scholarly journals Commentary: Ventriculo-ventricular interaction: A bad neighbor brings down the neighborhood

2020 ◽  
Vol 160 (4) ◽  
pp. 1016-1017
Author(s):  
David P. Bichell
Keyword(s):  
Ventricular Interaction

RV filling modulates LV function by direct ventricular interaction during mechanical ventilation

2005 ◽  
Vol 289 (2) ◽  
pp. H549-H557 ◽  
Author(s):  
Jamie R. Mitchell ◽  
William A. Whitelaw ◽  
Rozsa Sas ◽  
Eldon R. Smith ◽  
John V. Tyberg ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Left Ventricular Function ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Left Ventricular Volume ◽  
Venous Return ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Ventricular Interaction ◽  
Systemic Venous Return

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.

Ventricular Interaction via the Septum and Pericardium

2008 ◽  
pp. 41-52 ◽  
Author(s):  
Israel Belenkie ◽  
Eldon R. Smith ◽  
John V. Tyberg
Keyword(s):  
Ventricular Interaction

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.

Direct diastolic ventricular interaction gain measured with sudden hemodynamic transients

1989 ◽  
Vol 256 (2) ◽  
pp. H567-H573 ◽  
Author(s):  
B. K. Slinker ◽  
Y. Goto ◽  
M. M. LeWinter
Keyword(s):  
Confidence Interval ◽  
Right Ventricular ◽  
Diastolic Pressure ◽  
Direct Interaction ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Base Line ◽  
Right Ventricular Volume ◽  
Ventricular Interaction ◽  
Venae Cavae

Changes in right ventricular volume affect left ventricular function via direct ventricular interaction mediated by the septum, common myocardial fibers in the free wall, and the pericardium, and also via series interaction mediated by changes in right ventricular output reaching the left ventricle through the pulmonary circulation. To study direct interaction, series interaction must be held constant or removed from the experimental preparation. Because there has been no way to directly measure direct ventricular interaction in the intact circulation, we developed a new method to experimentally separate these two components of ventricular interaction by combining abrupt occlusion of both venae cavae and quick withdrawal of 10-15 ml of blood from the right ventricle. This procedure decreased right ventricular end-diastolic pressure (RVEDP) on the next beat without changing pulmonary venous flow, left ventricular end-diastolic segment lengths, or left ventricular systolic function. The direct interaction gains, quantified as delta LVEDP/delta RVEDP, where LVEDP is left ventricular end-diastolic pressure, and delta refers to the change between the beats before and after reducing right ventricular volume, were (means +/- SD) 0.32 +/- 0.32 at steady-state LVEDP = 5 mmHg, 0.38 +/- 0.23 at LVEDP = 10 mmHg, and 0.28 +/- 0.32 at LVEDP = 15 mmHg. These gains were not significantly different (P greater than 0.50). Therefore, we calculated an overall average gain by pooling data from the three base-line LVEDP conditions. This value is 0.33 with 95% confidence interval 0.16-0.51. This 95% confidence interval indicates our data are consistent with many previous reports of diastolic direct interaction.

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