CTG dan Hasil Sebagai

Prediksi Luaran Janin

Pembimbing: dr. Yuyun Lisnawati, SpOG(K)
PPDS Basic Obstetri-Ginekologi FKUI
 Pendahuluan
Kardiotokografi (KTG): Alat elektronik yang berfungsi untuk:
Menilai pola denyut jantung janin (kardiogram)
Menilai kontraksi atau aktivitas janin (tokogram)

Mekanisme pengaturan DJJ:

Sistem saraf simpatis, dipengaruhi: obat-obatan, stress
Sistem saraf parasimpatis , dipengaruhi a.l rangsang N.X
Baroreseptor, dipengaruhi tekanan N.X dan N.IX
Kemoreseptor, terdiri dari sentral (brainstem) dan perifer (karotid &
korpus aorta)
Susunan saraf pusat, dipengaruhi aktivitas otak & gerakan janin
Sistem hormonal, dipengaruhi a.l stress
 Pendahuluan (2)
Cara pemantauan:
Invasif (Fig 18.1)
Non-invasif (Fig 18.2)

Jenis pemeriksaan CTG:

Continuous CTG: pemeriksaan CTG yang dilakukan
terus menerus selama intrapartum
Intermittent CTG : pemeriksaan CTG yang dilakukan
secara periodik (umumnya 20”) selama intrapartum
 Figure 18–1.
Schematic representation of a bipolar electrode attached to fetal scalp for
detection of fetal QRS complexes (F). Also shown is the maternal heart and
corresponding electrical complexes (M) that are detected.

From: Chapter 18. Intrapartum Assessment. In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams
Obstetrics. 22nd ed, Mc. Graw Hill’s Company, 2005.
 Figure 18–2.
Schematic representation of fetal electrocardiographic signals used to
compute continuing beat-to-beat heart rate with scalp electrodes. Time
intervals (t1, t2, t3) in milliseconds between successive fetal R waves are
used by cardiotachometer to compute instantaneous fetal heart rate. (PAC
= premature atrial contraction.)

From: Chapter 18. Intrapartum Assessment. In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams
Obstetrics. 22nd ed, Mc. Graw Hill’s Company, 2005.
 Karakteristik DJJ
Denyut Jantung Janin (DJJ) basal

Frekuensi dasar (baseline rate) & variabilitas saat uterus dalam

keadaan istirahat (N : 120-160 dpm). Variasi :
o Takikardi (> 160 bpm)  hipoksia, kehamilan preterm, infeksi,
febris, tirotoksikosis, takiaritmia janin, obat-obatan (b-
adrenergik)
o Bradikardi (< 120 bpm)  hipoksia, hipotermi, bradiaritmia janin,
obat-obatan (b-blocker, anestesi lokal), janin dengan PJB

Periodisitas (reactivity)

Perubahan DJJ yang terjadi pada saat ada gerakan janin/kontraksi

 1. RATE
With increasing fetal maturation, the heart rate decreases.

This continues postnatally such that the average rate is 90 beats/min

by age 8.

Pillai and James (1990) longitudinally studied fetal heart rate

characteristics in 43 normal pregnancies.

The baseline fetal heart rate decreased an average of 24 beats/min

between 16 weeks and term, or approximately 1 beat/min per week.

It is postulated that this normal gradual slowing of the fetal heart rate
corresponds to maturation of parasympathetic (vagal) heart control.

The baseline fetal heart rate is the approximate mean rate rounded to
increments of 5 beats/min during a 10-minute tracing segment.

In any 10-minute window, the minimum interpretable baseline

duration must be at least 2 minutes.
 Bradycardia
During the third trimester, the normal mean baseline fetal heart rate has
generally been accepted to be between 120 and 160 beats/min.

The lower normal limit is disputed internationally with some investigators

recommending 110 beats/min.

Pragmatically, a rate between 100 and 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 head compression from occiput posterior or transverse positions,
particularly during second-stage labor.

Such mild bradycardias were observed in 2 percent of monitored pregnancies

and averaged about 50 minutes in duration.

Freeman and colleagues (2003) have concluded that bradycardia within the
range of 80 to 120 beats/min with good variability is reassuring.

Interpretation of rates less than 80 beats/min is problematic, and such rates

generally are considered nonreassuring
 Bradycardia
Some causes of fetal bradycardia include congenital heart block
and serious fetal compromise.

Figure 18–7 shows bradycardia in a fetus dying from placental

abruption.

Maternal hypothermia under general anesthesia for repair of a

cerebral aneurysm or during maternal cardiopulmonary bypass
for open-heart surgery also can cause fetal bradycardia.

Sustained fetal bradycardia in the setting of severe

pyelonephritis and maternal hypothermia also has been
reported.

These infants apparently are not harmed by several hours of such

bradycardia.
 Tachycardia
Fetal tachycardia is defined as a baseline heart rate in excess of 160 beats/min.

The most common explanation for fetal tachycardia is maternal fever from
amnionitis, although fever from any source can increase baseline fetal heart
rate.

Such infections also have been observed to induce fetal tachycardia before
overt maternal fever is diagnosed.

Fetal tachycardia caused by maternal infection typically is not associated with

fetal compromise unless there are associated periodic heart rate changes or
fetal sepsis.

Other causes of fetal tachycardia include fetal compromise, cardiac

arrhythmias, and maternal administration of parasympathetic (atropine) or
sympathomimetic (terbutaline) drugs.

The key feature to distinguish fetal compromise in association with tachycardia

seems to be concomitant heart rate decelerations.

Prompt relief of the compromising event, such as correction of maternal

hypotension caused by epidural analgesia, can result in fetal recovery.
 2. Wandering Baseline

This baseline rate is unsteady and "wanders" between 120

and 160 beats/min.

This rare finding is suggestive of a neurologically

abnormal fetus and may occur as a preterminal event.
 Karakteristik DJJ (2)
Variabilitas

 Gambaran osilasi tidak teratur pada DJJ

 Terdiri dari: short term (2-3 bpm) dan long term (≥ 5 bpm)
antara kontraksi
o Normal : amplitudo 6-25 bpm
o Berkurang : amplitudo 2-5 bpm
o Menghilang : amplitudo < 2 bpm
o Saltatorik (Fig 18.3) : amplitudo > 25 bpm

Berkurang, a.l. : fisiologis, kehamilan preterm, anensefalus,

blok n.X, PJB, pengaruh obat-obatan (narkotik, MgSO4, dll.)
 Figure 18–23.
Saltatory baseline fetal heart rate showing rapidly
recurring couplets of acceleration combined with
deceleration.

From: Chapter 18. Intrapartum Assessment. In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams
Obstetrics. 22nd ed, Mc. Graw Hill’s Company, 2005.
 Karakteristik DJJ (3)

Sau A, Langford K. Ante- and intrapartum assessment of the fetus. In: Anesthesia and intensive care
medicine. 2004
 Periodisitas DJJ
Akselerasi  peningkatan frek.DJJ, di mana bila normal amplitudo > 15
dpm, selama 15 s, selama ≥ 2 x/20’
Akselerasi seragam (uniform)
Akselerasi bervariasi (variable)
Disebabkan oleh a.l gerak janin, kontraksi uterus, prolaps tali pusat, stimulasi
janin

Deselerasi  respon parasimpatis (n.X) hasil stimulasi

baro/kemoreseptor.
Deselerasi dini :
Timbul & menghilang bersamaan dengan kontraksi (mirror image)
Penurunan amplitudo ≤ 20 bpm
Lama ≤ 90 s
Frek. Dasar & variabilitas normal
 Periodisitas DJJ (2)
Deselerasi lambat (Fig. 1) :
Timbul 20-30 s setelah kontraksi dan/atau berakhir 20-30 s setelah
kontraksi menghilang
Timbul berulang pada kontraksi dan berat sesuai intensitas kontraksi
Lama ≤ 90 s
Frek. Dasar & variabilitas normal
Deselerasi variabel :
Gambaran deselerasi bervariasi
Rule of 60  deselerasi berat bila ≥ 60 bpm di bawah baseline FHR
selama ≥ 60 s
Prolonged  berkurangnya frek.DJJ ≥ 30 bpm atau selama ≥ 2”,
patologis bila melewati 2 kontraksi
 Late Deceleration
Myers and associates (1973) studied monkeys in which they compromised
uteroplacental perfusion by lowering maternal aortic blood pressure.

The time interval, or lag period, from the onset of a contraction to the onset of a late
deceleration was directly related to basal fetal oxygenation.

They demonstrated that the length of the lag phase was predictive of the fetal PO 2 but
not fetal pH.

The lower the fetal PO2 prior to contractions, the shorter the lag phase to onset of late
decelerations.

This lag period reflected the time necessary for the fetal PO 2 to fall below a critical level
necessary to stimulate arterial chemoreceptors, which mediated decelerations.

Murata and co-workers (1982) also showed that a late deceleration was the first fetal
heart rate consequence of uteroplacental-induced hypoxia.

During the course of progressive hypoxia that led to death over 2 to 13 days, the monkey
fetuses invariably exhibited late decelerations before the development of acidemia.

Variability of the baseline heart rate disappeared as acidemia developed.

 Late Deceleration
A large number of clinical circumstances can result in late
decelerations.

Generally, any process that causes maternal hypotension, excessive

uterine activity, or placental dysfunction can induce late
decelerations.

The two most common causes are hypotension from epidural

analgesia and uterine hyperactivity caused by oxytocin stimulation.

Maternal diseases such as hypertension, diabetes, and collagen-

vascular disorders can cause chronic placental dysfunction.

A rare cause is severe chronic maternal anemia without hypovolemia.

Placental abruption can cause acute late decelerations (Fig. 18–17).

 Variable Decelerations
The most common deceleration patterns encountered during
labor are variable decelerations attributed to umbilical cord
occlusion.

Melchior and Bernard (1985) identified variable decelerations

in 40 percent of over 7000 monitor tracings when labor had
progressed to 5 cm dilatation and in 83 percent by the end of
the first stage.

Variable deceleration of the fetal heart rate is defined as a

visually apparent abrupt decrease in rate.

The onset of deceleration commonly varies with successive

contractions (Fig. 18–18).

The duration is less than 2 minutes.

 Figure 18–18.
Features of variable fetal heart rate decelerations. Characteristics include
abrupt decrease in the heart rate with onset commonly varying with
successive contractions. The decelerations measure 15 beats/min for 15
seconds or longer with an onset to nadir phase of less than 30 seconds.
Total duration is less than 2 minutes.

From: Chapter 18. Intrapartum Assessment. In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams
Obstetrics. 22nd ed, Mc. Graw Hill’s Company, 2005.
 Variable Decelerations

Very early in the development of electronic monitoring,

Hon (1959) tested the effects of umbilical cord compression
on fetal heart rate (Fig. 18–19).

Similar complete occlusion of the umbilical cord in

experimental animals produces abrupt, jagged-appearing
deceleration of the fetal heart rate (Fig. 18–20).

Concomitantly, fetal aortic pressure increases. Itskovitz

and co-workers (1983) observed that variable decelerations
in fetal lambs occurred only after umbilical blood flow was
reduced by at least 50 percent.
 Figure 18–21.
Varying (variable) fetal heart rate decelerations. Deceleration B
exhibits "shoulders" of acceleration compared with deceleration A.

From: Chapter 18. Intrapartum Assessment. In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams
Obstetrics. 22nd ed, Mc. Graw Hill’s Company, 2005.
 Figure 18–22.
Schematic representation of the fetal heart rate (FHR) effects of partial
occlusion (PO) and complete occlusion (CO) of the umbilical cord. (FSBP =
fetal systemic blood pressure; UA = umbilical artery; UC = uterine
contraction; UV = umbilical vein.)

From: Chapter 18. Intrapartum Assessment. In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams
Obstetrics. 22nd ed, Mc. Graw Hill’s Company, 2005.
 Variable Decelerations

Ball and Parer (1992) concluded that variable decelerations

are mediated vagally and that the vagal response may be
due to chemoreceptor or baroreceptor activity, or both.

Partial or complete cord occlusion produces an increase in

afterload (baroreceptor) and a decrease in fetal arterial
oxygen content (chemoreceptor).

These both result in vagal activity leading to deceleration.

In fetal monkeys the baroreceptor reflexes appear to be

operative during the first 15 to 20 seconds of umbilical
cord occlusion followed by decline in PO2 at
approximately 30 seconds, which then serves as a
chemoreceptor stimulus.
 Variable Decelerations

Thus, variable decelerations represent fetal heart rate reflexes that reflect
either blood pressure changes due to interruption of umbilical flow or
changes in oxygenation.

It is likely that most fetuses have experienced brief but recurrent periods of
hypoxia due to umbilical cord compression during gestation.

The frequency and inevitability of cord occlusion undoubtedly has provided

the fetus with these physiological mechanisms as a means of coping.

The great dilemma for the obstetrician in managing variable fetal heart rate
decelerations is determining when variable decelerations are pathological.

The American College of Obstetricians and Gynecologists (1995b) has defined

significant variable decelerations as those decreasing to less than 70
beats/min and lasting more than 60 seconds
 Prolonged Deceleration
Shown in Figure 18–24, this pattern is defined as an isolated deceleration
lasting 2 minutes or longer but less than 10 minutes from onset to return to
baseline.

Prolonged decelerations are difficult to interpret because they are seen in

many different clinical situations.

Some of the more common causes include cervical examination, uterine

hyperactivity, cord entanglement, and maternal supine hypotension.

Epidural, spinal, or paracervical analgesia may induce prolonged deceleration

of the fetal heart rate.

For example, Eberle and colleagues (1998) reported that prolonged

decelerations occurred in 4 percent of normal parturients given either
epidural or intrathecal labor analgesia.

Hill and colleagues (2003) observed prolonged deceleration in 1 percent of

women given epidural analgesia during labor at Parkland Hospital.
 Figure 18–24.
Prolonged fetal heart rate deceleration due to uterine hyperactivity.
Approximately 3 minutes of the tracing are shown, but the fetal heart rate
returned to normal after uterine hypertonus resolved. Vaginal delivery
later ensued.

From: Chapter 18. Intrapartum Assessment. In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams
Obstetrics. 22nd ed, Mc. Graw Hill’s Company, 2005.
 Karakteristik DJJ (4)

Sau A, Langford K. Ante- and intrapartum assessment of the fetus. In: Anesthesia and intensive care
medicine. 2004
 Karakteristik DJJ (5)
Interpretasi:
Akselerasi respons simpatetik, umumnya fisiologis
Deselerasi dini  persalinan normal sebagai respons
kontraksi/head compression
Deselarasi lambat  hipoksia janin
Semakin tidak terkompensasi, variabilitas <<<
Bila tidak terkompensasi, dapat timbul pola sinusoidal
(Fig.18.10)
Deselerasi variabel  penekanan tali pusat (lilitan atau
prolaps tali pusat, oligohidramnion)
Figure 18–10.
Grades of baseline fetal heart rate
variability (irregular fluctuations in
the baseline of 2 cycles per minute
or greater) together with a
sinusoidal pattern. The sinusoidal
pattern differs from variability in
that it has a smooth, sinelike
pattern of regular fluctuation and is
excluded in the definition of fetal
heart rate variability. (1)
Undetectable, absent variability; (2)
minimal 5 beats/min variability; (3)
moderate (normal), 6 to 25
beats/min variability; (4) marked, >
25 beats/min variability; (5)
sinusoidal pattern

From: Chapter 18. Intrapartum Assessment. In:

Cunningham FG, Leveno KJ, Bloom SL,et al.
Williams Obstetrics. 22nd ed, Mc. Graw Hill’s
Company, 2005.
 Modanlou and Freeman (1982), based on their
extensive review, proposed adoption of a strict
definition:

1. Stable baseline heart rate of 120 to 160 beats/min with

regular oscillations.

2. Amplitude of 5 to 15 beats/min (rarely greater).

3. Long-term variability frequency of 2 to 5 cycles per minute.

4. Fixed or flat short-term variability.

5. Oscillation of the sinusoidal waveform above or below a

baseline.

6. Absence of accelerations
 Sinusoidal Heart Rate
A true sinusoidal pattern such as that shown in panel 5 of Figure 18–10 may be
observed with serious fetal anemia, whether from D-isoimmunization,
ruptured vasa previa, fetomaternal hemorrhage, or twin-to-twin transfusion.

Insignificant sinusoidal patterns have been reported following administration

of meperidine, morphine, alphaprodine, and butorphanol.

Shown in Figure 18–13 is a sinusoidal pattern seen with maternal meperidine

administration.

An important characteristic of this pattern when due to narcotics is the sine

frequency of 6 cycles per minute.

A sinusoidal pattern also has been described with amnionitis, fetal distress,
and umbilical cord occlusion.

Young and co-workers (1980a) and Johnson and colleagues (1981) concluded
that intrapartum sinusoidal fetal heart patterns were not generally associated
with fetal compromise.
 Pemeriksaan CTG
Antepartum
Indikasi : high risk pregnancy, a.l:
Hipertensi gestasional & preeklamsia
Kehamilan dengan DM/DMG
Kehamilan postterm
IUGR
PROM
Gerak janin berkurang
Kehamilan dengan anemia
Kehamilan multipel
Oligohidramnion & polihidramnion
Riwayat obstetrik buruk
Kehamilan dengan penyakit penyerta
 Pemeriksaan CTG
Antepartum (2)
Non-stress test (NST)  penilaian gambaran DJJ dalam hubungannya dengan
aktivitas/gerak janin.

Interpretasi:
Reaktif:
≥ 2 x gerakan janin/20” yang disertai akselerasi normal
Frekuensi dasar DJJ di luar gerakan janin 120-160 dpm
Variabilitas 6-25 dpm
Non reaktif
Tidak didapatkan gerakan janin selama 20”/ tidak ditemukan akselerasi
Variabilitas dapat normal atau berkurang
Meragukan
Terdapat gerakan janin tapi < 2x/20” ATAU akselerasi < 10 dpm
Frekuensi dasar DJJ normal DAN variabilitas DJJ normal

Hasil pemeriksaan abnormal bila ditemukan bradikardia atau deselerasi ≥ 40 dpm di

bawah baseline FHR atau DJJ mencapai 90 bpm selama ≥ 60 s
 Pemeriksaan CTG
Antepartum (3)
Contraction stress test (CST)  pemeriksaan CTG pada saat kontraksi (in
partu)

Interpretasi:
Negatif bila frekuensi DJJ normal, variabilitas normal, tidak ada deselerasi
lambat, mungkin ada akselerasi/deselerasi dini
Positif bila deselerasi lambat rekuren pada ≥ 50% jumlah kontraksi ATAU
pada saat kontraksi dinilai tidak adekuat, variabilitas berkurang/menghilang
Mencurigakan bila deselerasi lambat < 50% jumlah kontraksi, deselerasi
variabel, frekuensi DJJ normal
Tidak memuaskan bila hasil rekaman tidak representatif atau tidak terjadi
kontraksi adekuat
Hiperstimulasi bila kontraksi > 5x/10”, lebih dari 90 s atau sering terjadi
deselerasi lambat atau bradikardi.
 Pemeriksaan CTG
Antepartum (4)
Kontraindikasi CST:
Absolut  risiko ruptur uteri, HAP, prolaps tali pusat
Relatif  PROM, preterm, kehamilan multipel,
inkompetensia serviks, CPD
 Table 18–1. NICHD Research Planning Workshop
(1997) Fetal Heart Rate Patterns

Pattern Workshop Interpretations

Normal Baseline 110–160 beats/min
  Variability 6–25 beats/min
  Accelerations present
  No decelerations
Intermediate No consensus
Severely abnormal Recurrent late or variable
decelerations with zero
variability
  Substantial bradycardia with
zero variability

From: Chapter 18. Intrapartum Assessment. In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams
Obstetrics. 22nd ed, Mc. Graw Hill’s Company, 2005.
 Table 18–5. Guidelines for Intrapartum Fetal Heart Rate
Surveillance
Surveillance Low-Risk Pregnancies High-Risk Pregnancies
Acceptable methods    
  Intermittent Yes Yes
auscultation
  Continuous electronic Yes Yes
monitoring (internal or
external)
Evaluation intervalsa    
 
  First-stage labor (active) 30 min 15 minb
 
  Second-stage labor 15 min 5 minb
 
a
Following a uterine contraction.
b
Includes tracing evaluation and charting when continuous electronic monitoring is used.

American College of Obstetricians and Gynecologists, 1995. From: Chapter 18. Intrapartum Assessment.
In: Cunningham FG, Leveno KJ, Bloom SL,et al. Williams Obstetrics. 22 nd ed, Mc. Graw Hill’s Company,
TERIMA KASIH
 Daftar Pustaka
Buku ajar ilmu kebidanan, ed.ke-2. Jakarta: PT Bina Pustaka
Sarwono Prawirohardjo; 2007

Cunningham FG, Leveno KJ, Bloom SL,et al, editors. Williams’

Obstetrics, 23rd ed. New York City (NY): McGraw-Hill; 2011

Macones GA, Hankins GDV, Spong CY, Hauth J, Moore T. The 2008
National Institute of Child Health and Human Development
Workshop Report on Electronic Fetal Monitoring. Curr Comm. VOL.
112, NO. 3, Sept 2008