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

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.

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

scholarly journals Sildenafil ameliorates right ventricular early molecular derangement during left ventricular pressure overload

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195528 ◽  
Author(s):  
Yousuke Imai ◽  
Taro Kariya ◽  
Masaki Iwakiri ◽  
Yoshitsugu Yamada ◽  
Eiki Takimoto
Keyword(s):  
Right Ventricular ◽  
Pressure Overload ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure

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.

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 regional ischemia and ventricular pacing on LV dP/dtmax-end-diastolic volume relation

1987 ◽  
Vol 252 (5) ◽  
pp. H933-H940 ◽  
Author(s):  
W. C. Little ◽  
R. C. Park ◽  
G. L. Freeman
Keyword(s):  
Coronary Artery ◽  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Ventricular Pressure ◽  
Free Wall ◽  
Ventricular Pacing ◽  
End Diastolic Volume ◽  
The Right

We investigated the effects of coronary artery occlusion and pacing from ventricular sites on the relation of the maximum rate of rise of left ventricular pressure (dP/dtmax) to the end-diastolic volume (VED) in dogs previously instrumented to measure left ventricular pressure and to determine left ventricular volume from three ultrasonically measured dimensions. The dP/dtmax-VED relation was generated by vena caval occlusion and compared with the simultaneously produced end-systolic pressure-end-systolic volume (PES-VES) relation. The dP/dtmax-VED relation was described by a straight line during all conditions. Occlusion of the left circumflex coronary artery produced a rightward shift of the dP/dtmax-VED relation, increasing the volume intercept by 11.3 +/- 5.3 (SD) ml (P less than 0.05). Compared with atrial pacing, the dP/dtmax-VED relation was shifted to the right with the volume intercept increasing by 4.8 +/- 4.4 ml (P less than 0.05) during pacing from the right ventricular free wall, 3.7 +/- 5.0 ml (P less than 0.05) during pacing from the right ventricular apex, and 3.7 +/- 2.4 ml (P less than 0.05) during pacing from the left ventricular free wall. Similar increases were observed in the volume intercepts of the PES-VES relations during coronary occlusion or ventricular pacing. These results are consistent with the predictions of the time-varying elastance model and support its use as a conceptual framework to understand left ventricular performance during isovolumic contraction and at end systole, both in the normal ventricle and the ventricle with regional abnormalities of contraction.

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