ANTENATAL FETAL SURVEILLANCE

1. Anterpartum Fetal Surveillance

2. • Assessment of fetal well being in utero before the onset
of labor
• Goal: To prevent fetal injury and fetal death..
ANTEPARTUM FETAL SURVEILLANCE

3. ANTEPARTUM FETAL SURVEILLANCE
• Improves long term neurologic outcome through
optimal timing of delivery
• equips us to avoid unnecessary intervention,
• such as cesarian delivery and preterm delivery.

4. The fetal heart rate results from the combined
effect of several fluctuating influences
mediated
through extrinsic and intrinsic cardiac control
mechanisms.

5. What regulates the Fetal Heart Rate

6. What regulates the Fetal Heart Rate

7. Physiology of Fetal Heart ResponsePhysiology of Fetal Heart Response
• FHR pattern, level of activity and degree of muscular
tone  sensitive to hypoxemia and acidemia.
• Redistribution of fetal blood flow in response to
hypoxemia  diminished renal perfusion and
oligohydramnios.

8. • However, acute, catastrophic changes in fetal status,
such as those that can occur with placental
abruption or an umbilical cord accident, are
generally not predicted by test of fetal well-being.

9. Adverse fetal and neonatal outcomes
associated with antepartum asphyxia

10. Patient selection
 Patients at risk for perinatal morbidity and/or mortality
 Not done where there are fetal abnormalities that are
incompatible with life.

11. Indications for Antepartum Fetal Surveillance Testing
MATERNAL CONDITIONS FETAL CONDITIONS
Severe hyperthyroidism Decreased fetal movement
Symptomatic hemoglobinopathy Oligohydramnios
Cyanotic heart disease IUGR
Chronic renal disease Post-term pregnancy
Type I diabetis Alloimunization
Marked uterine anomalies Macrosomia
Fetal anomalies or aneuploidy
PLACENTAL CONDITIONS Multiple gestation
APS
SLE OTHERS
Hypertensive disorders (PIH) IVF pregnancy
Thrombophilia Teratogen exposure
Marked placental anomalies Previous stillbirth
Prior neurologic injury
Previous recurrent abortion
Obesity

12. Frequency of testing
 It should be individualized.
 Usual testing is once to twice weekly
 Daily – aid in the timing of delivery to maximize gestational age
while avoiding significant intrauterine morbidity in preterm fetuses

13. Suggested Antenatal Fetal Surveillance
Condition Begin
Surveillance
Timing
Pregnancy-induced hypertension At diagnosis Weekly BPP ― + UA Doppler
Preeclampsia At diagnosis Twice weekly BPP ― + UA doppler
Chronic hypertension 28-32 wk Weekly BPP or MBPP
FGR At diagnosis Integrated fetal testing
Gestational diabetes
A1
A2
At 40 wk
At 36 wk
Weekly BPP or MBPP
Weekly BPP or MBPP
Pregestational diabetes At 28-32 wk Twice weekly BPP/MBPP
Diabetes with macrosomia At diagnosis Twice weekly BPP/MBPP
Vascular disease At 24-28 wk Integrated fetal testing
Postterm At 41 wk Twice weekly BPP/MBPP
Multiple gestation, concordant fetus FGR At 32-34 wk Weekly BPP/MBPP
Multiple gestation, discordant fetus FGR At diagnosis Integrated fetal testing
BMI >30 At 36 wk Weekly BPP or MBPP

14. Antenatal Fetal Testing Techniques
• Fetal movement counting
• Non-stress test
• Contraction stress test
• Biophysical profile
• Maternal – fetal doppler studies

15. Fetal Movement Counting
• The only antenatal surveillance technique
recommended for all pregnant women with or
without risk factors

16. Fetal Movement Counting
• Maximal activity is between 28-32 weeks
gestation
• Gradual reduction toward term
–due to the fetus/amniotic fluid volume ratio
–maturing fetus with longer sleep cycles.
• Highest incidence of fetal movement was in
the late evening.

17. Chronic hypoxia
↓
Attempt to reduce oxygen consumption
and
conserve energy
↓
Reduction or cessation of
fetal body movements

18. Fetal Movement Counting
• Normal daily fetal movement count was
associated with good outcome
• Low movement counts were associated with
fetal asphyxia and fetal death
• When stillbirth occurred, movements
diminished rapidly and stopped 12 to 24 hours
prior to fetal death

19. Reduced Fetal Movement
• Earlier warning of asphyxia
• Fetal compromise
• Nonreactive NST
• Positive CST
• Low Apgar score
• IUFD

21. Non-stress test
Principle: heart rate of a fetus that is not
acidotic or neurologically depressed will
temporarily accelerate with fetal movement.
- FHR accelerations reflect CNS alertness and
activity (fetal well being)

22. Non-stress test
• Use to determine the following:
a. Inadequate delivery of oxygen/ and or nutrition in
fetal tissue
b. Inadequate placenta exchange due to decrease
blood flow, decrease surface area or increased
membrane thickness
c. Inadequate maternal nutrients or oxygen to the
placenta

23. Baseline FHR
• Average FHR rounded to 5 bpm during a
10 minute period but excludes
• Periods of marked increased FHR
variability
• Segments of baseline that differs by more
than 25 bpm
• Normal: 110-160 bpm
• Bradycardia: <110 bpm
• Tachycardia: >160 bpm
• The minimum baseline duration must be
at least 2 minutes
• Always documented as range

24. Fetal Tachycardia
• Baseline FHR of >160 bpm
• Increased in sympa-parasympathetic tone,
sometimes associated with decrease in FHR
variability
• Etiology
– Fetal hypoxia
– Maternal fever
– Drugs amnionitis
– Hyperthyroidism
– Fetal anemia

25. Fetal Tachycardia
• Significance
– Usually hypoxemia is not the reason, especially in a
term fetus and a identifiable cause such as maternal
fever of drugs
– Can be non-reassuring sign if associated with late
decelerations or absent variability
• Intervention
– Maternal fever – can be reduced by antipyretics and
IV hydration
– Maternal oxygenation: supersaturation with O2 by
facemask
– NRFS: expeditiously deliver

26. Fetal bradycardia
• FHR of < 110 bpm for > 10 minutes
• Etiology
– Late (profound) fetal hypoxemia
– Beta blocker
– Anesthetics
– Maternal hypotension
– Prolonged umbilical cord compression

27. Fetal bradycardia
• Clinical significance:
– with loss of variability or late decelerations: NRFS
– Substantial bradycardia (90 bpm) especially if
prolonged and uncorrectable is a sign of impending
fetal acidemia
– Mild bradycardia: 90-110 bpm with moderate
variability and absence of late decelerations is
generally reassuring
• Intervention: correction of underlying etiology, if
not correctable usually emergent CS

28. Baseline Variability
• Fluctuations in the heart rate of more than 2 cycles
per minute.

29. Undetectable
Minimal variability
Moderate (normal) variability

30. Marked variability
Sinusoidal pattern

31. Variability
• Normal irregularity of cardiac
rhythm
• Balancing interaction of the
sympathetic and parasympathetic
nervous system
• Results from sporadic impulses
of the cerebral cortex

32. Variability
• Etiology of decreased variability
– Hypoxemia/acidemia
– Meds: narcotics, barbiturates, anesthetics,
parasympatholytics
– Fetal sleep cycle (20-40 minutes)
– Congenital anomalies
– Fetal cardiac arrhythmias
– Extreme prematurity

33. Variability
• Significance and intervention for decreased
variability
– Depends on the cause
– No intervention if transient secondary for fetal sleep cycle
or CNS depressants
– If hypoxemia is suspected: try to improve fetal blood
oxygenation:
• Maternal positioning
• Hydration
• Correcting maternal hypotension
• Maternal oxygenation
• Elimination of uterine stimulation

34. Sinusoidal Pattern
• Sine wave with undulating baseline
– Regular oscillation with an amplitude of 5-15 bpm
– 2-5 cycles per minute
– Minimal or absent short term variability
– Absence of accelerations
– Extreme regularity and smoothness
• Etiology: fetal hypoxemia from fetal anemia,
often secondary to Rh isoimmunization

35. Modanlou and Freeman proposed
adoption of a strict definition:
1. Stable baseline heart rate of 120 to 160 bpm with regular
oscillations,
2. Amplitude of 5 to 15 bpm (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, and
6. Absent accelerations.

36. Acceleration
• A visually apparent abrupt increase
(onset to peak in < 30 sec) in the FHR
• At > 32 weeks, a peak of >15 bpm
from baseline, with a duration of > 15
sec but < 2 min from onset to return
• < 32 weeks, a peak of > 10 bpm from
baseline, with a duration of ≥ 10 sec
but < 2 min from onset to return
• Prolonged acceleration lasts ≥ 2 min,
but < 10 min
• If an acceleration lasts 10 min, it is a
baseline change

37. Acceleration
• Etiology:
– Stimulation of sympathetic ANS
– Spontaneous fetal movement
– Vaginal examination
– Abdominal palpation
– Environmental stimuli ( noise)
– Scalp or vibroacoustic stimuli
– Uterine contractions
– Insertion of FSE

38. Acceleration
• Clinical Significance:
– Sign of fetal nervous system and reassuring FWB
– Repetitive accelerations: contractions compress
umbilical cord and cause transient fetal
hypotension -> baroreceptors -> increase in FHR

39. Decelerations
• Early deceleration
• Late deceleration
• Variable deceleration
• Prolonged deceleration

40. Early deceleration
• Gradual decrease (onset to nadir >30 sec) of FHR and return to
baseline
• Nadir at time of uterine contraction peaks
– Shape: uniform, mirror contraction of contraction phase
– Onset: early in contraction
– Recovery: with return of contraction to baseline
– Deceleration: rarely <110 bpm or 30 bpm below baseline
– Occurrence: repetitious with each contraction, usually in active
phase of labor or passive 2nd
stage

41. Early deceleration
• Etiology:
– Uterine contraction: fetal head compression  to
altered cerebral blood flow to vagal stimulation
– CPD (especially when occurs early in labor)
– POP
• Significance:
– No pathologic significance

42. Late Deceleration
• Visually apparent usually symmetrical
gradual decrease and return of the FHR
associated with a uterine contraction
• A gradual FHR decrease is defined as
from the onset to the FHR nadir of ≥ 30
sec
• The decrease in FHR is calculated from
the onset to the nadir of the deceleration
• The deceleration is delayed in timing,
with the nadir of the deceleration
occurring after the peak of the
contraction
• In most cases the onset, nadir, and
recovery of the deceleration occur after
the beginning, peak, and ending of the
contraction, respectively

43. Late Deceleration

44. Late Deceleration
• Etiology: uteroplacental insufficiency
– Uterine hyperstimulation
– Maternal supine hypotension
– Gestational hypertension
– Chronic hypertension
– Postterm gestation
– Amnionitis
– IUGR
– Poorly controlled maternal diabetis
– Placenta previa
– Abruption/maternal shock
– Spinal anesthesia

45. Late Deceleration
• Clinical significance:
– Non reassuring sign when persistent and uncontrollable
– When associated with decrease variability and/or
tachycardia: sign of fetal acidemia
– As myocardial depression increases, depth of late
deceleration decreases, becoming more subtle
– Single deceleration is not clinical significant if rest of
tracing is reassuring

46. Intervention for late deceleration
• Change maternal position to lateral
• Correct maternal hypotension
– Legs up, heads down
– IV fluid bolus
– Vasopressors
• Correct uterine hyperstimulation
– Stop oxytocin
– Consider tocolytic (0.2 – 0.5mg Terbutalin IV)
• Hyperoxygenate maternal blood with O2
• Cervical exam
– Labor status
– Fetal scalp stimulation (only when FHR at baseline)
– Consider FSE
• If repetitive and uncontrollable: expeditious delivery

47. Variable Deceleration
• Visually apparent abrupt decrease in FHR
• An abrupt FHR decrease is defined as
from the onset to the FHR nadir of <30 sec
• The decrease in FHR is calculated from
the onset to the nadir of the deceleration
• The decrease in FHR is ≥ 15 bpm, lasting
≥ 15 sec, and < 2 min in duration
• When variable decelerations are
associated with uterine contraction, their
onset, depth, and duration commonly vary
with successive uterine contractions

48. Three pathways involved with variable
decelerations

49. Variable Deceleration
• Etiology
– Maternal position (cord
between fetus and pelvis)
– Cord around fetal neck or
other part
– Short cord
– True knots
– Prolapsed cord
– Oligohydramnios
– After ROM

50. Variable Deceleration
• Reassuring fetus
– Mild to moderate variable decelerations
– Rapid return to baseline
– Normal, not increasing baseline
– Moderate variability
• Non reassuring features
– Severe variable deceleration
– Prolonged return to baseline
– Increasing baseline
– Absent or minimal variability

51. Recurrent decelerations
• Decelerations occur with 50% of uterine
contractions in any 20 minute segment.
– Recurrent variable deceleration – at least 3 in 20
minutes
– Recurrent late deceleration – would lead to
consideration of cesarian delivery unless the abnormal
results are believed to be a result of a reversible
maternal condition such as diabetic ketoacidosis or
pneumonia with hypoxemia

52. Prolonged deceleration
• > 15 bpm for >2 minutes, < 10
minutes
• Shape: Variable
• Variability: often lost
• Recovery: often followed by
period of late deceleration and
or rebound tachycardia
• Some fetuses don’t recover ->
terminal bradycardia

53. Prolonged deceleration
• Etiology
– Cord prolapse
– Maternal hypotension (supine or regional anesthesia)
– Tetanic uterine contractions
• Oxytocin
• Abruption
• Cocaine
– Maternal hypoxemia
• Seizures
• Narcotic overdose
• MgSO4 toxicity
• High spinal anesthesia
– Fetal head compression or stimulation can produce strong vagal response
• pelvic exam, sustained maternal Vasalva, rapid fetal descent

56. FIGO CTG classification criteria, interpretation
and recommended management

57. Normal NST

58. Abnormal NST

60. Contraction stress test
• Based on the response of the FHR to uterine
contractions
• Principle: fetal oxygenation will be transiently
worsened by uterine contractions

61. • According to ACOG, an adequate uterine
contraction pattern is present when at least 3
contractions persist for at least 40 seconds
each in a 10 minute period

62. • Uterine stimulation is not necessary if the patient is
having spontaneous uterine contractions of
adequate frequency.
• If fewer than three contractions of 40 seconds’
duration occur in 10 minutes, contractions are
induced with either nipple stimulation or intravenous
Oxytocin.

63. Contraindications to CST
• PROM
• Previous classical cesarean delivery
• Placenta previa
• Incompetent cervix
• History of premature labor in this pregnancy
• Multiple gestation

64. Negative CST
Negative: no late or significant variable decelerations

65. Negative CST

66. Positive CST - late decelerations after 50% or more of
contractions (even if the contraction frequency is fewer
than three in 10 minutes)

67. Positive CST

68. Hyperstimulation

69. • Equivocal–suspicious: intermittent late decelerations
or significant variable decelerations

70. • Equivocal: FHR decelerations that occur in the
presence of contractions more frequent than every 2
minutes or lasting longer than 90 seconds

71. • Unsatisfactory: fewer than three contractions in 10
minutes or an uninterpretable tracing

73. Biophysical Profile
• Between 24 and 28 weeks’ gestation,
approximately 50% of NSTs are non reactive.
• In contrast, sonographically evaluated variables are
valid early in gestation and account for 3 of the 5
components of BPP.
• The BPP may be used to verify fetal well being if
the NST is not reactive

74. Biophysical Profile
• Fetal movement and fetal tone develop between 7.5 and 9
weeks menstrual age,
• Fetal breathing movements are detectable by at least, 17-
18 weeks gestation.
• Amniotic fluid may be reduced as early as 17.5 weeks by
fetal acidosis.
• The components of BPP develop sequentially. In order of
appearance: tone, movement, breathing, reactivity.

75. Biophysical Profile
• Fetal state (wake-sleep cycle) plays an important role in
interpretation of the BPP.
• In quiet sleep, the average time to obtain a normal BPP is
26.3 minutes.
• The BPP is, therefore, continued for a maximum of 30
minutes.

76. Biophysical Profile
• The sonographic variables that develop last in gestation are
the most sensitive to acidosis and would be the first
components of the BPP to become abnormal.
• The NST, breathing and AFV are the most significant
variables.

77. Biophysical Profile
• The NST and fetal breathing movements are suppressed
when the pH falls below 7.2.
• If the pH falls below 7.10, fetal tone and fetal movements
become abolished.
• The presence of oligohydramnios with all of the other
variables of BPP being normal may reflect chronic
uteroplacental insufficiency.

78. Fetal Central Nervous System Centers
FT Cortex E
M H
FM Cortex nuclei B Y
R P
FBM Ventral surface Y O
of 4th
ventricle O X
G I
NST Posterior hypothalamus, E A
medulla N
E
S
I
S

79. Biophysical profile

80. Interpretation and Management of BPP

81. Modified Biophysical Profile
• NST and AFI
• If either the NST or the AFI is abnormal, a
complete BPP or a contraction stress test
(CST) is performed.

82. Factors Affecting the Biophysical Profile
Activity FHR
Acceleration
FT FM FBM AFV
Fetal sleep ↓ ↓ ↓ ↓
Early gestational age ↓ ↓
Late gestational age (>42 wk) ↓ ↓ ↓ ↓
Maternal glucose ingestion — — ↑
Maternal alcohol ingestion ↓/— ↑/—
Maternal magnesium
administration
↓ ↓
Artifical rupture of membranes ↓ ↓
PROM ↓
Labor ↓

83. Maternal and fetal causes of Stillbirth within one
week of a normal Biophysical Profile Score
Maternal Fetal
Placental abruption
Diabetic ketoacidosis
Sickle cell crisis
Drug overdose
Motor vehicle accident
Acute MI
Acute alcohol poisoning
Fetomaternal hemorrhage
Cord prolapse
Ruptured membranes
Vasa previa
Cord entanglement
Umbilical artery thrombosis

84. Biophysical Profile
• The observation of an abnormal BPP in an
anomalous fetus does not correlate very well
with the presence of hypoxia.
• The BPP cannot bee used in fetuses with
congenital muscular diseases or CNS conditions
that would affect muscular functions.
• If an anomalous fetus had a previously normal
BPP, a decreasing score should be considered an
indication of compromise.

85. Doppler studies
• allows assessment of placental status and,
therefore, helps to place other testing results
in context as well as helping to determine the
relative risk of sudden fetal deterioration

86. Doppler Abnormality Dictates Frequency of
Biophysical Profile Scoring
Abnormality BPP Frequency Decision to Deliver (Fetal)
Elevated
indices only
Weekly Abnormal BPP or term‖
or >36 wk with no fetal
growth
AEDV Twice weekly Abnormal BPP or >34 wk of
proven maturity
Conversion to REDV
REDV Daily Any BPP <10/10 or >32 wk
of dexamethasone given
REDV-UVP Three times daily Any BPP <10/10 or >28 wk
of dexamethasone given

88. Uterine Artery Doppler Velocimetry
• Uterine Artery is the branch of the internal iliac
artery originating close to the iliac bifurcation
• The uterine arteries cross the external iliac artery
on either side to reach the uterus at the cervico-
isthmic junction. At this point it divides into the
ascending and descending branches.
• The ascending branch divides into the arcuate,
radial and spiral arteries.

89. Anatomy of Uterine Artery

91. Normal Doppler waveform characteristics
• At the start of pregnancy, the uterine signal pattern
shows high pulsatility with high systolic and low
diastolic flow velocities in addition to an early diastolic
(postsystolic) notch.
• This notch represents a pulse wave reflection due to
an increased peripheral vascular resistance and is the
spectral counterpart of incomplete trophoblast
invasion.
• Under physiologic conditions, the end diastolic
velocities increased with continued gestation while
vascular resistance decreases as placentation
progresses.

92. • Beyond this period, the diastolic notch gradually disappeared
and is not seen after 23 weeks.
• Throughout the gestation there is steady increase in the
diastolic flow with lowering of the RI
Doppler spectra recorded
from the uterine artery at
different gestational ages.
The progressive increase in
diastolic flow velocity is a
result of normal
trophoblast invasion.

93. Effects of Medications on uterine artery
waveform
• Medications increased EDV and lower resistance
indices and hence improve uteroplacental circulation
- Betamimetics
- IV magnesium
- Methydopa and hydralazine
- Nifedipine
- Nitrate oxide

94. Clinical significance of uterine artery doppler
ultrasound
• Abnormal uterine blood flow velocities correlate well
with:
- Existing or impending fetal growth retardation
- Preeclampsia
- Increased rated of prematurity, placental abruption cesarean
section and low birth weight

95. Indication Of Uterine Artery Doppler
• Previous or present history of preeclampsia or any
other maternal disease like:
- Maternal collagen vascular disease
- Maternal hypertension DM with vasculopathy
- RPL – no work up or APL positive
• Previous child with IUGR
• Unexplained high maternal alpha fetoprotein level
• High hCG levels

96. Abnormal Uterine Artery Doppler
• Persistence of the diastolic notch (bilateral notch or
unilateral notch on placental side)
• High vascular resistance (increased indices)
• RI or PI >95th
percentile
• Difference between right and left uterine artery S/D
ratio >1.0
• Uterine artery S/D >2.6 after 22-24 weeks scan
• Important is normograph of PI of uterine artery. PI
should go down as the pregnancy advances.

97. Abnormal uteroplacental vascular system, with
lack of dilatation of the spiral arteries.
Normogram

98. • It is now understood that uterine artery doppler as a
screening test in the low risk pregnancy has little or
no value. Its value is limited to high risk pregnancies.
• If the PI values of both uterine arteries are both
normal, the patient can be informed that most likely
will not develop preeclampsia or have an IUGR fetus.
• This is because of the high negative predictive value
(>99%) of the test.

99. Flowchart for Doppler evaluation of the uterine
artery in high-risk patients

100. Treatment
• AIM – abnormal uterine artery doppler in early
pregnancy can be effectively treated before onset of
pregnancy complications
• Treatment options:
- Aspirin
- Vitamin C/E
- Low molecular weight heparin

101. Umbilical Artery Doppler Velocimetry
• Arise from the internal iliac artery of the fetus and course
along the umbilical cord in a long and winding path to reach
the placenta
• Intra placentally, they branch into the primary stem villous
arteries, which in turn branch into the secondary and tertiary
stem villous vessels
• The tertiary stem villi form the vascular bed of the umbilical
arteries
• As the pregnancy advance, there is increase in the tertiary
stem villi and small muscular arteries leading to decrease in
the placental vascular bed resistance

102. Color doppler image of a free loop of
umbilical cord demonstrating the two
arteries (red) and one vein (blue) at 28
weeks
Normal color doppler frequency
spectrum sampled from the
umbilical artery

103. Umbilical Artery (UA)
Doppler Velocimetry
• Nonivasive technique to assess blood flow
• UA reflects placental circulation
• UA resistance falls progressively through
pregnancy
• UA resistance increased in a number of
pathologic conditions such as infarction,
intervillous thrombosis, and damage from
villitis

104. UA Doppler Velocimetry
• As the UA resistance rises, diastolic velocities
fall, and ultimately become absent (absent
end-diastolic velocity) or reversed end-
diastolic velocity.

105. Umbilical Artery Doppler Velocimetry
• S/D ratio – most commonly used index
- abnormal if >95th
percentile for AOG
- Absent or reversed flow signify
increased impedance to UA blood
flow.
- Poorly vascularized placental villi

106. Normal umbilical artery waveforms
• Early weeks of gestation (till 12 weeks) – absent end diastolic
blood flow
• Between 12 to 14 weeks – end diastolic blood flow develops
• Beyond 14 weeks - end diastolic blood flow progressively
increases
• As pregnancy develops, there is increase in end diastolic
blood flow and the RI is low
• Umbilical artery sampling is not done in early pregnancy

107. Umbilical artery waveform patterns as a function of gestational age.
Note the steady, physiologic increase in peak systolic flow velocities and
especially in diastolic velocities with advancing gestational age. The
absence of diastolic flow at 10 weeks’ gestation is a normal finding.

108. Abnormal Waveforms
• Low diastolic flow (high resistance) i.e.
resistance indices above the 95th
percentile
• AEDF
• REDF
- above 3 types are an indication of increasing
resistance which correlates with FETAL
HYPOXIA

109. Normal UA Doppler Velocimetry

110. Elevated UA Doppler Velocimetry
• Suggest placental injury
• Correlate with IUGR in <60%
• Indicates continue monitoring fetal growth,
amniotic fluid volume and fetal well-being.

111. Elevated UA Doppler Velocimetry

112. Absent End-Diastolic Velocity

113. Reversed End-Diastoloc Velocity

114. Abnormal umbilical artery doppler
• Umbilical artery RI > 0.8 is always abnormal at any gestational age.
• PI values range from 2.0 to 1.5 in second trimester and 1.5 to 1.0 in
third trimester, Values above this is abnormal.
• S/D ratio >3 in umbilical artery beyond 30 weeks is abnormal.
Doppler waveform becomes abnormal 2 weeks earlier than
abnormal CTG.
• Transient AEDF may be due to cord compression or due to
myometrial contraction
• Changing patient’s position or examination after sometime can
show a normal doppler waveform
• Do not report the absence of EDV until this has been demonstrated
on 2 successive days.

115. • It is important to note that normal umbilical artery
waveforms after 34 weeks’ gestation do not exclude
fetal hypoxemia and acidemia
• Loss of end-diastolic frequencies occurs only when
over 70% of the placental vascular bed has been
obliterated. The latter is less likely to occur after 34
weeks’ gestation, hence the limitation of umbilical
artery doppler at later gestation

116. Treatment
• >32-34 weeks
Abnormal doppler contributes to decide to
deliver
• In second trimester
weigh risk of hostile intrauterine environment
vs risk of extreme prematurity

117. AEDF
• Uteroplacental insufficiency
• Will progress to REDV over time
• Altered brain blood flow
• IUGR
• Not compatible with term fetus
• Best rest, aggressive management of maternal disease
30 % improve within 48 hours
• Improvement supports continuation of pregnancy in
second trimester
• 80-100% are delivered by CS
• Perinatal mortality in AEDF: 9%

118. AEDV
• Indication for preparation for delivery
• Cortcosteroid administration
• Maternal evaluation for HPN, renal diseases,
connective tissue disorder or thrombophilias
• Congenital anomaly screening
• Immediate evaluation of fetal well-being

119. Absent End-Diastolic Velocity

120. REDV
• Delivery as soon as possible
• Associated with very significant abnormalities
of cerebral perfusion and often with abnormal
venous circulation.
• Associated with highest frequency of fetal
compromise, neonatal complications,
perinatal morbidity and mortality.

121. Reversed End-Diastolic Velocity

122. • REDF
Quantified by ratio of highest amplitude forward flow
(A)/maximum reverse flow (B)
- A/B ration >4.3 without venous pulsation in free loop
may support expectant management in second
trimester
- Perinatal mortality REDF : 36%
- REDF is associated with fetal demise within 1-7 days
- Addition of venous doppler – more information on
fetal response to adverse conditions

123. Middle cerebral artery doppler velocimetry
• The circle of Willis is formed by the anastomosis of the MCA,
ACA and PCA facilitated by their respective communicating
arteries.
• Why MCA is chosen for sampling?
• MCA has a conducive course and high reproducible, easy to
identify and can be studied easily with an angle of 0 degrees
between the ultrasound beam and the direction of the blood
flow, providing information on the true velocity of blood flow.

124. • Unlike the uterine and umbilical artery
vascular beds which constantly change with
advancing gestational age, the MCA vascular
bed resistance is almost constant throughout
pregnancy.
• RI = 0.75-0.85

125. • The MCA is most easily visualized in a transverse plane. First
the fetal head is imaged in the standard biometry plane, and
then the plane is shifted downward the skull base at the level
of sphenoid bone. This brings into the view the circle of Willis.
• The best site for recording a doppler spectrum is
approximately 2mm from the circle of Willis or at the origin of
the ICA.

126. • Hyperactivity of fetus, increase of intauterine
pressure (polyhydramnios) and external pressure to
the fetal head (e.g. by the probe) might erroneously
increase EDV velocities.

127. Abnormal MCA
• During hypoxia, fetal compensatory mechanisms
cause constriction of the splanchnic, renal and
pulmonary vascular beds with redistribution of the
arterial blood flow to the cerebrum, mycocardium,
adrenals. This is reflected in the MCA as increased
diastolic flow with reduced PI.

128. Cerebroplacental Ratio
• in normal fetus, the placental vascular
resistance decreases as pregnancy advances,
whereas the MCA resistance is almost
constant
• PI MCA/ PI UMB A >1
• If < 1, indicates fetal hypoxia

129. • Protective mechanism allows increased proportion of the
umbilical blood flow to go to brain
• With IUGR/ hypoxia up to 70% of flow is shunted to
brain/coronaries
• MCA diastolic flow increases – SD ratio decreases
• UA SD ration increased as placental resistance increases
• Eventually, UmA SD ratio > MCS SD ratio -= brain sparing
pattern

130. Abnormal MCA Doppler
• Brain edema sparing: high diastolic, decrease PI
• When O2 deficit is greater, PI tends to rise, which
presumably reflects development of brain edema
• Reversal in MCA: cerebral edema
• In growth retarded fetus the disappearance of
brain sparing or presence of reversed MCA flow is
a critical event for the fetus and precedes fetal
death

131. Abnormal frequency spectrum recorded from the MCA with color
doppler in a fetus with severe IUGR at 27 weeks. This waveform
pattern, called the brain-sparing effect, is characterized by increased
end diastolic flow velocities.

132. Absent Diastolic Blood Flow in MCA

133. REDF in MCA

134. MCA Flow
• MCA is more sensitive to hypoxia than
umbilical artery.
• MCA response to fetal hypoxia is instant.
• High systole in MCA – Fetal anemia
• High diastole in MCA – brain sparing effect in
fetal hypoxia

135. Recommendations of ACOG in antepartum fetal
surveillance (Level B)

136. Recommendations of ACOG in antepartum fetal
surveillance (Level B)