This document provides an overview of cardiotocography (CTG), which is the continuous monitoring of fetal heart rate and uterine contractions during pregnancy and labor. It discusses the history of CTG, indications for monitoring, CTG parameters including baseline heart rate, variability, accelerations, and decelerations. The different types of decelerations like early, late, variable and prolonged are defined. Interpretation of normal versus non-reassuring CTG tracings and management of non-reassuring tracings is covered. Supplementary procedures like fetal blood sampling that can further assess fetal wellbeing are also summarized.
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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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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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14.
15. FetalTachycardia (>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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18. BaselineVariability:
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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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.
25.
26. Causes of loss of Accelerations:
Sleeping fetus
CNS depressant drugs: Sedatives, Narcotic,
Analgesics
Hypertensive Crisis, Diabetic Keto Acidosis
Smoking
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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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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.
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:
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.
41.
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
43.
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 StressTest (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
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.
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
54.
55.
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
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)
60. DeadlyTrio:
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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63.
64.
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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