CTG - Cardiotocography or Non stress test A nonstress test is a screening test used in pregnancy to assess fetal status by means of the fetal heart rate and its responsiveness. A cardiotocograph is used to monitor the fetal heart rate and presence or absence of uterine contractions. The test is typically termed "reactive" or "nonreactive".

1. CARDIOTOCOGRAPH
CTG
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL
– BASAVANAGUDI, BANGALORE

2. ANTEPARTUM CARDIOTOCOGRAPHY
• GOAL: to prevent hypoxia related neurological damage and still births.
• There is also evidence that with antepartum monitoring , the risk of IUD in High
risk pregnancies can be reduced to levels even lower than in Low risk pregnancies.
• Antepartum risk factors :
► Socio-economic status
► Family history of seizures or neurological disease
► Conception after infertility treatment
► Maternal thyroid disease
► Severe preeclampsia
► Antepartum hemorrhage
► Viral infections
► Intrauterine growth restriction
► Post maturity
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE

3. WHO SHOULD BE MONITORED
Maternal indications Obstetric indication
§ Chronic HTN
§ Collagen vascular diseases
§ Diabetes
§ Impaired renal function
§ Significant cardiac disease
§ Asthma
§ Epilepsy
§ Antiphospholipid syndrome
§ Substance abuse
§ IUGR
§ Post- term pregnancy
§ Previous still birth
§ Decreased fetal movements
§ Pregnancy induced HTN
§ PPROM
§ Cholestasis of pregnancy
§ Multiple pregnancy
§ RH iso-immunisation
§ oligohydraminos
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE

4. WHEN SHOULD MONITORING BEGIN & HOW OFTEN
Risk benefit analysis for most indication suggest that
ü Optimal timing to begin fetal
monitoring
32-34 weeks.
ü In case of previous still birth monitoring to begin in 1 or 2week
before the previous fetal death or 32
week or earlier.
ü Twice weekly testing is recommended
ü If condition detoriates e.g
uncontrolled diabetes or HTN,
absent or reverse diastolic flow
on um. Artery Doppler
CTG performed daily, frequently as
twice a day.
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE

5. FETAL HEART RATE RECORDING
1.CTG – Cardiotocography
2.NST – Non-stress Test
3.Computerized CTG
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE

6. DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE

7. THE EQUIPMENT
• Electronic fetal monitoring or the cardiotocograph – a
device for recording the fetal heart rate (FHR) on a beat to
beat basis, and the uterine contractions.
• In 1960- Professor Hamacher & Hewlet-Packard –
developed non invasive Fetal monitor.

9. The Fetal heart rate
Non- Invasive
An external transducer placed
on the maternal abdomen with
an help of an abdominal belt.
Invasive
Internally by hooking a
fine electrode on to the
fetal scalp.
The technique for external
recording utilizes a pulse
Doppler with auto
correlation processing which
detects fetal heart motion.
The internal fetal scalp electrode
(FSE) uses a direct ECG input
from the fetus, the wires from the
electrode are connected to a leg
plate kept in place on the mothers
thigh with a strap, which in turn is
connected to the CTG machine .

10. • The uterine activity can be similarly recorded by
the internal and external transducers
• The external toco-transducer or tocodynamometer
detects the uterine activity by sensing a change in
a tension of the anterior abdominal wall .
• The tocodynamometer is strapped to the mothers
abdomen on the fundal area.
An internal transducer is introduced in to the uterine
cavity after the membranes are ruptured.

13. PHYSIOLOGICAL BASIS OF FETAL HEART
PATTERNS
• The fetal heart is innervated by nerve fibers from autonomic nervous system.
The efferents originate in both sympathetic as well as parasympathetic
system.
• In a well oxygenated fetus constant modulation of these impulses
reflected as fluctuations in the basal heart rate baseline varaibility.
• The parasympathetic system matures later than sympathetic system, usually
becoming fully functional by 32-34 weeks of gestation.
BP - Vagal tone FHR
BP - Vagal tone FHR
Sympathetic activity
Parasympathetic activity

14. BASELINE HEART RATE
• Mean level of FHR when stable, acceleration and
deceleration being absent
• Normal = 110-160 bpm
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE

15. ACCELERATION
• An abrupt increase in baseline FHR of 15 bpm or more
and lasting for 15 seconds or more. which occur
independent of uterine contractions , both in antepartum
and intrapartum traces.
• Prolonged acceleration : an acceleration lasting greater
than 2 min and less than 10 min.
• Acceleration lasting longer than or equal to 10 min should
be interpreted as a baseline change.
• SIGNIFICANCE – reassuring feature of FHR pattern
indicating fetal well being.

16. TO CALCULATE ACCELERATION

17. DECELERATION
• A transient episode of slowing of FHR below the baseline
level more than 15 bpm and lasting 15 seconds or more.

18. EARLY DECELERATION
• Onset of deceleration is at the onset of contraction.
Causes:
• Fetal head compression
• Seen in late first stage or second stage. (usually not indicative of
F.hypoxia/acedemia)
The nadir of the decelerations therefore corresponds to the peak of contractions and
the FHR starts picking up, as the contractions recedes, returning to the base line at
the end of contraction.
Exclude – CPD (action taken )

20. LATE DECELERATION
• Deceleration occur more than 15 seconds after the peak of contraction.
• Gradual decrease
• FHR below 15 bpm below baseline
• Lasting at least 15 sec
• Onset of deceleration at mid to end of contraction
• Baseline variability <5 bpm .
Causes:
• Reduction in placental blood flow (abruptio, hyperstimulation)
• Maternal related disease (PIH, pre-eclampsia)
• Fetal compromised (IUGR, premature)
• Supine hypotension
As the blood flow to the placenta is replenished after the uterine contractions are over
the FHR returns to the base line.

21. VARIABLE DECELERATION
• Variable, intermittent usually abrupt decrease in FHR below the baseline by
at least 15 bpm lasting 15 sec to 2 min from onset to return to the baseline .
• Deceleration that inconsistent in shape and in timing with uterine
contraction.
• They are variable in shape, size, timing in reference to the uterine
contractions, depending on the severity of the compression .
Causes :
• Umbilical cord entanglement/ cord compression
• Cord round neck
• True knot
• Cord prolapsed
Causes for cord compression
- Change in maternal posture
- Intensity of uterine contractions
- Amount of amniotic fluid.

22. Compression of cord- vein
occludes first
Loss of blood volume –
stimulates sym. Activity in
fetus
Increase in baseline FHR
Compression progress to
involve arteries
Systemic hypertension-
Inc. vagal activity
Fall in FHR
Manifesting Variable
deceleration
The brief period of increase in baseline
before the deceleration is called
“SHOULDERING” (Hump /
Overshoot).
Reflects – fetal compensatory
mechanisms are intact in so far well
oxygenated fetus.
When compression is released -
same chain of events occur in
reverse order
----arterial circulation is restored
first followed by venous &
shouldering at an end of
deceleration .
If the cord compression is
prolonged – shouldering may
disappear with flattening of the
baseline ----sugg. Impending
acidosis.

24. PROLONGED DECELERATION
• A consistent drop in fetal heart rate > 30bpm, lasting 2
min
Causes :
• Total umbilical cord occlusion
• Uterine hypertonic
• Maternal hypotension
• Cord compression

27. NATURE OF HYPOXIA & FHR PATTERN
Gradually developing hypoxia
Results in Deceleration
Metabolic acidosis & myocardial damage
Respiratory acidosis – initially
Hypoxia continues
Baseline variability due to brain stem hypoxia
Slowly FHR
Vagal tone
BP
Cardiac output

28. Acute hypoxic events
Chronic intrauterine hypoxia
Due to ..
• Fetal growth restriction
• Pre-eclampsia
• Chronic HTN………may show reduced baseline FHR on antepartum
CTG.
Note :
• Acute vagal stimulation
Placental abruption
Scar dehiscence
Cord prolapse
Decelerations or
bradycardia
Vagal stimulation
(parasympathetic)
rapid change in
baseline FHR
Deceleration/Bradycardia
Sympathetic activation Gradual change
In baseline Tachycardia

29. ANALYSIS OF FETAL HEART
PATTERNS
All FHR tracings hav a scaling speed of 1 cm per minute
i.e., each small square is equivaent to 30 seconds.
The individual components of the FHR tracigs that need to
be evaluated are :
ØBaseline FHR
ØBaseline variability
ØPresence of acceleration
ØPeriodic or episodic deceleration

30. BASELINE FHR
• Mean level of FHR when stable, acceleration and deceleration being absent
• Normal baseline - 110-160 bpm
• Moderate bradycardia - 100-109 bpm
• Moderate tachycardia - 161-180 bpm
• Abnormal bradycardia - <100 bpm
• Abnormal tachycardia - >180 bpm
TO CALULATE BASELINE FHR
A ten minute segment is chosen where the baseline is fairly stable. Periods of
marked baseline variability and significant accelerations & deceleration are excuded.
The max A and the min B FHR is marked as shown in graph, & its mean is calculated
& rounded to 5 bpm.
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE

32. VARIABILITY
• The amplitude of the fluctuations of the baseline FHR denotes a baseline
variability
• Degree to which the baseline varies with in a particular band width excluding
acceleration and deceleration (5-15bpm)
• Represent interaction of nervous system which determine the cardiac output
and heart rate, in response to venous return and metabolic demands of fetus.
• The criteria for normal, non reassuring or abnormal baseline variability are
as follows
Ø Normal baseline variability >5bpm
Ø Non-reassuring baseline variability <5bpm for > 40 min but less
than 90 min
Ø Abnormal baseline variability <5bpm for 90 min
TO CALCULATE THE BASELINE VARIABILITY
One min. segment on the graph which is stable is selected, the highest peak &
lowest nadir are marked & the differences between the two gives the baseline
variability.

39. REACTIVE TRACE
• Normal baseline heart rate, variability, presence of
acceleration (2 in 20 min’s trace) and absence of
deceleration.

43. Causes of fetal tachycardia Causes of fetal bradycardia
ØDrugs to Mother –
1)Beta-sympathomimetic agents
used to inhibit preterm labor
(isoxsuprine, ritodrine)
2) Vagolytic : atropine
ØInfection – both maternal & Fetal
ØAnemia – both maternal & Fetal
ØFetal hypoxia
ØFetal hypoxia, acidosis
ØFetal sepsis, anomalies
ØUse of local anesthetic drugs,
epidural analgesia
ØDrugs to mother eg. Pethedine,
antihypertensive (methyl dopa,
propranolol) MgSO4
ØFetal heart conduction defect
(SLE)
Changes of FHR pattern

44. BRADYCARDIA
• A baseline FHR persistently low than 110 bpm
Causes :
• Gestational age >40w
• Cord compression / prolapsed
• Congenital heart malformation
• Drugs
• Late fetal hypoxia
• Idiopathic

45. TACHYCARDIA
• Persistently baseline > 160 bpm
Causes :
• Maternal pyrexia
• Fetal infection
• Chronic hypoxia
• Hyperthyroidism or maternal stress
• Fetal hormones in response to stress
• Gestational age <32 w
• Drugs
• Excessive fetal movements

49. DECREASE VARIABILITY
• Variability <5bpm or absent
Causes :
• Severe hypoxia
• Fetal sleeping pattern
• Maternal sedation
• Gestational age <28-30w
• Congenital malformation

50. SINUSOIDAL
• A smooth , wave like baseline, absent beat to beat
variability
• It is seen as a regular oscillation of the baseline
resembling a sine wave with 3-5 cycles per minute and an
amplitude of 5-15 bpm above and below the baseline
lasting atleast 10 min.
• The baseline variability is absent
Causes:
• Severe hypoxia
• Anemic fetus/ fetal hemorrhage
• Idiopathic

52. PSEUDO-SINUSOIDAL PATTERN
• This has been observed after administration of pathedine
and epidural anesthesia.
• Usually short lasting , some baseline variability is
maintained as compared to the true sinusoidal which is
more smooth and , the rhythm aborts on stimulating the
fetus.

53. SUSPICIOUS / EQUIVOCAL CTG
• Absence of acceleration for >40 min
• BHR 160-170bpm or 100-110 bpm
• Absent BV for >40 min with normal baseline and no
deceleration
• Variable deceleration <60 bpm for 60 sec
• Transient bradycardia <100 bpm more than 2 min.

54. PATHOLOGICAL / OMINOUS
• BHR >160 bpm with absent variability & /or repetitive
late or variable deceleration
• Absent BV >90 min
• Complicated variable deceleration (>60 bpm lasting > 60
sec )
• Repetitive late deceleration
• Prolonged bradycardia
• Sinusoidal pattern

55. INTERPRETATION OF A
CARDIOTOCOGRAPHY
• Accelerations and normal baseline variability (5-25 bpm) denote a
healthy fetus.
• Absence of accelerations is the first feature to denote onset of
hypoxia.
• Absence of accelerations, reduced baseline variability of <5 bpm for
>90 minutes denotes a hypoxic fetus.
• Decreased baseline variability may be due to fetal sleep , infection,
hypoxia, anomalies or due to maternal medications.
• Repeated late decelerations increase the risk of low APGAR score
and CP
• Reduced baseline variability , with late or variable deceleration
increase the risk of CP

56. Feature Baseline (bpm) Variability
(bpm)
Deceleration Accelerations
Reassuring 110-160 >_5 None Present
Non-Reassuring 100-109
161-180
<5 for >40 to
<90minutes
• Early
deceleration
• Variable
deceleration
• Single
prolonged
deceleration
upto3 minutes
The absence of
accelerations
with an or
otherwise normal
CTG are of
uncertain
significance.
Abnormal <100
>180
Sinusoidal
pattern >- 90
minutes
<5 for >-90
minutes
Atypical variable
decelerations
Late
decelerations
Single prolonged
deceleration >3
minutes
CATEGORIZATION OF COMPONENTS OF CTG

57. CATEGORISATION OF FETAL HEART PATTERNS
Category Definition
NORMAL A CTG where all four feature all in to the
reassuring category
SUSPECIOUS A CTG whose features fall into one of the
non reassuring categories and the remainder
of the features are reassuring.
PATHOLOGICAL A CTG whose features fall in to two or more
non-reassuring categories or one or more
abnormal categories.

58. MANAGEMENT OF SUSPECIOUS/ PATHOLOGICAL CATEGORY.
v Correctable cause -> measures tried
Check the following
1. Is there a evidence of hyper stimulation ?
ØStop oxytocin
ØConsider tocolysis, give 0.25mg terbutaline sc /i.v
2. Maternal tachycardia / fever ?
Ø Check maternal PR, BP, T
Ø Treat maternal infection if any
Ø Correct dehydration
Ø To hydrate if an epidural has been sited or topped up.

59. 3. General resuscitative measures to improve fetal perfusion
Ø Change maternal posture to left lateral if supine
Ø Infuse 500ml of crystalloid if no contradiction
Ø To give maternal oxygen by mask at 8-10 lt/min.
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE

60. NST – NON STRESS TEST
• NST is also known as Antenatal Cardiotocography
PRINCIPLE :
To see for ..FHR tracing via external transducer
Fetal movements marked on the trace by the
mother using event marker.

62. THE TEST
• the test should be performed with the patient in semi-
recumbent or left lateral recumbent position
• A 20 min record is obtained
• The criteria of a normal & reactive test are :
I. Baseline – 110-160 bpm
II. Two accelerations > 15bpm lasting at least 15 sec.

65. FACTORS AFFECTING NST
• Besides fetal hypoxia, the NST is also affected by fetal behavior &
environmental factors they are :
ØPrematurity :
§ a higher baseline FHR (because of only sympathetic activity)
§ Reduced baseline variability
§ Isolated decelerations
§ Acceleration <15 bpm

67. ØFetal sleep activity cycle :
§ Quite sleep state or NREM sleep in the
fetus is associated with decreased level of fetal
activity with absence accelerations and reduced
FHR variability.
§ If CTG/NST is non-reactive in a 20 min
record, it should be continued for another 20
min which is referred to as “EXTENDED
NST”

68. ØMaternal state & medications : : eg,
§ Narcotics - prolong sleep pattern
§ Stimulants - dec. baseline FHR; decrease amplitude of
accelerations
§ Beta-blockers - dec. baseline FHR; dec. frequency of
acceleartion
§ Betamethasone - dec. baseline variability
ØAbnormal karyotype: particularly trisomy 21
(downs syndrome)

69. TWIN PREGNANCY
• Multiple pregnancies are associated with high risk of growth disorders,
prematurity & cerebral palsy.

70. COMPUTERIZED CTG
• Computer analysis of CTG is a step towards standardization of
the technology and to reduce the subjectivity in its interpretation
which results in high inter- & intra- observer variability..

72. THANK YOU
DR BHAVANA G
GUNASHEELA SURGICAL & MATERNITY HOSPITAL – BASAVANAGUDI, BANGALORE