Vol. 275, Issue 5, H1759-H1767, November 1998
Dilatation of the ductus venosus in human fetuses:
ultrasonographic evidence and mathematical modeling
M.
Bellotti1,
G.
Pennati2,
G.
Pardi1, and
R.
Fumero2
1 Department of Obstetrics and
Gynecology, San Paolo Biomedical Sciences Institute, University of
Milan, 20142 Milan; and
2 Department of Bioengineering
and Centro di Bioingegneria e Innovazioni Technologiche in
Cardiochirurgia, Politecnico di Milano and Hospital San Raffaele,
20132 Milan, Italy
 |
ABSTRACT |
Autonomic regulation of blood flow through the
fetal ductus venosus has been suggested, but the existence of a
sphincter at the ductal entrance in human fetuses has yet to be
established. In this paper two cases of apparent ductus venosus
dilatation in two growth-restricted human fetuses are reported.
Prolonged ultrasonographic analysis (45 min) showed rapid and
substantial changes (>80%) of ductal diameters. Pulsed Doppler
analysis was used to investigate flow velocity in the ductus venosus
and umbilical vein for both normal and dilated conditions. Dilated
conditions caused manifest modifications of velocity tracings. Systolic
peak velocity in the ductus did not change visibly, whereas velocity at
the atrial contraction showed evident reduction; consequently, pulsatility indexes increased. Furthermore, the umbilical vein presented flow velocity pulsations. The mean blood flow rate through the ductus seemed to increase substantially (>70%) for high
dilatation. To investigate these findings further, we performed
simulations of ductal dilatation by means of a lumped-parameter
mathematical model of the human fetal circulation. Model results agreed
with clinical evidence and confirmed the relationship between ductal dilatation and the observed velocity alterations. Simulated systolic peak velocity slightly increased for small dilatation (<30%), whereas atrial velocity was reduced when the ductus dilated.
Furthermore, the model indicated that umbilical venous pressure
decreases for increasing dilatation, whereas no change occurs in the
central venous pressure. The present results seem to indicate the
presence of active dilatation of the ductus venosus in human fetuses.
fetal circulation; model simulation; ultrasound; sphincter
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INTRODUCTION |
IN RECENT YEARS technological
advances in ultrasound imaging and color Doppler equipment allowed the
collection of new data on the complex morphology and hemodynamics of
the ductus venosus (DV) in the human fetus (13, 15, 17-21, 26,
30). Many studies demonstrated the role of the DV in shunting the
well-oxygenated blood from the umbilical vein (UV) through the foramen
ovale to the left atrium (LA) and to the cerebral and myocardial
circulation in both animals (2, 7, 31) and human fetuses (17). In animal studies, induced hypoxemia (8, 23) or severe acute hemorrhage
(22) results in a higher blood flow rate through this vessel. An
increased proportion of blood flow from the intrahepatic UV to the DV
was shown when umbilical blood flow decreased because of experimental
cord compression (16). In human growth-restricted fetuses, the DV peak
velocities are maintained within normal ranges even in the presence of
impaired umbilical circulation (18). In these fetuses a reverse flow
during atrial contraction in the DV has been supposed to be related to
augmented atrial pressure, suggesting myocardial compromise (18, 30).
The exact mechanism determining an increased flow shunt is still
unknown. The anatomic findings in animals of a muscular structure along
the DV and adrenergic activity suggested the presence of a sphincter
that could allow the DV to change its isthmic diameter and regulate the
blood flow throughout it (1, 4). Similar sphincteric activity was
speculated in the human fetus (11, 24), but this occurrence is quite controversial. To the best of our knowledge, no clinical evidence of
active ductal dilatation has been observed in human fetuses.
Obviously, modifications of the diameter of a vessel cause alterations
in the hydraulic resistance to blood flow through the vessel. The
effects of a change in a vascular parameter (i.e., flow resistance) on
the hemodynamic features of blood circulation can be evaluated by means
of model simulations. Huikeshoven and colleagues (14) applied a
mathematical model of the fetal lamb circulation to study the effects
of disturbances from the normal steady state produced by changes in DV
resistance. According to their model, mean ductal and umbilical flow
are substantially affected by ductal resistance changes, whereas
cardiac output, central oxygen tension, and central blood pressures in
fetal lambs are only slightly influenced. However, the simulated
changes in DV resistance were not related to changes in its diameter.
Furthermore, the influences of a resistance change on the morphology of
velocity time tracings were not investigated.
We previously developed a mathematical model to simulate the Doppler
tracings in the human fetal circulation (27). The model parameters are
related to the anatomic dimensions of the vessels; thus the model
allows us to simulate changes of the ductal diameter and to investigate
the subsequent hemodynamic variations.
In this paper two clinical cases of apparent DV dilatation are
presented. The ductal ultrasonographic and Doppler findings in two
growth-restricted human fetuses were compared with the results of
mathematical simulations of ductal dilatation to investigate a possible
active dilatation of the DV in human fetuses.
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MATERIALS AND METHODS |
Clinical study: Case reports.
Two fetuses (fetus A and
fetus B) affected by intrauterine
growth restriction (IUGR) were examined, fetus
A at 24 wk of gestation and fetus
B at 29 wk of gestation. Ultrasound examinations were carried out with a coaxial pulsed Doppler color flow imaging system (Esaote Biomedica AU4, Genoa, Italy) implemented with a 3.5-MHz probe.
Fetal biometry was plotted against our reference values for gestational
age. IUGR was defined as an abdominal circumference below the fifth
percentile of our reference limits. Fetal morphology was examined to
exclude structural abnormalities. Fetal karyotypes obtained after fetal
blood samplings were normal (46 XY for both fetuses).
Fetus A was delivered at 28 wk of
gestation by cesarean section performed for fetal distress, with a
birth weight of 900 g. Fetus B was
delivered at 29 wk of gestation by cesarean section, weighing 910 g.
At birth no major malformations and no infectious diseases were present
in the neonates. Fetus A is alive and
well at 12 mo of life. Fetus B died
after 15 days of life because of respiratory distress syndrome, and
autopsy did not evidence anatomic malformations. Histological
examinations of the two placentas revealed multiple vascular cysts for
fetus A and wide chronic hypoxic areas
for fetus B.
Each fetus was observed for ~45 min. During this period repeated
measurements of ductal dimensions were performed (Fig.
1), studying the DV in a near-midsagittal
section (Figs. 2,
A and D, and
3, A
and C). Measurements of the
diameters at the inlet (Disthmus) and
at the outlet portion of the vessel
(Doutlet) were obtained by positioning the calipers at the inner walls of the vessel.
Doppler investigations of the DV velocity were also performed for some
relevant values of diameters. Pulsed Doppler waveforms were recorded in
the absence of fetal active and breathing movements. Doppler tracings
of the maximal velocities
(Vmax) were
obtained with an insonation angle below 30°. The maximum velocity
at the systolic peak (S) and the minimum velocity during atrial
contraction (A) were measured at the isthmus of the DV (see Figs. 2,
B and E, and 3,
B and
D); time-averaged maximal velocity
during the cardiac cycle
(
max)
was also calculated.
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Fig. 1.
Modifications of measured diameters ( , outlet diameter;  , isthmic
diameter) of ductus venosus (DV) in fetus
A (A) and
fetus B
(B). Time instants at which Doppler
velocity recordings were also performed are shown.
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Fig. 2.
Ultrasonographic analysis of DV of fetus
A during dilated
(A-C; time of study, 10 h 27 min)
and normal (D-F; time of study,
11 h 13 min) conditions. A and
D: near-sagittal midsection showing DV
[inlet section (I) and outlet section (O)], which connects
umbilical vein (UV) to heart (H). B
and E: blood velocity tracings at
ductal isthmus evidencing large decrease of minimum of velocity at
atrial systole (A) when DV dilates
(B). Systolic peak velocity (S)
shows similar values in both conditions.
C and
F: blood flow velocity in intrahepatic
UV. Normally, time tracing is almost steady during cardiac cycle
(F), but some pulsations are present when DV dilates
(C). Because of position of fetus,
negative values of recorded Doppler tracings indicate a flow from UV
toward H.
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Fig. 3.
Ultrasonographic analysis of DV of fetus
B during normal (A and
B; time of study, 9 h 26 min) and
dilated (C and
D; time of study, 10 h 07 min)
conditions. A and
C: near-sagittal midsection showing DV
(I and O), which connects UV to H. B
and D: blood velocity tracings at
ductal isthmus evidencing a decrease of A during dilatation of DV. S
shows similar values in both conditions. Note that fetus changed
position between the 2 measurements; consequently, Doppler tracing
recorded during dilated conditions is reversed with respect to
nondilated conditions.
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With this velocity value and
Disthmus, we
estimated the blood flow rate through the DV according to the following
formula
|
(1)
|
where
the constant h (related to the spatial
velocity distribution) was assumed equal to 0.67 in agreement with a
previous study (28).
To assess the fetal ventricular function, peak velocities at the aorta
and pulmonary artery were obtained and compared with our normal
reference ranges (10). In addition, the intrahepatic UV was sampled
immediately before the ductal branching (Fig. 2, C and
F). The blood flow direction was
assessed using color Doppler imaging, and the exact site of the
isthmical flow of the DV was evidenced by the aliasing effect, at a low
pulse repetition frequency.
Angle-independent indexes were calculated at the level of the umbilical
artery and the middle cerebral arteries [pulsatility index (PI)
according to the Gosling formula (Ref. 12)] and the DV [DV
index (DVI) = (S 
A)/S, according to DeVore and Horenstein (Ref.
5)].
Mathematical model.
The fluid dynamics of the DV was investigated by means of a
mathematical model of the human fetal circulation that was primarily based on and validated using blood velocity data derived from the
Doppler analysis (27). It consists of two major parts, the heart and
the vascular bed (arteries and veins), that were described by means of
some lumped parameters. We adopted this model approach to have a simple
tool to study human fetal blood circulation and to identify the
relationship between vascular features and hemodynamic behavior. The
parameter values of the model refer to the final gestation period, when
fetal body weight is ~3 kg. The vascular bed is divided into 19 compliant vascular compartments. Figure 4
shows only the portion of the model close to the DV. The connection between the inferior vena cava and LA represents the blood flow path
that crosses the foramen ovale (17). A component that allows the flow
only in one direction was considered in the models of the cardiac
valves and the foramen ovale.
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Fig. 4.
Sketch of investigated anatomic region and block scheme of
lumped-parameter model. RV and LV, right and left ventricles; RA and
LA, right and left atria; SVC and IVC, superior and inferior venae
cavae; HE, hepatic circulation; Plac, placenta.
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Each compartment in the vascular model (blocks in Fig. 4) was described
by means of a constant compliance C = 
V(t)/P(t), where P(t) is the instantaneous
local pressure and V(t) is the instantaneous compartmental blood volume. Each compartment was mathematically modeled by the mass conservation law, which can be
expressed, according to the C definition, as follows
|
(2)
|
where
in(t)
and
out(t)
indicate the sum of the instantaneous volumetric flow rates at the
inlet and the outlet of the compartment, respectively.
The momentum conservation law for each interconnection (lines in Fig.
4) between two compartments can be expressed as
|
(3)
|
where
P(t) is the instantaneous
pressure difference applied to the line ends,
(t) is the
instantaneous volumetric flow rate,
Rvisc is the
viscous resistance, and L is the
inertance. The additional term
K · (t)
,
which depends on the flow rate, takes the local fluid dynamics into
account. In particular for the DV model, this term is related to the
convective acceleration and energy dissipations at the inlet of the
vessel (
= 2). The inertial phenomena were considered for the
cardiac valves and the large arteries close to the heart only. For the
model of each vessel the instantaneous hydraulic impedance
Z(t) = P(t)/(t)
can be calculated.
Mass and momentum conservation laws applied to all of the compartments
and connections, combined with the heart model equations, resulted in a
nonlinear algebraic differential equation system that was solved using
a backward differentiation formula implicit method (3); see Pennati et
al. (27) for extensive explanation and validation of the model assumptions.
Simulation of DV dilatation.
In the case of the DV Eq. 3 becomes
|
(4)
|
where
the values of
RviscDV and
KDV depend on the
blood properties (the blood was assumed as incompressible, viscous, and Newtonian fluid with a density 
= 1.06 g/ml and a viscosity µ = 4.0 cP) and on the DV dimensions, particularly the diameter (D) and length
(l).
As far as the resistive term related to the viscous friction along the
walls of a rigid cylindrical vessel is concerned, it can be calculated
according to the Poiseuille theory as
|
(5)
|
The dissipative term
KDV accounting
for the energy losses caused by irregular local fluid dynamics
(separation of flow and secondary flow at the abrupt changes of cross
section) can be related to the flow velocity
(v) according to traditional
hydraulic formulas. Pressure drops are usually calculated as P = kv2/2, where
k is a constant coefficient that for
the DV assumes a value slightly less than 1 (28). In the model we
assumed P = K · 2;
it then follows that
|
(6)
|
The DV has a conical shape: its diameter increases from the inlet to
the outlet. In any event, in our calculations the DV was considered as
a cylindrical vessel with a diameter equal to the average of
Disthmus and
Doutlet. Assuming
D = 2.1 mm and
l = 20 mm for a normal human fetus at
38 wk (21),
RviscDV = 1.3 mmHg · s · ml
1
and KDV = 0.26 mmHg · s2 · ml2.
According to Eqs. 5 and 6, a little modification in the DV
mean diameter D causes a large change
in both parameter values (RviscDV 
D4 and
KDV D4) and
strongly affects the local hemodynamics. In the present study we
simulated a progressive increase of the mean diameter of the vessel
(30, 60, 90, and 150% of the reference value), maintaining the same
values for all the other model parameters. Flows and velocities through
the DV as well as pressures at its ends were investigated. Furthermore,
the hydraulic impedance
ZDV(t)
of the DV was evaluated using the calculated values of
P(t) and
(t) for the DV.
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RESULTS |
Clinical study.
Fetus A evidenced changes in ductal
diameters within 40 min of observation, passing from wider to narrower
measures (Figs. 1A and 2,
A and
D) and successively recovering wider
dimensions. In fetus B the ductal
diameters dilated abruptly within 6 min of observation (Figs.
1B and 3,
A and
C) and then remained almost stable.
In both cases the maximal variation of the diameters exceeded 50%.
Measurements of the ductal diameters and velocities as well as
calculations of angle-independent indexes and flow rates are summarized
in Tables 1 and 2 for
fetus A and fetus
B, respectively. These tables also report the
velocities at the ventricular outlets and the PI at the peripheral
arteries. For fetus A UV flow velocity was also examined. Pulsations at the intrahepatic level were observed for dilated DV (Fig. 2C) but
disappeared when the diameters of the DV decreased (Fig.
2F). The time lag between the
maximum and minimum velocities at the UV was equal to the measured time
lag between the systolic peak velocity and the atrial contraction minimal velocity recorded in the DV. Furthermore, no pulsations were
seen in the UV at the placental end.
Diameter and velocity values were normalized on their respective values
in absence of dilatation (when the isthmic diameter assumed its minimum
value) and are examined in Figs. 5 and
6.
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Fig. 5.
Fetus A: changes of blood velocities
and flow through DV (A) and of
angle-independent index [DVI = (S A)/S;
B] consequent to modifications
of isthmic diameter
(Disthmus).
Velocity and flow are normalized to values corresponding to
minimum recorded diameter value
( ).
time-averaged maximal velocity;
, time-averaged blood flow rate.
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Fig. 6.
Fetus B: changes of blood velocities
and flow through DV (A) and of DVI
(B) consequent to modifications of
vessel diameter. Velocity and flow are normalized to values
corresponding to
.
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In fetus A, the normalized velocities
in the DV showed a slight decrease for the systolic peak velocity in
correspondence to larger diameters; on the other hand, the atrial
contraction wave largely decreased as the dilatation increased and
minimum velocity (A) became negative (Figs. 2,
B and
E, and
5A). As a consequence, the DVI value
notably increased (Fig. 5B). The
mean blood flow rate through the dilated DV increased; meanwhile, the mean velocity tended to decrease. (Fig.
5A).
Similar trends of modifications are shown for fetus
B (Figs. 3, B and
D, and 6,
A and
B) except for the systolic peak
velocities, which slightly increased.
Model simulations.
Figure 7 shows the simulated time tracings of velocity
in the DV and pressure at the vessel ends for a normal fetus. Two fetal cardiac cycles were presented for five different values of the ductal
mean diameter. Ductal dilatation causes a shift toward low values of
the velocity at the atrial contraction (A) and produces values near
zero for highly dilated DV. On the contrary, the computed systolic peak
velocities (S) substantially do not change. Umbilical venous pressure
decreases as much as ductal diameter increases, whereas the pressure in
the inferior vena cava present only small alterations. In addition,
pulsations of the pressure, synchronous to the atrial events, appeared
at the UV level when high dilatation was simulated. Figure
8 reports the changes of the blood velocities and flow
through the DV and of the DVI consequent to modifications of the vessel
diameter. The computed velocities show minor changes for the systolic
peak and important reduction of the atrial contraction velocity for
dilated diameter; ductal mean velocity decreases, even if blood flow
rate is notably augmented (Fig. 8A).
The related angle-independent index doubles its value when normalized
diameter reaches the maximum investigated value
(D/D* = 2.5, see Fig. 8 B). Table
3 summarizes absolute values of flow and velocity
calculated by means of model simulations. DV dilatation causes an
increase (<15% of its reference value) of the flow in the UV
(UV);
nevertheless, the proportion of umbilical flow shunted to the DV
significantly increases. The calculated impedance
ZDV(t
) showed small changes during the simulated cardiac cycle
(standard deviation <20% of mean value) and large variations with
ductal diameter modifications. Figure
9 illustrates the
relationships among normalized ductal diameter, ductal impedance (time
averaged), and mean flow rates through the UV and the DV. A diameter
increase of 30%
(D/D* = 1.3) causes a reduction of the ductal impedance over 50% of its reference value (from 0.031 to 0.013 mmHg · s · ml1)
and a 78% increase of the flow rate through the ductus (from 117 to
208 ml/min); when diameter dilates further on
(D/D* > 2) the impedance of the ductus falls to <10% of the reference
value and the ductal flow rate tends to equal
UV (445 vs. 479 ml/min for
D/D* = 2.5).
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Fig. 7.
Mathematical model: simulated time tracings of velocity in DV
(A) and pressure in UV
(B) and IVC
(C).
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Fig. 8.
Mathematical model: changes of blood velocities and flow through DV
(A) and of DVI
(B) consequent to modifications of
Disthmus.
Velocities and flow are normalized to values corresponding to reference
diameter value
(D*).
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Fig. 9.
Mathematical model: influence of ductal diameter (normalized value
D/D*)
on ductal impedance (time-averaged
ZDV) and mean
flow rates through UV
(UV) and DV
(DV).
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DISCUSSION |
The ductus venosus plays an important role in shunting highly
oxygenated blood to the brain and the myocardial cells, both in animals
and in human fetuses (2, 6, 7, 17). Experimental studies suggested that
an increased proportion of blood flow passes from the umbilical vein to
the ductus venosus, in the presence of hypoxic conditions and reduced
umbilical blood flow volume (2, 8, 29). Similarly, the observed
maintenance of high velocities at the systolic and diastolic peak of
the ductus venosus in growth-retarded human fetuses, despite reduced
umbilical vein blood flow, was associated with higher flow rate through
the vessel (18). However, up to now, this hypothesis has not been
supported by measurements of vessel diameter and evaluations of blood
flow rate.
Anatomic findings in animals suggested the presence of a sphincter at
the level of the ductal isthmus (1, 4), and its muscular activity would
represent the physiopathological basis of the redistribution of blood.
Determination of a similar muscular activity in the human fetus is
quite controversial because of the lack of anatomic evidence of such a
structure and in vivo observations of diameter dilatation.
In our clinical observations on two growth-retarded fetuses examined
for a prolonged period of time, we evidenced variation of the ductus
venosus diameters in both fetuses. Because our reproducibility of the
ductus venosus diameters showed a mean coefficient of variation within
10% (25) both at the isthmus and at the outlet, the changes of the
ductus diameters measured during fetal observations are caused by an
unstable condition of ductal dilatation rather than by large
variability in measurements. In addition, the extent of diameter
increase (as high as 100% for fetus
B) was unlikely to have been caused by a passive
enlargement for augmented venous pressure because the pressure should
reach values inconsistent with the observed normal cardiac function.
Hence, in our opinion, it is reasonable to affirm that in IUGR fetuses,
active dilatation of the ductus venosus could occur and that specific
Doppler waveforms are related to different diameter conditions.
However, we cannot exclude the possibility of transient dilatation of
the ductus venosus in normal fetuses, although such evidence of ductal
dilatation should have a different pathophysiological basis. In any
event, in our experience prolonged echographic examinations in normal fetuses never demonstrated dilatation of the ductus venosus with peculiar modifications of the velocity tracing. The ultrasonographic and Doppler studies cannot evaluate the anatomic basis and the physiopathological mechanism of such a dilatation. Biochemical or
neurological factors could be involved in determining an active enlargement of ductal diameters, even in early gestation
(4).
In dilated ductus venosus, we observed a large reduction of the
velocities at the atrial contraction, leading to a reverse flow in some
instances (fetus A). However, the
velocities recorded at the systolic peak were maintained at normal
values for both fetuses, even if slightly different trends with
diameter values were noted. In any event, the DVI manifestly increased
in both fetuses when ductal diameter enlarged. The values of the DVI
measured for fetus A and
fetus B with small diameter (DVI = 0.52 and DVI = 0.59 for fetuses A and
B, respectively) fell within the
normal range according to DeVore and Horenstein (5), whereas they clearly exceeded normal values in dilated conditions (DVI > 1 and DVI = 0.79 for fetuses A and
B, respectively).
Mathematical simulation of ductal dilatation showed quite similar
behavior of the velocity time tracings at the ductus compared with
clinical observations. This good agreement, although qualitative, confirms the dependence that exists between diameter increase and
alterations of Doppler velocity waveforms. Negative values for velocity
at the atrial contraction were never found in the simulations with
highly dilated diameters. This discrepancy with experimental data is
probably caused by the different features of the model with respect to
the examined fetuses. First, the model was scaled for a fetus at 38 wk
of gestation (body wt = 3 kg), whereas the gestational ages of
fetus A and fetus
B were both <30 wk (body wt < 1 kg). In addition,
the model refers to normal conditions, whereas the two investigated
fetuses were IUGR fetuses. In any event, the accord of trends between
model and clinical data was enough so as to not be considered trivial.
A large reduction of the A wave velocity with absent or reverse flow
during atrial contraction was observed in many pathological conditions
(20), all suggesting an impairment of myocardial function. Furthermore,
in IUGR fetuses velocities close to zero or negative, recorded at the
atrial contraction, were related to probable high atrial pressures
following fetal myocardial impairment (18).
In the present study we observed a large reduction of the A wave during
the ductus venosus dilatation, even in the presence of normal cardiac
function. Indeed, normal peak velocities both in the pulmonary artery
and in the aorta were recorded, although the fetuses under study were
severe, true IUGR fetuses. According to our previous study, in IUGR
fetuses the peak velocity at the ascending aorta level is well
correlated with normal acid-base state and myocardial function (9). The
transient effect of ductal dilatation and the return to normal
dimensions and normal Doppler waveforms at the isthmus of the ductus
could be explained by a temporary fetal distress, in the presence of
impaired placental function, as documented by the observed Doppler
velocimetric indexes (high PI in the umbilical artery) and fetal
cerebral vasodilatation (low PI in the middle cerebral artery) (10).
Impaired placental function of both fetuses was confirmed by
histological examination at birth. Furthermore, we can speculate that
more severe placental diseases and related hypoxic conditions could
determine a lasting dilatation of the ductus venosus in IUGR fetuses,
not only transient modifications of the ductal diameters.
The mathematical simulations confirmed the hypothesis that low velocity
during atrial contraction could occur without myocardial dysfunction
but caused solely by an enlargement of the diameter of the ductus
venosus. Indeed, simulations with progressive increase of the ductal
diameter evidenced almost constant pressure values in the inferior vena
cava in presence of low A velocities. According to the model, these
velocity reductions were related to a reduced pressure in the umbilical
vein, consequent to the lower flow resistance of the dilated ductus.
The mean impedance of the ductus venosus seems to become very low for
diameter dilatations similar to those detected in the investigated
fetuses (increase of 40-60% in the isthmic diameter). Actually,
the calculated impedance decreases below 30% of the reference value
when a 50% increase in the ductal diameter is simulated. The reference
value calculated for the mean ductal impedance (0.031 mmHg · s · ml1)
is very close to the resistance (0.0355 mmHg · s · ml1)
assumed by Huikeshoven and colleagues (14) in their model of the
circulation of a 3-kg fetal lamb. It is interesting to note that in the
present work the value of impedance of the ductus results from the
lumped model parameters
(RDV and
KDV) calculated using the anatomic dimensions of the vessel and the properties of the
fetal blood.
Model simulations showed that ductus dilatation causes an increase of
the flow in both the umbilical vein and the ductus venosus, but the
proportion of umbilical flow shunted to the ductus venosus notably
increases. The trends of the volume flow rates through the umbilical
vein and the ductus venosus (Fig. 9) calculated for various impedance
values (i.e., various ductal diameters) are quite similar to those
simulated by Huikeshoven and colleagues (14).
The blood flow rate through the ductus venosus in both fetuses under
study, evaluated from the measured velocities and diameters, evidenced
an increase of the mean blood flow for the maximum dilatation of the
ductal diameters around 80% of the values associated to the minimum
recorded diameters.
In conclusion, the present study seems to indicate that in human IUGR
fetuses, an active dilatation of the ductus venosus could occur.
Further investigations are required to confirm this clinical evidence.
The observed dilatation suggests a compensatory effect for which a
higher proportion of the umbilical flow is shunted through the ductus
to the brain and the myocardium. As yet, we cannot know whether this
condition is temporary in acute distress or steady in chronic placental
impairment. For dilated conditions the Doppler indexes of the ductus
venosus used in the clinical routine show notable augmentation.
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ACKNOWLEDGEMENTS |
This work was partially supported by Grant 6-FY97-0174 from
the March of Dimes Birth Defects Foundation.
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FOOTNOTES |
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement"
in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: M. Bellotti, Dept. of Obstetrics and
Gynecology, San Paolo Biomedical Sciences Inst., Univ. of Milan, Via di
Rudini 8, 20142 Milan, Italy.
Received 17 February 1998; accepted in final form 19 July 1998.
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The "sphincter" of the ductus venosus.
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C. W. de Lannoy,
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Distribution of the circulation in the normal and asphyxiated fetal primate.
Am. J. Obstet. Gynecol.
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956-969,
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Am J Physiol Heart Circ Physiol 275(5):H1759-H1767
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Abstract
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