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Dr Majaz Ahmed Khan
Neonatology fellow
Done by-
1. Fetal heart rate (FHR) monitoring
2. Fetal blood sampling (FBS).
3. Fetal pulse oximetry
4. Fetal electrocardiograpy Supplementary methods
5. Ultrasound
Fetal heart rate (FHR) monitoring
 Fetal parasympathetic nervous system Matures
by Term.
 Sympathetic nervous system development is still
ongoing even after delivery.
 Fetus is conditioned to thrive in a mildly hypoxic and
acidic environment.
 Change in fetal heart rate, caused by the impact of
hypoxia and acidosis which forms the premise of FHR
it is based on the assumption that fetal heart rate is a
reflection of fetal oxygenation status.
 Electronic fetal monitoring (EFM)> Doppler> Auscultation.
 Electronic fetal monitoring (EFM)-Is a paper record of FHR
pattern plotted simultaneously in relation to uterine activity.
 So-
i. Intermittent auscultation alone for low-risk pregnancies
ii. Continuous EFM for pregnancies with higher risk.
FHR
surface transducers
on the maternal
abdomen
Not feasible in morbid
obesity.
small electrode into
the skin of the fetal
presenting part
Requires dilatation of the
cervix and rupture of the fetal
membranes
Mild infection at the
electrode site.(4%)
Uterine
activity
Tocodynamometer
strapped to maternal
abdomen
Intrauterine pressure
catheter following
rupture of
membranes.
Uterine
contractions
Healthy
fetoplacental unit
tolerate
unhealthy fetus
there will be fetal
hypoxia
Reduce or eliminate
perfusion of the
intervillous space
Image of CTG monitor and routinely recorded parameters, including fetal heart
rate, maternal heart rate, and strength and frequency of uterine contractions
 Fetal heart rate is assessed for four features-
i. Baseline rate
ii. Baseline variability
iii. Presence or absence of decelerations
iv. Presence of accelerations
Baseline heart rate
Between 110 and 160 bpm
Fetal bradycardia, defined as an FHR <110 bpm.
Fetal tachycardia, defined as an FHR >160 bpm.
Fetal dysrhythmias are typically associated with FHR
>200 bpm.
The base line is judged by looking at the mean heart
rate over 10min.
FETAL BRADYCARDIA FETAL TACHYCARDIA
 congenital heart block
i. congenital heart
malformation
ii. Maternal systemic lupus
erythematosus
iii. Maternal medications(β-
antagonists—Labetalol)
iv. Fetal acidosis.
i. Maternal fever
ii. Infection
iii. Stimulant medications
(atropine)
iv. Drugs(β2-agonists)
v. Hyperthyroidism
Baseline variability
 Between 5 to 25 bpm.
 Measured from the peak to a trough of a recording during 1
min.
 Reduced baseline variability-
1. Depression of the fetal CNS(fetal immaturity, hypoxia)
2. Fetal sleep,
3. Maternal medications such as narcotics, sedatives, β-
blockers, corticosteroids, intravenous magnesium
sulfate.
 Marked variability-
1. Thumb sucking.
2. Fetal Hypoxia
Persistent absence of variability is considered a pre-
terminal feature and carries with it high probability of
a hypoxic fetus.
Sinusoidal variability is an oscillating pattern of three
to five cycles per minute-
1. fetal anemia.
2. Severe fetal hypoxia.
Accelerations
Accelerations of the FHR in response to movements
(To mechanical stimulation of the fetal Scalp/
vibroacoustic stimulation) are reassuring.
>15 beats min for at least 15 sec
Decelerations
Decelerations
Early
decelerations
Late
decelerations
Variable
decelerations
uncomplicated
(<60 s)
complicated
(>60 s)
Prolonged
deceleration
(>3 min)
(>15 beats min for at least
15 s)
Early decelerations Late decelerations Variable decelerations
Symmetric in shape
Benign in nature.
Variable in their shape
Mirror uterine
contractions in time of
onset, nadir, duration,
and termination
“late” in relation
to uterine contractions.
No specific relationship
with contractions
Seen in active labor when
the fetal head is
compressed
in the pelvis
Result of uteroplacental
insufficiency
Result from fetal
umbilical cord
compression.
Late decelerations
 A fall in the heart rate of 15 bpm below baseline (even if still within the
range of 110 to 160 bpm) and lasting for >15 seconds is significant.
 As the uteroplacental insufficiency/hypoxia worsens-
(i) baseline variability will be reduced and then lost,
(ii) decelerations will last longer
(iii) they will begin sooner following the onset of a contraction
(iv) they will take longer to return to baseline
(v) the rate to which the fetal heart slows will be lower.
 Repetitive late decelerations demand action.
Variable decelerations
 “Concerning characteristics” include –
i. Deceleration lasting more than 60 seconds
ii. Reduced baseline variability within the deceleration
iii. Failure to return to the baseline
iv. Biphasic (W) shape
v. Absence of shouldering (transient increase in the
heart rate before the start of deceleration).
Classification and Interpretation of Intrapartum
Monitoring
Classification and Interpretation of Intrapartum
Monitoring
EVIDENCE
 A 2009 systematic review of 12 randomized trails
including > 37,000 women(both low and high risk)
comparing continuous electronic FHR monitoring and
intermittent auscultation showed-
i. Intrapartum fetal death rate approximately 0.5/1000
births with either approach
ii. Use of electronic FHR monitoring instead of
intermittent auscultation did not result in a
significant reduction in overall risk of perinatal
death(RR 0.85,95% CI 0.59-1.23)
iii. APGAR scores and NICU admission rates were
similar for both modalities
iv. Electronic FHR monitoring instead of intermittent
auscultation did not-reduce the risk of hypoxic
ischemic encephalopathy, long –term neurologic
impairment , or cerebral palsy.
v. Frequency of neonatal seizure was reduced in the
electronically monitored group(RR 0.50, 95% CI
0.31-0.80)
vi. Use of electronic FHR monitoring instead of
intermittent auscultation increased the frequency of
operative delivery (cesarean delivery RR 1.66, 95% CI
1.30-2.13; instrumental vaginal delivery RR 1.16, 95%
CI 1.01-1.32)
Fetal blood sampling (FBS)
 Done when cesarean section is being planned for fetal
distress.
 Rationale- Acidosis or rise in lactate is considered as a
marker of fetal hypoxia.
 Falsely reassuring in the presence of chorioamnionitis or
thick meconium
 Interpretation of FBS:
i. pH-
 Normal: ≥7.25
 Borderline: 7.21 to 7.24
 Abnormal: ≤7.20
ii. Lactate
 Normal: ≤4.1 mmol/L
 Borderline: 4.2 to 4.8 mmol/L
 Abnormal: 4.9 ≥mmol/L
FETAL BLOOD
SAMPLE
Normal
No accelerations
in response to
fetal scalp
stimulation
second fetal
blood sample no
more than 1 hour
later
Borderline
No accelerations
in response to
fetal scalp
stimulation
fetal blood
sample no more
than 30 minutes
later
still abnormal
Assisted
NVD/LSCS
Fetal scalp electrode
The fetal heart rate is derived from the R-R interval of
the fetal electrocardiographic (fECG) trace
Carries the risk of infection
May allow more reliable recording of fetal heart rate
Fetal pulse oximetry
 The literature suggests that fetal saturations 30% are
reassuring(usually associated with PH> 7.13), whereas
<30% should prompt consideration of intervention.
 A Cochrane review of fetal pulse oximetry (FPO) to
supplement CTG concluded that its use did not appear
to enhance clinical practice.
Fetal electrocardiograpy
 Rationale- Hypoxaemia alters characteristics of the f
ECG (P-R interval, T:Q.RS ratio and ST segment).
 Automated ST analysis (STAN) software which looks at
the CTG and fECG concurrently. The analysis of the
fECG using STAN requires a scalp electrode to be
placed.
 The current NICE guideline does not make a
recommendation on the use of STAN.
Ultrasound
 Trans abdominal ultrasound scanning for fetal distress
in labour.
 Has ability to visualize fetal cardiac activity rapidly.
Intrapartum assessment of fetal well being (1)

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Intrapartum assessment of fetal well being (1)

  • 1. Dr Majaz Ahmed Khan Neonatology fellow
  • 2. Done by- 1. Fetal heart rate (FHR) monitoring 2. Fetal blood sampling (FBS). 3. Fetal pulse oximetry 4. Fetal electrocardiograpy Supplementary methods 5. Ultrasound
  • 3. Fetal heart rate (FHR) monitoring  Fetal parasympathetic nervous system Matures by Term.  Sympathetic nervous system development is still ongoing even after delivery.  Fetus is conditioned to thrive in a mildly hypoxic and acidic environment.  Change in fetal heart rate, caused by the impact of hypoxia and acidosis which forms the premise of FHR it is based on the assumption that fetal heart rate is a reflection of fetal oxygenation status.
  • 4.  Electronic fetal monitoring (EFM)> Doppler> Auscultation.  Electronic fetal monitoring (EFM)-Is a paper record of FHR pattern plotted simultaneously in relation to uterine activity.  So- i. Intermittent auscultation alone for low-risk pregnancies ii. Continuous EFM for pregnancies with higher risk.
  • 5.
  • 6.
  • 7.
  • 8. FHR surface transducers on the maternal abdomen Not feasible in morbid obesity. small electrode into the skin of the fetal presenting part Requires dilatation of the cervix and rupture of the fetal membranes Mild infection at the electrode site.(4%)
  • 9. Uterine activity Tocodynamometer strapped to maternal abdomen Intrauterine pressure catheter following rupture of membranes.
  • 10. Uterine contractions Healthy fetoplacental unit tolerate unhealthy fetus there will be fetal hypoxia Reduce or eliminate perfusion of the intervillous space
  • 11. Image of CTG monitor and routinely recorded parameters, including fetal heart rate, maternal heart rate, and strength and frequency of uterine contractions
  • 12.  Fetal heart rate is assessed for four features- i. Baseline rate ii. Baseline variability iii. Presence or absence of decelerations iv. Presence of accelerations
  • 13. Baseline heart rate Between 110 and 160 bpm Fetal bradycardia, defined as an FHR <110 bpm. Fetal tachycardia, defined as an FHR >160 bpm. Fetal dysrhythmias are typically associated with FHR >200 bpm. The base line is judged by looking at the mean heart rate over 10min.
  • 14. FETAL BRADYCARDIA FETAL TACHYCARDIA  congenital heart block i. congenital heart malformation ii. Maternal systemic lupus erythematosus iii. Maternal medications(β- antagonists—Labetalol) iv. Fetal acidosis. i. Maternal fever ii. Infection iii. Stimulant medications (atropine) iv. Drugs(β2-agonists) v. Hyperthyroidism
  • 15. Baseline variability  Between 5 to 25 bpm.  Measured from the peak to a trough of a recording during 1 min.  Reduced baseline variability- 1. Depression of the fetal CNS(fetal immaturity, hypoxia) 2. Fetal sleep, 3. Maternal medications such as narcotics, sedatives, β- blockers, corticosteroids, intravenous magnesium sulfate.  Marked variability- 1. Thumb sucking. 2. Fetal Hypoxia
  • 16.
  • 17. Persistent absence of variability is considered a pre- terminal feature and carries with it high probability of a hypoxic fetus. Sinusoidal variability is an oscillating pattern of three to five cycles per minute- 1. fetal anemia. 2. Severe fetal hypoxia.
  • 18.
  • 19. Accelerations Accelerations of the FHR in response to movements (To mechanical stimulation of the fetal Scalp/ vibroacoustic stimulation) are reassuring. >15 beats min for at least 15 sec
  • 21.
  • 22. Early decelerations Late decelerations Variable decelerations Symmetric in shape Benign in nature. Variable in their shape Mirror uterine contractions in time of onset, nadir, duration, and termination “late” in relation to uterine contractions. No specific relationship with contractions Seen in active labor when the fetal head is compressed in the pelvis Result of uteroplacental insufficiency Result from fetal umbilical cord compression.
  • 23.
  • 24. Late decelerations  A fall in the heart rate of 15 bpm below baseline (even if still within the range of 110 to 160 bpm) and lasting for >15 seconds is significant.  As the uteroplacental insufficiency/hypoxia worsens- (i) baseline variability will be reduced and then lost, (ii) decelerations will last longer (iii) they will begin sooner following the onset of a contraction (iv) they will take longer to return to baseline (v) the rate to which the fetal heart slows will be lower.  Repetitive late decelerations demand action.
  • 25.
  • 26. Variable decelerations  “Concerning characteristics” include – i. Deceleration lasting more than 60 seconds ii. Reduced baseline variability within the deceleration iii. Failure to return to the baseline iv. Biphasic (W) shape v. Absence of shouldering (transient increase in the heart rate before the start of deceleration).
  • 27.
  • 28. Classification and Interpretation of Intrapartum Monitoring
  • 29. Classification and Interpretation of Intrapartum Monitoring
  • 30.
  • 31. EVIDENCE  A 2009 systematic review of 12 randomized trails including > 37,000 women(both low and high risk) comparing continuous electronic FHR monitoring and intermittent auscultation showed- i. Intrapartum fetal death rate approximately 0.5/1000 births with either approach ii. Use of electronic FHR monitoring instead of intermittent auscultation did not result in a significant reduction in overall risk of perinatal death(RR 0.85,95% CI 0.59-1.23)
  • 32. iii. APGAR scores and NICU admission rates were similar for both modalities iv. Electronic FHR monitoring instead of intermittent auscultation did not-reduce the risk of hypoxic ischemic encephalopathy, long –term neurologic impairment , or cerebral palsy. v. Frequency of neonatal seizure was reduced in the electronically monitored group(RR 0.50, 95% CI 0.31-0.80) vi. Use of electronic FHR monitoring instead of intermittent auscultation increased the frequency of operative delivery (cesarean delivery RR 1.66, 95% CI 1.30-2.13; instrumental vaginal delivery RR 1.16, 95% CI 1.01-1.32)
  • 33. Fetal blood sampling (FBS)  Done when cesarean section is being planned for fetal distress.  Rationale- Acidosis or rise in lactate is considered as a marker of fetal hypoxia.  Falsely reassuring in the presence of chorioamnionitis or thick meconium  Interpretation of FBS: i. pH-  Normal: ≥7.25  Borderline: 7.21 to 7.24  Abnormal: ≤7.20 ii. Lactate  Normal: ≤4.1 mmol/L  Borderline: 4.2 to 4.8 mmol/L  Abnormal: 4.9 ≥mmol/L
  • 34. FETAL BLOOD SAMPLE Normal No accelerations in response to fetal scalp stimulation second fetal blood sample no more than 1 hour later Borderline No accelerations in response to fetal scalp stimulation fetal blood sample no more than 30 minutes later still abnormal Assisted NVD/LSCS
  • 35. Fetal scalp electrode The fetal heart rate is derived from the R-R interval of the fetal electrocardiographic (fECG) trace Carries the risk of infection May allow more reliable recording of fetal heart rate
  • 36. Fetal pulse oximetry  The literature suggests that fetal saturations 30% are reassuring(usually associated with PH> 7.13), whereas <30% should prompt consideration of intervention.  A Cochrane review of fetal pulse oximetry (FPO) to supplement CTG concluded that its use did not appear to enhance clinical practice.
  • 37. Fetal electrocardiograpy  Rationale- Hypoxaemia alters characteristics of the f ECG (P-R interval, T:Q.RS ratio and ST segment).  Automated ST analysis (STAN) software which looks at the CTG and fECG concurrently. The analysis of the fECG using STAN requires a scalp electrode to be placed.  The current NICE guideline does not make a recommendation on the use of STAN.
  • 38. Ultrasound  Trans abdominal ultrasound scanning for fetal distress in labour.  Has ability to visualize fetal cardiac activity rapidly.