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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5772_Библиотеки_им_академика_М_И_Перельмана.pdf
Normal Fetomaternal Doppler Indices in the Second and Third Trimesters of Pregnancy
1.0
0.8
0.6
S/D
0.4
Middle cerebral artery
0.2
0
28 30 34
26
32 36 38 40 42
Weeks of gestation
p95
p90
p50
p10
p5
Fig. 15.10 Reference curves for the RI of the middle cerebral
artery, based on 581 measurements in normal pregnancies and
grouped by even gestational weeks. The curves were smoothed by
cubic regression.
15
3.5
3.0
2.5
Uterine artery
2.0
S/D
1.5
1.0
0.5
0
26
28 30 34
32 36 38 40 42
p95
p90
p50
p10
p5
Weeks of gestation
3.5
3.0
2.5
2.0
PI
1.5
Middle cerebral artery
1.0
0.5
0
28 30 34
26
32 36 38 40 42
Weeks of gestation
p95
p90
p50
p10
p5
Fig. 15.11 Reference curves for thePI of the middle cerebral artery,
smoothed by cubic regression.
1.0
0.8
Uterine artery
0.6
RI
0.4
0.2
0
28 30 34
26
32 36 38 40 42
Weeks of gestation
p95
p90
p50
p10
p5
132
Fig. 15.12 Reference curves for the S/D ratio of the uterine artery,
smoothed by cubic regression.
1.4
1.2
1.0
Uterine artery
0.8
PI
0.6
0.4
0.2
0
26
28 30 34
32 36 38 40 42
Weeks of gestation
p95
p90
p50
p10
p5
Fig. 15.14 Reference curves for the PI of the uterine artery,
smoothed by cubic regression.
Fig. 15.13 Reference curves for the RI of the uterine artery,
smoothed by cubic regression.
2.0
1.6
1.2
0.8
0.4
0
28 30 34
26
Middle cerebral artery/umbilical artery
ratio (C/U-ratio)
32 36 38 40 42
Weeks of gestation
p95
p90
p50
p10
p5
Fig. 15.15 Reference curves for the cerebroplacental ratio, based
on 580 measurements of the RI of the middle cerebral artery and
umbilical artery in normal pregnancies and grouped by even gestational weeks. The curves were smoothed by cubic regression.
Discussion
Discussion
The advent of Doppler sonography has opened up a new
functional dimension in diagnostic ultrasound. For the first
time, we are able to evaluate both the physiology and the
pathophysiology of uterofetoplacental hemodynamics during
the course of pregnancy using a noninvasive, largely standardized method. The evaluation of fetal well-being is an important
prerequisite for obstetric risk assessment.
ROC curves and cutoff values. The goal of establishing normal
reference curves is to be able to classify the course of pregnancy as normal or abnormal on the basis of measured values.
By establishing normal values, we are able to create receiver
operating characteristic (ROC) curves to define cutoff values
that discriminate between normal and abnormal pregnancies
with an optimum degree of specificity and sensitivity. This can
be accomplished with the reference curves shown above. From
a formal statistical standpoint, however, it must be considered
that the curves shown are regression-optimized graphic interpolations, and so the curves and their deviation values cannot
be used as mathematical equations.
Problems with repeat measurements. Because the database is
that of a cross-sectional study and not a longitudinal study, our
methodology does not allow us to evaluate a change that occurs in repeat measurements. This can lead to difficulties in
Doppler flowmetry, the purpose of which is to measure a
change in the functional properties of the uteroplacental unit.
The problem is that it cannot be determined whether the
measured change reflects an individual physiological progression or a steady decline in the functional capacity of the fetoplacental unit with pathophysiological significance.
Progression of Doppler Indices during the
Course of Pregnancy
The Doppler indices recorded from maternal and fetal vessels
show a variable pattern of progression during the course of
pregnancy as a result of anatomical and histological changes.
Umbilical artery. The S/D ratio of the umbilical artery falls continuously with advancing gestation owing to the increase in
arterial blood flow during the course of pregnancy. This leads
to persistent flow throughout the cardiac cycle with a steady
increase in end-diastolic flow. Comparative data from two
longitudinal studies by Fogarty et al.
numerous cross-sectional studies
progression. Trudinger et al.
25
mechanisms:
➤
Continuous maturation of the fetal placental villous system
➤
Increase in the cross-sectional area of the fetal placental vessels, causing a progressive decline of fetoplacental vascular
resistance
➤
Increase in fetal cardiac output
➤
The changing compliance and resistance of the vessel wall
➤
Rise of fetal blood pressure
10
and Hünecke et al.15and
1,2, 21, 23
indicate a similar
attributed this to the following
Interestingly, these highly individual developmental processes
lead to a very large scatter of normal values by the start of the
third trimester. This variability is strongly reflected in the S/D
ratio (Figs. 15.
2,15.3) and less so in the PI (Fig. 15.5). It has little
effect on the RI, which cannot exceed 1, and so the rangeof variance of this index remains almost constant from the 28th
week of gestation until term (Fig. 15.
4).
Fetal descending aorta. It has become routine practice to scan
the fetal descending aorta in addition to the umbilical artery.
The S/D ratio of the fetal aorta shows a slight, insignificant decline with advancing gestational age. Our results in this area
are comparable to those of Hecher et al.
12
. The waveform of the
fetal aorta exhibits forward flow throughout the cardiac cycle,
but the diastolic flow velocity is lowerin relation to the systolic
flow velocity than in the umbilical artery. As a result, higher
normal values are generally measured for the S/D ratio of the
fetal aorta than for the umbilical artery. The total crosssectional area of all the vessels increases tremendously during
the course of pregnancy. This is accompanied by a falling peripheral resistance and a rising diastolic flow velocity, although
there is only a slight resulting decrease in the S/D ratio of the
fetal aorta (Fig. 15.
6). This progression is weakly reflected in
the PI and RI and, as in the umbilical artery,the scatters of these
two indices are considerably smaller and more stable over the
course of the pregnancy (Figs. 15.
7,15.8).
Middle cerebral artery. The middle cerebral artery is the most
commonly selected cerebral supply artery for antenatal Doppler investigation. The cerebral supply arteries show a large
range of biological variability, as these vessels reflect the
degree of activity of the individual fetus. The resistance indices
decline with advancing gestation
26
(Figs. 15.9–15.11). The dias-
tolic flow in the cerebral supply arteries is normally low but increases toward the end of pregnancy. Vigorous fetal movements can cause a false elevation of diastolic flow, which can
also result from increased intrauterine pressure (e.g., hydramnios) or from extrinsic pressure on the fetal skull
28
.
Uterine artery. In contrast to the arcuate arterial system, the
measurement of uteroplacental perfusion in the uterine artery
permits an overall assessment of uterine perfusion
6
. Higher
values are measured than in the arcuate system, however, and
so the site of the measurement should be carefully noted when
the reference curves are used. This is easily accomplished with
the aid of color-flow imaging.
The blood flow conditions depend on the location of the
placenta and on gestational age
20
. With a lateralized placenta,
the ipsilateral uterine artery reflects the flow conditions in the
distal vascular bed and is therefore preferred for clinical evaluation. The differences between the sides are quite pronounced in the early weeks of pregnancy. But in the final
trimester, the difference between the S/D ratios of the right and
left uterine arteries decreases and averages only 0.4–0.3
6
. The
detection of abnormal waveforms in both uterine arteries signifies a high risk for the development of preeclampsia
4
or of in-
Obstetric Ultrasound
133
Normal Fetomaternal Doppler Indices in the Second and Third Trimesters of Pregnancy
trauterine growth retardation when accompanied by abnormal perfusion of the fetal vessels.
The uteroplacental vessels at the start of pregnancy show a
high pulsatility with high systolic flow velocities and very low
end-diastolic velocities
6
. With increasing trophoblastic invasion and transformation of the uteroplacental vascular bed, a
high-impedance vascular system is transformed into a low-impedance system after the second trimester
5
. After 20 weeks the
parameters show largely constant values with a stable biological scatter from the 30th week on (Figs. 15.
12 –15.14 ).
The early diastolic notch that is normally present in the
uterine artery waveformbefore the 24th week is attributed to a
pulse-wave reflection in the vascular periphery, relating to the
fact that adaptation of the uteroplacental vascular bed is still
incomplete. If the notch persists after 24 weeks’ gestation, this
should be considered pathognomonic for pregnancy-induced
hypertension
3, 14, 25
.
Summary. In normal pregnancies, constant values of uteroplacental blood flow are found from the middle of the second
trimester until term. Meanwhile, the fetal vessels continue to
exhibit changes as the pregnancy progresses. Thus, the S/D
ratio of the umbilical artery declines with advancing gestation,
15
as does the S/D ratio of the middle cerebral artery.The values in
the fetal descending aorta tend to remain constant, but like the
other fetal vessels they show a decreasing scatter with advancing gestational age. It is important, therefore, to develop gestational-age-based reference curves for all of these vessels and to
evaluate them for the definition of cutoff limits that can discriminate between normal and abnormal pregnancies.
References
1 Arabin B, Bergmann PL, Saling E: Simultaneous assessment of blood
flow velocity waveforms in uteroplacental vessels, the umbilical
artery, the fetal aorta and the fetal common carotid artery. Fetal Therapy 2 (1987) 17–26
2 Arduini D, Rizzo G: Normal values of pulsatility index from fetal ves-
sels: A cross-sectional study on 1556 healthy fetuses. J. Perinat. Med.
18 (1990) 165–172
3 Campbell S, Pearce JMF, Hackett G, Cohen-Overbeek T, Hernandez C:
Qualitative assessment of uteroplacental blood flow: Early screening
test for high-risk pregnancies. Obstet. Gynecol. 68 (1986) 649–653
4 Bower S, Schuchter K, Campbell S: Doppler ultrasound screening as
part of routine antenatal scanning: Prediction of pre-eclampsia and
intrauterine growth retardation. Brit. J. Obstet. Gynaecol. 100 (1993)
989–994
5 Brosens I, Dixon HG, Robertson WB: Fetal growth retardation and the
arteries of the placental bed. Brit. J. Obstet. Gynaecol. 84 (1977) 656–
664
6 Deutinger J: Physiologie des Doppler-Flusses in maternalen Gefäßen
während der Schwangerschaft. Gynäkologe 25 (1992) 284–291
7 Ertan AK, Rühle W, Gnirs J, Schmidt W: Doppler-Sonographie; Ver-
gleich der Aussagekraft von “A/B-Ratio“, “RI“ und “PI“ bei Aorta fetalis
und Nabelarterien. Berichte Gynäkologie Geburtshilfe. 128(8) (1991)
611
8 Erz W, Franz HBG, Gonser M: Dopplersonographie des utero- und feto-
plazentaren Kreislaufs: Plazentalateralität, Normalwerte und Referenzkurven. Ultrasch. Med. 19 (1998) 108–113
9 Fendel H, Giani G, Fendel M, Jung H: Die Bestimmung des Gesta-
tionsalters mit der Scheitelsteißlänge und dem biparietalen Kopfdurchmesser in der ersten Schwangerschaftshälfte – Gegenüberstellung zweier Methoden. Z. Geburtsh. u. Perinat. 188 (1984) 161–166
10 Fogarty P, Beattie B, Harper A, Dornan J: Continuous wave Doppler
flow velocity waveforms from the umbilical artery in normal pregnancy. J. Perinat. Med. 18 (1990) 51–57
11 Gosling RG, King DH: Arterial assessment by Doppler shift ultrasound.
Proc. Roy. Soc. Med. 67 (1977) 447–449
12 Hecher K, Spernol R, Szalay S, Stettner H, Ertl U: Referenzwertefür den
Pulsatilitätsindex und den Resistanceindex von Blutflusskurven der
Arteria umbilicalis und der fetalen Aorta im dritten Trimenon. Ul-
trasch. Med. 10 (1989) 226–229
13 Hendrik HJ: Sonographische Untersuchungen – erweiterte fetale Bio-
metrie und semiquantitative Bestimmung der Fruchtwassermenge.
Inaug. Diss. Med. Fak. Univ. Heidelberg 1988
14 Hoffmann H, Chaoui R, Bollmann R, Bayer H: Klinische Anwendungs-
möglichkeiten des Doppler-Ultraschalls in der Geburtshilfe. Zentralbl.
Gynäkol. 111 (1989) 1277–1284
15 Hünecke B, Holst A, Schröder HJ, Carstensen MH: Normalbereiche für
die relativen Doppler-Indizes A/B-Ratio, Resistance-Index und Pulsatilitäts-Index der Arteria uterina und Arteria umbilicalis bei ungestörter Schwangerschaft. Geburtsh. u. Frauenheilk. 55 (1995) 616–
622
16 Mires GJ, Christie AD, Leslie J: Are notched uterine arterial waveforms
of prognostic value for hypertensive and growth disorders of pregnancy? Fetal Diagn. Ther. 10 (1995) 111–118
17 Pourcelot L: Application clinique de l‹examen Doppler transcutane. In
Peronneau P (ed.): Velocimetrie ultrasonore Doppler. Inserm. 34
(1974) 213–240
18 Roemer VM, Bühler K, Kieback DG: Gestationszeit und Geburts-
gewicht. Z. Geburtsh. u. Perinat. 194 (1990) 241
19 Rühle W, Graf von Ballestrem CL, Ertan AK, Schmidt W: Doppler-
Sonographie der fetalen Gefäße – Optimierung der Aussagekraftdurch
ein Kombinationsdiagramm. Z. Geburtsh. u. Perinat. 197 (1993) 95–98
20 Schneider KTM: Standards in der Perinatalmedizin – Dopplersonogra-
phie in der Schwangerschaft. Der Frauenarzt 38 (1997) 452–458
21 Schulman H, Fleischer A, Stern W, Farmakides G, Jagani N, Blattner P:
Umbilical velocity wave ratios in human pregnancy. Amer. J. Obstet.
Gynecol. 148 (1984) 985–990
22 Stuart B, Drumm J, Fitzgerald DE, Duignan NM: Fetal blood velocity
waveforms in normal pragnancies. Brit. J. Obstet. Gynecol. 87 (1980)
780–785
23 Thompson RS, Trudinger BJ, Cook CM: Doppler ultrasound waveform
indices: A/B-Ratio, pulsatility index and Pourcelot Ratio. Brit. J. Obstet.
Gynaecol. 95 (1988) 589
24 TrudingerBW, Giles WB, Cook CM: Uteroplacentalblood flow velocity-
time waveforms in normal and complicated pregnancy. Brit. J. Obstet.
Gynaecol. 92 (1985) 39–45
25 Trudinger BW: Umbilical Artery Blood Flow.In Chervenak FA, Isaacson
GC, Campbell S (eds.): Ultrasound in Obstetrics and Gynecology. Vol.
1. Little, Brown and Company, Boston 1993, 597–604
26 Vetter K, Gonser M, Gasiorek-Wiens A: Dopplersonographie in der
Schwangerschaft. In Sohn C, Holzgreve W (eds.): Ultraschall in Gynäkologie und Geburtshilfe. Thieme, Stuttgart 1995, 501–540
27 Voigt M, Schneider KTM, Jährig K: Analyse des Geburtengutes des
Jahrgangs 1992 der Bundesrepublik Deutschland. Teil 1: Neue Perzentilwerte für die Körpermaße von Neugeborenen. Geburtsh. u. Frauenheilk. 56 (1996) 550–558
28 Vyas S, Campbell S, Bower S, Nicolaides KH: Maternal abdominal pres-
sure alters fetal cerebral blood flow. Brit. J. Obstet. Gynaecol. 97 (1990)
740–747
134
16 Venous Doppler Sonography
F. Bahlmann
Historical Development
Since its initial description by Fitzgerald in 197713, the Doppler
ultrasound assessment of the fetomaternal vascular system
has become widely utilized in the surveillance of high-risk
pregnancies. In the past, scientific and clinical attention was
focused primarily on examination of the uteroplacental vascular system and on the arterial system of the fetus. In recent
years, there have been increasing numbers of Doppler ultrasound studies of the physiological and pathophysiological
changes in the fetal heart and circulatory system, with special
emphasis on the cardiac and venous vascular systems. Al-
Physiology
Streaming effect. The ductus venosus represents the first of
three specific shunts in the fetal circulation and appears to be
an important regulator in the distribution of oxygen-enriched
blood. Studies in experimental animals have demonstrated the
existence of two different directions of blood flow (streaming
effect) in the thoracic portion of the inferior vena cava
in fetal lambs showed that approximately 50% of oxygenated
umbilical venous blood flows through the ductus venosus. The
narrow ductal lumen causes marked acceleration of the blood
flow, creating a stream in the left dorsal portion of the inferior
vena cava with the preferential direction of flow through the
foramen ovale into the left atrium and left ventricle. This
streaming mechanism ensures an optimum oxygen supply to
the brain and myocardium.The considerablyslower blood flow
in the distal inferior vena cava forms a stream in the right ventral portion of the inferior vena cava that is directed into the
right atrium and then into the right ventricle (Fig. 16.
This streaming effect appears to be supported by the crest-
like caudal border of the foramen ovale
9
. Similar findings were
made in color Doppler studies of human fetuses
mately 70% increase of blood flow through the ductus venosus
was documented in response to hypoxemia in fetal lambs
The exact pathophysiological mechanism of this effect is still
uncertain.
Umbilical Vein
Quantitative determination of blood flow. Eik-Nes and Gill
used Doppler ultrasound to evaluate fetal blood volume in the
early 1980 s. They found a relatively constant mean volume
flow of 110–125 ml/(kg min) in the third trimester, which
9
. Studies
1).
42
. An approxi-
10
11, 18
though Doppler studies of volume flow in the intrahepatic
umbilical vein were already being done in the early 1980 s, this
method has not become widely established because of its poor
reproducibility
11,12,18,19, 20, 35, 36, 41
. With technical advances in
ultrasound instrumentation and especially the advent of color
Doppler sonography, it became possible to make a detailed
evaluation of the fetal venous system. Besides the umbilical
vein, inferior vena cava, and hepatic veins, Doppler examination of the ductus venosus has become a particular object of
current scientific interest.
Superior vena cava
Tricuspid valve
Foramen ovale
Right hepatic vein
Left hepatic vein
Ductus venosus
Portal vein
Fig. 16.1 “Streaming effect” demonstrated by experimental studies
.
in fetal sheep
9
.
Inferior vena cava
decreased to 90 ml/(kg min) toward the end of pregnancy
(Fig. 16.2). The following formula (equation 1) is used for the
quantitative determination of blood flow in the umbilical
47
vein
:
Q
= V ⫻ (D/2)2⫻ π ⫻ 0.6 ml/min (1)
VU
Venous umbilical blood flow in this equation (Q
VU
ent on the blood flow velocity (V) and the vascular cross-
Obstetric Ultrasound
Umbilical vein
11, 12, 18
135
) is depend-
136
Venous Doppler Sonography
500
n=118
400
300
200
100
0
Blood flow in the umbilical vein (ml/min)
26 32
28 30 34 36 4038
Weeks of gestation
Fig. 16.2 Mean volume flow in theumbilical vein during pregnancy19.
16
Fig. 16.3 Normal and abnormal umbilical venous Doppler spectra.
sectional area (D/2)2⫻ π. The quantitative analysis of umbilical
blood flow is problematic, however, in that even slight deviations in the vessel diameter lead to a large scatter of flow
47
values
method of blood volume determination is not widely utilized
Locating the umbilical vein. Doppler spectra are recorded from
either the intra-amniotic or intrahepatic segment of the
umbilical vein. The intrahepatic segment is preferred for its
better reproducibility
abdomen in a transverse plane and placing the sample volume
at an acute angle (⬍30⬚) in the central part of the intrahepatic
umbilical vein
Findings. The umbilical venous waveform generally shows a
monophasic pattern with a mean flow velocity of 10–15cm/s.
. Because of its poor reproducibility, this quantitative
12
.
11, 12, 18
. It is sampled by imaging the fetal
11
.
90%
50%
10 %
Under physiological conditions, umbilical vein pulsations
occur until the end of the first trimester or in response to fetal
breathing movements
33, 58
and normally are no longer seen
after 13 weeks’ gestation. Umbilical vein pulsations in the second or third trimester may signify a cardiac anomaly or congestive heart disease, or they are commonly associated with
absent end-diastolic flow in the umbilical artery as a result of
chronic placental insufficiency
22, 49
(Fig. 16.3). Umbilical vein
pulsations in these cases show a temporal correlation with
atrial systole and are an expression of myocardial insufficiency.
Pulsations in the umbilical vein may take the form of single
pulsations, double pulsations, or a triphasic Doppler spec-
1,3, 22, 49
trum
reported when these flow patterns are detected
. A markedly increased mortality rate of 50–60% is
22, 33, 49
.
Ductus venosus
Locating the ductus venosus. The ductus venosus and its flow
pattern can be demonstrated with two-dimensional real-time
ultrasound and also with color Doppler (Fig. 16.
precardial veins, the ductus venosus yields the best and most
reliable information on the myocardial hemodynamics and
function of the fetal heart, with good reproducibility of the
Doppler spectra
61
. Doppler signals are recorded most easily
and quickly when the fetus is in a dorsoposterior lie. For rapid
venous orientation, the intrahepatic portion of the umbilical
vein should be imaged first. The best view is obtained in either
a midsagittal plane or oblique transverse plane of the fetal abdomen
24, 30, 42, 43
. The entry of the intrahepatic umbilical vein
into the ductus venosus is located in continuity with the vein.
The diameter of the ductus venosus rarely exceeds 2 mm and
shows a slight funnel-shaped expansion up to 20 mm long
A marked difference in blood flow velocities between the
umbilical vein and ductus venosus can be recognized with
color Doppler. The 3–4 times higher flow velocity in the ductus
venosus causes aliasing, which appears as an area of color reversal (Figs. 16.
5,16.6). Flow signals are acquired by position-
ing the Doppler sample volume directly at the entrance to the
ductus venosus, at the site of the color reversal
The width of the sample volume should just cover the vessel
lumen to avoid detecting signals from the adjacent hepatic
veins and umbilical vein. The use of color Doppler makes it
much easier to locate the ductus venosus and accurately position the sample volume. Owing to the funnel shape of the ductus venosus, the flow velocities directly at the entrance are
higher than at the outlet
53
. An insonation angle less than 30⬚
(or 50⬚) is recommended to obtain an optimum waveform
The wall filter should be set as low as possible—between
125Hz and 100 Hz, depending on the type of equipment used.
Waveforms and indices. A sonographer experienced in Doppler ultrasound can obtain clear Doppler signals from the ductus
venosus in 94% of cases
24
. The normal velocity waveform of the
ductus venosus exhibits continuous, triphasic forward flow
throughout the cardiac cycle. Absent or low pulsatility is noted
in 3 % of cases and is considered a normal variant
waiting period is recommended in these cases. The maximum
flow velocities in the ductus venosus are the highest in the
venous system and appear to be responsible for the “streaming
4). Of all the
24, 42
(Fig. 16.7).
44
; a brief
44
.
44
.
Physiology
컅 Fig. 16.4 B-mode image of the portal sinus with the origin of the
ductus venosus. Dorsoposterior lie (27th week).
effect.” As in the arterial system, the flow velocities in the ductus venosus are dependent upon gestational age, fetal breathing and body movements, and the fetal heart rate
mum blood flow velocity rises on average from 65 cm/s to
75 cm/s between 18 and 40 weeks’ gestation
velocity in the ductus venosus can rise to double or triple the
normal value during inspiration, depending on the intensity of
the breathing movements.
The quantities that are determined for ductus venosus
waveform analysis are the maximum flow velocities during
ventricular systole (S), ventricular early diastole (D), and
ventricular late diastole (atrial contraction [a]) (Fig.16.
Hemodynamically, these phases reflect the rapidly time-varying pressure gradient between the umbilical vein and right
atrium. The highest pressure gradient between the ductus ve-
44
. The maxi-
44
. The blood flow
8).
Fig. 16.5 Midsagittal scan through the fetal abdomen demonstrates
the course of the umbilical vein (blue) and its junction with the ductus
venosus (yellow). Thecolor reversal (aliasing) marks the site where the
flow velocities are highest. Dorsoposterior lie (30th week).
Obstetric Ultrasound
Fig. 16.6 Oblique transverse scan through the fetal abdomen (34th
week) demonstrates the course of the umbilical vein (blue) and its
junction with the ductus venosus (yellow).
Fig. 16.7 Color recording of the Doppler spectrum at the entry of the
umbilical vein into the ductus venosus shows the typical triphasic,
antegrade flow pattern.
137
Fig. 16.8 Normal triphasic waveform of the ductus venosus: maximum antegrade blood flow velocities during ventricular systole (S),
early ventricular diastole (D), and atrial contraction (a).
Venous Doppler Sonography
1.4
PVIV
1.2
1.0
0.8
0.6
0.4
0.2
0
20
22 24
26
28 30 34
32 36 38 40
Weeks of gestation
95%
50%
5%
Fig. 16.9 Ductus venosus. Preload index (S–a)/D of Hecher (1994).
PVIV = peak velocity index for veins.
nosus and right atrium occurs during ventricular systole. This
gradient is produced by the descent of the atrioventricular(AV)
16
valve plane, resulting in antegrade flow that fills the atria. Subsequent early diastole is marked by opening of the AV valves
and passive filling of the ventricles. This phase corresponds to
the E component of the biphasic atrioventricular waveform.
During atrial contraction, which coincides with the A component of the atrioventricular waveform, the foramen ovale
closes and the rest of the atrial blood volume is actively
pumped into the right ventricle. By analyzing these patterns,
the sonographer can obtain information on the end-diastolic
right ventricular pressure and the central venous pressure. The
angle-independent parameters listed in Table 16.
1 are used for
the qualitative assessment of pulsatility. These parameters can
be used to evaluate the cardiac preload
8
.
1.4
PIV
1.2
1.0
0.8
0.6
0.4
0.2
0
20
22 24
26
28 30 34
32 36 38 40
Weeks of gestation
95%
50%
5%
Fig. 16.10 Ductus venosus. Preload index (S–a)/Tamx of Hecher
(1994). PIV = pulsatility index for veins.
138
Normal and abnormal changes duringthe course of pregnancy.
The end-diastolic ventricular pressuredeclines with advancing
gestational age as a result of placental maturation processes
that lower the placental resistance. This decrease is manifested
by a decline of venous pulsatility and falling preload indices
and is due mainly to the rising flow velocity during atrial contraction (Figs. 16.
9,16.10). A rise in the preload indices reflects
an increased end-diastolic ventricular pressure in the heart. In
a healthy fetus, the umbilical venous pressure during atrial
Table 16.1 Doppler indices in the venous vascular system for qualitative evaluation of the cardiac preload and central venous pressures
Index Author
a/S Kanzaki (1990)
S/D Huisman (1991)
(S–a)/S De Vore (1993)
(S–a)/D Hecher (1994)
(S–a)/Tamx Hecher (1994)
S = systole, D = diastole, a = atrial contraction, Tamx= time-averaged maximum velocity.
37
29
8
24
24
Fig. 16.11 Normal and abnormal ductus venosus Doppler spectra in
fetuses with severe asymmetrical intrauterine growth retardation due
to chronic placental insufficiency. The increase in pulsatility caused by
a slowing or reversal of flow during atrial contraction reflects the increasing degree of fetal compromise.
contraction is higher than the central venous pressure. When
there is severe centralization of the fetal circulation due, for example, to chronic placental insufficiency or hypovolemia, a
hypoxia-induced myocardial insufficiency develops, leading
to a rise of central venous pressure in the fetal right heart. The
result is a fall of maximum flow velocities in the ductus
venosus or even reverse flow during atrial contraction
(Fig. 16.
23, 25, 27, 46, 62
11)
. Complete cardiac exhaustion and decompensation are manifested by sinus bradycardia, which is
marked by a decrease in systolic and early diastolic antegrade
flow velocities and an increase in retrograde late diastolic flow
velocities.
Physiology
Fig. 16.12 Color-flow image of the inferior vena cava in a parasagittal
plane.
Inferior Vena Cava
Locating the inferior vena cava. There is disagreement in the
literature concerning the best site for sampling flow velocity
waveforms from the inferior vena cava
pling directly below the right atrium appears to adversely affect the inferior vena cava waveform owing to venous flows
merging in different directions from subdiaphragmatic tribu-
31
taries
. Rizzo et al. compared various sampling sites for recording flow velocity waveforms from the inferior vena cava
In this study, sites between the renal vessels and subdiaphragmatic venous tributaries and also below the ductus venosus
provided the best reproducibility, the most favorable insonation angle, and the least variation
inferior vena cava is imaged in a parasagittal longitudinal
plane, and the sample volume is positioned at the lowest
possible angle (⬍30⬚) (Fig. 16.
12). Another option is toplace the
sample volume just below the entrance to the right atrium
but this leads to greater variability of the velocity waveforms
Fetal body and breathing movements in particular can lead to
marked changes in the Doppler frequency spectrum
Waveforms and indices. The flow velocity waveform of the inferior vena cava, like that of the ductus venosus, reflects the
systolic and diastolic phases of the cardiac cycle and thus the
intracardiac pressure changes
57
. Unlike the ductus venosus,
the inferior vena cava exhibits a bidirectional, triphasic flow
pattern with a retrograde component during atrial contraction
and 2–3 times lower flow velocities (Fig. 16.
tus venosus, the indices shown in Table 16.
tative analysis of the inferior vena cava waveform.
Normal and abnormal changes duringthe course of pregnancy.
The percentage of retrograde flow during atrial contraction de-
clines with advancing gestational age
with a decrease in pulsatility and related indices and is attributable to both a decrease in fetoplacental resistance and an increasing differentiation of diastolic ventricular function. In-
24, 29, 37,54, 59
59
. With this technique the
. Flow sam-
32, 34
.
13). As in the duc-
1 are used for quali-
29, 60, 65
. This is associated
59
54
29
Fig. 16.13 Color Doppler scan of the inferior vena cava (blue) below
the ductus venosus (red). Note the bidirectional flow velocity
waveform with typical antegrade S- and D-phases and a retrograde a-
phase.
.
Fig. 16.14 Increased retrograde flow during atrial contraction in a
fetus with significant pulmonic stenosis (29th week, no hydrops).
,
creased pulsatility and retrograde flow are commonly found in
.
hypoxemic fetuses with a severe centralization of blood flow,
congestive heart disease, and cardiac arrhythmias (Fig. 16.
Simultaneous Doppler sampling of the inferior vena cava and
descending aorta can be performed to evaluate fetal arrhyth-
4, 38, 54
mia
. For this purpose, the sample volume is enlarged to
detect the flow velocities in both vessels.
Hepatic Veins
To date, only a few reports have been published on Doppler ul-
trasound studies of the hepatic veins and their clinical signifi-
24, 48, 64
cance
waveform of the hepatic veins shows a triphasic, bidirectional
pattern (Fig. 16.
what lower, however. The left hepatic vein is most easily located in a parasagittal plane just below the diaphragm. As in all
other fetal vessels, the Doppler spectrum of the hepatic veins is
modulated by fetal body and breathing movements (Fig. 16.
. As in the inferior vena cava, the flow velocity
15). The maximum flow velocities are some-
Obstetric Ultrasound
14).
139
16).
Venous Doppler Sonography
Fig. 16.15 Color-flow image and corresponding Doppler spectrum of
the left hepatic vein. The color reversal (yellow) reflects the area of the
ductus venosus.
Clinical Applications
16
Intrauterine Growth Retardation Due to Chronic Placental Insufficiency
Fetal compensatory mechanisms. Hypoxemia and acidemia
trigger a compensatory centralization of the fetal circulation in
which peripheral vascular resistance rises and blood flow is
routed preferentially to the brain, myocardium, and adrenal
glands
appears that a growth-retarded fetus can compensate for its
chronic hypoxemic state for some time through specific adaptive processes that include an increase in maximum myocardial blood flow, the formation of new blood vessels in the
myocardium, and changes in myocardial energy metabolism
The hemodynamic changes, along with increased erythropoie-
5, 10, 47,63
. In a setting of chronic placental insufficiency, it
Fig. 16.16 Effect of fetal breathing movements on the Doppler spec-
trum of the left hepatic vein. The maximum velocities are two to three
times higher during inspiration.
sis and increasing anaerobic glycolysis, are logical adaptive responses by the fetus aimed at the prevention of serious injury.
When this compensatory capacity has reached its limit, a
further increase in acidemia will cause irreversible damage
that is reflected in high rates of perinatal morbidity and mor-
27, 39, 62
tality
Centralization of the fetal circulation. Rising resistance to
blood flow in the placental vascular bed evokes an increasing
centralization of the fetal circulation. The Doppler manifestations of this oxygen-sparing response include elevated resistance indices in the umbilical artery and fetal aorta and a fall
2
of the cerebral resistance indices. As resistance in the fetal
.
aorta continues to rise (increased afterload), there is a corresponding rise in the end-diastolic right ventricular pressure,
.
140
Fig. 16.17 Severely abnormal
Doppler waveforms in the arterial
(left side) and venous (right side)
vascular systems in a severely
growth-retarded fetus at 30 weeks
4 days. The FHR trace shows a silent
pattern with a late deceleration.
Clinical Applications
whose persistence leads to greater pulsatility in the venous
vessels and the occurrence of umbilical vein pulsations
55, 56
These Doppler changes reflect a hypoxia-induced myocardial
insufficiency and are especially pronounced in cases with progressive acidemia. It appears that abnormally increased preload indices in the ductus venosus and inferior vena cava as
well as umbilical vein pulsations precede definite changes in
fetal heart rate (FHR) tracings
6, 25
(Fig. 16.17).
Use of venous Doppler sonography. Venous Doppler sonography is particularly indicated in cases with absent or reverse
end-diastolic flow in the umbilical artery
22, 25, 46, 62
. The goal of
this examination is to gain additional, noninvasive information
on fetal cardiac performance so that the optimum timing of the
delivery can be determined. This appears to be particularly
crucial in severely growth-retarded fetuses below 30 weeks in
a setting of chronic placental insufficiency
21
. Clinical studies
are currently underway to determine the extent to which these
findings can be confirmed and clinical management principles
can be derived from them.
Growth Discordance in Multiple Pregnancy
In cases where malformations and chromosome abnormalities
can be excluded, a growth discordance in a multiple pregnancy
is most commonly related to intrauterine growth retardation
based on chronic placental insufficiency or a fetofetal transfusion syndrome.
Fetofetal transfusion syndrome. Although the pathogenesis of
fetofetal transfusion syndrome is not yet fully understood, the
chronic shunting of blood from one twin (donor) to the other
twin (recipient) through placental vascular anastomoses appears to be the cause of the syndrome. This leads to increasing
hypervolemia in the recipient and varying degrees of hypovolemia in the donor. The result is increased diuresis in the
recipient and decreased diuresis in the donor, promoting the
development of polyhydramnios or oligohydramnios (“stuck
twin”). When this process outstrips the compensatory capacity
of the recipient, the hypervolemia leads to congestive heart
.
failure. The resulting elevation of central venous pressure in
the heart leads to cardiomegaly, which in turn is reflected in
elevated preload indices in the venous vessels or even pulsations in the umbilical vein (Figs. 16.
18,16.19). When congestive
failure has become established in the recipient, tricuspid insufficiency can be demonstrated in 56% of cases and increased
preload indices in 40 %
66
. By contrast, increased venous preload
indices are found in the donor twin in only 8 % of cases. They
may be an expression of hypovolemia and increased placental
resistance. Tricuspid insufficiency is not invariably associated
with increased pulsatility in the venous vessels. This is due to
the time difference between the valvular and venous flows:
whereas the regurgitation in tricuspid insufficiency occurs
mainly during ventricular systole, reverse flow (a) in venous
vessels occurs during late ventricular diastole or atrial contraction. Depending on the adaptive capacity of the heart, hydrops
fetalis can develop in 8% of cases, usually in the recipient twin.
Interestingly, these cases often display normal resistance indices in the arterial vessels
28
.
Hydrops fetalis
Some fetuses with nonimmune hydrops are found to have a
low right ventricular stroke volume, which is manifested by
elevated preload indices in the venous vessels and the presence of umbilical vein pulsations
22
. The examination of venous
vessels can be helpful in these cases for the etiological and
prognostic evaluation of the various forms of fetal hydrops.
Fetal Arrhythmias
Supraventricular extrasystoles. Supraventricular extrasystoles
(premature beats) may occur singly or at regular intervals and
account for approximately 95 % of all fetal arrhythmias. This
type of arrhythmia is considered to have a very good overallintrauterine and neonatal prognosis. Only about 10% of extrasys-
Obstetric Ultrasound
Fig. 16.18 Fetofetal transfusion syndrome at 17 weeks 4 days. A normal Doppler spectrum is recorded from the ductus venosus of the
donor twin.
Fig. 16.19 Fetofetal transfusion syndrome at 17 weeks 4 days. An abnormal Doppler spectrum is recorded from the ductus venosus of the
recipient twin.
141