End-systolic pressure-volume, pressure-length, and stress-strain relations in canine hearts

1985 ◽  
Vol 249 (3) ◽  
pp. H648-H654 ◽  
Author(s):  
S. Kaseda ◽  
H. Tomoike ◽  
I. Ogata ◽  
M. Nakamura
Keyword(s):  
Systolic Pressure ◽  
Wall Stress ◽  
Regional Wall Motion ◽  
Stress Strain ◽  
Contractile State ◽  
Inotropic State ◽  
Inferior Caval Vein ◽  
Strain Relationship ◽  
Pressure Volume Relationship ◽  
Lv Volume

End-systolic pressure-volume relationship (ESPVR) of the in situ heart in the dog was measured during changes in contractile state and was compared with end-systolic pressure-length (ESPLR) or stress-strain relationship (ESSSR). Circumferential segmental length and wall thickness at the equator and external long and short axis diameters of the left ventricle (LV) were determined sonomicrometrically, and LV volume was calculated by an ellipsoidal model. Circumferential wall stress at the equator was calculated by a very thin shell model. Contractile state was enhanced by an intravenous infusion of dobutamine and was suppressed by propranolol. ESPVR, ESPLR, and ESSSR were determined during a reduction of arterial pressure by occluding temporarily the inferior caval vein (IVC). ESPVR, ESPLR, and ESSSR during changes in end-systolic pressure from 108 +/- 3 to 71 +/- 2 mmHg were linear, irrespective of inotropic states (r greater than 0.92). Slopes of these relationships increased similarly in case of dobutamine and were reduced after propranolol, yet the extrapolated X-axis intercept of ESPVR, ESPLR, and ESSSR remained unchanged. Thus the slope of ESPVR is unique to the inotropic state, and both ESPLR and ESSSR are useful as a substitute for ESPVR when there is no regional wall motion abnormality.

Bending of Blood Vessel Wall: Stress-Strain Laws of the Intima-Media and Adventitial Layers

1995 ◽  
Vol 117 (1) ◽  
pp. 136-145 ◽  
Author(s):  
Jiaping Xie ◽  
Jianbo Zhou ◽  
Y. C. Fung
Keyword(s):  
Experimental Data ◽  
Stress State ◽  
Beam Theory ◽  
Nonlinear Least Squares ◽  
Wall Stress ◽  
Wall Material ◽  
Stress Strain ◽  
Strain Relationship ◽  
Residual Strains ◽  
Residual Stresses And Strains

In order to determine the stress-strain relationship of the inner (intima and media) and outer (adventitia) layers of blood vessels in the neighborhood of the zero-stress state, bending experiments were performed on aortic strips of rats. In the experiments, one end of a strip was clamped, and a force was applied on the other end. The deflection curves of the strips were measured. By regarding the aortic strip as a curved beam, the classical beam theory was employed to analyze the strain distribution from the experimental data. A computer program dealing with nonlinear equations and nonlinear least squares optimization was developed. Strains were referred to the zero-stress state. The load-deflection relationship was then used to determine the stress-strain relationship. Certain forms of the stress-strain laws were assumed. The linear laws fit the experimental data accurately, probably because the strains during bending are quite small, although the rotations are large. The Young’s modulus of the inner layer, which consists of endothelial and smooth muscle cells and elastic lamina, was found to be three to four times larger than that of the outer layer which consists of collagen with a small amount of fibroblasts and elastin. The residual stresses and strains at the no-load state were calculated from the deduced stress-strain relationship. It is shown that large errors (up to 50 percent) in the values of the residual strains will occur if the wall material was treated as homogeneous, i.e., if the layered constitution was ignored.

A New Non-Invasive Method for Assessing the Intrinsic Active Strength of Human Left Ventricular Tissue

2007 ◽  
Author(s):  
Tom E. Claessens ◽  
Ernst R. Rietzschel ◽  
Marc L. De Buyzere ◽  
Dirk De Bacquer ◽  
Guy De Backer ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Contractile State ◽  
Non Invasive ◽  
Left Ventricular Tissue ◽  
Ventricular Tissue ◽  
Volume Relationship ◽  
Invasive Method ◽  
Pressure Volume Relationship ◽  
Human Left Ventricle

The contractile state of the human left ventricle (LV) is often assessed by its end-systolic elastance (Ees) [1]. This index is calculated as the slope of the linear end-systolic pressure-volume relationship (ESPVR), which connects the upper left corners of pressure-volume loops obtained under various loading conditions (figure 1).

Single-beat evaluation of left ventricular inotropic state in conscious dogs

1989 ◽  
Vol 256 (1) ◽  
pp. H56-H65 ◽  
Author(s):  
E. C. Lascano ◽  
J. A. Negroni ◽  
J. G. Barra ◽  
A. J. Crottogini ◽  
R. H. Pichel
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Time Data ◽  
Inotropic State ◽  
Volume Relationship ◽  
Pressure Volume Relationship ◽  
Experimental Findings ◽  
Parameter Values

Two competing left ventricular elastic-resistive (ER) models were used to predict parameter values from pressure, volume, and time data of a single ejective beat in conscious dogs during control, enhanced (dobutamine), and decreased (propranolol) inotropic states. The animals were instrumented with three pairs of microcrystals and a transducer to measure intraventricular volume and pressure. Results showed that with the ER nonlinear model (ERNL), parameter values in all animals lay within the physiological range. These were the slope (Emax) and the intercept (V0) of the isovolumic end-systolic pressure-volume relationship (ESPVR), the slope of the end-diastolic pressure-volume relationship (Ed), the time to Emax (Tmax), the normalized time to end of activation (A), and the resistive constant (K). In the two models, the normalized SE of the estimate of data fitting was below 0.2 Emax, as estimated from a single beat, responded to changes in contractility in a significantly more consistent fashion than the slope of ESPVRs (Ees) generated by preload maneuvers in conscious dogs. Single-beat estimated Tmax and K with the ERNL model did also respond consistently to contractility changes, whereas with the elastic resistive linear (ERL) model, K did not reproduce the experimental findings with decreased inotropic state. We conclude that 1) the ERNL model can be employed to assess contractility changes in conscious dogs from data of a single ejective beat, and 2) these changes are better indicated by single-beat estimated Emax than by Ees calculated from conventional ESPVRs.

Loading determinants of isovolumic pressure fall in closed-chest dogs

1991 ◽  
Vol 260 (3) ◽  
pp. H690-H697 ◽  
Author(s):  
J. B. Su ◽  
L. Hittinger ◽  
M. Laplace ◽  
B. Crozatier
Keyword(s):  
Systolic Pressure ◽  
Wall Stress ◽  
Load Level ◽  
Aortic Constriction ◽  
Autonomic Blockade ◽  
Loading Sequence ◽  
Lv Volume ◽  
Control State ◽  
Pressure Fall

The respective roles of load level and loading sequence of the left ventricle (LV) are controversial in the in situ heart. They were analyzed under autonomic blockade and sedation in 17 dogs previously instrumented with a pressure micromanometer and ultrasonic crystals measuring LV diameters and wall thickness for computation of LV volume and stress. The time constant of isovolumic pressure fall (T) and end-systolic pressure (ESP) were calculated during the control state, caval occlusion, aortic constriction obtained by inflation of a hydraulic cuff occluder positioned around the aorta, and during the inflation of an intra-aortic balloon. Caval occlusion significantly decreased both ESP (from 124.0 +/- 6.6 to 88.7 +/- 3.7 mmHg; P less than 0.005) and T (from 29.0 +/- 2.2 to 18.8 +/- 2.4 ms; P less than 0.005), which were linearly correlated (mean r = 0.90 +/- 0.03) and inflation of an intra-aortic balloon increased both ESP (from 107.3 +/- 7.1 to 150.6 +/- 10.4 mmHg; P less than 0.005) and T (from 24.6 +/- 2.1 to 32.7 +/- 2.3 ms; P less than 0.005). Both interventions did not modify the loading sequence (analyzed by the evolution of systolic wall stress vs. time). In contrast, aortic constriction delayed to midsystole the time to which wall stress reached its peak and, for matched ESP with intra-aortic balloon inflation, T was not significantly different from control. We conclude that both the level of afterload and the loading sequence of LV are the determinants of T when contractility is not modified.

Abstract 12880: A Clinical Index of Myocardial Afterload Can Replace Wall Stress Calculations

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nathaniel Reichek ◽  
Jonathan Weber ◽  
Madhavi Kadiyala ◽  
Marie Grgas ◽  
Tazim Merchant ◽  
...  
Keyword(s):  
Treatment Guidelines ◽  
Systolic Pressure ◽  
Wall Stress ◽  
Stress Index ◽  
Stress Indices ◽  
Lv Volume ◽  
And Gender ◽  
Brachial Systolic Pressure ◽  
Myocardial Level

Introduction: Afterload at the myocardial level is a principal determinant of LV chamber and myocardial wall function, generated by interplay of LV pressure, volume, and mass. Quantitation has relied on wall stress indices which require additional measurements and calculations as well as incorrect assumptions. Unfamiliar to most clinicians, they have largely fallen out of use, but the role of myocardial afterload in contemporary heart failure pathophysiology and therapy merits reevaluation given the roles of EF and myocardial strains in prognostic indices and treatment guidelines. Hypothesis: A simple clinical afterload index using variables fundamental to wall stress indices (systolic pressure(mmHg) * LV volume(ml))/LV mass(g)) or PV/M correlates closely with stress indices and relates similarly to LV EF and myocardial strains. Methods: In 277 normals (54% female, mean age 50.9±12.9 yrs) and small cohorts with dilated non-ischemic cardiomyopathy(35), aortic stenosis(12) and cancer chemotherapy(43), each with matched controls, we used CMR LV volumes, mass and brachial systolic pressure during imaging to compare end-systolic PV/M to stress indices and systolic pressure alone using correlations and correlation standard errors(SEs). Results: There were extremely close correlations (r= 0.97-0.99, all p< 0.001) with minimal SEs between PV/M and Arts and Alters stress indices with similar slopes in all groups and in normal subgroups by age and gender. Negative correlations with EF, global strains and strain rates were also present and extremely similar in all groups. But Mirsky’s stress index and brachial pressure performed less well. Conclusions: A simple clinical afterload index correlates closely with wall stress indices and similarly with LV ejection fraction and strains. It can support efficient reassessment of the role of afterload at the myocardial level in research and potentially, in clinical practice.

Ventricular stroke work and efficiency both remain nearly optimal despite altered vascular loading

1993 ◽  
Vol 264 (6) ◽  
pp. H1817-H1824 ◽  
Author(s):  
P. P. De Tombe ◽  
S. Jones ◽  
D. Burkhoff ◽  
W. C. Hunter ◽  
D. A. Kass
Keyword(s):  
Oxygen Consumption ◽  
Animal Studies ◽  
Myocardial Oxygen Consumption ◽  
Systolic Pressure ◽  
Theoretical Models ◽  
Stroke Work ◽  
Windkessel Model ◽  
Arterial Elastance ◽  
Inotropic State ◽  
Pressure Volume Relationship

Recent clinical and animal studies have suggested that ventricular-vascular coupling normally operates at either optimal ventricular efficiency (EFF = stroke work/myocardial oxygen consumption) or stroke work (SW) and that efficiency in particular is compromised by cardiac dysfunction. These distinctions between coupling states at maximal work vs. efficiency are largely based on theoretical models. To date, there are few direct experimental data defining optimal conditions for each parameter, respectively, in the same heart or tests of whether changes from these conditions must produce significant declines in both parameters. Therefore, 10 isolated blood-perfused canine hearts were studied at varying contractilities, with the heart ejecting into a simulated three-element Windkessel model of arterial impedance. For a given inotropic state [indexed by the slope of the end-systolic pressure-volume relationship (Ees)], myocardial oxygen consumption and SW were measured over a broad range of afterload resistances. The latter was indexed by the effective arterial elastance (Ea) and ventricular-vascular interaction expressed by the ratio of Ea to Ees (Ea/Ees). On average, maximal SW occurred at Ea/Ees = 0.80 +/- 0.16, whereas EFF was maximal at Ea/Ees = 0.70 +/- 0.15 (P < 0.01). However, these differences were small, and both SW and EFF were > or = 90% of their respective optima over a broad overlapping range of Ea-to-Ees ratios (0.3-1.3, corresponds with ejection fractions ranging from approximately 40 to 80%). These data show that both SW and efficiency are nearly maximal under many conditions of ventricular-vascular interaction.(ABSTRACT TRUNCATED AT 250 WORDS)

End-systolic pressure-length relations during changes in regional contractile state

1984 ◽  
Vol 247 (5) ◽  
pp. H768-H774
Author(s):  
S. Kaseda ◽  
H. Tomoike ◽  
I. Ogata ◽  
M. Nakamura
Keyword(s):  
Coronary Artery ◽  
Systolic Pressure ◽  
Circumflex Coronary Artery ◽  
Caval Vein ◽  
Contractile State ◽  
Inferior Caval Vein ◽  
Length Relationship ◽  
Group 2 ◽  
Contracting Heart ◽  
Group 1

End-systolic pressure-length relationship (ESPLR) was examined in the heterogenously contracting heart in open-chest dogs. Regional length was measured sonomicrometrically in the areas of both the left circumflex coronary artery (LCX) and left anterior descending coronary artery (LAD). ESPLR was linear during a transient reduction in arterial pressure following occlusion of the inferior caval vein (IVC). In group 1 (12 dogs), saline as a control condition (Cont) and isoproterenol (Iso, 0.05 microgram/min) to enhance the regional contractile state were infused into the LCX. Percent shortening in the LCX area increased from 13 to 16% (P less than 0.01) in Iso. The slope (Ees) of ESPLR increased from 57 to 71 mmHg/mm (P less than 0.01) in Iso. The extrapolated X-axis intercept (Lo) of ESPLR was unchanged. In the LAD area, Ees and Lo remained constant. In group 2 (13 dogs), lidocaine (1 mg/min, Lid 1; 5 mg/min, Lid 5) was infused into the LCX to induce mild and severe hypokinesis, respectively. Percent shortening in the LCX area was reduced from 14 to 8% (P less than 0.01 vs. Cont) in Lid 1 and 5% (P less than 0.01 vs. Cont, P less than 0.05 vs. Lid 1) in Lid 5. Ees tended to decrease in Lid 1 but to increase in Lid 5 (statistically not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Curvilinearity of LV end-systolic pressure-volume and dP/dtmax-end-diastolic volume relations

1993 ◽  
Vol 265 (3) ◽  
pp. H910-H917 ◽  
Author(s):  
T. Noda ◽  
C. P. Cheng ◽  
P. P. De Tombe ◽  
W. C. Little
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Aortic Constriction ◽  
Contractile State ◽  
End Diastolic Volume ◽  
Open Chest ◽  
Geometric Factors ◽  
Lv Volume ◽  
Length Dependent Activation

We investigated the effect of contractile state (CS) on the curvilinearity of the left ventricular (LV) end-systolic pressure-volume (Pes-Ves) and the dP/dtmax-end-diastolic volume (dP/dtmax-Ved) relations in eight anesthetized open-chest dogs. LV volume was determined from three orthogonal diameters measured by sonomicrometry. The Pes-Ves relation and dP/dtmax-Ved relation were assessed during transient vena caval occlusion and aortic constriction, while CS was altered with dobutamine. At all CS, both relations were linear when volumes were decreased by caval occlusion. However, at higher volumes obtained by aortic constriction, the relations became nonlinear. At enhanced CS, the nonlinearity of both the Pes-Ves relation and the dP/dtmax-Ved relation increased. The dP/dtmax-Ved relation began to deviate from linearity at larger volumes, but closer to baseline operating volume, than the Pes-Ves relation. The relation between end-systolic mean circumference stress and wall strain (sigma es-epsilon es) was linear at control CS when the Pes-Ves relation was nonlinear but became nonlinear with enhanced CS. We conclude that both the Pes-Ves relation and the dP/dtmax-Ved relation are nonlinear, saturating at higher volumes. With increased CS, the nonlinearity of both relations increases. This CS-dependent curvilinearity of the Pes-Ves relation is due to both CS-dependent nonlinearity of the sigma es-epsilon es relation (consistent with length-dependent activation) and geometric factors that alter the relation between Pes and sigma es.

Chronic hypoxia augments uterine artery distensibility and alters the circumferential wall stress-strain relationship during pregnancy

2006 ◽  
Vol 100 (6) ◽  
pp. 1842-1850 ◽  
Author(s):  
Stephanie N. Mateev ◽  
Rhonda Mouser ◽  
David A. Young ◽  
Robert P. Mecham ◽  
Lorna G. Moore
Keyword(s):  
Blood Flow ◽  
Guinea Pigs ◽  
Uterine Artery ◽  
Chronic Hypoxia ◽  
Wall Stress ◽  
Myogenic Tone ◽  
Stress Strain ◽  
Circumferential Wall Stress ◽  
Strain Relationship ◽  
Resting Tone

Pregnancy-associated increases in uterine artery (UA) blood flow are due, in part, to vasoactive and growth-related changes that enlarge UA diameter. Although active and passive mechanical factors can contribute to this enlargement, their role is less well understood. We hypothesized that pregnancy increased UA distensibility and/or decreased myogenic tone. Given the fetal growth restriction and lower UA flow seen under chronic hypoxia, we further hypothesized that chronic hypoxia opposed these normal active and passive mechanical changes. UA were isolated from 12 nonpregnant and 12 pregnant (0.7 gestation) guinea pigs housed under normoxia or chronic hypoxia (3,960 m) and studied by pressure myography. Pregnancy increased UA diameter similarly under normoxia and hypoxia. Although chronic hypoxia raised resting tone in UA from nonpregnant guinea pigs to ∼20% and tone was greater in preconstricted pregnant chronically hypoxic vs. normoxic UA (both P < 0.01), there was an absence of myogenic response (i.e., an increase in tone with rising pressure) in all groups. Pregnancy increased UA distensibility 1.5-fold but did not change stiffness or the stress-strain relationship. Compared with vessels from normoxic pregnant animals, hypoxic pregnancy raised UA distensibility fourfold, decreased stiffness (rate constant b = 3.80 ± 1.06 vs. 8.92 ± 1.25, respectively, P < 0.01), lowered elastin by 50%, and shifted the stress-strain relationship upward such that four times as much strain was present at a given stress. We concluded that increased distensibility and low myogenic tone contribute to enlarging UA diameter and raising UA blood flow during pregnancy. Chronic hypoxia exaggerates the rise in distensibility and alters the stress-strain relationship in ways that may provoke vascular injury.

End-systolic pressure-volume relationships in dogs during ventilation with PEEP

1988 ◽  
Vol 254 (4) ◽  
pp. H664-H670 ◽  
Author(s):  
A. J. Crottogini ◽  
P. Willshaw ◽  
J. G. Barra ◽  
G. J. Breitbart ◽  
R. H. Pichel
Keyword(s):  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Positive End Expiratory Pressure ◽  
Closed Chest ◽  
Inotropic State ◽  
Anesthetized Dogs ◽  
Lv Volume

Whether left ventricular (LV) contractility changes during ventilation with positive end-expiratory pressure (PEEP) remains controversial. To assess LV inotropic state during PEEP using a load-independent index, we generated end-systolic pressure-volume relationships (ESPVRs) in eight closed-chest, chronically instrumented, anesthetized dogs undergoing 0 [zero end-expiratory pressure for the 1st time (ZEEP1)], 5 (PEEP-5), 10 (PEEP-10), and again 0 (ZEEP2) cmH2O PEEP. LV volume was calculated from three orthogonal internal diameters (sonomicrometry), and LV pressure was measured using an implanted transducer. ESPVRs at each level of PEEP were generated by transient inflation of a vena caval occluder. Despite significant decreases in cardiac output with PEEP-5 (1.81 +/- 0.38 l/min, means +/- SE; P less than 0.05) and PEEP-10 (1.70 +/- 0.46; P less than 0.01) with respect to ZEEP1 (2.12 +/- 0.41), no change was found in the slope (ZEEP1: 6.99 +/- 1.03 mmHg/ml; PEEP-5: 7.48 +/- 1.20; PEEP-10: 7.17 +/- 1.02; ZEEP2: 7.38 +/- 1.02), the volume intercept (ZEEP1: 7.4 +/- 3.4 ml; PEEP-5: 6.6 +/- 3.0; PEEP-10: 7.2 +/- 4.0; ZEEP2: 6.6 +/- 3.6), or the new index area beneath the ESPVR (ZEEP1: 304 +/- 98; PEEP-5: 329 +/- 104; PEEP-10: 310 +/- 98; ZEEP2: 343 +/- 114). We conclude that these levels of PEEP do not affect LV contractility as assessed by the ESPVR.

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