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(Circulation. 1997;95:2407-2415.)
© 1997 American Heart Association, Inc.
Articles |
Serial Assessment of the Cardiovascular System in Normal Pregnancy
Role of Arterial Compliance and Pulsatile Arterial Load
the Departments of Medicine and Obstetrics and Gynecology and the Committee on Clinical Pharmacology, University of Chicago (Ill) Medical Center.
Correspondence to Sanjeev G. Shroff, PhD, Section of Cardiology, University of Chicago Medical Center, 5841 S Maryland Ave, MC5084, Chicago, IL 60637. E-mail sshroff{at}medicine.bsd.uchicago.edu
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Abstract |
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Background Temporal changes in systemic arterial compliance and wave propagation properties (pulsatile arterial load) and their role in ventricular–systemic arterial coupling during gestation have not been explored. Noninvasive methods combined with recently developed mathematical modeling techniques were used to characterize vascular and left ventricular (LV) mechanical adaptations during normal gestation.
Methods and Results Fourteen healthy women were studied at each trimester of pregnancy and again postpartum. Experimental measurements included instantaneous aortic pressure (subclavian pulse tracings) and flow (aortic Doppler velocities) and echocardiographic imaging of the LV. A small increase in LV muscle mass and end-diastolic chamber dimension occurred by late gestation, with no significant alterations in myocardial contractility. Cardiac output increased and the steady component of arterial load (total vascular resistance) decreased during pregnancy. Several changes in pulsatile arterial load were noted: Global arterial compliance increased (
30%) during the first trimester and remained elevated thereafter. The magnitude of peripheral wave reflections at the aorta was reduced. The mathematical model-based analysis revealed that peripheral wave reflections at the aorta were delayed and that both conduit and peripheral vessels contributed to the increased arterial compliance. Finally, coordinated changes in the pulsatile arterial load and LV properties were responsible for maintaining the efficiency of LV-to–arterial system energy transfer.
Conclusions The rapid time course of compliance changes and the involvement of both conduit and peripheral vessels are consistent with reduced vascular tone as being the main underlying mechanism. The pulsatile arterial load alterations during normal pregnancy are adaptive in that they help to accommodate the increased intravascular volume while maintaining the efficiency of ventricular-arterial coupling and diastolic perfusion pressure.
Key Words: contractility • hemodynamics • arteries • ventricles • pregnancy
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Introduction |
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Extensive human data are available regarding the hemodynamic alterations during pregnancy, eg, increased intravascular volume, cardiac output, and heart rate, with a marked fall in vascular resistance and a tendency toward decreased mean blood pressure.1 2 3 4 5 6 7 8 9 10 11 12 13 14 A comprehensive assessment of changes in the intrinsic vascular and cardiac mechanical properties is the crucial first step for elucidating the mechanisms of these alterations, especially in abnormal gestation. TVR has been the predominant parameter used to characterize the systemic arterial circulation under a variety of physiological and pathophysiological conditions in humans; pregnancy is no exception. However, this parameter describes only one of the components of vascular afterload, ie, the opposition to steady flow. Since ventricular ejection is intermittent, other components of vascular afterload, collectively called pulsatile arterial load, should be considered also. These include ACA (a measure of arterial reservoir-like properties), aortic characteristic impedance (determined by local vessel wall stiffness and geometric properties), and indices of wave propagation and reflection (eg, pulse wave velocity and global reflection coefficient). Although striking reductions in TVR have been described during gestation, little is known about the role of pulsatile arterial load. Thus, the first goal of the present study was to characterize serial changes in pulsatile arterial load during normal pregnancy and to examine their physiological relevance by use of a mathematical model–based analysis.
As stated above, it is important to assess LV properties as well. Although a general consensus exists regarding LV structural alterations during pregnancy (eg, increased end-diastolic volume and LVM), the effects on myocardial contractile state are less clear, mostly because of the use of load-dependent indices of contractility. Since both LV and systemic arterial mechanical properties change in pregnancy, it is relevant to examine whether ventricular-arterial coupling is altered. Quantification of various aspects of LV-to–arterial circulation mechanical energy transfer can be used for this purpose.15 16 No human data are available regarding this issue. Accordingly, the second goal was to characterize serial changes in LV properties and indices of ventricular-arterial coupling during normal pregnancy.
Until recently, these more encompassing cardiovascular characterizations could not be obtained serially throughout pregnancy because they required invasive measurements of aortic pressure and flow. However, we and others have described and validated noninvasive techniques to acquire instantaneous aortic pressure and flow using calibrated SPTs or carotid pulse tracings and aortic Doppler velocities, respectively.17 18 These noninvasive techniques are ideally suited for serial assessment of the vascular and cardiac changes that occur during gestation. Thus, a serial study was designed to characterize both the LV and the systemic arterial circulation during pregnancy. Our initial hypothesis was that ACA increases considerably during pregnancy and that this increase in compliance, together with the concomitant changes in LV properties, is responsible for maintaining the efficiency of ventricular-arterial coupling. Given the generalized state of smooth muscle relaxation during pregnancy, as indicated by decreased vascular resistance and increased vascular volume without a significant change in mean pressure, it is reasonable to expect the increase in arterial compliance.
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Methods |
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Study Population
Sixteen healthy, normotensive women (age range, 18 to 40 years) carrying single fetuses were recruited from the University of Chicago obstetrics clinic during the first trimester of pregnancy. Gestational age was estimated by crown-rump measurements obtained during the first trimester ultrasound examination. Two of the 16 women were excluded before completion of the protocol, 1 because of clinical complications leading to an abortion and another because of premature labor requiring tocolytic therapy (ie, inhibition of uterine contractions) during the third trimester. The remaining 14 subjects had uneventful pregnancies and delivered infants of normal birth weights (Table 1
). One woman developed gestational diabetes requiring insulin in the third trimester; this was after her last study visit, and her data are included. No subjects had any significant structural heart disease. Except for 1 woman receiving appropriate replacement thyroid hormone, none were taking medications other than prenatal vitamins, and all denied the use of alcohol, tobacco, or recreational drugs. There were no trained athletes, although some women exercised recreationally. All volunteers gave informed consent to a protocol approved by the Institutional Review Board of the Pritzker School of Medicine, University of Chicago.
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Data Acquisition Protocol
Data were collected serially at four times: first trimester (12±1 weeks, n=14), second trimester (20±3 weeks, n=14), third trimester (31±2 weeks, n=14), and 8 weeks postpartum (8±2 weeks, n=14). In a subset of these subjects (n=10), additional data were acquired at >6 months postpartum (57±29 weeks). At each visit, subjects were weighed, and the following data were acquired simultaneously: (1) ECG, (2) two-dimensional targeted M-mode echocardiogram of the LV, (3) ascending aortic blood velocity by Doppler, (4) brachial artery blood pressure, and (5) SPTs (Fig 1). All studies were performed in the left lateral decubitus position, and all data were acquired after the patient had been resting for 10 minutes.
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Aortic Pressure-Flow Data
BPS and BPD were measured in the left arm every 2 minutes with an oscillometric sphygmomanometer (Dinamap Vital Signs Monitor, model 1846 SX, Critikon, Inc). It was assumed that aortic and subclavian pressure wave morphologies are similar, an assumption that has been validated.18 In addition, carotid and central aortic pressure waveforms have been shown to be alike in humans over a wide range of pulse pressures and vasoactive states.17 19 Although subclavian and central aortic pressure wave morphologies have not been examined experimentally during pregnancy, existing data cited above suggest that pregnancy should be no exception. SPTs were recorded with a small plastic funnel positioned over the point of maximal impulse in the right supraclavicular fossa and connected by Silastic tubing to a strain-gauge transducer (model 03040170, Cambridge Instrument Co, Inc). The pressure waveform was recorded with a physiological recording system (frequency bandwidth of the pressure transducer-amplifier system, 0.05 to 50 Hz) and calibrated as follows. First, BPD was assigned to the nadir of the pulse tracing, and the mean brachial artery pressure (=2/3 BPD+1/3 BPS) was assigned to the electronic mean of the pulse tracing. Pressure values at other time points during the cardiac cycle were then calculated by linear interpolation or extrapolation. This calibration procedure has been validated in human subjects by use of carotid pulse recordings.17
Instantaneous aortic flow was determined noninvasively from the aortic Doppler velocity recordings combined with the two-dimensional echocardiographic measurement of LVOT diameter (Fig 1
). Ascending aortic blood velocity was obtained from the apical window first with a steerable pulsed-Doppler (2.5-MHz, Hewlett-Packard, Inc) and then with a Pedoff continuous-wave Doppler (1.9-MHz, Hewlett-Packard, Inc) transducer. Both data sets were recorded at paper speeds of 100 mm/s, and tracings from the technique yielding the highest velocities and continuous maximum velocity envelope were used in the subsequent analysis. From the parasternal long-axis view, aortic annular diameter was measured during systole at the base of the leaflets. Diameters were remeasured at each visit. Aortic cross-sectional area was calculated from the measured aortic annular diameter, assuming a circular orifice. Instantaneous aortic flow was calculated as the product of aortic Doppler blood velocity and the aortic annular cross-sectional area. Instantaneous aortic flows determined in this manner correlate well with measurements obtained invasively by electromagnetic flow probes in experimental animals and human subjects.18 20
The following criteria were used to select three representative cardiac cycles for each subject at each visit: RR interval variation 
15%; baseline drift in SPT due to respiration 10%; and well-demarcated envelope of the Doppler signal with peak velocity variations 10%. The subclavian pulse transmission time delay relative to the aortic Doppler velocity recording was corrected by aligning the incisura of the pressure tracing with the closing click of the aortic Doppler signal.
Doppler echocardiographic tracings and SPTs were digitized at 200 Hz with a digitizing tablet (Bit Pad Two, Summagraphics Corp) and custom software. Three cardiac cycles were averaged and the digital data stored on a personal computer for subsequent off-line analysis.
LV Data
M-mode tracings of the LV were obtained at held end expiration from the parasternal short-axis view with the beam directed at the mid–papillary muscle level (2.5-MHz transducer, Sonos 1500 and 2000, Hewlett-Packard, Inc). Two-dimensional imaging facilitated proper alignment of the imaging axis. Tracings were recorded on videotape and a strip-chart recorder at a paper speed of 100 mm/s. LV end-systolic and end-diastolic chamber dimensions and respective posterior wall thicknesses were measured from the M-mode recordings according to the recommendations of the American Society of Echocardiography.21
The following criteria were used to select three representative cardiac cycles for data analysis from each subject at each visit: RR interval variation 15% and well-delineated LV endocardium during both systole and diastole. Echocardiographic tracings and SPTs were digitized, averaged, and stored for subsequent off-line analysis as described above.
Data Analysis
General Hemodynamics
Heart rate was determined from the RR interval on the ECG recording. The MAP was calculated from brachial artery systolic and diastolic pressures as described above. Stroke volume was calculated as the aortic blood velocity–time integral multiplied by the annular cross-sectional area and cardiac output as the product of stroke volume and heart rate.
LV Parameters
LV shortening fraction (SF) was calculated as the difference between end-diastolic (DED) and end-systolic (DES) chamber dimensions divided by DED. LV ejection time (LVET) was measured from the SPT as the time from the initial upstroke to the dicrotic notch. Rate-corrected mean velocity of VcfC was calculated as follows22 : VcfC=SF/[LVET/(TRR½)], where TRR is RR interval on the ECG recording.
Assuming negligible LV-aortic pressure gradient, LV end-systolic pressure (PES) was estimated from the dicrotic notch of the calibrated SPT. LV end-systolic meridional wall stress (
ES) was calculated from PES, DES, and end-systolic LV wall thickness (hES) by the following formula23 : ES=1.35PESDES/{4hES[1+(hES/DES)]}. LV myocardial contractility was assessed in terms of VcfC relative to ES.22 LVM was calculated from the M-mode measurements using the regression-corrected American Society of Echocardiography cube formula.24 In these structurally normal hearts, interventricular septal wall and posterior wall thicknesses were assumed to be equal: LVM=0.8{1.04[(DED+2hED)3-(DED)3]}+0.6.
Systemic Arterial Parameters
TVR was calculated from MAP and cardiac output. ACA was estimated from the diastolic decay of the aortic pressure waveform by the area method described by Liu et al25 : ACA=AD/TVR(P1-PD), where P1 and PD are peak aortic pressure after the dicrotic notch and minimum diastolic pressure, respectively, and AD is the area under the pressure curve bounded by P1 and PD. Aortic input impedance spectrum was derived by calculating the Fourier transforms of aortic pressure and flow signals and then dividing the pressure coefficient by the flow coefficient at each harmonic.15 Since we used subclavian pressure as a surrogate for ascending aortic pressure, our calculations should be considered an estimate of the true aortic input impedance. Aortic characteristic impedance was calculated as the average of input impedance magnitudes over the frequency range of 4 to 12 Hz.15 Those frequencies with flow magnitude <5% of the first harmonic were excluded from the averaging process; this eliminates impedance values that are prone to estimation errors due to insufficient energy in the flow harmonic.
Arterial wave reflections were characterized by two parameters: reflection index (RI), calculated as the ratio of the backward and forward pressure wave peak-to-peak amplitudes,26 and the amplitude of the first harmonic of global reflection coefficient (
1), derived from the estimated aortic input impedance spectrum and aortic characteristic impedance.15 Instantaneous aortic pressure [P(t)] and flow [Q(t)] data were used to calculate total (
TOT), steady (STD), and oscillatory (OSC) powers15 16:
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| (1) |
where T is cardiac cycle duration; STD=MAPxCO, where CO is cardiac output; and OSC=&TOT-STD. Because OSC is the power wasted in pulsations, the ratio (%OSC) of OSC and TOT was used as a measure of the inefficiency of LV-arterial coupling.
Statistical Analysis
For each parameter, a one-way repeated-measures ANOVA was used to compare data gathered at various times. When data did not satisfy the normality constraint, a nonparametric test (Friedman repeated-measures ANOVA on ranks) was used. If the differences among the groups were found to be statistically significant (P<.05), a pairwise comparison was performed by the Student-Newman-Keuls method. The 8-week postpartum measurement was designated as the control. Unless stated otherwise, all statistical comparisons for changes during pregnancy are made with respect to this control state. Data are presented as mean±SD.
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Results |
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General hemodynamic data measured at each of the three trimesters and at postpartum are presented in Table 2
. Compared with the postpartum control, heart rate was higher only in the second and third trimesters. Both cardiac output and stroke volume were significantly higher at each of the three gestational times. However, only cardiac output continued to increase from the first to the second trimester; thereafter, it did not change significantly. MAP, BPS, and peak-systolic and minimum diastolic aortic pressures were unchanged throughout gestation. End-systolic aortic pressure decreased slightly (6 mm Hg) but significantly in the second trimester and did not change thereafter.
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LV structural and functional data are shown in Table 3. There was a small but significant increase in LVOT diameter during late gestation. LV end-diastolic chamber diameter and LVM tended to increase during mid to late gestation, but these changes were significant only with respect to the late postpartum (>6 months) measurement. There were no significant changes in LV posterior wall thickness (both end-diastolic and end-systolic) and end-systolic chamber diameter during pregnancy.
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Measures of LV systolic performance (shortening fraction and VcfC) were not significantly altered during gestation (Table 3). These data, together with invariant end-systolic wall stress (Table 3), indicate that myocardial contractile state did not change significantly during gestation.
Systemic arterial parameters during and after pregnancy are presented in Table 4. Compared with the postpartum control, TVR decreased significantly at each of the three gestational time points, with the response leveling off beyond the second trimester (Fig 2). ACA significantly increased in the first trimester; thereafter, it remained high throughout gestation (Fig 2). Aortic characteristic impedance tended to decrease during gestation, but the changes did not achieve statistical significance. The magnitude of the first (fundamental) impedance harmonic (Z1) decreased during gestation, and the corresponding phase (
1) was less negative. These observations are consistent with increased arterial compliance and with pressure and flow becoming more in phase. Both reflection index and reflection coefficient tended to decrease during gestation, with the decrement in reflection coefficient reaching statistical significance in the third trimester.
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P<.05, second or third vs first trimester).
Total hydraulic power increased significantly throughout pregnancy, attaining a peak value during the third trimester (Table 4). Increments in both steady and oscillatory components contributed to this increase in total power (Fig 3). Consequently, the ratio of oscillatory to total power, a measure of energy wasted in pulsations, was not significantly affected by pregnancy (Table 4).
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;STD) and oscillatory (&
Although peak-systolic and diastolic aortic pressures did not change significantly with pregnancy (Table 2), several characteristic differences in pressure and flow wave morphologies occurred (Fig 4): (1) Despite a significant decrease in cycle duration (930±120 ms at postpartum control versus 760±90 ms at third trimester, P<.05), time to peak flow (103±12 versus 93±18 ms) and ejection time (330±20 versus 308±26 ms) did not decrease significantly. (2) Instantaneous values of aortic flow, including peak flow, were higher with pregnancy. (3) Despite similar time to peak flow, time to peak pressure was shorter during pregnancy (214±56 ms at postpartum control versus 142±46 ms at third trimester, P<.05). (4) Dicrotic notch (or end-systolic) pressure was significantly lower during pregnancy (PES in Table 2). In brief, pressure and flow wave morphologies were more in phase during late pregnancy than those observed during the postpartum control.
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A model-based analysis of aortic pressure and flow waveforms was performed to gain additional insights into changes in arterial compliance and wave propagation properties. A lumped representation of the arterial system (eg, three-element Windkessel) was inadequate to reproduce experimental observations, especially the changes in the morphological features (Fig 4). Therefore, an asymmetrical T-tube model was used to represent the arterial circulation.27 28 Details regarding this model and the parameter estimation technique have been described elsewhere.28 Briefly, the model consisted of two parallel circulations, bodyward (subscript b) and headward (subscript h), each having a lossless tube terminated with a complex load. By use of a prespecified cardiac output distribution between the two circulations, TVRb and TVRh were calculated directly from measured mean aortic pressure and flow. It was assumed that the bodyward circulation received 70% of total cardiac output under control conditions, and this increased to 74% during pregnancy.29 30 With the measured aortic flow as the input, six parameters (three for each circulation) were estimated by fitting to measured aortic pressure: one-way tube transmission times, 
b and h; tube compliances, Ctb and Cth; and load compliances, Clb and Clh. Pressure wave morphologies were accurately reproduced by the T-tube model for both control and pregnancy states (Fig 5). The estimated model parameters are listed in the legend of Fig 5. As indicated by tube transmission times, especially b, wave reflections were delayed during pregnancy. Both tube and load compliances increased with pregnancy, a result that is consistent with the generalized state of vascular relaxation.
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Discussion |
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An understanding of cardiovascular alterations during normal pregnancy is crucial to interpret the adaptive mechanisms that bring about these changes and to establish a reference for comparison when pregnancy is complicated by pathological conditions. The basic hemodynamic parameters, heart rate, blood pressure, vascular resistance, and cardiac output, have been studied extensively by both invasive and noninvasive methods.1 2 3 4 5 6 7 8 9 10 11 12 13 14 Our data confirm some of the previous observations and extend them by characterizing the serial changes in the pulsatile arterial load and their physiological role in ventricular-vascular coupling during normal pregnancy.
Methodological Considerations
Preconception data would be the most ideal control measurement for assessing changes during pregnancy. In the absence of such data, a long-term postpartum point (eg, 6 months postpartum) should be used as the control state.31 32 However, because our >6 months postpartum data were limited and the time of measurement was variable (24 to 100 weeks), we elected to use the 8-week postpartum condition as control. This appears reasonable because most hemodynamic parameters return to preconception values within 8 to 12 weeks, as evidenced by our data (Tables 2 through 4, 8-week postpartum versus >6 months) and those of others.8
We found a small (5%) but systematic increase in LVOT area during pregnancy, an observation reported by others as well.8 10 Therefore, it is better to remeasure the LVOT diameter at each visit during pregnancy when calculating stroke volume from Doppler-based velocity measurements. The use of ejection phase indices of performance to describe LV contractile state may be problematic because factors other than contractility (eg, heart rate, preload, afterload) are known to affect these indices. Therefore, in the present and a previous study,33 we used a load- and heart rate–independent measure (VcfC relative to ES) to assess LV contractility during gestation. Finally, since compression of the inferior vena cava by the enlarged gravid uterus may cause significant hemodynamic alterations,6 all cardiovascular measurements should be made with the subjects in the left lateral position.
LV in Normal Pregnancy
We found small increases in LV end-diastolic chamber diameter (5%) and LVM (10%) during late gestation, but these were significant only compared with late (>6 months) postpartum values, possibly reflecting the increased time required for ventricular remodeling. Most previous studies have reported similar LV structural alterations in normal pregnancy.6 13 34 In contrast, Robson et al8 10 have reported greater (40%) increases in LVM, mostly due to a significant (20%) LV wall thickening. However, we (Table 3) and others did not find such changes.11 12 34
We did not detect changes in LV systolic performance (eg, shortening fraction or VcfC), an observation similar to that of Katz et al.6 Although Robson et al8 10 and Rubler et al5 reported an increase in Vcf, had they corrected their data for heart rate, it probably would not have increased. Mone et al34 observed an increase in VcfC; however, this was associated with a reduction in LV afterload (ES).
Our data of invariant VcfC and ES indicate no significant alterations in LV myocardial contractility at any time during pregnancy, confirming observations made at term in a previous study.33 On the basis of the Vcf–mean wall stress relationship, Buttrick et al35 observed increased LV contractility during late pregnancy in rats; however, this appears to be related to changes in myosin isozymes, an observation that may be limited to smaller mammals. Most previous inferences regarding LV contractility in pregnant women are problematic because they are based on shortening fraction or Vcf alone. On the basis of the shortening fraction–ES relationships, Mone et al34 recently concluded that LV myocardial contractility progressively falls throughout gestation. However, this relationship is sensitive to preload and heart rate. In fact, their own VcfC–ES data indicated that LV contractility remains within the normal range throughout pregnancy. We conclude that if pregnancy affects LV myocardial contractility, this effect is modest at best.
Systemic Arterial Circulation in Normal Pregnancy
In agreement with previous studies,8 9 10 34 the steady component of arterial load (ie, TVR) decreased with pregnancy, with the decrement leveling off beyond the second trimester (Fig 2). Regarding the pulsatile arterial load, ACA significantly increased with pregnancy, with most of the increase occurring early during gestation (Fig 2). Both increased vascular distensibility and the presence of the uteroplacental circulation could contribute to observed increase in ACA. The second mechanism is unlikely to be the major factor, for two reasons. First, the compliance changes occur very rapidly (by the first trimester). Second, studies with animal models (guinea pigs) have shown that most of the pregnancy-associated hemodynamic changes can be reproduced simply by sex steroid administration36 and that the uteroplacental circulation contributes only 20% to the overall drop in TVR.30 Hemodynamic changes similar to those occurring with pregnancy have been reported in male transsexuals subjected to exogenous estrogen administration.37 Increased vascular distensibility has been observed by both direct (eg, rightward shift of vascular pressure-volume relationships)36 38 39 and indirect (eg, decreased pulse wave velocity in large arteries)40 41 measures. As a result of increased heart rate, peripheral vasodilation, and the tendency for aortic characteristic impedance to fall, the magnitude of arterial wave reflections was reduced during late pregnancy. On the basis of decreased pulse wave velocity40 41 and the results of the model-based analysis presented above, we conclude that the timing of reflected waves is also affected during pregnancy, such that their arrival at the heart is delayed.
Potential mechanisms for increased arterial distensibility can be divided into three categories: (1) passive changes in vessel wall properties secondary to reduced distending pressure, (2) vascular wall remodeling, and (3) reduced smooth muscle tone. Since systolic and diastolic aortic pressures did not change significantly (Table 2), the first possibility can be ruled out. The rapid time course of change in ACA (Fig 2) suggests that vessel wall remodeling probably plays a minor role, although direct measurements are necessary to address this issue. Thus, reduced smooth muscle tone appears to be the likely mechanism responsible for increased vascular distensibility, although the contribution of vessel wall remodeling cannot be completely ruled out. Estrogen levels are elevated during pregnancy, and estrogen receptors have been found in both the vascular smooth muscle and endothelium. Estrogen administration causes vasodilation by potentiating endothelium-dependent (related to acetylcholine) and endothelium-independent (nipride-responsive) pathways, both in humans42 43 and experimental animals.44 In addition to direct hormonal effects, increased aortic blood velocities noted early in pregnancy could enhance the shear stress–induced release of endothelial relaxing factors (eg, nitric oxide and prostaglandin I2).
Performance of the Coupled LV-Arterial System in Normal Pregnancy
The basic hemodynamic parameters of heart rate, stroke volume, and cardiac output increased throughout gestation and peaked in the third trimester, and MAP did not change. These findings are similar to previously reported data.
The steady component of hydraulic power increased during pregnancy, a result of increased cardiac output with little change in MAP. The oscillatory component of hydraulic power also increased. However, the ratio of oscillatory to total power did not change significantly during pregnancy, indicating no adverse effects on the efficiency of LV-to–arterial system mechanical energy transfer. Since a reduction in TVR by itself is known to increase this ratio, concomitant changes in other arterial and LV mechanical properties must be responsible for this observation.16 45
The model-based analysis revealed that wave reflections at the aorta are delayed and arterial compliance increases for both conduit (ie, tube compliance) and peripheral (ie, load compliance) vessels. This observation is consistent with the above-stated conclusion that a generalized reduction in vascular tone is the factor most responsible for pulsatile arterial load changes during pregnancy. The model-based analysis also indicated that TVR alone is inadequate to reproduce the experimental observations; concomitant alterations in pulsatile arterial load (ie, wave propagation properties, including arterial compliances) are necessary. A decrement in TVR alone would cause, besides marked hypotension, a significant increase in the ratio of oscillatory to total power (by 50%). Thus, during normal pregnancy, various LV and arterial mechanical properties change in a coordinated manner such that the efficiency of the coupled system is preserved.
Physiological Perspective
The increase in ACA during pregnancy is relevant from several physiological perspectives. First, this appears to be one of the body's adaptive mechanisms to accommodate greater intravascular volume without increasing MAP. Other investigators, using animal models, have described similar changes in total vascular compliance during gestation.38 39 Second, increased arterial compliance, along with other factors discussed above, counterbalances the effects of reduced TVR and helps maintain the efficiency of LV-to–arterial system mechanical energy transfer. Third, increased compliance also offsets the effect of reduced TVR on aortic diastolic pressure decay, thus preserving perfusion pressure to the coronary arteries and other vital organs. It should be noted, however, that reduced TVR is an important adaptive response that maintains MAP within the normal range at the time of greatly increased cardiac output. Concomitant changes in arterial pulsatile load during normal pregnancy, including arterial compliance, are such that the potentially deleterious effects of TVR reduction alone are mitigated. Future studies will be designed to evaluate abnormal gestations, such as those complicated by chronic hypertension or preeclampsia in relation to these normative data.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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We are grateful to Hetal Amin for help with data processing and statistical analyses.
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Footnotes |
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Preliminary results of this study were presented at the 67th Scientific Sessions of the American Heart Association, Dallas, Tex, November 14-17, 1994, and published in abstract form (Circulation. 1994;90[pt 2]:I-555).
Received September 16, 1996; revision received December 2, 1996; accepted December 14, 1996.
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