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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) Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 10 140 140 120 120 100 100 so so to so 40 40 20 20 0 101 201 301 401 101 201 301 401 51f 200 150 1100 51 1 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 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 1135 UNLOAD 200.0 L DRIVE F -100.0 100.0 LVP 0.0 40.0 RYP 0.0 15.0 0 PA -4.0, 0.0 deI LVP IU oc:- n _.nn -& O% ..*F 0.0 - - ----- - -- - del RVP 0.0 0.0 del ape - -5.0 1-_~ -T -.- . I. :*_ - i-- I -_ 0.5 4.5 Sec 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) Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 RA-RV 60 MSEC LV PRESSURE RA-RV 240 MSEC RA-RV 180 MSEC RA-RV 120 MSEC Mr 0L (mmHg) RV PRESSURE 5 f\fVf\fVA~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ (mmHg) PA FLOW I f\JVVf%AIf\rw\J-\x 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 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 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) Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 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 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 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) Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 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 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 1141 10 45 160 40 140 35 120 30 T 100 25 60 20 60 15 40 10 20 5 0 0 1 101 201 301 401 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) Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21712/ on 05/05/2017 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. 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