The ratio of right ventricular volume to left ventricular volume reflects the impact of pulmonary regurgitation independently of the method of pulmonary regurgitation quantification

2012 ◽  
Vol 81 (10) ◽  
pp. e977-e981 ◽  
Author(s):  
Mateusz Śpiewak ◽  
Łukasz A. Małek ◽  
Joanna Petryka ◽  
Łukasz Mazurkiewicz ◽  
Barbara Miłosz ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Left Ventricular Volume ◽  
Pulmonary Regurgitation ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Right Ventricular Volume ◽  
The Impact

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.

scholarly journals Altered biventricular hemodynamic forces in patients with repaired tetralogy of Fallot and right ventricular volume overload because of pulmonary regurgitation

2018 ◽  
Vol 315 (6) ◽  
pp. H1691-H1702 ◽  
Author(s):  
Pia Sjöberg ◽  
Johannes Töger ◽  
Erik Hedström ◽  
Per Arvidsson ◽  
Einar Heiberg ◽  
...  
Keyword(s):  
Blood Flow ◽  
Right Ventricular ◽  
Tetralogy Of Fallot ◽  
Flow Direction ◽  
Pulmonary Regurgitation ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Hemodynamic Forces ◽  
Control Subjects ◽  
Repaired Tetralogy Of Fallot

Intracardiac hemodynamic forces have been proposed to influence remodeling and be a marker of ventricular dysfunction. We aimed to quantify the hemodynamic forces in patients with repaired tetralogy of Fallot (rToF) to further understand the pathophysiological mechanisms as this could be a potential marker for pulmonary valve replacement (PVR) in these patients. Patients with rToF and pulmonary regurgitation (PR) > 20% ( n = 18) and healthy control subjects ( n = 15) underwent MRI, including four-dimensional flow. A subset of patients ( n = 8) underwent PVR and MRI after surgery. Time-resolved hemodynamic forces were quantified using 4D-flow data and indexed to ventricular volume. Patients had higher systolic and diastolic left ventricular (LV) hemodynamic forces compared with control subjects in the lateral-septal/LV outflow tract ( P = 0.011 and P = 0.0031) and inferior-anterior ( P < 0.0001 and P < 0.0001) directions, which are forces not aligned with blood flow. Forces did not change after PVR. Patients had higher RV diastolic forces compared with control subjects in the diaphragm-right ventricular (RV) outflow tract (RVOT; P < 0.001) and apical-basal ( P = 0.0017) directions. After PVR, RV systolic forces in the diaphragm-RVOT direction decreased ( P = 0.039) to lower levels than in control subjects ( P = 0.0064). RV diastolic forces decreased in all directions ( P = 0.0078, P = 0.0078, and P = 0.039) but were still higher than in control subjects in the diaphragm-RVOT direction ( P = 0.046). In conclusion, patients with rToF and PR had LV hemodynamic forces less aligned with intraventricular blood flow compared with control subjects and higher diastolic RV forces along the regurgitant flow direction in the RVOT and that of tricuspid inflow. Remaining force differences in the LV and RV after PVR suggest that biventricular pumping does not normalize after surgery. NEW & NOTEWORTHY Biventricular hemodynamic forces in patients with repaired tetralogy of Fallot and pulmonary regurgitation were quantified for the first time. Left ventricular hemodynamic forces were less aligned to the main blood flow direction in patients compared with control subjects. Higher right ventricular forces were seen along the pulmonary regurgitant and tricuspid inflow directions. Differences in forces versus control subjects remain after pulmonary valve replacement, suggesting that altered biventricular pumping does not normalize after surgery.

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.

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.

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