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.

Right and left ventricular pressure-volume response to respiratory maneuvers

1984 ◽  
Vol 57 (5) ◽  
pp. 1520-1527 ◽  
Author(s):  
W. P. Santamore ◽  
J. L. Heckman ◽  
A. A. Bove
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Valsalva Maneuver ◽  
Left Ventricular Pressure ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Left Ventricular Volumes ◽  
Right Ventricular Volume ◽  
Ventricular Volumes ◽  
End Diastolic Volume

With respiration, right ventricular end-diastolic volume fluctuates. We examined the importance of these right ventricular volume changes on left ventricular function. In six mongrel dogs, right and left ventricular volumes and pressures and esophageal pressure were simultaneously measured during normal respiration, Valsalva maneuver, and Mueller maneuver. The right and left ventricular volumes were calculated from cineradiographic positions of endocardial radiopaque markers. Increases in right ventricular volume were associated with changes in the left ventricular (LV) pressure-volume relationship. With normal respiration, right ventricular end-diastolic volume increased 2.3 +/- 0.7 ml during inspiration, LV transmural diastolic pressure was unchanged, and LV diastolic volume decreased slightly. This effect was accentuated by the Mueller maneuver; right ventricular end-diastolic volume increased 10.4 +/- 2.3 ml (P less than 0.05), while left ventricular end-diastolic pressure increased 3.6 mmHg (P less than 0.05) without a significant change in left ventricular end-diastolic volume. Conversely, with a Valsalva maneuver, right ventricular volume decreased 6.5 +/- 1.2 ml (P less than 0.05), and left ventricular end-diastolic pressure decreased 2.2 +/- 0.5 mmHg (P less than 0.05) despite an unchanged left ventricular end-diastolic volume. These changes in the left ventricular pressure-volume relationship, secondary to changes in right ventricular volumes, are probably due to ventricular interdependence. Ventricular interdependence may also be an additional factor for the decrease in left ventricular stroke volume during inspiration.

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.

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.

Alterations in left ventricular compliance due to changes in right ventricular volume, pressure and compliance

1988 ◽  
Vol 22 (11) ◽  
pp. 768-776 ◽  
Author(s):  
W. P SANTAMORE ◽  
M. CONSTANTINESCU ◽  
J. VINTEN-JOHANSEN ◽  
W. E JOHNSTON ◽  
W. C LITTLE
Keyword(s):  
Right Ventricular ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Right Ventricular Volume ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance

Normal myocardial function in severe right ventricular volume overload hypertrophy

2001 ◽  
Vol 280 (1) ◽  
pp. H11-H16 ◽  
Author(s):  
Yuji Ishibashi ◽  
Judith C. Rembert ◽  
Blase A. Carabello ◽  
Shintaro Nemoto ◽  
Masayoshi Hamawaki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Tricuspid Regurgitation ◽  
Contractile Function ◽  
Right Heart Failure ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Right Ventricular Volume ◽  
Right Heart ◽  
Severe Tricuspid Regurgitation

Severe left ventricular volume overloading causes myocardial and cellular contractile dysfunction. Whether this is also true for severe right ventricular volume overloading was unknown. We therefore created severe tricuspid regurgitation percutaneously in seven dogs and then observed them for 3.5–4.0 yr. All five surviving operated dogs had severe tricuspid regurgitation and right heart failure, including massive ascites, but they did not have left heart failure. Right ventricular cardiocytes were isolated from these and from normal dogs, and sarcomere mechanics were assessed via laser diffraction. Right ventricular cardiocytes from the tricuspid regurgitation dogs were 20% longer than control cells, but neither the extent (0.171 ± 0.005 μm) nor the velocity (2.92 ± 0.12 μm/s) of sarcomere shortening differed from controls (0.179 ± 0.005 μm and 3.09 ± 0.11 μm/s, respectively). Thus, despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function was normal. This finding for the severely volume-overloaded right ventricle stands in distinct contrast to our finding for the left ventricle severely volume overloaded by mitral regurgitation, wherein intrinsic contractile function is depressed.

Sign in / Sign up

Export Citation Format

Share Document