ライフサイエンスコーパス: stroke volume

1 at bedside (0.9 x systolic femoral pressure/stroke volume).

2 pulmonary artery pulse pressure, and reduced stroke volume.

3 lar coupling, and decreased left ventricular stroke volume.

4 and contractility influence left ventricular stroke volume.

5 iance correlated with lower left ventricular stroke volume.

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

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

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

9 increase in both maximal cardiac output and stroke volume.

10 vere malaria have rapid ejection of a normal stroke volume.

11 oppler left ventricular outflow minus inflow stroke volume.

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

13 filling pressure during exercise to maintain stroke volume.

14 5.4 and 8.4 mL increases in left ventricular stroke volume.

15 flow volume from the total left ventricular stroke volume.

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

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

18 ion in hemispheric, cortical and subcortical stroke volumes.

19 1 mm/mL; P=0.01), and lower left ventricular stroke volume (-0.01 mm/mL; P<0.05).

20 gnificant (P < 0.05) decreases vs. ageing in stroke volume (13% OVX and 15% for OVF), stroke work (34

21 h corresponding increases in mean aqueductal stroke volume (14.6 muL; P = .045) and mean CSF peak-to-

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

23 +31 +/- 13 mL; p = 0.004), right ventricular stroke volume (+23 +/- 10 mL; p = 0.009), cardiac output

24 -7, -1; P=0.03) gradients, without affecting stroke volume 3 mL/m(2) (-2, 8; P=0.16).

25 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

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

27 -84 +/- 11 mL; p < 0.001), right ventricular stroke volume (-40 +/- 6 mL; p = 0.001), cardiac output

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

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

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

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

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

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

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

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

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

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

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

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

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

41 ver, after an induced myocardial infarction, stroke volume and cardiac output were reduced in Plin2(-

42 Stroke volume and cardiac output were significantly incr

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

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

45 namic" study, fluid administration increased stroke volume and end-systolic pressure, whereas effecti

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

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

48 her peak workload, VO2 peak, cardiac output, stroke volume and leg blood flow.

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

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

51 tio of systolic pulmonary artery pressure to stroke volume and right atrial pressure significantly im

52 c volume (p = 0.020) while right ventricular stroke volume and right ventricular ejection fraction we

53 ly associated with 4D flow derived tricuspid stroke volume and RV blood flow KE E/A ratio.

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

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

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

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

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

59 h the presence of SAM, presence of MR, total stroke volume, and cardiac mass were assessed.

60 Upright posture reduces venous return, stroke volume, and cardiac output (CO) while causing ref

61 s also assessed by measuring the heart rate, stroke volume, and cardiac output, as cardiac performanc

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

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

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

65 Among measures of LV functioning, stroke volume, and ejection fraction were associated wit

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

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

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

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

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

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

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

73 arge respiratory changes in left ventricular stroke volume, and thus pulse pressure, occur in cases o

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

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

76 tio of systolic pulmonary artery pressure to stroke volume) before left ventricular assist device, we

77 anges in hemodynamic parameters (heart rate, stroke volume, blood pressure, and peripheral blood flow

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

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

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

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

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

83 stemic vascular resistance, which constrains stroke volume, cardiac output and O(2) delivery thereby

84 stemic vascular resistance, which constrains stroke volume, cardiac output and O(2) delivery, thereby

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

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

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

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

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

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

91 Stroke volume changes after fluid challenge were +28.6%

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

93 ac output was associated with an increase in stroke volume compared to monotonic pacing (P = 0.03) an

94 ystemic vascular resistance and increases in stroke volume compared with placebo (all, P < 0.01).

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

96 d pressure, total peripheral resistance, and stroke volume compared with white participants, who disp

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

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

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

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

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

102 13.3 mL per decade, respectively; P < .001), stroke volume decreased (-8.8 and -8.6 mL per decade, re

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

104 /A ratio and 4D flow derived tricuspid valve stroke volume demonstrated independent association to he

105 Stroke volume did not correlate with resistive index cha

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

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

108 EW was calculated as stroke volume (echo)xend-systolic pressurexheart rate.

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

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

111 9 mm Hg and an increase in left ventricular stroke volume from 42 ml at baseline to 72 ml.

112 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.

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

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

115 e arterial elastance = end-systolic pressure/stroke volume in critically ill patients.

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

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

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

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

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

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

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

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

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

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

126 absence of preload dependence (increases in stroke volume index >= 15%).

127 left ventricular ejection fraction >=50% and stroke volume index >=35 mL/m(2)) and LG.

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

129 was defined by Doppler echocardiography as a stroke volume index <30 mL/m(2) (n=131) or a stroke volu

130 (adjusted HR 2.17 [1.51-3.13]; P<0.0001 for stroke volume index <30 mL/m(2) and adjusted HR 1.86 [1.

131 Flow status was defined according to stroke volume index <35 mL/m(2) (low flow, LF) or >=35 m

132 left ventricular ejection fraction >=50% but stroke volume index <35 mL/m(2)) and LG; and normal-flow

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

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

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

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

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

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

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

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

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

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

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

144 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

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

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

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

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

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

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

151 t pulmonary artery diastolic pressure (PAD), stroke volume index (SV index), systolic blood pressure

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

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

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

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

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

157 ersus 22+/-2% and 38+/-5% versus 21+/-2% for stroke volume index and stroke volume, respectively, bot

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

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

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

161 max correlated with fluid-induced changes in stroke volume index in preload-dependent cases (r = 0.61

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

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

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

165 Stroke volume index was obtained by transpulmonary therm

166 c index, extravascular lung water index, and stroke volume index were also overestimated (853 +/- 240

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

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

169 Optimal thresholds of stroke volume index were obtained for men (40 ml/m(2)) a

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

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

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

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

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

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

176 c index, extravascular lung water index, and stroke volume index, especially when double-lumen 5F per

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

178 In a subsample of 200 patients with HF, LV stroke volume index, LV filling pressure estimation, tri

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

180 We compared LF (stroke volume index, SVI < 35 ml/m(2)) and NF severe AS.

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

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

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

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

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

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

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

188 8%) had PLF as defined by LVEF of >/=50% but stroke volume indexed to body surface area (SVi) of </=3

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

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

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

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

193 stroke volume index <30 mL/m(2) (n=131) or a stroke volume <55 mL (n=136).

194 d adjusted HR 1.86 [1.29-2.68]; P=0.001, for stroke volume <55 mL).

195 diastolic volume, LV end-systolic volume, LV stroke volume, LV ejection fraction, LV mass, and LV mas

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

197 articipants because of tachycardia; however, stroke volume, LV internal diameter in diastole (LVIDd),

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

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

200 2): -4.2 mL/m(2) [-6.8 to -1.7], P=0.001, LV stroke volume/m(2): -3.0 mL/m(2) [-4.5 to -1.5], P<0.001

201 ) [-4.5 to -1.5], P<0.001; right ventricular stroke volume/m(2): -3.8 mL/m(2) [-6.5 to -1.1], P=0.005

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

203 were associated with significant changes in stroke volume (mean decrease of 4.2% [95% CI = 0.8-7.6;

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

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

206 Neither annual stroke volume nor primary stroke center designation was

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

208 10 mug/kg/min; this was significant only for stroke volume, not for other parameters.

209 2 L/min ( P<0.001) because of an increase in stroke volume of 20+/-2 mL ( P<0.001) and heart rate of

210 cardiac motion, and better adherence to the stroke volume of the heart.

211 urrence of bradycardia, though no changes in stroke volume or cardiac output were observed.

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

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

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

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

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

217 0.009), right atrial pressure (P=0.037), and stroke volume (P=0.043).

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

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

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

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

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

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

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

225 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;

226 50 ml/m(2) to 36 ml/m(2), respectively) with stroke volume remaining constant (49 ml/m(2) vs. 51 ml/m

227 Stroke volume reserve during exercise correlates with ex

228 % versus 21+/-2% for stroke volume index and stroke volume, respectively, both P<0.0001).

229 1.9% and 2.0% for left and right ventricular stroke volumes, respectively) than gated (coefficient of

230 nd more severely impaired cardiac output and stroke volume responses to exertion, but similar pulmona

231 Stroke volume showed no correlations with resistive inde

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

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

234 rdiovascular function (cardiac output ( Q ); stroke volume (SV) acetylene rebreathing) were examined

235 n right ventricle (RV) ejection fraction and stroke volume (SV) at 12 weeks of age and decreased left

236 racic echocardiography we measured f(H), and stroke volume (SV) during voluntary surface apneas at re

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

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

239 RV-arterial coupling ratio using stroke volume (SV) to end-systolic volume (ESV) has been

240 LV end-diastolic volume (EDV) and stroke volume (SV) were decreased upon ascent to high al

241 volume (LVSV), 21 mL (LVSV/BSA, 13 mL/m(2)); stroke volume (SV), 19 mL (SV/BSA, 12 mL/m(2)); and ejec

242 lume (RVSV), 198 mL (RVSV/BSA, 124 mL/m(2)); stroke volume (SV), 64 mL (SV/BSA, 40 mL/m(2)); and ejec

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

244 ic volume (ESV), end-diastolic volume (EDV), stroke volume (SV), and ejection fraction (EF), were mea

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

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

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

248 died the parameters determining BP, that is, stroke volume (SV), heart rate (HR), and total periphera

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

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

251 stroke, which had higher predictive power of stroke volume than the movement components defined by hu

252 The effect of flow rate (ratio of stroke volume to ejection time) on prognostic value of A

253 d led to increased cardiac preload, and high stroke volumes, ultimately resulting in high-output hear

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

255 Stroke volume variation >8.7% predicted the increase in

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

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

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

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

260 The new stroke volume variation algorithm is designed to restore

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

262 Stroke volume variation and pulse pressure variation do

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

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

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

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

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

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

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

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

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

272 . 12% +/- 3%, p < .05), whereas the standard stroke volume variation was similar in the two groups (2

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

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

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

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

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

278 norepinephrine can be predicted by baseline stroke volume variation.

279 0.95; 95% confidence interval 0.82-0.99) and stroke volume variations (0.60; 95% confidence interval

280 A 12.6% stroke volume variations threshold discriminated between

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

282 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

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

284 < 0.05) but not in LT (ANOVA P > 0.05), and stroke volume was lower in LT relative to HT at all leve

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

286 tio of systolic pulmonary artery pressure to stroke volume was the strongest hemodynamic predictor.

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

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

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

290 eleration time (AAT)/AET, cardiac output and stroke volume were decreased compared to controls.

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

292 Cardiac output and stroke volume were increased in rats paced with respirat

293 ak-to-peak velocity amplitude and aqueductal stroke volume) were quantified for each phase.

294 ht ventricular preload and right ventricular stroke volume, whereas diuretics decreased right ventric

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

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

297 tio of systolic pulmonary artery pressure to stroke volume with right atrial pressure may be most hel

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

299 ht ventricular preload and right ventricular stroke volume without affecting mean arterial pressure.

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