1. Intrapartum CTG

2. Which is the most important factor that influence the FHR?
There are many factors that can influence the fetal heart rate; hypoxia is potentially the most important factor

3. What is hypoxia?
Hypoxaemia  - low level of oxygen content in arterial blood
Hypoxia  - deficiency of oxygen in tissue
Asphyxia - impairment of tissue oxygenation with accumulative carbon dioxide and anaerobic metabolism, thereby causing metabolic acidosis.
IT IS MAINLY ACIDOSIS WHICH HARMS THE FETUS

4. Why is it we need to known about fetal hypoxia?
Fetal hypoxia is a major cause for perinatal death, neonatal morbidity and neurodevelopmental disability.
It can lead to complex medico–legal consequences. 

5. What are the causes of fetal hypoxia?

6. What are the intrapartum risk factors for development of fetal hypoxia?
preterm labour
suspected chorioamnionitis or sepsis, or temperature of 38°C or above
intrapartum pyrexia – infection
thick meconium with scanty fluid
prolonged rupture of the membranes
intrapartum haemorrhage
induced/augmented labour, hyperstimulation
cord prolapse
scar rupture
epidural anaesthesia

7. How does fetal hypoxia affect FHR pattern?
Brain stem centres influence acceleration of FHR with movement.
Baseline variability is a reflection of the integrity of the autonomic nervous systems.
These centres are sensitive to hypoxia, and changes in the FHR pattern may suggest hypoxia.

8. What are the types of fetal hypoxia?
Gradually developing hypoxia
Long-standing (chronic) hypoxia
Acute hypoxia
Sub-acute hypoxia

9. When is gradually developing hypoxia seen?
Gradually developing hypoxia is seen in normal fetus to begin with
It can be due to
oligamnios causing repeated episodes of occlusion of the umbilical cord
prolonged pregnancy with reduced placental perfusion

10. What are the Stages of Gradually developing hypoxia?

11. Stage 1
Stress pattern
Reactive FHR pattern → Decelerations without a rise in baseline rate or reduction in baseline variability

13. Stage 2 Stress to distress pattern
Absence of accelerations →rise in the baseline rate up to the possible maximum (20-30)→ reduction in baseline variability <2 (hypoxia of the autonomic nervous system)
The fetus has no capacity to increase the cardiac output by increasing the stroke volume
surge of catecholamine → increases heart rate and causes vaso-constriction in the peripheral circulation to divert the blood to the brain, heart and the adrenal glands.

15. Stage 3 Distress to collapse pattern
In the absence of timely intervention, the FHR may suddenly decline in a stepwise manner leading to terminal bradycardia

16. This period is termed distress to collapse (or death) interval and is usually short (20–60 minutes) once the FHR starts to decrease

17. How does the fetus with long standing (chronic) hypoxia present?
Already hypoxic fetus presents with a nonreactive trace with baseline variability of less than 5 bpm (usually <2 bpm).
It may also exhibit shallow late decelerations of less than 15 beats from the baseline, with the onset of uterine contractions.
With the contractions of labour, there may be sudden bradycardia and fetal death within a relatively short time (1–2 hours) because of rapidly developing metabolic acidosis. 

19. How does acute hypoxia present?
In acute hypoxia – such as that due to abruption, scar dehiscence or cord prolapse – there may be prolonged deceleration of less than 80 beats per minute.

20. What are the three types of acute hypoxia?
single prolonged deceleration – the acute hypoxia lasts for less than 3 minutes and then recovers to normal baseline
prolonged decelerations – lasting for more than 3 minutes
prolonged baseline bradycardia – the FHR remains below 100 bpm (80 bpm in severe cases of hypoxia) for over 10 minutes.

21. What are the reversible iatrogenic causes of acute bradycardia?
Hypoperfusion due to maternal hypotension or epidural top-up
vaginal examination
Uterine hyperstimulation due to oxytocin infusion
In more than 50% of cases no cause may be identified

22. What is the effect of acute hypoxia?
The fetal pH drops at the rate of 0.01 per minute

23. What do you do with this brady trace?
Rule out abruption, scar dehiscence or cord prolapse → the variability during the episode of deceleration or bradycardia is normal and the CTG prior to the deceleration was normal → wait
In the absence of the these three major accidents, over 90% of CTGs with prolonged bradycardia are likely to recover to normal baseline in 6 minutes and up to 95% in 9 minutes.

24. What is 3-, 6-, 9- and 12-minute rule?
However, a delivery conducted within 12 minutes of the development of a fetal bradycardia does not always guarantee a good outcome
The 3-, 6-, 9- and 12-minutes rules for a prolonged fetal bradycardia were originally proposed by Gibb and Arulkumaran (2008) and are as follows

25. What is subacute hypoxia?
Fetus spends 2-3times more time at decelerations than at the base line rate, and the drop of the FHR is below 80 bpm → circulation may not be sufficient for optimal gas exchange → this leads to fetal hypoxia and acidosis at a fast rate.
This type of FHR pattern is called the 'sub-acute hypoxic' pattern

27. Predictability of hypoxia?
A normal reactive trace indicates that the fetus is not hypoxic
A pathological trace is associated with a large number of false positives
Intervention on the basis of an abnormal trace alone will increase the caesarean section and instrumental delivery rate with only a 50% chance of fetal acidosis

28. Intra-uterine resuscitation
Alteration of maternal position
Hydration
Use of oxygen
Intravenous hypertonic dextrose
Amnioinfusion
Reduction or abolition of uterine activity/acute tocolysis.

29. Alteration of maternal position
A 15° lateral tilt can increase cardiac output by 20–25% and stroke volume by 25–30%, and decrease heart rate by 5–6 bpm

30. Hydration
In hypovolemic or hypotensive women, fluid boluses of 500 ml/hr over 20 minutes have been shown to improve fetal oxygenation
after administration of an epidural
in antepartum haemorrhage
after the administration of hydralazine

31. Use of oxygen
Maternal facial oxygen therapy should not be used for intrauterine fetal resuscitation in well oxygenated mother because it may harm the baby
Maternal facial oxygen is for maternal indications such as hypoxia or as part of preoxygenation before a potential anaesthetic.

32. Intravenous hypertonic dextrose
Bolus doses of dextrose is of little value and there is evidence that it could be harmful, particularly in a growth restricted fetus.

33. Amnioinfusion in meconeum stained liquor
There is a reduction in the rate of caesarean section due to fetal distress
No statistically significant difference in overall caesarean section rate
No improvement in neonatal outcomes

34. Summary Remember the SPOILT mnemonic: Stop oxytocin
Position – adopt left lateral position
Oxygen – before anaesthesia
IV fluid bolus
Low BP – consider vasopressors, ephidrine
Tocolysis