intrapartum fetal monitoring

1. • Basic CTG features
• Tracing classification
Tracing analysis
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2. Mean level of the most horizontal and less oscillatory
FHR segments. Estimated in 10-min periods, expressed
in bpm
Baseline
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3. Normal 110-160 bpm
Tachycardia
> 160 bpm for more than 10 min (pyrexia,
epidural, early stages of non-acute hypoxemia,
β agonist or parasympathetic drugs, arrhythmias)
Bradycardia < 110 bpm for more than 10 min
(hypothermia, beta-blockers and fetal arrhythmias)
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4. Average bandwidth amplitude in 1-min
segments
Variability
1 min
120
125
115
Subjectivity in visual evaluation
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5. Reduced
variability
< 5 bpm for more than 50 min in baseline
or more than 3 min in decelerations
• Hypoxia/acidosis of CNS, previous cerebral injury, infection, CNS
depressants or parasympathetic blockers
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6. Increased
variability
(saltatory)
Bandwidth > 25 bpm for more than 30 min
• Incompletely understood
• Hypoxia/acidosis of rapid evolution
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7. Abrupt increases in FHR above baseline, > 15 bpm
amplitude, > 15 secs
Accelerations
• Most coincide with fetal movements
• Reactive fetus without hypoxia/acidosis
150
130
140
120
>15 s
>15 bpm
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8. Abrupt decreases in FHR below baseline, > 15 bpm
amplitude, > 15 secs
Decelerations
150
130
140
120
>15 s
>15 bpm
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9. Early
decelerations
Shallow, short-lasting, with normal
variability and coincident with contractions
• Believed to be caused by fetal head compression
• Do not indicate fetal hypoxia/acidosis
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10. Variable
decelerations
Rapid drop (onset-nadir in < 30 sec), rapid
recovery, good variability. Varying size,
shape and relation to uterine contractions
• Baroreceptor-mediated response to ↑ BP (cord compression)
• Seldom associated with important hypoxia/acidosis
• Majority of decelerations
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11. Late
decelerations
Gradual onset and/or gradual return to
baseline, and/or reduced variability.
Onset > 20 sec after start of contraction, nadir
after acme and return to baseline after end
• Chemoreceptor-mediated response to hypoxemia
• With  variability and no accelerations, amplitude only > 10 bpm
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12. Prolonged
deceleration
> 3 min
• Likely to include a chemoreceptor-mediated component
• If > 5 min,  variability, and FHR < 80 bpm  emergency intervention
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13. • Severe anemia, acute hypoxia/acidosis, infection, cardiac
malformations, hydrocephalus, gastroschisis
Sinusoidal
pattern
Regular, smooth, undulating, resembling
sine wave. Amplitude 5-15 bpm, frequency
3-5 cycles/min, > 30 min, no accelerations
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14. Pseudo-sinusoidal pattern
• Analgesic administration, fetal sucking and other mouth movements
Pseudo-
sinusoidal
pattern
Jagged “saw-tooth” appearance. Duration
seldom exceeds 30 min. Normal patterns
before and after
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15. Tachysystole
> 5 contractions in 10 min in two successive
10-min periods, or averaged over 30 min.
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16. Body
movements
Eye
movements
+ +
Active sleep
-
-
CTG
Deep sleep
+++ +
Active awakeness
• Cycling represents the hallmark of neurological responsiveness
• Transitions become clearer > 32-34 weeks
• Deep sleep may last 50 min
Behavioural states
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17. Deep sleep Active sleep
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18. Active awakeness (difficulty in baseline estimation)
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19. Tracing classification
*Decelerations are repetitive when associated with > 50% contractions.
Absence of accelerations in labour is of uncertain significance.
Baseline
Variability
Decelerations
Interpretation
Clinical
Management
Normal
110-160 bpm
5-25 bpm
No repetitive*
decelerations
Suspicious
Lacking at least one
characteristic of
normality, but with
no pathological
features
Pathological
< 100 bpm
Reduced variability.
Increased variability.
Sinusoidal pattern.
Repetitive* late or prolonged
decelerations for > 30 min (or > 20
min if reduced variability).
Deceleration > 5 min
No
hypoxia/acidosis
No intervention
necessary to
improve fetal
oxygenation state
Low probability of
hypoxia/acidosis
Action to correct
reversible causes if
identified, close
monitoring, or
adjunctive methods
High probability of
hypoxia/acidosis
Immediate action to correct
reversible causes, adjunctive
methods or if this is not possible
expedite delivery.
In acute situations, immediate
delivery should be accomplished.
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20. Clinical decision
• gestational age
• medication administered to the mother
• integrated with clinical information
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21. Baseline 130 bpm
Accelerations
Non-repetitive decelerations
Normal variability
Case 1
Normal
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22. Baseline 154 bpm
No accelerations
Non-repetitive decelerations
Normal variability
Normal
Case 2
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23. Baseline 180 bpm
No accelerations
Repetitive late decelerations (> 30 min)
Reduced variability (> 50 min)
Pathological
Case 3
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24. Baseline 140 bpm
No accelerations
Repetitive variable decels. (1 late+ prol)
Normal variability
Suspicious
Case 4
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25. Baseline 148 bpm
Accelerations
Repetitive decelerations, one > 5 min
Reduced variability at the end
Case 5
Pathological
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26. Baseline 130 bpm
Accelerations
Repetitive decels (not late/prolonged)
Normal variability
Case 6
Suspicious
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27. Baseline 132 bpm
Acceleration
Deceleration > 5 min
Reduced variability in deceleration
Case 7
Pathological
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28. Baseline 146 bpm
No accelerations
Repetitive variable decels (1 prolonged)
Normal variability
Case 8
Suspicious
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29. Reversible causes
Excessive uterine activity ( oxytocics,
tocolysis)
Supine position (change maternal positions)
Sudden hypotension (fluids, ephedrine)
Irreversible causes
Uterine rupture
Major placental abruption
Umbilical cord prolapse
Maternal or mechanical complications
Fetal haemorrhage
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30. Intravenous
salbutamol started
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31. Limitations of CTG
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32. Signal loss
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33. MHR monitoring
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34. CTG analysis is subject to considerable
intra- and interobserver disagreement
(decelerations, variability, suspicious-pathological)
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35. High predictive
value for NO
hypoxia/acidosis
Low predictive
value for
hypoxia/acidosis
Limited predictive value of abnormal CTGs
BJOG 1993;100(suppl 9):4-7
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36. Cochrane Database Syst Rev. 2013 May 31;5:CD006066
12 trials (circa 37,000 women)
↓ neonatal seizures (RR=0.50, 95%CI 0.31-0.80)
↑ c-sections (RR=1.66, 95%CI 1.30-2.13)
↑ instrumental deliveries (RR=1.16, 95%CI 1.01-1.32)
= perinatal mortality (RR=0.85, 95%CI 0.59-1.23)
= cerebral palsy (RR=1.20, 95%CI 0.52-2.79)
RCTs comparing CTG with IA
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37. • Trials carried out > 25 years ago
• Different CTG monitor technologies
• Different interpretation guidelines
• Different experience with CTG
• Different use of adjunctive methods
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38. The evidence for the benefits of CTG
when compared to IA is inconclusive
Difficult to establish how these RCTs
relate to current clinical practice
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39. CTG monitoring should not be
regarded as a substitute for good
clinical observation and judgement,
or as an excuse for leaving the
mother unattended
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40. 2nd BREAK
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