Download Reservoir and conduit function of right atrium: impact on - AJP

Am J Physiol Heart Circ Physiol 288: H2140 –H2145, 2005.
First published December 9, 2004; doi:10.1152/ajpheart.00566.2004.
Reservoir and conduit function of right atrium: impact
on right ventricular filling and cardiac output
Sydney L. Gaynor,1 Hersh S. Maniar,1 Sunil M. Prasad,1 Paul Steendijk,2 and Marc R. Moon1
1
Division of Cardiothoracic Surgery, Washington University School of Medicine, St. Louis, Missouri;
and 2Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
Submitted 22 June 2004; accepted in final form 3 December 2004
right atrial function; conductance catheter; right ventricular afterload;
inotropic stimulation; pulmonary artery occlusion
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
THE RIGHT ATRIUM
Address for reprint requests and other correspondence: M. R. Moon,
Division of Cardiothoracic Surgery, Washington Univ. School of Medicine,
3108 Queeny Tower, #1 Barnes-Jewish Plaza, St. Louis, MO 63110-1013
(E-mail: [email protected]).
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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 (36) 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. Others
have predicted that early ventricular filling increases directly
with atrial compliance (16, 33, 38); however, data from intact
subjects are limited to support these theories. In addition, it
remains completely unknown what factors influence the RA
conduit-to-reservoir ratio and how physiological 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.
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 then intubated and ventilated (Siemens, Munich, Germany) with
supplemental inhalational isoflurane (1.5–3%). A median sternotomy
was performed, leaving the pericardium intact. Ultrasonic flow probes
(10- to 12-mm perivascular probes with a T206 flowmeter; Transonic
Systems, Ithaca, NY) were placed around the superior (SVC) and
inferior vena cava (IVC) ⬃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).
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Gaynor, Sydney L., Hersh S. Maniar, Sunil M. Prasad, Paul
Steendijk, and Marc R. Moon. Reservoir and conduit function of
right atrium: impact on right ventricular filling and cardiac output.
Am J Physiol Heart Circ Physiol 288: H2140 –H2145, 2005. First
published December 9, 2004; doi:10.1152/ajpheart.00566.2004.—
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 11 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 (SD 0.13) of RA inflow, early conduit for
0.29 (SD 0.07), and late conduit (during RA contraction) for 0.16 (SD
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 (SD 0.11) (P ⬍ 0.04), and the conduit-to-reservoir ratio
decreased by 41% (P ⬍ 0.03). Similarly, after pericardiotomy, early
conduit function fell to 0.14 (SD 0.09) (P ⬍ 0.004), reservoir function
increased to 0.72 (SD 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 than a conduit in a
dynamic manner. The RA conduit-to-reservoir ratio was directly
related to the right ventricular pressure-RA pressure 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.
RA RESERVOIR AND CONDUIT FUNCTION
AJP-Heart Circ Physiol • VOL
Fig. 1. Typical hemodynamic data recorded with the pericardium intact during
the baseline state in 1 animal from this study. Three steady-state beats are
illustrated. The reservoir phase extends from the ECG R wave to the time of
maximum right atrial (RA) volume (corresponding to tricuspid valve opening).
The conduit phase contains 2 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 right ventricular (RV) filling (the subsequent
ECG R wave). RAP, RA pressure; RVP, RV pressure.
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 Fishers 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, Chicago, IL).
RESULTS
Table 1 summarizes the steady-state hemodynamic data
during baseline (pericardium closed), inotropic stimulation
(calcium chloride bolus), and partial PA occlusion and after
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). After a pericardiotomy was
performed, 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 RAP (P ⬎ 0.28), total RA inflow (stroke volume,
P ⬎ 0.40), or cardiac output (P ⬎ 0.32).
Table 2 and Figs. 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
(SD 0.13) of RA inflow [21.1 ml (SD 6.8)], early conduit
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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 steadystate data were obtained. Acute pulmonary hypertension was 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 10-min stabilization period,
the pericardium was opened, and data were again recorded during
steady-state conditions. Complete data with the pericardium intact
were available in 9 of the 11 animals, and complete data with the
pericardium open were available in 7 of the 11 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 change in pressure over time (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) and then subtracted from the pressure differential as
follows: RVP-RAP gradient ⫽ RVP(t) ⫺ RAP(t) ⫺ ⌬PH.
RA reservoir and conduit function. Reservoir and conduit functions
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). Because 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
R wave). 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.
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RA RESERVOIR AND CONDUIT FUNCTION
Table 1. Hemodynamic effects of inotropic stimulation with calcium chloride, acute
partial PA occlusion, and pericardiotomy
Pericardium Closed
Heart rate, beats/min
RA filling time, ms
RA emptying time, ms
Mean RA pressure, mmHg
Maximum RV pressure, mmHg
Maximum RA dP/dt, mmHg/s
Maximum RV dP/dt, mmHg/s
Total RA inflow, ml/beat
Cardiac output, ml/min
Baseline
Calcium
PA occlusion
Pericardium Open Baseline
104 (SD 32)
342 (SD 67)
208 (SD 91)
4.1 (SD 1.7)
25 (SD 6)
177 (SD 56)
1,245 (SD 423)
37.3 (SD 9.6)
3.7 (SD 1.2)
105 (SD 12)
344 (SD 71)
235 (SD 64)
4.6 (SD 1.7)
35 (SD 9)*
225 (SD 73)
1,563 (SD 188)*
36.8 (SD 9.8)
3.8 (SD 0.8)
101 (SD 20)
349 (SD 31)
228 (SD 62)
4.7 (SD 1.7)
38 (SD 10)*
214 (SD 68)
1,472 (SD 274)
33.5 (SD 6.5)
3.3 (SD 0.8)
119 (SD 22)
363 (SD 43)
205 (SD 51)
5.2 (SD 2.1)
22 (SD 3)
223 (SD 94)
997 (SD 173)*
38.8 (SD 6.7)
4.5 (SD 0.9)
function for 0.29 (SD 0.07) [11.2 ml (SD 5.5)], and late conduit
function for 0.16 (SD 0.11) [5.3 ml (SD 2.4)]. Inotropic
stimulation decreased RA inflow volume during the late conduit phase to 3.0 ml (SD 1.0) (P ⬍ 0.02), but the fall in late
conduit function to 0.09 (SD 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
(SD 0.22) at baseline to 0.33 (SD 0.22) (P ⬍ 0.03). After
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 (SD 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) (Fig. 4).
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 include 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 (SD 0.69) to 0.40 (SD 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 conduitto-reservoir ratio from 0.43 (SD 0.49) to 0.62 (SD 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 (SD 0.50) to 0.64 (SD 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 (24), it was noted that RA contractility (atrial kick) fell by 54% and RA compliance rose by 39%
after pericardiotomy. 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 (SD 0.22)
to 0.21 (SD 0.15) (P ⬍ 0.006). Likely, the pericardium has a
greater effect on the thin-walled atria than on the thick-walled
Table 2. Effects of inotropic stimulation with calcium chloride, acute partial PA occlusion, and
pericardiotomy on RA reservoir and conduit function
Pericardium Closed
Baseline
Calcium
PA occlusion
Pericardium Open Baseline
Reservoir volume, ml
Early conduit volume, ml
Late conduit volume, ml
21.1 (SD 6.8)
11.2 (SD 5.5)
5.3 (SD 2.4)
23.2 (SD 6.7)
11.0 (SD 6.0)
3.0 (SD 1.0)*
21.5 (SD 4.3)
7.0 (SD 4.7)*
5.4 (SD 1.3)
27.4 (SD 3.9)
5.8 (SD 4.3)*
5.9 (SD 2.6)*
Reservoir function
Early conduit function
Late conduit function
0.56 (SD 0.13)
0.29 (SD 0.07)
0.16 (SD 0.11)
0.63 (SD 0.10)
0.29 (SD 0.11)
0.09 (SD 0.04)
0.64 (SD 0.08)
0.20 (SD 0.11)*
0.17 (SD 0.06)
0.72 (SD 0.08)*
0.14 (SD 0.09)*
0.15 (SD 0.07)
Early conduit-to-reservoir
0.56 (SD 0.22)
0.50 (SD 0.26)
0.33 (SD 0.22)*
0.21 (SD 0.15)*
Values are means ⫾ SD; n ⫽ 9 for pericardium closed and 7 for pericardium open. *P ⬍ 0.05 vs. pericardium closed baseline. Repeated-measures ANOVA
was used for all comparisons.
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Values are means ⫾ SD; n ⫽ 9 for pericardium closed and 7 for pericardium open. PA, pulmonary artery; RA, right atrial; RV, right ventricular; dP/dt, change
in pressure overtime. *P ⬍ 0.05 vs. pericardium closed baseline. Repeated-measures ANOVA was used for all comparisons.
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RA RESERVOIR AND CONDUIT FUNCTION
ventricles. Nagano et al. (28) found in normal subjects that the
left atrium was less compliant than the left ventricle, facilitating blood transfer between the chambers during the early
conduit phase. 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 Gabel (14) 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). 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 and Gabel’s study was inadequate to maintain
cardiac output, which fell by 20%. In the current study, cardiac
output was inversely related to the conduit-to-reservoir ratio,
Fig. 4. Linear regression analysis comparing the RA conduit-to-reservoir
(C:R) ratio to cardiac output (CO). As the RA conduit-to-reservoir ratio
increased, cardiac output decreased.
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 physiological 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 et al. (21), using myocardial markers on the mitral
valve, demonstrated that the mitral valve moves toward its
Table 3. Effects of RA and RV hemodynamics at the time of
maximum RA volume on RA reservoir and conduit function
Reservoir
Fig. 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 vs. pericardium closed (baseline) (repeatedmeasures ANOVA).
AJP-Heart Circ Physiol • VOL
RA pressure at maximum
RA volume
⬍4.2 mmHg
⬎4.2 mmHg
RV pressure at maximum
RA volume
⬍5.8 mmHg
⬎5.8 mmHg
RV-RA pressure at
maximum RA
volume
⬍0.53 mmHg
⬎0.53 mmHg
Early Conduit
Late Conduit
0.58 (SD 0.18) 0.28 (SD 0.16) 0.15 (SD 0.13)
0.65 (SD 0.15)* 0.21 (SD 0.11)* 0.15 (SD 0.12)
0.64 (SD 0.16) 0.22 (SD 0.12) 0.15 (SD 0.15)
0.59 (SD 0.17)* 0.27 (SD 0.16)* 0.15 (SD 0.09)
0.66 (SD 0.14) 0.22 (SD 0.12) 0.13 (SD 0.10)
0.57 (SD 0.18)* 0.27 (SD 0.16)* 0.17 (SD 0.14)*
Values are means ⫾ SD; n ⫽ 254 including all baseline, calcium chloride,
and partial PA occlusion runs with and without pericardial integrity. *P ⬍ 0.05
for higher values vs. lower values. ANOVA was used for all comparisons.
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Fig. 2. Effects of inotropic stimulation with calcium chloride, acute partial
pulmonary artery (PA) occlusion, and pericardiotomy on RA reservoir and
conduit function. Data represent mean values for reservoir, early conduit, and
late conduit contributions as a percentage of total RA inflow during each
intervention.
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AJP-Heart Circ Physiol • VOL
but future studies are 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, although 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.
Although 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 –20% (30, 34), a
contribution that increases via the Frank-Starling mechanism
after ventricular ischemia (25) and becomes more important to
maintain filling with advanced age and when the ventricle
either dilatates or hypertrophies (14, 34). Work at this laboratory has previously shown (24) that atrial contraction increases
with acute pulmonary hypertension to support ventricular filling but falls when pericardial integrity is lost. 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 et al. (30) found that
the minimum pulmonary venous flow rate rose progressively
with increasing levels of exertion. 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 and 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 physiological
changes but also 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. Although this study examined subjects exposed to acute physiological 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
We gratefully acknowledge Martha L. Lester and Celeste M. Chu for
assistance with the surgical preparation, as well as the technical assistance of
Diane Toeniskoetter and Kathy Fore.
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open position in the isovolumic phase but that the leaflets do
not separate until minimum left ventricular pressure is obtained. A similar phenomenon could occur on the right side of
the heart with the tricuspid valve, and the RA appendage also
may play a role. Hoit et al. (17) elegantly demonstrated the
impact of the left atrial appendage on left atrial compliance and
left ventricular filling. 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, although there was a shift toward
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 et al. (30) demonstrated that with exercise, left
atrial reservoir function increased by 37% and left atrial conduit function decreased by 23%. Although Nishikawa et al. 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 et al.
(32) noted that peak exercise produced a 90% increase in mean
PA pressure with a threefold rise in RAP. In the current study,
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. 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
(SD 0.13) to 0.33 (SD 0.22) (P ⬍ 0.03). Grant et al. (10)
demonstrated that the left atrium acts as a short-term storage
reservoir and that atrial reservoir function is four times more
important than active atrial contraction in providing energy for
the work of ventricular filling. 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,
RA RESERVOIR AND CONDUIT FUNCTION
GRANTS
This study was supported by National Heart, Lung, and Blood Institute
(NHLBI) Grant HL-69949 and by a Foundation Research Grant from the
Thoracic Surgery Foundation for Research and Education. S. L. Gaynor and
H. S. Maniar were also supported in part by NHLBI Grant T32-HL-07776.
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