Mechanical interaction between the ventricles during systole

1977 ◽  
Vol 55 (3) ◽  
pp. 373-382 ◽  
Author(s):  
B. Lowell Langille ◽  
David R. Jones
Keyword(s):  
Left Ventricle ◽  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Mechanical Interaction ◽  
Rigor Mortis ◽  
Ventricular Performance ◽  
Ventricular Afterload

The immediate effect of abrupt alteration in the function of either ventricle on pressures in both ventricles has been examined in rabbits. Increasing left ventricular afterload, by aortic occlusion, caused a marked increase in peak left ventricular pressure (an increase of 44.0 ± 5.7 mmHg, from a mean of 79.4 ± 3.4 mmHg) and simultaneously a significant increase (an increase of 3.8 ± 0.6 mmHg, from a mean of 24.2 ± 1.4 mmHg) in right ventricular pressure. On the other hand, when similar increases in left ventricular pressure were induced by sudden changes in preload no alteration in right ventricular pressure was seen. High-frequency oscillatory infusion of saline into the left ventricle produced coincident oscillations in both ventricular pressures during systole. Left ventricular pressure generation was affected by interventions with right ventricular performance which altered afterload or preload and, although interaction was minimal at normal physiological pressures, a significant interaction was observed during induced systemic hypotension. A direct transference of pressure from right to left ventricle, comparable with that seen in vivo, was also observed when the ventricles of excised hearts in rigor mortis were inflated with saline. It is concluded that mechanical interaction occurs between the ventricles during systole and, consequently, the ventricles cannot be treated as mechanically independent pumps.

Effects of left ventricular pressure reductions on right ventricular systolic performance

1989 ◽  
Vol 257 (6) ◽  
pp. H1878-H1885 ◽  
Author(s):  
E. Chow ◽  
D. J. Farrar
Keyword(s):  
Right Ventricular ◽  
Interventricular Septum ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Segment Length ◽  
Stroke Work ◽  
Ventricular Performance ◽  
Right Ventricular Performance ◽  
Intact Heart

Reductions in left ventricular pressure (LVP) have been shown to produce a leftward shift of the interventricular septum and to reduce left ventricular contribution to right ventricular performance. To evaluate the magnitude of this contribution in the intact heart, five anesthetized pigs were implanted with a left prosthetic ventricle to gradually decrease LVP while maintaining arterial systemic pressure. Three descriptors of RV global and regional systolic function were studied in the septum to free wall (RVSFW) and anterior to posterior (RVAP) dimensions and in an outflow tract segment length (RVSL), during both steady state and transient inferior vena cava occlusion. LVP gradual reduction from 102 +/- 4 to 11 +/- 3 mmHg (90% decrease in peak systolic pressure) produced no changes in the RV global stroke work curve or in the RVAP and RVSL pressure-dimension relationships. However, the reduction in LVP resulted in parallel shifts in the RVSFW dimension, with 16.6 +/- 6.7% increase in the intercept D(o) of the end-systolic relationship and 16.5 +/- 2.5% increase in D(o) of the dimensional stroke work relationship, with no significant changes in their respective slopes as calculated by linear regression. Therefore, in the normal intact heart, large reductions in left ventricular pressure affect the geometry of the right ventricle because of septal shifting, but there is a negligible net effect of this anatomic ventricular interaction on overall right ventricular performance.

In vivo safety and accuracy of a clinically applicable telemetered left ventricular pressure module: intermediate-term results

2004 ◽  
Vol 10 (4) ◽  
pp. S67 ◽  
Author(s):  
Patrick I. McConnell ◽  
Daise de Cunha ◽  
Tanya Shipkowitz ◽  
Justin Van Hee ◽  
Phillip H. Long ◽  
...  
Keyword(s):  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure

Levels of brain natriuretic peptide in children with right ventricular overload due to congenital cardiac disease

2005 ◽  
Vol 15 (4) ◽  
pp. 396-401 ◽  
Author(s):  
Thomas S. Mir ◽  
Jan Falkenberg ◽  
Bernd Friedrich ◽  
Urda Gottschalk ◽  
Throng Phi Lê ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Brain Natriuretic Peptide ◽  
Right Ventricular ◽  
Natriuretic Peptide ◽  
Cardiac Disease ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Congenital Cardiac Disease ◽  
The Right

Objective:To evaluate the role of the concentration of brain natriuretic peptide in the plasma, and its correlation with haemodynamic right ventricular parameters, in children with overload of the right ventricle due to congenital cardiac disease.Methods:We studied 31 children, with a mean age of 4.8 years, with volume or pressure overload of the right ventricle caused by congenital cardiac disease. Of the patients, 19 had undergone surgical biventricular correction of tetralogy of Fallot, 11 with pulmonary stenosis and 8 with pulmonary atresia, and 12 patients were studied prior to operations, 7 with atrial septal defects and 5 with anomalous pulmonary venous connections. We measured brain natriuretic peptide using Triage®, from Biosite, United States of America. We determined end-diastolic pressures of the right ventricle, and the peak ratio of right to left ventricular pressures, by cardiac catheterization and correlated them with concentrations of brain natriuretic peptide in the plasma.Results:The mean concentrations of brain natriuretic peptide were 87.7, with a range from 5 to 316, picograms per millilitre. Mean end-diastolic pressure in the right ventricle was 5.6, with a range from 2 to 10, millimetres of mercury, and the mean ratio of right to left ventricular pressure was 0.56, with a range from 0.24 to 1.03. There was a positive correlation between the concentrations of brain natriuretic peptide and the ratio of right to left ventricular pressure (r equal to 0.7844, p less than 0.0001) in all patients. These positive correlations remained when the children with tetralogy of Fallot, and those with atrial septal defects or anomalous pulmonary venous connection, were analysed as separate groups. We also found a weak correlation was shown between end-diastolic right ventricular pressure and concentrations of brain natriuretic peptide in the plasma (r equal to 0.5947, p equal to 0.0004).Conclusion:There is a significant correlation between right ventricular haemodynamic parameters and concentrations of brain natriuretic peptide in the plasma of children with right ventricular overload due to different types of congenital cardiac disease. The monitoring of brain natriuretic peptide may provide a non-invasive and safe quantitative follow up of the right ventricular pressure and volume overload in these patients.

Fluid-Structure Interaction Simulation of Blood Flow Inside a Diseased Left Ventricle With Obstructive Hypertrophic Cardiomyopathy in Early Systole

2009 ◽  
Author(s):  
Ahmad Moghaddaszade-Kermani ◽  
Peter Oshkai ◽  
Afzal Suleman
Keyword(s):  
Blood Flow ◽  
Hypertrophic Cardiomyopathy ◽  
Left Ventricle ◽  
Fluid Structure Interaction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Fluid Structure ◽  
Structure Interaction ◽  
Systolic Phase

Mitral-Septal contact has been proven to be the cause of obstruction in the left ventricle with hypertrophic cardiomyopathy (HC). This paper presents a study on the fluid mechanics of obstruction using two-way loosely coupled fluid-structure interaction (FSI) methodology. A parametric model for the geometry of the diseased left ventricular cavity, myocardium and mitral valve has been developed, using the dimensions extracted from magnetic resonance images. The three-element Windkessel model [1] was modified for HC and solved to introduce pressure boundary condition to the aortic aperture in the systolic phase. The FSI algorithm starts at the beginning of systolic phase by applying the left ventricular pressure to the internal surface of the myocardium to contract the muscle. The displacements of the myocardium and mitral leaflets were calculated using the nonlinear finite element hyperelastic model [2] and subsequently transferred to the fluid domain. The fluid mesh was moved accordingly and the Navier-Stokes equations were solved in the laminar regime with the new mesh using the finite volume method. In the next time step, the left ventricular pressure was increased to contract the muscle further and the same procedure was repeated for the fluid solution. The results show that blood flow jet applies a drag force to the mitral leaflets which in turn causes the leaflet to deform toward the septum thus creating a narrow passage and possible obstruction.

Hypotensive mechanism of [Leu13]motilin in dogs in vivo and in vitro

1998 ◽  
Vol 76 (12) ◽  
pp. 1103-1109 ◽  
Author(s):  
Takeshi Iwai ◽  
Hiroyuki Nakamura ◽  
Hisanori Takanashi ◽  
Kenji Yogo ◽  
Ken-Ichi Ozaki ◽  
...  
Keyword(s):  
Mesenteric Artery ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Gastric Antrum ◽  
Ventricular Pressure ◽  
High Dose ◽  
Aortic Blood Flow ◽  
Arterial Blood

The effects of [Leu13]motilin were examined in vivo after its intravenous administration into anesthetized dogs and in vitro with isolated preparations of canine mesenteric artery. [Leu13]Motilin (0.1-10 nmol·kg-1, i.v.) induced both strong and clustered phasic contractions in the gastric antrum and duodenum. At doses of over 1 nmol·kg-1, [Leu13]motilin also produced transient decreases in arterial blood pressure, left ventricular pressure, maximum rate of rise of left ventricular pressure, and total peripheral resistance, and an increase in aortic blood flow and heart rate. A selective motilin antagonist, GM-109 (Phe-cyclo[Lys-Tyr(3-tBu)-betaAla]betatrifluoroacetate), completely abolished the gastric antrum and duodenal motor responses induced by [Leu13]motilin. In contrast, hypotension induced by [Leu13]motilin (1 nmol·kg-1) was unchanged in the presence of GM-109. In isolated mesenteric artery preparations precontracted with U-46619 (10-7 M), [Leu13]motilin (10-8-10-5 M) induced an endothelium-dependent relaxation, and this was inhibited by a pretreatment with Nomega-nitro-L-arginine, a competitive inhibitor of NO synthase (10-4 M). A high dose (10-4 M) of GM-109 slightly decreased [Leu13]motilin-induced relaxation, and shifted the concentration-response curve of [Leu13]motilin to the right. However, the pA2 value (4.09) of GM-109 for [Leu13]motilin in the present study was conspicuously lower than that previously demonstrated in the rabbit duodenum (7.37). These results suggest that [Leu13]motilin induces hypotension via the endothelial NO-dependent relaxation mechanism and not through the receptor type that causes upper gastrointestinal contractions.Key words: motilin, gastrointestinal motility, hypotension, hemodynamics, anesthetized dog, mesenteric artery, endothelium, nitric oxide.

Malignant Hyperthermia Phenotype

2000 ◽  
Vol 92 (6) ◽  
pp. 1777-1788 ◽  
Author(s):  
Daniel C. Sigg ◽  
Paul A. Iaizzo
Keyword(s):  
Malignant Hyperthermia ◽  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
High Dose ◽  
Central Venous ◽  
Induced Hypotension ◽  
Arterial Blood ◽  
Left And Right

Background Succinylcholine causes immediate and severe arterial hypotension in swine with the malignant hyperthermia phenotype. The underlying mechanisms are unknown. Methods Malignant hyperthermia-susceptible (MHS; n = 10) and normal swine (n = 5) were anesthetized with thiopental. The following were monitored: electrocardiogram; arterial blood pressure; pulmonary artery, central venous, and left and right ventricular pressure; cardiac output; end-tidal carbon dioxide; core temperature; peripheral-blood flows; and arterial blood gases. After a control period, 2 mg/kg succinylcholine was given intravenously. Three MHS animals received 1 mg/kg vecuronium and two MHS animals received 2.5 mg/kg dantrolene intravenously. The effects of succinylcholine on left and right ventricular pressure and contractility were analyzed in isolated hearts. The effects of 0.06 mm succinylcholine on isometric tension development were recorded in isolated femoral artery rings. Results Succinylcholine caused an early, severe decrease in blood pressure, cardiac output, left ventricular pressure, and left ventricular contractility in MHS swine but not in normal swine; no significant differences were found in heart rate, right ventricular parameters, systemic vascular resistance, and preload (pulmonary diastolic pressure, central venous pressure). The succinylcholine-induced hypotension and associated effects were not prevented by dantrolene. However, pretreatment with high-dose vecuronium prevented not only the cardiovascular depression, but also MH. In addition, no phenotypic differences of succinylcholine on contractility or left ventricular pressure were observed in the isolated working hearts. Similary, succinylcholine did not cause a significantly different relaxation in rings in either phenotype. Conclusion Succinylcholine-induced hypotension occurred before muscle hypermetabolism in MHS swine. Succinylcholine had no differential physiologic effects on either the isolated heart or on isolated arteries. This hypotension could not be prevented by dantrolene but was prevented by pretreatment with high-dose vecuronium. Thus, an indirect mechanism such as the release of a cardiac depressant from skeletal muscle may have caused this hypotensive response.

scholarly journals Influence of Right Ventricular Filling Pressure on Left Ventricular Pressure and Dimension

1974 ◽  
Vol 34 (4) ◽  
pp. 498-504 ◽  
Author(s):  
CHARLES E. BEMIS ◽  
JUAN R. SERUR ◽  
DAVID BORKENHAGEN ◽  
EDMUND H. SONNENBLICK ◽  
CHARLES W. URSCHEL
Keyword(s):  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Ventricular Pressure ◽  
Ventricular Filling Pressure ◽  
Right Ventricular Filling ◽  
Ventricular Filling

In vivo murine left ventricular pressure-volume relations by miniaturized conductance micromanometry

1998 ◽  
Vol 274 (4) ◽  
pp. H1416-H1422 ◽  
Author(s):  
Dimitrios Georgakopoulos ◽  
Wayne A. Mitzner ◽  
Chen-Huan Chen ◽  
Barry J. Byrne ◽  
Huntly D. Millar ◽  
...  
Keyword(s):  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Genetically Engineered ◽  
Ventricular Pressure ◽  
Stroke Work ◽  
Time Varying ◽  
End Diastolic Volume ◽  
Novel Approach ◽  
Preload Reduction

The mouse is the species of choice for creating genetically engineered models of human disease. To study detailed systolic and diastolic left ventricular (LV) chamber mechanics in mice in vivo, we developed a miniaturized conductance-manometer system. α-Chloralose-urethan-anesthetized animals were instrumented with a two-electrode pressure-volume catheter advanced via the LV apex to the aortic root. Custom electronics provided time-varying conductances related to cavity volume. Baseline hemodynamics were similar to values in conscious animals: 634 ± 14 beats/min, 112 ± 4 mmHg, 5.3 ± 0.8 mmHg, and 11,777 ± 732 mmHg/s for heart rate, end-systolic and end-diastolic pressures, and maximum first derivative of ventricular pressure with respect to time (dP/d t max), respectively. Catheter stroke volume during preload reduction by inferior vena caval occlusion correlated with that by ultrasound aortic flow probe ( r 2 = 0.98). This maneuver yielded end-systolic elastances of 79 ± 21 mmHg/μl, preload-recruitable stroke work of 82 ± 5.6 mmHg, and slope of dP/d t max-end-diastolic volume relation of 699 ± 100 mmHg ⋅ s−1 ⋅ μl−1, and these relations varied predictably with acute inotropic interventions. The control normalized time-varying elastance curve was similar to human data, further supporting comparable chamber mechanics between species. This novel approach should greatly help assess cardiovascular function in the blood-perfused murine heart.

Left ventricular pressure effects on right ventricular pressure and volume outflow

1990 ◽  
Vol 19 (4) ◽  
pp. 269-278 ◽  
Author(s):  
Ralph J. Damiano ◽  
James L. Cox ◽  
James E. Lowe ◽  
William P. Santamore
Keyword(s):  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Pressure Effects ◽  
Ventricular Pressure
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