(Circulation. 1995;92:1026-1033.)
© 1995 American Heart Association, Inc.
Articles |
Automated Echocardiographic Measures of Right Ventricular Area as an Index of Volume and End-Systolic Pressure-Area Relations to Assess Right Ventricular Function
From the Divisions of Cardiothoracic Surgery and Cardiology, University of Pittsburgh (Pa) Medical Center, and the VA Medical Center, Pittsburgh.
Correspondence to John Gorcsan III, MD, Division of Cardiology, University of Pittsburgh Medical Center, 200 Lothrop St, Pittsburgh, PA 15213-2582.
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Abstract |
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Background On-line determination of right ventricular (RV) volume to assess its function is clinically difficult. Echocardiographic automated border detection measures of left ventricular (LV) cavity area have been shown to reflect changes in volume, and pressure-area relations have been used to estimate LV contractility. The potential for RV cavity area to estimate changes in volume and to assess RV function, however, has not been evaluated. Accordingly, the objective of this study was to determine the relation between echocardiographic automated border-detected RV cross-sectional area and true volume and to assess the potential for end-systolic pressure-area relations to estimate RV function in an isovolumically contracting isolated canine heart preparation.
Methods and Results Eight excised dog hearts with both right and left intraventricular balloons were perfused in an ex vivo apparatus in which both ventricular volumes were controlled independently. RV area data from the level of the left midventricular short-axis plane and pressure data were recorded on a computer through a customized hardware and software interface with the ultrasound system. RV volumes were varied from 9.4±3.9 to 43.8±6.9 mL at each of three different LV volume ranges (low range, 12.5±3.8 mL; medium range, 23.9±5.6 mL; and high range, 37.5±5.4 mL). The variation of RV area during isovolumic contraction, which we called deformational area change, was considerable (1.49±0.68 cm2 mean±SD) but did not change significantly with changing RV and LV volumes. Linear regression analysis correlated the maximum, minimum, and mean automated border-detected RV area during isovolumic contraction with absolute volume. A predominantly linear relation was observed, with the group mean r=.98 (y=0.16x+0.97; SEE=0.21 cm2). The effect of LV volume on RV area-volume relation was a significant parallel downward shift (P<.05) by increases in LV volume. End-systolic pressure-area and pressure-volume relations using simultaneously RV pressure were both highly linear and covaried with changing LV volume.
Conclusions Echocardiographic automated border-detected RV area reflects changes in RV volume under a constant LV volume, and the derived end-systolic pressure-area relation has potential for on-line assessment of RV function.
Key Words: echocardiography • ventricular performance • ventricular interaction • ultrasound
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Although the right ventricle was previously considered a passive volume conduit or a low-pressure booster pump,1 recent studies have shown the importance of right ventricular (RV) function for global cardiac performance and maintenance of stable hemodynamics.2 3 4 An established method of determining ventricular function requires assessment of the end-systolic pressure-volume relation (ESPVR). RV chamber volume, however, is technically difficult to determine because of its complex anatomic geometry. Echocardiographic automated border detection is a new technique capable of continuously measuring ventricular cavity area by differentiating the acoustic backscatter characteristics of blood from myocardial tissue.5 6 Pressure-area relations obtained with automated border detection were previously reported to assess left ventricular (LV) contractility in both animal and human studies, with LV cavity area as a surrogate for volume.7 8 9 Because no clinically applicable on-line method exists to assess changes in RV volume, it is attractive to attempt to apply similar pressure-area analyses to assess RV function. Accordingly, the objectives of this study were to evaluate the potential utility of the RV end-systolic pressure-area relation (ESPAR) as a means to assess RV function by determining the RV area-volume relation over a wide range of physiological values, the effects of LV volume on this RV area-volume relation, and the potential effects of isovolumic conformational changes on RV area10 11 in an isolated perfused canine heart preparation, with biventricular volumes controlled independently by intraventricular balloons.
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Methods |
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Preparation
Eight adult mongrel dogs weighing from 16.4 to 26.8 kg (22.7±3.8 kg) were included in the study. The study was approved by the Institutional Animal Care and Use Committee and conformed to the Position of the American Association on Research Animal Use. The dogs were anesthetized with halothane (1% to 2%) delivered in 50% oxygen/50% nitrous oxide after induction with thiamylal sodium (25 mg/kg IV). The hearts were excised after being arrested by cold crystalloid cardioplegic solution and placed in an isolated perfused heart preparation as previously described.7 Briefly, both atria were opened wide, the mitral and tricuspid valves and chordae tendineae were excised, and thin latex balloons attached to rigid plastic cannulas were inserted into both ventricles. The sewing rings linked to the cannula were sutured to the mitral and tricuspid valve annuli. The main pulmonary artery was ligated to prevent prolapse of the RV balloon during inflation. Prolapse of the LV balloon into the aorta was prevented by a flange on the mitral sewing ring that extended under the aortic valve. Two micromanometer catheters (MPC-500, Millar) were positioned into each ventricular balloon through the cannulas. The balloons were filled with saline, with volume controlled by 50-mL calibrated syringes. Small catheters inserted through stabs in the apexes were set to decompress the interspace between the balloons and the endocardium and to drain any thebesian flow. The hearts were perfused with autologous blood pumped by a centrifugal pump (Biomedicus) and oxygenated by a membrane oxygenator (ECMO 0600, AVECOR Cardiovascular Inc). The temperature was held constant at 37°C with a heat exchanger. Coronary perfusion pressure was monitored in the aortic root and maintained at 80 to 100 mm Hg. The hearts were paced at a rate of 120 beats per minute with pacing electrodes on the remnant of right atrial wall.
Echocardiography
Epicardial two-dimensional (2D)
echocardiographic images were recorded with a
Hewlett-Packard Sonos 1500 ultrasound system with automated
border-detection capabilities (model 77035A). A 2.5-MHz transducer was
used to maximize the difference in backscatter characteristics of blood
and tissue and was held in contact with the lateral LV epicardium
opposite the right ventricle by a mechanical support
apparatus. This location eliminated near-field transducer
artifacts within the right ventricle and possible mechanical RV
compression. Images were recorded from a midventricular
short-axis plane, with the LV midpapillary level as an anatomic
landmark and the transducer oriented to obtain the most circular LV
geometry with uniform wall thickness as previously
described.7 8 The backscatter data along each scan
line
were used to discriminate the blood-tissue interface of the
endocardium.5 6 The threshold for determination of
this
border was manually set by adjustment of the overall transmit, time
gain compensation, and lateral gain controls to optimize tracking of
the endocardium as previously
described7 8 9 12 Briefly,
these gain settings were adjusted as a compromise between cavity
clutter from excessive gain and wall dropout from insufficient gain
through visual inspection of the blood-tissue interface displayed as a
colored line superimposed on the 2D image. A region of interest was
then drawn manually immediately beyond the RV endocardial border to
exclude the LV cavity and low-density ultrasound signals that may
appear within the lateral myocardium. Once established, the
same region of interest was maintained throughout each experiment. The
interobserver and intraobserver variabilities for these
echocardiographic automated border detection measures
were reported previously by our group and others to be low (<5%) and
similar to those for manual echocardiographic
methods.12 13 The on-line cavity area signal was
continuously digitized at a sampling rate of 150 Hz for display and
storage on a computer workstation (model DN3550, Apollo Computer Inc)
directly interfaced with the ultrasound system.
Protocol
RV volume within the intraventricular
balloon was manually varied by saline injection or withdrawal through
the attached calibrated syringe at 1-mL increments every 3 seconds for
the first two dogs and at 5-mL increments every 10 seconds for the last
six dogs. This was done within physiological ranges
from a small volume (5 to 20 mL; 9.4±3.9 mL, mean±SD) to a large
volume (30 to 50 mL; 43.8±6.9 mL) according to the heart size and then
back to the small volume. Increases in LV or RV volume above 50 mL in
our preparation resulted in LV or RV end-diastolic
pressures exceeding 25 mm Hg and ensuing ventricular
arrhythmias. Larger fixed LV or RV volume ranges that may be
encountered with disease states could not be studied, and these data
reflect volumes within the low to normal
physiological ranges. The small volume for each dog
was determined by the minimal volume above which the artifact on the
echo image from RV collapse was eliminated. The protocol of the RV
volume alterations was repeated at four or five different LV volumes.
Simultaneous measurements of RV pressure and LV pressure
were digitized and recorded with automated border-detected RV area
on the computer workstation in a similar manner during RV volume
infusion and withdrawal.
Data Analysis
RV pressure, area, and LV pressure data were
transferred to a
customized program written in ASYST (ASYST Software
Technologies, Inc) that separated data into cardiac cycles by using a
threshold of the LV pressure for each 10-second run of RV volume. The
maximum, minimum, and mean values for the RV area and RV and LV
pressures were automatically calculated from each cardiac cycle. In
this isovolumically contracting preparation, RV deformational changes
were assessed as the difference between the maximum and minimum RV
cross-sectional area within the cardiac cycle. These values were then
averaged for 10 to 20 beats. Data with ventricular
arrhythmias were discarded from subsequent analyses. To
determine the relation between changes in RV area and in true volume,
first-order linear regression analysis was used to correlate
each of the maximum, minimum, and mean RV automated border-detected
areas with RV volume for each LV volume. Thirty area-volume coordinates
were used for linear regression analysis of these relations
from each run in the first two dogs with variation in RV volume of 1-mL
increments; 10 area-volume coordinates were used for each run in six
dogs with RV volume variation of 5-mL increments. Variability of
maximum, minimum, and mean RV area-volume relations in each dog was
determined by calculation of the maximal percent differences in slope
values between two or three runs of varying RV volume at constant LV
volume. LV volumes were then grouped into three ranges for each
ventricle based on the size of the heart: low (10 to 20 mL; 12.5±3.8
mL), medium (15 to 30 mL; 23.9±5.6 mL), and high (25 to 40 mL;
37.5±5.4 mL) range of LV volume.
To further evaluate the potential utility of RV area as an index of RV volume in assessing RV function, we compared simultaneous pressure-area relations with pressure-volume relations during alterations in LV volume. Using RV pressure and area signals, we obtained ESPAR, which was a modification of the method of Suga and Sagawa.14 RV ESPAR was estimated by linear regression analysis of the averaged minimum RV area and the maximum RV pressure from the entire range of RV volumes with our automated ASYST program. The RV ESPVR was also calculated with the same methods. These equations were then calculated for each LV volume level. LV function for each heart was also assessed by LV ESPVR calculated from the peak LV pressure and the LV intraventricular volume at each LV volume level.
Statistical Methods
Measured values were expressed by mean
and standard deviation.
Slopes and intercepts between maximum area-volume and minimum
area-volume relations were compared with the paired t test.
RV ESPVRs and ESPARs were fitted by multiple linear regression
analysis (least squares). Effects of LV volume on the mean
area-volume relations, deformational area changes, ESPVRs, and ESPVRs
were compared by ANOVA for repeated measures, with P<.05
considered to be statistically significant.15
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Results |
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Fig 1
shows representative tracings
of RV area, RV pressure, and LV pressure. Under each constant LV volume
level, a series of RV volume loading runs was repeated. Increasing RV
volume led to increases in RV area, RV pressure, and LV pressure. At
higher LV volumes, however, changes in RV area and LV pressure were
slightly attenuated.
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RV Area-Volume Relations
Highly significant and reproducibly
linear relations between
maximum, minimum, and mean RV cross-sectional area and RV volume were
observed over the range of RV volumes studied. Table 1
gives the results from individual preparations. Because of the
deformational area changes under the constant RV volume, the
area-volume relation varied throughout the cardiac cycle (Fig
2). However, the relation of each of the maximum,
minimum, and mean RV area during cardiac cycle to true RV volume was
highly linear in each dog. The slopes of the maximum and minimum
area-volume relations were not different, but the intercepts were
significantly different (P<.01), and the deformational area
changes did not change significantly with increasing both RV and LV
volumes (Table 2), indicating the parallel shift during
the cardiac cycle (Fig 3).
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Effects of LV Volume on the RV Area-Volume Relations
The
linearity of the RV area-volume relation was unaffected by
alterations in LV volumes over the physiological
range of volumes studied. Table 3 gives the effects of
LV volume on individual mean RV area-volume relations. Although the
slopes of the area-volume relation varied among the dogs, they were
relatively constant over the changing LV volume levels in each dog (Fig
4). The slope values from repeated RV area-volume
relations from all dogs demonstrated a maximal variability of
10.1±3.6% with constant LV volumes. Increases in LV volume appeared
to result in parallel downward shifts with decreasing intercept values
(P<.05).
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Effects of LV Volume on ESPVR and ESPAR
The group mean values
for RV and LV ESPVR were 1.04±0.40 and
2.28±0.58 mm Hg/mL, respectively. Both RV ESPVRs and RV ESPARs were
highly linear at each LV volume level studied (Tables 4 and
5). The slopes of both RV ESPVR and ESPAR increased
slightly but significantly with increasing LV volume (Fig 5),
which is consistent with previously
described increases in RV ESPVR with increases in LV volume. The area
and volume axis intercepts of both the relations did not change
significantly with increasing LV volume. Simultaneous
changes in RV ESPVR and ESPAR that occurred with alterations in LV
volume were of a similar magnitude. This was demonstrated by a
significant correlation of the percentile change of ESPVR with the
percentile change in ESPAR during LV volume change (Fig 6).
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Discussion |
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This study demonstrates that on-line measures of RV cross-sectional area by echocardiographic automated border detection are related to changes in RV volume in a highly linear fashion within the range of physiological volumes studied. Furthermore, the linearity of the RV area-volume relation was unaffected by alterations in LV volume. Cardiac cycle–related deformational changes in RV area did occur in this isovolumically contracting preparation. These changes, however, remained similar throughout the range of RV volumes studied and were unaffected by alterations in LV volume. The RV ESPAR was linear like the RV ESPVR and varied in a similar fashion with changes in LV volume, although the absolute values of the area-volume relation differed between ventricles. These findings suggest that RV cross-sectional area may be used as an index of RV volume and that ESPAR may be used to assess RV function, particularly for serial assessment of individual ventricles.
RV mechanical function was described previously in a similar fashion as the left ventricle with load-insensitive parameters such as the ESPVR14 16 17 and preload recruitable stroke work relations.18 These assessments require measuring beat-to-beat changes in ventricular volume in situ. However, complex RV geometry has made determination of RV volume and thus assessment of RV mechanical function difficult. Previous estimates of RV volume included angiographic, echocardiographic, radionuclide, and multiple markers techniques.19 20 21 22 23 24 The shell subtraction model by Feneley et al,23 the multiple marker method by Schweip et al,22 and the three-dimensional (3D) echocardiographic method by Jiang et al24 provide precise estimates of RV volume. These methods, however, either are invasive or require substantial off-line digitization. Although the conductance catheter has been extensively used to acquire on-line LV volume data, potential problems exist with estimation of RV volume, such as parallel conductance from the left ventricle, and its use with the right ventricle has not been fully validated.25 26 Other studies used a one-dimensional (1D) length of the RV chamber for the pressure-length relation.27 28 RV free wall dimension showed a consistent temporal and quantitative relation with changes in RV chamber pressure and volume during the cardiac cycle. Slinker et al29 showed the RV septal–free wall dimension to represent more consistent changes in RV volume with positive-pressure ventilation than the base-apex or anterior-posterior dimension.30 However, Feneley et al23 cautioned about the possibility of an independent relation between RV free wall dimensions or septal–free wall dimension and LV volume and showed the significant effect of the changes in LV volume on the RV geometry because of ventricular interaction. They suggested that the use of free wall dimensions and septal–free wall dimension as indexes of RV volume might not be entirely valid because LV volume varies significantly during the cardiac cycle. Furthermore, 1D analysis to reflect RV volume is limited because an increase in LV volume at a constant RV volume reduces the RV septal–free wall dimension, while the RV free wall dimension is increased as the RV becomes more crescent-shaped.23 31 The present study measures cross-sectional area from a tomographic plane that includes both septal and free wall portions of the body of the right ventricle, thus representing a compromise between these two 1D regions. Consequently, the effect of change in LV volume appears to be partly offset by measuring RV area as an index of volume. In terms of the RV ESPVR, increasing LV volume shifts the relation upward and leftward.31 Although we failed to observe the reported consistent change in volume axis intercepts of the RV ESPVR, we obtained the result that increasing LV volume increased the slope of the RV ESPVR. Increasing LV volume also increased the slope of the RV ESPAR, which suggests covarying characteristics of the RV ESPVR with the RV ESPAR with regard to changing LV volume. These findings support the possible utility of the RV ESPAR as an index of RV systolic function. A potential advantage of this on-line echocardiographic technique is that area as an index of RV volume may be obtained noninvasively. Although an invasive pressure-sensing catheter and load alteration are still required to construct ESPAR, this method may potentially eliminate one step of invasive instrumentation, such as placement of myocardial crystals or a conductance catheter.
RV Deformational Changes
The RV deformational changes
apparent in all the hearts studied
during isovolumic contraction are of potential importance.
Deformational area changes during contraction were also observed with
the LV in previous studies7 32 but to a lesser extent
than
that of the RV in the present study. The deformational
characteristics of the RV have not been previously analyzed as
in the LV. Unlike the LV, RV electric activation and mechanical
contraction progress in a sequential, peristaltic manner from apex to
outflow tract.33 34 This asynchronous contraction
mode of
RV may partly be responsible for relatively large deformational changes
during isovolumic contraction. However, this deformational area change
did not preclude the linear correlation of each of the maximum,
minimum, and mean values of the RV area and the true RV volume.
Although this deformational change tended to decrease with increasing
both RV and LV volumes (Figs 1
and 2), these
changes did not reach
statistical significance within the physiological
ranges of RV volume (Table 2). As a result, statistical
analysis showed no consistent difference between the
slopes of the maximum and minimum area-volume relations. The slopes of
RV area-volume relations at each LV volume level were relatively
constant, and y intercepts decreased with increasing LV
volume. Accordingly, automated border detection measurements of the RV
area can be used to assess the change in the RV volume with regard to
end-systolic and end-diastolic points under the relatively
constant LV volume.
Limitations
A fundamental limitation of this technique, as in
all other
tomographic techniques, is the use of cross-sectional area to reflect
the 3D volume of the anatomically complex RV. This method, however,
does not attempt to determine the absolute value of RV volume but
rather demonstrates the linearity of the relation of changes in area
with changes in volume. By providing more on-line data than 1D
techniques previously used, our method theoretically should be
superior, although a direct comparison between 1D and 2D techniques
does not exist. Because the assessment of RV function by use of
end-systolic relations reflects relative changes in volume over a range
of values, pressure-area relations appear potentially useful for
predicting RV function. The present study used only normal hearts
with normal geometry and physiological ranges of
volumes for canine ventricles and was used to serially detect only
relative changes in RV function. Alterations in RV shape or geometry by
diseases resulting in RV volume and/or pressure overload, including
congenital diseases, may significantly affect the RV area-volume
relation throughout the cardiac cycle. Coronary artery disease
resulting in regional RV dysfunction or fibrosis may also affect this
relation. Accordingly, the findings of the present study may apply
only to hearts without major regional geometric or global geometric
shape alterations as encountered in disease states. In addition, the
utility of RV pressure-area relations as a measure of global RV
function would be strengthened by applying these methods to a wider
range of RV functional variations. Despite these limitations, RV
pressure-area relations have potential clinical utility in assessments
of RV function in patients with heart disease, and preliminary data
suggest that RV ESPAR respond in a predictable manner to
pharmacological inotropic
modulation.35 36 37
Another limitation of this study is that we examined the effect of altering LV volume on the RV area-volume relation of the heart in an ex vivo apparatus without the pericardium. The diastolic pressure-volume relation of either ventricle, but in particular the right ventricle, is affected by the presence of the pericardium.38 Systolic ventricular interaction may also depend to some degree on the anatomic constraints imposed by the pericardium. Although the absolute magnitude of the effects of diastolic and systolic ventricular interaction remains unclear, the RV area-volume relation may be influenced to some degree by the intact pericardium. Another limitation of this preparation was that the AV valves were removed and replaced with intraventricular support rings, which may have altered cardiac geometry. Also, the reported values for the slopes of the RV ESPVR of similar-sized dog hearts in either isolated or in situ were from 1.20 to 4.14 mm Hg/mL.16 17 22 23 31 The volume axis intercepts of the relation were from 2.87 to 15.1 mL. Both the average slope and volume axis intercepts (1.04 mm Hg/mL and 0.41 mL, respectively) in the present study were lower than the reported values. Because the average slope of the LV ESPVR (2.28 mm Hg/mL) for the studied hearts was also lower than the reported values,14 the hearts might be somewhat damaged by the preparation. The blood was removed from the dog before the heart was arrested with cardioplegia and severed chordae tendineae of both ventricles. These preparation methods might be partly responsible for relatively depressed function.39 However, this relatively depressed functional state was considered not to influence the results of the area-volume relation.
In addition, the automated border detection algorithm analyzes backscatter data, which are affected by ultrasound gain settings. Because these gain settings involve manual adjustment based on visual inspection, complete objectivity of settings cannot be ensured, and this is a limitation of this technique. Finally, the method of measuring echocardiographic area is dependent on the direction and placement of the echo probe. Although we can obtain relatively constant high-quality cross-sectional images of the right ventricle in the present isolated perfused hearts, technically adequate automated border detection data may be acquired by transthoracic or transesophageal echocardiography in clinical settings.36 37
In summary, the relation between RV cross-sectional area and volume was predominantly linear and varied little with changing LV volume. Therefore, echocardiographic automated border detection may have potential to measure RV area as an index of RV volume. With simultaneous measured RV pressure, ESPARs can be constructed and may have potential for measuring RV function on-line, although further study and validation are required.
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Acknowledgments |
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This work was supported in part by a Veterans Administration Merit Award, US Department of Veterans Affairs.
Received January 3, 1995; revision received February 14, 1995; accepted February 27, 1995.
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