Contribution of systemic vascular resistance and total arterial compliance to effective arterial elastance in humans

2003 ◽  
Vol 285 (2) ◽  
pp. H614-H620 ◽  
Author(s):  
Denis Chemla ◽  
Isabelle Antony ◽  
Yves Lecarpentier ◽  
Alain Nitenberg
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Reliable Estimate ◽  
Arterial Elastance ◽  
Total Arterial Compliance ◽  
Arterial Load ◽  
Effective Arterial Elastance

The respective contribution of systemic vascular resistance ( R) and total arterial compliance ( C) to the arterial load remains to be established in humans. Effective arterial elastance ( Ea), i.e., the left ventricular end-systolic pressure (LVESP)-over-stroke volume ratio, is a reliable estimate of arterial load. It is widely accepted that Ea mainly relates to mean aortic pressure (MAP) and thus to the R-to- T ratio ( R/ T ratio), where T is cycle length. We tested the contribution of R/ T and 1/ C to Ea in 20 normotensive and 46 hypertensive subjects (MAP range: 84–160 mmHg). The multilinear model applied ( Ea = 1.00 R/ T + 0.42/ C – 0.04; r2 = 0.97). The sensitivity of Ea to a change in R/ T was 2.5 times higher than to a similar change in 1/ C in both normotensive and hypertensive adults. The LVESP was more strongly related to systolic aortic pressure (SAP; r2 = 0.94) than to MAP ( r2 = 0.83), and LVESP matched 90% SAP (bias = 0 ± 5mmHg). An alternative model of Ea is proposed, in which Ea is proportional to the heart rate × SAP product-over-cardiac index ratio whatever the MAP.

scholarly journals Systemic arterial compliance, systemic vascular resistance, and effective arterial elastance during exercise in endurance-trained men

2008 ◽  
Vol 295 (1) ◽  
pp. R228-R235 ◽  
Author(s):  
Takeshi Otsuki ◽  
Seiji Maeda ◽  
Motoyuki Iemitsu ◽  
Yoko Saito ◽  
Yuko Tanimura ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Vascular Resistance ◽  
Maximal Oxygen Uptake ◽  
Doppler Ultrasonography ◽  
Arterial Compliance ◽  
Left Ventricular ◽  
Dependent Manner ◽  
Arterial Elastance ◽  
Effective Arterial Elastance ◽  
The Difference

Systemic arterial compliance (C) and vascular resistance (R) regulate effective arterial elastance (Ea), an index of artery load. Increases in Ea during exercise are due primarily to reductions of C and maintain optimal ventricular-arterial coupling. Because C at rest and left ventricular functional reserve are greater in endurance-trained (ET) compared with sedentary control (SC) humans, we hypothesized that reductions of C and increases in Ea are greater in ET than SC individuals. The aim of this study was to investigate C, R, and Ea during exercise in ET and SC humans. C, R, Ea, and cardiac cycle length (T) were measured at rest and during exercise of 40, 60, and 80% maximal oxygen uptake using Doppler ultrasonography in 12 SC and 13 ET men. C decreased in an exercise intensity-dependent manner in both groups, but its reductions were greater in the ET than SC subjects. Consequently, although C at rest was greater in the ET than SC group, the intergroup difference in C disappeared during exercise. Exercise-related changes in R/T were relatively slight and R/T was lower in the ET than the SC group, both at rest and during exercise. Although Ea at rest was lower in the ET than SC group, there were no intergroup differences in Ea at 40, 60, or 80% maximal oxygen uptake. We conclude that the reductions of C from rest to exercise are more marked in ET than SC humans. This may be related to the exercise-associated disappearance of the difference in Ea between ET and SC humans.

scholarly journals Relaxin Modifies Systemic Arterial Resistance and Compliance in Conscious, Nonpregnant Rats

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3289-3296 ◽  
Author(s):  
Kirk P. Conrad ◽  
Dan O. Debrah ◽  
Jackie Novak ◽  
Lee A. Danielson ◽  
Sanjeev G. Shroff
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Therapeutic Potential ◽  
Muscle Tone ◽  
Arterial Compliance ◽  
Renal Arteries ◽  
Conscious Rat ◽  
Systemic Hemodynamic ◽  
Arterial Load ◽  
Passive Mechanics

Abstract Relaxin emanates from the corpus luteum of the ovary and circulates during pregnancy. Because the hormone is a potent renal vasodilator and mediates the renal vasodilation and hyperfiltration of pregnancy in conscious rats, we reasoned that it might also contribute to the broader cardiovascular changes of pregnancy. We began investigating this concept by testing whether relaxin can modify systemic arterial hemodynamics and load when chronically administered to nonpregnant rats. The major objectives of the present work were to determine whether relaxin administration to nonpregnant rats 1) modifies cardiac output (CO), systemic vascular resistance, and global arterial compliance (AC), and 2) regulates the passive mechanics of isolated arteries. To accomplish the first objective, we developed a conscious rat model for assessment of global AC. Passive mechanics of small renal arteries were assessed using a pressure arteriograph. Chronic administration of recombinant human relaxin by sc osmotic minipump to conscious, female, nonpregnant rats reduced the steady arterial load by decreasing systemic vascular resistance, increased CO, and reduced the pulsatile arterial load by increasing global AC as quantified by two indices—AC estimated from the diastolic decay of aortic pressure and CO and AC estimated by the ratio of stroke volume-to-pulse pressure. In another group of rats, relaxin administration also regulated the passive mechanics of small renal arteries, indicating that, in addition to reduction in vascular smooth muscle tone, modification of the vascular structure (e.g. extracellular matrix) contributes to the increase in global AC. These findings suggest a role for relaxin in the systemic hemodynamic changes of pregnancy, as well as novel therapeutic potential for relaxin in modifying arterial stiffness and cardiac afterload.

Hemodynamic correlates of effective arterial elastance in mitral stenosis before and after balloon valvotomy

1997 ◽  
Vol 83 (4) ◽  
pp. 1083-1089 ◽  
Author(s):  
Patrice Colin ◽  
Michel Slama ◽  
Alec Vahanian ◽  
Yves Lecarpentier ◽  
Gilbert Motté ◽  
...  
Keyword(s):  
Mitral Stenosis ◽  
Arterial Compliance ◽  
Aortic Pressure ◽  
Pulse Interval ◽  
Wave Reflections ◽  
Arterial Elastance ◽  
Before And After ◽  
Hydraulic Load ◽  
Balloon Valvotomy ◽  
Effective Arterial Elastance

Colin, Patrice, Michel Slama, Alec Vahanian, Yves Lecarpentier, Gilbert Motté, and Denis Chemla. Hemodynamic correlates of effective arterial elastance in mitral stenosis before and after balloon valvotomy. J. Appl. Physiol. 83(4): 1083–1089, 1997.—This study had the purpose of documenting the hemodynamic correlates of effective arterial elastance (Ea; i.e., an accurate estimate of hydraulic load) in mitral stenosis (MS) patients. The main hypothesis tested was that Ea relates to the total vascular resistance (R)-to-pulse interval duration ( T) ratio (R/ T) in MS patients both before and after successful balloon mitral valvotomy (BMV). High-fidelity aortic pressure recordings were obtained in 10 patients (40 ± 12 yr) before and 15 min after BMV. Ea value was calculated as the ratio of the steady-state end-systolic aortic pressure (ESAP) to stroke volume (thermodilution). Ea increased after BMV (from 1.55 ± 0.63 to 1.83 ± 0.71 mmHg/ml; P < 0.05). Throughout the procedure, there was a strong linear relationship between Ea and R/ T: Ea = 1.09R/ T − 0.01 mmHg/ml, r = 0.99, P = 0.0001. This ultimately depended on the powerful link between ESAP and mean aortic pressure [MAP; r = 0.99, 95% confidence interval for the difference (MAP − ESAP) from −18.5 to +4.5 mmHg]. Ea was also related to total arterial compliance (area method) and to wave reflections (augmentation index), although to a lesser extent. After BMV, enhanced and anticipated wave reflections were observed, and this was likely to be explained by decreased arterial compliance. The present study indicated that Ea depended mainly on the steady component of hydraulic load (i.e., R) and on heart period (i.e., T) in MS patients.

Peripheral circulatory control of preload-afterload mismatch with angiotensin in dogs

1987 ◽  
Vol 253 (1) ◽  
pp. H126-H132
Author(s):  
R. W. Lee ◽  
L. D. Lancaster ◽  
D. Buckley ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Peripheral Circulation ◽  
Aortic Pressure ◽  
Venous Compliance ◽  
Mean Aortic Pressure

To determine whether changes in the venous circulation were responsible for preload-afterload mismatch with angiotensin, we examined the changes in the heart and the peripheral circulation in six splenectomized dogs after ganglion blockade during an angiotensin infusion to increase mean aortic pressure 25 and then 50%. The peripheral circulation was evaluated by measuring mean circulatory filling pressure (MCFP), arterial compliance, and venous compliance. A 25% increase in mean aortic pressure increased MCFP from 6.2 +/- 0.3 to 7.6 +/- 0.3 mmHg (P less than 0.001) but did not change cardiac output, heart rate, or stroke volume. Systemic vascular resistance increased (P less than 0.01) from 0.50 +/- 0.02 to 0.59 +/- 0.03 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.03 to 0.06 +/- 0.03 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.6 +/- 0.1 ml X mmHg-1 X kg-1, respectively. A 50% elevation in mean aortic pressure increased MCFP from 7.1 +/- 0.4 to 9.5 +/- 0.9 mmHg (P less than 0.001) but did not change heart rate. At this level of aortic pressure, cardiac output and stroke volume decreased (P less than 0.01) 12 and 19%, respectively, whereas systemic vascular resistance increased (P less than 0.001) from 0.48 +/- 0.03 to 0.83 +/- 0.05 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.01 to 0.05 +/- 0.01 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.4 +/- 0.1 ml X mmHg-1 X kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Influence of critical closing pressure on systemic vascular resistance and total arterial compliance: A clinical invasive study

2017 ◽  
Vol 110 (12) ◽  
pp. 659-666 ◽  
Author(s):  
Denis Chemla ◽  
Edmund M.T. Lau ◽  
Philippe Hervé ◽  
Sandrine Millasseau ◽  
Mabrouk Brahimi ◽  
...  
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Total Arterial Compliance ◽  
Critical Closing Pressure ◽  
Closing Pressure

Arterial Stiffness Is Associated With QTc Interval Prolongation in Patients With Heart Failure

2017 ◽  
Vol 20 (3) ◽  
pp. 255-263
Author(s):  
Salah Al-Zaiti ◽  
Samir Saba ◽  
Rodolfo Pike ◽  
Jennifer Williams ◽  
Fadi Khraim
Keyword(s):  
Heart Failure ◽  
Arterial Stiffness ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Qtc Interval ◽  
Interval Prolongation ◽  
Indirect Measure ◽  
Total Arterial Compliance ◽  
Qtc Interval Prolongation

Background: A prolonged corrected QT (QTc) interval is a known risk factor for adverse cardiac events. Understanding the determinants and physiologic correlates of QTc is necessary for selecting proper strategies to reduce the risk of adverse events in high-risk patients. We sought to evaluate the role of arterial stiffness in heart failure as a determinant of QTc prolongation. Method: This was an observational study that recruited ambulatory heart failure patients (New York Heart Association Classes I–II) from an outpatient heart failure clinic. In the supine resting position, consented patients underwent noninvasive 12-lead electrocardiograph (ECG) and hemodynamic monitoring using BioZ Dx impedance cardiography. ECGs were evaluated by a reviewer blinded to clinical data, and QTc interval was automatically computed. Patients with pacing or bundle branch block (BBB) were analyzed separately. Strengths of associations were evaluated using Pearson’s r coefficients and multivariate linear regression. Results: The final sample ( N = 44) was 62 ± 13 years of age and 64% male with ejection fraction of 34% ± 12%. At univariate level, QTc interval moderately ( r > .50) correlated with cardiac output, left cardiac work index, systemic vascular resistance, and total arterial compliance in patients with intrinsically narrow QRS complexes. At the multivariate level, increasing systemic vascular resistance and decreasing total arterial compliance remained independent predictors of widening QTc interval in this group ( R2 = .54). No significant correlations were seen in patients with pacing or BBB. Conclusions: In the absence of conduction abnormalities, magnitude of arterial stiffness, an indirect measure of endothelial dysfunction, is associated with QTc interval prolongation.

scholarly journals Pulmonary vascular resistance and compliance relationship in pulmonary hypertension

2015 ◽  
Vol 46 (4) ◽  
pp. 1178-1189 ◽  
Author(s):  
Denis Chemla ◽  
Edmund M.T. Lau ◽  
Yves Papelier ◽  
Pierre Attal ◽  
Philippe Hervé
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Arterial Compliance ◽  
Pulmonary Arteries ◽  
Transpulmonary Pressure ◽  
Total Arterial Compliance ◽  
Arterial Load ◽  
Pulmonary Arterial

Right ventricular adaptation to the increased pulmonary arterial load is a key determinant of outcomes in pulmonary hypertension (PH). Pulmonary vascular resistance (PVR) and total arterial compliance (C) quantify resistive and elastic properties of pulmonary arteries that modulate the steady and pulsatile components of pulmonary arterial load, respectively. PVR is commonly calculated as transpulmonary pressure gradient over pulmonary flow and total arterial compliance as stroke volume over pulmonary arterial pulse pressure (SV/PApp). Assuming that there is an inverse, hyperbolic relationship between PVR and C, recent studies have popularised the concept that their product (RC-time of the pulmonary circulation, in seconds) is “constant” in health and diseases. However, emerging evidence suggests that this concept should be challenged, with shortened RC-times documented in post-capillary PH and normotensive subjects. Furthermore, reported RC-times in the literature have consistently demonstrated significant scatter around the mean. In precapillary PH, the true PVR can be overestimated if one uses the standard PVR equation because the zero-flow pressure may be significantly higher than pulmonary arterial wedge pressure. Furthermore, SV/PApp may also overestimate true C. Further studies are needed to clarify some of the inconsistencies of pulmonary RC-time, as this has major implications for our understanding of the arterial load in diseases of the pulmonary circulation.

Abstract 323: Acute Reduction of Ambient Air Pressure Lowers Systemic Vascular Resistance and Improves Cardiac Output in Mice in-vivo

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Anmol Shahid ◽  
Vaibhav B Patel ◽  
Gavin Y Oudit ◽  
Michael S McMurtry
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Atmospheric Pressure ◽  
Arterial Compliance ◽  
Ambient Air ◽  
Left Ventricular ◽  
Air Pressure

Background: Humans have lower risk for myocardial infarction and stroke at higher altitudes. The mechanism is unknown. We previously demonstrated that acute reductions in ambient air pressure result in enhanced arterial vasodilation ex vivo using a myograph model of murine resistance arteries. Enhanced vasodilation might increase effective arterial compliance in vivo , thus we further hypothesized a reduction in systemic vascular resistance in vivo as a result of lowered ambient air pressure. Methods: In-vivo Pressure Volume Loops: A novel hypobaric chamber was designed and constructed with the capacity to hold a single anaesthetized mouse and simulate a variety of lowered air pressures within the chamber. The design of the chamber allowed for monitoring of murine heart rate, respiratory rate, & blood oxygen saturation at all times. Using inhaled isoflurane to anesthetize the animal, a closed-chest left-ventricular catheterization procedure was performed within the chamber on free-breathing adult male C57-WT mice (n=8) during consecutive acute exposures to the three air pressure steps: 754 mmHg (control or room atmospheric pressure), 714 mmHg (p1) and 674 mmHg (p2). Results: In-vivo : Total systemic vascular resistance was reduced by acute exposure to lower air pressure (10.09±0.15 mmHg*min/μL at control vs. 8.11±1.45 and 8.18±1.24 mmHg*min/μL at p1 and p2, respectively; p<0.05). Cardiac output was significantly improved by lowering atmospheric pressure below room pressure (7.36±0.15 mL/min at control versus 9.71±1.45 mL/min and 9.59±1.77 mL/min at p1 and p2, respectively; p<0.05). Significant increases in stroke volume with a reduction in air pressure were also observed (p<0.05 for p1 and p2 vs. control). We did not note significant changes in heart rate, mean arterial pressure, or contractility of the mice with lowered atmospheric pressure. Conclusion: Acute reductions in ambient air pressure lower systemic vascular resistance, and increase cardiac output and stroke volumes in vivo .

Effects of enhanced ventricular filling on cardiac pump performance in exercising dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1886-1890 ◽  
Author(s):  
L. D. Horwitz ◽  
J. Lindenfeld
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Increase Stroke Volume ◽  
Normal Increase ◽  
Ventricular Filling

The extent to which the normal increase in stroke volume during exercise can be augmented by increasing preload by dextran infusion was studied in seven dogs. Each dog ran 3 min on a level treadmill at mild (3–4 mph), moderate (6–8 mph), and severe (9–13 mph) loads during the control study and immediately after 10% dextran 14 ml/kg iv. During severe exercise dextran-augmented stroke volume (+5.4 ml or 19% vs. exercise without dextran, P less than 0.01) and left ventricular end-diastolic diameter and pressure did not change heart rate, aortic pressure, or maximum derivative of left ventricular pressure but decreased systemic vascular resistance by 16%. Similar increases in stroke volume and preload after dextran occurred during mild and moderate exercise when arterial pressure and heart rate were unchanged or increased and systemic vascular resistance was decreased. Thus altering preload above those levels normally encountered during exercise is a potential mechanism to increase stroke volume and cardiac output.

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