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Articles in PresS. Am J Physiol Heart Circ Physiol (December 9, 2004). doi:10.1152/ajpheart.00566.2004
Reservoir and Conduit Function of the Right Atrium:
Impact on Right Ventricular Filling and Cardiac Output
Sydney L. Gaynor, MD, Hersh S. Maniar, MD, Sunil M. Prasad, MD,
Paul Steendijk, PhD,* Marc R. Moon, MD
From the Division of Cardiothoracic Surgery,
Washington University School of Medicine, St. Louis, Missouri,
and the Department of Cardiology,
Leiden University Medical Center, Leiden, The Netherlands*
Address for Correspondence:
Marc R. Moon, MD
Division of Cardiothoracic Surgery
Washington University School of Medicine
3108 Queeny Tower
#1 Barnes-Jewish Plaza
St. Louis, Missouri 63110-1013 (314) 362-0993 FAX: (314) 362-0328
E-mail: [email protected]
Short Running Title: RA Reservoir & Conduit Function …
Keywords: Right Atrial Function, Conductance Catheter, Right Ventricular Afterload, Inotropic
Stimulation, Pulmonary Artery Occlusion
Copyright © 2004 by the American Physiological Society.
Gaynor et al …
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ABSTRACT
The purpose of this study was to investigate the relationship between right atrial (RA) reservoir
and conduit function and to determine how hemodynamic changes influence this relationship and
its impact on cardiac output. In eleven open-chest sheep, RA reservoir and conduit function were
quantified as RA inflow with the tricuspid valve closed versus open, respectively. Conduit
function was separated into early (before A-wave), and late (after A-wave) components. The
effects of inotropic stimulation, partial pulmonary artery occlusion, and pericardiotomy were
tested. At baseline with the pericardium intact, reservoir function accounted for 0.56 ± 0.13
(mean ± one standard deviation) of RA inflow, early conduit for 0.29 ± 0.07, and late conduit
(during RA contraction) for 0.16 ± 0.11. Inotropic stimulation decreased conduit function and
increased reservoir function, but these effects did not reach statistical significance. With partial
pulmonary artery occlusion, early conduit function fell to 0.20 ± 0.11 (P<0.04), and the conduitto-reservoir ratio decreased by 41% (P<0.03). Similarly, after pericardiotomy, early conduit
function fell to 0.14 ± 0.09 (P<0.004), reservoir function increased to 0.72 ± 0.08 (P<0.04), and,
consequently, the early conduit-to-reservoir ratio decreased by 63% (P<0.006). Cardiac output
was inversely related to the conduit-to-reservoir ratio (r = 0.39, P<0.001).
This study
demonstrated that the right atrium adjusts its ability to act more as a reservoir versus a conduit in
a dynamic manner. The RA conduit-to-reservoir ratio was directly related to the RVP-RAP
gradient at the time of maximum RA volume, with increased ventricular pressures favoring
conduit function, but it was inversely related to cardiac output, with an increase in the reservoir
contribution favoring improved cardiac output.
Gaynor et al …
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The right atrium is a dynamic structure whose role is to assist filling of the right ventricle.
Ideally, the right atrium should transfer a high volume of blood rapidly to the ventricle at low
pressure to prevent peripheral edema and hepatic congestion. The three components of atrial
function are: 1) reservoir function, storing blood when the tricuspid valve is closed and releasing
stored blood when it opens, 2) conduit function, passive blood transfer directly from the coronary
and systemic veins to the right ventricle when the tricuspid valve is open, and 3) booster pump
function, atrial contraction in late diastole to complete ventricular filling (10,13,31). Previous
studies have demonstrated that pathologically altered left atrial conduit-to-reservoir function is an
important determinant of left-heart function and can profoundly affect cardiac performance
(2,4,14-17,30,33,34,38), but studies examining right atrial (RA) reservoir and conduit function
are limited.
The mechanics of the right atrium are complex (5,8,24,26). In 1628, William Harvey
was the first to identify the atrium as a “receptacle and store-house” and reported that the right
atrium was “the first to live, and the last to die” (12). In an elegant computer model, Suga found
that increased atrial compliance markedly improved cardiac performance and concluded that a
“flexible atrium” (increased receptacle capabilities) would substantially improve the heart’s
output (36). Others have predicted that early ventricular filling increases directly with atrial
compliance (16,33,38); however, data is limited from intact subjects to support these theories. In
addition, it remains completely unknown what factors influence the RA conduit-to-reservoir ratio
and how physiologic adaptations impact this ratio to accommodate right ventricular (RV) needs
in times of stress. The purpose of the current investigation was to examine the relationship of
conduit-to-reservoir function in the normal right atrium and to determine how loss of pericardial
integrity, increased inotropic state, acute pulmonary hypertension, and, ultimately, the
atrioventricular (AV) pressure gradient influenced the composite functions of the right atrium and
its impact on cardiac output.
Gaynor et al …
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Methods
Eleven adult sheep (25-30 kg) were anesthetized with ketamine hydrochloride (27 mg/kg
im) and pentothal sodium (6.8 mg/kg iv), and intubated and ventilated (Siemens; Munich,
Germany) with supplemental inhalational isoflurane (1.5-3%).
performed, leaving the pericardium intact.
A median sternotomy was
Ultrasonic flow probes (10-12-mm perivascular
probes with a T206 Flowmeter, Transonic Systems; Ithaca, NY) were placed around the superior
(SVC) and inferior (IVC) vena cava approximately 1-cm from the caval-atrial junction to
measure RA inflow. Micromanometer-tipped pressure catheters (Millar Instruments, Houston,
TX) were zeroed in a 37°C water bath for 30 min before insertion. A 1-cm incision was made in
the pericardium over the anterior RV free wall, and a 7-Fr micromanometer was positioned in the
mid-RV cavity to record RV pressure (RVP).
A second 1-cm incision was made in the
pericardium over the RA appendage, and a 6-Fr combined pressure-volume conductance catheter
(Millar SPR-766) was positioned along the long axis of the right atrium so that its tip rested at the
RA-IVC junction. This catheter was connected to a signal conditioner processor (Sigma 5DF,
CD Leycom; Zoetermeer, The Netherlands) to convert instantaneous conductance measurements
into relative RA volume as previously described (24). A micromanometer 2-cm from the distal
end of the catheter allowed simultaneous measurement of RA pressure (RAP). A tourniquet was
positioned around the distal main pulmonary artery (PA) to permit acute RV afterload
manipulation via partial PA occlusion. A third 1-cm incision was made over the AV groove to
place a vascular loop around the coronary sinus so that it could be occluded during data collection
to prevent coronary venous return.
Experimental Protocol.
With the pericardium intact, data were recorded during steady-state baseline conditions.
Between 3 and 10 steady-state beats were recorded during each study intervention, and data
acquisition runs were repeated in triplicate. To alter inotropic state, a calcium chloride bolus (10
mg/kg iv) was given, and steady-state data were obtained. Acute pulmonary hypertension was
Gaynor et al …
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created by partial PA occlusion to produce a 50% rise in maximum RVP, and steady-state data
were recorded. The PA tourniquet was released, and RVP returned to its baseline level. After a
ten minute stabilization period, the pericardium was opened, and data were again recorded during
steady-state conditions. Complete data with the pericardium intact was available in nine of the
eleven animals, and complete data with the pericardium open was available in seven of the eleven
animals. At the conclusion of the experiment, the animals were euthanized using pentothal
sodium (1 g iv) followed (after 2 min) by potassium chloride (80 meq iv), and proper positioning
of the catheters was confirmed. All animals received humane care in compliance with the
“Principles of Laboratory Animal Care” formulated by the National Society for Medical Research
and the “Guide for the Care and Use of Laboratory Animals” prepared by the National Academy
of Sciences and published by the National Institutes of Health. The study was approved by the
Washington University School of Medicine Animal Studies Committee and conducted according
to Washington University policy.
Data Analysis.
During each data acquisition run, ECG, RAP, RVP, SVC flow, IVC flow, and RA
conductance signals were acquired at 200 Hz and processed using custom-designed computer
software. The RAP and RVP signals were differentiated with respect to time to calculate
maximum RA dP/dt and RV dP/dt, and relative RA volume was determined using the
conductance catheter as previously described (24,35). The instantaneous pressure gradient across
the tricuspid annulus (RVP-RAP gradient) was corrected for differences in the height of the RAP
and RVP sensors (hydrostatic pressure gradient) (20). The average hydrostatic pressure gradient
( PH) was calculated as the difference between RAP and RVP at the time immediately before the
electrocardiographic P wave (during diastasis), then subtracted from the pressure differential as
follows: RVP-RAP gradient = RVP(t) – RAP(t) - PH.
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RA reservoir and conduit function. Reservoir and conduit function of the right atrium
were calculated by integrating RA inflow (combined SVC and IVC flow) during RV systole
(reservoir) and RV diastole (conduit) (16,17,30). Since the tricuspid valve is closed during RV
systole, all blood that enters from the cavae during this period is reserved in the atrium (coronary
sinus return was temporarily interrupted during data collection). Thus, RA reservoir volume
equals integrated RA inflow from the ECG R-wave to the time of maximum RA volume, which
corresponds to the initiation of RA emptying and approximates the time of tricuspid valve
opening (17). In contrast, RA conduit volume equals integrated RA inflow during RV filling
when the tricuspid valve is open. Total conduit volume was separated into an early component,
from the time of maximum RA volume to the beginning of atrial contraction (A-wave, time of
maximum RA dP/dt), and a late component, from the A-wave to the end of RV filling (ECG Rwave). The late conduit component quantifies blood entry into the atrium against the force of the
RA kick. Figure 1 illustrates typical hemodynamic data obtained from one animal at baseline.
Integrated RA inflow volume during the reservoir and conduit phases was divided by total RA
inflow volume (stroke volume) to yield reservoir and conduit (both early and late) function as a
percentage of total RA inflow.
Statistical Analysis.
All data are reported as means ± SD. Hemodynamic data obtained during steady-state
baseline conditions with the pericardium closed and after calcium chloride bolus, partial PA
occlusion, and pericardiotomy were compared using repeated-measures ANOVA.
When
indicated by a significant F statistic (P<0.05), differences were isolated using Fischer’s protected
least significant difference test. Multiple linear regression analysis was used to determine which
hemodynamic factors most influenced reservoir and conduit function, and linear regression was
used to determine the relationship between the conduit-to-reservoir ratio and cardiac output
(stroke volume times heart rate). All statistical analyses were performed using SigmaStat 2.03
(SPSS Inc., Chicago, IL).
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Results
Table 1 summarizes the steady-state hemodynamic data during baseline (pericardium
closed), inotropic stimulation (calcium chloride bolus), partial PA occlusion, and following
pericardiotomy. With inotropic stimulation, maximum RVP increased by 38% (P<0.04), RV
dP/dt increased by 26% (P>0.05), and there was a tendency for RA dP/dt to rise (P=0.06). With
partial PA occlusion, maximum RVP similarly increased by 51% (P<0.004), but the changes in
RV dP/dt and RA dP/dt did not reach statistical significance (P=0.10 and P=0.09, respectively).
Following pericardiotomy, maximum RV dP/dt fell by 20% (P=0.06). There were no significant
changes with any intervention in heart rate (P>0.60), P-R interval (P>0.13), RA filling time
(reservoir time, P>0.75), RA emptying time (total conduit time, P>0.96), mean RA pressure
(RAP) (P>0.28), total RA inflow (stroke volume, P>0.40), or cardiac output (P>0.32).
Table 2 and Figures 2 and 3 summarize changes in reservoir and conduit function with
each intervention. At baseline with the pericardium closed, reservoir function accounted for 0.56
± 0.13 of RA inflow (21.1 ± 6.8 mL), early conduit function for 0.29 ± 0.07 (11.2 ± 5.5 mL), and
late conduit function for 0.16 ± 0.11 (5.3 ± 2.4 mL). Inotropic stimulation decreased RA inflow
volume during the late conduit phase to 3.0 ± 1.0 mL (P<0.02), but the fall in late conduit
function to 0.09 ± 0.04 did not reach statistical significance (P=0.11). With partial PA occlusion,
early conduit function fell by 31% (P<0.04) and there was a tendency for reservoir function to
increase (p=0.09), resulting in a fall in the early conduit-to-reservoir ratio from 0.56 ± 0.22 at
baseline to 0.33 ± 0.22 (P<0.03). Following pericardiotomy, there was a small increase in RA
inflow during the late conduit phase (+0.6 mL, P<0.05) but a larger decrease during the early
conduit phase (-5.4 mL, P<0.003). This coupled with a 29% increase in reservoir function
(P<0.04), resulted in a fall in the early conduit-to-reservoir ratio to 0.21 ± 0.15 with the
pericardium open (P<0.006). Linear regression analysis demonstrated that cardiac output was
inversely related to the conduit-to-reservoir ratio (r = 0.39, P<0.001) (Figure 4).
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In multilinear regression analysis, heart rate (P>0.10), stroke volume (P>0.10), maximum
RA dP/dt (P>0.09), maximum RV dP/dt (P>0.30), and maximum RA volume (P>0.16) did not
significantly influence reservoir and conduit function.
Significant factors included RAP
(P<0.004), RVP (P<0.003), and the RVP-RAP gradient (P<0.004) at the time of maximum RA
volume, which corresponds to the initiation of RA emptying. Table 3 summarizes the impact of
each significant factor on reservoir, early conduit, and late conduit function. The cutoff values
analyzed included RAP at maximum RA volume = 4.2 mmHg, RVP at maximum RA volume =
5.8 mmHg, and RVP-RAP gradient at maximum RA volume = 0.53 mmHg, representing the
median value for each parameter across all interventions in all animals. With increased RAP at
maximum RA volume, reservoir function rose by 12% (P<0.001) and early conduit function fell
by 25% (P<0.001), resulting in a fall in the early conduit-to-reservoir ratio from 0.65 ± 0.69 to
0.40 ± 0.49 (P<0.001). In contrast, with elevated RVP at maximum RA volume, reservoir
function fell by 8% (P<0.02) and early conduit function rose by 23% (P>0.006), resulting in a rise
in the early conduit-to-reservoir ratio from 0.43 ± 0.49 to 0.62 ± 0.69 (P<0.02). The RVP-RAP
gradient at maximum RA volume had a similar effect, increasing the early conduit-to-reservoir
ratio from 0.42 ± 0.50 to 0.64 ± 0.69 (P<0.004).
Discussion
Previous studies have demonstrated that pericardial integrity can have a profound effect
on the interplay between various cardiac chambers and, when lost, can decrease the adaptive
capacity of the atrium to stress (1,3,11,16). In an earlier report from this laboratory, it was noted
that RA contractility (atrial kick) fell by 54% and RA compliance rose by 39% following
pericardiotomy (24). In the current study, without pericardial restraint, the atrium acted more as a
reservoir than a conduit; the RA early conduit-to-reservoir ratio fell from 0.56 ± 0.22 to 0.21 ±
0.15 (P<0.006). Likely, the pericardium has a greater effect on the thin-walled atria than on the
thick-walled ventricles. Nagano and coauthors found in normal subjects that the left atrium was
Gaynor et al …
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less compliant than the left ventricle, facilitating blood transfer between the chambers during the
early conduit phase (28). It is not surprising, however, that others have suggested that increased
atrial compliance, which promotes reservoir function (17,37), would have a greater positive
impact on cardiac output than would supplementation of conduit function (2,36). Hoit and
colleagues examined left atrial mechanics during left ventricular dysfunction, comparing the
compensatory response with a normal atrium versus a failing atrium (induced with rapid atrial
pacing) (14). With a normal atrium, reservoir function increased by 19% and booster pump
function (atrial contraction) nearly doubled to maintain cardiac output despite a fall in left
ventricular ejection fraction from 0.57 to 0.32. In contrast, with a failing atrium, reservoir
function fell by 30%, conduit function increased by 33%, and the atrial kick disappeared. The
shift from reservoir to conduit function in Hoit’s study was inadequate to maintain cardiac output,
which fell by 20%. In the current report, cardiac output was inversely related to the conduit-toreservoir ratio, increasing as the reservoir contribution increased (p<0.03).
These findings
support the theory of Suga and others that a “flexible atrium” would substantially improve the
heart’s output (2,16,33,36,38).
The proper physiologic explanation of right heart AV valve mechanics is that the valve
leaflets open when ventricular pressure drops below atrial pressure and coapt and close when
ventricular pressure exceeds atrial pressure during systole (9,39). In the current study, RA
volume reached its maximum and began to fall when the RVP-RAP gradient was 0.53 mmHg on
average. It is important to note, however, that the time of maximum RA volume does not
necessarily correspond to the time of tricuspid valve opening. On the left side of the heart,
Karlsson and associates, using myocardial markers on the mitral valve, demonstrated that the
mitral valve moves towards its open position in the isovolumic phase, but that the leaflets do not
separate until minimum LV pressure is obtained (21). A similar phenomenon could occur on the
right side of the heart with the tricuspid valve, and the RA appendage may also play a role. Hoit
and colleagues elegantly demonstrated the impact of the LA appendage on LA compliance and
Gaynor et al …
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LV filling (17). In the current study, the RA conductance catheter was placed into the atrium via
the appendage and secured with a purse string. With this technique, we could not be certain that
the entire contents contained within the appendage were included in the volume measured using
the conductance catheter. Thus, it is possible that at the time of maximum RA volume, blood
may have been moving from the chamber into the appendage, giving the illusion of RA emptying.
In the current study, while there was a shift towards reservoir function with partial PA
occlusion, it was noted that as the RVP-RAP gradient at the time of maximum RA volume
increased, the atrium functioned more as a conduit than a reservoir. As the atrium fills during the
reservoir phase, it has been suggested that, like the ventricle, the atrial myocardium stores elastic
energy that is released when the tricuspid valve opens to aid early ventricular filling (2,10).
Presumably, as the RVP-RAP gradient at the time of maximum RA volume increases, the atrium
has to work harder to move the same amount of blood across the tricuspid valve. Acutely, the
right atrium has not had time to adapt, and the elastic recoil stored during the reservoir phase may
not be adequate to support ventricular filling. Potentially through a rise in RV suction, the
ventricle could actively draw blood into itself through the atrium directly from its inflow source,
the systemic venous circulation, expressed as an increase in RA early conduit function. Pressure
clamping studies on the right side of the heart would be necessary to prove these theories
(19,20,27,29).
Nishikawa and coauthors demonstrated that with exercise, LA reservoir function
increased by 37% and LA conduit function decreased by 23% (30). Although Nishikawa did not
measure PA pressures, others have demonstrated that substantial pulmonary hypertension can
develop during exercise, especially in subjects with abnormal hearts (7,18,23,32). For example,
in heart transplant recipients, Pflugfelder and colleagues noted that peak exercise produced a 90%
increase in mean PA pressure with a three-fold rise in RAP (32). In the current report, when RAP
at the time of maximum RA volume exceeded 4.2 mmHg, reservoir function rose by 12%, early
conduit function fell by 25%, and the early conduit-to-reservoir ratio decreased from 0.65 to 0.40.
Gaynor et al …
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The redistribution of conduit to reservoir function during exercise was similar to the findings of
the current study during partial PA occlusion, in which the atrium acted more as a reservoir than a
conduit. With partial PA occlusion, the early conduit-to-reservoir ratio fell from 0.56 ± 0.13 to
0.33 ± 0.22 (P<0.03). Grant and associates demonstrated that the left atrium acted as a short-term
storage reservoir and that atrial reservoir function was four times more important than active
atrial contraction in providing energy for the work of ventricular filling (10). Reservoir function
also provides capacitance to dampen irregularities of atrial filling and prevent acute elevations of
central venous pressure. With chronic exposure to elevated pulmonary pressures, changes in the
biochemical properties and myocardial fiber structure of the right atrium likely occur to make it a
more efficient capacitor, but future studies will be necessary to delineate the mechanistic adaptive
response of the right atrium to chronic pulmonary hypertension (6,22).
Potential Limitations. As with all open-chest physiology studies in anesthetized animals,
there are potential difficulties in translating results to the closed-chest human clinical setting.
However, pericardial integrity was maintained through most of the preparation in an attempt to
best mimic the natural in vivo state, and although pericardial pressures were not measured, we
suspect that the use of transmural pressures (subtracting pericardial pressure from intracavitary
pressure) would have demonstrated similar results. In addition, while this study examined only
subjects with acute pulmonary hypertension, we anticipate that subjects with chronic pulmonary
hypertension and other diseases that impair the right heart may be even more dependent on the
atrium’s ability to variably function more as a reservoir or a conduit.
While we did not quantify booster pump function (atrial contraction) in the current report,
its contribution to ventricular filling and cardiac output can be quite important. Active atrial
contraction increases stroke volume by 10% to 20% (30,34), a contribution that increases via the
Frank-Starling mechanism following ventricular ischemia (25) and becomes more important to
maintain filling with advanced age and when the ventricle either dilatates or hypertrophies
Gaynor et al …
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(14,34).
We have previously shown that atrial contraction increases with acute pulmonary
hypertension to support ventricular filling, but falls when pericardial integrity is lost (24). The
late conduit phase reported in the current study quantifies RA inflow during atrial contraction.
On the left side of the heart, reversed flow is common in the pulmonary veins during the atrial
kick, but it disappears with exercise (30). Nishikawa and associates found that the minimum
pulmonary venous flow rate rose progressively with increasing levels of exertion (30). In the
current report examining the right side of the heart, reversal of flow in the vena cavae was rare,
occurring during the late conduit phase in only 29 of 653 (4%) steady-state beats, more often
during inotropic stimulation (7 of 45 beats, 16%) and partial PA occlusion (12 of 166, 7%) than
during baseline with the pericardium closed (8 of 267, 3%) or open (2 of 175, 1%).
In summary, this study demonstrated that the right atrium adjusts its ability to act more as
a reservoir versus a conduit in a dynamic manner, dependent not only on global physiologic
changes, but on beat-to-beat changes in the pressure differential between the right-sided
chambers. The RA conduit-to-reservoir ratio was directly related to the RVP-RAP gradient at the
time of maximum RA volume, with increased ventricular pressures favoring conduit function, but
it was inversely related to cardiac output, with an increase in the reservoir contribution favoring
increased cardiac output. While this study examined subjects exposed to acute physiologic
changes, we anticipate an even more profound impact of RA reservoir and conduit function on
RV filling and cardiac output during chronic disease states that impair right heart mechanics.
ACKNOWLEDGMENTS
This study was supported by grant HL-69949 from the National Heart, Lung, and Blood Institute
of the National Institutes of Health and by a Foundation Research Grant from the Thoracic
Surgery Foundation for Research and Education. Drs. Gaynor and Maniar were also supported in
part by grant T32-HL-07776 from the National Heart, Lung, and Blood Institute. The authors
gratefully acknowledge Martha L. Lester, BS and Celeste M. Chu, BS for their assistance in the
surgical preparation as well as the technical assistance of Diane Toeniskoetter and Kathy Fore.
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TABLE 1. Hemodynamic effects of inotropic stimulation with calcium chloride, acute partial
PA occlusion, and pericardiotomy.
Baseline
Pericardium Closed
Pericardium Open
Calcium
PA Occlusion
Baseline
Heart rate (beats/min)
104 ± 32
105 ± 12
101 ± 20
119 ± 22
RA filling time (msec)
342 ± 67
344 ± 71
349 ± 31
363 ± 43
RA emptying time (msec)
208 ± 91
235 ± 64
228 ± 62
205 ± 51
Mean RA pressure (mmHg)
4.1 ± 1.7
4.6 ± 1.7
4.7 ± 1.7
5.2 ± 2.1
Maximum RV pressure (mmHg)
25 ± 6
35 ± 9*
38 ± 10*
22 ± 3
Maximum RA dP/dt (mmHg/s)
177 ± 56
225 ± 73
214 ± 68
1563 ± 188*
1472 ± 274
997 ± 173*
37.3 ± 9.6
36.8 ± 9.8
33.5 ± 6.5
38.8 ± 6.7
3.7 ± 1.2
3.8 ± 0.8
3.3 ± 0.8
4.5 ± 0.9
Maximum RV dP/dt (mmHg/s) 1245 ± 423
Total RA inflow (mL/beat)
Cardiac output (mL/min)
223 ± 94
Values are means ± SD. n = 9 for pericardium closed and 7 for pericardium open. PA,
pulmonary artery; RA, right atrial; RV, right ventricular. *P<0.05 versus pericardium closed
baseline. Repeated measures ANOVA was used for all comparisons.
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TABLE 2. Effects of inotropic stimulation with calcium chloride, acute partial PA occlusion,
and pericardiotomy on RA reservoir and conduit function.
Baseline
Pericardium Closed
Pericardium Open
Calcium
PA Occlusion
Baseline
reservoir volume (mL)
21.1 ± 6.8
23.2 ± 6.7
early conduit volume (mL)
11.2 ± 5.5
11.0 ± 6.0
late conduit volume (mL)
5.3 ± 2.4
reservoir function
21.5 ± 4.3
27.4 ± 3.9
7.0 ± 4.7*
5.8 ± 4.3*
3.0 ± 1.0*
5.4 ± 1.3
5.9 ± 2.6*
0.56 ± 0.13
0.63 ± 0.10
0.64 ± 0.08
0.72 ± 0.08*
early conduit function
0.29 ± 0.07
0.29 ± 0.11
0.20 ± 0.11*
0.14 ± 0.09*
late conduit function
0.16 ± 0.11
0.09 ± 0.04
0.17 ± 0.06
0.15 ± 0.07
0.56 ± 0.22
0.50 ± 0.26
0.33 ± 0.22*
0.21 ± 0.15*
--------------------------------------
-------------------------------------early conduit-to-reservoir
Values are means ± SD. n = 9 for pericardium closed and 7 for pericardium open. PA,
pulmonary artery; RA, right atrial. *P<0.05 versus pericardium closed baseline. Repeated
measures ANOVA was used for all comparisons.
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TABLE 3. Effects of RA and RV hemodynamics at the time of maximum RA volume on RA
reservoir and conduit function.
Reservoir
Early conduit
Late conduit
RA pressure at maximum RA volume
< 4.2 mmHg
0.58 ± 0.18
0.28 ± 0.16
0.15 ± 0.13
> 4.2 mmHg
0.65 ± 0.15*
0.21 ± 0.11*
0.15 ± 0.12
RV pressure at maximum RA volume
< 5.8 mmHg
0.64 ± 0.16
0.22 ± 0.12
0.15 ± 0.15
> 5.8 mmHg
0.59 ± 0.17*
0.27 ± 0.16*
0.15 ± 0.09
RV-RA pressure at maximum RA volume
< 0.53 mmHg
0.66 ± 0.14
0.22 ± 0.12
0.13 ± 0.10
> 0.53 mmHg
0.57 ± 0.18*
0.27 ± 0.16*
0.17 ± 0.14*
Values are means ± SD. n = 254 including all baseline, calcium chloride, and partial pulmonary
artery occlusion runs with and without pericardial integrity. PA, pulmonary artery; RA, right
atrial; RV, right ventricular. *P<0.05 for higher values versus lower values. ANOVA was used
for all comparisons.
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FIGURE LEGENDS
FIGURE 1: Typical hemodynamic data with the pericardium intact during the baseline state in
one animal from this study. Three steady-state beats are illustrated. The reservoir phase extends
from the ECG R-wave to time of maximum RA volume (corresponding to tricuspid valve
opening).
The conduit phase contains two components, the early phase, from the time of
maximum RA volume to the A-wave (maximum RA dP/dt), and the late phase, from the A-wave
to the end of RV filling (the subsequent ECG R-wave).
FIGURE 2: Effects of inotropic stimulation with calcium chloride, acute partial PA occlusion,
and pericardiotomy on RA reservoir and conduit function. Data represent mean values for
reservoir (black, bottom), early conduit (white, middle), and late conduit (grey, top) contribution
as a percentage of total RA inflow during each intervention.
FIGURE 3: Effects of inotropic stimulation with calcium chloride, acute partial PA occlusion,
and pericardiotomy on RA early conduit-to-reservoir ratio. Values are means ± SD.
*
P<0.05
versus pericardium closed baseline (repeated measures ANOVA).
FIGURE 4: Linear regression analysis comparing the RA conduit-to-reservoir ratio to cardiac
output. As the RA conduit-to-reservoir ratio increased, cardiac output decreased.
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Figure 1:
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Figure 2:
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Figure 3:
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Figure 4: