Resetting of regional preload due to ventricular shape change alters diastolic and systolic performance

1993 ◽  
Vol 265 (5) ◽  
pp. H1629-H1637 ◽  
Author(s):  
S. Yamaguchi ◽  
Y. Tamada ◽  
H. Miyawaki ◽  
Y. Niida ◽  
A. Fukui ◽  
...  
Keyword(s):  
Shape Change ◽  
Interventricular Septum ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Chamber Pressure ◽  
Right Ventricular Free Wall ◽  
Active Length ◽  
Wall Area ◽  
Ventricular Interaction ◽  
Regional Area

The diastolic and systolic pressure of one ventricle is increased by an increase in volume and/or pressure of the opposite ventricle; however, a mechanism for the ventricular interaction remains unclear. We hypothesized that the shape change of one ventricle elicited by the opposite ventricle would lead to resetting of the regional length, which may explain the ventricular interaction. We used 15 cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were independently controlled. Diastolic regional segment area was calculated by multiplying circumferential and longitudinal lengths on right ventricular free wall (RVFW; n = 6), interventricular septum (IVS; n = 11), and left ventricular (LV) FW (n = 12). The regional area at relatively small volumes of both ventricles were expressed as 100%. With constant RV volume, increasing LV from 7 to 19 ml increased RV diastolic and systolic pressures by 2.7 and 5.5 mmHg, respectively. Conversely, increasing RV volume increased LV diastolic and systolic pressures by 2.3 and 7.5 mmHg, respectively. Increasing LV volume increased RVFW regional area from 121.0 to 124.6% (P < 0.01) and increased IVS regional area from 103.3 to 108.7% (P < 0.01), whereas the RV volume was held constant. Increasing RV volume also increased LVFW and IVS regional areas from 109.9 to 111.6% (P < 0.01) and from 106.8 to 108.9% (P < 0.05), respectively. Ventricular shape change elicited by ventricular interaction will increase the regional wall area, even though the volume of the chamber is unchanged. The increase in the regional area alters the position of the tissue on its resting and active length-tension relations and, thus, leads to enhancement of the chamber pressure.

Chronic pressure overload hypertrophy decreases direct ventricular interaction

1987 ◽  
Vol 253 (2) ◽  
pp. H347-H357 ◽  
Author(s):  
B. K. Slinker ◽  
A. C. Chagas ◽  
S. A. Glantz
Keyword(s):  
Interventricular Septum ◽  
Systolic Pressure ◽  
Pressure Overload ◽  
Direct Interaction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Size ◽  
Left Ventricular Size ◽  
Concentric Hypertrophy ◽  
Ventricular Interaction

We studied the relative roles of direct (via the interventricular septum) and series (via the pulmonary circulation) ventricular interaction in hearts with concentric left ventricular hypertrophy by using statistical models to analyze the transient responses in right and left ventricular pressures and dimensions to occlusions of the venae cava and pulmonary artery in five open-chest anesthetized dogs. The left ventricles of these dogs had moderate concentric hypertrophy (31% increase in mass) induced by 3 mo of renovascular hypertension [peak left ventricular pressure = 160 +/- 13 (SD) mmHg]. At end diastole we found that direct interaction was only about one-tenth as important as series interaction in determining left ventricular size with the pericardium around the heart. At end systole we found that direct interaction was about one-fifth as important as the end-systolic pressure-volume relationship in determining left ventricular size. Removing the pericardium decreased the importance of direct interaction. Direct interaction is less important in these hearts than in normal hearts, probably because the septum is thicker and, hence, less distensible. This change in the relative importance of direct ventricular interaction with hypertrophy complicates comparison of pressure-volume relationships between normal and hypertrophied hearts.

Left-to-right systolic ventricular interaction in patients undergoing biventricular stimulation for dilated cardiomyopathy

2010 ◽  
Vol 109 (2) ◽  
pp. 418-423 ◽  
Author(s):  
Giuseppe Osculati ◽  
Gabriella Malfatto ◽  
Roberto Chianca ◽  
Giovanni B. Perego
Keyword(s):  
Right Ventricular ◽  
Dilated Cardiomyopathy ◽  
Biventricular Pacing ◽  
Interventricular Septum ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Data Set ◽  
Ventricular Interaction ◽  
Left And Right ◽  
The Right

Left-to-right systolic ventricular interaction (i.e., the phenomenon by which the left ventricle contributes to most of the flow and to two-thirds of the pressure generated by the right ventricle) originates from transmission of systolic forces between the ventricles through the interventricular septum and from the mechanical effect of the common muscle fibers encircling their free walls. As a consequence, any reduction of left ventricular free wall function translates in lower right ventricular pressure or function. We investigated whether systolic ventricular interaction could be evidenced in nine patients with dilated cardiomyopathy in whom a biventricular pacemaker was implanted. Changes in right and left ventricular pressures were measured with high-fidelity catheters, before and after periods of biventricular pacing from the right atrium with different stimulation intervals to the right and left ventricles, respectively. The steady-state changes of left and right ventricular systolic pressure obtained from any single pacing interval combination were considered. We then calculated, with a two-level mixed regression analysis of the entire data set, the relation between changes in left and right systolic pressures: the presence of a statistically significant slope was assumed as evidence of ventricular interaction. The slope of the regression replaced the crude pressure ratio as an estimate of the gain of the interaction; its value compared with values observed in experimental studies. Moreover, its dependence on septal elastance and on right ventricular volume was similar to that already demonstrated for ventricular interaction gain. In conclusion, the linear relationship we found between systolic pressure changes in the two ventricles of patients with dilated cardiomyopathy during biventricular pacing could be explained in terms of ventricular interaction.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

End-systolic and end-diastolic ventricular interaction

1986 ◽  
Vol 251 (5) ◽  
pp. H1062-H1075 ◽  
Author(s):  
B. K. Slinker ◽  
S. A. Glantz
Keyword(s):  
Right Ventricular ◽  
Interventricular Septum ◽  
Systolic Pressure ◽  
Direct Interaction ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Physiological Mechanisms ◽  
In Series ◽  
The Right ◽  
Transient And Steady State

Right ventricular volume affects left ventricular volume via direct interaction across the interventricular septum and series interaction because the right and left hearts are connected in series through the lungs. Because it is difficult to sort out complex physiological mechanisms in the intact circulation, the relative importance of these two effects is unknown. We used statistical analyses of transient changes in left and right ventricular pressures and dimensions following pulmonary artery and venae caval constrictions to separate and quantitate the direct (immediate) from the series (delayed) interaction effects on left ventricular size at end systole and end diastole. With the pericardium closed, direct interaction was one-half as important as series interaction at end diastole and was one-third as important at end systole. With the pericardium removed, direct interaction was one-fifth as important as series interaction at end diastole and one-sixth as important at end systole. These results suggest that differences between transient and steady-state end-systolic pressure-volume relationships are largely explained by direct interaction and that direct end-systolic interaction is important for maintaining balanced right and left heart outputs.

Effects of free wall ischemia and bundle branch block on systolic ventricular interaction in dog hearts

1994 ◽  
Vol 266 (3) ◽  
pp. H1087-H1094 ◽  
Author(s):  
H. Yaku ◽  
B. K. Slinker ◽  
S. P. Bell ◽  
M. M. LeWinter
Keyword(s):  
Right Ventricular ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Free Wall ◽  
Ventricular Pacing ◽  
Aortic Constriction ◽  
Bundle Branch Block ◽  
Ventricular Interaction ◽  
Right Ventricular Stroke Volume

Systolic direct ventricular interaction is thought to occur via the ventricular septum and the coordinated contraction of common fibers shared by both ventricles. The purpose of the present study was to evaluate the effects of transient free wall ischemia and bundle branch block, which disrupt the coordinated contraction of shared common fibers, on left-to-right systolic ventricular interaction. We produced transient right and left ventricular free wall ischemia by 2-min coronary artery occlusions and bundle branch block by ventricular pacing in nine in situ dog hearts. To eliminate any confounding effect of series interaction, we used an abrupt hemodynamic perturbation (aortic constriction), and we measured systolic interaction gain (IG) as delta right ventricular peak systolic pressure/delta left ventricular peak systolic pressure (IG(peak)) and instantaneous delta right ventricular pressure/delta left ventricular pressure at matched data sampling times (IG(inst)), along with changes in right ventricular stroke volume and stroke work before and on the beat immediately after the aortic constriction. To achieve equivalence of the interventricular septal pressure transmission contribution to ventricular interaction, the delta left ventricular peak systolic pressure produced by the aortic constriction was matched under all experimental conditions [average increase: 64 +/- 19 (SD) mmHg]. Control IG(peak) was 0.12 +/- 0.05, and control IG(inst) was 0.11 +/- 0.05. These values did not change with either free wall ischemia or ventricular pacing, with or without an intact pericardium. The changes in right ventricular stroke volume and stroke work produced by the aortic constriction were not different from zero, during either ischemia or ventricular pacing, with or without an intact pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of pacing site on canine left ventricular contraction

1986 ◽  
Vol 251 (2) ◽  
pp. H428-H435 ◽  
Author(s):  
D. Burkhoff ◽  
R. Y. Oikawa ◽  
K. Sagawa
Keyword(s):  
Right Ventricular ◽  
Time Course ◽  
Peak Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Free Wall ◽  
Ventricular Pacing ◽  
Right Ventricular Free Wall ◽  
Isolated Hearts

We investigated the influence of pacing site on several aspects of left ventricular (LV) performance to test the hypothesis that "effective ventricular muscle mass" is reduced with direct ventricular pacing. All studies were performed on isolated supported canine hearts that were constrained to contract isovolumically. To determine the influence of pacing site on magnitude and time course of isovolumic LV pressure (P) generation, LVP waves were recorded in eight isolated hearts paced at 130 beats/min. Pacing was epicardially from atrium, LV apex, LV free wall, right ventricular free wall (RVF), and endocardially from right ventricular endocardium. In a given heart, peak LVP was greatest with atrial pacing and smallest with RVF pacing, the difference being on average 26 +/- 10% (mean +/- SD) of the former pressure. The other pacing sites produced intermediate peak LVPs. When instantaneous LVP waves, obtained while pacing from each of the five sites, were normalized by their respective amplitudes, they were virtually superimposable up to the time of peak pressure and only slightly different during the remainder of the cardiac cycle. With changes in pacing site there was a linear negative correlation (r = 0.971) between changes in peak pressure and changes in duration of the QRS complex of a bipolar epicardial electrogram with an average slope of -0.51 mmHg/ms. Compared with atrial pacing, the slope of the end-systolic pressure-volume relation, Ees, was decreased with ventricular pacing, but Vo, the volume axis intercept, was relatively constant.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Septal flash and septal rebound stretch have different underlying mechanisms

2016 ◽  
Vol 310 (3) ◽  
pp. H394-H403 ◽  
Author(s):  
John Walmsley ◽  
Peter R. Huntjens ◽  
Frits W. Prinzen ◽  
Tammo Delhaas ◽  
Joost Lumens
Keyword(s):  
Pressure Gradient ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Early Systole ◽  
Underlying Mechanisms ◽  
Activation Times ◽  
Septal Flash

Abnormal left-right motion of the interventricular septum in early systole, known as septal flash (SF), is frequently observed in patients with left bundle branch block (LBBB). Transseptal pressure gradient and early active septal contraction have been proposed as explanations for SF. Similarities in timing (early systole) and location (septum) suggest that SF may be related to septal systolic rebound stretch (SRSsept). We aimed to clarify the mechanisms generating SF and SRSsept. The CircAdapt computer model was used to isolate the effects of timing of activation of the left ventricular free wall (LVFW), right ventricular free wall (RVFW), and septum on SF and SRSsept. LVFW and septal activation times were varied by ±80 ms relative to RVFW activation time. M-mode-derived wall motions and septal strains were computed and used to quantify SF and SRSsept, respectively. SF depended on early activation of the RVFW relative to the LVFW. SF and SRSsept occurred in LBBB-like simulations and against a rising transseptal pressure gradient. When the septum was activated before both LVFW and RVFW, no SF occurred despite the presence of SRSsept. Computer simulations therefore indicate that SF and SRSsept have different underlying mechanisms, even though both can occur in LBBB. The mechanism of leftward motion during SF is early RVFW contraction pulling on and straightening the septum when unopposed by the LVFW. SRSsept is caused by late LVFW contraction following early contraction of the septum. Changes in transseptal pressure gradient are not the main cause of SF in LBBB.

A dynamic model of ventricular interaction and pericardial influence

1997 ◽  
Vol 272 (6) ◽  
pp. H2942-H2962 ◽  
Author(s):  
D. C. Chung ◽  
S. C. Niranjan ◽  
J. W. Clark ◽  
A. Bidani ◽  
W. E. Johnston ◽  
...  
Keyword(s):  
Time Course ◽  
Interventricular Septum ◽  
Dynamic Interaction ◽  
Chamber Pressure ◽  
Experimental Investigations ◽  
Free Wall ◽  
Ventricular Mechanics ◽  
Hemodynamic Variables ◽  
Ventricular Interaction ◽  
Left And Right

A mathematical model describing the dynamic interaction between the left and the right ventricle over the complete cardiac cycle is presented. The pericardium-bound left and right ventricles are represented as two coupled chambers consisting of the left and right free walls and the interventricular septum. Time-varying pressure-volume relationships characterize the component compliances, and the interaction of these components produces the globally observed ventricular pump properties (total chamber pressure and volume). The model 1) permits the simulation of passive (diastolic) and active (systolic) ventricular interaction, 2) provides temporal profiles of hemodynamic variables (e.g., ventricular pressures, volumes, and flow) that agree well with reported observations, and 3) can be used to examine the effect of the pericardium on ventricular interaction and ventricular mechanics. It can be reduced to equivalency with models previously reported by invoking simplifying assumptions. Furthermore, model-generated "dynamic interaction gains" are employed to quantify the mode and degree of ventricular interaction. The model also yields qualitative predictions of septal and free wall displacements similar to those detected experimentally via M-mode echocardiography. Such analogies may be extended easily to the study of pathophysiological states via appropriate modifications to 1) the pressure-volume characteristics of the component walls (and/or pericardium) and/or 2) the specific time course of activation of the ventricular free wall or the septum. A limited number of examples are included to demonstrate the utility of the model, which may be used as an adjunct to new experimental investigations into ventricular interaction.

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