
a. Revealed abruption, unrecognized placenta praevia, local causes and vasa
praevia.
b. Yes, it is important to exclude fetal hypoxia if bleeding was of fetal origin.
c. Abruption – recurrent late decelerations with loss of baseline FHR variability.
Vasa praevia – atypical sinusoidal pattern (‘poole shark teeth pattern’).
d. Atypical sinusoidal pattern (poole shark teeth pattern) and therefore fetomaternal
haemorrhage.
Apply 8Cs while interpreting CTG traces:
Clinical picture – unexplained vaginal bleeding and reduced fetal movements
Cumulative uterine activity (frequency and duration) – 5 in 10 minutesCycling of FHR – none
Central organ oxygenation – baseline is stable but loss of variability with
atypical sinusoidal pattern, also called the ‘poole shark teeth pattern’
Catecholamine surge – yes, baseline is higher than expected at 40 weeks
Chemo- or baroreceptor decelerations – none
Cascade – High risk with evidence of CNS hypoxia likely from fetomaternal
haemorrhage – needs immediate delivery
Consider next change – myocardial decompensation and terminal bradycardia
e. Clear explanation to the woman regarding the possibility of ongoing fetal
hypoxia and hypotension secondary to fetal bleeding. Immediate delivery (category
1 C-section) and inform the neonatal team regarding the need to check haemoglobin
and for immediate fluid resuscitation and blood transfusion in view of likely fetal
hypotension.
This patient had an emergency caesarean section and a ruptured vasa praevia
(Figure 14.4).
Figure 14.4 Note the ruptured vasa praevia in a case with an atypical sinusoidal patternwith a ‘jagged edge’ resembling ‘Poole Shark Teeth’.
Chapter 15. Labour with a Uterine Scar: The
Role of CTG
1. A 36-year-old gravida 2 para 1 with a previous caesarean section for failure to
progress in labour was admitted with spontaneous onset of labour. Cervix was 6 cm
dilated and the presenting part was at 0 station and the CTG trace was classified as
normal. Oxytocin was commenced at 23:00 hours for failure to progress in labour as her
cervix had remained 6 cm 2 hours after artificial rupture of membranes.
a. Classify the CTG trace (using the ‘8C’ format).
Figure 15.1
b. What are effects of oxytocin on myometrial contractions and what changes would you
observe on the CTG trace?
c. Consider the CTG trace from 02:58 hours.Figure 15.2
1. What is the type of hypoxia?
2. What are the differential diagnoses?
3. What immediate actions would you take?
d. What is the likelihood of the observed CTG change to return back to normal in this
case?
e. What would you expect to see in the umbilical cord gases if delivery was
accomplished within 20 minutes of the onset of this acute, prolonged decelerations?
Answers
1.
a. Apply 8Cs while interpreting CTG traces.
Clinical picture – previous caesarean section, oxytocin augmentation
Cumulative uterine activity (frequency and duration) – no contractions
recorded at present
Cycling of FHR – present; presence of periods of accelerations and good
variability alternating with periods of quiescence with reduced variability
Central organ oxygenation – good variability reflecting good oxygenation of
the central nervous system (brain)
Catecholamine surge – no, baseline is about 145 bpm
Chemo- or baroreceptor decelerations – no decelerations presentCascade – risk of uterine rupture in the presence of a uterine scar and oxytocin
augmentation
Consider next change – In the presence of oxytocin augmentation, if there is a
uterine dehiscence, repetitive decelerations will be recorded; however, if there is a
complete uterine, a prolonged deceleration with loss of variability within the first
3 minutes will appear.
b. Oxytocin produces stronger and more frequent contractions. If oxytocin continues
to be increased, uterine tachysystole/hypertonia on the ‘toco’ component may be
observed and presence of decelerations on the ‘cardiograph’.
If there is uterine dehiscence, repetitive decelerations and loss of variability
will appear; and if it is a complete rupture, a prolonged deceleration would be
observed.
c.
1. Acute hypoxia
2. Differential diagnosis includes:
• Uterine scar rupture
• Cord prolapse
• Abruption
• Iatrogenic causes (oxytocin causing hypertonia, epidural causing
hypotension)
3. Stop oxytocin, prepare for an immediate delivery as there is loss of baseline
variability within the first 3 minutes of deceleration and the clinical diagnosis is
uterine rupture. In this case, the ‘3, 6, 9, 12, 15’ rule cannot be applied.
Immediate delivery is the appropriate management in this clinical scenario.
d. In the presence of one of the three major accidents, prolonged deceleration
would not be expected to recover as fetal hypoxia can only get worse over time.
If a prolonged deceleration is due to iatrogenic causes and in the absence ofthree major accidents, 90 percent of these decelerations will recover in 6
minutes within the onset of deceleration and 95 percent by 9 minutes.
e. The rate of fall in pH during acute hypoxia is 0.01 per minute. The CTG prior
to the onset of prolonged deceleration was normal, and we would expect a
normal pH of around 7.25. If the delivery is accomplished within 20 minutes, the
pH will drop by 0.2 unit (0.01 × 20 = 0.2), and therefore the umbilical cord
arterial pH at birth would be expected to be around 7.05.
Chapter 16. Impact of Maternal Environment
on Fetal Heart Rate
Figure 16.1
1. A 31-year-old primigravida presents to the labour ward at 37 weeks of gestation with
a history of regular contractions. She was diagnosed with type 1 diabetes at the age of
11 and uses insulin pump therapy. Her HBA1c at booking was 56 mmol/mol and control
has been difficult during pregnancy. She appears dehydrated and urine dipstick shows
>3 ketones. On admission she is found to be 3 cm dilated and CTG monitoring is
commenced. The following trace is observed:
a. How would you classify the CTG?
b. What do you need to consider given her history and how might it impact upon the
CTG?
c. How will you manage her?Answers
1.
a. The CTG can be described using the 8Cs technique:
Clinical picture: The mother is a poorly controlled type 1 diabetic in early
labour. She is showing signs of diabetic ketoacidosis, a form of metabolic
acidosis.
Cumulative uterine activity: Contraction frequency is 2 in 10, and each
contraction is lasting approximately 60 seconds in duration.
Cycling: There is no evidence of cycling on this portion of the CTG.
Central organ oxygenation: Baseline variability is reduced (between 3 and 5),
indicating that central nervous system centres (sympathetic and parasympathetic)
are depressed. Causes include fetal sleep, drugs (opiates), hypoxia and acidosis.
Chemoreceptor/baroreceptor decelerations: There is no evidence of
decelerations mediated by either chemo- or baroreceptors. However, in cases of
severe maternal acidosis, loss of variability may occur before the onset of
decelerations.
Catecholamine surge: The baseline heart rate is stable, without the rise that
usually appears in cases of gradually evolving hypoxia. However, in cases of
severe maternal acidosis, reduced baseline variability may be the first change seen
on the CTG trace, even in the absence of acidosis.
Compute and cascade: There is evidence of severe maternal acidosis in the
form of diabetic ketoacidosis, which may be causing the CTG changes. A full
assessment of the mother is required, and treatment of ketoacidosis should be
urgently instituted to optimize maternal condition
Consider next change: Given that central nervous system centres are already
depressed secondary to passive transfer of maternal acidosis, any further hypoxic
stress will cause myocardial decompensation and prolonged deceleration.
b. There is evidence of severe maternal acidosis; in such fetuses, baseline
variability may be lost before the onset of decelerations and a rise in baseline
FHR.c. Management involves treatment of the cause of CTG change. A full assessment of
the mother must be made by performing blood glucose and blood gas testing. Urea
and electrolytes should also be checked and IV (intravenous) access obtained. If
diabetic ketoacidosis is confirmed, the mother should be treated using an
insulin/dextrose infusion, with careful monitoring of potassium levels. Care should
be multidisciplinary, with involvement from anaesthetic and medical teams.
Chapter 17. Use of CTG with Induction and
Augmentation of Labour
1. A 30-year-old, G2 P1, previous caesarean section is being induced for postdates (41
+ 4 weeks of gestation). She had prostaglandin pessary inserted for 24 hours, following
which she had an artificial rupture of membranes (ARMs) that showed meconium grade
1. Two hours later, she was started on oxytocin infusion. Oxytocin has been augmented
every 30 minutes as per protocol. CTG trace before the ARM was normal with a
baseline FHR of 130 bpm, variability of 10–15 bpm, presence of accelerations with no
decelerations and she had two contractions in 10 minutes.
CTG after 8 hours of oxytocin augmentation shows the following features.
Figure 17.2
a. What is your diagnosis?
b. What is your management?
c. What other complications do you expect?Answers
1.
a. Apply 8Cs while interpreting CTG traces:
Clinical picture: induction of labour followed by oxytocin augmentation;
previous caesarean section; meconium grade 1; postterm fetus
Cumulative uterine activity (frequency and duration): 6 in 10 minutes
Cycling of FHR: none
Central organ oxygenation: good variability in between decelerations
reflecting good oxygenation of the central nervous system (brain)
Catecholamine surge – yes, baseline is higher than expected (160 bpm) at 41 +
4 weeks and was previously recorded.
Chemo- or baroreceptor decelerations – baroreceptor deceleration due to
umbilical cord compression; note the shouldering before and after deceleration,
sharp fall of the FHR followed by a quick recovery to the normal baseline.
Cascade – risk of uterine rupture, meconium aspiration and fetal hypoxia if
oxytocin augmentation continues
Consider next change – decelerations will become longer-lasting with delayed
recovery, and there may be loss of shouldering. Onset of metabolic acidosis would
result in delayed recovery to the baseline due to chemoreceptor-mediated
response.
b. Stop/reduce oxytocin infusion. Consider tocolysis if frequency of contractions
persists and there is no improvement on the CTG trace.
c. Uterine rupture as patient has a previous caesarean section. Meconium aspiration
syndrome and if above interventions are delayed and if fetal decompensation
ensues, fetal hypoxic-ischaemic encephalopathy (HIE).
Chapter 19. Unusual Fetal Heart Rate Patterns:
Sinusoidal and Saltatory Patterns1. A 35-year-old primigravida presents at 38 weeks of gestation with abdominal pain
for 3 hours and reduced fetal movements with no vaginal bleeding. On examination,
uterine contractions were palpated and the cervix was fully effaced, 2 cm dilated.
a. What is your differential diagnosis?
b. Is a CTG indicated?
c. She was re-examined in 4 hours and established to be in labour. She was later
commenced on oxytocin for confirmed delay in the first stage of labour. Vaginal
examination after 4 hours of oxytocin demonstrated that she was 8 cm dilated. Describe
the CTG at this stage (Figure 19.3). Do you have any concerns?
Figure 19.3
d. She opted for an epidural anesthesia and is now fully dilated and has had a 2-hour
passive descent. A repeat vaginal examination suggests that she is fully dilated with the
fetal head in occipito-anterior position, at station +1. A decision has been made to start
active pushing. She has been actively pushing for 20 minutes and CTG is given below
(Figure 19.4). How would you describe the CTG?
Figure 19.4
e. What is your management plan based on the features observed on the CTG (Figure
19.4)?Answers
1.
a. Early labour or a concealed placental abruption
b. Yes – to exclude fetal hypoxia due to the history of reduced fetal movements
c. No – baseline 130 bpm, variability 5–10 bpm, accelerations present, no
decelerations. Overall normal CTG trace as autonomic and somatic nervous
systems are well oxygenated with the presence of accelerations and cycling.
d. Saltatory pattern – baseline FHR not defined, fetal heart baseline amplitude
changes of >25 bpm with an oscillatory frequency of >6 per minute, occurring for
15 minutes
e. Stop or reduce oxytocin to improve utero-placental circulation. In view of
persisting saltatory pattern, the woman should be advised to stop active pushing in
the second stage of labour to improve fetal oxygenation. CTG trace should be
carefully observed for improvement (i.e. reappearance of a stable baseline FHR
and reassuring variability). If no improvement is seen on the CTG trace, delivery
should be accomplished. If immediate delivery is not possible, terbutaline should
be administered while the woman is transferred to the operating theatre.
Apply 8Cs while interpreting CTG traces:
Clinical picture: 38 weeks presenting with abdominal pain and reduced fetal
movements
Cumulative uterine activity: 7 out of 10 minutes
Cycling of FHR: absent
Central organ oxygenation: absent stable baseline with variability >25 bpm
Catecholamine surge: Yes, there are attempts to increase FHR to 180 bpm
Chemo- or baroreceptor decelerations: Yes – repeated baroreceptor
decelerations
Cascade: Rapidly evolving hypoxia may lead to fetal overshoots and saltatory
patterns; therefore, stop or reduce oxytocin or consider intravenous fluids or
tocolysis.Consider next change: Myocardial decompensation and terminal bradycardia
Chapter 20. Intrauterine Resuscitation
1. A 29-year-old primigravida presented with spontaneous early labour at 39 + 4 weeks
of gestation. She was commenced on oxytocin at 5 cm dilation for failure to progress.
One hour later, her CTG trace (Figure 20.2) shows the following features.
Figure 20.2
a. What is your diagnosis?
Two hours later, the CTG trace shows the following features (Figure 20.3):
Figure 20.3
b. What is your diagnosis?
c. What action will you take?Answers
1.
a. Uterine tachysystole – frequent/excessive uterine contractions with a normal
cardiograph
b. Uterine hyperstimulation – frequent/excessive uterine contractions with
associated changes in the cardiograph (i.e. decelerations and/or changes in
baseline)
c. Stop oxytocin, consider fluid infusion to dilute oxytocin in systemic circulation,
then reassess the CTG trace. If decelerations do not improve and a stable baseline
FHR and variability are not maintained within 3–5 minutes (half-life of oxytocin),
consider administration of tocolytics.
Apply 8Cs to interpreting CTG traces:
Clinical picture: oxytocin administration for failure to progress
Cumulative uterine activity: 15 in 20 minutes
Cycling of FHR: none
Central organ oxygenation: initially good variability and return to baseline
heart rate indicating good fetal reserve; however, with repeated stress, the baseline
heart rate falls, suggestive of myocardial hypoxia and acidosis, and there is
reduced variability within deceleration (hypoxia to the central nervous system)
Catecholamine surge: attempts at increasing the baseline heart rate, but due to
repeated decelerations, a progressive reduction in baseline fetal heart rate is
observed.
Chemo- or baroreceptor decelerations: baroreceptor decelerations with a
sharp fall and a rapid recovery to the baseline. However, some decelerations
demonstrate a delayed recovery suggestive of a co-existing chemoreceptor
response as well. This is because, in addition to umbilical cord compression,
oxytocin-induced sustained uterine contractions may also reduce utero-placental
circulation leading to acidosis within the placental venous sinuses.
Cascade: suspected fetal compromise due to excessive uterine contractionsConsider next change: If no action is taken, due to progressive myocardial
hypoxia and acidosis, prolonged deceleration culminating in a terminal
bradycardia would ensue.
Management: Stop oxytocin, consider fluid infusion to dilute oxytocin in
systemic circulation, and if CTG changes, do not normalize within 3–5 minutes
(half-life of oxytocin), then consider administration of tocolytics.
Chapter 21. Management of Prolonged
Decelerations and Bradycardia
Figure 21.4
1. A primigravida is induced at 41 + 5 weeks of gestation for postdates after a normal
pregnancy. The CTG up to this point has been entirely normal with a baseline rate of
130 bpm and variability of 5–15 bpm. At 11:49, a deceleration begins and the attending
midwife appropriately moves the mother into the left lateral position.
You are called to the room at 11:54.
a. What are the first steps you would take to assess the patient?
b. What is the likely cause of this prolonged deceleration?c. What would your management be?
d. What features on the CTG are reassuring?
e. What features on the CTG are concerning?
Now consider the trace again (Figure 21.5).
Figure 21.5 CTG trace from 11:55 to 11:56.
f.
What phenomenon is demonstrated at 11:55–11:56?
g. Terbutaline is administered at 11:57. At 11:58 what would your next action be?
Figure 21.6 CTG trace after administration of terbutaline.Figure 21.6 shows the full trace indicating first recovery of the baseline and second
restoration of normal variability suggesting an intact neurological system. The
tocograph clearly demonstrates that the uterine activity has been temporarily
abolished.
h. What might you expect to see next on the CTG?
Answers
1.
a. Examine the patient – BP and pulse, abdominal palpation and vaginal
examination particularly for signs of abruption, cord prolapse or uterine rupture.
b. Barring any evidence on physical examination of one of the three accidents, this
deceleration is clearly in response to the prolonged uterine activity recorded on the
tocograph and represents the fetal response to uterine hyperstimulation.
c. Stop any syntocinon or consider removing prostaglandins if still present. Keep
the patient in left lateral and correct any hypotension with intravenous fluids. Give
terbutaline 250 mg subcutaneously as soon as possible.
d. The preceding CTG was normal and the variability in the first 3 minutes is
normal.
e. The variability is lost as deceleration progresses and the FHR drops < 80.
f.
The FHR here is being doubled to give a falsely high reading. This would be
clear to clinicians in the room if the ‘sound’ is turned on as a lower heart rate
would be audible.
g. At 1158, one should know that the fetus was normally oxygenated at the onset of
deceleration and that the cause of deceleration is uterine tone, and therefore
management of the underlying cause should be undertaken (i.e. uterine relaxation)while remaining prepared for an emergency delivery. It is expected that the
baseline will recover within the next 1–2 minutes.
h. After deceleration, one would expect to see a rebound tachycardia; however, a
strong fetus with good reserves will rapidly settle back down to the original
baseline unless another source of stress causes need for further adrenaline release.
Terbutaline itself may cause a transient fetal tachycardia.
Chapter 30. Medico-legal Issues with CTG
1. A 28-year-old gravida 2 is in spontaneous normal labour. She has no high-risk factors
and she is in the active second stage of labour. She was monitored for audible
abnormality of the FHR. Abdominally the fetus was estimated to be 3.8 kg and the head
was 0/5th palpable. Vaginally there was clear amniotic fluid, she was fully dilated, and
the occiput was in left occipito transverse position at station 0 to +1. There is ++ caput
and ++ moulding. The CTG trace is shown in Figure 30.6.
Figure 30.6
Describe your plan of action.
a. Observe for another hour
b. Perform FBS
c. Perform caesarean section
d. Perform instrumental deliverye. Give acute tocolysis and await further descent
Answer
The decelerations are getting more and more prolonged (>2 minutes), and the FHR
remains at the baseline rate only for about 30 seconds. The baseline variability has
become salutatory suggestive of possible acute hypoxia. This would warrant
immediate instrumental vaginal delivery in the next 15 to 30 minutes.
Nhận xét
Đăng nhận xét