a tertiary facility is best since the mother’s uterus is still

NON-INVASIVE ANTEPARTUM the “best incubator” rather than transferring a preterm

ASSESSMENT OF FETAL neonate. It must be pointed out that acute compromise
such as abruptio or cord accidents cannot be detected by
WELL-BEING the methods that will be described.

 Generally, all antepartum fetal testing has negative

predictive value (True negative) of 99.8%, while positive
GENERAL PROFILE OF MATERNAL HEALTH
predictive value is only 10-40%.
ANTENATAL EVALUATION OF FETAL HEALTH

Fetal Movement Counting

GENERAL PROFILE OF MATERNAL
Electronic Fetal Monitoring
HEALTH
Fetal Heart Rate

Control (Sympathetic and Parasympathetic)

 Assessment of fetal well being starts with the general
Baseline Rate (Tachycardia, Bradycardia) profile of maternal health as early as the preconceptional
stage, during the time of conception, and as the
Variability (Absent, Minimal, Moderate, Marked
pregnancy progresses. Data from the history, physical
(Saltatory), Sinusoidal, Causes of Decreased FHR
examination and laboratory examinations will identify a
Variability
pregnancy that is at risk.
Accelerations
 Pre-existing maternal conditions such as diabetes I and II,
Decelerations (Early, Late, Variable, Prolonged) cardiac problems, chronic lung disease, asthma,
hypertension, thyroid problems, chronic renal disease,
NON-STRESS TEST (NST) SLE, thrombosis (Anti Phospholipid Antibody Syndrome),
malnutrition, anemia and obesity complicate pregnancy
Reactive, Non-Reactive
outcome.
Fetal Acoustic Stimulation Test (FAST)
 Pregnancy- related conditions such as gestational
Causes of False Positive NST hypertension, pre-eclampsia, oligohydramnios,
polyhydramnios, intrauterine growth restriction,
Causes of False Negative NST post-term pregnancy, multiple gestation and perinatal
infections add to the perinatal mortality and morbidity.
CONTRACTION STRESS TEST (CST)

Negative, Positive, Suspicious, Hyperstimulation,

Unsatisfactory
ANTENATAL EVALUATION OF FETAL
Contraindication to perform CST (Computerized HEALTH
Interpretation of FHR Monitoring, Biophysical Profile
(BPP), Modified Biophysical Profile, Umbilical Cord Artery
Doppler Velocimetry, Middle Cerebral Artery Velocimetry)
 FETAL MOVEMENT COUNTING (FETAL KICK
Other Non-Invasive Modalities (Magnetocardiography,
COUNT)
Venous Doppler Ultrasound Waveform)
 Fetal activity can be appreciated as early as 7 weeks, and
becomes sophisticated and coordinated as pregnancy
 Ideally, the ultimate goal of fetal assessment is to detect advances. At 36 weeks, the fetal behavior status is
chronic and intermittent fetal compromise to prevent established as observed in ultrasound:
stillbirth, decrease neonatal mortality and morbidity,
and minimize long term sequelae.
STAGE 1F: quiescent state, with a narrow oscillatory
 Testing is usually started at 32-34 weeks, when the fetal
bandwidth of the fetal heart rate (quiet sleep)
autonomic nervous system can be considered mature. It is
done on a weekly basis or earlier and more frequently
depending on the clinical situation. Maternal transport to

CHAPTER 18 TEXTBOOK OF OBSTETRICS 3RD EDITION

STAGE 2F: frequent gross body movements, continuous eye
movements, wider oscillation of fetal heart rate
(active sleep)
STAGE 3F: continuous eye movements, absent body
movements, no accelerations of the fetal heart
rate
STAGE 4F: vigorous body movement, continuous eye
movement, fetal heart rate accelerations (awake
state)
 Fetus spends most of the time in States 1F and 2F.
 Fetal activity has sleep-wake cycles. It may last longer
than 20-80 minutes. It is also dependent on the amniotic
fluid volume. When there is diminished amniotic fluid,
fetal activity may be restricted.
1. Maternal perception of 10 fetal movements in 2 hours is
reassuring. A decrease in movement from the maternal
norm should be evaluated with the non-stress test (NST) and
the biophysical profile (BPS).
2. Fetal movement may also be observed 1 hour after meals
by the mother lying down on the left lateral position. Four
fetal movements should be felt in 1 hour. If movements are
less than 4, continue observation for another hour. If there is
still no improvement, do further testing by NST or by BPS.
3. Fetal movement counting may be done 3 times per week
for 1 hour. The count is reassuring if it equals or exceeds the
previously established baseline.
 THE ELECTRONIC FETAL MONITOR
 Electronic fetal monitoring was pioneered by Edward
Hon (USA) in 1958. The phonocardiogram was the first
instrument used to record fetal heart sounds. However,
this method was abandoned since it also recorded
extraneous sounds producing inferior quality tracings.
 Electronic fetal monitoring can be EXTERNAL
(NON-INVASIVE) or INTERNAL (INVASIVE). The word
external connotes a non-invasive manner of evaluating
fetal heart rate patterns in response to uterine activity as
recorded by the electronic fetal monitor.
 The introduction of the Doppler ultrasound transducer
improved the quality of these tracings. After locating the
fetal heart by auscultation, the Doppler ultrasound
transducer, secured by an elastic strap, is applied to the
maternal abdomen. It emits ultrasound waves in the
direction of the fetal heart.
CHAPTER 18 TEXTBOOK OF OBSTETRICS 3RD EDITION
 According to the Doppler shift principle, the ultrasound
wave undergoes a shift in frequency as it is reflected from
the moving fetal heart valves and from blood ejected
during systole. These ultrasound Doppler signals are
electronically microprocessed by the electronic fetal
monitor through the process of auto-correlation.
 AUTO-CORRELATION is based on the premise that fetal
heart rate has regularity unlike noise which comes at
random without regularity. After electronic editing, a
much improved print out of the tracing is made available.
 The uterine contractions are indirectly assessed by a
toco-transducer placed at the uterine fundus where
strongest uterine contractions are felt. Like the FHR
ultrasound transducer, it is held in place by an elastic strap.
The transducer has a button or “plunger” that is sensitive
to the changes in abdominal contour brought about by the
uterine contractions. The button or plunger moves in
proportion to the strength of the contraction. This is
converted into an electronic signal giving a relative
intensity of the contraction. A print-out is made available
and changes in the fetal heart rate with or without
contractions are recorded.
 CONTROL OF THE FETAL HEART RATE (FHR)
 Fetal heart rate motion is demonstrated by transvaginal
ultrasound as early as day 23. By day 55, the sinoatrial
(SA) and atrioventricular (AV) nodes develop and begin
to control the rate of contractions. As the heart
continues to develop, the conducting systems become
more innervated with autonomic fibers, first sympathetic
and later parasympathetic, which matures at around 32
weeks. As the neural control of the fetal heart matures,
fetal heart rate variability appears.
SYMPATHETIC REGULATION
 Stimulation of the sympathetic innervations of the fetal
heart increases the heart rate due to catecholamine
release from sympathetic nerve endings and from
chromaffin tissues of the adrenal glands. With
catecholamine release, the cardiac effect is acceleration.
However, these agents also induce compensatory fetal
vasoconstriction and fetal hypertension.
PARASYMPATHETIC REGULATION
 This is the most important controlling mechanism of
the FHR. The parasympathetic supply to the heart travels
from the cardio-regulatory center in the ventral surface of
the brainstem to the heart via the cardiac fibers of the
vagus nerve. Stimulation of this vagus nerve releases
 acetylcholine from its nerve endings in the region of the
SA and AV nodes. The net effect is slowing of the fetal
heart rate.
 In the youngest fetus <23 weeks, FHR patterns and
responses will reflect immaturity of the parasympathetic
control of the FHR. The FHR baseline is faster (170-180
bpm) since at this early gestational age, the sympathetic
control predominates.
THE CARDIOREGULATORY CENTER
 The integration of the FHR is the cardioregulatory
center at the ventral and lateral surface of the medulla
in the region of the 4th ventricle. The connections
between the fetal cardioregulatory center and the fetal
heart rate are both direct and indirect.
 The direct parasympathetic pathways are via the vagal
nuclei and the afferent cardiac vagal fibers. The direct
sympathetic control travels from the cardioregulatory
center to the spinal cord, the cervical and thoracic
sympathetic ganglia then to the fetal heart via the cardiac
sympathetic fibers. The indirect control is via sympathetic
discharge and release of catecholamines from the fetal
adrenals.
 Pressure changes (baroreceptors), oxygen concentration
(chemoreceptors) and volume receptors located in the
fetal heart, aorta and carotids also play significant roles in
the control of the FHR and the cardiovascular system.
 Reflex arcs governing the FHR initiated by (1)
HYPOXEMIA, (2) HYPERTENSION, and (3)
HYPOVOLEMIA.
 ELECTRONIC FETAL HEART RATE: BASIC
PATTERNS
BASELINE FHR
 The approximate mean fetal heart rate over a
10-minute segment excluding decelerations,
accelerations and periods of marked variability. NORMAL
VALUE: 110-160 BPM
 FHR BRADYCARDIA: VALUES LESS THAN 110 BPM
 FHR TACHYCARDIA: VALUES MORE THAN 160 BPM
 VARIABILITY
 Fluctuations above and below the FHR baseline; 4
categories used to quantify variability are the following:
CHAPTER 18 TEXTBOOK OF OBSTETRICS 3RD EDITION
 ABSENT FLUCTUATIONS
 MINIMAL (Detectable fluctuations to 5bpm)
 MODERATE (6 bpm- 25 bpm)
 MARKED- SALTATORY (>25 bpm)
 ACCELERATION
 A peak in the FHR above baseline at least 15 bpm
lasting 15 seconds but less than 2 minutes. Before 32
weeks, accelerations increase only 10 bpm lasting 10
seconds.
 DECELERATION
 A decrease in FHR with reference to uterine contractions.
It has 3 categories:
 EARLY DECELERATION (head compression)
 VARIABLE DECELERATION (cord compression)
 LATE DECELERATION (uteroplacental insufficiency)
EARLY DECELERATION (HEAD COMPRESSION)
 A gradual decrease in FHR associated with a uterine
contraction, with return to baseline by the end of the
contraction.
LATE DECELERATION (UTEROPLACENTAL
INSUFFICIENCY)
 Similar to early deceleration but the timing is delayed,
30 seconds or more after the onset of the contraction.
The nadir occurs after the contraction peak and return to
baseline when the contraction is over.
VARIABLE DECELERATION (CORD COMPRESSION)
 Abrupt decrease in FHR below baseline varies in shape,
duration, depth and timing, can occur with or without
contractions; shapes can present as U, V, or W. Variable
decelerations are classified as MILD, MODERATE or
SEVERE.
 MILD VARIABLE DECELERATIONS: have a duration of
less than 30 seconds, regardless of level or a deceleration
below 70-80 bpm, regardless of duration.
 MODERATE VARIABLE have a level less than 80 bpm
regardless of duration
 SEVERE VARIABLES are less than 70 bpm for greater 2. Maternal hypothermia
than 60 seconds.
3. Prolonged hypoglycemia
 The depth and duration of the deceleration correlate to
4. Beta-blocker therapy
the degree of hypoxia and other parameters of the FHR
tracing (loss of variability, baseline tachycardia) 5. Second stage of labor

6. Maternal heart rate being recorded in a case of fetal

demise
PROLONGED DECELERATION

 A decrease in FHR that lasts >2 minutes but <10 minutes;

a decrease > 10 minutes is considered a change in  CAUSES OF DECREASED FHR VARIABILITY
baseline FHR.
1. Fetal sleep cycles

2. Hypoxia/ Acidosis
 SINUSOIDAL PATTERN
3. Extreme prematurity
1. Stable baseline heart rate 120-160 bpm with regular
oscillations 4. Congenital anomalies

2. Amplitude of 5-15 bpm 5. Fetal tachycardia

3. Frequency of 2-5 cycles/ min (as long term variability) 6. Preexisting neurological abnormality

4. Fixed or flat short term variability 7. Drugs: CNS depressants, parasympatholytics (atropine),
beta-blockers
5. Change of FHR accelerations

CAUSES: SEVERE FETAL ANEMIA, ANALGESICS

NON-STRESS TEST (NST)
(Demerol, etc.), AMNIONITIS
 The NST is based on the premise that the heart rate of the
fetus that is not acidotic or neurologically depressed will
temporarily accelerate with fetal movements (reactivity).
 CAUSES OF FETAL TACHYCARDIA Loss of reactivity may be associated with fetal sleep cycles,
acidosis or central nervous system depression. The NST is
1. Fetal hypoxia initiated at 32 weeks AOG on a weekly basis, or earlier
2. Fetal anemia and more frequent in very high risk situations.

3. Fetal sepsis  In the OPD setting, the patient is positioned in a left

lateral tilt manner. With the electronic fetal monitor, the
4. Fetal heart failure FHR is observed with the Doppler ultrasound external
transducer. The patient should not have smoked
5. Fetal tachyarrhythmia
recently because this may affect the test results. The
6. Maternal fever FHR tracing is observed for FHR accelerations that peak
at least 15 beats per minute above the baseline, lasting
7. Maternal hyperthyroidism for 15 seconds, at least 2 or more accelerations, in a 20
8. Beta-sympathomimetic drugs minute period should be observed. It may be necessary
to extend to 40 minutes taking into account fetal
9. Parasympatholytic drugs: atropine, hydroxyzine HCL sleep-wake cycles.
(Iterax), Phenothiazines
 For the term fetus, it has the following characteristics:

1. Adequate FHR baseline of 110-160 bpm

2. Acceleration in the FHR baseline of 15 bpm for 15 seconds

 CAUSES OF FETAL BRADYCARDIA 3. Absence of decelerations
1. Fetal hypopituitarism with brainstem injury

CHAPTER 18 TEXTBOOK OF OBSTETRICS 3RD EDITION

 A REACTIVE NST is re-assuring if the to using does not
have variables, late or prolonged decelerations.
 For the preterm fetus, it has the following characteristics:
1. Adequate FHR baseline, 110-160 bpm
2. Acceleration in the FHR baseline 10bpm for 10 seconds
3. Absence of decelerations
 FETAL ACOUSTIC STIMULATION TEST (FAST)
 The non-reactive NST due to fetal sleep (State 1F) is a
major source of false-alarming test. Stimulating the fetus
with a noxious vibration/ noise (100-105 dB) will startle the
fetus and produce FHR acceleration. The source of the
acoustic stimulation may come from an electronic
artificial larynx delivering 100-105 dB. This is an
accessory part of the fetal monitor set. In its absence, an
electronic driven toothbrush may serve the same
purpose. Either of the 2 sources is positioned on the
maternal abdomen in the area where the fetal head is.
 A stimulation by 1-2 seconds is applied and may be
repeated 3 times up to 3 seconds to elicit FHR
acceleration. Interpretation is the same as regular NST.
This whole procedure reduces over all testing time.
 Preterm infants may require louder sounds to elicit
significant responses, which may produce hearing injury
before 33 weeks AOG.
 CAUSES OF FALSE NEGATIVE NST (NORMAL
TEST IN AN ABNORMAL FETUS)
1. Prematurity
2. Maternal smoking and stress
3. Malnutrition
4. Medications
5. Glycemic levels
6. Fetal sleep states
 CAUSES OF FALSE POSITIVE TEST
(ABNORMAL TEST IN A NORMAL FETUS)
1. Caffeine
2. Cocaine
3. Morphine
4. Sedatives
5. Alcohol
CHAPTER 18 TEXTBOOK OF OBSTETRICS 3RD EDITION
 The Non-Stress Test alone will not detect
oligohydramnios, lethal anomalies, cord and placental
abnormalities, growth disorders, and twin demise.
 The positive predictive value of NST in detecting
metabolic acidosis at birth is only 44%. A non-reactive
NST should be further evaluated by CST or BPS (standard
or modified)
CONTRACTION STRESS TEST (CST)
 The goal of CST is to identify a fetus at risk for
compromise by observing the fetus in the presence of
stress. Stress is introduced through uterine contractions
which interrupt maternal-fetal blood flow. A fetus that is
compromised does not have the oxygen reserve needed to
tolerate this interruption. A compromised fetus will have a
positive CST, meaning a late deceleration pattern will be
displayed.
 In the labor or delivery unit, with the patient in the left
lateral recumbent position. FHR and uterine contractions
are recorded by the external electronic fetal monitor. The
first 30 minutes is recorded to assess FHR baseline, to
identify presence or absence of periodic change and to
determine if there is spontaneous uterine activity. If
there are 3 adequate spontaneous contractions within a 10
minute period, and the FHR recording is of sufficient
quality (without decelerations), the test is finished.
 If there are no contractions, nipple stimulation is done.
This releases endogenous oxytocin from the posterior
pituitary, and uterine contractions are elicited. The patient
initially rolls or tugs on one nipple through the clothing
until contractions occur. If no contractions result following
2-3 minutes, the patient is asked to perform bilateral
nipple stimulation, following a 5 minute rest period. This
cycle of stimulation is then repeated until adequate
activity is documented. Once adequate contractions are
achieved, the nipple stimulation is stopped.
 Dilute exogenous oxytocin IV infusion may also be used
to induce uterine contractions. An infusion pump is used
starting at a dose of 0.5-1.0 mU/min, increasing every
15 minutes by 1.0 mU/min until adequate contractions
are achieved. It is unusual to require an infusion rate of
more than 10 mU/min.
INTERPRETATION:
NEGATIVE TEST: 3 uterine contractions in a 10 minute
period without late decelerations; average baseline
variability and accelerations of FHR with fetal movements

POSITIVE TEST: persistent late decelerations or late
decelerations in more than half of the contractions; minimal
or absent variability
EQUIVOCAL
SUSPICIOUS: late deceleration occurring in less than half of
the uterine contractions
HYPERSTIMULATION: contractions occurring more often
than every 2 minutes or lasting longer than 90 seconds. If no
decelerations in spite of this, the test is negative. If late
decelerations occur, the test is not interpretable and is
classified as hyperstimulation.
UNSATISFACTORY: the quality of the tracing is poor or no 3
contractions occurred in 10 minutes.
 The correlated perinatal mortality within 1 week of a
negative contraction stress test is 1.2/1000 births, negative
contraction value of >99.9% and a positive predictive
value of <35%. When variable decelerations are seen, they
are suggestive of oligohydramnios or cold entrapment.
Sonogram should verify this. The test should be repeated
the next day.
 CST is repeated weekly unless there are some changes in
the clinical situation such as deterioration in diabetic
control, worsening hypertension and decreased fetal
movement.
 Equivocal test results should be repeated the next day.
Positive results are acted on in the context of the clinical
condition and verified by biophysical profile.
 CONTRAINDICATIONS TO PERFORM CST
1. Previous classical C-section or other uterine surgery that
has left a scar to the uterine fundus (danger of uterine
rupture),
2. Premature rupture of membranes before term
3. Placenta previa
4. Incompetent cervix
5. History of preterm labor
6. Multiple gestations
CHAPTER 18 TEXTBOOK OF OBSTETRICS 3RD EDITION
 COMPUTERIZED INTERPRETATION OF FHR
MONITORING
 There are systems available by computerized storage and
interpretation of FHR records obtained from conventional
monitors. There are differences in the visual interpretation
of FHR baseline, variability, accelerations, thus minimizing
inter- and intra- observer interpretations (“eyeballing”).
This gives a more quality information, however, this
methodology has not gained practical acceptance. There
are not many fetuses for whom such precision is required.
More fetuses with equivocal testing on heart rate
evaluation will be referred to ultrasound backup testing.
 BIOPHYSICAL PROFILE (BPP)
 Using real-time B-mode ultrasound, the fetal behavioral
and physiologic characteristics are observed. This is an
adjunct to NST and CST since these two methods have
high false positive results. The test lasts 30-60 minutes
observing 5 variables:
1. NST (which, if all 4 ultrasound components are normal,
may be omitted)
2. Fetal breathing movements, FBM (one or more episodes
of rhythmic fetal breathing movements of 30 seconds or
more within 30 minutes)
3. Fetal movement, FM (3 or more discrete body or limb
movements within 30 minutes)
4. Fetal tone, FT (one or more episodes of extension of a
fetal extremity with return to flexion or opening and
closing of hand within 30 minutes)
5. Amniotic fluid volume (single vertical pocket >2cm or
AFI>5cm)
INTERPRETATION
 Composite score of 8-10 is normal, 6 is equivocal and 4
or less is abnormal. Regardless of the composite score, in
the presence of oligohydramnios, further evaluation is
warranted.
 Manning and colleagues reported a false normal test rate
of 1 per 1000 (antepartum death of a structurally normal
fetus). Causes of death mainly due to fetomaternal
hemorrhage, umbilical cord accidents, and placental
abruption.
 FACTORS INFLUENCING BPP PERFORMANCE
1. DRUGS, ex: sedatives- decrease activity; cocaine- bizarre
fetal movement; indomethacin- oligohydramnios
2. MATERNAL CIGARETTE SMOKING- FBM abolished or
attenuated; FM reduced
3. MATERNAL HYPERGLYCEMIA- sustained FBM/ acidosis;
diminution or abolition of FM/ FT/ CTG reactivity
4. MATERNAL HYPOGLYCEMIA- abnormal behavior
 MODIFIED BIOPHYSICAL PROFILE
 During the 2nd and 3rd trimesters, the amniotic fluid
volume is mainly composed of fetal urine indicating an
adequate renal perfusion. When it becomes low, it can
mean a chronic low uteroplacental perfusion whereby
blood is diverted to more vital organs particularly the brain,
myocardium and adrenals.
 Amniotic fluid volume determination together with
NST is known as the MODIFIED BIOPHYSICAL PROFILE.
It is much easier to do and time of observation is
shortened. A reactive NST with an amniotic fluid index >5
cm is reassuring. If the modified BPP is non-reassuring,
the full BPP or CST should be done.
 Like the NST, CST and BPP, the modified BPP is done
weekly, but may be done more frequently depending on
the clinical situation. (DM, IUGR, HPN)
 UMBILICAL CORD ARTERY DOPPLER
VELOCIMETRY
 DOPPLER VELOCIMETRY is particularly useful in
assessment of pregnancies complicated by growth
restriction or pregnancy associated hypertension/
pre-eclampsia.
 The umbilical arteries reflect placental circulation. Normal
umbilical artery resistance falls progressively through
pregnancy, reflecting increased number of tertiary villi.
Resistance increases in conditions such as infarction,
partial abruption, placental scarring from intervillous
thrombosis, villitis, viral or bacterial.
 Umbilical cord artery flow is done using Doppler
real-time ultrasound. A free floating loop of umbilical
cord is identified, either continuous or pulsed wave
Doppler is used to identify arterial flow. The waveform
pattern is recorded and interpreted. The most frequent
waveform used is the systolic/diastolic ratio (S/D). The
S/D ratio declines as pregnancy continues. The presence
of diastolic flow is better interpreted than the absolute
value of the S/D ratio.
 Normally growing fetuses have high-velocity diastolic flow
in the umbilical artery. Growth restricted fetuses have
diminished, absent or reversed end-diastolic flow.
CHAPTER 18 TEXTBOOK OF OBSTETRICS 3RD EDITION
Reversal of flow is associated with perinatal morbidity and
mortality.
 MIDDLE CEREBRAL ARTERY DOPPLER
STUDIES (MCA)
 Measuring the fetal middle cerebral artery peak systolic
velocity is very sensitive for detecting fetal anemia. This
is usually done in the RH-sensitized fetus. It is less costly,
no risk to worsening fetal anemia due to fetomaternal
bleed from invasive procedures like amniocentesis. There
is also no risk for infection.
 Low levels of fetal hemoglobin causes a decrease in
cardiac output and a decline in blood viscosity. A fetus is
considered anemic if MCA values is > 1.5 multiple of the
median (MOM). The mother undergoes cordocentesis to
obtain fetal hemoglobin and hematocrit to estimate blood
for transfusion.
OTHER NON-INVASIVE MODALITIES
 The following are non-invasive modalities to assess fetal
health but are still under investigation:
1. MAGNETOCARDIOGRAPHY: the instrument, a
magnetocardiogram, contains biomagnet meter channels
that permit examination of the fetal cardiac conduction
system on the basis of electrophysiological signals. The
instrument is compact and easy to handle. It is claimed to
be helpful in detecting fetal arrhythmias, IUGR, and fetal
acidosis. This can supplement fetal electrocardiography.
At present, there is not enough data to establish standards
for its acquisition and analysis.
2. VENOUS DOPPLER ULTRASOUND WAVEFORM: the
use of color and pulsed Doppler ultrasound to identify
normal and abnormal venous waveforms may predict
adverse outcome in high risk fetuses. This will add to the
knowledge provided by the umbilical artery blood flow
studies and will give a clear perspective of the
hemodynamic changes of the fetal cardiovascular system.
This is still under investigation.