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Departments of Medicine and Physiology and Biophysics, The University of Calgary, Calgary, Alberta, Canada T2N 2T9
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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In the intact animal, it is difficult to
discriminate between the independent effects of series and direct
ventricular interaction (DI) or the individual contributions of the
pericardium and septum to DI. Left ventricular (LV) venous return
(LVVR) and right ventricular (RV) end-diastolic pressure (RVEDP) were
varied independently in a right-heart bypass model. LV minor-axis
diameters were measured, and the product of the two diameters was used
as an index of LV volume (LVVI). At each RVEDP (0, 5, 10, and 15 mmHg),
increased LVVR caused an increased LVVI. When RVEDP was increased,
increased pump output was required to maintain a given LVVI. RV-to-LV
pressure gain (
LVEDP/RVEDP) reflects coupling and DI. With the
pericardium closed, the gain was dependent on RVEDP; when RVEDP was
increased from 0 to 5 mmHg, the gain was not statistically different
from zero, indicating little or no DI. When RVEDP was increased from 10 to 15 mmHg, the gain was not statistically different from 1.0, indicating ~1:1 coupling of the ventricles. Opening the pericardium reduced the gain, but significant interaction remained. When the septal
contribution was accounted for, the remaining interaction was
eliminated. In conclusion, DI substantially affects LVEDP-volume relations. Considerable increases in RV output may be required to
counterbalance increased constraint to LV filling. With the pericardium
closed, RV-to-LV coupling is minimal when RVEDP is low and increases to
1:1 coupling when RVEDP is high. Opening the pericardium reduces DI,
but significant septum-mediated interaction remains.
ventricular interdependence; ventricular mechanics; diastole; diastolic interaction
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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BECAUSE THE RIGHT and left ventricles (RV and LV, respectively) function in series, share a common septum, and are enclosed in a relatively nondistensible pericardium, changes in function of one ventricle can affect that of the other. Diastolic ventricular interaction involves two components. Interaction via RV output (equal to LV venous return, LVVR) is termed series interaction, and interaction via the septum and pericardium is termed direct ventricular interaction (DI). Diastolic interaction has been studied extensively, and many of its characteristics have been clarified (4, 6, 9, 11, 13, 15, 16, 22, 24, 30). Normally, series interaction is the dominant physiological mechanism. However, increased LV constraint due to increased pericardial pressure (PP) and/or RV end-diastolic pressure (RVEDP) may have substantial hemodynamic effects. The importance of series interaction vs. DI and the relative contributions of the septum and pericardium to DI are not yet clear.
We have previously shown that DI plays an important role in determining the hemodynamic response to acute pulmonary embolism (1-3). After severe acute pulmonary embolization with the pericardium closed, volume loading decreased LV end-diastolic volume and stroke work, although with the pericardium opened, volume loading increased LV end-diastolic volume and stroke work (3). These studies demonstrated that although RV output (i.e., series interaction) is clearly important, constraint to LV filling (i.e., DI) may contribute significantly to the hemodynamic responses to acute pulmonary embolism and subsequent volume loading and unloading.
The relative contributions of series vs. direct ventricular interaction were not addressed in our previous work. In the intact heart, this question has been difficult to resolve because most interventions affect both mechanisms. For example, pulmonary artery constriction or embolism increases RVEDP but also decreases LVVR. In the present study, we used a canine right-heart bypass model in which both pump output (the series component) and RVEDP (a determinant of DI) could be controlled independently to separate the effects of the series and direct components of ventricular interaction. We applied the interventions while the pericardium was closed and again when it was open to discriminate between the pericardial and septal contributions to DI.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Animal preparation.
After premedication with 0.75 mg/kg morphine sulfate, 11 dogs weighing
19-29 kg were anesthetized, initially with thiopental sodium
(10-15 mg/kg iv), and then maintained with fentanyl citrate (50 µg/kg iv over 5 min followed by 20-50
µg · kg
1 · h1).
Additional boluses were administered and infusion rates were adjusted
as necessary. The animals were ventilated with a 70% nitrous
oxide-30% oxygen mixture using a constant-volume respirator (model
607, Harvard Apparatus, Natick, MA).
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Experimental protocol. The right-heart bypass model used in this study allowed for independent control of LVVR and RVEDP. Thus series interaction was controlled by adjusting pump output (i.e., LVVR), and DI was varied by changing the height of the RV reservoir (i.e., RVEDP). Initially, LVVR was adjusted so that LV end-diastolic pressure (LVEDP) was ~8 mmHg.
While RVEDP was maintained at 0 mmHg by adjusting the height of the reservoir above the RV, pump output was varied over a wide range. Over a period of ~4 min, LVVR was first decreased by reducing the pump output until systemic aortic pressure decreased to ~60 mmHg and then increased incrementally until LVEDP was at least 20 mmHg. Pump output was then returned to the control rate. To assess the effects of increasing degrees of DI, the height of the reservoir above the RV was then raised to maintain RVEDP at 5 mmHg. LVVR was then varied over the same range as described above. The procedure was then repeated with RVEDP maintained at 10 and at 15 mmHg. To assess the pericardial and septal contributions to DI, the pericardium was opened and the entire protocol was repeated.Data analysis.
Only data collected at end expiration were analyzed. Transmural
LVEDP was calculated in two ways:
1)
LVEDPTM as LVEDP minus PP, and
2)
LVE
as LVEDP minus the sum of
two-thirds PP and one-third RVEDP (20). The product of the LV
minor-axis diameters (anteroposterior septum-to-free wall diameter) was
used as an index of LV area and, hence, volume (LVVI). LVVR was
measured as pump output, and stroke volume (SV) was calculated as pump output per beat. End-diastolic pressure-volume curves (LVEDP-LVVI) were
plotted for each dog, and the curves were fitted to second-order equations. Normalized data from each dog were combined for analysis. Baseline LVVI (i.e., 100%) was defined as the LVVI observed at an
LVEDP of 5 mmHg with the pericardium open (PP = 0) and RVEDP was 0 mmHg
(i.e., LVEDPTM = LVE = 5 mmHg). For a single dog,
because of missing data when the pericardium was open and RVEDP was 0 mmHg, 100% LVVI was defined as the volume observed at an LVEDP of 5 mmHg and RVEDP of 5 mmHg with the pericardium open. Other values of
LVVI were expressed as percentages of the above-defined baseline value
to compare data from different dogs. To assess the relationship between
LVVR and external constraint, these data were summarized by recording
the SV at each level of RVEDP at LVVI values of 94, 100, and 106%. SV
of 100% was defined as the LVVR per beat when the LVVI was 100%,
RVEDP was zero, and the pericardium was closed. RV-to-LV end-diastolic
pressure gain (i.e., the ratio of the change in LVEDP to the change in
RVEDP, a measure of ventricular coupling) was determined at an LVVI of 100% for each increase in RVEDP. With the pericardium closed, pressure
gains were calculated for each incremental change in RVEDP (i.e., RVEDP = 0-5, 5-10, and 10-15 mmHg). The pressure gains for
each 5-mmHg change in RVEDP were calculated as mean values
from paired data points. Pressure gains were also calculated for the
pericardium-open data, but because there was no statistical difference
between the gains for every 5-mmHg increase in RVEDP, these gains were
calculated using linear regression for the entire range of RVEDP values
(i.e., RVEDP = 0-15 mmHg).
Statistical analysis.
For the pericardium-closed data, to determine if the pressure
gain for each incremental change in RVEDP (i.e., 0-5, 5-10, and 10-15 mmHg) was different from each other, different from zero, and different from one, the mean differences from the paired data
for each segment were compared using the Student's paired t-test. To determine if opening the
pericardium decreased DI, the RV-to-LV end-diastolic pressure gains for
pericardium-closed and pericardium-open data over the interval between
RVEDP = 10 and RVEDP = 15 mmHg were compared using the Student's
paired t-test. To determine if the
remaining DI was signficiant, we compared the slope of the
pericardium-open data to zero. The slope of the pericardium-open data
was also compared with the slope of the LVE data using two-way
repeated-measures ANOVA to determine whether the gain indicated by the
slope of the pericardium-open data was because of RVEDP. A
P value <0.05 was considered
significant.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Independent effects of increasing pump output vs. increasing RVEDP.
As illustrated in Fig. 2, the series
contribution to ventricular interaction was characterized by the
end-diastolic pressure-volume relations (LVEDP-LVVI) when LVVR was
varied at constant RVEDP values (0, 5, 10, and 15 mmHg), whereas the
direct component was charactered by the shifts in these curves when
RVEDP was increased. When RVEDP was maintained constant at 0, 5, 10, or
15 mmHg, increasing LVVR increased LVVI along separate single
LVEDP-LVVI curves, reflecting the contribution of the series component
of ventricular interaction (Fig.
2A). Each increment in RVEDP shifted
the LVEDP-LVVI curve upward and to the left, reflecting the
contribution of the direct component of ventricular interaction.
Transmural LVEDP-LVVI relations (calculated both ways, Fig. 2,
B and
C) eliminated the effects of
constraint to LV filling by DI (pericardial and septal), and the curves
became superimposed. In contrast to the pericardium-open behavior (see
below), there was no significant difference between the
LVEDPTM-LVVI and
LVELVVI curves with the
pericardium closed.
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Contributions of the pericardium and septum to DI.
When the pericardium was open (i.e., PP = 0 mmHg), increases in RVEDP
still shifted the pressure-volume relations upward, but the shifts were
smaller (Fig.
5A). To
evaluate the degree to which the remaining shift could be attributed to
a septum-mediated mechanism, we subtracted the theoretical contribution
of the septum to constraint (20); this eliminated the shifts in the
LVE-LVVI relations (Fig.
5B), illustrating that the
constraint that was still present with the pericardium open was septum
mediated.
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RV-to-LV end-diastolic pressure gain. Figure 6 shows the combined RV-to-LV end-diastolic pressure gains from all dogs at normalized LVVI values of 100%. With the pericardium closed (Fig. 6, solid circles), RV-to-LV pressure gain was not statistically different from zero when RVEDP was increased from 0 to 5 mmHg (0.22 ± 0.13). As RVEDP increased, the gain also increased, reaching a slope of 0.9 ± 0.15 (not statistically different from 1) when RVEDP was increased from 10 to 15 mmHg, indicating 1:1 coupling of the ventricles. The gain when RVEDP was increased from 5 to 10 mmHg fell in between these two extremes (0.57 ± 0.18). The difference in the pericardium-closed (Fig. 6, solid circles) vs. pericardium-open gains (Fig. 6, open circles) when RVEDP was 10-15 mmHg was statistically significant (P < 0.005). When the theoretical contribution of the septum was eliminated by subtracting one-third of the value of RVEDP (20) (Fig. 6, open triangles), the pericardium-open pressure gain was not significantly different from zero, indicating that the interaction remaining with the pericardium open could be explained by the septum.
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The relationships between the series and direct mechanisms of diastolic ventricular interaction have not been adequately characterized previously because of the difficulty in controlling each component independently. We have previously shown that DI is an important determinant of the hemodynamic response to acute RV pressure loading and subsequent volume loading, but we could not quantify the effects of each component of ventricular interaction because both the series and direct mechanisms were affected simultaneously by our interventions (1-3). In the present study, our right-heart bypass model allowed us to manipulate and therefore assess the series and direct mechanisms independently, and by opening and closing the pericardium, we were also able to discriminate between the pericardial and septal contributions to DI. At each different RVEDP, the LV end-diastolic pressure-volume relation reflects the results of independent changes in RV output and, thus, series interaction. The shifts in these relations when RVEDP was increased reflect the results of changes in constraint to LV filling (i.e., DI). The shifts with the pericardium closed reflect constraint due to the pericardium plus septum, whereas shifts with the pericardium open are due to the septum alone.
Series vs. direct interaction. The contributions of the series component of ventricular interaction are illustrated by the LVEDP-LVVI relation at each RVEDP (Fig. 2A). When RVEDP was held constant and pump output was increased, LVEDP and volume both increased monotonically along a single curve. The effects of DI are illustrated by the upward and leftward shifts of these relations when RVEDP and therefore PP were increased, defining a family of LVEDP-LVVI relations with each curve corresponding to a given RVEDP.
During acute interventions that affect series interaction and DI simultaneously, the responses are a composite of the effects on both mechanisms. For example, during pulmonary artery constriction, there is a decrease in RV output and an increase in RVEDP; this results in decreased venous return to the LV and increased constraint to LV filling, both mechanisms tending to reduce LV end-diastolic volume. In the present model, we were able to demonstrate the impact of increased constraint to LV filling. Thus we had to increase RV output substantially to maintain a given LV end-diastolic volume (i.e., the same transmural pressure) when constraint was increased. For example (see Fig. 3), to maintain an end-diastolic volume index of 92%, pump output per beat had to be increased from 10 to 20 ml/beat when RVEDP was increased from 0 to 5 mmHg, to 30-40 ml/beat when RVEDP was increased to 10 mmHg, and to 50-60 ml/beat when RVEDP was increased to 15 mmHg, illustrating the dramatic increase in LVVR required to counterbalance the increasing DI. To further quantify the relationship between LVVR and different degrees of external constraint, we calculated the required LVVR to maintain representative smaller, normal, and larger LV end-diastolic areas at different levels of RVEDP (Fig. 4). As an illustration of the importance of this interaction, to maintain a normal LV end-diastolic volume (i.e., LVVI = 100%), when RVEDP was increased from 0 to 15 mmHg, LVVR had to be doubled. This demonstrates the interdependence of the series and direct mechanisms of ventricular interaction in that, as RVEDP is increased, more LVVR is required to maintain the same LVVI. Also, as a reflection of the curvilinear pressure-volume relations, a greater change in LVVR was required to change the LVVI from 100 to 106% than from 94 to 100%. Thus, as we have reported previously in acute pulmonary embolism, direct ventricular interaction can play a pivotal role in the hemodynamic response, although both the series and direct components of the interaction contribute to the associated decrease in LV end-diastolic volume (1-3). To fully compensate for the adverse DI on LV end-diastolic volume, it would be necessary for RV output to increase substantially. The quantitative data from the present study underscore the potential importance of DI in the response to acute RV pressure loading.Pericardial and septal contributions to DI. After the pericardium was opened (i.e., PP remained 0 throughout), increases in RVEDP resulted in smaller, but definitely present, shifts in the LVEDP-LVVI relations. Thus removal of pericardial constraint reduces but does not eliminate DI. This is consistent with the model proposed previously by Mirsky and Rankin (20). They suggested that the effective external pressure of the LV is a function of both RV and pericardial pressure, each weighted according to the respective surface areas over which they apply. Because the LV free wall constitutes approximately two-thirds of the LV surface and the interventricular septum one-third, the effective external pressure equals approximately two-thirds PP plus one-third RVEDP. Despite our not having measured surface areas or radii of curvature of the septum and LV free wall, application of this formula to our pericardium-open data still appeared to account for the differences between the LV pressure-volume curves, thus providing experimental support for their model. With the pericardium closed, the transmural LVEDP-LVVI relation (calculated using PP only) demonstrated little or no shift and was similar when we calculated transmural LVEDP using the Mirsky and Rankin algorithm (Fig. 2B). This is consistent with the fact that, when the pericardium was closed, RVEDP and PP were similar (1, 28, 29, 31). However, if RVEDP and PP are different, as was the case in our model when the pericardium was open and as can occur in acute RV or LV pressure loading (29), both should be considered when calculating LV transmural pressure.
RV-to-LV end-diastolic pressure gain.
RV-to-LV end-diastolic pressure gain is the ratio of the change in
end-diastolic pressure in the LV produced by change in pressure in the
RV (LVEDP/RVEDP). As indicated by our results, the degree of
coupling (RV-to-LV pressure gain) between the two ventricles is
dependent on the degree of external constraint, with greater coupling
observed at higher RVEDP values than at low RVEDP values. Our data
indicate that at low RVEDP values (0-5 mmHg) there is little or no
coupling of the ventricles (i.e., the slope was 0.22 ± 0.13 and not
statistically different from 0). As RVEDP increases, the heart expands,
external constraint increases, and the pressure-volume curve becomes
steeper. When RVEDP was increased from 10 to 15 mmHg, our analysis
indicated that coupling was effectively complete (i.e., the slope of
the RV-to-LV pressure gain was 0.90 ± 0.15 and not statistically
different from 1). Not surprisingly, there was an intermediate degree
of coupling at intermediate values of RVEDP (5-10 mmHg).
Therefore, as external constraint increases, the RV-to-LV end-diastolic
pressure gain increases to approximately one. This relationship may be particularly relevant in patients with severe congestive heart failure
when ventricular filling pressures frequently exceed those produced in
our experimental model. Indeed, Janicki (12) has provided such evidence
of pericardial constraint during exercise in patients with varying
severity of heart failure.
"Natural" end-diastolic pressure-volume relation. Each LVEDP-LVVI curve generated using our protocol represents manipulations of the individual components of ventricular interaction. Under normal physiological conditions, however, both the series and direct mechanisms operate simultaneously. For example, volume loading simultaneously increases both RV output and RVEDP. The pressure-volume relation obtained during volume loading represents a composite of curves such as ours (Fig. 2A). Boettcher et al. (5) defined such a curve in the intact dog. Compared with the curves from the present study, their pressure-volume relation is very steep. This is consistent with the concept that the steepness of the curve during volume loading in an intact animal reflects a simultaneous increase in both the series and direct effects (as volume increases, pressure increases, not only as predicted by our RVEDP-constant single curves but as a result of moving upward from one RVEDP-constant curve to another) with the direct effects proportionately greater at higher volumes. In addition, in the intact animal, the curve becomes even steeper because the tachycardia induced by volume loading tends to decrease end-diastolic volume.
Evaluation of the method. Various approaches have been used to study ventricular interaction. Because of the difficulty in separating the direct and series components, one approach has been to eliminate the series contribution to ventricular interaction by using isolated (9, 10, 19, 25) or arrested hearts (21, 30) in which the ventricles were no longer coupled in series. The contributions of DI were evaluated as the pressure or volume in one ventricle was held constant while the pressure-volume relation of the other ventricle was determined. These models allowed for precise control of the ventricular pressures and volumes but were not physiological because the hearts were removed from the circulatory system and often were arrested. Another approach has been a statistical one involving analysis of beat-to-beat changes over a number of cycles in response to manipulations such as caval occlusion or pulmonary artery constriction (17, 26). This did not allow the direct description of ventricular pressure-volume relations. Using a third approach, Slinker et al. (27) have studied ventricular interaction in a dog model in which they separated direct from series interaction by occluding both vena cavas while simultaneously withdrawing blood from the RV and analyzing the change in LVEDP on the next beat. However, they did not have independent control of ventricular volume and, when the pericardium was open, they were unable to remove volume fast enough to decrease RVEDP substantially.
Our method allowed us to separately and independently control and assess the series and direct mechanisms of ventricular interaction in the beating heart in an in situ system over a wide range of ventricular pressures and volumes. We were also able to quantitate the pericardial and septal contributions to direct ventricular interaction by doing the same interventions with the pericardium closed and open. Clearly, this model only describes the results of acute hemodynamic changes, and the results cannot be assumed to reflect what might occur in chronic disease states. Under chronic conditions, the pericardium is capable of enlarging and increasing its unstressed volume; changes in ventricular chamber size and wall thickness may also occur. Although we focused primarily on diastolic interaction, any implications regarding systolic interaction would be derived from data obtained when the RV was not loaded physiologically, the pulmonary outflow tract was obstructed, and some degree of tricuspid incompetence may have been caused by the cannula. Finally, LVVR was assumed to be represented by the pump output. Changes in vascular volume of the lungs during the interventions could alter this relationship; however, pump output was altered slowly, allowing for stability to be achieved, and there was little or no hysteresis in the curves obtained first by decreasing and then by increasing pump output. In summary, we have devised a right-heart bypass model in which series and direct ventricular interaction can be independently controlled. We demonstrated that the position of each LVEDP-volume curve reflects DI and the position along each constant-RVEDP curve is a function of series interaction. LV end-diastolic volume is augmented by LVVR and diminished by pericardium- and septum-mediated constraint; to maintain a given LV end-diastolic transmural pressure and volume, RV output must increase to offset increasing external constraint. In addition, if LV end-diastolic volume is increased, increasingly greater RV outputs are required to increase LV end-diastolic volume further. When the pericardium was closed, RV-to-LV end-diastolic pressure gain depended on RVEDP. When RVEDP was high, coupling was complete. When RVEDP was low, coupling was absent. When RVEDP was intermediate, coupling was intermediate. The pericardium contributes importantly to DI in this model. However, opening of the pericardium resulted in a reduced but still significant RV-to-LV pressure gain that was entirely accounted for by RV pressure. This suggests that the residual DI observed after the pericardium was opened was septum mediated.| |
ACKNOWLEDGEMENTS |
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We thank Gerry Groves and Cheryl Meek for skillful technical assistance. We also thank Dr. Rollin Brant of the Centre for the Advancement of Health for expert guidance in the statistical analysis.
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FOOTNOTES |
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J. V. Tyberg is a Medical Scientist of the Alberta Heritage Foundation for Medical Research (Edmonton). The study was supported by grants-in-aid from the Heart and Stroke Foundation of Alberta (Calgary) (to I. Belenkie and J. V. Tyberg).
Address for reprint requests: I. Belenkie, Dept. of Medicine, Foothills Hospital, 1403-29th St. NW, Calgary, Alberta, Canada T2N 2T9.
Received 7 April 1997; accepted in final form 6 April 1998.
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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pericardial pressure (PP)], shift in curves was eliminated,
indicating that DI had been accounted for.
C: calculated LV transmural
pressure using both RV and PP
[LVE
