ライフサイエンスコーパス: stroke volume

1 increase in both maximal cardiac output and stroke volume.

2 oppler left ventricular outflow minus inflow stroke volume.

3 (MR) as total left ventricular minus forward stroke volume.

4 filling pressure during exercise to maintain stroke volume.

5 flow volume from the total left ventricular stroke volume.

6 at 6 hours, corresponding with the nadir of stroke volume.

7 5.4 and 8.4 mL increases in left ventricular stroke volume.

8 ion by decreasing systemic venous return and stroke volume.

9 ocardial oxygen consumption for a particular stroke volume.

10 dance cardiogram (dZ/dt) is used to indicate stroke volume.

11 pulmonary artery pulse pressure, and reduced stroke volume.

12 lar coupling, and decreased left ventricular stroke volume.

13 and contractility influence left ventricular stroke volume.

14 iance correlated with lower left ventricular stroke volume.

15 essures, with no effect on cardiac output or stroke volume.

16 me as well as a higher ejection fraction and stroke volume.

17 aine group was due to a two-fold increase in stroke volume.

18 nd 30% reduction in hemispheric and cortical stroke volumes.

19 ion in hemispheric, cortical and subcortical stroke volumes.

20 1 mm/mL; P=0.01), and lower left ventricular stroke volume (-0.01 mm/mL; P<0.05).

21 n, HFpEF patients showed a lower increase in stroke volume (+10 +/- 16% vs. +21 +/- 12%) despite a gr

22 =0.99 by dose), associated with increases in stroke volume (15 [2] mL), fractional shortening (8% [1]

23 t ventricular mass [1.6%, P=0.008]), resting stroke volume (2.0%, P=0.002), left ventricular diastoli

24 per unit mean hemoglobin A(1c) percent) and stroke volume (-2.3 mL per unit mean hemoglobin A(1c) pe

25 dence interval [CI], -3.3 to -4.9; P<0.001), stroke volume (-2.7 ml; 95% CI, -2.2 to -3.3; P<0.001),

26 te patients with IPAH and DD decreased their stroke volume (-25% and -30%; P < 0.05) and failed to in

27 -7, -1; P=0.03) gradients, without affecting stroke volume 3 mL/m(2) (-2, 8; P=0.16).

28 jection time 25 ms (95% CI 18-32, p<0.0001), stroke volume 3.6 mL (0.5-6.7, p=0.0217), left ventricul

29 models, older age was associated with lower stroke volume (-3.6 mL per decade; P<0.001) and higher L

30 astolic pressure (19+/-5 mm Hg), and reduced stroke volume (33+/-8 mL/m(2)).

31 illion MultiStem resulted in improved EF and stroke volume 4 months later.

32 e (77 +/- 18 ml vs. 77 +/- 17 ml; p = 0.51), stroke volume (48 +/- 9 ml vs. 46 +/- 9 ml; p = 0.83), o

33 en epoetin alfa and placebo, but declines in stroke volume (-5+/-8 versus 2+/-10 mL; P=0.09) without

34 al/noise ratio was 3-fold better for BP than stroke volume (6.8+/-3.5 versus 2.3+/-1.4; P<0.001).

35 produced a significant acute reduction in LV stroke volume (63.9 +/- 12.0 vs. 49.4 +/- 7.8 ml, P < 0.

36 Ejection fraction (60%) and stroke volume (77 mL) were normal, while diastolic dysfu

37 rison with conventional CS site stimulation (stroke volume, 83 [79-112] mL versus 73 [62-89] mL; P=0.

38 x+LV and LV-only pacing resulted in improved stroke volume (85+/-32 mL and 86+/-33 mL versus 58+/-23

39 vq-1, that affected limb muscle survival and stroke volume after femoral artery or middle cerebral ar

40 ining venous return, central venous pressure,stroke volume and (.)Q or maintaining muscle blood flow

41 lume reduction in the context of a preserved stroke volume and an increased ejection fraction.

42 Accurate beat-to-beat stroke volume and BF were estimated using VMHDVCG extrac

43 mic brain damage was measured by determining stroke volume and by stereologic quantifications of surv

44 r how venous return is augmented to increase stroke volume and cardiac output during exercise.

45 mpensatory mechanism to maintain an adequate stroke volume and cardiac output in the face of the prog

46 r in HFpEF (p < 0.0001), and improvements in stroke volume and cardiac output were each approximately

47 Stroke volume and cardiac output were significantly incr

48 n the ML than EF phase; however, heart rate, stroke volume and cardiac output were similar between ph

49 peripheral resistance were greater, whereas stroke volume and cardiac output were smaller in patient

50 pling intervals were associated with greater stroke volume and dP/dtmax despite more pronounced dyssy

51 have significantly reduced left ventricular stroke volume and ejection fraction (LVEF) and tend to d

52 ume and decreased chest compliance decreased stroke volume and increased arterial pressure variations

53 12 h after experimental stroke reduced both stroke volume and inflammatory cytokines associated with

54 unted response to dobutamine with respect to stroke volume and kinetic energy.

55 sing blood pool images and applied to obtain stroke volume and LV ejection fraction (LVEF).

56 Despite normalization of LV stroke volume and LV end-diastolic volume/mass ratio, th

57 Hemispheric stroke volume and neural deficit scores were quantitated

58 In Fontan patients, the largest increases in stroke volume and stroke volume index were during zero-r

59 ationship between increased vagal tone, high stroke volumes and incident AF, and particularly so in p

60 LV outflow tract area, indexed stroke volume, and AVA correlated well between echocardi

61 ce to acute stroke care performance metrics, stroke volume, and bed size was not associated with down

62 as associated with worse systolic (lower EF, stroke volume, and cardiac index) and diastolic (shorter

63 ed to left ventricular end-diastolic volume, stroke volume, and cardiac output among persons without

64 Baseline blood pressure, stroke volume, and cardiac output were greater in HFpEF

65 was associated with an increased heart rate, stroke volume, and cardiac output, as well as increased

66 dary reductions in left ventricular filling, stroke volume, and cardiac output.

67 LV short-axis echocardiographic images, LV stroke volume, and dP/dtmax were obtained during all ect

68 d-diastolic volume and end-systolic volume), stroke volume, and EF were measured by 3D echocardiograp

69 r end-diastolic volume, end-systolic volume, stroke volume, and ejection fraction were determined.

70 timing demonstrated differences in preload, stroke volume, and ejection fraction.

71 with LV mass, volume, mass-to-volume ratio, stroke volume, and ejection fraction.

72 core was linearly associated with LV volume, stroke volume, and ejection fraction: for each +1-U diff

73 t gain in ejection fraction, cardiac output, stroke volume, and fractional area change in mice treate

74 d low left ventricular diastolic volume, low stroke volume, and greater severity of mitral regurgitat

75 o impaired left ventricular filling, reduced stroke volume, and lower cardiac output without changes

76 LV mass, stroke volume, and LV ejection fraction (LVEF) were meas

77 re to enhance cardiac venous return, improve stroke volume, and reduce heart rate in these patients.

78 bell-shaped improvements in cardiac output, stroke volume, and systemic oxygen delivery (p < .05 vs.

79 end-diastolic volumes, end-systolic volumes, stroke volumes, and masses with increasing doses of life

80 e permeability assays, we observed increased stroke volumes, BBB breakdown and edema formation, reduc

81 ody surface area, a 0.43-mL/m(2) decrease in stroke volume/body surface area, and a 0.21% decrease in

82 BP and stroke volume both increased immediately (P<0.001, withi

83 ventricular mass, end diastolic volume, and stroke volume, but not with ejection fraction.

84 ared with a treatment strategy of maximizing stroke volume by fluid loading, leads to less vascular e

85 calculated by dividing left ventricular (LV) stroke volume by LV myocardial volume, and long-axis str

86 he difference in automated mitral and aortic stroke volumes by real-time 3D volume color flow Doppler

87 ials evoked similar increases in heart rate, stroke volume, cardiac output and a reduction in mean ar

88 PLM-induced increases in heart rate, stroke volume, cardiac output and reductions in mean art

89 e left ventricular total isovolumic time and stroke volume, cardiac output, and cardiac index in all

90 bo 2.5 +/- 1.6 EF units; p = 0.0009), as did stroke volume, cardiac output, and diastolic strain only

91 as evidenced by decreased ejection fraction, stroke volume, cardiac output, and peak ejection rate.

92 rrelation between changes in RR interval and stroke volume, cardiac output, or cardiac index in the o

93 or stroke volume variation and the change in stroke volume/cardiac index after a fluid or positive en

94 ), pulse pressure variation (one trial), and stroke volume change with passive leg raise/fluid challe

95 Stroke volume changes after fluid challenge were +28.6%

96 Ventriculoarterial coupling implies that stroke volume changes little while preserving ventricula

97 The ITD also improved stroke volume compared with the sham device (35+/-2 vers

98 nd Gorlin methods under 7 different in vitro stroke volume conditions.

99 lunted peripheral vasoconstriction and lower stroke volume contribute to compromised orthostatic tole

100 The increase in stroke volume correlated with the increase in estimated

101 MHD, we hypothesized that a method to obtain stroke volume could be derived from extracted VMHD vecto

102 Stroke volume decreased (-21 +/- 19%; p < 0.001) and cor

103 13.3 mL per decade, respectively; P < .001), stroke volume decreased (-8.8 and -8.6 mL per decade, re

104 +/- 2.2 ml min(-1) mmHg(-1); P = 0.001) and stroke volume (Delta 9.1 +/- 2.1 ml beat(-1); P < 0.001)

105 d-diastolic volume plotted against neoaortic stroke volume demonstrated a Frank-Starling-like curve t

106 Stroke volume did not correlate with resistive index cha

107 t; r=0.95 [95% CI, 0.86-0.98]); in contrast, stroke volume did not decline (P=0.87).

108 in cardiac output, and greater likelihood of stroke volume drop with vasodilators.

109 circulation increases in cardiac output and stroke volume during Ex were due to the muscle pump, wit

110 maging revealed decreases in cardiac output, stroke volume, ejection fraction, and fractional shorten

111 tion of zebrafish, including the ventricular stroke volume, ejection fraction, cardiac output, heart

112 An average error of 7.22% and 3.69% in stroke volume estimation, respectively, was found during

113 nisms, we measured simultaneous beat-to-beat stroke volume (flow) using Doppler echocardiography, and

114 9 mm Hg and an increase in left ventricular stroke volume from 42 ml at baseline to 72 ml.

115 e 68-79) to 80 mm Hg (75-86; p < 0.0001) and stroke volume from 50 mL (30-77) to 55 mL (39-84; p < 0.

116 Multivariate analysis was performed to fit stroke volumes from gated myocardial perfusion imaging s

117 ardiogram system could detect differences in stroke volumes from gated myocardial perfusion imaging s

118 dZ/dt was the best predictor of reduction in stroke volumes from gated myocardial perfusion imaging s

119 l/min (p = 0.003); 2) an increase in forward stroke volume (FSV) from 57 +/- 17 ml to 65 +/- 18 ml (p

120 ing improved hemodynamic indexes at all AVD (stroke volume >76 mL at all fixed intervals and 88+/-31

121 tenosis patients had smaller valve areas and stroke volumes, higher mean gradients, and comparable de

122 creased during pregnancy because of a higher stroke volume in early pregnancy and a late increase in

123 es in systolic pressure, pulse pressure, and stroke volume in patients undergoing mechanical ventilat

124 ution of the muscle and ventilatory pumps to stroke volume in patients without a subpulmonic ventricl

125 evelop a technique to noninvasively estimate stroke volume in real time during magnetic resonance ima

126 aw, a mechanism by which the heart increases stroke volume in response to an increase in venous retur

127 ractional shortening, ejection fraction, and stroke volume in the EMU group.

128 ardiac electromechanics, cardiac output, and stroke volume in the perioperative setting.

129 of cardiac contractility prompted increased stroke volume, in turn increasing cardiac output, which

130 infusion of 50 mug/kg/min, left ventricular stroke volume increased (from 43.22+/-21.5 to 51.84+/-23

131 implantation, systemic arterial pressure and stroke volume increased and pulmonary pressure decreased

132 In post hoc analysis, right ventricular stroke volume increased by 4.87 ml/m(2) (P = 0.003); rig

133 ugh multiple mechanisms including depressing stroke volume, increasing fluid loss into the intestine,

134 te BP increment correlated strongly with the stroke volume increment (r=0.74, P<0.001).

135 as similar in 125 patients with normal flow (stroke volume index >35 mL/m2; P=0.22).

136 ts with evaluable echocardiograms (92%), LF (stroke volume index </=35 mL/m(2)) was observed in 530 (

137 flow and gradient: low flow was defined as a stroke volume index </=35 mL/m(2), low gradient as a mea

138 ction, including paradoxical low-flow (i.e., stroke volume index <35 ml/m(2)), low-gradient (LF-LG) a

139 tricular ejection fraction [LVEF] >/=50% but stroke volume index <35 ml/m(2)), low-gradient (mean gra

140 reduced aortic valve area (<1 cm(2)), normal stroke volume index (>/=35 mL/m(2)), and either high mea

141 Patients were stratified by stroke volume index (<35 mL/m(2) [low flow, LF] versus >

142 levosimendan increased cardiac index (22%), stroke volume index (15%), and heart rate (7%) and decre

143 es mellitus (25% versus 41%, P=0.009), lower stroke volume index (36.4+/-8.4 versus 34.4+/-8.7 mL/m2,

144 ents with LF compared with those with normal stroke volume index (47% versus 34%; hazard ratio, 1.5;

145 ats per minute; P<0.001) and to reduced peak stroke volume index (47+/-10 mL/min per m(2) versus 54+/

146 confidence interval, 0.2-0.5; P=0.0001) and stroke volume index (5.2 mL.m(-2); 95% confidence interv

147 onary (45%; P<0.001) vascular compliance and stroke volume index (8%; P=0.01).

148 ludes important subsets of patients with low stroke volume index (low flow) and low-gradient with red

149 ce index (p < 0.001; 95% CI, 0.97-0.99), and stroke volume index (p < 0.01; 95% CI, 0.96-0.99) in pre

150 esistance index (P < .01), right ventricular stroke volume index (P </= .01), and pulmonary artery ca

151 ion (P<0.001 and P=0.0007, respectively), RV stroke volume index (P<0.0001), and left ventricular end

152 nce between noninvasive and invasive AVA was stroke volume index (P<0.01).

153 ), decreased heart rate (P(group)=0.01), and stroke volume index (P(group)=0.004) compared with TTM36

154 nafil increased cardiac index (P<0.0001) and stroke volume index (P=0.003), especially at high-intens

155 Stroke volume index (P=0.015) and end-diastolic volume i

156 on functional class, 6-minute walk distance, stroke volume index (SVI), and right atrial pressure wer

157 Forty-one subjects (25 with low flow [LF], stroke volume index [SVI] </=35 ml/m(2), 16 with normal

158 Low flow (i.e., reduced stroke volume index [SVi]) can occur with both reduced a

159 SAS, but the patients with LGSAS had reduced stroke volume index and cardiac index (P=0.003 for both)

160 We measured stroke volume index and collapsibility index of the infe

161 citonin, and waveform analysis of changes in stroke volume index and systemic vascular resistance ind

162 1 .9 vs. 37.7 +/- 15.4; p = .03), plus lower stroke volume index and worse cardiac function with high

163 stroke volume index, and in the study group, stroke volume index assessed prior to severe acute pancr

164 dex with a regime using individual values of stroke volume index assessed prior to severe acute pancr

165 After volume expansion, a relevant (>/= 10%) stroke volume index increase was recorded in 56% patient

166 Stroke volume index increased after first fluid bolus in

167 ide, systemic vascular resistance index, and stroke volume index on days 3-7.

168 ts with reduced aortic valve area and normal stroke volume index undergoing AVR underwent echocardiog

169 , the largest increases in stroke volume and stroke volume index were during zero-resistance cycling.

170 cular ejection fraction and left ventricular stroke volume index were most strongly predictive of sur

171 e effects of such consequent maximization of stroke volume index with a regime using individual value

172 Doxycycline improved cardiac and stroke volume index with no chronotropic effect in doxyc

173 A measure of flow (stroke volume index) should be included in the evaluatio

174 was associated with lower ejection fraction, stroke volume index, and aortic valve mean gradient up t

175 admission, including severe tachycardia, low stroke volume index, and high inferior vena cava collaps

176 up, fluid therapy was directed by maximizing stroke volume index, and in the study group, stroke volu

177 rain natriuretic peptide, ejection fraction, stroke volume index, E/E', and left ventricular mass ind

178 iac MRI measurements included cardiac index, stroke volume index, global and regional contractile fun

179 ctors, LV mass index, aortic valve area, and stroke volume index, LVEF was independently predictive o

180 For stroke volume index, the median AUC for esmolol was 4 mL

181 ulmonary resistance index and an increase in stroke volume index.

182 lar resistance, while increasing cardiac and stroke volume index.

183 asures of arterial afterload were related to stroke volume index.

184 etween central venous pressure and change in stroke volume index/cardiac index and the percentage of

185 seline central venous pressure and change in stroke volume index/cardiac index was 0.18 (95% CI, 0.1-

186 e AS were defined in CG-AS with normal flow (stroke-volume-index >35 ml/m(2)).

187 8%) had PLF as defined by LVEF of >/=50% but stroke volume indexed to body surface area (SVi) of </=3

188 and myocardial 3-nitrotyrosine content with stroke volume indexes (r = -.701; p = .004).

189 myocardial function, as suggested by higher stroke volume indexes and left ventricular stroke work i

190 During Ex plus expiratory load, stroke volume indexes were reduced to baseline, non-exer

191 the heart (cardiac output, left ventricular stroke volume, isovolumic relaxation, E' septal annulus,

192 A PLF (indexed stroke volume </=35 mL/m(2)) was found in 26%, and after

193 prevalence of LFLG (indexed left ventricular stroke volume <35 mL/m(2) and mean gradient <40 mm Hg),

194 Using <40 mm Hg and indexed stroke volume <35 mL/m(2) by echocardiography as criteri

195 H2RA use was associated with preserved stroke volume, LV end-diastolic volume, and mass/volume

196 sure planimetric AVA, phase-contrast indexed stroke volume, LV mass, and focal fibrosis.

197 abnormal stress changes in left ventricular stroke volume (LVSV) and aortic stiffness predict future

198 gitant orifice area [EROA], left ventricular stroke volume [LVSV]) and quality-of-life (QoL) measurem

199 on, those with low gradient (LG) and reduced stroke volume may have an adverse prognosis.

200 Automated 3D stroke volume measurement can also be used as an adjunct

201 ventricular stroke volume (right ventricular stroke volume minus pulmonary regurgitant volume) after

202 disease or pharmacologic reasons, changes in stroke volume must compensate, but the capacity to do so

203 Neither annual stroke volume nor primary stroke center designation was

204 yielded total TKEsys and by normalizing for stroke volume, normalized TKEsys was obtained.

205 10 mug/kg/min; this was significant only for stroke volume, not for other parameters.

206 Patients were defined as responders if stroke volume obtained using echocardiography increased

207 A marked decrease in the stroke volume occurred with increased afterload in the f

208 s the result of an (undesirable) decrease in stroke volume or a (desirable) compensatory relief of pe

209 There was no reduction in stroke volume or neural deficit following the IV adminis

210 LBNP and LBPP had no heart rate, stroke volume, or blood pressure effects (P>0.05).

211 ulmonary arterial capacitance (PAC, ratio of stroke volume over pulmonary pulse pressure), in relatio

212 associated with lower RVEDV (p = 0.005) and stroke volume (p < 0.001), as was the presence of centri

213 ed with lower RVEDV (p = 0.004) and lower RV stroke volume (p < 0.001).

214 ss and septal thickness (both P<0.05); lower stroke volume (P<0.0001); and lower peak lateral and sep

215 0.009), right atrial pressure (P=0.037), and stroke volume (P=0.043).

216 nd higher indexed left and right ventricular stroke volumes (P=0.007 and P=0.015) and ejection fracti

217 patients was associated with maintenance of stroke volume, preserved microvascular blood flow, and a

218 ]; P < 0.0001) and in improvements in median stroke volume/pulmonary pulse pressure ratio (2.6 ml/mm

219 cular resistance as co-primary endpoints and stroke volume/pulmonary pulse pressure ratio, tricuspid

220 p < 0.0001), right ventricular outflow tract stroke volume (r = 0.660; p < 0.0001), and pulmonary vas

221 d slightly lower correlations were found for stroke volume (r = 0.74), LVEF (r = 0.81), and thickness

222 , R(2)=0.43; end-systolic volume, R(2)=0.35; stroke volume, R(2)=0.30), while EF was unaffected.

223 /dt (between 1.5 and 4.5 Hz) correlated with stroke volume (r2 = .3, p < .001).

224 5; 5.3] vs 3.1 [2.6; 3.9] L/min/m; p<0.001), stroke volume remained unchanged (34 [37; 47] vs 40 [31;

225 50 ml/m(2) to 36 ml/m(2), respectively) with stroke volume remaining constant (49 ml/m(2) vs. 51 ml/m

226 Stroke volume reserve during exercise correlates with ex

227 1.9% and 2.0% for left and right ventricular stroke volumes, respectively) than gated (coefficient of

228 Effective right ventricular stroke volume (right ventricular stroke volume minus pul

229 Stroke volume showed no correlations with resistive inde

230 tricular systolic and diastolic volumes, low stroke volume, smaller EOA, and prosthesis-patient misma

231 A showed increased LV diameters, LV volumes, stroke volume, stroke work, and septal peak systolic tis

232 e while heat stressed, a greater decrease in stroke volume (SV) for a similar decrease in ventricular

233 However, beat-to-beat stroke volume (SV) has not been assessed in response to

234 ise intolerance is associated with a reduced stroke volume (SV) in POTS, and that the high heart rate

235 attenuates orthostatic-induced decreases in stroke volume (SV) via altering the operating position o

236 TGA patients had lower peak VO2, Qc, and stroke volume (SV), a blunted Qc/VO2 slope, and diminish

237 diastolic volume (EDV), end systolic volume, stroke volume (SV), cardiac output (CO), LV mass, ejecti

238 ed with novel magnetic resonance measures of stroke volume (SV), cardiac output (CO), total periphera

239 lic volume (EDV), end-systolic volume (ESV), stroke volume (SV), ejection fraction (EF), cardiac outp

240 Blood pressure was measured by arm cuff; stroke volume (SV), ejection fraction, and end-diastolic

241 Cardiac output (CO), heart rate (HR), stroke volume (SV), mean arterial pressure (MAP), and fe

242 lic volume (EDV), end-systolic volume (ESV), stroke volume(SV), and myocardial mass, were derived.

243 face area (PISA) (in vitro and patients) and stroke volume technique (patients) to assess mitral regu

244 CT showed significantly better agreement for stroke volume than 2D Echo, 3D Echo, and CVG.

245 (up to an 80 ms increase from baseline) and stroke volume (up to 9.7 mL) were recorded, associated w

246 We investigated the prognostic impact of stroke volume using the recently proposed flow-gradient

247 Stroke volume variation >8.7% predicted the increase in

248 nship between hypotension with normovolemia (stroke volume variation < 12%) and sepsis.

249 used to assess fluid responsiveness included stroke volume variation (nine trials), pulse pressure va

250 olute change in pulse pressure variation and stroke volume variation after increasing tidal volume fr

251 olute change in pulse pressure variation and stroke volume variation after increasing tidal volume fr

252 The new stroke volume variation algorithm is designed to restore

253 he standard stroke volume variation, the new stroke volume variation algorithm was able to predict fl

254 Stroke volume variation and pulse pressure variation do

255 variation, pulse pressure variation, and/or stroke volume variation and the change in stroke volume/

256 te, central venous pressure, cardiac output, stroke volume variation and, with use of inspiratory hol

257 d resistance for venous return increased and stroke volume variation decreased.

258 e devices to report dynamic left ventricular stroke volume variation has never been validated.

259 are superior to pulse pressure variation and stroke volume variation in predicting fluid responsivene

260 Prevalences of stroke volume variation less than 12% (normovolemia) wit

261 ng volume therapy, including cardiac output, stroke volume variation monitoring, and global end-diast

262 The changes in pulse pressure variation or stroke volume variation obtained by transiently increasi

263 Median [interquartile range, 25% to 75%] stroke volume variation values at baseline were not diff

264 cteristic curve analysis showed that the new stroke volume variation was an accurate predictor of flu

265 rterial pressure waveforms were recorded and stroke volume variation was computed from the new and fr

266 The new stroke volume variation was higher in responders than in

267 Baseline stroke volume variation was higher in those in whom card

268 the curve = 0.892 +/-, whereas the standard stroke volume variation was not (area under the curve =

269 . 12% +/- 3%, p < .05), whereas the standard stroke volume variation was similar in the two groups (2

270 the changes in pulse pressure variation and stroke volume variation will predict fluid responsivenes

271 The pulse pressure variation, stroke volume variation, and cardiac index were recorded

272 baseline cardiac function, as quantified by stroke volume variation, and the subsequent changes in m

273 en the baseline systolic pressure variation, stroke volume variation, and/or pulse pressure variation

274 The pulse pressure variation, stroke volume variation, central venous pressure, and en

275 udies that evaluated the association between stroke volume variation, pulse pressure variation, and/o

276 variation and 0.82, 0.86, and 27.34 for the stroke volume variation, respectively.

277 tween the baseline pulse pressure variation, stroke volume variation, systolic pressure variation, an

278 In contrast to the standard stroke volume variation, the new stroke volume variation

279 norepinephrine can be predicted by baseline stroke volume variation.

280 pressure variation and 11.6 +/- 1.9% for the stroke volume variation.

281 0.95; 95% confidence interval 0.82-0.99) and stroke volume variations (0.60; 95% confidence interval

282 Stroke volume variations and cardiac output obtained wit

283 Stroke volume variations obtained with a pressure record

284 A 12.6% stroke volume variations threshold discriminated between

285 ariations, systolic pressure variations, and stroke volume variations; and cardiac output were obtain

286 mL higher (95% CI: 0.0, 0.8 mL higher), the stroke volume was 0.5 mL higher (95% CI: 0.2, 0.8 mL hig

287 timing of echocardiography, although reduced stroke volume was an indicator of adverse prognosis.

288 < 0.05) but not in LT (ANOVA P > 0.05), and stroke volume was lower in LT relative to HT at all leve

289 eterization showed modest agreement, whether stroke volume was measured by oxymetry (0.69 +/- 0.16 cm

290 cTfRMAb-EPO fusion protein, the hemispheric stroke volume was reduced 81% and the neural deficit was

291 variable, pulse distension (a surrogate for stroke volume) was improved in the neurokinin-1 receptor

292 (EF, end-systolic and end-diastolic volumes, stroke volumes) was not different in 371 subjects with C

293 city, left ventricular systolic pressure and stroke volume were blunted in dysferlin-deficient mouse

294 During PEI, LV end-diastolic volume and stroke volume were increased in both groups (P < 0.001),

295 cular ejection fraction, cardiac output, and stroke volume were modestly lower in the RA group compar

296 2)max, LV mass, LV end-diastolic volume, and stroke volume were significantly smaller and the LV was

297 amine deficiency, including elevated cardiac stroke volume with decreased vascular resistance, and el

298 kely than HFrEF to experience a reduction in stroke volume with nitroprusside (p < 0.0001), suggestin

299 curs in an attempt to limit the reduction in stroke volume, with uncoupling and increased wall stress

300 led to concentric LV remodeling and reduced stroke volume without impaired LV contractility determin