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Blood Flow Analysis During Pregnancy
1
Reference Values
During an uncomplicated pregnancy the end-diastolic
flow in the uterine aa. or the arcuate aa. is 쏜50% of sys-
Fig.
tolic peak maximal velocity (
4.4). The resistance
index (RI) is nearly constant at 0.35 after the 20th week
of pregnancy, with a maximal value near RI = 0.50.
After the middle of pregnancy a persistent postsystolic
notch, especially on the placental side of the uterus
must be considered to be abnormal.
Physiological Flow Changes
Brief maternal exertion may be followed by an increase
in impedance in the uteroplacental aa., which may be
enhanced in a complicated pregnancy (Campbell and
Cohen-Overbeek 1987).
Uterine contractions are accompanied by reduction
of the blood supply to the intervillous space (
(Fendel and Sohn 1989).
Studies of the uteroplacental aa. showed marked reduction in flow velocities, especially in diastole,
without a dicrotic late systolic notch in a previously
normal waveform (Fendel 1986, Fendel et al. 1984,
1986, 1987, Fleischer et al. 1987, Janbu et al. 1985). This
is probably due to summation. Experimental data suggest that during a contraction some of the vessels
piercing the myometrium are completely compressed
(Borrell et al. 1965). Medications that delay labor may
contribute to increased diastolic blood flow.
Fig. 4.5)
70
60
50
40
RI
30
20
10
0
24-27 28-31 32-35 36 -39 ≥ 40
Weeks of gestation
Fig. 4.4 Changes in the RI of a uteroplacental a. during pregnancy. Box and whisker plot. Boxes: 25th, 50th, and 75th per-
centiles; whiskers 10th and 90th percentile (reproduced from
Vetter 1991b).
The position of the mother during the procedure influences the pulsatility index (PI) of the uterine a. The
PI falls significantly when changing from the supine to
the left lateral position. The explanation for this may
be that the contractions diminish at the same time,
suggesting an indirect effect of the tone of the uterine
wall, which is dependent on position (Park and Hidaka
1991).
Brief maternal heat stress, for example, in a sauna,
does not lead to flow changes in the uteroplacental and
fetoplacental aa. Only in a few cases where the blood
pressure fell could a rise in the S/D ratio be demonstrated (Vaha et al. 1991).
54
kHz
2
0
kHz
2
0
kHz
2
0
1 sec 1 sec
1 sec
70
mmHg
60 sec
Fig. 4.5 Doppler sonogram of
a utero-placental a. during a
contraction (reproduced from
Fendel and Sohn 1989).
kHz
2
0
kHz
2
0
Fetoplacental Vessels
Abnormal Flow Changes
Vascularization of the placental bed is marked not only
by trophoblast invasion (Pijnenborg et al. 1980), but
also by considerable dilatation of the vascular lumina
due to humoral factors. High levels of estrogens have
been identified as one of the responsible factors (Moll
et al. 1988). Their mode of action is probably a rise in
nitrogen monoxide (NO) (Campbell 1993). This would
explain the rise in the diastolic flow velocities in the
uteroplacental aa. that may be seen from the beginning
of the second trimester, and the disappearance of the
late systolic notch in the waveform by the 26th week of
pregnancy at the latest (Fleischer et al. 1986). If these
necessary anatomical adaptations to an increased
demand for perfusion do not occur, the pregnancy is at
risk. Often the result is preeclampsia, or pregnancy-induced hypertension (PIH) (Brosens 1977), or in-
trauterine growth retardation (IUGR) resulting from the
placental hypoperfusion (Campbell et al. 1983, Cohen-
Fetoplacental Vessels
Overbeek et al. 1985, Hackett et al. 1986). Occlusive
vascular lesions in the spiral aa. can lead to a similar result (Sheppard and Bonnar 1980). A close connection
between changes in the placental bed and those in the
uteroplacental flow curves has been demonstrated by
postpartum biopsies of the placental bed (Voigt and
Becker 1992). Vascular spasms or morphological
changes in the vessels are marked by a clearly elevated
flow impedance in the vessels (Fleischer et al. 1986,
Trudinger et al. 1985, Vetter et al 1986).
Medications
β1-sympathomimetic drugs probably facilitate dias-
tolic blood flow by reducing uterine muscle tone (Vetter et al. 1989). On the other hand, atenolol, a selective
-blocker, raises the PI in the uteroplacental vascular
β
1
bed and in the fetal aorta if blood flow volume in the
aorta and the umbilical v. is maintained (Montan et al.
1987).
Basic Concepts
Umbilical Vessels
Blood flow in the umbilical aa. is analyzed qualitatively, because quantitative analysis is impractical due
Fig.
to problems with the presence of two vessels (
The evaluation covers systolic/diastolic changes. Ele-
vated flows are taken as a sign of adequate villous stem
vessel architecture. As pregnancy progresses, the villi
mature and impedance declines, leading to an increase
in diastolic flow rate (Trudinger 1987). The major decline in pressure responsible for this occurs in the
small arteries and arterioles of the tertiary villi (Becker
1981).
4.6).
Reference Values
The RI of the umbilical aa. tends to diminish as pregnancy progresses, declining from ca. 0.70, maximally
0.80 at 24 weeks of gestation, to 0.55, maximally 0.65
at term. The values then remain constant (
Early in pregnancy diastolic flow is absent in all
cases up to the 10th week of pregnancy. The proportion
of fetuses in whom diastolic flow is present then rises
continuously to 100% at week 15 (Arduini and Rizzo
1991, Jauniaux et al. 1992).
Fig. 4.7).
Fig. 4.6 Doppler sonogram of an umbilical a.
100
90
80
70
RI
60
50
*
*
*
*
during pregnancy. Box and whisker plot. Boxes: 25th, 50th, and
75th percentiles; whiskers 10th and 90th percentile. Confidence level: * p 쏝 0.05, ** p 쏝 0.01 (reproduced from Vetter
1991b).
30
컄Fig. 4.7 Changes in the resistance index of an umbilical a.
20
24-27 28-31 32-35 36-39 ≥ 40
Weeks of gestation
55
Blood Flow Analysis During Pregnancy
56
1
Physiological Flow Changes
The waveforms of the umbilical aa. are quite variable.
For one thing each artery may supply a terminal bed
that differs materially from the other. Therefore, before
prematurely interpreting marked fluctuations between two readings, the two arteries should be analyzed separately. But even fetal factors can influence
the extent of these fluctuations materially. Movements
of the extremities or respiratory movements are accompanied by noticeable changes in the flow curves
(van der Mooren et al. 1991).
Some indications of increased impedance in the fetoplacental circulation have been found when the
mother was supine (Marx et al. 1986). This led to the
hypothesis of a “sluice flow” in the villous stem vessels.
The flow was thought to be brought about by compression of vessels resulting from backflow from the dilated intervillous space. Other authors were unable to
confirm any change in umbilical blood flow (Fitzgerald
et al. 1984, Park and Hidaka 1991). There is no change
in the fetoplacental circulation in a healthy pregnant
woman when standing. A rise in the S/D ratio was only
found in hypertensive gravid women, especially those
in whom an increase in peripheral resistance had been
ascertained (Sørensen et al. 1992).
Elevated maternal blood pressure readings without
changes in the placenta or fetus are accompanied by
normal flow patterns in the umbilical aa. (Fitzgerald et
al. 1984, Fleischer et al. 1986, Milliez et al. 1983).
Changes in the total viscosity of cord blood have at
most a minor influence on umbilical a. impedance
(Steel et al. 1991). Even when plasma viscosity was examined separately no connection with the Doppler
sonogram could be found (Fairlie et al. 1991).
Small changes in oxygen supply do not influence the
flow indices in the fetal and fetoplacental vessels significantly (Meyenburg et al. 1991).
Pathological Flow Changes
Deviations from the norm in the flow curve are an indication of changes in the placental vessels. The total
developmental disorders and pathological changes in
the vessels must be considerable to be detectable in
the waveform. In animal experiments at least half the
placental vessels had to be embolized before the PI
rose (Muijsers et al. 1991). One should also note that
areas of infarction can have no further influence on the
waveform. They are invisible to Doppler sonography.
Pressure changes, however, do seem to have an influence on blood flow through the umbilical aa.: A re-
duction in the amount of amniotic fluid of itself can increase the impedance in the fetoplacental circulation,
probably by mechanical compression. In pronounced
oligohydramnion the rise in impedance in the umbilical aa. was suppressed temporarily by instilling fluid
(Wladimiroff 1988).
Morphological Changes
Morphological changes in the fetoplacental bed correlate with changes in the course of flow velocity
changes in the umbilical aa. (Giles et al. 1985, Jimenez
et al. 1988, McCowan et al. 1987). Such changes may
come about primarily in the fetal vessels, but they may
also be a consequence of uteroplacental problems. In
such cases diastolic flow velocities decline. Histologically, normal Doppler sonograms correspond either to
normal vascular and villous architecture, or to focal lesions compensated by degenerative vascular disease or
growth. In the absence of compensatory changes, diastolic flow in the umbilical aa. diminishes (Hitschold et
al. 1992, Nordenvall et al. 1991). In fetuses with growth
retardation and normal Doppler sonogram vascularization in the terminal villi was found to take its normal
course (Hitschold et al. 1993).
The unusual biological situation of multiple pregnancy in a woman with several gestational sacs induced Giles et al. (1993) to look for disturbances in
blood supply. The distinguishing criteria were blood
flow and S/D ratio on the one hand, and proportion of
small arteries in the placenta on the other. There were
clear-cut differences in microvascular supply between
siblings with different Doppler sonograms. The
authors interpreted this finding as suggesting that
vascular problems derive from the fetal rather than the
uteroplacental circulation. This interpretation needs
confirmation.
Extreme changes in the waveformpresent a separate
category: diastolic or end-diastolic flow may be absent
ig.
F
4.8) or even reversed (Fig. 4.9) (absent or reversed
(
diastolic flow = ARED flow). These are signs of significant or even extreme general change in the placental
circulation. Reverse flow signifies that a part of the
blood between the fetus and the placenta simply oscillates between fetus and placenta. In sum such flow
patterns are “ominous signs of grave impairment of
fetal blood supply” (Battaglia et al. 1993) or warnings
of “catastrophic perinatal end-results” (Brar and Platt
1988).
Perinatal mortality in such cases is considerable and
runs between 30% and 60 % depending on the proportion of very small premature babies (maximum 100 %)
(Schmidt et al. 1991). Most often this coincides with
considerable growth retardation (Chaoui et al. 1991,
Graca et al. 19991) and, last but not least, many of these
babies have chromosomal aberrations. Whether it is
correct to classify reverse flow as an indication for aggressive as opposed to conservative management in
view of its successes (Hadi et al. 1991) requires confirmation before such a procedure is universally adopted.
Detailed analyses of flow distribution in cases with
reverse flow in the umbilical a. show that reverse flow
is also present in the aortic arch, while flow in the
carotid a. is forward. Evidently in this situation it is not
the placenta but the brain that is the vascular bed with
the lowest flow resistance. The reverse flow is often
more marked in the aortic arch than more distally in
the descending aorta. This fact may be explained by
the additional diastolic filling from the pulmonary a.
through the ductus arteriosus (Fouron et al. 1993).
This assertion is supported by the observation that
in growth-retarded fetuses with absent diastolic flow
the flow volume over the tricuspid and pulmonary
valves is increased when compared to the flow in fe-
tuses of normal size. The ratio of left to right flow
volumes is 2.15:1 instead of an expected ratio of about
1.33:1 (Reed et al. 1987).
One observation clarifies the possible mechanism of
the pathology of reverse flow: High pressure impedes
the fetoplacental flow so severely that the incoming
blood is, as it were, reflected. Concurrent Doppler
analysis during active labor, in which variable decelerations occurred in the cardiotocogram (CTG),
showed reverse flow, where the flow curve was normal
before and after contraction (Weiss et al. 1991). A complication involving the umbilical cord could be the
basis on which this event might be explained.
The contribution of Doppler sonography in determining risk in postterm fetuses is small. While at one
time a significant but irrelevant difference in the S/D
ratio of 2.42 was found in children with an abnormal
pregnancy outcome as opposed to 2.19 for a normal
one (Fischer et al. 1991), other authors were unable to
use waveforms to elicit differences that might have
had prognostic value (Malcus et al. 1991, Stokes et al.
1991, Weiner et al. 1993).
The notch in the aortic waveform described by us,
which we called “term effect” in the Doppler sonogram, was observed prominently in a Swedish clinic,
where the length of observation was extended signifi-
cantly beyond 294 days (Malcus et al. 1991). This phe-
4.10) often occurs in the last days before
nomenon (
spontaneous delivery. It is a reflection of the complex
circulatory changes that occur at the end of pregnancy
and that at times coincide with dilatation of the aorta
simultaneously with the diastolic increase in flow in
the vessels supplying the brain. Whether the trigger
for these changes is increased flow resistance in the
systemic circulation of the fetus, or whether there is an
active reduction in flow impedance in the vessels of
the brain remains to be determined.
In individual cases with premature separation of the
normal placenta, and coincidentally with placental infarcts, unequal blood flow images were obtained from
the two umbilical aa., indicating major differences in
the terminal vascular beds of the two arteries (Harper
and Murnaghan 1986a). Arteriovenous shunts are
special placental disorders that can accompany
placental angiomata. It is to be expected that in these
cases the total flow resistance will be reduced, leading
to a correspondingly elevated diastolic flow. The most
Fig.
Fetoplacental Vessels
Fig. 4.8 Doppler sonogram of an umbilical a. with end-diastolic block.
Basic Concepts
Fig. 4.9 Doppler sonogram of an umbilical a. with reverse diastolic flow.
57
Fig. 4.10 Doppler sonogram of a descending aorta with postsystolic notch.
Blood Flow Analysis During Pregnancy
1
significant feature, however, is the massively increased
flow volume through the umbilical v., which eventually leads to the manifestations of decompensation in
the fetus (Arbenz and Real 1986, Kaplan and Assali
1972, Vetter 1991b). This might take the form of a
functional atrioventricular valvular insufficiency due
to excessive dilatation of the heart from volume overload.
A special case is the feto−fetal transfusion syndrome
(FFTS), which has given rise to some very contradictory
opinions in the literature. The question is: Under what
circumstances can transfusion from one twin to the
other take place? In fact, abnormal flow waveforms can
be observed in the terminal stage in both twins. All
other study results are so controversial that they cannot be summarized conclusively in brief.
Fig. 4.11 Doppler sonogram of an umbilical vein running next
to an umbilical a.
Umbilical Vein
Blood flow in the umbilical v. is constant and slow
4.11). Readings from this vessel may be inter-
(Fig.
preted in two ways: 1. The whole perfusion of the
placenta can be determined quantitatively, and 2. Deviations from the continuous flow waveform indicate
cardiac pathology, or intra-abdominal or intrathoracic
pressure fluctuations.
Reference Values
The fetal side of placental perfusion has been determined quantitatively from the intra-abdominal portion of the umbilical v. In the last trimester the mean
flow velocity (V
relatively constant. The diameter of the umbilical v. increases up to the 34th week of pregnancy, so that from
the 35th week of pregnancy on the volume of flow
stagnates and actually decreases significantly in proportion to the fetal weight (from 139 to 65 mL/min/kg).
This demonstrates that the part of cardiac minute
volume played by the placenta diminishes with increasing gestational age (Lingman and Maršál 1986b).
Hence about 50−35% of the blood in the descending
aorta flows through the umbilical v.
During the first trimester pulsations in the waveform
of the umbilical v. are normal up to the eighth week of
pregnancy.Usually they can no longer be seen after the
13th week of pregnancy (Rizzo et al. 1992).
The umbilical v. is especially liable to be influenced
by pressure fluctuations between it and the right
atrium. Significant rhythmic reverse flow occurs as a
result of respiratory movements. Absolute flow velocities can therefore only be determined when the fetus is
at rest or asleep.
(TA) or TASAV) is 12−13 cm/s and
mean
58
Fig. 4.12 Doppler sonogram of an umbilical vein with marked
pulsations.
Physiological and Pathological Flow Alterations
An influence of active labor in significantly reducing
blood flow in the fetal intra-abdominal umbilical v.
could only be demonstrated in cases in which the heart
rate changed concurrently. In such cases the CTG
showed variable decelerations. In late deceleration
pulsations synchronous with heart rate were observed
Fig. 4.12) (Murakami et al. 1985). In another study the
(
same phenomenon was seen during hypoxia (Lingman
et al. 1986). Venous pulsations are observed preponderantly in cases with cardiac insufficiency
(Gonser 1992, Gudmundsson et al. 1991, Indik et al.
1991). Hydrops fetalis often ensues if the pulsations
persist. Such cases carry a very high perinatal mortality. An influence of contractions on blood flow on the
Fetal Vessels
umbilical v. was not demonstrated during normal
pregnancies (Fendel et al. 1987, Fleischer et al. 1987,
Stuart et al. 1981).
Fetal Vessels
Aorta
The pulsatile blood flow in the descending aorta shows
more systolic/diastolic variability than that in the
umbilical aa., which carry a significant part of the
F
blood flow (
ig. 4.13).
riphery of the fetus are normally much greater than
those in the placenta, and this explains the distinct
difference between the two vascular beds.
Evaluation Criteria
Criteria used to evaluate blood flow include:
왘 The range of systolic/diastolic variations, quantifia-
ble, e.g., by the RI,
왘 The shape of the waveform, which may show a
notch with impaired compliance,
왘 The absolute flow velocities, such as the peak maxi-
mal velocity,
왘 The volume flow, which can be calculated from the
mean flow velocity and the diameter of the vessel.
Because the course of the vessel is straight, because
the angle of the transducer can be determined, and
because of the size of the vessel, quantitative blood
flow measurements can be performed on the aorta
as well as on the umbilical v.
Reference Values
After the 24th week of pregnancy the aortic RI changes
only fractionally. Eventually it rises somewhat toward
the end of pregnancy concurrently with other changes.
The mean RI is 0.80; the maximum 0.90 (
The systolic peak maximum velocity also rises. At 26
weeks it is barely 80 cm/s (range: 65−95), and rises
until the 38th week to 100 cm/s (range: 80−130), then
declines slightly to 90 cm/s (range: 70−115) (
Mean flow velocity (V
second half of pregnancy is about 30 cm/s with a range
of 25 to about 36 cm/s. In the last days of pregnancy
these values decline slightly. In the thoracic part of the
descending aorta the mean velocity of flow is just
35 cm/s. This value is therefore constantly about 2 cm/s
higher than that in the abdominal part of the descending aorta, which is just 33 cm/s.
The volume flow increases quantitatively in propor-
tion to weight in the course of pregnancy, together
with the almost linear increase in aortic diameter. It is
about 200−250 mL/min/kg body weight. However,
The resistances to flow in the pe-
4.14).
Fig.
4.1).
Table
(TA) or TASAV) during the
mean
In cases of maternal anemia before and after treatment no equivalent change was demonstrated in
umbilical v. flow (Jouppila and Kirkinen 1984).
Fig. 4.13 Doppler sonogram of a descending aorta.
100
95
90
85
80
RI
75
70
65
60
55
24-27 28-31 32-35 36-39 ≥ 40
Weeks of gestation
Fig. 4.14 Changes in the RI of a descending aorta during pregnancy. Box and whisker plot. Boxes: 25th, 50th, and 75th percentiles; whiskers 10th and 90th percentile (reproduced from
Vetter 1991b).
when related to fetal weight it declines slightly from
241−213 mL/min/kg body weight (Lingman and Maršál
1986b). The total volume flow is about 200 mL/min
(range: 140−300) at 26 weeks and rises to 700 mL/min
(range: 400−900) at term. In large fetuses the amount
of blood pumped through the aorta each minute corresponds to the size of the fetus, though the qualitative
flow parameters, including those of the fetoplacental
and uteroplacental vessels, do not change. Only the diameter of the vessel corresponds to the greater size of
the fetus (Vetter et al. 1992).
The waveform indices of Doppler sonograms of the
aorta do not change significantly during the last three
months of pregnancy (Lingman and Maršál 1986c).
Maršál and co-workers published an overview of the
flow measurements in the fetal aorta (1987a). Their
Basic Concepts
59
1
Blood Flow Analysis During Pregnancy
Tabelle 4.1 Reference values for the uteroplacental arteries, umbilical arteries, and descending aorta, determined by ADRKranzbühler instrument (reproduced from Vetter 1991b)
Value 24 weeks to term 24−27 weeks 28−31 weeks 32−35 weeks 36−39 weeks >39 weeks
Descending aorta
RI 71-79-87 73-77-90 74-80-87 73-79-85 69-77-86 70-79-88
Pulse 120-144-158 130-146-153 130-143-162 130-142-158 127-145-159 127-145-158
(TA) 24-30-36 21-26-32 25-30-36 27-31-34 25-30-38 21-28-37
v
mean
(TA) 24−30-36 21−26-32 25−30-36 27−31-34 25−30-38 21−28-37
V
mean
Diameter 4.4-6.1-7.9 3.5-3.9-4.8 4.6-5.2-6.1 4.8-5.8-6.6 5.2-6.6-7.9 5.7-7.4-8.1
mL/min 254-495-797 138-204-301 281-400-544 369-480-686 404-638-850 407-694-901
(TP) 73-93-115 64-78-94 73-91-115 79-97-112 82-100-129 71-92-115
v
max
(TA) 35-46-59 32-45-53 32-44-54 33-46-53 37-48-62 33-45-59
v
max
PI 10-90 1.27-2.20 1.27-2.16 1.37-2.01 1.31-2.20 1.19−2.23 1.26-2.26
PI
med
rMRT 0.36-0.40-0.43 0.36-0.39-0.45 0.37-0.38-0.44 0.37-0.40-0.43 0.35-0.41-0.43 0.33-0.39-0.43
Umbilical arteries
RI 47-58-70 59-67-78 53-63-70 46-60-67 46-55-68 47-55-64
PI 10-90 0.67-1.25 0.87-1.38 0.91-1.38 0.71-1.32 0.63-1.11 0.68-0.96
PI
med
rMRT 0.43-0.45-0.47 0.40-0.45-0.46 0.43-0.45-0.48 0.43-0.45-0.47 0.44-0.46-0.48 0.45-0.46-0.47
Uteroplacent arteries
RI 23-34-49 25-34-47 23-33-51 23-35-48 26-34-49 22-35-48
Maternal
puls
PI 0.29-0.54-0.79 0.35-0.59-2.17 0.21-0.52-0.86 0.25-0.45-0.74 0.38-0.55-0.79 0.22-0.54-0.80
rMRT 0.46-0.47-0.49 0.45-0.47-0.48 0.47-0.47-0.50 0.45-0.47-0.48 0.46-0.47-0.48 0.46-0.47-0.49
N 256 32 42 59 74 49
1.68 1.73 1.77 1.62 1.59 1.66
0.89 1.25 1.03 1.00 0.77 0.81
71-86-104 60-91-95 75-80-104 70-86-116 73-85-100 74-89-103
60
compilation showed that the mean trends of the results converged increasingly also for quantitative
measurements, thus probably approaching their actual
values.
Physiological Flow Changes
Changes in the circulatory conditions in the fetus depend on a variety of well-defined “behavioral states”
according to Nijhuis et al. (1982). Not taking these conditions into account may to some extent explain the
scatter of the data. A condition of high activity, labeled
2F by Nijhuis, accompanies a diminished impedance in
the descending aorta (van Eyck et al. 1985) as well as
the internal carotid a. (van Eyck et al 1987), while the
Fig. 4.15 Doppler sonogram of descending aorta with arrhythmia.
flow pattern in the umbilical aa. remains unchanged.
This shows that with increased movement impedance
is diminished in the fetal vessels, but not in the placental circulation (Conners et al. 1991). These results confirm the data previously known from animal experiments (Jensen et al. 1985).
Brief maternal exercise has no effect on mean blood
flowvelocity in the fetal aorta, despite a rise in maternal
pulse rate and blood pressure (Pijpers et al. 1984).
Changesin heart rate offrom 120−160 beats/min had no
significant effect on the parameters of the waveform
(Lingman and Maršál 1986c). On the other hand, filling
time of the atria influences the stroke volume in accordance with the Frank−Starling principle (Lingman and
Maršál 1986a, Tonge et al 1986). The fetal heart is so
adaptable that no hemodynamic changes can be demonstratedin thefetus with pulserates between50 and
almost 250 (Lingman and Maršál 1987). The interpretation is more complex with arrhythmias, for the stroke
volume changes with diastolic f illing, influencing the
Fig.
Doppler sonogram (
4.15).
Arteries Supplying the Brain
The internal carotid a. and the middle cerebral a. are
the main cerebral vessels that have been studied. Because the system primarily used today is a duplex system with an integrated Doppler built into the transducer, the preferred recording is from the middle cerebral a., which lies along the axis of the sound beam in
late pregnancy (Fig. 4.16). The evaluation is based on
the systolic/diastolic velocity changes in the blood flow
through these vessels and the absolute value of the
peak systolic velocity.
Reference Values
The arteries supplying the brain show considerable biological variability, since they reflect mainly the current activity of the child. The RIs decline initially
during the course of the pregnancy, but rise again
slightly toward term. To make comparisons it is important to know in which vessel the Doppler window lies,
for the waveforms differ distinctly from each other.The
PI is considerably higher in the middle cerebral (2.25)
than in the anterior cerebral a. (1.82), while the latter
in turn is higher than the internal carotid a. (1.51) (Mari
et al. 1989).
The internal carotid a. shows no changes in its flow
pattern between the 26th and 36th weeks. As pregnancy proceeds the diastolic flow velocities increase, a
sign of decreased impedance or increased flow resistance in the systemic circulation (Kirkinen et al.
1987, Wladimiroff and Van Bel 1987).
Such changes have not yet been described in the
common carotid a. (
Fig. 4.17) (Arabin et al. 1987).
Fetal Vessels
Fig. 4.16 Doppler sonogram of middle cerebral a.
Basic Concepts
Physiological Flow Changes
Fetal activity powerfully influences cerebral perfusion.
Movementis accompaniedby aconsiderable increasein
diastolic flow, i. e., diminished impedance parameters.
Inhalation of air containing 3 % carbon dioxide resulted in a rise in diastolic flow only in the middle cerebral a. All other vessels showed no changes (Veille and
Penry 1992).
Cerebral blood flow depends on the intrauterine and
intracerebral pressures. Increased pressure on the fetal
skull is accompanied by increased impedance (Ueno
1992). In extreme cases pressure on the fetal skull, for
example, by a transducer, can cause reverse diastolic
4.18) (Vyas et al.
flow similar to cerebral edema (
1990a).Pressurerelief, forexample, byamniocentesis to
relieve hydramnios can lead to a distinct increase in diastolicflow (Mariet al. 1992).However,whether control
of cerebral perfusion by amniocentesis can be used as a
basis for regulation remains an open question. In fetal
anemia systolic peak velocity in the middle cerebral a.
has been used as a valuable noninvasive parameter
since March 2000.
Fig.
Renal Arteries
In the beginning Doppler sonography of the renal aa.
was thought to be a promising avenue for the diagnosis
of disturbances in the blood supply and general condi-
Fig. 4.17 Doppler sonogram of common carotid a.
Fig. 4.18 Doppler sonogram of middle cerebral a. with cerebral edema.
tion of the fetus. However, the integration of the renal
blood supply into the greater circulation appears to be
more complex than at first thought, frustrating the
hope that this parameter might be key in pregnancies
at risk.
61
Blood Flow Analysis During Pregnancy
1
Evaluation Criteria
The renal aa. were evaluated by blood flow pulsatility
4.19). In a few cases diastolic flow was absent
(Fig.
during the whole pregnancy, making it impossible to
note changes using a 2-point index. In this situation
calculating the PI is mandatory.
Reference Values
The PI declines on average from 3 in the 20th week to 2
in the 40th week (Mari et al. 1993, Vyas et al. 1989,
Zimmermann et al. 1993).
Ductus Arteriosus
The criteria to be evaluated are the systolic/diastolic
variability and the peak maximal velocity.
Physiological flow changes have not been examined
to any great extent. Blood flow is influenced by fetal
movement.
Inferior Vena Cava
Evaluation Criteria
Blood flow in the central v.’s depends to a large extent
on cardiac function, especially tricuspid competence.
The waveform shows three significant points:
1. Systolic peak maximal velocity (S),
2. Diastolic peak maximal velocity (D) at the beginning of diastole, and
3. The low point in velocity (A) at the time of atrial
contraction.
The resulting waveform shows two peaks, beginning with the low point A and showing the two
4.20). The available criteria are:
peaks S and D (
1. The S/D ratio,
2. The ratio of the time velocity integrals for S and D
(time velocity integral for S [STVI]/time velocity integral for D [DTVI]),
3. The percentage of reverse flow (PRF) related to systolic peak velocity (Reed et al. 1986, 1990, Rizzo et
al. 1992a, Wladimiroff et al. 1992).
Fig.
Reference Values
62
Fig. 4.19 Doppler sonogram of renal artery and vein.
Fig. 4.20 Doppler sonogram of inferior vena cava.
The S/D ratio rises between the 18th to the 40th week
linearly from a mean of 1.5 to nearly 2. The ratio of the
time velocity integrals STVI/DTVI rises only minimally
from 2.5 to 2.8, while the PRF declines significantly
from 16% to 5 % (Rizzo et al. 1992a).
Physiological Flow Changes
Marked changes occur especially in this vascular bed in
early pregnancy (Wladimiroff et al. 1992).
Pathological Flow Changes
In cases of cardiac insufficiency distinct changes occur
in the waveforms of the central v.’s. A sign considered
prognostically very unfavorable is marked diastolic
reverse flow, as it were a measure for the inefficiency
of cardiac performance (Gudmundsson et al. 1991).
These changes are propagated into the umbilical v. and
cause venous pulsations (Indik et al. 1991).
Ductus Venosus Arantii
The ductus venosus is currently the subject of research.
Its central position in the complex distribution of oxygenated blood is undisputed. The technical problems
related to its function in the human fetus have been
overcome. Its diameter has been measured at a maximum of 2 mm. The waveform shows forward flow
throughout. It shows two peaks, one in systole and one
in diastole, and a minimum at the end of diastole
4.21). The peak velocity is relatively high. In the
(Fig.
course of pregnancy it increases on average from 65 to
75 cm/s. These high velocities may play a role in
streamlining (Kiserud et al 1991, 1992). In cases where
cardiac function was markedly disturbed diminished
flow velocities or reverse flow (especially A-wave)
have been observed.
Hepatic Veins
Quite different flow waveforms may be observed not
far from the ductus venosus, for example, in the hepatic v.’s: Reverse flow is normal as the pressure
gradient to the heart is much lower than that of the
4.22).
ductus venosus (
Fig.
Effect of Therapeutic Measures
Fig. 4.21 Doppler sonogram of ductus venosus
Basic Concepts
Effect of Therapeutic Measures
Doppler sonography makes it possible to evaluate the
effect of various treatments on uteroplacental
hemodynamics.
Prostaglandins
왘 Prostacyclin could not be shown to have a positive
effect on abnormal intervillous blood flow (determined by xenon) or blood flow in the umbilical v.
(Jouppila et al. 1985b).
왘 Prostaglandin E
tion of the cervix, did not influence blood flow in
the uterus, the placenta, or the child (Rayburn et al.
1991).
, which is used to induce matura-
2
Fig. 4.22 Doppler sonogram of a hepatic vein.
Antihypertensives
왘 By contrast dihydralazine increased minute volume
in the umbilical v. while intervillous blood flow remained constant (Jouppila et al. 1985a). In a more
recent study the drug showed no effect on the
shape of the Doppler sonogram of the uteroplacen-
tal and fetoplacental vessels (Duggan et al. 1992).
왘 Methyldopa has no significant effect on blood flow
in the uterus, placenta, or fetus (Montan et al.
1993).
63