ライフサイエンスコーパス: elastance

1 of respiratory resistance and low-frequency elastance).

2 with increased elastic artery stiffness (or elastance).

3 lung compliance, tissue damping, and tissue elastance).

4 l pressure and the other based on chest wall elastance.

5 olic elastance (Eed), and effective arterial elastance.

6 had increased lung compliance and decreased elastance.

7 buted to increased tissue damping and tissue elastance.

8 onary valve resistance and systemic arterial elastance.

9 om the frequency responses of resistance and elastance.

10 orrelated with body mass index or chest wall elastance.

11 cle contraction, lung resistance and dynamic elastance.

12 ey were not reliable for determining maximum elastance.

13 artery pressure, resistance, compliance, and elastance.

14 uction in small airway resistance and tissue elastance.

15 oup experienced a change in dynamic arterial elastance.

16 nsitivity, without changing dynamic arterial elastance.

17 ere recorded to compute driving pressure and elastance.

18 ements in oxygenation and respiratory system elastance.

19 w is applied to overcome lung and chest wall elastance.

20 l pressure and the other based on chest wall elastance.

21 2); P=0.029) and pulmonary systemic arterial elastance (0.32+/-0.20-0.25+/-0.19 mm Hg/mL per m(2); P<

22 and increased right ventricular end-systolic elastance (+0.72 +/- 0.2 mm Hg/mL; p < 0.001) and system

23 626 +/- 153 dyn.s/cm; p = 0.714), effective elastance, (0.63 +/- 0.22 vs 0.58 +/- 0.17 mm Hg/mL; p =

24 with impaired LV contractility (end-systolic elastance 1.74 mm Hg/mL vs 2.35 mm Hg/mL [P = 0.024]; ma

25 55+/-122 mm Hg/s, P=0.006), and end-systolic elastance (1.03+/-0.57 versus 0.89+/-0.38 mm Hg/mL, P=0.

26 LV ventricular elastance (1.31+/-0.93-1.23+/-0.72 mm Hg/mL per m(2); P=

27 EF >60% had higher increases in end-systolic elastance (1.85 versus 0.82 mm Hg/mL; P=0.023), attenuat

28 /m(2)) and increased arterial load (arterial elastance, 1.51 mm Hg/mL) were evident.

29 gher baseline LV contractility (end-systolic elastance, 1.85 vs 1.33 mm Hg/mL; P<0.001) and passive d

30 Hg; p = 0.01) and greater effective arterial elastance (2.77 +/- 0.84 mm Hg .

31 , P=0.009]), and arterial function (arterial elastance [2.1%, P=0.002] and systemic arterial complian

32 post-MR versus post-PVA, P=nonsignificant), elastance (3.5+/-1.4 versus 2.9+/-1.3; post-MR versus po

33 e (27%), tissue resistance (48%), and tissue elastance (30%).

34 6+/-7 mm Hg; P<0.001) and effective arterial elastance (5.9+/-3.1 to 9.2+/-3.9 mm Hg/microl; P<0.001)

35 e-area relations were variable: end-systolic elastance, 6.5+/-3.4 to 4.3+/-2.5 mm Hg/cm2 and preload

36 9 br/mm, P=0.043) and lung mechanics (static elastance 61 +/- 36 cmH2O /mL vs 113 +/- 40 cmH2O/mL, P=

37 br/mm2, P=0.043) and lung mechanics (static elastance 61 +/- 36 cmH2O /mL vs 113 +/- 40 cmH2O/mL, P=

38 Mesenchymal stem cell mitigated changes in elastance, alveolar collapse, and inflammation at days 2

39 tions of this approach due to variability in elastance among mice, suggesting that the constancy obse

40 dynamic Starling mechanism, dynamic arterial elastance and arterial-cardiac baroreflex function were

41 dynamic Starling mechanism, dynamic arterial elastance and arterial-cardiac baroreflex function.

42 dynamic Starling mechanism, dynamic arterial elastance and arterial-cardiac baroreflex function.

43 ge compression slightly worsened static lung elastance and cardiac output (p = 0.0391).

44 at rest and improved arterial compliance and elastance and central hemodynamics during exercise.

45 rdiac function judged by reduced ventricular elastance and decreased cardiac output.

46 expiratory pressure levels minimizing global elastance and driving pressure, electrical impedance tom

47 the groups did not differ in terms of static elastance and dynamic intrinsic positive end-expiratory

48 ing, defined by the quotient of end-systolic elastance and effective arterial elastance, was preserve

49 or a potentially deleterious effect (reduced elastance and ejection fraction).

50 However, it reduced arterial elastance and improved Vo(2)max by 19% (22.8+/-3.4 versu

51 i, which is associated with decreased tissue elastance and increased quasi-static compliance of Sepn1

52 ices of force-generation, e.g., end-systolic elastance and invasive indices of diastolic properties,

53 VV sheep also displayed lower-lung elastance and mechanical heterogeneity in comparison wit

54 nonaerated lung tissue, reestablishing lung elastance and oxygenation while avoiding increased pulmo

55 Global LV systolic function (end-systolic elastance and preload recruitable stroke work) were not

56 eased contractility assessed by end-systolic elastance and provided venoarterial dilation.

57 nhanced contractility, doubling end-systolic elastance and raising fractional shortening similarly in

58 ic elastance, and left ventricular diastolic elastance and relaxation noninvasively in consecutive HF

59 ignificantly decreased perturbations in lung elastance and resistance, resulting in faster resolution

60 RV elastance and stiffness both increased (P<0.05), suggest

61 approximately 40% fall in effective arterial elastance and systemic resistance.

62 ic pressure and decreased effective arterial elastance and systemic vascular resistance (each p < 0.0

63 eased (p < 0.05), whereas effective arterial elastance and systemic vascular resistance remained unch

64 fluid-induced changes in effective arterial elastance and systemic vascular resistance were correlat

65 At days 1, 2, and 7, static lung elastance and the amount of alveolar collapse were simil

66 LV systolic (end-systolic elastance and twist) and diastolic functional profiles (

67 Arterial elastance and ventricular end-systolic elastance were si

68 tion, as well as pulmonary/systemic arterial elastance and ventriculoarterial coupling, were assessed

69 ontractility (eg, +33+/-4.2% in end-systolic elastance) and lowered afterload (-14.2+/-2% in systemic

70 ally quasi-static lung compliance and tissue elastance) and reduced mucus production in airways.

71 rs of ventricular contractility (ventricular elastance) and ventricular compliance function, as well

72 ffness (total aortic compliance and arterial elastance), and maximal exercise testing.

73 otal arterial compliance, effective arterial elastance, and aortic characteristic impedance were deri

74 mputed tomography scans, oxygenation, static elastance, and dynamic respiratory resistance and elasta

75 ontrol mice, but that lung tissue dampening, elastance, and hysteresivity were significantly elevated

76 ial elastance, left ventricular end-systolic elastance, and left ventricular diastolic elastance and

77 Throughout 4 years, blood pressure, arterial elastance, and LV mass decreased, coupled with significa

78 s of alveolar capillary barrier injury, lung elastance, and mortality than WT mice with ALI.

79 tly improve lung volumes, respiratory system elastance, and oxygenation.

80 n the restoration of normal lung compliance, elastance, and pressure-volume loops (tissue recoil).

81 eft ventricular diastolic function, arterial elastance, and ventricular-arterial coupling in hyperten

82 in ventricular diastolic function, arterial elastance, and ventricular-arterial coupling.

83 , including arterial compliance, resistance, elastance, and wave reflection.

84 tion fraction, stroke work, and end-systolic elastance are significant (P<0.01) between groups.

85 Ventriculo-arterial coupling (end-systolic elastance/arterial elastance) at rest was in the range o

86 Measuring respiratory resistance and elastance as a function of time, tidal volume, respirato

87 eased end-diastolic and end-systolic chamber elastance, as well as diastolic dysfunction seen at the

88 rd shift in V100 [the volume of end-systolic elastance at 100 mm Hg], 24+/-9 to 16+/-5 microL; P<0.00

89 als, and an estimated normalized ventricular elastance at arterial end diastole.

90 ervals, and estimated normalized ventricular elastance at end diastole.

91 2 hrs of treatment, left ventricular maximum elastance at end systole increased and was unchanged in

92 systolic elastance (left ventricular maximum elastance at end systole), cardiac output, circumflex ar

93 ance, and dynamic respiratory resistance and elastance at end-expiratory pressure levels of 7.5-20 cm

94 ntrol hearts reached only 42+/-4% of maximum elastance at the onset of ejection, with substantial fur

95 al coupling (end-systolic elastance/arterial elastance) at rest was in the range of optimized stroke

96 Esophageal pressure and chest wall elastance-based methods for estimating pleural pressure

97 Esophageal pressure and chest wall elastance-based methods for estimating pleural pressure

98 Esophageal pressure and chest wall elastance-based methods for estimating pleural pressure

99 of 0 cm H2O and targeting an end-inspiratory elastance-based transpulmonary pressure of 26 cm H2O can

100 O and the other targeting an end-inspiratory elastance-based transpulmonary pressure of 26 cm H2O.

101 O and the other targeting an end-inspiratory elastance-based transpulmonary pressure of 26 cm H2O.

102 o t/t mutants, which reached 77+/-3% of peak elastance before ejection of peak.

103 MyBP-C t/t ventricles displayed reduced peak elastance, but more strikingly a marked abbreviation of

104 e and magnitude of left ventricular systolic elastance (chamber stiffening), and assessed mechanisms

105 urve shapes allow to detect regions in which elastance changes during inflation.

106 k power, ejection fraction, and end-systolic elastance changes reduced by 32+/-34%, 66+/-64%, and 56+

107 lation improved oxygenation and reduced lung elastance compared with volume-controlled ventilation in

108 s), airspace enlargement, and decreased lung elastance compared with wild-type lungs.

109 nt of pulmonary artery resistance, effective elastance, compliance, and reflected pressure waves.

110 y artery resistance (Z0), effective arterial elastance, compliance, and reflected pressure waves.

111 RA and RV elastance (contractility) and diastolic stiffness were c

112 at is based on normalized human time-varying elastance curves [EN(tN)].

113 Time-varying elastance curves were generated from 72 PV loops (52 pat

114 regions of presumed tidal recruitment (i.e., elastance decrease during inflation, pressure-volume cur

115 d tissue damping after albuterol, but tissue elastance decreased only in the Type B group.

116 In Group I, lung elastance decreased, and blood oxygenation increased sig

117 In some, total arterial elastance decreases to maximize LV work and maintain LV

118 ; CI = 0.0 to -0.9; P = 0.047), end-systolic elastance (Delta: 0.15 mmHg mL(-1); CI = 0.05-0.25; P =

119 86 +/- 50 torr; p < 0.01) and decreased lung elastance (Delta5 +/- 5 cm H2O/L; p < 0.01).

120 A concomitant decrease in effective arterial elastance (DeltaEa: -0.094 mm Hg/mL, P=0.004) yielded un

121 ial compliance and higher effective arterial elastance despite similar mean arterial pressures in con

122 load-recruitable stroke work and ventricular elastance did not change.

123 Contractility as end-systolic elastance did not decrease from the chronic MI to the ac

124 Static elastance did not demonstrate any significant pressure d

125 Baseline elastance distribution was estimated in 8-week-old wild

126 IVA was compared with elastance during contractility modulation by esmolol and

127 IVA was compared with elastance during contractility modulation by esmolol and

128 pproach to continuously track resistance and elastance during Variable Ventilation (VV), in which fre

129 Group mean RV end-systolic elastance (E'es) and maximal elastance (E'max) increased

130 RV end-systolic elastance (E'es) and maximal elastance (E'max) increased with augmented dobutamine in

131 ruitable stroke work (PRSW) and end-systolic elastance (E(es)) were calculated to assess global LV sy

132 elastance (EaI) to left ventricular systolic elastance (E(LV)I), and its components, at rest and duri

133 flow; LVOT(Acc) was compared with LV maximal elastance (E(m)) acquired by conductance catheter under

134 f intraventricular pressure, volume, maximal elastance (e(max)), preload recruitable stroke work, and

135 by systemic vascular resistance and arterial elastance (Ea) and preload as determined by end-diastoli

136 temic arterial load was assessed by arterial elastance (Ea) and right ventricular afterload by pulmon

137 afterload was measured by effective arterial elastance (Ea) and systemic vascular resistance index (S

138 rterial coupling indices, effective arterial elastance (Ea) and the coupling ratio Ea/Eessb, without

139 Effective arterial elastance (Ea) end-systolic elastance (Ees) and ventricu

140 The effective arterial elastance (Ea) represents resistive and pulsatile afterl

141 that diastolic stiffness (Eed) and arterial elastance (Ea) were increased, end-systolic elastance (E

142 tance (Ees), peripheral resistance, arterial elastance (Ea), arterial compliance, aortic pulse wave v

143 ime (max -dP/dt), filling rate, and arterial elastance (Ea), respectively.

144 (CO), arterial and end-systolic ventricular elastance (Ea, Ees,) and ventriculoarterial coupling (V/

145 rial elastance/left ventricular end-systolic elastance [Ea/Ees]) after adjustment for potential confo

146 e work [Msw]), measures of RV load (arterial elastance [Ea]), and RV pulmonary artery coupling (Ees/E

147 d intercept [V0]); and VA coupling (arterial elastance [Ea]/Eessb).

148 temic arterial afterload (effective arterial elastance, Ea; total arterial compliance, Ca; and system

149 r coupling, defined by the ratio of arterial elastance (EaI) to left ventricular systolic elastance (

150 dt) by 49 +/- 8% (p < 0.001) and ventricular elastance (Ecs) by 53 +/- 16% (p < 0.03).

151 breathing, and higher values of dynamic lung elastance (EdynL) (p < 0.01) and intrinsic positive end-

152 lic RV function was defined as end-diastolic elastance (Eed) >= median (0.19 mm Hg/mL).

153 End-diastolic elastance (Eed) was 0.14 (0.06-0.24) mm Hg/mL.

154 end-systolic elastance (Ees), end-diastolic elastance (Eed), and effective arterial elastance.

155 fective arterial elastance (Ea) end-systolic elastance (Ees) and ventricular-arterial coupling (defin

156 e were significant increases in end-systolic elastance (Ees) from 0.74+/-0.11 to 0.90+/-0.16 mm Hg/ml

157 elastance (Ea) were increased, end-systolic elastance (Ees) was decreased, and arterioventricular (A

158 arterial compliance (TAC), and end-systolic elastance (Ees) were calculated at baseline and after 8

159 us peak pressure (dP/dtmax) and end-systolic elastance (Ees) were preserved in both groups compared t

160 tionship was determined to give end-systolic elastance (Ees), a load-independent measure of contracti

161 cluding ejection fraction (EF), end-systolic elastance (Ees), and preload-recruitable stroke work (PR

162 ate paired data to determine LV end-systolic elastance (Ees), end-diastolic elastance (Eed), and effe

163 y: left ventricular volumes and end-systolic elastance (Ees), peripheral resistance, arterial elastan

164 parameter of systolic function, end systolic elastance (Ees), requires invasive catheterization.

165 fined by a ratio of end-systolic to arterial elastances (Ees/Ea).

166 end-systolic elastance to effective arterial elastance [Ees/Ea]: SHF: 1.05 +/- 0.25; P = 0.002; DHF:

167 to derive contractile indexes (end-systolic elastance [Ees] and preload recruitable stroke work [Msw

168 Systolic (end-systolic elastance, Ees) and diastolic (tau) function were assess

169 h prognosis in systolic HF, but end-systolic elastance (Eessb) is not.

170 from shortening fraction, end-systolic fiber elastance (Ef(es)) measured at resting heart rates, and

171 was caused by an increase in total arterial elastance, effectively double loading the LV, contributi

172 ndexes (maximal power index and end-systolic elastance), ejection fraction, and measures of diastolic

173 tor waveform was used to measure RL and lung elastance (EL) in 21 asthmatics from approximately 0.1 t

174 Peak elastance (Emax) was determined as the slope of end-syst

175 f intraventricular pressure, volume, maximal elastance (Emax), and dP/dtmax by conductance catheteriz

176 The reference index, maximal elastance (Emax), was calculated from pressure-volume lo

177 ociated with a lowering of systemic arterial elastance (end-systolic pressure/stroke volume) and syst

178 date bedside estimates of effective arterial elastance = end-systolic pressure/stroke volume in criti

179 sensitivity (resistance, tissue damping, and elastance), eosinophilic inflammation, and airway remode

180 cted to vary according to respiratory system elastance (Ers).

181 that results in increased respiratory system elastance (Ers); however, the extent of this increase va

182 ystolic pressure, whereas effective arterial elastance (femoral estimate) and systemic vascular resis

183 ndividual breaths, calculates resistance and elastance for each breath, bins them according to freque

184 nd load-independent measures of end-systolic elastance from pressure-area loops (r = 0.90, SEE 10.6 m

185 Chest wall and respiratory system elastances grew with increases in positive end-expirator

186 scillation perturbations to determine tissue elastance (H) and damping (G) were performed.

187 nstant, kappa, decreased (P=0.02), LV volume elastance improved (P=0.04), and the myocardial stiffnes

188 There was no change in dynamic arterial elastance in either of the two groups.

189 suggesting higher right ventricular systolic elastance in HFpEF.

190 and had negative effects on left ventricular elastance in the postjet ventilation period in both norm

191 h upward curvature) or overdistension (i.e., elastance increase during inflation, downward curvature)

192 distress syndrome, Z0 and effective arterial elastance increased (from 218 +/- 94 to 444 +/- 115 dyn.

193 In response, RA contractility improved (elastance increased from 0.28+/-0.12 to 0.44+/-0.13 mm H

194 affected by PPVI although systemic arterial elastance increased significantly (0.83+/-0.26-0.90+/-0.

195 Left ventricular systolic elastance increased to a greater extent in young versus

196 Chest wall and respiratory system elastances increased with increases in positive end-expi

197 ll recruitment maneuvers reduced static lung elastance independent of acute lung injury etiology.

198 arterial afterload as evidenced by a higher elastance index (3.3+/-0.9 versus 2.9+/-0.7 mm Hg/mL.m(2

199 ed with SBP (beta=0.24 [95% CI, 0.02-0.45]), elastance index (beta=20.2 [95% CI, 15.8-44.1]) and tota

200 Elastance index (but not SBP) was predictive of longitud

201 erload was assessed using effective arterial elastance index and total arterial compliance index.

202 MR imaging-derived elastance index correlates with ICP over a wide range of

203 The mean of the fractional SD of the elastance index in humans was 19.6%.

204 The elastance index in the five patients with intraventricul

205 The reproducibility of the elastance index measurement was established from four to

206 An elastance index was derived from the ratio of pressure t

207 The elastance index was measured and compared with invasive

208 ties (systemic vascular resistance index and elastance index) and changes in vasopressor support afte

209 ed arterial load indices (effective arterial elastance index, total arterial compliance index, system

210 ppearance, but a marked increase in arterial elastance, indicating increased afterload, and elevated

211 ysfunction" to indicate that RV end-systolic elastance is depressed or diastolic elastance is increas

212 systolic elastance is depressed or diastolic elastance is increased.

213 ed increase in afterload (effective arterial elastance), L-NMMA increased preload (end-diastolic dime

214 easure left ventricular maximum end-systolic elastance (left ventricular maximum elastance at end sys

215 left ventricular volume, effective arterial elastance, left ventricular end-systolic elastance, and

216 In all patients, nitroprusside reduced elastance, left ventricular filling pressures, and pulmo

217 icular-arterial coupling (effective arterial elastance/left ventricular end-systolic elastance [Ea/Ee

218 These two elastances limit RV filling and stroke volume and conseq

219 atory pressure PaO2/FIO2, respiratory system elastance, lung weight, normally aerated tissue, collaps

220 critically ill patients, effective arterial elastance may be reliably estimated at bedside (0.9 x sy

221 ung-distending pressure, and that chest wall elastance may vary among individuals, a physiologically

222 Finally, chest wall and respiratory system elastances may vary unpredictably with changes in positi

223 h as driving pressure and respiratory system elastance, may be predictive of those most likely to ben

224 tricular (RV) systolic pressure and arterial elastance (measure of vascular resistance) more than tri

225 and 10 days, mice were anesthetized and lung elastance measured.

226 After PPVI, both RV ventricular elastance (median [interquartile range], 0.26 [0.16-0.83

227 ressure-volume relationship and time-varying elastance model provide a foundation for understanding c

228 levant to the discussion of the time-varying elastance model, cardiogenic shock, and sepsis were retr

229 transalveolar pressures, heavily affected by elastance of the chest wall and lung, respectively, play

230 ed after surgery (p < 0.02), whereas dynamic elastance of the chest wall did not change.

231 Dynamic elastance of the lung (Edyn,L) decreased after surgery (

232 The failure group had a higher dynamic elastance of the lung than the success group (p < 0.01),

233 d-expiratory pressure resulted in the lowest elastance of the respiratory system (18.6 +/- 6.1 cm H2O

234 stroke output is caught between the passive elastance of the RV walls during diastolic filling and t

235 In 60 patients, elastances of lung and chest wall were computed, and lun

236 chest wall components or in terms of dynamic elastances of the respiratory system and chest wall.

237 teral annular diameter, but not end-systolic elastance or regional myocardial function.

238 increased respiratory system resistance and elastance (p < 0.05).

239 ance (p = 0.008), right ventricular arterial elastance (p = 0.003), and right ventricular end-systoli

240 ction to exercise due to pathologic arterial elastance (p = 0.04).

241 of a significant decrease in total arterial elastance (P<0.01 versus Group I).

242 atter inversely correlated with end-systolic elastance (P=0.0001).

243 ompliance (P=0.03), and decrease in arterial elastance (P=0.02).

244 nt PR (>=25%; n=10) had lower RV ventricular elastance (P=0.043) before and higher LV compliance (P=0

245 utrophilic infiltration, tissue damping, and elastance parameters, in association will less peribronc

246 or Crs (<40 ml/cm H(2)O; phenotype with high elastance ["phenotype H"]).

247 ed Crs (>=50 ml/cm H(2)O; phenotype with low elastance ["phenotype L"]), and 827 (74%) patients had p

248 Ventilation at lowest elastance positive end-expiratory pressure preceded by a

249 preload adjusted maximal power, end-systolic elastance, preload recruitable stroke work) and produced

250 alls during diastolic filling and the active elastance produced by the RV in systole.

251 n (17% reduction in PVR, 12% reduction in PA elastance [pulmonary Ea], and 24% increase in PA complia

252 ation, systemic resistance, pulmonary venous elastance, pulmonary resistance, pulmonary arterial elas

253 ce, pulmonary resistance, pulmonary arterial elastance, pulmonary valve resistance and systemic arter

254 s also correlated significantly with maximal elastance (r = .85 +/- .04) from pressure-volume relatio

255 PRSW (r = 0.730; P = 0.001), and NI maximum elastance (r = 0.706; P = 0.002) strongly correlated wit

256 n three key assumptions: constant normalized elastance (ratio of pressure over volume) across individ

257 RMACS classes, and higher pulmonary arterial elastance (ratio of systolic pulmonary artery pressure t

258 hemodynamics, stroke work, and end-systolic elastance return to preinfarction values 1 week after in

259 Measurements of lung resistance and elastance (RL and EL) from 0.1 to 8 Hz reflect both the

260 m Hg (+28.1+/-5.3%; P=0.02), and ventricular elastance rose from 6.0+/-1.6 to 10.5+/-2.2 mm Hg/mm (P=

261 RV afterload assessed by effective arterial elastance rose similarly in both groups; thus, ventricul

262 Conversely, effective arterial elastance should not be used in isolation as an index of

263 gest that left ventricular (LV) and arterial elastance (stiffness) increase with age, but data examin

264 stolic (Ees), and ventricular diastolic (Ed) elastance (stiffness) may contribute to the pathogenesis

265 End-systolic elastance (stiffness) was higher in patients with HF-nlE

266 piratory lung gas volume, respiratory system elastance, strain, and oxygenation significantly worsene

267 systolic properties, namely EF, end systolic elastance, stroke work, and preload recruitable stroke w

268 re pronounced effects of weight loss on lung elastance suggest that the distal lung is inherently mor

269 on with lower Vt in ARDS varies according to elastance, suggesting that lung-protective ventilation s

270 ic data, left ventricular ejection fraction, elastance, tau (relaxation constant), left ventricular s

271 udinal strain; and higher effective arterial elastance than patients without hypertension.

272 The abbreviated elastance time course and lower peak were consistent wit

273 kingly a marked abbreviation of the systolic elastance time course, which peaked earlier (27.6+/-2.1

274 including respiratory system resistance and elastance, tissue damping, inspiratory capacity, total l

275 g was worse in Cpc-PH patients (end-systolic elastance to effective arterial elastance [Ees/Ea]: SHF:

276 tion (i.e., pressure change/volume change or elastance), transmural left ventricular end-systolic pre

277 e of myocytes, but it depresses end-systolic elastance; under conditions of exercise, the beneficial

278 culation of the reference effective arterial elastance value (1.73 +/- 0.62 mm Hg/mL).

279 toring of dynamic respiratory resistance and elastance ventilator settings can be used to optimize ve

280 ationship held across a wide range of atrial elastance, ventricular relaxation and systolic function,

281 Effective arterial elastance was also higher (2.6+/-0.5 versus 1.9+/-0.5 mm

282 After jet ventilation, left ventricular elastance was decreased 36 +/- 8% in normal hearts and 3

283 End-systolic elastance was determined using blood pressure, stroke vo

284 The femoral estimate of effective arterial elastance was more accurate and precise than the radial

285 group, whereas left ventricular end-systole elastance was preserved at baseline levels.

286 Effective arterial elastance was related to systemic vascular resistance at

287 Right ventricular end-systole elastance was significantly improved in the HOX group co

288 atio of ventricular end-systolic to arterial elastances) was approximately 0.25 at baseline and doubl

289 nd-systolic elastance and effective arterial elastance, was preserved throughout all stages of exerci

290 red compliance, and increased resistance and elastance were observed in subjects with HFpEF.

291 The lung and chest wall elastance were similar between groups.

292 erial elastance and ventricular end-systolic elastance were similarly increased in hypertensive contr

293 re levels, chest wall and respiratory system elastances were calculated at each positive end-expirato

294 e, collapsed tissue, and lung and chest wall elastances were similar between the two groups.

295 ic input impedance, compliance, and arterial elastance), were significantly modified by TAVR, exhibit

296 his validated estimate of effective arterial elastance when coupled with an index of left ventricular

297 did not augment contractility (end-systolic elastance) whereas IPAH did (P<0.001).

298 cument the added value of effective arterial elastance, which is increasingly used as an index of lef

299 s, ZVV detected a decrease in resistance and elastance with time by 12.8% and 6.2%, respectively, sug

300 The proposed method is based on time-varying elastance, with experimentally optimized model parameter