Maisuri T.

Chalid
Divisi Fetomaternal
Bagian Obstetri dan Ginekologi FK UNHAS

 Indirect (external monitoring)

 Direct (internal)

Detect fetal hypoxia i.e reduce and avoid harm to

the fetus and improve fetal and baby out-come.
Severe acidosis may result in FHR changes.
Could occur in Normal physiological response in
labor.
Misunderstanding the physiological and
pathphysiological CTGs will improve the Mx.

 Electronic Intra-partum FHR

Monitoring is now considered
mandatory for high-risk pregnancies.
Difficulties with interpretation include
over confidence and not-only
difference in opinion between
practitioners but, also when the same
practitioner examines the same CTG
twice.
Increases CS rates 1.41%rr.

 Increases operative vaginal delivery

1.20%rr.
And no change in incidence of C
Palsy.
Reduction in Neonatal seizures rates
0.51%
No difference in APGAR scores.
? About the efficacy.

 Reliability of interpretation-50-75%
are false positive .
False positive Dx reduces to 105
with FBS.
FBS 93% sensitivity, 6% false
positive.
PH Vs Lactate -39% Vs 2.3(rr 16.7).

Indications for the continuous

EFM

High risk pregnancies

IOL and Augmentation
of Labour.

Reduced FM.
Premature labour/TPL.
APH/IPH

Oligohydramnios
Hypertension.
Abnormal FHR
detected.
Malpresentation
and in labour.
DM,Multiple
Gestation.
Previous CS.
Abdominal Trauma.
Prolonged ROM.
Meconium Liq.

Consider :

Intrapartum/antepartum trace.
Stage of labour.
Gestation.
Fetal presentation, ? Malpresentation.
Any augmentation,? IOL Medications

Direct or indirect monitoring/

*Done using the cardiotocometry with the

patient in left lateral position
**Record for 20 minutes

Howtomeassure

UltrasoundProbe

PressureTransducer

The ultrasound probe transmits the

fetal heart rate in beats per minute.
Each small vertical square is 10
beats.
Each small horizontal square is 10
seconds .
Each large horizontal square is 1
minute .

The pressure transducer

transmits the pressure generated
by uterine contractions in mm Hg.
Each small vertical square is 5 mm
Hg
Each small horizontal square is 10
seconds .
Each large horizontal square is 1
minute .

*The base line 120-160 beats/minute

*Reactive:
At least two accelerations from base line of 15 bpm
for at least 15 sec within 20 minutes
Non reactive:
No acceleration after 20 minutes- proceed for
another 20 minutes

If non reactive in 40 minutes---proceed for

contraction stress test or biophysical profile
The positive predictive value of NST to predict fetal
acidosis at birth is 44%

 Contraction is initiated by nipple stimulation or by

oxytocin I.V.

The objective is 3 contractions in 10 minutes

If late deceleration occur-----positive CST

InterpretationoftheFetalHeartTracing
Theinterpretationofthefetalheartratetracingshouldfollow
asystematicapproachwithafullqualitativeandquantitative
descriptionofthefollowing:
Baselinerate
Baselinefetalheartrate(FHR)variability
Presenceofaccelerations
Periodicorepisodicdecelerations
ChangesortrendsofFHRpatternsovertime
Frequencyandintensityofuterinecontractions

BaselineFetalHeartRate
ThebaselineFHRistheheartrateduringa10minute
segmentroundedtothenearest5beatperminuteincrement
excludingperiodsofmarkedFHRvariability,periodicor
episodicchanges,andsegmentsofbaselinethatdifferby
morethan25beatsperminute.
Theminimumbaselinedurationmustbeatleast2
minutes.
Ifminimumbaselinedurationis<2minutesthenthe
baselineisindeterminate.

BaselineFetalHeartRate

TwoMinutes

BaselineFetalHeartRate

Baselinechange:
Thedecreaseorincreaseinheartratelastsforlongerthan10
minutes.

Baseline FHR - Mean level of FHR when this is

stable, excluding Accelerations and Decelerations
(110-160 bpm)
-Tachycardia
-Bradycardia
Baseline Variability-5 bpm or greater than or equal
to 5bpm, between contractions
-Normal
-Non-reassuring-Less than 5 bpm or less but less
than 30 min
-Abnormal-less than 5 bpm for 90 min or more.

FHRVariability
Gradesoffluctuationarebasedon
amplituderange(peakto
trough)
Asinusoidalpatternhas
regularamplitudeand
frequencyandisexcluded
inthedefinitionof
variability.
Thetracingtotherightshows
anamplituderangeof~10
BPM(moderatevariability).

DevelopmentofFHRVariability
Earlyingestationthefetalheartrateispredominatelyunderthe
controlofthesympatheticnervoussystemandarterial
chemoreceptors.
Asthefetusdevelopsitsheartratedecreasesinresponseto
parasympathetic(vagalstimulation)nervoussystemmaturation
andvariabilitybecomesmorepronounced.

 Definitions
Short term
Long term

 The minor fluctuations on baseline

FHR at 3-5 cycles p/m produces
Baseline variability.
Examine imin segment and estimate
highest peak and lowest trough.
Normal is more than or equal to 5
bpm.

 Para-Sympathetic affects short term

variability whilst Long Term is more
Symp.
CNS ,Drugs reduce Variability
High gestation increases variability
Mild Hypoxia may cause both S and
para S stimulation.

 NRCTGs- reduced or less than 5

bpm for 40 min or more but less
than 90 mins..
B-B or short Term V is varying
intervals between successive heart
beats .
Long Term v is irregular waves on
the CTG 3-5 bpm.
Normal is 5-25 bpm this indicates
N-CNS.

HowHypoxia(LowOxygen)LeadstoAcidosisand
DecreasedFHRVariability

Thefetususesoxygento"burn"moleculesandreleaseenergy.
Thereaction:glucose+oxygen>>carbondioxide+water+
energy
Poorbloodflowfromtheuterusandplacentacausesthefetusto
constrictbloodvesselsinnonvitalperipheralareassuchasthe
armsandlegsinordertosupplymorebloodflowtovitalorgans
suchastheheartandbrain.

HowHypoxia(LowOxygen)LeadstoAcidosisand
DecreasedFHRVariability
Withalimitedsuppliesofoxygen(hypoxia)theperipheral
tissuescanonlypartiallybreakdownthesugarandconvertsit
tolacticacid.
Significantlevelsofacidintheblood(acidemia)maysuppress
thefetalnervoussystemandeventuallyleadto

cardiovascularcollapse.

ThePresenceofModerateFHR
VariabilityisReassuring.
PersistentlyminimalorabsentFHRvariabilityappearstobe
themostsignificantintrapartumsignoffetalcompromise.
OntheotherhandthepresenceofgoodFHRvariabilitymay
notalwaysbepredictiveofagoodoutcome(suchasmayoccur
withanabruption).

CausesofDecreasedVariability

Fetal metabolic
acidosis
CNS depressants
Fetal sleep cycles
Congenital anomalies
Prematurity

Fetaltachycardia
Preexistingneurologic
abnormality
Normalvariant
Betamethasone

SinusoidalandPseudosinusoidalPatterns

Sinusoidalpattern:
Asmooth,undulatingpattern,
lastingatleast10minuteswitha
fixedperiodofthreetofivecycles
perminuteandanamplitudeof515
bpm.

Pseudosinusoidal:
Usuallycausedbydrugssuch
asSedativedrugs

Accelerations
An acceleration is an abrupt increase in FHR above baseline with
onset to peak of the acceleration less than < 30 seconds and
less than 2 minutes in duration. The duration of the
acceleration is defined as the time from the initial change in
heart rate from the baseline to the time of return to the FHR to
baseline.
<32 weeks' : >10 BPM above baseline for >10 seconds [3]
>32 weeks' : >15 BPM above baseline for > 15 seconds[3].
Prolonged acceleration: Increase in heart rate lasts for 2 to
10 minutes.
The absence of accelerations for more than 80 minutes
correlates with increased neonatal morbidity.

Reactivity
A NST is considered reactive
when two or more fetal heart
rate accelerations peak (but do
not necessarily remain) at least
15 beats per minute above
the baseline and last 15
seconds from baseline to
baseline within a 20 minute
period with or
without fetal movement
discernible by the woman.

Vibroacousticstimulation(VAS)
If the pattern is nonreactive after 20 minutes of
observation then vibroacoustic stimulation
(VAS)
The acoustic stimulator should be positioned on the
maternal abdomen and a stimulus of 3 seconds or
less applied near the fetal head. If the NST remains
nonreactive, the stimulus is repeated at 1-minute
intervals up to three times.

HowReassuringisaReactiveNST?

A reactive NST has been associated with a perinatal

mortality of approximately 5/1,000.
The false-positive rate (the test indicates fetal
compromise when the fetus is actually O.K.)
associated with the nonreactive NST is
approximately 75 to 90 percent
Malformed fetuses have a higher incidence of
nonreactive NSTs.

LikelihoodofaNonreactiveNST
A nonreactive NST is one that lacks sufficient fetal heart rate
accelerations as described above over a 40-minute period.
Overall, on initial testing, 85 percent of NSTs will be reactive and
15 percent will be nonreactive
Most fetuses exhibiting a nonreactive NST will not be
compromised but will simply fail to exhibit heart rate reactivity
during a 40-minute period of testing .
~50 percent of NSTs are nonreactive between 24 and 28 weeks'
gestation.
~15 percent of NSTs remain nonreactive between 28 and 32
weeks.

AnonreactiveNSTrequiresthata
biophysicalprofilebedone.

PeriodicorEpisodicDecelerations
Episodic patterns are those not associated with uterine
contractions
Periodic patterns are those associated with uterine contractions.
Early and late decelerations (with some exceptions-i.e., supine
hypotension) are periodic.
Variables can also be periodic.

Quantitated by the depth of the nadir in BPM below the baseline.

Duration is quantitated in minutes and seconds from the
beginning to the end of the deceleration.
(Accelerations are quantitated similarly.)

 Accelerations- transient increase in

FHR of 15 bpm or more lasting for 15
sec.
Absence of accelerations on an
otherwise normal CTG remains
unclear.
Presence of FHR Accelerations have
Good outcome.

 Decelerationstransient slowing of
FHR below the
baseline level of
more than 15 bpm
and lasting for 15
sec.
or more.

Decelerations
The type of the deceleration is distinguished on the
basis of its waveform.
Abrupt (variables) decrease in FHR below baseline
with onset to nadir < 30 seconds.
Gradual decrease and return to baseline with time
from onset of the deceleration to nadir >30 seconds.
Further subclassified based on their relation to the
contraction.

Early decelerations: The nadir occurs with the

peak of a contraction.
Late decelerations:The nadir occurs after the
peak of a contraction.

EarlyDeceleration

GradualdecreaseinFHR
withonsetofdecelerationto
nadir>30seconds.The
nadiroccurswiththepeakof
acontraction.

a) Early Decelerations (fig 3)

Head compression
Begins on the onset of
contraction and returns to
baseline as the contraction ends.
Should not be disregarded if they
appear early in labor or
Antenatal.
Clinical situation should be r/v

Fig 3 Early Decelerations

LateDeceleration

GradualdecreaseinFHR
withonsetofdecelerationto
nadir>30seconds.The
nadirofthedeceleration
occursafterthepeakofthe
contraction

 Uniform periodic slowing of FHR

with the on set of the
contractions .
Repetitive late decels increases
risk of Umbilical artery acidosis
and Apgar score of less than 7 at
5 mins and Increased risk of CP.

Fig 4 Late Decelerations

LateDecelerations
LateDecelerationsassociatedwithpreservationofbeattobeatvariability

These decelerations appear to be mediated by

arterial chemo receptors in mild hypoxia.
Below a pO2 of 15-20 mm Hg chemoreceptors
are triggered causing reflex alpha adrenergic
stimulation leading to hypertension.
The hypertension stimulates a baroreceptor
mediated vagal response (deceleration)
The onset of reflex late decelerations typically
precedes the loss of accelerations

LateDecelerations
Lates associated with no variability (where loss of variability has
not been caused by drug administration)
With progressing hypoxia, the decelerations become deeper.
As acidosis develops the brain stem reflexes become blunted and direct
myocardial depression causes shallow decelerations [20,22].
If myocardial depression is severe enough, lates may be absent all together
Reduces Baseline variability together with Late Decelerations or
Variable Decelerations is associated with increased risk of CP.

CAUSES
Excessive uterine contractions (hyperstimulation), maternal hypotension, or
maternal hypoxemia.
Reduced placental exchange as in hypertensive disorders, diabetes, IUGR,
abruption.

LateDecelerations

From:SwehaA,HackerTW,NuovoJ.Interpretationoftheelectronicfetalheartrateduringlabor.
AmFamPhysician.1999;59:2487500

LateDecelerations
Management
Thesemaneuversareprimarilyintendedtoalleviate"reflex"lates.
Placepatientonside
AdministerO2bytightfacemask
Discontinueoxytocin.
Correctanyhypotension
IVhydration.
Ifhyperstimulationispresentconsiderterbutaline0.25mgSC
Iflatedecelerationspersistformorethan30minutesdespite
theabovemaneuvers,fetalscalppHisindicated.
ScalppH>7.25isreassuring,pH7.27.25maybe
repeatedin30minutes.
DeliverforpH<7.2orminimalbaselinevariabilitywith
lateorprolongeddecelerationsandinabilitytoobtainfetal
scalppH

VariableDeceleration
AbruptdecreaseinFHRof>15
beatsperminutemeasuredfrom
themostrecentlydetermined
baselinerate.Theonsetof
decelerationtonadirislessthan
30seconds.Thedecelerationlasts
>15secondsandlessthan2
minutes.Ashoulder,ifpresent,is
notincludedaspartofthe
deceleration.
Variabledecelerationsmaybe
observedinupto50%ofNSTs.If
nonrecurrentand<30seconds,
theyareofnoclinical
significance.

 Variable intermittent periodic slowing

of FHR with rapid onset recovery and
isolation.
They can resemble other types of
deceleration in timing and shape.
Atypical VD are associated with an
increased risk of umbilical artery
acidosis and Apgar score less than 7 at
5 min

Additional components:
Loss of 1 degree or 2 degree rise in baseline Rate
Slow return to baseline FHR after and end of
contraction.
Prolonged secondary rise in Base FHR
Biphasic deceleration
Loss of variability during deceleration
Continuation of base line at a lower level.

c) Variable Deceleration (Vagal activity) (Fig 5)

Inconsistent in configuration,
No uniform temporal r-ship to the onset of
contraction, are variable and occur in isolation.
Worrisome when Rule of 60 is exceeded (i.e.
decrease of 60 bpm,or rate of 60 bpm and longer
than 60 sec)
Caused by cord compression of the umbilical cord
Often associated with Oligo-hydroaminos with or
without ROM
Can cause short lived RDS if they MILD
Acidosis if prolonged and Recurrent.

Fig 5 Variable Decelerations

RecurrentDecelerations
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.

ProlongedDecelerations

Patients with a fall in the fetal hear rate of 15 PBM below

thebaselinefor1minuteorlongershouldbeconsideredfor
transfer to Labor and Delivery for further observation and
physiciannotified

ProlongedDecelerations
AdecreaseinFHRof>15beatsperminutemeasuredfromthemost
recentlydeterminedbaselinerate.Thedecelerationlasts>=2minutes
butlessthan10minutes.

Causes:
Maternal hypotension

Rapiddescentoffetalhead

Uterine hyperactivity

Abruption

Cord prolapse

Artifact(maternalheartrate

Cord compression*

Maternalseizure

 Cord prolapse.
Maternal hypertension
Uterine Hypertonia
Followed by a VE or ARM or SROM
with High PP.

Fig 6 Prolonged Deceleration

Prolonged Deceleration (Fig 6)

Drop in FHR of 30 bpm or More lasting for at least 2
min
Is pathological when crosses 2 contractions i.e 3
mins.
Reduction in O2 transfer to placenta.
Associated with poor neonatal outcome.

Maternal position
IV fluids
V.E to exclude cord prolapse
Assess BP
FBS if cx dilated and well applied PP
Mx Depending on the clinical situation.

Bradycardia
MeanFHR<110BPM
Arateof100119BPMintheabsenceofothernonreassuring
patternsisnotusuallyasignofcompromise
Causes
Heartblock(littleornovariability)
Occiputposteriorortransverseposition
Seriousfetalcompromise.
Patientswithnewonsetbradycardiashouldbetransferredto
LaborandDeliveryforfurtherobservationandphysician
notified

FH below 110bpm(FIGO ).
less than 100bpm (RANZCOG).
Causes :
Postdates, Drugs, Idiopathic,
Arrythmias, hypothermia(increased Vagal Tone)
Cord Compression (Acute Hypoxia, congenital
H/disease and Drugs).
Mx depends on the clinical situation.(FBS,VE
Observation or expedite delivery)

 Moderate Bradycardia 100-109 bpm

Abnormal bradycardia less than
100bpm.
Tachycardia 161-180 bpm
Abnormal Tachycardia more than
180 bpm
Ranzcog Australian more than 170
bpm

Tachycardia
MeanFHR>160BPM
Inthepresenceofgoodvariabilitytachycardiaisnotasignof
fetaldistress
Causes:
Maternalfever
Fetalhypoxia
Fetalanemia
Amnionitis
Normalvariant
Fetaltachyarrhythmia
(usually>200BPMwith
abruptonsetlittletono
variability)

SVT (200-240 BPM)

Fetal heart failure
Drugs
Beta sympathomimetics
Vistaril
Phenothiazines
Rebound transient tachycardia
following a deceleration
accompanied by
decreased variability)

Asphyxia
Drugs
Prematurity
Maternal Fever
Maternal thyrotoxicosis
Maternal Anxiety
Idiopathy
Mx depends on the clinical situation

Tachycardia

 Uncomplicated baseline
tachycardia 161-180 bpm or
bradycardia 101-109 do not appear
to be associated with poor NN
outcome.

Regular Oscillation of the Baseline long-term

Variability resembling a Sine wave ,with no Bb Variability (Fig 2),
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
haemorrhage)

Sinusoidal pattern - distinctive smooth undulating

Sine-wave baseline with no B-b variability ( Fig 2 )
0.3 % (Young 1980)
cord compression
hypovolemia
ascites
idiopathic(fetal thumb sucking)
Analgesics
Anaemia
Abruption
Mx r/v clinical situation

 Seen During Fetal thumb sucking.

Could be associated with Hypoxia.

 Difficult to interpretation,leads to Increased rate

of C Section.
50% CTG in Labour have 1 abnormal feature
15-20% Nr CTGs (pathological).
?? To reduce CS.

 Normal - CTG with all 4 Features

Suspicious -one non reassuring category and
reminder are reassuring
Pathological -2 or more non-reassuring
categories or one or more abnormal categories.

Manual Obs and Gyn. by Niswander, MD

Fetal Monitoring RCOG UK
CTGs RANZCOG
Literature review articles American Family
Physician
CTG Made Easy
D. Lata Sharma, MD, FRANZCOG, Senior
Lecturer, University Of Queensland, Australia
Charles Kawada, M.D,Harvard Medical School