Doppler in obstetric power point presentation (4)

Doppler Ultrasound in Obstetrics
DR.RIYADH AL ESAWI
DMRD, MSc, PhD
assist .Prof. Diagnostic Radiology
Faculty of Medicine/Kufa University
The Doppler effect, which was first reported
by Christian Doppler in 1842, describes the
apparent variation in frequency of a light
or a sound wave as the source of the wave
approaches or moves away, relative to an
observer.

 SGA and IUGR are too often used synonymously
though there is a degree of overlap.
 SGA fetus is not necessarily growth retarded.
Baby may be constitutionally small not at increase
risk.
 Late onset of pathological cessation of growth
may produce a baby with typical feature of IUGR--
-increase perinatal mortality and morbidity.

FETAL DYSMATURITY
Incidence
Dysmaturity compromises one third of
LBW babies.
 In developed countries about 3-10%
 Term babies 5%
 Post term 15%

LOW BIRTH WEIGHT
 WHO has defined LBW as one whose
birth weight is less than 2500 g irrespective
of gestational age.
 Very low birth weight =<1500 g
 Extremely low birth weight < 1000 g.

Fetal growth
 Up to 16 weeks there is cellular hyperplasia
 16-32 weeks –hyperplasia and hypertrophy
 After 32 weeks– hypertrophy.
 Most of fetal weight gain ( two third) occur
beyond 24th week of gestation.

types
 Based on clinical evaluation and U.S
examination.
 1-fetuses those are small and healthy.
Birth weight is less than 10th percentile for
gestational age, they have normal ponderal
index, normal subcutaneous fat and usually have
uneventful neonatal course.

 2-fetuses where growth is restricted by
pathological process –true IUGR.
 Depend on relative size of their head,
abdomen and femur, they are subdivided
into.
 Symmetrical , type 1
 Asymmetrical ,type 2

Symmetrical 20%
 Effect involve cellular hyperplasia
 Reduced total cell number.
 Most often caused by structural or chromosomal
abnormalities or congenital infection (TORCH).
 Pathological process is intrinsic to the fetus and
involve all organs including the head.

Asymmetrical 80%
 Affect cellular hypertrophy in later months of
gestation.
 Total cell number is normal but small size.
 Pathological process is maternal, extrinsic to the
fetus.
 Placental cause with shunting of oxygen and
nutrients to the brain.

Biophysical
 First examination 16-20 weeks should confirm
gestational age , anomalies.
 USG 2-3 weekly
 Diagnosis of IUGR type
 Head circumference/abdominal circumference ratios
 > 1- before 32weeks, elevated—asymmetrical IUGR.
 =1, 32-34 weeks– asymmetrical IUGR
 <1 after 34 weeks- 85% IUGR fetuses are detected
 AC – single most sensitive parameter.

 Serial measurements of AC and fetal weight are
more diagnostic.
 Femur length , is not affected in asymmetrical IUGR
 FL/AC=22 from 21 weeks to term
 FL/AC> 23.5-IUGR.
 Amniotic fluid volume
 Vertical pocket of amniotic fluid <1 cm suggest IUGR.
 Four quadrant technique measuring vertical diameter
of largest pockets of fluid in each of 4 quadrants of
uterus , the sum of results is AFI
 AFI 5-25 cm is normal.
 Anatomical survey to exclude fetal abnormalities.
 BPD measurement.

Placental grading
 Grade 0; seen in less than 18 weeks
 Uniform echogenecity with smooth chorionic plate.
 Grade 1 ;18-29 weeks, occasional parenchymal
calcification/ hyper-echoic area.
 Grade II. >30 weeks, occasional basal
calcification/hyper-echoic areas may also have
comma type densities at the chorionic plate.
 Grade III > 39 weeks
 Significant basal calcification.
 Chorionic plate interrupted by indentations.
An early progression to grade III placenta is some
times associated with placental insufficiency.

Doppler indices that are commonly used in
obstetrics. D, diastole; PI, pulsatility index;
RI, resistive index;
S, systole
Quantative analysis
Qualitative analysis
Diastolic notch
Absent EDF
Reverse EDF

Fetal circulation (Moore KL, Persaud TVN 1998 and Whitaker, Kent
2007) 4

Fetal circulation
There are three major vascular shunts
Ductus venosus -between umbilical vein and IVC
Foramen ovale- between right and left atria
Ductus arteriosus-between pulmonary artery and
descending aorta.

Doppler studies
Maternal side– uterine arteries
Placental side----umbilical arteries
Fetal side---MCA+ descending aorta
venous circulation ----DV, hepatic ,
umbilical veins
fetal heart.

 The uterine arteries branch into arcuate which lead
to spiral arteries within the myometrium.
 With advancing gestation due to trophoblastic
invasion of uterine spiral arteries , it dilates and
result in fall in the resistance to blood flow.
 Uterine artery flow in non pregnant women is 50
ml/min, and increase to 700 ml/min in 3rd trimester.
 Hence , in normal pregnancy diastolic component is
transformed from one of low peak flow and diastolic
notch to one of high flow and no diastolic notch by
18-22 weeks, PI < 1.2 is normal.
 PI> 1.45 with bilateral notches , sign of clinically
significant uteroplacental vascular ischemia.

Uterine artery score
Abnormal uterine artery flow
Increase resistance , high RI and PI
Persistent of early diastolic notch.
Score ¼-4/4

Placental side;Umbilical
arterial circulation
The umbilical arterial circulation is normally a low
impedance circulation , with an increase in the
amount of end diastolic flow with advancing
gestation . Umbilical arterial Doppler waveforms
reflect the status of the placental circulation, and
the increase in end diastolic flow that is seen
with advancing gestation is a direct result of an
increase in the number of tertiary stem villi that
takes place with placental maturation . Diseases
that obliterate small muscular arteries in
placental tertiary stem villi result in a progressive
decrease in

end-diastolic flow in the umbilical arterial Doppler waveforms
until absent, and then reverse flow during diastole is noted.
Reversed diastolic flow in the umbilical arterial circulation
represents an advanced stage of placental compromise, and
is associated with more than seventy percent of placental
arterial obliteration .
The presence of absent or reversed end diastolic flow in the
umbilical artery is commonly associated with severe
intrauterine growth restriction and oligohydramnios .
Doppler waveforms of the umbilical arteries can be obtained
from any segment along the umbilical cord.Waveforms
obtained from the placental end of the cord show more end
diastolic flow than

waveforms obtained from the abdominal cord
Insertion . Differences in Doppler indices
of arterial waveforms obtained from different
anatomic locations of the same umbilical cord
are generally minor and have no significance on
clinical practice.

Umbilical artery Doppler
Abnormalities
Increase resistance , RI, PI, S/D
Absent diastolic flow
Reverse diastolic flow

Blood flow class (BFC)
BFC=I , mean+2 SD
BFC=II , mean=3SD
BFC=III a
BFC=IIIb

Fetal side; Middle cerebral
circulation
The cerebral circulation is normally a high
impedance circulation with continuous
forward
flow throughout the cardiac cycle.
The middle cerebral artery is the most
accessible
cerebral vessel to ultrasound imaging in the
fetus,
and it carries more than 80% of cerebral blood
flow.

In the presence of fetal hypoxemia, central
redistribution of blood flow occurs, resulting in an
increased blood flow to the brain, heart, and
adrenals, and a reduction in flow to the
peripheral and placental circulations.
This blood flow redistribution is known as the
brain-sparing reflex, and plays a major role in
fetal adaptation to oxygen deprivation.

Middle cerebral artery Doppler waveforms,
obtained from the proximal portion of the
vessel, immediately after its origin from the
circle ofWillis, have shown the best
reproducibility.

Late third trimester MCA Doppler spectrum
 At the late third trimester, the PI, RI, and S/D decrease and
the AT increases due to decrease of vascular resistance which
may be attributed to the increase of deoxyribonucleic acid in
the fetal brain (Chandra et al).

34 weeks viable fetus with normal umbilical artery blood flow.

 In the hypoxic fetus, the cerebral vasculature dilates
and this causes a reduction in the MCA pulsatility
index in a phenomenon known as “brain sparing”.
With disease progression the fetus is no longer able to
compensate, and resistance in the MCA increases.
 In the preterm (<32 weeks) small for gestational age
fetus, MCA Doppler has limited accuracy in predicting
acidaemia in the absence of other Doppler
abnormalities.
 In the term small for gestational age fetus with
normal umbilical artery Doppler, an abnormal MCA
Doppler (PI < 5th centile) has moderate predictive
value for acidosis at birth and should be used to time
delivery.

 Transient MCA-REDF likely occurs due to
excessive external probe pressure and is an
artifact that is of no clinical consequence.When
this occurs, it is suggested that the
measurements are repeated and confirmed by a
second operator with attention to minimizing
transducer pressure.
 Rarely, persistent MCA-REDF occurs , which
indicate severe fetal morbidity and mortality.

example
 30 yrs pregnant leady with 32 weeks gestation
 USG, shows HC/AC> 1.3
 Liquor amount- severe oligohydramnios
 AFI=3.5 cm.
 MCA PI=1.27
 UA PI=1.4
 CPR=0.9
 impression-fetal hypoxia/IUGR.

 Sonographic criteria for diagnosis of IUGR
 1-elevated HC/AC ratio PPV 62%.
 Elevated ratio of FL/AC
 Presence of oligohydramnios without
ruptured membranes.
 Presence of advanced placental grade
(Grannum grade III).

 MCA Doppler in fetal anaemia

 In 1990 G.Mari proposed the use of MCA Doppler
for the diagnosis of fetal anaemia.
 The sensitivity of PSV for the prediction of
moderate –severe anaemia without hydropse
was 100% with a false positive 12%.
 The PPV and NPV were 65 % and 100 %
respectively.

 The risk of anaemia was high in fetuses with
a PSV of 1.5 times the median or higher.
 Fetuses with values below 1.5 either did not
have anaemia or had only mild degree.

Fetal Aorta
Thoracic aorta has higher PI&RI than abdominal
aorta
Time average mean velocity is constant 35_+
5.5 cm/s

Thoracic descending aorta in
healthy fetus

IUGR IN 27 WEEK descending
aorta

Fetal side, venous Doppler
Doppler waveforms obtained from the central
venous circulation in the fetus reflect the
physiologic status of the right ventricle. Specific
information with regards to right ventricular
preload, myocardial compliance, and right
ventricular end-diastolic pressure can be derived
from Doppler flow studies of the inferior vena
cava and ductus venosus in the fetus .

Inferior vena cava Doppler waveforms can be obtained from
a coronal plane of the chest and abdomen.
In this view, the inferior vena cava can be imaged as it
enters into the right atrium, joined by the ductus venosus
and the left hepatic vein .
The inferior vena cava can be studied at two locations: at
the inlet into the right atrium, or in the segment between
the entrance of the renal vein and the ductus venosus.
A good correlation coefficient exists between these two
measurement sites, and the location that provides the
smallest angle of insonation with the blood flow should
be chosen .

Inferior vena cava Doppler waveforms are
triphasic in shape, with the first phase
corresponding to ventricular systole, the second
phase to early diastole, and the third phase to
late diastole or the atrial kick.

Doppler velocity waveforms of the
inferior vena cava in a normal fetus in
the third trimester of pregnancy.

DUCTUS VENOSUS
the ductus venosus can be identified as it branches
from the umbilical vein,Turbulence is commonly
seen within the ductus venosus given its narrow
lumen,The presence of turbulence on color flow
Doppler helps in identifying the ductus venosus in
early gestations. Ductus venosus Doppler
waveforms are biphasic in shape, with the first
phase corresponding to ventricular systole, the
second phase to early diastole, other consider
second phase to late diastole or the atrial kick.

Doppler velocity waveforms of the ductus venosus
in a normal fetus in the third trimester of
pregnancy.

Ductus venosus
Abnormal ductus venosus
Doppler in a trisomy 21 .
shows retrograde flow
during atrial contractions

twin pregnancy
 Growth in multiple pregnancy
 Most of these fetuses are constitutionally small
and are not suffering from uteroplacental
insufficiency.
 An inter- twin growth discrepancy 20-25% is
considered to be significant.
 Twin –to -twin transfusion syndrome
(TTTS)color Doppler finding in the donor are
susally typical of utero-placental insufficiency.

Example
 USG findings in early onset severe IUGR at 28 weeks, anatomical finding
short femurs and echogenic bowel..
 Biometry
 EFW 640 g< 10th centile. HC/AC ratio 1.35 (normal <1.2)
 AFI =7 cm
 Doppler finding
 Uterine arteries B/L early diastolic notches
 Lt.uterine artery PI 1.97, RT PI 1.65
 UA absent EDF in both.
 Smooth umbilical venous cord flow, peak velocity 16 cm/s.
 MCA PI 1.12 (redistribution).
 Ductus venosus positiveA wave 32 cm/s, normal.
 biophysical profile score-8/8 normal.

 Cerebro-placental ratio is better predictor of
IUGR, than MCA or UA alone
 Diagnostic accuracy for CPR was 90%,
compared with 78>8% for MAC and 83.3 for
umbilical artery.
 normal CPR> 1.08.

 Protocol (after 28W)
 Step (1) : Assess fetoplacental circulation (Umb.A)
 If abnormal >>> Fetoplacental insufficiency.
 Step (2) : Assess fetal arterial circulation (M.C.A)
 If abnormal >>> arterial redistribution (Brain sparing
mechanism).
 Step (3) : Assess fetal venous circulation(D.V)
 If abnormal >>> (Impending) Fetal heart failure.

Table (1) Middle CerebralArtery (MCA), UmbilicalArtery( UA)
and CPR (MCA/UA) DopplerWaveform Parameters at 16-20
Weeks Gest.Age. 17
Parameter
No=60
Mean Range SD SEM
95% Confidence Interval
Lower limit Upper limit
MCPI 1.64 1.27-1.96 0.16 0.021 1.60 1.68
MC RI 0.77 0.62-0.86 0.042 0.0054 0.76 0.78
MC S/D 4.53 3.0-7.0 0.88 0.11 4.30 4.76
MC AT(ms) 70.13 32-96 16.61 2.140 65.84 74.42
UA PI 1.35 0.9-1.74 0.171 0.022 1.31 1.39
UA RI 0.72 0.57-0.8 0.050 0.006 0.71 0.737
UA S/D 3.73 2.34-5.13 0.62 0.080 3.57 3.89
UAAT(ms) 96.78 56-120 14.49 1.870 93.03 100.52
MC PI/UA PI 1.22 0.92-1.62 0.164 0.021 1.18 1.26
MC RI/ UA RI 1.06 0.91-1.29 0.090 0.016 1.04 1.08
MC S.D/ UA
S.D
1.23 0.9-2.01 0.32 0.041 1.15 1.32
MC AT/UAAT 0.73 0.4-1.11 0.17 0.022 0.68 0.77

Table (2) DopplerWaveforms of MCA, UAand MCA/UARatio
18 Parameters at the 24-28Weeks GestationalAge (Week).
Parameter
No= 60
Mean Range SD SEM
95% Confidence Interval for Mean
MCPI 1.82 1.25-2.43 0.26 0.034 1.75 1.89
MC RI 0.81 0.68-1.0 0.058 0.0075 0.80 0.83
MC S/D 5.81 3.1-12.6 1.80 0.23 5.34 6.27
MC AT(ms) 60.23 40-88 10.07 1.30 57.63 62.83
UA PI 1.13 0.6-1.45 0.18 0.023 1.08 1.17
UA RI 0.67 0.44-0.8 0.062 0.008 0.65 0.68
UA S/D 3.14 1.79-4.64 0.62 0.080 2.98 3.31
UAAT(ms) 101.31 80-136 12.96 1.67 97.95 104.67
MCPI/UAPI 1.64 1.1-2.55 0.30 0.039 1.56 1.72
MC RI/UA
RI
1.22 0.97-1.81 0.13 0.018 1.18 1.25
MC S.D/
UA S.D
1.88 0.91-5.08 0.65 0.084 1.71 2.05
MC AT/UA
AT
0.59 0.35-0.9 0.12 0.016 0.56 0.63

Table (3) Dopplerwaveforms of MCA, UAand MCA/UARatio
Parameters at the 36-40Weeks GestationalAge (Week). 19
Parameter
No=60
Mean Range SD SEM
95% Confidence Interval for Mean
MCPI 1.62 0.95-2.59 0.35 0.045 1.53 1.71
MCRI 0.78 0.6-0.92 0.071 0.0092 0.746 0.78
MC S/D 4.67 2.47-8.1 1.37 0.18 4.31 5.02
MC AT(ms) 66.58 48-96 10.00 1.29 63.99 69.16
UA PI 0.92 0.52-1.23 0.16 0.021 0.87 0.96
UA RI 0.58 0.42-0.7 0.069 0.009 0.57 0.60
UA S/D 2.48 1.74-3.3 0.40 0.051 2.38 2.60
UAAT(ms) 98.05 56-144 16.99 2.19 93.65 102.44
MCPI/UAPI 1.80 1.03-3.26 0.48 0.061 1.68 1.93
MCRI/UARI 1.30 1.01-1.71 0.16 0.021 1.25 1.34
MC S.D/ UAS.D 1.91 1.02-3.54 0.62 0.084 1.75 2.07
MC AT/ UAAT 0.69 0.31-1.0 0.15 0.020 0.65 0.73

Fetal cardiac Doppler
Doppler indices in fetal echocardiography are
quantitative parameters, and are for the majority,
angle dependent.To obtain accurate Doppler
indices in fetal echocardiography, the sample
volume is placed distal to the respective valves, the
insonating angle 15-20 degree.

Doppler waveforms should be obtained during fetal
apnea, and multiple measurements should be
made. Color Doppler is used to direct placement of
the sample volume; placing the sample volume at
the brightest colors of the blood flow segment will
ensure the best measurements.

The fetal circulation is different from the adult
circulation in many aspects.The fetal
circulation is in parallel, rather than in series,
and the right ventricular cardiac output is
greater than the left ventricular cardiac output .
The progressive development of organs during
gestation influences blood distribution and
vascular impedance .

 With advancing gestation, ventricular
compliance is increased, total peripheral
resistance is decreased, preload is increased, and
combined cardiac output is increased .
Compliance of the fetal left heart increases more
rapidly than compliance of the fetal right heart
with advancing gestation .

The pulmonary vascular resistance is high in the
fetus and the pulmonary arterial pressure is
almost systemic. Flow to the pulmonary
vascular bed is maintained at a low rate with
a noted increase toward the end of gestation
. Cardiac output in the fetus is mainly affected
by preload and ventricular compliance .The
presence of right to left shunts at the level of
the foramen ovale and ductus arteriosus has
a significant impact on cardiac flow patterns
and affects the distribution of blood and
oxygen to various organs.

Flow across the foramen ovale contributes
to the majority of blood entering the left
ventricle and more than two thirds of right
ventricular output is directed to the ductus
arteriosus .This shunting mechanism ensures
the delivery of blood with high oxygen content
to the coronary and cerebral circulations

Doppler waveforms across the atrioventricular valves
are biphasic in shape.The first peak (E wave),
corresponds to early ventricular filling of diastole,
and the second peak (A wave) corresponds to atrial
systole or the atrial kick. Unlike in postnatal life,
the velocity of the A wave is higher than that of the
E wave in the fetus .This highlights the importance
of the role that atrial systole plays in cardiac filling
in the fetus. E/A ratio increases with advancing
gestation and reflects ventricular diastolic function
. E and A velocity peaks are higher in the right
ventricle, and this right ventricular dominance is
noted from the first trimester.

Shifting to left ventricular dominance starts in utero
toward the end of gestation . E/A ratio is an index
of ventricular preload and compliance .
Doppler waveforms across the semilunar valves
are uniphasic in shape. Indices most commonly
used for the semilunar Doppler waveforms include
the peak systolic velocity (PSV) and the time to
peak velocity (TPV). PSV andTPV increase with

advancing gestation across the semilunar
valves. PSV is higher across the aorta than
across the pulmonary artery because of a
decreased after load and a smaller diameter
across the aorta .These Doppler indices
reflect ventricular contractility, arterial
pressures, and after loads.

Mitral valve
Pulsed-Doppler study showing
normal mitral inflow. apical
image with the sample volume
(S) placed in the mitral orifice
between left atrium (LA) and
left ventricle (LV). normal inflow
pattern with an initial large
passive flow (E) followed by a
later smaller active flow (A)
produced by atrial systole.

Echo indices in semilunar
valve
Doppler indices that are commonly used in fetal echocardiography. (A) Peak
systolic velocity (PSV) is the peak velocity achieved during one cardiac cycle.
(B) Acceleration time (AT) is the time it takes the velocity to reach its peak in
one cardiac cycle. (C )Time velocity integral (TVI) is the integral of the
planimetric area under the curve.TVI expresses the distance that the red
blood cells would have to cover with a constant area of the flow section.

Fetal Doppler and intrauterine
growth
restriction
Arterial Doppler abnormalities, at the level of the
umbilical and middle cerebral arteries (brain-
sparing reflex), confirm the presence of
hypoxemia in the growth-restricted fetus, and
present early warning signs. Once arterial
centralization occurs, however, no clear trend is
noted in the observational period, and thus
arterial redistribution may not be helpful for the
timing of the delivery

On the other hand, the presence of reversed
diastolic flow in the umbilical arteries is a sign of
advanced fetal compromise, and strong
consideration should be given for delivery, except
for extreme prematurity. Cesarean section should
be given preference in this setting, because labor
may cause further fetal compromise

The current literature suggests that venous Doppler
abnormalities in the inferior vena cava and ductus
venosus and abnormal fetal heart rate
monitoring, even in its computerized version,
follow arterial Doppler abnormalities and are thus
associated with a more advanced stage of fetal
compromise.

Furthermore, in the majority of severely growth
restricted fetuses, sequential deterioration of
arterial and venous Doppler precedes
biophysical profile score deterioration . At
least one third of fetuses show early signs of
circulatory deregulation-

1 week before biophysical profile deterioration,
and that in most cases, Doppler deterioration
preceded biophysical profile deterioration by
1 day.

The occurrence of such abnormal late stage changes
of vascular adaptation by the intrauterine growth-
retarded (IUGR) fetus appears to be the best
predictor of perinatal death, independent of
gestational age and weight In a longitudinal study
on Doppler and IUGR fetuses, all intrauterine
deaths and all neonatal deaths had late Doppler
changes at the time of delivery, whereas only a
few of the surviving fetuses showed such changes
.

This sequential deterioration of the hypoxemic,
growth-restricted fetus is rarely seen at gestations
beyond 34 weeks . Indeed, normal umbilical artery
Doppler is common in growth restricted
fetuses in late gestations, and cerebroplacental
ratios have poor correlation with outcome of
IUGR fetuses at greater than 34 weeks of gestation.

Caution should therefore be exercised when Doppler is
used in the clinical management of IUGR fetuses
beyond 34 weeks of gestation.The pathophysiology of
fetal growth restriction has not been fully described
because recent studies have highlighted the presence
of significant variation in fetal adaptation to
hypoxemia.The pattern of incremental deterioration
of arterial Doppler abnormalities, followed by venous
Doppler abnormalities, then followed by fetal heart
tracings and biophysical profile abnormalities, is not
seen in about 20% of preterm fetuses

Furthermore, only 70% of IUGR fetuses show
significant deterioration of all vascular beds by the
time they were delivered, and about 10% showed
no significant circulatory change by delivery time .
In a prospective, observational study, more than
50% of IUGR fetuses delivered because of abnormal
fetal heart rate tracings did not have venous
Doppler abnormalities . In view of these findings,
the universal introduction of venous Doppler in the
clinical management of the growth-restricted fetus
should await the results of randomized trials on this
subject.

IUGR is associated with several changes at the level
of the fetal heart involving preload, afterload,
ventricular compliance, and myocardial
contractility. An increase in afterload is seen at
the level of the right ventricle because of
increased placental impedance . A decrease in
afterload is noted at the level of the left ventricle
because of decreased cerebral impedance
associated with the brain-sparing reflex .These
changes in afterload result in a redistribution of
the cardiac output from right to left ventricle .
Preload is reduced at both atrioventricular valves
because of

hypovolemia and decreased filling associated with
IUGR.This decrease in preload is reflected by a
decrease in the E/A ratio, decreased atrial peak,
and decreased time velocity integral at the mitral
and tricuspid valves.

myocardial contractility
Reduced myocardial contractility in the presence of
severe IUGR has also been reported.
Ventricular ejection force, an index of ventricular
systolic function that is independent of preload and
after load is decreased at the level of the right and
left ventricle in fetal growth restriction . IUGR fetuses
that have reduced ventricular ejection force have a
shorter time to delivery, a higher incidence of non
reassuring fetal heart rate tracing, and a lower pH at
birth when compared with controls.

A significant correlation between the severity of
fetal acidosis at cordocentesis and ventricular
ejection force values validates the association
of this index and the severity of fetal compromise.
Myocardial cell damage, demonstrated
by elevated levels of cardiac troponin-T, is seen in
some fetuses that have severe growth restriction .
This advanced stage of fetal compromise is
associated with signs of increased systemic
venous pressure,

a change in the distribution of cardiac output, a rise
in right ventricle afterload, and a high incidence of
tricuspid regurgitation .These findings suggest
that Doppler abnormalities in the proximal venous
system of the growth restricted fetus suggest fetal
myocardial cell damage and increased systemic
venous Pressure.

The fetal heart plays a central role in the adaptive
mechanisms for hypoxemia and placental
insufficiency. Studies showed umbilical artery and
middle cerebral artery are the first variables to
become abnormal .These arterial Doppler
abnormalities are followed by abnormalities in the
right cardiac diastolic indices, followed by the right
cardiac systolic indices, and finally by both left
diastolic and systolic cardiac indices . Preserving
the left systolic function as the last variable to
become abnormal ensures an adequate left
ventricular output, which supplies the cerebral and
coronary circulations.

Several of the Doppler changes seen in association
with fetal IUGR in the peripheral circulation
are directly related to the adaptation of the
fetal heart.The current management of IUGR
involves Doppler at the peripheral arterial circulation(
middle cerebral and umbilical arteries), central
venous vessels (ductus venosus and inferior vena
cava), and cardiotocography. Adding cardiac
Doppler may improve management of the IUGR

Fetus, however, changes in the central venous
circulation reflect an advanced stage of fetal
compromise, commonly associated with
myocardial dysfunction and damage.

Doppler in obstetric power point presentation (4)

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