KARDIOTOCOGRAPHY-interpretation and

MANAGEMENT

FETAL DISTRESS
( NEW ERA OF FHR TRACINGS
what is the difference ? )
Jaya Kusuma,dr,Obgyn Spec, MFM
Subsepecialist
Head Of MFM Division Obgyn Dept.Udayana
Faculty of Med/Sanglah Hospital.

dr. A.A.N Jaya Kusuma, SpOG(K), MARS

Maternal fetal Medicine Division
Obstetrics and Gynecology Department
Faculty of medicine Udayana University
Sanglah Hospital Bali

INCREASINGLY
DEFENSIVE
MEDICAL
BEHAVIOURS ???
?

.. Being born is one of the most crucial events in human life..

After intra uterine growth and development a fetus, must adapt to a new environment
and is going to estbalish itself with its own nutritional supply and pattern of reactions
As an independent individu
During pregnancy and labour..a fetus can suffer frOm oxygen insufficiency which is
normal..
But --For fetuses with weakend defence mechanism ..a fetal distress and metabolic acidosis
could be developed
Can lead neuro-developmental disability,cerebarl palsy,neonatal encephalopathy,and
death
To cope this event fetuses are equipped with defence mechanism..
That is why..we should know what is the signs and symptoms of defence meachanism
failure..
To react before the long term consequencies developed..

Spilka, 2013

Fetal Distress
Often used without evidence of Acidosis
Fetal distress. . Pogressive fetal asphyxia that if
not corrected will result in decompensation of the
physiological respones and can cause permanent
nervous system,damage and death ..
( Kither,2012)

Lungs
Heart
Fetal oxygenation involves the tansfer of
oxygen from the environment to the fetus
along the oxygen pathway

Vaculature
Uterus
Placenta
MATERNAL -FETAL
OXYGEN PATHWAY

Umbilical Cord
FETUS( Fetal Circulation)
Hypoxemia

Fetal oxygenation also involves the fetal

physiologic response to interruption of the
oxygen pathway

Hypoxia
Metabolic Acidosis
Metabolic Acidemia
HYPOTENSION

Clinical Signs/Symptomps- Organ dysfunction- Organ Failured

Courtesy by Jaya Kusuma,2015

DEATH

ACOG/AAP CRITERIA FOR DEFINING NEONATAL ENCEPHALOPATHY AND

CEREBRAL PALSY(2003)

1.
2.
3.
4.

1.

Essensital criteria( must meet all 4) :

Evidence of metabolic acidosis in intrapartum fetal,umb.cord arterial blood obtained at
delivery pH <7.00 and base deficit > 12 mmol/L
Early onset of severe or moderat neonatal encephalopathy in infants born at >34 weeks
Cerebral palsy of the spastic quadriplegia or dyskinetic type
Exclusion of other identifiable etiologies, such as trauma,infections,genetic etc
Nonspecific criteria :
A sentinel(signal) hypoxuc event occurring immediately before or during labor

2. A sudden and sustained fetal bradycardia or the absence of FHR

variability in the presence of persistent,late or variable decelerations
usually after a hypoxic sentinel event when pattern was previuosly
normal
3. Apgar Score 0-3 beyond 5 minutes
4. Onset of multisystems involvement withi 72 hours

PHYSIOLOGY OF FETAL OXYGENATION

Aerobic metabolism required oxygen and glucosa
(main sources of energy) all cells need
Glucose usually be stored and mobilized when needed
Oxygen : if supplies is not enough cell at risk
Complication occurred in any levef of oxygen supply
may result decreased fetal oxygenation in fetal arterial
blood(hypeoxemia) and fetal tissues hypoxia
The severity of hypoxia depend on :
intensity,duration,repetitive,and placental capacity

FETAL HYPOXIA RESULT FROM :INTERRUPTED

OXYGEN TRANSFER
Hypoxia may result from ( Miller, 2013)
(1) Reduced placental perfusion with maternal blood and consequent
decrease in fetal arterial blood oxygen content due to low pO2 (hypoxemic
hypoxia);
(2) Reduced arterial blood oxygen content due to low fetal hemoglobin
concentration (anemic hypoxia);
(3) Reduced blood flow to the fetal tissues (ischemic hypoxia).

PLACENTA AS FETAL GAS EXCHANGE ORGAN ( HOW

IMPORTANT) PLACENTA WORKS AS THE FETAL LUNG

CO2 eleminate across the placenta diificulties in

CO2 elimination increase CO2 concentration +
H20 increase H2CO3 respiratory acidemia no
injury because CO2 diffuses rapidly across the
placenta
When hyoxia occurred anaerobic metabolism to
maintain cell energy production but 20 time less
accumulation of lactic acid inside the cellfetal
circulation and extra cellular fluid.
H+ ion of lactic acidtransferred very slowly
accros the placenta but they are buferred by
circulating bases( bicarbonate) if buffering
agents fail to neutralize H+ion( base deficit or base
excess in nega number) tissue injury- cell death

O2 is transferred to the fetus via passive

diffusion

FETAL PHYSIOLOGY : BLOOD SHORT CUTS

Guyton & Hall,2005

Oxygenated
blood

Deoxygenated
blood

HEART RATE
SENSITIVE TO
OXYGEN
CONTENT

FETAL RESPONSE TO INTERRUPTED OXYGEN

TRANSFER ?

FETAL RESPONSE TO INTERRUPTED OXYGEN TRANSFER(2)

Fetus normally able to maintain aerobic metabolism until the
avalaible oxygen in the intervillous space falls to 50% of normal
levels
- Compensatory mechanisme vasocnstriction + increase
blood pressure ( Chemoreceptor) TACHYCARDA
hypertension( barroreceptor) vagal stimulation fetal
BRADICARDIA
FETAL HEART TRACING/MONITORING ASSESS FETAL
OXYGENATION
FETAL INJURY DUE TO INTERRUPTED OXYGENATION DOESNT
OCCUR UNLESS FETAL RESPONSE PROGRESS AT LEAST TO THE
STAGE OF SIGNIFICANT MEATBOLIC ACIDEMIA ( UMBILICAL
ARTERY pH < 7,0 and Base Deficit > 12 mmol/L) ( Miller,2013)

FHR tracing as a tool to detection fetal hypoxia :

what is the evidence ? ( ACOG,2012)
Interpretation of FHR tracings has been difficult lack of
agreement in definition,nomenclature and/or
recommendations
Abnormality of FHR tracing likely labelled as foetal distress

Subjectivity when intepreted the pictures of tracings and

implementation increasing SC rate/medical management
of pregnancy
Still leave some question how to definitely label each
tracing ?

The History of FHR Tracings

EFM > 50 years old USA > 4 million women giving birth have continous
EFM during labor CS rates higher than women who do not EFM
JA Le Jumeau,V de Kergaradecused Stethoscope to hear the noise of the
water in uterus and identified as the FHR
Evory Kennedy(1833) term of Fetal distress bardicardia as poor
prognosis of born baby due to fetal head compression
Head Fetoscope David Hillis (1917) and Joseph de Lee (1922)
Edward Hon,1958,Caldeyro Barcia,Hammacher FHR monitoring by
electronic devices Cardiotocography

Research at the end of the 20th Century on EFM

The Issues : What went wrong with EFM ?

Fetal Heart rate patterns reflecting fetal distress varied among the different
sudies they used varied parameter to identified outcome of neonates who
being asphyxia( Apgars,perinatal mortality,CP)
1996 National Institute of Child Health and Human development (NICHD)
made recommendations three important aspects of FHR monitoring for
research and clinical practice : 1) standard definitions of FHR
pattern,2)absence of asphyxia described with normal baseline rate,moderate
variability,presence of accelerations,and no decelerations, 3) predictive of
current or impending asphyxia if we there are any recurrent late or varaible
decelarations or substatial bradicardia with absent variability.

Fetal Monitoring in the 21 th Century

1997, NICHD defeinitions used in research
investigating the relationship between FHR and fetal
acidemia and in 2008 new NICHD panel on FHR
monitoring wa s convened ( as clarifications the
old/tarditional terme reassurung/non reassuring )
ACOG,AWHONN,ACNM endorsed NICHD for daily use of
FHR monitoring
The research still ongoing to predict abnoramlitiess of
FHR with poor neonato outcame/fetal acidemia ( fetal
scalp/pulsed oxymetry and ST segment analysies)

Pattern Recognition and Interpretation

Clinical Aplication of e-FHR consists of three main component :
1)Definition
2)Interpretation
3)Management

Standar Interpretasi Garis Monitor Janin Pada kertas rekam

KTG

Kertas monitor KTG diatur dengan kecepatan 1 cm/menit (atau 3

cm/mt ) dan dapt merekam Djj interval 30-24 dpm
Kertas KTG dibagi menjadi 2 bagian atas merekam grafik DJJ dan
bagian bawah merekam kontraksi/aktiftas uterus
Bagian atas (grafik Djj) dibagi garis horisontal tebal dan garis
horisontal tipis, jarak antar dua garis tebal = 30-40 dpm dan jarak
antar 2 garis tipis 2-5 dpm dan garis vertikal dibagi dalam garis
tebal dan tipis, interval antara 2 garis tebal 1 menit dan antara
dua garis tipis 10 detik.
Bagian bawah (kontraksi uterus): interval dua grais tebal 1menit

GAMBARAN REKAMAN KTG BERDASARKAN

KECEPATAN KERTAS KTG

Definitions of fetal heart-rate

patterns

Pattern
Baseline

Definition
. The mean FHR rounded to increments of 5 bpm during a 10-min segment, excluding:
Periodic or episode changes
Periods of marked FHR variability
Segments of baseline that differ by more than 25 bpm
. The baseline must be for a minimum of 2 min in any 10-min segment
Baseline variability
. Fluctuations in the FHR of 2 cycles per min or greater
. Variability is visually quantitated as the amplitude of peak-to-trough in bpm
Absent amplitude range undetectable
Minimal amplitude range detectable but 5 bpm or fewer
Moderate (normal) amplitude range 625 bpm
Marked amplitude range > 25 bpm
. A visually apparent increase (onset to peak in < 30 sec) in the FHR from the most recent calculated baseline
. The duration of an acceleration is defined as the time from the initial change in FHR from the baseline to the return of the
Acceleration
FHR to the baseline
. At 32 wks of gestation and beyond, an acceleration has an acme of 15 bpm or more above baseline, with a duration of 15
sec or more, but < 2 min
. Before 32 wks of gestation, an acceleration has an acme of 10 bpm or more above baseline, with a duration of 10 sec or
more, but < 2mi
. Prolonged acceleration lasts 2 min or more but < 10 min
. If an acceleration lasts 10 min or longer, it is baseline change
Bradycardia
. Baseline FHR < 110 bpm
. In association with a uterine contraction, a visually apparent, gradual (onset to nadir 30 sec or more) decrease in FHR with
Early deceleration
return to baseline
Tachycardia
. Baseline FHR > 160 bpm
Variable deceleration
. An abrupt (onset to nadir 30 sec or more), visually apparent decrease in the FHR below the baseline
. The decrease in FHR is 15 bpm or more, with a duration of 15 sec or more, but < 2 min
Prolonged deceleration
. Visually apparent decrease in the FHR below the baseline
. Deceleration is 15 bpm or more, lasting 2 min or more but less than 10 min from onset to return to baseline
FHR, fetal heart rate; bpm, beats per minute. Reprinted from the ACOG Practice Bulletin No. 70. American College of Obstetricians and Gynecologists. Obstet
Gynecol 2005; 106: 145361.

The Causes of Absent varibaility

1.Fetal metabolic acidosis
2.Neurologic abnormality
3.Marked prematuriity
4.Drug effect
5.Fetal quit sleep ( 15-30 mnt/ not more 60 mnts)
6.Fetal inactvity

1.Recurrent VD with atypia

2. Recurrent VD +Mixed
featrures(Late/variable)
associated with absent var3. Prolonged dec without
recovery/ recurrent with
progresive depth,duration
4. Checkmark pattern

Atypia Var deceleration :

1.Absent primary accl
2.Absent secundary accl
3.Overshoot
4.Slow return to baseline
5.Biphasic wave( W Shape with second componen
late )
- hati- hati..bila berulang dan persisten !!

Hati-hati : tidak ada akselerasi,menurunya variabilitas dan ada deselerasi,bedakan

rebound tachycardia dengan ovrshoot (rebund accelerations )

Hati- hati : electromechanical dissociation/ electrical activity of the heart might

continue despite cessation of muscular cardiac activity : perhatikan variabilitas

The presence of moderate varibility is a signicant indicator of fetal

oxygention,particularly when accompanied by accelerations, it reflects
an intact autonomic nervous system

Hati-hati : bedakan dengan Sinusoidal

pattern

DESELERASI DINI

Penurunan DJJ sesaat bersamaan

dengan timbulnya kontraksi.

Penurunan DJJ biasanya tidak

mencapai 100 dpm.

Penurunan DJJ merupakan bayangan

cermin dari kontraksi.

Terjadi akibat kompresi kepala

di dasar pelvik.

Tidak mempunyai arti patologis.

DESELERASI DINI (HEAD COMPRESSION)

DESELERASI LAMBAT

Penurunan DJJ yang terjadi

beberapa saat setelah kontraksi
dimulai.

Deselerasi lambat yang berulang

merupakan keadaan patologis:
- insufisiensi plasenta
- hipoksia/asfiksia janin.

PROLONGED DECELERATION

DESELERASI VARIABEL

Deselerasi yang bervariasi dalam

bentuk, lama, dan saat terjadinya.

Jenis deselerasi yang paling sering

dijumpai (terutama dalam partus kala
II).

Terjadi akibat kompresi tali pusat.

Kebanyakan tidak berbahaya bagi janin.

Beratnya derajat deselerasi variabel

berhubungan langsung dengan
beratnya derajat hipoksia janin.

KLASIFIKASI DESELERASI VARIABEL

Deselerasi variabel ringan:
- penurunan DJJ tidak mencapai 80 dpm.
- lamanya kurang dari 30 detik.
Deselerasi variabel sedang:
- penurunan DJJ mencapai 70 - 80 dpm.
- lamanya 30 60 detik.
Deselerasi variabel berat:
- penurunan DJJ sampai di bawah 70 dpm.
- lamanya lebih dari 60 detik.

DESELERASI VARIABEL
Deselerasi variabel yg tidak patologis (tidak berbahaya bagi janin):
- timbul dan menghilangnya berlangsung cepat.
- variabilitas DJJ normal.
- terdapat akselerasi pra- dan pasca-deselerasi
(bahu deselerasi).
Deselerasi variabel yg patologis (berbahaya bagi janin):
- terjadinya lebih lambat dari saat timbulnya kontraksi.
- menghilangnya deselerasi berlangsung lambat.
- variabilits DJJ berkurang/hilang, atau meningkat secara berlebihan.
- menghilangnya akselerasi pra- dan pasca-deselerasi.
- semakin beratnya derajat deselerasi variabel.

KONTRAKSI UTERUS
Komponen kontraksi uterus

Frekuensi

Lama

Amplitudo

Tonus

Irama

Konfigurasi

PATTERN RECOGNITION(nichd)
--Note: patterns not defined by
NICHD: Wandering baselien, lambda,
overshoot, W Shape, etc.

Miller,2013

The Management of (ACOG) : NEW THREE

TIERED CLASSIFICATION OF FHR TARCINGS

Category I : Normal Tracing which are not associated with

fetal asphyxia ( Common in labor)
Category II : Indeterminate tracing,including a wide
variety of possible tracings that do not fit in
Categogry I and IIICommon in labor)
Category III : Abnormal tracing and indicative of hypoxic
risk to the fetus and possible fetal acidemia.

80% OF FHR TRACINGS FALL IN TO

CATEGORY II CRITICISM TO THE
BROAD DEFINITION OF CATEGORY II
WHAT THE EXPERTS DO ?

FHR SCORE VS 5-TIERS : LOOK

SIMILAR ?

DYNAMIC PHYSIOLOGIC RESPONSE MODEL

NORMAL FETAL
ACID BASE STATUS
:Well Oxygenated
Fetus
-Baseline rate :110160pm
Baseline var:
moderate
Late/Var desc :
Absent
Early desc:+/Accelreations :+/-

INDETERMINATE
Compensatory
Response
-Moderate Var with
recurent Late/Var
Decel.
-Minimal Var without
variable decl
-Absent Var without
Recurrent Decel-Bradicardia with
Mod.var-Prolonged DeclTachycardia

King T , Maternal Fetal neonatal Physiology, Blacburn 4 th Ed, 2013

ABNORMAL FETAL
ACID-BASE
STATUS:
-absent Var with :
-Recurrent late
decl,or
-recurrent var,or
-Bradicardia
OR
Sinusoidal pattern

STOPLIGHT
ALGORITHM

Jaya Kusuma,2015

TAKE HOME MESSAGES:

We have to speaking a common language when descrbing FHR
Tracing- Category I( Normal-well oxygenated fetus)-category II
(Indeterminate )- category III (Abnormal )
E-FHR as a High FP for predicting adverse outcome
Increased Operative Interventions, delivery or continue assesment
cannot be directed by CTG alone
Knowing the limitations, Clinical Condition and Close Monitoring
IMPROVED QUALITY OF CARE

(Denpasar Society of MFM /HKFM Denpasar- Collaboration with Women N

Children Harapan Kita Hospital, Prof Ananda/Singapore and Dr
Japaraj/Malaysia)