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J Thorac Cardiovasc Surg 2001;121:0116-0124
© 2001 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Effect of acutely increased left ventricular afterload on work output from the right ventricle in conscious dogs

From The Victor Chang Cardiac Research Institute and Cardiology Department, St Vincent's Hospital, Sydney, Australia.

Supported by a Project Grant from the National Health and Medical Research Council of Australia.

Received for publication Jan 18, 2000. Revisions requested March 14, 2000; revisions received May 1, 2000. Accepted for publication Aug 7, 2000. Address for reprints: Michael P. Feneley, MD, FRACP, FACC, Cardiology Department, St Vincent's Hospital, Darlinghurst, NSW 2010, Australia (E-mail: M.Karunanithi{at}unsw.edu.au).

	Abstract

Top Abstract Introduction Materials and methods Results Discussion References

 
Objective: To determine the effect of acute increments in left ventricular afterload on the stroke work output of the right ventricle in vivo.
Methods: After pharmacologic attenuation of autonomic reflexes, left and right ventricular pressure-volume data were obtained in 9 conscious dogs during vena caval occlusions performed before and during aortic constriction.
Results: The relationship between right ventricular stroke work and end-diastolic volume during vena caval occlusion was highly linear (r = 0.97 ± 0.02), but the slope decreased by 20% ± 13% during aortic constriction sufficient to increase left ventricular mean ejection pressure by 25% ± 14% (P < .05). The volume-axis intercept remained constant. Similarly, the slope of the linear relationship between right ventricular free wall regional segment work and end-diastolic segment length declined by 22% ± 10% during aortic constriction (P < .05), without significant change in the length-axis intercept. The reduction in both global and regional right ventricular stroke work at any given preload with increased left ventricular afterload was due entirely to decreased right ventricular stroke volume and free wall shortening, because right ventricular mean ejection pressure was unchanged. Additional experiments were performed in 5 open-chest dogs to produce a greater reduction in left ventricular free wall shortening than observed with aortic constriction by transient constriction of the left circumflex coronary artery. However, this intervention had no effect on right ventricular free wall segment work output.
Conclusion: Increased left ventricular afterload decreases global and regional right ventricular stroke work at any given preload, a direct, negative systolic ventricular interaction.

	Introduction

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Interactions between the left ventricle (LV) and the right ventricle (RV) during diastole are well characterized: increased filling of either ventricle displaces the interventricular septum toward the opposite ventricle, thereby decreasing the latter's diastolic compliance, ^1-4 an effect enhanced by the intact pericardium. ^3,5,6 Systolic ventricular interactions are less well characterized ⁷ but are of potential significance to the design and operation of ventricular assist devices. ⁸ There is considerable evidence that LV contraction contributes to RV systolic function, ^9-13 but the mechanism of this interaction remains speculative.

Feneley and colleagues ¹⁴ demonstrated previously that acute increments in RV afterload increase the work output from the LV at any given end-diastolic volume (preload), a direct, positive systolic ventricular interaction. Leftward systolic displacement of the interventricular septum due to the increase in RV systolic pressure during increased RV afterload contributes to this interaction. ¹⁴

In this study, we tested the converse hypothesis that acute increments in LV afterload would increase RV stroke work at any given preload. Because the two ventricles are connected in series via the pulmonary and systemic circulations, alterations in LV afterload might influence RV work output by altering RV end-diastolic volume (preload). ¹⁵ To examine the direct ventricular interactive effect of increased LV afterload on RV work output, therefore, we performed transient vena caval occlusions to cause wide variations in RV end-diastolic volume before and during aortic constriction. This experimental approach allowed us to express RV stroke work as a linear function of RV end-diastolic volume ¹⁶ before and during increased LV afterload, thereby accounting for any in-series effects on preload. ¹⁵ We found that increased LV afterload decreased RV stroke work at any given end-diastolic volume: a direct, negative systolic ventricular interaction.

	Materials and methods

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The experiments described herein were approved by our institutional ethics committee and conformed to the guidelines of the National Health and Medical Research Council of Australia.

Experiment 1
Experimental preparation
Nine healthy adult dogs (22-42 kg) were anesthetized (halothane 1%-2% and succinylcholine 0.3 mg · kg^-1 intravenously [iv] after thiamylal sodium 20 mg · kg^-1 iv). Through a left thoracotomy, pulse-transit ultrasonic dimension transducers were positioned across the base-apex (a) and anteroposterior (b) axes of the LV and across the septal–free wall axes of the LV (c) and RV (d). ^14,16,17 An additional pair of transducers was positioned to measure a regional segment length on the RV mid–free wall, perpendicular to the major axis. ¹⁷ Pneumatic occluders were positioned around the inferior vena cava and the descending thoracic aorta. Heparin-filled silicone catheters (2.6 mm in inner diameter) were secured in the base of the left atrial appendage and the apex of the RV. Another catheter with multiple side holes was positioned adjacent to the ventricular epicardium. Because surgical closure of the pericardium over the various devices on the surface of the heart was expected to produce an unphysiologic degree of pericardial constraint, the pericardium was left wide open, and the thoracotomy was repaired. After 7 to 10 days, the transducer leads, catheters, and occluder tubing were exteriorized from a subcutaneous pouch. Each animal, lying quietly on its right side, was studied in the conscious state 1 hour after light sedation (morphine sulfate, 10 mg intramuscularly).

Data acquisition and experimental protocol
Micromanometer-tipped catheters (model MPC-500; Millar Instruments, Inc, Houston, Tex) were passed via the implanted catheters to obtain RV, LV, and pleural pressures. Autonomic reflexes were attenuated with intravenous propranolol (1 mg · kg^-1) and atropine (0.2 mg · kg^-1). Data were recorded under steady-state conditions and during transient vena caval occlusion induced by inflation of the implanted occluder for approximately 10 seconds. After return of all variables to their baseline levels, the descending aortic occluder was inflated sufficiently to achieve a stable increment in LV systolic pressure of approximately 30%. After a 60-second wait to ensure stabilization of all variables at their new levels, thereby excluding any transient effects of increased afterload on LV contractile function, ¹⁸ transient vena caval occlusion was repeated while the aortic constriction was maintained.

Experiment 2
Experimental preparation
We examined the direct influence of reduced LV free wall shortening on RV free wall function in separate open-chest experiments. Five healthy adult dogs (29-40 kg) were anesthetized (fentanyl 0.05 µg · kg^-1 · min^-1 iv and halothane 0.5% after thiopenthal sodium 20 mg · kg^-1 iv). Through a left thoracotomy, a pair of ultrasonic transducers was positioned to measure lateral LV free wall segment shortening in the distribution of the largest ventricular branch of the circumflex coronary artery. The transducers were positioned parallel to the minor-axis plane of the LV. A similar pair of transducers was positioned directly opposite to measure RV free wall segment shortening, as described for experiment 1. A polyester tape was placed around the main circumflex coronary artery to permit controlled reduction in blood flow, which was measured with a flow probe (Transonic Systems Inc, Ithaca, NY). Pneumatic occluders were positioned around the inferior vena cava and the descending thoracic aorta. LV and RV pressures were measured with micromanometers (Millar model MPC-500) introduced through the apex.

Data acquisition and experimental protocol
The same sequence of vena caval and aortic constrictions after pharmacologic attenuation of autonomic reflexes described for experiment 1 was performed. This sequence was then repeated during constriction of the circumflex coronary artery sufficient to achieve approximately 50% reduction in LV free wall segmental shortening.

Data analysis
Data were digitized in real time at 200 Hz. LV chamber volume was calculated from the ultrasonic dimension measurements according to the formula for a general ellipsoid (/6 a · b² – LV wall volume). ¹⁹ RV chamber volume was calculated according to an ellipsoidal shell subtraction model (/6 a · b · d – RV free wall volume). ¹⁷ Postmortem wall volumes were determined by water displacement. LV and RV transmural pressures were calculated as chamber pressures minus pleural pressure. End-systolic pressure was defined at the time when the instantaneous pressure-volume ratio was maximal. The end-systolic pressure-volume relationship (ESPVR) of each ventricle was determined by linear regression analysis. ²⁰

Stroke work for each ventricle was calculated as the pressure-volume loop area for each beat. LV or RV free wall regional segment work was calculated as the pressure-dimension loop area for each beat. Global preload recruitable stroke work (PRSW) relationships between stroke work and end-diastolic volume and regional PRSW relationships between regional segment work and end-diastolic segment length during each vena caval occlusion were determined by linear regression analyses. ^16,17,19

Results are summarized as mean ± SD. Multiple comparisons were performed by analysis of variance. Paired comparisons were made with paired t tests. The effects of increased LV afterload on the ESPVR and PRSW relationships were determined by multiple linear regression analyses. ²⁰

	Results

Top Abstract Introduction Materials and methods Results Discussion References

 
Experiment 1
Representative dynamic data recordings obtained under control conditions and during aortic constriction are shown in Fig 1. Mean baseline data are presented in Table I. RV pressure-volume loops obtained during runs of vena caval occlusion before and during aortic constriction are shown in Fig 2, A and B, together with the corresponding RV PRSW relationships (Fig 2, C). The mean linear regression data are presented in Table II.

View larger version (29K): [in this window] [in a new window]   Fig. 1. Representative cardiac dimensions and pressures recorded under control conditions and during aortic constriction.

View larger version (17K): [in this window] [in a new window]   Fig. 2. RV pressure-volume loops recorded during vena caval occlusions before (panel A, VCO) and during aortic constriction (panel B, AC+VCO), together with the corresponding RV stroke work-end-diastolic volume relationships derived from these loops (panel C).

The RV PRSW relationship was highly linear (Table II), as was the LV PRSW relationship (r = 0.93 ± 0.12). During aortic constriction, the slope of the RV PRSW relationship decreased 20% ± 13% without significant change in the volume-axis intercept (Fig 2). That is, an acute increase in LV afterload decreased RV stroke work at any given end-diastolic volume. This reduction in RV stroke work was due to the reduction in RV stroke volume because there was no significant reduction in RV mean ejection pressure for any given end-diastolic volume (Table II). The slope of the LV PRSW relationship (78.0 ± 13.0 erg ·10³ · mL^-1) decreased slightly with increased LV afterload (71.4 ± 21.7 erg · 10³ · mL^-1) without significant change in the volume-axis intercept (7.3 ± 11.3 mL and 1.1 ± 14.6 mL, respectively).

RV free wall regional pressure-segment length loops obtained during runs of vena caval occlusion before and during aortic constriction are shown in Fig 3, A and B, together with the corresponding RV regional PRSW relationships (Fig 3, C). The results of the regional work analysis mirror those of the global work analysis (Table II). Increased LV afterload decreased the slope of the RV regional PRSW relationship 22% ± 10%, without significantly changing the length-axis intercept.

View larger version (15K): [in this window] [in a new window]   Fig. 3. RV free wall regional pressure-segment length loops recorded during vena caval occlusions before (panel A, VCO) and during aortic constriction (panel B, AC+VCO), together with the corresponding RV regional segment work-end-diastolic segment length relationships derived from those loops (panel C).

Increased LV afterload was associated with a significant increase in all 3 LV end-diastolic dimensions, but the RV septal–free wall dimension at end-diastole did not change significantly (Table I). The reduction in RV stroke volume during increased LV afterload was associated with a significant reduction in shortening of all 3 LV dimensions and the RV septal–free wall dimension. For each of the dogs studied, we computed the steady-state RV stroke work that would have been generated if shortening of the RV septal–free wall dimension had remained unaltered by the increase in LV afterload (Table III), so that the reduction in RV stroke work was due only to the reduction in shortening of the base-apex and anteroposterior dimensions. This analysis indicated that the reduction in shortening of the RV septal–free wall dimension accounted for 34% of the observed reduction in RV stroke work, on average.

View larger version (24K): [in this window] [in a new window]   Fig. 4. Representative dynamic waveforms demonstrating reduction of LV free wall segment shortening with constriction of circumflex coronary artery flow, but no significant change in RV free wall segment shortening or pressure.

	Discussion

Top Abstract Introduction Materials and methods Results Discussion References

Three mechanisms of systolic ventricular interaction have been proposed. First, contraction of either ventricle may displace the interventricular septum toward the opposite ventricle. ^21-24 Second, the attachment of the RV free wall to the LV may permit RV chamber compression by LV contraction, analogous to the action of a bellows. ²⁵ Third, because common muscle fiber pathways encircle both ventricular free walls and others cross through the septum, forming a figure-of-8 pattern, ²⁶ contraction of either ventricle might exert force on the opposite ventricular chamber by axial transmission along these common pathways.

The septal interaction mechanism is operative under conditions of both RV volume and RV pressure overload. ^21-24 The leftward diastolic septal displacement due to RV volume overload is reversed during early systole, resulting in paradoxic systolic motion of the septum into the RV. ²¹ Conversely, leftward systolic septal displacement is a hallmark of RV pressure overload, reflecting the reduced left-to-right systolic transseptal pressure gradient due to the increased RV systolic pressure. ^14,22-24 This mechanism contributes to increased LV stroke work and systolic pressure with increased RV afterload ^14,27 and the leftward shift of the LV ESPVR with increased RV volume. ^5,12,28

The reduction in RV stroke work with increased LV afterload in this study, however, cannot be attributed to a septal mechanism. Shortening of the LV septal–free wall dimension and leftward systolic motion of the septum were impeded by increased LV afterload (Table I). Consequently, the reduced shortening of the RV septal–free wall dimension with increased LV afterload was due entirely to reduced shortening of the RV free wall toward the septum rather than increased motion of the septum away from the free wall.

The fact that increased LV afterload impeded RV free wall fiber shortening might suggest that RV free wall muscle fibers share some of the load "seen" by LV muscle fibers during contraction. Santamore and colleagues ²⁹ demonstrated that incision or ischemia of the LV free wall in the isolated heart caused an immediate fall in RV isovolumic pressure, but these interventions also reduced LV pressure generation. In contrast, we observed no significant reduction in RV free wall shortening, stroke volume, mean ejection pressure, or regional stroke work during an ischemic reduction in regional LV shortening that caused no significant change in LV pressure generation. This finding suggests that the more modest reduction in LV fiber shortening observed with increased LV afterload cannot account directly for the reduction in RV free wall fiber shortening, thus discounting a role for the common fiber pathway mechanism of ventricular interaction.

The more probable explanation is altered RV free wall geometry during increased LV afterload. The increased anteroposterior and base-apex end-diastolic dimensions but unchanged RV free wall end-diastolic fiber length during increased LV afterload imply a flatter RV free wall, as demonstrated by Yamaguchi and colleagues ³⁰ by increasing LV volume relative to RV volume. The increased radius of RV free wall curvature would result in greater systolic stress for the same developed pressure, with a consequent reduction in systolic shortening.

Because septal curvature toward the RV is near maximal under normal loading conditions, ¹⁴ the increment in the transseptal pressure gradient caused by increased LV afterload can cause little increase in septal curvature. The septum is more sensitive to leftward displacement by increased RV afterload because this displacement is associated with a reduction in septal curvature: septal compliance varies with septal position (see Fig 6 of reference 14). This also may explain the absence of a reduction in RV end-diastolic volume or RV end-diastolic septal–free wall dimension with increased LV afterload, particularly in the absence of an intact pericardium. ^3,5,6,15

A reduction in the "bellows" action of LV contraction on the RV ²⁵ also appears to be implicated in the reduction in RV stroke work with increased LV afterload. Increased LV afterload impeded shortening of the anteroposterior and base-apex cardiac dimensions(Table I). It is via its effects on shortening of these dimensions that LV contraction exerts its "bellows" action on the RV. ²⁵ We estimated the contribution of this mechanism to the reduction in RV stroke work by computing the stroke work that would have been generated if shortening of the RV septal–free wall dimension had remained unaltered by the increase in LV afterload(Table III); thus, the reduction in RV stroke work would have been due entirely to reduced shortening of the anteroposterior and base-apex dimensions. This analysis indicated that 34% of the reduction in RV stroke work, on average, could be accounted for by reduced RV septal–free wall shortening, suggesting that the "bellows" mechanism might account for the remaining two thirds of the reduction in RV stroke work.

The ellipsoidal shell subtraction model used to determine RV volume in this study has been validated previously under much more extreme conditions of altered RV and LV geometry than were encountered in the present study. ¹⁷ In that previous study, ¹⁷ the volumes of intracavitary RV and LV balloons were varied independently over the range from 0 to 60 mL. Despite the gross distortions of biventricular geometry and interventricular septal position produced by this procedure, the estimates of RV volume by the ellipsoidal shell subtraction method were shown to be independent of LV volume changes.

The pericardium was deliberately left open in our experiments to avoid an unphysiologic degree of pericardial constraint due to surgical closure and subsequent healing during the 7 to 10 days before data collection. The normal intact pericardium enhances diastolic ^3,5,6,15 and, to a lesser extent, systolic ventricular interaction. ¹⁵ Because we observed a direct ventricular interactive effect of increased LV afterload on RV work output with the pericardium open, it seems likely that this interaction would be greater, if anything, with the pericardium intact.

The data presented in this report provide the first experimental evidence of a direct, negative systolic ventricular interaction. The increment in LV mean ejection pressure induced by aortic constriction was quite modest (25% ± 14%), yet RV stroke work fell by 20% ± 13% for any given end-diastolic volume. This marked sensitivity of RV stroke work to LV afterload contrasts with the fact that proportionately larger increments in RV afterload (a 71% ± 26% increase in RV mean ejection pressure) caused no reduction in RV stroke work for any given end-diastolic volume. ¹⁶ Thus, RV stroke work is more sensitive to LV afterload than to RV afterload, reflecting the normal dependence of RV work output on LV contraction.

	References

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