CTG lecture for undergraduates by Associate Prof.Dr Aisha Elbareg

Educational materials

1. Cardiotocography (CTG)
For undergraduates
Associate Clinical Prof. Dr. Aisha M. El-Bareg, MD, PhD
Senior Consultant in (Obs & Gyn)/ Reproductive Medicine
Faculty of Medicine, Misurata .LIBYA

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Eye doesn’t see
what mind doesn’t know
-- Osler

3. History
1818-Francios Major in Geneva-DDx between FH and Maternal Pulse
1827- John C Ferguson –described FHR sounds.
1849-Killian indicated FHr parameters requiring interventions.
1876-Pinard produced his design for a fetal stethoscope.
1893-Winkel set normal FHR120-169 bpm.
1958-Hon in USA and Hammacher in Europe introduced first EFM.
1964- Doppler ultrasound scan replaced phonocord.
1966- Saling in Berlin introduced FBS.
1968-Hamacher and Hewitt-Packard developed first fetal monitor.
1985- Dublin RCT changed terminology for the CTG interpretation.
Pioneered in 1958 by Hon.in USA and Hammacher in Europe
 Commercially available 1968

4. Timeline of FHM: Summery
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Mayor described
hearing Fetal heart
sounds & association
of slow rate with SB &
NND
1818 1841
Kennedy described
association of
Meconium with SB &
NND
1958
Honn reported
EFM
1966
1966- Saling introduced
FBS

5. Why fetal assessment ?
The goal of fetal surveillance
is:
1.To detect fetal hypoxia at
early stage
2.To prevent CP & IUFD
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6. Fetal heart monitoring

External fetal heart monitoring

Internal electronic FH monitoring- QRS wave
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7. External FHR monitoring
Continuous FHR monitoring :
using CTG.
Intermittent FHR Auscultation
using:
Pinard stethoscope.
Sonicaid

8. (CTG)???
External Fetal Monitoring

9. Internal Fetal Monitoring

10. Indications for Continuous Monitoring of Fetal Heart Rate:
Maternal medical illness:
-Gestational diabetes.
-Hypertension.
-Asthma.
Obstetric complications:
-Multiple gestation.
-Post-date gestation.
-Previous cesarean section.
-Intrauterine growth restriction.
-Oligohydramnios.
-Premature rupture of the membranes.
-Congenital malformations.
-Third-trimester bleeding- Antepartum hemorrhage.
-Oxytocin induction/augmentation of labor
-Preeclampsia.
-Meconium stained liquor.

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1. Baseline heart rate:
CTG parameters

12. Baseline FHR (110 – 160):
FHR occurs between contractions, regardless to
acceleration or deceleration.
Decrease gradually from 16 weeks gestation to
term as the parasympathetic system develops.
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13. Fetal Bradycardia:
FHR between < 110 beats/min for a period of 10
min or more.
In the absence of other changes, is not considered
significant.
Causes
1.Hypoxia, Drugs (eg. Beta-blocker)
2.Autonomic effect (pressure on fetal head)
3.Fetal heart block
4.Severe Pyelonephritis
5.Hypothermia, Maternal hypotension



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15. Fetal Tachycardia (>160):
FHR > 160 bpm for a period of 10 min or more.
Causes:
1.Prematurity
2.Hypoxia
3.Maternal Fever, Maternal Hypotension
4.Maternal thyrotoxicosis
5.Chorioamnionitis
6.Fetal Cardiac arrhythmias
7.Drugs: Atropine, Ventolin, Hydralazine,
Nifedipine.
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17. 2. Baseline variability
(BLV)
CTG parameters

18. Baseline Variability:
Best indicators of intact integration between
fetal CNS & heart .
Normal BLV 5-25 bpm
Increased> 25 bpm.
Absent < 3bpm







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•The oscillatory changes that occur during the
course of 1 min and result in the waviness of the
baseline (3 – 5 /min).
•Result from the continuous interaction between
symp & parasymp nervous system.

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22. Factors Affecting Baseline Variability:
↓ Variability:
1.Prematurity, fetal sleep
2.Fetal heart abn.,
arrhythmias
3.Fetal CNS abn.
4.Drugs: Sedatives,
Analgesics, & MgSO
4
↑ Variability:
1.High gestation
2.Early, Mild Hypoxia

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3. Periodic Changes
•Acceleration
•Deceleration
CTG parameters

24. Accelerations:
Accelerations: Transient, abrupt, increase in FHR of
≥ 15 bpm lasting for ≥ 15 sec , return to baseline <
2 min.

Occurs with fetal activity.

Presence of FHR Accelerations have Good
outcome.

Absence of accelerations on an otherwise normal
CTG remains unclear.

26. Causes of loss of Accelerations:
Sleeping fetus
CNS depressant drugs: Sedatives, Narcotic,
Analgesics
Hypertensive Crisis, Diabetic Keto Acidosis
Smoking
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27. Accelerations:
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Please
Consider my
Age for
interpretation
of
Accelerations

28. Decelerations:
Transient slowing of FHR ≥
15 bpm and lasting for ≥15
sec.

4 types are described:
1.Early
2.Late
3.Variable
4.Prolonged
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29. Early Decelerations:
Begins with the onset of contraction and returns to
baseline as the contraction ends.
Mostly due to Head compression
Considered physiologic, not associated with fetal
acidosis.
Significant, if appear during early labor or
Antenatal.
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30. Early decelerations:
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31. Early Decelerations:
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32. Late decelerations:
Occurs after the peak and past the length of
uterine contraction, often with slow return to the
baseline.
Due to acute and chronic feto-placental
vascular insufficiency.
Associated with respiratory and metabolic
acidosis
Common in PIH, DM, IUGR, Post maturity,
abruption placenta, maternal anemia & sepsis
uterine hyperstimulation.

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Late decelerations:

34. Late decelerations:
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36. Deceleration occurs before, during, or after the
onset of uterine contraction.
Caused by umbilical cord compression between
fetal parts and uterine wall.
Common in oligohydramnios.
Variable Decelerations:

37. Variable Deceleration:
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Significant if
recurrent

38. Variable Decelerations:
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40. Recurrent Decelerations:

Decelerations occur with > 50% of uterine contractions in any 20
minute segment.

Recurrent variable decelerations (at least 3 in 20 minutes) may be
observed. However, close follow up is recommended because cord
accidents with subsequent fetal death may occur even in the
presence of normal amounts of amniotic fluid.
Recurrent late decelerations should lead to consideration of
cesarean delivery unless the abnormal results are believed to be the
result of a reversible maternal condition such as diabetic
ketoacidosis or pneumonia with hypoxemia.

42. Prolonged decelerations:
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•A deceleration of 30 bpm or more for 2-10 min.
•Reduced oxygen transfer to the placenta
•Associated with poor outcome

44. Causes of Prolonged Deceleration:
1. Impending birth (head compression).
2. Fetal hypoxia:
Uterine hyperactivity- hypoperfusion/hypoxia
Placental abruption
Umbilical cord knots or prolapse.
Maternal hypotension
Maternal seizures including eclampsia and epilepsy.
Sympathetic blockade (regional anesthesia)
Maternal Valsalva maneuver.

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45. The Contraction Stress Test (CST):

The Contraction stress test is used by some antepartum testing
centers to evaluate placental function under stress. The test is
performed by placing transducers (ultrasound and toco), on patient's
abdomen as with the non-stress test.

The tracing is then observed for late decelerations.

The test requires three contractions in 10 minutes to be
present with the contractions lasting 40 to 60 seconds.

If uterine activity is absent then oxytocin is infused or nipple
stimulation is used.

46. CST:
The test is positive if late decelerations are consistent and present
with more than 50% of the contractions.

A positive CST has been associated with an increased incidence of
intrauterine death, late decelerations in labor, low 5-minute Apgar
scores, and intrauterine growth restriction.

The CST is equivocal or suspicious if there are intermittent late
decelerations
A suspicious or equivocal CST should be repeated in 24 hours

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CTG interpretation:

49. CTG Features:
Baseline(beats per minute)
Short term variability( beats per minute)
Phase rectified signal averaging (beats per minute)
Signal stability index
Number of decelerations in 15 min
Number of contractions in 15 min
Contraction duration (seconds)
Resting time between contractions (seconds)

50. CTG Interpretation:
Consider :
1.Intranatal or Antenatal
2.Stage of labour
3.Gestational Age
4.Fetal presentation ?Malpresentation
5.Induction or augmentation of labour
6.Medicines (especially OTC)
7.Maternal Vitals & medical disorders

51. CTG Interpretation:
It has to be taken into consideration the
following:
There are different differences in the way clinicians
interpret CTG tracings, depending on the guidelines they
use.
Differences in guideline structure as well as in clarity and
complexity of definitions, have a profound effect on inter-
observer agreement and reliability, as well as on the
sensitivity and specificity of CT classifications in
predicting acidemia.

52. Normal Antenatal CTG

53. Features of reassuring (Normal) CTG:
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Normal Base line FHR (110 – 160)
Normal
BLV
(6 to 25)
≥ 2 Accelerations in 20 minutes
No
Significant
Deceleration

56. Non reassuring (Nonreactive) CTG:
Absence of one or more features of normal CTG
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Normal Base line FHR
Normal
Base line
Variability
Presence of Acceleration
No
Significant
Deceleration

57. Sinusoidal pattern

58. Sinusoidal pattern
Regular Oscillation of the Baseline long-term
Variability resembling a Sine wave ,with no B-b
Variability.
Has fixed cycle of 3-5 p min. with amplitude of 5-
15 bpm and above but not below the baseline.
Should be viewed with suspicion as poor outcome
has been seen (eg Feto-maternal hemorrhage)

59. Sinusoidal pattern - distinctive smooth undulating
Sine-wave baseline with no B-b variability.
0.3 % (Young 1980)
cord compression
Hypovolemia
ascites
idiopathic(fetal thumb sucking)
Analgesics
Anemia
Abruption

60. Deadly Trio:
Accelerations absent

Loss of BLV

Recurrent late decelerations at least for 20 minutes
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61. Management of non reassuring CTG
Change maternal position.
Provide oxygen by face mask
Reversal of anesthetic effect.
Regulation of uterine activity:
 Stop oxytocin
Good hydration
Correction of cord compression
Change maternal position
Amnioinfusion

62. Supplementary Procedures:
Allow further assessment of fetal wellbeing

Vibro acoustic stimulation (VAS)
Scalp Stimulation:
With Fingers
With Allis Forceps


If both negative: do Fetal blood sampling (FBS)

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65. Fetal Blood Sampling:
Useful in the presence of a non reassuring CTG.
A scalp blood sample for pH or lactate
determination.
Specificity is high ( normal value rules out
asphyxia).
The sensitivity and positive predictive value of a
low scalp pH in identifying a newborn with
Hypoxic-ischemic encephalopathy is low.

66. FBS Contraindications
Premature –less than 34 weeks
Active Herpes
Known HIV, Hep B,C positive status.
Thrombocytopenia.
Maternal-
Unfavorable Cx
Mobile PP
Malpresentation(face etc.) uncertain??
Pl Praevia or APH
Sepsis

67. FBS-Sampling errors:
Between decelerations if possible
Avoid Excess pressure on PP reduces perfusion
Do not sample on the caput.
Failure of scalp to bleed –due to peripheral shut
down.

68. FBS:
•Normal pH 7.25—7.35
•If <7.20 – significant
acidosis/ immediate
delivery
Fetal blood oximetry
False positive diagnosis is reduced to 10 %

69. Problems with CTG:
1-Has a high sensitivity but with limited specificity
in the prediction of fetal hypoxia/acidosis.
2.Increases operative vaginal delivery
3.No change in incidence of CP
4.Reduction in Neonatal seizures rates only 0.51%
5.No significant difference in APGAR scores
6.? About the efficacy
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