Abnormal Cardiotocography

CTG

 commonly known as an electronic fetal monitor or

external fetal monitor (EFM) or non-stress test
(NST)
measures simultaneously both the fetal heart rate
and the uterine contractions,
two separate disc-shaped transducers laid against
the woman's abdomen.
- ultrasound transducer measures the fetal heartbeat.
- pressure-sensitive transducer (tocodynamometer
(toco) - measures the strength and frequency of
uterine contractions

A Normal Antenatal CTG

Features of a CTG
Baseline
Short term
variability
Accelerations
Decelerations
Response to stimuli
Contractions
Fetal movements
Other

Baseline Fetal Heart Rate

Mean level of fetal heart rate when stable
excluding acceleration and deceleration
110 to 150 bpm at term
Faster in early pregnancy
Below 100 = baseline bradycardia
Below 80 = severe bradycardia
Tachycardia common with maternal fever
Tachycardia with reduced STV = early
hypoxia
Look for a rising baseline

Accelerations
Must be >15 bpm and >15 sec above
baseline
Should be >2 per 15 min period
Always reassuring when present
May not occur when fetus is sleeping
Should occur in response to fetal movements
or fetal stimulation
Non reactive periods usually do not exceed
45 min
(>90 min and no accelerations is worrying)

Short Term Variability

(or Beat to Beat Variability with a Scalp Clip)

Should be >5 bpm

The most important feature of any CTG
Is a reflection of competing acceleratory
and decelerating CNS influences on the
fetal heart
And therefore represents the best measure
of CNS oxygenation
Will be affected by drugs
Will be reduced in the pre term fetus

Decelerations
Early: mirrors the contraction
Typically occurs as the head enters the pelvis and is
compressed, i.e. it is a vagal response

Late: Follows every contraction and exhibits a

slow return to baseline
Is quite rare but is the response of a hypoxic myocardium

Variable: Show no relationship to contractions

Mild
Moderate
Severe

In practice many decels or dips are

MIXED

An Abnormal Antenatal CTG

An Abnormal Antenatal CTG

contd

Abnormal CTG Features

Reduced STV
No accelerations
Decelerations after
most contractions
with a slow return
to baseline

In Practice a CTG is best regarded as a

screening tool:
High negative predictive value
>98% of fetuses with a normal CTG will be OK

Poor positive predictive value

50% of fetuses with an abnormal CTG will be
hypoxic and acidotic but 50% will be OK

Therefore the CTG should always be

interpreted in its clinical context
And backed by fetal blood sampling
PRN

The RCOG Classification of

CTGs
Normal = all 4 features are reassuring
Suspicious = One non reassuring
feature
Pathological = Two or more non
reassuring features or a abnormal
pattern

Suspicious CTG trace

Accelerations: absent for >40 minutes-first
to become apparent, and any of the following
Baseline heart rate
bradycardia<110 bpm
Tacycardia>150 bpm
Baseline variability:<10 bpm lasting for>
40 min, greater significant if < 5 bpm
Decelerations: variable decelerations
without ominous features

Abnormal CTG tracing

Accelerations: absent for>40 min and any of the
following
Baseline heart rate: abnormal
Baseline variability:less than 5 bpm lasting for >90
min
Deceleration
Repetitive late decelerations
Variable deceleration with ominous
features( duration >60s; beat loss>60 bpm;late
recovery; late deceleration component;poor
baseline variability btwn and/or during deceleration

Baseline fetal heart rate

normal FHR at term 110 160 bpm
average fetal heart rate is considered to be
the result of tonic balance between
accelerator ( sympathetic ) and decelerator
(parasympathetic) influences on
pacemaker cells mediated via vagal
slowing of heart rate
Heart rate also is under the control of
arterial chemoreceptors such that both
hypoxia and hypercapnia can modulate
rate.

Alteration of FHR
Fetal tachycardia baseline >160 bpm over 10 minutes or
more
- can be nonpathologic, considered a normal rate in the
premature fetus
Causes :
- maternal :
- chorioamnitis
- other causes of infection causing fever
- use of B-sympathomimetics
-

fetal
cardiac arrhythmias
fetal anemia
acute fetal blood loss
abnormal fetal conduction system

FIGURE 4. Fetal tachycardia that is due to fetal

tachyarrhythmia associated with congenital
anomalies, in this case, ventricular septal defect.
Fetal heart rate is 180 bpm. Notice the "spike"
pattern of the fetal heart rate.

Alteration n fetal heart rate

Fetal bradycardia baseline heart rate <
110bpm for greater than 10 minutes.
Rate : 100 - 119 beats/min, in the absence
of other changes, usually is not considered
to represent fetal compromise.
Such low but potentially normal baseline
heart rates also have been attributed to
vagal response to head compression from
occiput posterior or transverse positions,
particularly during second-stage labor
(Young and Weinstein, 1976).

 Adverse effect on fetal circulation

severe acute bradycardia
- acute hypoxemia chemoreceptor reflex
bradycardia
- cord occlusion fetal hypertension
baroreceptor reflex vagal response
bradycardia

Causes of fetal bradycardia

Beat to beat variability

Defined as fluctuations in the FHR
baseline of 2 cycles/min or greater with
irregular amplitude and inconstant
frequency.
The time interval between 2 heartbeats
in a healthy fetus is seldom the same.
Normal : 5 15 bpm
This variability is secondary to the
interaction of the sympathetic and
parasympathetic reflexes

 Causes of loss of variability :

- fetal sleep
- administration of drugs
- narcotics, barbiturates,
phenothiazines
- MgSO4
- gestational age (28-30wks)
- metabolic acidemia

Accelerations
Upward deflection in the baseline
fetal heart rate of at least 15 bpm
lasting for at least 15 seconds.
In pregnancies of fewer than 32
weeks of gestation, accelerations are
defined as having a peak 10 beats
per minute or more above the
baseline and duration of 10 seconds
or longer.

Decelerations
Reductions in fetal heart rate of at
least 15bpm lasting for at least 15
seconds
4 types :
- Type 1 (early)- physiological
- Type 2 (late)- pathological
- variable
- prolonged

Early deceleration
consists of a gradual decrease and return
to baseline associated with a contraction.
Result of a physiologic chain of events
that begins with head compression
during a uterine contraction
the degree of deceleration is generally
proportional to the contraction strength
and rarely falls below 100 to 110
beats/min or 20 to 30 beats/min below
baseline.

 early decelerations are not

associated with fetal hypoxia,
acidemia, or low Apgar scores

FIGURE 5. Early deceleration in a patient with an

unremarkable course of labor. Notice that the onset
and the return of the deceleration coincide with the
start and the end of the contraction, giving the
characteristic mirror image.

Late deceleration (type 2)

smooth, gradual, symmetrical decrease in
fetal heart rate beginning at or after the peak
of the contraction and returning to baseline
only after the contraction has ended.
The magnitude of late decelerations is rarely
more than 30 to 40 beats/min below baseline
and typically not more than 10 to 20
beats/min.
Late decelerations usually are not
accompanied by accelerations.

 associated with uteroplacental

insufficiency
Causes :
- placental dysfunction
- placenta abruptio
- maternal hypotension
- uterine hyperactivity
- maternal disease DM, HPT, Collagenvascular disease
Repetitive late decel increases risk of umbilical
artery acidisis and apgar score less than 7 at
5min

Variable deceleration
Inconsistent time of onset when
compared to uterine contraction
The onset of deceleration commonly
varies with successive contractions .
The duration is less than 2 minutes.
represent fetal heart rate reflexes that
reflect either blood pressure changes
due to interruption of umbilical flow or
changes in oxygenation

 significant variable decelerations are

those decreasing to less than 70
beats/min and lasting more than 60
seconds.
Causes :
- Umbilical cord entanglement
- Eg:
- Umblilical around body or neck
- True knot in the umbilical cord
- Prolapsed umbilical cord

Prolonged deceleration
isolated deceleration lasting 2 minutes
or longer but less than 10 minutes
from onset to return to baseline.
Causes :
1)Total umbilical cord occlusion (cord
prolapse)
2)Maternal hypotension
3)Uterine hypertonia
4)VE or artificial ruptured of membrane

Sinusoidal pattern
regular, smooth, undulating form typical
of a sine wave that occurs with a
frequency of 2-5/minute and an
amplitude range of 5-15 bpm
also characterized by a stable baseline
heart rate of 120 to 160 bpm and absent
beat-to-beat variability
Occurs in severe fetal anemia, as occurs
in cases of Rh disease or severe hypoxia

Sinusoidal Pattern

 Saltatory pattern :
- rapidly recurring couplets of
acceleration and deceleration causing
relatively large oscillations of the
baseline fetal heart rate
- sympathetic stimulation overrides
parasympathetic dominance in response
to acute but temporary hypoxemia
( umbilical cord compression )
- almost exclusively seen during labour

FIGURE 2. Saltatory pattern with

wide variability. The oscillations of
the fetal heart rate above and below
the baseline exceed 25 bpm.

Goal of intrapartum monitoring is to distinguis fetus who is

hypoxemic but well compensated from one which is acidotic
and at risk for neurological sequelae.
1.Determine the likely cause of abnormality, if possible
(abruptio, cord prolapse, maternal medication, rapid descent of
fetal head)
2.Attempt to correct problem or initiate general measures to
improve fetaal oxygenation (supplemental oxygen, change in
position, increase hydration, treatment of hypotension,
discontinue any uterotonic)
3.If FHR does not improve, perform ancillary test to determine
fetal condition (vibroacustic stimulation, fetal scalp
stimulation,fetal blood sampling)
4.Determine wheher operative intervention is needed