Download Right Ventricular Systolic Function

Significant Left Ventricular Contributions to
Right Ventricular Systolic Function*
Mechanism and Clinical Implications
William P. Santamore, PhD; and Laman Gray, Jr, MD, FCCP
(Chest 1995; 107:1134-45)
dP/dt=rate of change of pressure
Key words: hemodynamics; myocardial infarction; pressure overload; ventricular interdependence; volume overload
Abnormalities of right ventricular function have
been classically attributed to primary abnormalities of the right ventricular myQcardium, excessive
load imposed on the right ventricular during systole,
diastole, or both, or obstruction to right ventricular
inflow. Recent studies, however, have also suggested
that, in addition to the above mechanisms, left ventricular function may significantly affect right ventricular function. This so-called ventricular interdependence is defined herein as the forces that are
transmitted from one ventricle to the other ventricle
through the myocardium and pericardium, independent of neural, humoral, or circulatory effects.1 These
ventricular independent effects are immediate as
compared with circulatory changes, which require
several beats. Ventricular interdependence is a consequence of the close anatomic association between
the ventricles: the ventricles are encircled by common muscle fibers, share a septal wall, and are
enclosed within the pericardium.
In this article, we will first briefly review the
mechanisms for diastolic ventricular interaction,
followed by a more in-depth review of recent data
showing the importance of systolic ventricular interaction. This will be followed by a brief review of
several clinical pathophysiologic conditions wherein
ventricular interaction is thought to significantly influence right ventricular function.
DIASTOLIC VENTRICULAR INTERACTION
The evidence for diastolic ventricular interaction
*From the Division of Thoracic and Cardiovascular Surgerv,
University of Louisville, Ky.
This study was supported in part by a grant from the Heart and
Lung Institute of Jewish Hospital.
Reprint requests: Dr. Santamore, Dept of Surgery, University of
Louisville, 550 S Jackson Street, Louisville, KY 40202
1134
is indisputable and has been the source of in-depth
reviews.12 Briefly, the volume or pressure in one
ventricle can directly influence the volume and
pressure in the other ventricle. This phenomenon,
ventricular interdependence, was probably first observed by Henderson and Prince3 in 1914 and later
verified in postmortem4'5 and in isolated heart preparations.6-10 Increased distention of either ventricle
during diastole alters the compliance and geometry
of the opposite ventricle. Taylor et a15 and Laks et al,4
in postmortem hearts, and Santamore et a19 and
Elzinga et al7 in isolated beating hearts observed
acute changes in ventricular distensibility caused by
changing the volume of the opposite ventricle. As left
(or right) ventricular volume and pressure increased,
the right (or left) ventricular pressure-volume curve
shifted to the left and became steeper. This diastolic
interaction occurred even with the pericardium
open, although the coupling was stronger with it
closed.8"11'14
Diastolic ventricular interdependence is present
on a moment-to-moment, beat-to-beat basis, ie, part
of the measured diastolic ventricular pressure is
caused by the opposite ventricle. Although always
present, ventricular interdependence is most apparent with sudden changes in ventricular volume. For
example, during spontaneous inspiration, right ventricular dimensions and volume increase.15-18 Concomitant with these changes, left atrial transmural
pressure increases and the septum moves toward the
left ventricle in diastole.18 Left ventricular enddiastolic volume remains either unaltered or decreases. This increase in filling pressure with a
decrease in left ventricular volume is consistent with
a change in left ventricular distensibility. Thus,
diastolic interaction is always present and the interactions are large enough to be of physiologic and
pathophysiologic importance.
SYSTOLIC VENTRICULAR INTERACTION
In recent years, the evidence for systolic ventricular interaction is becoming indisputable. In the sections that follow, we review the studies showing the
existence, magnitude, and mechanisms of systolic
Significant LV Contributions to RV Systolic Function (Santamore, Gray)
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FIGURE 1. From an acute canine study. A, Plot of left and right ventricular pressure. A partial
constriction of the pulmonary artery was released in diastole. On the subsequent systolic contraction,
both left and right ventricular systolic decrease. B, left ventricular pressure plotted before (solid line)
and after (dashed line) pulmonary artery release. C and D, A partial constriction of the aorta was released during diastole, leading to a decrease in both left (,panel C) and right (panel D) ventricular systolic (from reference 2, with permission).
ventricular interdependence.
Existence
Figure 1 (top, A and B) shows
a very simple way
show systolic ventricular interdependence. Left
and right ventricular pressures are recorded, while
suddenly in diastole, a partial constriction of the
pulmonary artery is released (Fig 1, top panels). On
the subsequent systole, not only does right ventricular systolic pressure decrease, but left ventricular
systolic pressure also decreases slightly. Because preload was not altered, only systolic ventricular interdependence can explain this decrease in left ventricular pressure. Figure 1 also shows the complementary
study for the right ventricle. An aortic constriction is
released in diastole, leading on the subsequent systolic contraction to a decrease in left ventricular systolic pressure and also, through ventricular interdependence, to a decrease in right ventricular systolic
to
pressure.
A number of studies have revealed similar observations.7 9 19-26 Initial studies used isolated heart
preparations to break the circulatory connections and
thus show ventricular interdependence. These studies
showed that increasing the pressure or volume in one
ventricle leads to an increase in both the diastolic and
systolic pressure in the other ventricle. Because circulatory connections were disrupted, only a direct
mechanical effect can explain these results.
Further evidence of systolic ventricular interdependence has been presented experimentally by
Oboler et a127 and clinically by Feneley et al.28 These
studies demonstrated the influence of left ventricular
isovolumic pressure on right ventricular pressure.
With normal ventricular conduction, the right ventricular rate of change of pressure (dP/dt) curve is
broad or double-peaked, with one of the peaks corresponding in time to the maximum left ventricular
dP/dt. This relationship between right and left ventricular dP/dt was accentuated during right and left
ventricular endocardial pacing.
Experimental studies have also shown that this
systolic interaction is an immediate effect: rapid
withdrawal or injections into the left ventricle caused
immediate changes in right ventricular pressure and
volume outflow."2129 In an isolated rabbit heart
preparation, Bove and Santamore1 used a high-speed
injector to rapidly infuse 1.5 mL of water into the left
ventricular balloon. This rapid left ventricular volume increase caused an immediate increase in right
ventricular pressure. Similarly, a rapid withdrawal of
fluid from the left ventricular balloon caused an immediate decrease in right ventricular pressure.' Langille and Jones21 showed similar results in an openchest rabbit heart preparation in which the aorta was
rapidly occluded and fluid rapidly infused into the
left ventricle. Sudden aortic constriction in diastole
increased right ventricular systolic pressure and
CHEST / 107 / 4 / APRIL, 1995
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1135
UNLOAD
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FIGURE 2. The upper four tracings are ventricular assist device pneumatic drive pressure (L drive P),
left and right ventricular pressure (LVP and RVP, respectively), and pulmonary artery flow (Qpa). The
lower three tracings are the differences between each beat and the preceding beat (del). During left
ventricular unloading, right ventricular pressure and flow are markedly reduced as a result of systolic
ventricular interaction (from reference 29, with permission).
dP/dt in the subsequent systolic contraction. Small,
rapid oscillations in left ventricular volume produced
left ventricular pressure oscillations with coincident
oscillations in right ventricular pressure. In whole
animal studies, Woodard et a129 used a ventricular
assist device to withdraw rapidly blood from the left
ventricle. This withdrawal occurred in systole during
a single cardiac cycle. Figure 2 shows the typical response. The withdrawal of blood from the left ventricle caused a rapid decrease in left ventricular
pressure. Right ventricular pressure and flow outflow
also decreased, resulting in a large change in developed pressure and outflow.
These studies show that systolic ventricular interdependence can have a purely systolic component.
Injection or withdrawal of fluid from the left ventricle during systole caused immediate changes in right
ventricular pressure.
Magnitude
Although these studies proved the existence of
systolic ventricular interdependence, they did not
quantify the magnitude of systolic interdependence
on right ventricular function. Are these observations
just interesting phenomena or are they physiologically important with significant clinical implications?
Two studies addressed this question and quantified
the magnitude of this left ventricular assistance, us1136
ing a unique electrically isolated right heart preparation.30'31 The electrically isolated right heart preparation allowed for wide variations in the timing interval between right and left ventricular contractions.
Double-peaked waveforms for right ventricular pressure and pulmonary artery blood flow occurred over
a wide range (0 to 300 ms) of pacing intervals
between the left and right ventricles (Fig 3). Numeric
analysis indicated that these pressures and volume
waveforms were due to two components.29 One
component could be directly related to right ventricular contraction, while the other component was
directly related to left ventricular contraction (Fig 4).
Left ventricular systolic pressure was due primarily
to left ventricular contraction. For left ventricular
pressure, the left ventricular component was significantly larger than the right ventricular component
(92.7% ± 3.2% vs 7.3% ± 3.2% peak-to-peak value,
p<0.01; 95.2% ± 1.8% vs 4.8% ± 1.8% root-meansquare value, p<0.01). Right ventricular systolic
pressure and pulmonary artery blood flow were
composed of both right ventricular and left ventricular components, with the left ventricular component dominating. For right ventricular pressure, the
left ventricular component was significantly greater
than the right ventricular component (63.5% ± 10.9%
vs 36.5% ± 10.9% peak-to-peak value, p<0.05;
65.2% ± 10.4%
vs
34.8% ± 10.4% root-mean-square
Significant LV Contributions to RV Systolic Function (Santamore, Gray)
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RA-RV
60 MSEC
LV
PRESSURE
RA-RV
240 MSEC
RA-RV
180 MSEC
RA-RV
120 MSEC
Mr
0L
(mmHg)
RV
PRESSURE 5
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(mmHg)
PA
FLOW
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FIGURE 3. LV pressure, RV pressure, and volume outflow are presented at 60-, 120-, 180-, and 240-ms
delay between RA and RV pacing. At 60-ms delay, RV pressure and volume outflow are double-peaked
waveforms with one peak occurring before LV pressure. At 240-ms delay, RV pressure and volume
outflow are again double-peaked waveforms but with one peak occurring after LV pressure (from reference 30, with permission).
A
B
CASE 5216
LEFT COIPONENT OF LEFT PRESSURE
CASE 5216
LEFT COIPOENT OF RIGHT PRESSURE
125mm Hg-
0
RIGHT COMPONENT OF RIGHT PRESSURE
RIGHT COIPONENT OF LEFT PRESSURE
75mm Hg
15mm
Hg
0-
I
400 ms
l
400
ms
FIGURE 4. Computer analysis of the data in Figure 3. With the use of numeric analysis, left and right
ventricular pressure waveforms were separated into left and right components. A, Left and right components for LV pressure. As is apparent, most LV pressure can be associated with left component. B,
Left and right components for RV pressure and volume outflow, respectively. RV pressure has significant left and right components (from reference 30, with permission).
value, p<0.05).
Similarly, for pulmonary artery blood flow, the left
ventricular component was significantly greater than
the right ventricular component (67.5% ±9.0% vs
32.5% ± 9.0% peak-to-peak value, p<0.05; 68.3% ±
3% vs 31.8% ± 8.9% root-mean-square value, p<0.05).
This study shows that left ventricular contraction is
very important and may be the primary source for
right ventricular developed pressure and volume
outflow.30
With the same type of experimental preparation,
Goldstein et a13' examined the mechanism for right
ventricular contraction when the right ventricular
free wall was electrically silent. Ultrasound showed
that right ventricular free wall dyskinesis increased
right ventricular end-diastolic size (155% ± 13% of
control), but decreased left ventricular size
(69% ± 11 % of control). The septum showed reverse
curvature in diastole and bulged paradoxically into
the right ventricle in early systole, generating the
initial peak in right ventricular pressure and reducing its volume. Later, posterior septal motion coincided with maximal left ventricular pressure and the
second peak of the right ventricular pressure waveCHEST /10714/APRIL, 1995
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1137
form. Therefore, when contractility of the right
ventricular free wall is acutely depressed, right ventricular performance is dependent on left ventricleseptal contraction.
Mechanism
The above studies have shown clearly that ventricular interdependence exists, and that a significant
portion of right ventricular developed pressure and
volume outflow depends on left ventricular function.
Further, these studies have shown that this systolic
interaction is immediate: rapid withdrawal or injection of fluid into the left ventricle causes immediate
changes in right ventricular pressure and volume
outflow 1,21,29
Because of its position between the two ventricles,
the septum has been identified as a key element for
ventricular interaction. Several studies have demonstrated alterations in the normal end-systolic septal
shape and position with alterations in systolic loading
conditions. For instance, right ventricular hypertension caused a progressive leftward shift in septal position during systole.32 Pulmonary artery constriction
caused a leftward septal shift.3335 In human subjects,
increased right ventricular loading, by the Mueller
maneuver18 or by pulmonary embolism,36 caused
end-systolic septal flattening and leftward shift. It has
been inferred from such studies that the end-systolic
septal shape and position depend on the transseptal
pressure gradient. Such a view is also supported by
the tight linear relationship between the transseptal
pressure gradient and the end-systolic septum to right
ventricular free wall distance.37
The fact that systolic flattening and leftward shift
exist at end-systole, however, even though the left
ventricular end-systolic pressure exceeds the right
ventricular end-systolic pressure,32 suggests that additional factors are involved. One such factor is the
end-diastolic position of the septum, which has been
shown to determine both the magnitude and direction of septal motion during systole.38-40 In addition,
right ventricular volume loading, which shifts the
septum leftward in diastole, causes passive stretching
of the septal muscle fibers, which, in turn, induces an
increased active systolic shortening.41 Such an alteration in contraction can alter the end-systolic septal
position, regardless of the transseptal pressure.
Based on the concept that ventricular interdependence occurs primarily through the septum, several
models have been developed to explain interaction.
Elzinga et a17 described the shape of both ventricles
by a combination of ellipsoids and showed that right
ventricular volume was inversely related to left ventricular volume. Mirsky and Laks42'43 proposed a
model in which the effective left ventricular external
138
pressure was expressed as a weighted average of the
right ventricular and pericardial pressures. Maughan
et al,24 Little et al,44 and Santamore et al45'46 developed models based on simple definitions for volume
and regional elastances.
The above models imply that all interactions occur
through the septum, and that no direct transfer of
forces between the left and right ventricular free
walls occurs. However, this view is not consistent with
experimental results. Yamaguchi et a147 observed that
increasing left ventricular volume altered the diastolic dimension of the right ventricular free wall and
that increasing right ventricular volume not only alters septal position and dimensions but also caused
regional deformation in the left ventricular free wall.
Goto et a148 showed that increasing right ventricular
pressure by pulmonary artery constriction caused
nonuniform regional changes in systolic shortening in
the anterior, posterior, and lateral walls of the left
ventricle and the septum. In an isolated rabbit heart
preparation, Santamore et a120 produced left ventricular free-wall ischemia by ligating the anterior ventricular branches of the left coronary artery. This ligation caused a rapid decrease in right ventricular
developed pressure. In an isolated rabbit heart preparation, the left ventricle was vented, and thus, left
ventricular cavity pressure was zero.49 Cutting the
left ventricular free wall from the atrioventricular
orifice to the apex prevented the left ventricle from
generating wall stress during systole and thereby
eliminated left ventricular free wall contributions to
right ventricular developed pressure. After cutting
the left ventricular free wall, right ventricular developed pressure fell dramatically. Suturing the left
ventricular free wall reestablished right ventricular
developed pressure.
These findings imply that interaction causes overall ventricular deformation. Thus, although we agree
that the septum is important in systolic interaction,
we think that ventricular interdependence affects the
whole heart: the right ventricular free wall, the left
ventricular free wall, and the septum. In 1977, Seki
et al50 proposed the first model that attempted to
explain ventricular interdependence by considering
wall stress. Seki et a150 modeled the biventricular
cross-section as a circular left ventricle with the right
ventricular free wall as a portion of a circle overlapping part of the left ventricle. Forces at the interventricular sulcus were computed. However, the
analysis did not allow deformation.
To model ventricular interdependence, Beyar et
al5l and Taher52 expanded the ideas of Seki et aM50 and
developed an analytical model based on the balance
of forces at the sulcus (Fig 5). This configuration
highlights forces at the sulci and is useful in analyzing the mechanical interplay of forces at these juncSignificant LV Contributions to RV Systolic Function (Santamore, Gray)
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RV Free Wall
aspects of this interaction.
HEMODYNAMIC CONSEQUENCES OF SYSTOLIC
VENTRICULAR INTERDEPENDENCE
~-'--~
5' LV Free Wall
y
A
Ti
FIGURE 5. Balance of forces at the interventricular sulcus. Top
panel shows cross section of heart. The summation of the forces
at the sulcus is zero. The bottom panel shows how the stress or
tension (TI) in the left ventricular free wall is balanced by the
tension in both the septum (Ts) and right ventricular free wall
(Tr).
tions. Beyar et al5l compared the model with data
from animal experiments subjected to aortic and
pulmonary constriction. The model predicted the
observed shift in the pressure-area relationship of
each ventricle by a change in loading of the opposite
ventricle and predicted that large transmural gradients in stress and strain are associated with septal inversion. Thus, the model and the experimental data
agree and describe the important factors that modulate diastolic septal mechanics during acute differential ventricular loading.
The model shows that interactions are sensitive to
the material properties of the heart wall as well as to
cardiac dimensions. For example, diastolic interaction, similar to that measured experimentally, appears to be possible only if the material nonlinearities
of the three walls are different. Taher52 applied this
model to study systolic ventricular interdependence
and was able to simulate most of the important
Right Ventricular Volume Overload
Right ventricular volume overload provides a great
example of both diastolic and systolic ventricular interdependence. Right ventricular volume overload,
resulting from atrial septal defect, tricuspid insufficiency, or pulmonary insufficiency, causes an increase in right ventricular end-systolic and enddiastolic volumes with normal right ventricular ejection fraction.53'54 Left ventricular end-diastolic
volume is decreased with normal left ventricular
end-diastolic pressure53'5.5'56 and left atrial systolic
contribution to late diastolic filling is reduced compared with normal subjects.57'58 Left ventricular
stroke volume and stroke work indexes are decreased.5559 In younger children, left ventricular
ejection fraction is decreased53'56'59 while in older
patients, the left ventricular ejection fraction and
circumferential fiber shortening are normal or only
slightly depressed.55'60 Analysis of systolic time intervals showed a decrease in the left ventricular
ejection time index, an increase in the preejection
period index, and an increase in the preejection period index divided by the left ventricular ejection
time index.59'61 Left ventricular response to exercise
can be depressed.
Thus, with right ventricular volume overload,
there is evidence for left ventricular dysfunction, although left ventricular failure probably does not occur until right ventricular failure is evident. The
mechanism for the left ventricular dysfunction is
thought to be a mechanical interaction between the
ventricles.40'60'62-65 This mechanism has been documented in patients by Weyman et al.40 Using crosssectional echocardiography, they observed a change
in the diastolic shape of the left ventricle with right
ventricular volume overload. The change in configuration was confined mainly to the interventricular
septum and ranged from a slight flattening of the
normal septal curvature to a complete reversal of the
direction of curvature with the septum concave
toward the right ventricle and convex toward the left
ventricle. In systole, the left ventricle reassumed a
normal or relatively normal circular shape (Fig 6).
This change in the interventricular septum from a
flattened or inverted shape during diastole to normal
in systole resulted in a net motion of the septum away
from the normal center of curvature in the left ventricle and toward the anterior chest wall and right
ventricle.66
The alteration in the left ventricular diastolic
configuration appears to be the reason for the deCHEST/ 107/4/APRIL, 1995
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1139
FIGURE 6. This figure illustrates the changes in diastolic septal
position that occur with right ventricular volume overload (from
reference 40, with permission).
creased left ventricular distensibility and the reduced
left ventricular end-diastolic and stroke volumes. It is
interesting to speculate that the net motion of the
interventricular septum into the right ventricular
cavity in systole provides a left ventricular assist to
right ventricular function. Since the right ventricle
has a large surface area to volume ratio, small changes
in the septum-to-free-wall distance will cause a large
volume displacement.67 Thus, the interventricular
septum moving from a flattened or inverted position
in diastole to a normal position in systole would cause
a considerable amount of blood to be ejected from the
right ventricle. This mechanism might account for
the normal right ventricular ejection fraction and the
slight depression in left ventricular systolic function
in patients with right ventricular volume overload.
Right Ventricular Pressure Overload
Right ventricular pressure overload also provides
an example of both diastolic and systolic ventricular
interdependence. Right ventricular pressure over1140
load caused by pulmonary constriction or pulmonary
embolism decreases cardiac output. In experimental
studies in which the pulmonary artery is progressively constricted, right ventricular systolic pressure
initially increases. Right ventricular end-diastolic
and end-systolic volume also increase, and most
studies show an inverse relationship between right
ventricular ejection fraction and afterload (pulmonary artery pressure or pulmonary vascular resistance).68-72 Eventually, with further pulmonary artery constriction, right ventricular failure occurs with
a definable end point: right ventricular systolic pressure increases until a point at which right ventricular systolic pressure fails to rise further, and a
progressive decline in function is initiated. This coincides with large decreases in cardiac output and
systemic pressure.73-77
Right ventricular pressure overload also affects left
ventricular function: left ventricular ejection fraction, stroke volume, end-diastolic volume, and endsystolic volume decrease and the isovolumic relaxation time of the left ventricle is prolonged.34'78'79
The left ventricular volume decreases are associated
with a greater reduction in the left ventricular septal-lateral axis both at end-diastole and end-systole, as
compared with anterior-posterior axis. Total axis excursion or degree of systolic shortening also decreased. Thus, similar to right ventricular volume
overload, right ventricular pressure overload distorts
left ventricular end-diastolic geometry. However, in
contrast to right ventricular volume overload, with
right ventricular pressure overload, the left ventricle
does not return to its normal shape in systole.34'80'81
For instance, pulmonary artery constriction significantly decreased the end-systolic septum to left ventricular free wall distance, indicating a leftward
septal shift.335 In human subjects, increased right
ventricular loading, by the Mueller maneuver18 or by
pulmonary embolism,36 caused end-systolic septal
flattening and leftward shift. However, this abnormal
septal motion is reversible. In a patient who sustained
massive pulmonary embolism,82 paradoxic septal
motion in the left ventricle immediately returned to
normal after embolectomy.
In an experimental model of chronic severe emphysema, left ventricular ejection fraction, mean
velocity of circumferential shortening, and rate of
anterior-posterior dimensional shortening were reduced compared with baseline values.83 The endsystolic volume was increased for a given end-systolic
pressure or stress at the post-i-year study compared
with baseline values, while fractional shortening was
decreased. In dogs, chronic right ventricular hypertrophy altered left ventricular geometry, mass, and
material properties.84 In humans, chronic cor pulmonale caused pathologic changes in both ventricles,
Significant LV Contributions to RV Systolic Function (Santamore, Gray)
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ie, increased wall thickness, myocyte diameter, and
the percent of fibrosis in the walls.85
Angiographic and echocardiographic data from
patients with chronic pulmonary hypertension have
also shown comparable abnormalities in septal geometry and motion.86'87 In children, right ventricular hypertension caused a progressive leftward shift
in septal position during systole, with resultant septal flattening and a decrease in curvature.32 In these
patients, the septal free wall axis was shortened at
end-diastole; the septum was flattened and posteriorly displaced.86 During systole, brisk anterior motion of the septum occurred initially and was followed by more gradual posterior displacement during ejection.87 Thus, the available data suggest that
perturbations in dynamic left ventricular geometry
can occur during either acute or chronic pressure
overload of the right ventricle.
The series circulatory connections and ventricular
interdependence help to explain the observed responses to right ventricular pressure overload. Left
ventricular filling is compromised by the decrease in
right ventricular output: the series connection. Left
ventricular filling is further compromised by the increased right ventricular diastolic volume: the ventricular interdependence component. The increased
right ventricular diastolic volume alters left ventricular compliance, making it harder to fill the left
ventricle. The observed changes in left ventricular
isovolumic relaxation, shape, and septal position reflect this altered compliance. With reduced filling,
left ventricular systolic pressure and stroke volume
decrease, and left ventricular ejection fraction decreases slight. Again, this is reflected in the observed
changes in left ventricular septal position that persist
throughout systole.
In turn, via ventricular interdependence, the decrease in left ventricular systolic function decreases
left ventricular assistance to right ventricular function. This sets up a positive feedback mechanism: the
decreased left ventricular assistance decreases right
ventricular systolic pressure and stroke volume, which
decrease left ventricular filling leading to a decrease
in left ventricular systolic pressure. This leads to a
further decrease in left ventricular assistance and
right ventricular systolic pressure and stroke volume.
This ventricular interdependence-positive feedback
mechanism is partially the cause for the circulatory
failure. A corollary of ventricular interdependence
mechanism is that if left ventricular systolic function
(and its assistance to the right ventricle) could be
maintained, then the right ventricle could reach
greater systolic pressure levels before circulatory
failure would occur.
The early studies on right ventricular pressure
overload attributed failure primarily to the inability
of right ventricular myocardial blood flow to increase. These studies suggested that the maximal
right ventricular systolic pressure is determined primarily by myocardial perfusion pressure. Increasing
myocardial blood flow helped to restore or maintain
function. Most studies, however, increased flow by
increasing aortic, and thus left ventricular, pressure.
For example, Salisbury73 produced recovery from
afterload-induced right ventricular failure by occluding the aorta. He postulated that this occlusion
raised coronary artery driving pressure, produced
recovery from ischemia, and therefore improved
function. Similar results were obtained by other investigators who produced similar recovery from
failure by mechanically or pharmacologically increasing aortic pressure.74-77
More recent studies suggest that, independent of
blood flow, reestablishing left ventricular systolic
pressure can restore right ventricular function.88'89 In
pulmonary embolic shock, which showed a fall in left
ventricular pressure to about 60 mm Hg and cardiac
output to about 40% of control, the leftward displacement of interventricular septum became
marked, and the cooperative movement of interventricular septum to left ventricular contraction disappeared. Ligating the descending aorta or norepinephrine administration improved the deteriorated
hemodynamics with restoration of biventricular ge-
ometry.88
In an acute canine preparation, with progressive
pulmonary artery constriction, maximal generated
right ventricular pressure was studied with the right
coronary artery cannulated and maintained at constant perfusion pressure.89 In all preparations, the
maximal pressure the right ventricle could generate
was linearly related to left ventricular systolic pressure. Maintaining constancy of right coronary artery
perfusion pressure, either at high or low values, did
not alter these findings. These results suggested that
right ventricular perfusion may not be the sole
determinant of maximal right ventricular function.
These results suggest the importance of the maintenance of systemic pressure for the restoration of
failed right ventricular function.88
Right Ventricular Myocardial Infarction
Acute right coronary artery occlusions proximal to
the right ventricular branches compromise right
ventricular free wall perfusion, resulting in right
ventricular dysfunction in nearly 50% of patients
with transmural inferoposterior myocardial infarctions.90-93 Acute ischemia leads to right ventricular
free wall dyskinesis and depressed global right ventricular performance,94-98 resulting in diminished
peak pressure, delayed relaxation, and right ventricular enlargement. A spectrum of hemodynamic
CHEST / 107 / 4 / APRIL, 1995
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1141
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1
51
FIGURE 7. From the same study as Figure 1. A and B, An acute myocardial infarction, restricted solely
to the left ventricular free wall, was created. Suddenly releasing the aortic constriction causes a much
smaller decrease in right ventricular pressure (from reference 2, with permission).
perturbations is manifest in about 50% of patients
with ischemic right ventricular involvement. In its
severe form, acute right ventricular infarction can
cause severe circulatory instability and life-threatening hypotension. The clinical syndrome of predominant right ventricular infarction develops, characterized by right heart failure with clear lung
fields.91-93'99"100 Hemodynamic evaluation in such
patients typically reveals disproportionate elevation
of right-sided filing pressures, equalization of rightand left-sided diastolic pressures, and low cardiac output despite preserved left ventricular contractility.
Ventricular interdependence helps to explain the
observed hemodynamic responses due to right ventricular infarction. For example, Calvin101 showed
the impact of right ventricular volume changes on
left ventricular compliance following right ventricular free wall ischemia. In mongrel dogs, right ventricular infarction increased right ventricular diastolic size, but reduced stroke volume by 30%. Left
ventricular end-diastolic segment length decreased,
while left ventricular end-diastolic pressure increased. Volume loading restored cardiac output to
baseline values. This was achieved by increasing right
ventricular end-diastolic pressure from 9 to 16 mm
Hg. Complete opening of the pericardium significantly decreased right and left ventricular end-diastolic pressures, increased end-diastolic segment
lengths, resulting in an increase in cardiac output and
stroke volume. Thus, via ventricular interdependence, left ventricular diastolic pressure-segment
length relations were shifted upward by right ventricular infarction. This effect was augmented by the
pericardium and contributed to the reduced left
ventricular filling and cardiac output following right
ventricular infarction.
Systolic coupling between the ventricles, and thus
left ventricular assistance, is also depressed by right
ventricular free wall ischemia.102 In eight acute canine studies, ventricular coupling was assessed by
measuring the changes in pressure caused by aortic
constriction during diastole. Measurements were obtained in control, after right coronary artery occlu1142
sion, and then after injecting glutaraldehyde into the
right ventricular free wall. Left-to-right ventricular
coupling decreased from control (11%) to ischemia
(8%) and increased with glutaraldehyde (15%). Thus,
acute ischemia in right ventricular free wall decreased the magnitude of systolic ventricular interdependence from left ventricle to right ventricle,
while glutaraldehyde, which stiffens the right ventricular free wall, increased the magnitude.
From this canine study, Figure 7 shows the effects
of a right ventricular infarction on systolic ventricular interdependence. A purely right ventricular freewall infarction was created by occluding the right
coronary artery and collateral vessels. The animal
was given a volume infusion of dextran to partially
restore the ventricular pressure. Releasing the aortic
constriction in diastole still resulted in a decrease in
right ventricular systolic pressure on the subsequent
systolic contraction; however, the magnitude of systolic ventricular interdependence was decreased.
Systolic right ventricular pressure decreased by 2.2
mm Hg; only 2.9% of the left ventricular pressure
change was transmitted to the right ventricle. Considering the beat before aortic release, if we assume
that all the left ventricular systolic pressure (129 mm
Hg) is transmitted (XO.029) to the right ventricle,
then 5.2 mm Hg, or 16%, of the total measured right
ventricular pressure (32 mm Hg), was generated by
the left ventricle.
Despite diminished coupling, interventions that
depress left ventricular function further depress right
ventricular function, and conversely interventions
that increase left ventricular function augment right
ventricular function. Goldstein et a198 showed that, in
dogs, right coronary branch occlusions led to right
ventricular dilation and free wall dyskinesia, reversed septal curvature, and reduced left ventricular
diastolic volume. In systole, the septum returned to
its normal position, thereby bulging into the right
ventricle generating an active but depressed right
ventricular systolic pressure (29 to 22 mm Hg), with
associated decreases in right ventricular stroke work
(5.7 to 1.9 g inm/m2) and left ventricular systolic
Significant LV Contributions to RV Systolic Function (Santamore, Gray)
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pressure (123 to 80 mm Hg). Septal ischemia induced
systolic septal thinning, left ventricular dilation, and
decreased left ventricular systolic pressure (80 to 55
mm Hg) and stroke work. There were further
decrements in right ventricular systolic pressure (22
to 19 mm Hg) and stroke work (1.9 to 0.7 g m/mi2).
Dopamine infusion augmented left ventricular free
wall contraction and increased left ventricular systolic pressure (55 to 172 mm Hg) and stroke work.
The extent of septal displacement into the right
ventricle increased strikingly and, despite continued
right ventricular free wall dyskinesia, right ventricular systolic pressure increased (19 to 40 mm Hg) as
did right ventricular stroke work (0.7 to 7 g im/mi2).
Therefore, left ventricular function is an important
determinant of right ventricular performance during
right heart ischemia. Septal dysfunction, which depresses left ventricular function, diminishes this
interaction, whereas inotropic stimulation, which
augments left ventricular function, increases this
compensatory mechanism.
Thus, ventricular interdependence helps to explain
the observed hemodynamic responses due to right
ventricular myocardial infarction. Via interdependence, right ventricular diastolic volume increase
changes effective left ventricular compliance, making it harder to fill the left ventricle. With reduced
filling, left ventricular systolic pressure decreases,
which leads to a decrease in left ventricular assistance
to right ventricular function. Additional right ventricular ischemia, by altering right ventricular free
wall elastance, can decrease ventricular coupling and
left ventricular assistance. The left ventricle, however, still helps to maintain right ventricular function, and interventions that improve left ventricular
function also improve right ventricular function.
ACKNOWLEDGMENT: The authors thank Jennifer Skerrett for
her expertise and careful preparation of this manuscript.
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