Vol. 274, Issue 5, H1605-H1612, May 1998
Venous and arterial behavior during normal pregnancy
D. A.
Edouard1,
B. M.
Pannier2,
G. M.
London2,
J. L.
Cuche2, and
M. E.
Safar2
1 Department of Anesthesiology,
A. Béclère Hospital, 92140 Clamart; and
2 Department of Internal Medicine
(Medicine 1) and Institut National de la Santé et de la Recherche
Médicale, U 337, Broussais Hospital, 75674 Paris Cedex 14, France
 |
ABSTRACT |
To assess the contribution of the arterial and
venous systems in the hemodynamic changes of normal pregnancy, we
studied blood flow, vascular resistance, venous tone, and the
viscoelastic properties ("creep") of the upper and lower limbs
(using plethysmography), aortic distensibility (using pulse wave
velocity measurements), and cardiac dimensions (using echocardiography)
in nine healthy women. Studies were longitudinally performed at the
first (10-13 wk) and third (33-38 wk) trimesters of pregnancy
in comparison with the period between the third and sixth month after
delivery. From the first trimester, heart rate significantly increased
while systemic blood pressure and limb vascular resistances did not change significantly and aortic distensibility increased
(P < 0.05). Lower limb viscoelastic
properties decreased at the third trimester
(P < 0.05) and venous tone increased
from the first trimester (P < 0.01),
whereas little changes were observed at the site of upper limbs. The
decrease in calf venous tone was significantly correlated with the
increase in left ventricular diastolic diameter at the first
(P < 0.001) and the third trimester (P < 0.05). The study provides
evidence that during normal pregnancy, changes in the arterial and
venous sides of the circulation occur independently of pressure
alterations. The increase in venous tone, contributing to preload
augmentation, and the decrease in aortic stiffness, reducing afterload,
both optimize cardiac function until delivery.
venous tone; aortic compliance; arterial distensibility; cardiac
function
| |
INTRODUCTION |
IT IS WELL ACCEPTED that a normal pregnancy is
characterized by a large increase in total blood volume and in cardiac
output (31, 32, 48). Blood volume expansion appears early during the
pregnancy and rises up to 50%. Cardiac output rises up to 40-50%
above nonpregnant values, and the highest increase is reached halfway
through gestation. Cardiac output is the product of heart rate and
stroke volume. Heart rate is known to reach a 10-27% increase
between weeks 4 and
36 of pregnancy (10). However, an
increase in stroke volume might also play an important role at the
early phase. Stroke volume appears elevated at least until weeks 28-32 (31). The
mechanism(s) causing the increase in stroke volume are not yet well
established. In pregnant rats and women, an increased cardiac
contractility has been suggested (13, 36, 44), but the differentiation
between the contractile properties of cardiac muscle itself and the
contractile changes that result from altered preload and afterload is
difficult to establish. The possibility should be
considered that an increase in venous return also plays a major role.
In the literature, numerous data indicate a significant increase in
venous capacitance (11, 17, 18, 28, 35, 47). However, significant
discrepancies have also been reported, depending mainly on the site of
measurement of venous variables (40, 46). Furthermore, the early venous changes could not be adequately detected because pregnant women were
not studied longitudinally and because there was a large measurement
error associated with the method used. Finally, the venous system was
often investigated alone in pregnant women. No simultaneous evaluation
of vascular resistance and of arterial distensibility was performed,
thus allowing a concomitant evaluation of the consequences of the
arterial and venous changes on the cardiac structure and function
during pregnancy. Our working hypothesis is that alterations of both
the arterial and venous sides of the circulation contribute to optimize
cardiac structure and function in pregnant women.
The aim of this work was 1) to
investigate the upper and lower limb behavior throughout a normal
pregnancy in terms of venous tone and viscoelastic properties of the
venous wall ("creep," as derived from the hysteresis of the
pressure-volume curve), 2) to
analyze in parallel the aortic distensibility, and, finally, 3) to evaluate the cardiac function
and dimensions using echocardiography. Because of the well-established
role of neurohumoral factors during pregnancy (4, 9, 16, 19, 27, 30,
37, 42), plasma levels of estrogens, progesterone, and several hormones
related to the autonomic and renin-angiotensin systems were also
repeatedly measured.
| |
METHODS |
Subjects. Our subjects were drawn from
a specialized obstetrical outpatient visit to A. Béclère
Hospital. From 1989 to 1991, 70 women having a confirmed pregnancy of
<14 wk were selected. Of the 70 women, 15 were normotensive, accepted
the protocol, and were enrolled in the study after providing written
consent and reviewing a complete description of the procedure,
according to the ethical committee of the hospital. In these 15 women,
blood pressure measured before pregnancy constantly indicated values equal to or lower than 140/90 mmHg. No patient suffered or had suffered
from varicose veins or lower limb venous disease, as confirmed by
clinical history and examination and Doppler investigation. Three of
these 15 patients became hypertensive during pregnancy and therefore
were finally excluded, and three withdrew before the end of the study
for personal reasons. Consequently, nine women were investigated during
the entire protocol, and for them all measurements were completed. All
newborns were healthy and ranged in normal body weight (between 3,020 and 3,600 g). Five of these women were nulliparous. Mean age and height
were, respectively, 28 ± 4 yr (±1 SD of the mean) and
159 ± 5 cm. At each hemodynamic period and throughout the clinical
follow-up of the pregnancy, the supine or sitting blood pressures
recorded by mercury sphygmomanometer were below or equal to 130/85
mmHg. The repeated determinations of proteinuria were constantly
negative. The hemodynamic study was performed during three outpatient
visits in the center, in the same temperature-controlled room (22 ± 1°C), at the first (10-13 wk) and third trimesters (33-38
wk) of their pregnancy and after the third month following their
delivery, which was considered the control period. During this control
period, no woman was breast-feeding.
Study design. The investigations began
at 8:30 AM after the women ate a standard breakfast without tea or
coffee. The women were placed in a 30° left lateral recumbent
position to avoid any compression of the vena cava during the
investigation periods. An indwelling intravenous catheter was
immediately placed in a left forearm vein to permit blood sampling. A
cuff connected to a semiautomatic oscillometric blood pressure recorder
(Dinamap, Critikon, Chatenay Malabry, France) was placed on the left
arm to measure blood pressure every 3 min throughout the entire
procedure, except during the 15 min before blood sampling. Mean blood
pressure (MBP) was calculated from systolic (SBP) and diastolic blood
pressure (DBP) as MBP = DBP + (SBP 
DBP)/3. Measurements began
after a 30-min supine resting period and involved successively the
measurement of aortic distensibility, then upper and lower limb
plethysmography, and finally echocardiography.
Aortic distensibility determination.
The characteristic impedance of an arterial segment is directly related
to regional pulse wave velocity (PWV) according to the widely accepted
Moens-Korteweg equation: PWV = 
, where
E is Young's modulus of the arterial
wall, h is wall thickness, R is lumen arterial radius, and µ is
blood density (29). Aortic PWV was determined as the foot-to-foot wave
velocity measured from the carotid and femoral arteries. Two pulse
transducer heads (Electronics for Medicine) were fixed to the skin over
the most prominent part of the right common carotid artery and the
right common femoral artery in the groin. The distance between the two sites (D) was measured on the skin.
The time delay [or transit time (TT)] was measured on paper
between the feet of the two simultaneously recorded pulse waves (at a
speed of 150 mm/s). The foot, which contains the high-frequency
information, was defined as the point obtained by extrapolating the
wavefront downward and measured from the intersection of this line with
the straight line extrapolation of the last part of the diastolic
curve. PWV was calculated as D/TT.
This was averaged over at least one respiration cycle, that is to say,
about 10 beats.
The variability coefficient (SD/mean) and the repeatability coefficient
(RC) were calculated according to the British Standards Institution (7)
and the Bland and Altman recommendations (6). RC was calculated as
, where D is
the difference within each pair of measurements and N is sample size. The intraobserver
variability coefficient of this method was previously evaluated as
6.2% (3), and the short-term repeatability coefficient was 0.94 m/s
(2). We measured the carotid-to-femoral pulse wave velocity over 2 mo
in eight normotensive patients (not included in this study). For a mean
value of 8.08 ± 0.88 m/s, the repeatability coefficient was 0.80 m/s.
Hemodynamic investigations of upper and lower
limbs. Upper and lower limb blood flow, vascular
resistance, and venous variables were determined using strain-gauge
occlusion plethysmography with gauges placed around the right forearm
and calf and pressure controlled with a mercury sphygmomanometer
(Perivein, Société Européenne des Techniques
Avancées, Noisy-le-Grand, France) (49). The right forearm was
placed in 90° abduction, 5-10 cm above heart level (taking
into consideration the left lateral recumbent position). An adjustable
arm rest ensured that the forearm remained in the same position
relative to the heart. The mercury-in-Silastic strain gauge was applied
on the right forearm 6 cm distal to the lateral epicondyle of the
humerus and then calibrated. The right leg was placed in an adjustable
leg rest, ensuring that the calf was maintained 5-10 cm above
heart level. The gauge was placed on the prominent part of the calf and
then calibrated. Pneumatic cuffs were placed around the right arm and
thigh for venous occlusion. Both cuffs were connected to the same air
compressor and mercury manometer for measurement of cuff pressure
during inflation and deflation. Venous distensibility was first
measured simultaneously on the upper and lower limbs, and thereafter
blood flow (BF) simultaneously on both limbs. Local resistances
(RL) were
calculated as RL = (MBP/BF)/60
(mmHg · ml
1 · s1).
The venous distensibility was determined by a method adapted from Wood
and Eckstein (50), as already published (21, 25, 34). Volume changes
measured by the gauge are well correlated with radionuclide
plethysmography and highly reproducible (26). The cuff pressures were
simultaneously increased by steps of 2-3 mmHg until the volume of
the limbs started to increase. The cuff pressure just below that value
was considered the zero level of effective venous pressure (minimal
occluding pressure). The cuff pressure was increased to 5 mmHg, then to
7.5 mmHg, and then by steps of 5 mmHg to 10, 15, 20, 25, and 30 mmHg of
effective venous pressure. At each step the pressure was kept constant
for a delay corresponding, for each subject, to 10 heartbeats. The
plateau corresponding to the last five heartbeats was then recorded on paper. The same technique was used in the deflation phase, during which
cuff pressures were decreased by identical steps from 30 to 0 mmHg. The
pressure-volume relationship showed a typical hysteresis and then was
analyzed to define simple quantitative parameters of venous
viscoelastic properties. The first hemodynamic variable was the venous
tone, expressed as the slope of the linear part of the volume-pressure
relationship (from 5 to 30 mmHg of cuff pressure) during the inflation
phase. The slope of this correlation was expressed in millimeters of
mercury per milliliter times 100 ml and represented an
index of the elasticity of the veins (VdP/dV), where dP and dV are the
change in pressure and in volume, respectively, and V is the baseline
volume. The second variable was the extent of isotonic relaxation
(creep) determined as the difference in limb volume between inflation
and deflation phases at 20 mmHg. The creep [volume increment at a
pressure of 20 mmHg
(
VP20)] was expressed in milliliters per 100 ml and quantified the hysteresis of the venous pressure-volume curve. The third parameter was the relative change of limb volume observed at the second 30-mmHg step of
pressure (the 1st step of the deflation) and corresponded to a global
index: the venous capacitance [volume variation at a pressure of
30 mmHg (VV30)]. This
variable depends on both the venous tone and the width of the curve
hysteresis. For each patient three recordings were performed at 5-min
intervals, permitting a return to baseline conditions. The mean value
of these three consecutive measures was taken as characteristic for
each subject and for statistical evaluation. In a previous study (38)
we showed that forearm venous tone determined according to this
noninvasive method was strongly correlated in humans with total
effective compliance of the vascular bed evaluated from rapid volume
expansion.
Forearm and calf blood flows were measured just after the determination
of venous distensibility with the same mercury-in-Silastic strain
gauges. Venous occlusion was achieved by cuff inflation to 50 mmHg at a
constant rate of 5 mmHg/s. Three consecutive flow curves were recorded,
the mean value being taken as characteristic for each subject and
statistical evaluation. Because no arterial occlusion was performed at
the site of wrist or ankle, changes in hand or foot blood flow were
included in the measurements. The results are expressed in milliliters
per minute per 100 ml of tissue.
The reproducibility of the plethysmographic method was evaluated on six
young normal women (not belonging to this population). Two measurements
were performed over a 4-wk interval, exactly at the same menstrual
date. For the lower limb venous tone, the averaged value was 16.56 ± 1.89 mmHg · ml1 · 100 ml, the SD of the difference was 4.72 mmHg · ml1 · 100 ml, and the repeatability coefficient (7) was 4.57 mmHg · ml1 · 100 ml. For the creep (VP20), the
RC was 0.19 ml/100 ml and for the capacitance
(VV30), the RC was 0.64 ml/100
ml.
Echocardiographic measurements. M-mode
echocardiography was performed with an echocardiograph V3280
(Electronics for Medicine) with a 2.25-MHz transducer and a continuous
recorder at a paper speed of 50 mm/s. Each woman was studied in the
30° left lateral position. Incidences were obtained through the
standard left parasternal site. The measurements of aortic diameter,
left atrium (LA), left ventricular systolic (LVSD) and diastolic
diameter (LVDD), interventricular septal thickness (IVST), and
posterior wall thickness (PWT) were taken on at least three heart beats
following the usual recommendations of the Pennsylvania Convention
(12). Left ventricular ejection time (LVET) was measured on a
simultaneously recorded carotid pulse tracing. The mean velocity of
circumferential fiber shortening (VCF) was
calculated as the percent change of left ventricular diameter divided
by the LVET (expressed as circumference/s). Repeatability of the method
has been previously published (3) and is in agreement with the commonly
admitted values (24).
Hormonal determinations. Blood
sampling was performed after a 30-min supine resting period following
the intravenous catheter setting. The plasma protein level and the
following hormones were measured: norepinephrine, epinephrine, dopamine
(radioenzymatic technique), estradiol (competitive immunoassay
technique, Johnson & Johnson), progesterone [radioimmunoassay
(RIA), Bio Merieux, Lyon, France], atrial natriuretic factor
(ANF, RIA), plasma renin activity, and aldosterone (RIA). Because of
technical problems, hormonal levels were determined only in six women.
Statistical analysis. Results are
expressed as means ± SD of the mean. One-way analysis of variance
(ANOVA) for repeated measures was performed to analyze the parameter
changes throughout the study. The value recorded at the end of the
first trimester after the delivery was considered the baseline control
period value. If ANOVA was significant, a Fisher's least
significant difference post hoc test was performed. A
P value < 0.05 was considered
significant.
| |
RESULTS |
Table 1 shows the values of
body weight, blood pressure, heart rate, and pulse wave velocity. Body
weight was increased significantly at the third trimester of pregnancy,
but postpartum weight remained slightly but significantly higher than
the first trimester body weight. Blood pressures did not change
throughout the study, whereas heart rate increased as early as the
first trimester (P < 0.01). PWV
significantly decreased throughout the pregnancy. This was due to a
significant increase in the pulse wave TT (control period: 7.1 ± 0.6 102 s; 1st trimester:
7.8 ± 0.8 102 s; 3rd
trimester: 8.4 ± 0.8 102 s;
P < 0.01) without any significant
change in distance between each recording site (data not shown). Thus
there was a significant increase in aortic distensibility of up to 10%
at the third trimester compared with the postdelivery value.
Figure 1,
A and
B, shows the venous pressure-volume
recorded curves at the site of the lower and the upper limbs. The
values of the venous parameters are indicated in Table
2 for both the upper and lower
limbs. For the lower limb venous changes (Fig. 1B), there was a significant
(P < 0.001) decrease in curve width (VP20) on the third trimester
corresponding to decrease in the viscoelasticity, and an early increase
in the venous tone (P < 0.01) from
the first trimester. These results indicate a global reduced venous
distensibility of the lower limb, as shown by the significant decrease
(P < 0.01) in
VV30. For the forearm (Fig. 1A), only the width of the curve
hysteresis (VP20)
significantly increased at the third trimester. Note that whereas at
the delivery control period, venous tone and
VP20 differed significantly
(P < 0.01) between the upper and the
lower limbs, no difference was observed at the third trimester (Table
2).
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Fig. 1.
Upper limb (A) and lower limb
(B) pressure (P)-volume (V) curves
recorded at 1st and 3rd trimesters and control period (postpartum) (see
RESULTS). dV, change in venous volume.
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During the pregnancy, blood flows and local resistances did not change
in both the upper and lower limbs (Table 2).
Table 3 shows the echocardiographic
changes. The aorta annulus diameter was increased at the third
trimester (P < 0.05). The LVDD also
slightly increased at the third trimester
(P < 0.05), whereas no significant
change in cardiac thickness was observed.
Table 4 indicates the hormone results.
Plasma catecholamine and ANF levels did not change, whereas the sex
hormone levels (estradiol and progesterone), plasma renin
activity, and aldosterone levels increased markedly during the
pregnancy, particularly at the third trimester. Plasma proteins
decreased during pregnancy. Thus, when the hormonal levels were
analyzed relative to the plasma protein level (data not shown), only
plasma estradiol, progesterone, renin activity, and aldosterone were
shown to be significantly elevated along the pregnancy. There was no
significant correlation relating hormonal plasma levels to the measured
hemodynamic variables. In the overall population, we observed a
significant positive relationship between the changes in the lower limb
venous tone and the change in LVDD between the control period and the
first trimester (r = 0.91, P < 0.001) (Fig.
2). For the two variables, a similar
relationship was observed between the control period and the third
trimester (r = 0.68, P < 0.05) (Fig.
3). LVDD did not correlate with any other
variable related to the viscoelastic properties of the veins either for
the upper or the lower limbs.
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Fig. 2.
Scatterplot of correlation between changes in lower limb venous tone
(VT) and change in left ventricular diastolic diameter (DD) between
control period and 1st trimester (r = 0.91, P < 0.001).
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Fig. 3.
Scatterplot of correlation between changes in lower limb VT and change
in left ventricular DD between control period and 3rd trimester
(r = 0.68, P < 0.05).
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Results in Tables 1-4 did not differ when the patients were
divided into two subgroups: multiparity
(n = 4) and nulliparity (n = 5).
| |
DISCUSSION |
The principal findings of this longitudinal study of normal pregnancy
were that 1) all the distensibility
and viscoelastic components of the lower limb veins significantly
decreased, whereas no comparable finding was observed in the upper
limb, 2) the changes in lower limb
venous tone were strongly correlated with the changes in left
ventricular diastolic diameter, and
3) aortic distensibility and
diameter significantly increased, whereas at the same period of
observation, there was no significant change in the concomitant measurements of systemic blood pressure.
Considerations of methods.
Important discrepancies have been previously reported for the study of
the peripheral venous system during normal pregnancy. Most of the
investigations did not analyze the upper and lower limbs in parallel,
did not involve longitudinal measurements, or did not include a control
period. Furthermore, in most investigations, the venous system of the
upper or the lower limbs was analyzed in terms of global indexes of
venous capacitance. With this procedure, the cuff was usually inflated
at one level of pressure between 30 and 60 mmHg. Subsequently, venous
compliance has been shown to be significantly decreased (17) or
increased in both limbs (4) and either increased (39) or decreased (20)
in the forearm. In the present study, the variability of measurements was considerably improved by the determination of a more complete pressure-volume relationship, thus enabling the
calculation of the slope of the curve with a high degree of
reproducibility.
An important consideration is that, in most studies of the literature,
the time dependency of the venous vessel behavior was not taken into
consideration. Indeed, it is important to distinguish between the tonic
part of the venous wall (the venous tone) and the time-dependent
viscoelastic part of the venous system, which both participate in
determining venous capacitance (Fig. 1). An important feature of the
venous tissue is the marked time dependency in its elastic behavior,
sometimes referred to as elastic hysteresis, delayed compliance, or
stress relaxation, the latter term implying that the pressure falls
after sudden distension at a constant volume (1, 43). As a result,
pressure-volume curves observed on injection or filling and
pressure-volume curves on withdrawal of fluid or emptying form a loop
(Fig. 1). The width of this loop for each level of pressure (Fig. 1)
shows time dependency, i.e., it becomes narrower at very fast and
larger at very slow rates of injection or filling. Stretch relaxation
implies that the later stretch curve differs greatly from the initial
stretch unless sufficient time is allowed between measurements for
complete return to the resting distensibility state. For this reason,
in the present study we attempted to minimize errors due to stress
relaxation and uneven filling by studying volume changes during both a
relatively slow increase and decrease in distension. Thus the creep
could be determined as a variable characterizing the changes in the venous wall itself. Most of the studies of veins in vitro referring to
the viscous component of the passive properties of the venous wall show
that, in addition to functional changes, it involves principally
structural changes of smooth muscle and connective tissues rather than
water and electrolyte changes (1, 43).
Several limitations of this study should be mentioned. First, the
control period was considered to be the third month after delivery. It
might be possible that the physiological changes after the delivery
were not complete at this period as suggested by the higher body weight
in comparison with the first trimester of pregnancy, as already pointed
out for the cardiac parameters at 12 wk postpartum (8). Our period of
examination was chosen to avoid withdrawals, which are particularly
frequent after pregnancy. Furthermore, most cardiovascular parameters
show their greatest changes within 2 wk postpartum (14). Second, the
determinations were performed at the first and the third trimester, but
the determination of a third midpregnancy study point would have been
more advisable because a rise in cardiac output has been noted in the
last or midtrimester and might play a role in the regional observed
changes. This point could account for the observed lack of change in
MBP. Finally, the relatively small number of subjects participating in
the overall investigation might have contributed to reduce the
statistical power, particularly for cardiac mass determination (33).
However, such a difficulty was partly challenged by the use of
longitudinal measurements, a point that is detailed below.
Considerations of findings. The
principal finding in this study was that all the measured indexes of
venous distensibility and viscoelastic properties were decreased in the
lower limbs but not in the upper limbs. At the site of the lower limb,
the width of the pressure-volume loop, expressed as the creep (or VP20), was significantly
decreased at the third trimester. The tonic venous tone increased from
the end of the first trimester. The mechanics of such venous changes
are difficult to elucidate. The venous alterations appear as a
consequence of two different factors:
1) the distending force applied on
the vessel wall (which is here largely dependent on the inward
arteriolar flow), and 2) the local
muscle tone. In the present study, we did not identify a change in limb
blood flow or in systemic blood pressure during the pregnancy. Thus the
venous changes could not be considered a passive consequence of
arteriolar vasodilatation. On the other hand, venous changes differed
markedly at the site of lower and upper limbs, suggesting that changes
in venous pressure could not explain per se the substantial differences
in behavior of the two limbs. Thus the contribution of intrinsic
structural and/or functional alterations of the venous wall
should be considered (43). It is important to mention that the density
of smooth muscle cell (SMC) in the vein wall differs greatly from upper limb to lower limb; it is higher in lower limb and higher in the distal
part of the limb. Thus it is clear that, with a larger amount of SMC,
the same constrictor stimulus will produce a higher degree of
constriction of the vein wall. Furthermore, in the venous system, the
degree of innervation is considerably less than in the resistance
arteries. Moreover, the amount of innervation differs from saphenous
veins to iliac veins and is higher in the former. Thus a smaller amount
of reactive muscle in the forearm will produce smaller variations in
venous viscoelasticity and/or distensibility during pregnancy.
One of the major results of this study was the significant increase in
aortic distensibility observed during normal pregnancy, as evidenced
from the average 10% decrease in PWV that occurred at the third
trimester. Similar findings have been reported in rats (45). The PWV
change could not be related to changes in systemic blood pressure,
which was unmodified during the pregnancy. Because aortic
distensibility is the ratio between aortic compliance and volume, and
because an increase in aortic diameter and volume (Table 3) was also
observed during the pregnancy, the increase in distensibility indicates
intrinsic change in the aortic wall. As for veins, structural
and/or functional factors may be implicated in the observed
aortic changes. Because estrogens were increased during the pregnancy
and because estrogen receptors are present on SMC in arterial wall (5,
22), it might be suggested that this hormone was responsible for the
distensibility changes. In humans, arterial vasodilation may be
obtained from acute administration of estrogen (15). In postmenopausal
women, the loss of estrogens is associated with increased rigidity of
the arterial wall (23). In the present study, we did not observe any
correlation between estrogens and hemodynamic variables. We found a
positive correlation between the increase in the venous tone of the
lower limbs and the changes in the LVDD studied both at the end of the
first and the third trimesters. Because we found a decrease in lower
limb tonic and viscoelastic distensibilities, it is clear that venous return was markedly augmented during pregnancy, a mechanism involving an increase in the filling of the heart and contributing to the increase or maintenance of cardiac output. On the other hand, because a
decrease in aortic PWV and an increase in aortic diameter were
concomitantly observed, aortic compliance was substantially decreased.
Thus both arterial and venous adjustments contributed to optimize
cardiac function during normal pregnancy.
In conclusion, throughout normal pregnancy, the lower limb venous
distensibility and viscoelastic properties were decreased and induced
and/or maintained the increase in cardiac filling and cardiac
output. In contrast, the upper limb venous system showed a late and
small increase in wall time-dependent viscoelasticity. This hemodynamic
pattern was observed without any change in limb local vascular
resistances or change in mean blood pressure. In addition, although
aortic distensibility is often dependent on blood pressure level, we
observed an increase in aortic distensibility unrelated to mechanical
stress and probably due to intrinsic modifications of the arterial
wall. This change contributed to preserve heart vessel adjustment
during normal pregnancy. The mechanisms by which both the reduced
venous distensibility and the increased aortic distensibility may be
observed simultaneously in normal pregnancy remain unexplained and
require further investigations.
| |
ACKNOWLEDGEMENTS |
We are indebted to Prof. Frydman for providing the patients for the
study. We gratefully thank Brigitte Laloux for excellent technical
assistance and Joelle Taïeb and Dr. Eric Puissart for biochemical assistance.
| |
FOOTNOTES |
This study was performed with grants from Institut National de la
Santé et de la Recherche Médicale (France) and Mise Au Point en Anesthésie-Réanimation (France).
Address for reprint requests: M. Safar, Medecine 1, Hôpital
Broussais, 96 rue Didot, 75674 Paris Cedex 14, France.
Received 4 August 1997; accepted in final form 10 December 1997.
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Abstract
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