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 ◽  
...  

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.

2003 ◽  
Vol 285 (2) ◽  
pp. H614-H620 ◽  
Author(s):  
Denis Chemla ◽  
Isabelle Antony ◽  
Yves Lecarpentier ◽  
Alain Nitenberg

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Maxime Nguyen ◽  
Jihad Mallat ◽  
Julien Marc ◽  
Osama Abou-Arab ◽  
Bélaïd Bouhemad ◽  
...  

BackgroundFluid responsiveness has been extensively studied by using the preload prism. The arterial load might be a factor modulating the fluid responsiveness. The norepinephrine (NE) administration increases the arterial load and modifies the vascular properties. The objective of the present study was to determine the relationship between fluid responsiveness, preload, arterial load, and NE use. We hypothesized that as a preload/arterial load, NE use may affect fluid responsiveness.MethodsThe retrospective multicentered analysis of the pooled data from 446 patients monitored using the transpulmonary thermodilution before and after fluid expansion (FE) was performed. FE was standardized between intensive care units (ICUs). The comparison of patients with and without NE at the time of fluid infusion was performed. Stroke volume (SV) responsiveness was defined as an increase of more than 15% of SV following the FE. Pressure responsiveness was defined as an increase of more than 15% of mean arterial pressure (MAP) following the FE. Arterial elastance was used as a surrogate for the arterial load.ResultsA total of 244 patients were treated with NE and 202 were not treated with NE. By using the univariate analysis, arterial elastance was correlated to SV variations with FE. However, the SV variations were not associated with NE administration (26 [15; 46]% vs. 23 [10; 37]%, p = 0.12). By using the multivariate analysis, high arterial load and NE administration were associated with fluid responsiveness. The association between arterial elastance and fluid responsiveness was less important in patients treated with NE. Arterial compliance increased in the absence of NE, but it did not change in patients treated with NE (6 [−8; 19]% vs. 0 [−13; 15]%, p = 0.03). The changes in total peripheral and arterial elastance were less important in patients treated with NE (−8 [−17; 1]% vs. −11 [−20; 0]%, p &lt; 0.05 and −10 [−19; 0]% vs. −16 [−24; 0]%, p = 0.01).ConclusionThe arterial load and NE administration were associated with fluid responsiveness. A high arterial load was associated with fluid responsiveness. In patients treated with NE, this association was lower, and the changes of arterial load following FE seemed to be driven mainly by its resistive component.


2000 ◽  
Vol 92 (6) ◽  
pp. 1769-1776 ◽  
Author(s):  
Kazuko Hayashi ◽  
Kenji Shigemi ◽  
Toshiaki Shishido ◽  
Masaru Sugimachi ◽  
Kenji Sunagawa

Background The ratio of ventricular end-systolic elastance (Ees) to effective arterial elastance (Ea) is known to reflect not only ventricular mechanical performance but also energetic performance. Despite these useful features, technical difficulties associated with estimating Ees make the clinical application of Ees/Ea impractical. We developed a framework to estimate Ees/Ea without measuring ventricular volume or altering the loading condition. Methods To achieve this goal, we approximated the ventricular time-varying elastance curve with two straight lines, one for the isovolumic phase and the other for the ejection phase, and characterized the curve with the slope ratio, k, of these two straight lines. Using the concept of the pressure-volume relationship, Ees/Ea is algebraically expressed as Ees/Ea = Pad/Pes (1 + k. ET/PEP) - 1, where Pes is end-systolic pressure, Pad is aortic diastolic pressure, ET is ejection time, and PEP is pre-ejection period. In 11 anesthetized dogs, we recorded arterial and ventricular pressures and ventricular volume and estimated Ees and Ea under various contractile states and loading conditions. Results An empirical relation between k and Ees/Ea was found as k = 0.53 (Ees/Ea)0.51. Simultaneous solution of these two equations yielded Ees/Ea as a function of Pad/Pes and ET/PEP. The estimated Ees/Ea values correlated well with the measured Ees/Ea values ([Measured Ees/Ea] = 0.96 [Estimated Ees/Ea] + 0.098, r = 0.925, SEE = 0.051). Conclusions The proposed framework is capable of estimating Ees/Ea from ventricular and aortic pressure.


2008 ◽  
Vol 295 (1) ◽  
pp. R228-R235 ◽  
Author(s):  
Takeshi Otsuki ◽  
Seiji Maeda ◽  
Motoyuki Iemitsu ◽  
Yoko Saito ◽  
Yuko Tanimura ◽  
...  

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.


1992 ◽  
Vol 263 (4) ◽  
pp. H1300-H1305
Author(s):  
J. T. Colston ◽  
G. L. Freeman

The effect of vasoactive intestinal peptide (VIP) on ventriculovascular coupling in the intact cardiovascular system has not been defined. We studied seven dogs chronically instrumented with left ventricular (LV) pressure manometers and three sets of diameter gauges before and after infusions of 0.02, 0.05, and 0.10 microgram.kg-1.min-1 VIP. The dogs were studied after autonomic blockade, anesthesia, and intubation, with a fixed heart rate of 160 beats/min. Contractility was assessed using LV elastance at end systole (Ees) and the slope of the stroke work-end-diastolic volume relation. The vascular influence of VIP was quantified by determining effective arterial elastance (Ea) under steady-state conditions. The overall effect on ventriculovascular coupling was assessed using the transfer of mechanical energy from LV to the arterial system (TransPVA) quantified as the percentage of pressure-volume area (PVA) expressed as stroke work. LV relaxation was measured using the time constant of LV pressure decay. The results showed that VIP increased contractility (Ees increased to 129, 156, and 181% of control; P < 0.01 for all vs. control) and decreased effective arterial elastance (Ea fell to 84, 68, and 64% of control; P < 0.0155 vs. control for the two higher doses). VIP had no consistent effects on LV relaxation. Thus, in addition to its positive ventricular effects (increased contractility), VIP has beneficial vascular effects (reduced Ea). These properties combine to improve ventriculovascular coupling, such that VIP enhances delivery of mechanical energy from the LV to the circulatory bed.


2002 ◽  
Vol 282 (3) ◽  
pp. H1041-H1046 ◽  
Author(s):  
Patrick Segers ◽  
Nikos Stergiopulos ◽  
Nico Westerhof

Effective arterial elastance ( E a), defined as the ratio of left ventricular (LV) end-systolic pressure and stroke volume, lumps the steady and pulsatile components of the arterial load in a concise way. Combined with E max, the slope of the LV end-systolic pressure-volume relation, E a/ E max has been used to assess heart-arterial coupling. A mathematical heart-arterial interaction model was used to study the effects of changes in peripheral resistance ( R; 0.6–1.8 mmHg · ml−1 · s) and total arterial compliance (C; 0.5–2.0 ml/mmHg) covering the human pathophysiological range. E a, E a/ E max, LV stroke work, and hydraulic power were calculated for all conditions. Multiple-linear regression analysis revealed a linear relation between E a, R/ T (where T is cycle length), and 1/C: E a= −0.13 + 1.02 R/ T + 0.31/C, indicating that R/ T contributes about three times more to E a than arterial stiffness (1/C). It is demonstrated that different pathophysiological combinations of R and C may lead to the same E a and E a/ E max but can result in differences of 10% in stroke work and 50% in maximal power.


2006 ◽  
Vol 38 (Supplement) ◽  
pp. S185
Author(s):  
Takeshi Otsuki ◽  
Seiji Maeda ◽  
Motoyuki Iemitsu ◽  
Yoko Saito ◽  
Yuko Tanimura ◽  
...  

1991 ◽  
Vol 67 (2) ◽  
pp. 162-168 ◽  
Author(s):  
Thomas Wisenbaugh ◽  
Martin Berk ◽  
Rafique Essop ◽  
Shirley Middlemost ◽  
Pinhas Sareli

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