ライフサイエンスコーパス: venous pressure

1 ng lung compliance without impacting central venous pressure.

2 he pulmonary circulation at a normal central venous pressure.

3 tions of IFN-gamma, TNF-alpha, and increased venous pressure.

4 d tonographic outflow facility or episcleral venous pressure.

5 hemangioma, and signs of elevated episcleral venous pressure.

6 aortic pressure, both subtracted by central venous pressure.

7 ongenital heart disease and elevated central venous pressure.

8 syndrome patients with a low initial central venous pressure.

9 ay differ based on patients' initial central venous pressure.

10 when compared to guiding therapy on central venous pressure.

11 tic pressure both subtracted by mean central venous pressure.

12 coupled with elevated systemic and pulmonary venous pressures.

13 ectively, compared with 0.55 for the central venous pressure, 0.56 for the global end-diastolic volum

14 AD support for >/=30 days had higher central venous pressures (11+/-6 versus 8+/-5 mm Hg, P=0.04), lo

15 = 78) had significantly higher mean central venous pressure (15 vs. 13 mm Hg; p = 0.001), pulmonary

16 12 mm Hg (median = 8, p = .005); and central venous pressure -2 mm Hg (median = -1, p = .04).

17 mm Hg vs. 33 +/- 8 mm Hg, p = 0.002, central venous pressure: 20 +/- 6 mm Hg vs. 16 +/- 8 mm Hg, p =

18 creased blood pressure (+6% +/- 1%), central venous pressure (+245% +/- 65%), cardiac output (+11% +/

19 ry capillary wedge pressure 33%, and central venous pressure 27% while increasing cardiac output 34%,

20 +/- 4 beats min(-1)), while reducing central venous pressure (5.5 +/- 07 to 0.2 +/- 0.6 mmHg) accompa

21 +/- 0.6 to 14.3 +/- 0.8 mm Hg), and central venous pressure (6.6 +/- 0.7 to 10.7 +/- 0.9 mm Hg).

22 pressure gradient added to invasive central venous pressure accurately estimates systolic pulmonary

23 ous ANP and observations of elevated central venous pressure after a similar volume expansion in mice

24 was not an independent predictor of central venous pressure after adjusting for inferior vena cava d

25 Central venous pressure, airway pressure, pericardial pressure,

26 atients with heart failure, elevated jugular venous pressure and a third heart sound are each indepen

27 We measured heart rate, central venous pressure and arterial pressure during all trials,

28 ion coefficient between the baseline central venous pressure and change in stroke volume index/cardia

29 coefficient, and/or the AUC between central venous pressure and change in stroke volume index/cardia

30 ccurred in the face of reductions in central venous pressure and circulating blood volume.

31 omes included greater intraoperative central venous pressure and greater transfusion volumes.

32 the brain, leading to increased intracranial venous pressure and increased intracranial pressure.

33 Portal venous pressure and intrahepatic endothelial dysfunction

34 ation remains low, despite achieving central venous pressure and mean arterial pressure targets, pack

35 few years have paid attention to peripheral venous pressure and more specifically its pressure wavef

36 ystemic and leg oxygen delivery, but central venous pressure and muscle metabolism remained unchanged

37 ly with respect to the monitoring of central venous pressure and oxygen and the use of intravenous fl

38 ergic receptor inhibition normalized central venous pressure and partly restored glymphatic and cervi

39 r variability in the measurements of central venous pressure and pulmonary artery occlusion pressure

40 signal (Paw) to pressure tracings of central venous pressure and pulmonary artery occlusion pressure

41 in HFpEF because of both elevated pulmonary venous pressure and some element of pulmonary vasoconstr

42 ary capillary wedge pressure (PCWP), central venous pressure and SV (via thermodilution) were obtaine

43 rated an interaction between initial central venous pressure and the effect of fluid strategy on mort

44 the mean systemic filling pressure - central venous pressure and the number of cardiac index-responde

45 eractions: patients without elevated jugular venous pressure and those without ascites showed directi

46 PICCs can be used to measure central venous pressure and to follow trends in a clinical setti

47 Central venous pressure and velocity-time integral were measured

48 sociated with increased postoperative portal venous pressure and von Willebrand factor antigen levels

49 iled only if nocturnal changes in episcleral venous pressure and/or uveoscleral flow occurred.

50 aracterized by chronically elevated systemic venous pressures and decreased cardiac output.

51 , both toxins decreased arterial and central venous pressures and systemic vascular resistance and in

52 pulmonary artery occlusion pressure, central venous pressure) and end-diastolic ventricular volumes/c

53 iver tissue, mean arterial pressure, central venous pressure, and CI were analyzed.

54 variation, stroke volume variation, central venous pressure, and end-expiratory occlusion test obtai

55 ory pressure (PEEP), flow rate, pH, hypoxia, venous pressure, and flow pulsatility on NOe were determ

56 rrelated with cool extremities, high central venous pressure, and low 24-hr fluid output; and low mix

57 elevated serum creatinine, increased central venous pressure, and red blood cell transfusion were fac

58 , cerebral perfusion pressure (CPP), central venous pressure, and urine output before and after the a

59 Aortic pressures, central venous pressures, and heart rates were not different at

60 produced higher survival (P = .008), central venous pressures, and left ventricular ejection fraction

61 = 21) displayed higher central and pulmonary venous pressures, and more severely impaired cardiac out

62 both, independently, been implicated in high venous pressure- and fluid shear stress-induced vascular

63 ing techniques supplemented with low central venous pressure anesthesia, availability of novel device

64 Low central venous pressure anesthetic technique was used intraopera

65 p, calculated as (occlusive pressure-central venous pressure)/(aortic pressure-central venous pressur

66 Current measurements of episcleral venous pressure are either invasive or provide highly va

67 turn (mean systemic filling pressure-central venous pressure), arterial load properties (systemic vas

68 bjects were passively tilted to increase the venous pressure at the level of the calf by 47.4 +/- 2.4

69 ry distress syndrome patients with a central venous pressure available at enrollment, 609 without bas

70 hen alveolar pressure (PA) exceeds pulmonary venous pressure because alveolar capillaries collapse an

71 10 eyes, was associated with higher central venous pressure before treatment (P = 0.03), prolonged f

72 s of intravascular volume, including central venous pressure, brain-natriuretic-peptide concentration

73 ry artery pressure (sPAP) and higher central venous pressure, but not with other clinical or hemodyna

74 rrelated with knee mottling and high central venous pressure, but these correlations were not found t

75 ntral venous pressure more than CICC central venous pressure by 1.0 + 3.2 mm Hg (p = 0.02).

76 dy was to assess whether reduction of portal venous pressure by terlipressin improves postoperative l

77 cinine-induced effect on heart rate, central venous pressure, cardiac index, or stroke index.

78 s equilibrium pressure, arterial and central venous pressure, cardiac output (LiDCOplus; LiDCO, Cambr

79 mean arterial pressure, heart rate, central venous pressure, cardiac output, stroke volume variation

80 uous aortic, pulmonary arterial, and central venous pressures, cardiac output by thermodilution, arte

81 cluding intra-arterial catheters and central venous pressure catheters, and more technological therap

82 from previously placed arterial and central venous pressure catheters.

83 tion, intra-arterial blood pressure, central venous pressure, chest wall movement, electrocardiograph

84 ngenital heart disease with elevated central venous pressure complicated by PLE.

85 ecisions regarding fluid management, central venous pressure continues to be recommended for this pur

86 A low central venous pressure (CVP) (mean threshold <8 mm Hg) was asso

87 gnal used to detect right atrial and central venous pressure (CVP) abnormalities in cardio-vascular d

88 ents who developed WRF had a greater central venous pressure (CVP) on admission (18 +/- 7 mm Hg vs. 1

89 determine the effects of changes in central venous pressure (CVP) on upper airway size.

90 Central venous pressure (CVP) provides information regarding rig

91 t postganglionic muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patients durin

92 cal study, SNA, blood pressure (BP), central venous pressure (CVP), and heart rate were recorded duri

93 a-arterial blood pressure (BP), ECG, central venous pressure (CVP), and muscle sympathetic nerve acti

94 Arterial blood pressure (BP), central venous pressure (CVP), and peripheral muscle sympathetic

95 Arterial blood pressure (BP), central venous pressure (CVP), and SNA were recorded during 3 mi

96 eripheral venous pressure (PVP) with central venous pressure (CVP), as well as other invasive hemodyn

97 lood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity

98 capillary wedge pressure (PCWP) and central venous pressure (CVP).

99 he emergency department: a) initiate central venous pressure (CVP)/central venous oxygen saturation (

100 Estimated central venous pressure decreased with LBNP (P<0.05), increased

101 ximal pressure gradient added to the central venous pressure demonstrated the best correlation with t

102 monary artery occlusion pressure and central venous pressure did not correlate significantly with ini

103 However, subclinical increases in pulmonary venous pressure due to left ventricular diastolic dysfun

104 Marked increase in central venous pressure during passive leg raising cannot identi

105 The changes in central venous pressure during passive leg raising did not diffe

106 Venous pressure elevation from 0 to 5 and 10 mm Hg decre

107 Episcleral venous pressure (EVP) was measured by gradually lowering

108 Measurements of IOP, episcleral venous pressure (EVP), conventional outflow facility (C(

109 ation in IOP is due to changes in episcleral venous pressure (EVP).

110 tions in IOP, suggesting elevated episcleral venous pressure (EVP).

111 to diastolic duration), and elevated central venous pressure (expressed as right atrial [RA] area, RA

112 s determined by subtracting the free hepatic venous pressure (FHVP) from the wedged hepatic venous pr

113 r vena caval pressure (SVCP) and femoroiliac venous pressure (FIVP) measurements by using short (<20

114 knee mottling, or cool extremities), central venous pressure, fluid output, and central venous oxygen

115 ned the relationship between initial central venous pressure, fluid strategy, and 60-day mortality in

116 monary artery occlusion pressure and central venous pressure following saline infusion also did not c

117 pressure, splanchnic blood flow, and portal venous pressure following treatment with ET and selectiv

118 allow brief retrograde transmission of high venous pressure from the arms to the cerebral venous sys

119 Mean central venous pressure from the CICCs was 11 + 7 mm Hg, and fro

120 RV function improved as measured by central venous pressure (from 23.4 +/- 4.9 to 10.5 +/- 3.1 mm Hg

121 iver operating characteristic of the central venous pressure, global end-diastolic volume index, and

122 s in good overall agreement with the hepatic venous pressure gradient (HVPG) (R = 0.82).

123 emains unclear whether a decrease in hepatic venous pressure gradient (HVPG) after cure of hepatitis

124 Hepatic venous pressure gradient (HVPG) and systemic hemodynamic

125 A hepatic venous pressure gradient (HVPG) decrease of 20% or more

126 t by transient elastography (TE) and hepatic venous pressure gradient (HVPG) in patients with chronic

127 The hepatic venous pressure gradient (HVPG) is becoming increasingly

128 Hepatic venous pressure gradient (HVPG) is the best indicator of

129 ears +/- 8) who underwent DCE US and hepatic venous pressure gradient (HVPG) measurement and four hea

130 ssessed whether guiding therapy with hepatic venous pressure gradient (HVPG) monitoring may improve s

131 nships between DIA, Ishak stage, and hepatic venous pressure gradient (HVPG) reflecting severity of f

132 The hepatic venous pressure gradient (HVPG) was determined 5 days af

133 te with portal pressure, measured by hepatic venous pressure gradient (HVPG), and predict clinically

134 itudinal changes in liver histology, hepatic venous pressure gradient (HVPG), and serum markers of fi

135 Hepatic venous pressure gradient (HVPG), the difference between

136 iameter covered stent vs those given hepatic venous pressure gradient (HVPG)-based medical therapy pr

137 utes to the postprandial increase in hepatic venous pressure gradient (HVPG).

138 nsion is the invasive acquisition of hepatic venous pressure gradient (HVPG).

139 al hypertension as determined by the hepatic venous pressure gradient (HVPG).

140 er changes in PLT correlate with the hepatic venous pressure gradient (HVPG).

141 gnificant portal hypertension (CSPH, hepatic venous pressure gradient 10 mm Hg) at FU assigned most (

142 n age 54 years (range 38-73), median hepatic venous pressure gradient 18 mmHg (range 12-37)), and 18

143 ated cirrhosis, portal hypertension (hepatic venous pressure gradient [HVPG] >/=6 mm Hg), and body ma

144 cirrhosis, and portal hypertension (hepatic venous pressure gradient [HVPG] >= 6 mm Hg) from 36 cent

145 gnificant portal hypertension (CSPH, hepatic venous pressure gradient [HVPG] 10 mmHg or greater), des

146 measured against the gold standards (hepatic venous pressure gradient [HVPG] measurement and upper en

147 sis and portal hypertension (minimal hepatic venous pressure gradient [HVPG] of 6 mm Hg) to receive t

148 correlation was observed between the hepatic venous pressure gradient and the velocity of the magnet

149 ls that demonstrate the value of the hepatic venous pressure gradient in predicting these complicatio

150 ith severity of portal hypertension (hepatic venous pressure gradient measurement) and outcome.

151 et-spleen ratio [PSR]) and endoscopy/hepatic venous pressure gradient measurement.

152 Hepatic venous pressure gradient measurements, when properly per

153 nt with rifaximin did not reduce the hepatic venous pressure gradient or improve systemic hemodynamic

154 lic hepatitis and cirrhosis, in whom hepatic venous pressure gradient was higher (P = 0.001) than cir

155 The hepatic venous pressure gradient was measured in all patients at

156 etection of EVs, and measurements of hepatic venous pressure gradient were used as the standard for i

157 Measurements of hepatic venous pressure gradient, cardiac output, and systemic v

158 Rifaximin had no effect on hepatic venous pressure gradient, mean 16.8 +/- 3.8 mm Hg at bas

159 Pugh-Turcotte scores, as well as the hepatic venous pressure gradient.

160 ortal pressure (as determined by the hepatic venous pressure gradient; HVPG) and were independent pre

161 ective evaluation revealed increased hepatic-venous pressure gradients in 2 patients with progressive

162 t baseline shock, those with initial central venous pressure greater than 8 mm Hg experienced similar

163 Taking an increase in central venous pressure greater than or equal to 3 or greater th

164 An increase in central venous pressure greater than or equal to 4 mm Hg during

165 we hypothesized that an increase in central venous pressure greater than or equal to 5 cm H2O (i.e.,

166 RV dysfunction was defined as central venous pressure >15 mmHg and consistent echocardiographi

167 rial pressure >70 mm Hg; ScvO2 <70%; central venous pressure >8 mm Hg.

168 Banding has not been compared with hepatic venous pressure-guided medical therapy (beta-blockers an

169 monary artery occlusion pressure and central venous pressure have been considered to be reliable meas

170 Arterial pressure, venous pressure, heart rate, and mean circulatory fillin

171 tionally, central arterial pressure, central venous pressure, heart rate, arterial blood gas, and pul

172 monary arterial pressure (Ppa) and pulmonary venous pressure (i.e., in Zone 1 conditions), indicating

173 s and can be associated with elevated portal venous pressure, impaired hepatic regeneration, and post

174 y decreased splanchnic blood flow and portal venous pressure in portal hypertensive rats.

175 procedure, the inability to monitor central venous pressure in the emergency department, and challen

176 er enalaprilat despite reductions in central venous pressure in this group.

177 In retinal vein occlusion, venous pressures in a segmental retinal circulatory bed

178 ow about how the blood flow and arterial and venous pressures in giraffes change when they stop to dr

179 onary artery occlusion pressure, and central venous pressure, increased and SVR decreased in GV (p <

180 paroscopy with pneumoperitoneum, low central venous pressure, intermittent pedicle clamping, anterior

181 bal effect of the fluid challenge on central venous pressure is greater in nonresponders, but not the

182 Elevated intracranial venous pressure is thought by some authors to be the "un

183 essure, pulmonary arterial pressure, central venous pressure, kaolin and celite activated clotting ti

184 With a cut-off value<8 mm Hg for central venous pressure, kappa was 0.33 [-0.03;0.69].

185 thesized that chronically increased systemic venous pressures lead to adaptive changes in regional an

186 ena cava diameter < 2 cm predicted a central venous pressure < 10 mm Hg with a sensitivity of 85% (95

187 test, targeting the following goals: central venous pressure <12 mm Hg, pulmonary capillary wedge pre

188 der the curve) to discriminate a low central venous pressure (< 10 mm Hg) was 0.91 for inferior vena

189 remaining 14 patients who all had a central venous pressure<12 mm Hg.

190 eting three physiological variables: central venous pressure, mean arterial pressure, and either cent

191 group was resuscitated to normalize central venous pressure, mean arterial pressure, and lactate cle

192 group was resuscitated to normalize central venous pressure, mean arterial pressure, and ScvO2 of at

193 ed hypoperfusion, specific levels of central venous pressure, mean arterial pressure, urine output, c

194 widening the range of cardiac index:central venous pressure measurements and increasing the accuracy

195 IRV significantly increased central venous pressure measurements from both catheter sites bu

196 METHODS AND PVP-HF (Peripheral Venous Pressure Measurements in Patients With Acute Deco

197 rauma patient, or FAST, is replacing central venous pressure measurements to detect hemopericardium a

198 study, three to 12 paired, digital, central venous pressure measurements were recorded from each of

199 Paired central venous pressure measurements were taken from 19-gauge du

200 atient comfort and relaxation during hepatic venous pressure measurements, without significantly affe

201 m tests, histologic examination, and hepatic venous pressure measurements.

202 ption for patients undergoing serial hepatic venous pressure measurements.

203 After TIPS, central venous pressure (median, 11 vs 15 cm H(2)O; P < .001), c

204 were instrumented for arterial and systemic venous pressure monitoring and blood sampling, and a spl

205 nursing staff, problems in obtaining central venous pressure monitoring, and challenges in identifica

206 sis by repeated measures showed PICC central venous pressure more than CICC central venous pressure b

207 Neither central venous pressure nor left ventricular end diastolic press

208 Neither central venous pressure nor pulmonary artery occlusion pressure

209 included arterial, intraocular, and orbital venous pressures obtained by direct cannulation, to asse

210 mm Hg, heart rate of >120 beats/min, central venous pressure of >15 mm Hg, stroke volume index of <30

211 pericardial pressure, and change in central venous pressure of 1.1 +/- 0.7, 1.1 +/- 0.8, 0.7 +/- 0.4

212 A central venous pressure of 10 mm Hg was chosen a priori as a cli

213 an arterial pressure >/=65 mm Hg and central venous pressure of 10 to 15 mm Hg were hemodynamic treat

214 18%; p = 0.928), whereas those with central venous pressure of 8 mm Hg or less experienced lower mor

215 inistering fluid boluses to attain a central venous pressure of 8 to 12 mm Hg, vasopressors to attain

216 Systemic venous pressures of >15 mm Hg, stent dysfunction, and co

217 pendent prognostic value of elevated jugular venous pressure or a third heart sound in patients with

218 The presence of elevated jugular venous pressure or a third heart sound was ascertained b

219 s, and disorders involving increased central venous pressure or mesenteric lymphatic obstruction.

220 are exertion-related increase in episcleral venous pressure or ocular compression from sleeping on t

221 Pullers reduce central venous pressures or renal venous pressures to increase r

222 l fluid outflow resistance and high cerebral venous pressure, or a combination of the three.

223 have dyspnea, tachycardia, elevated jugular venous pressure, or cardiomegaly on chest radiograph.

224 ther changes in outflow facility, episcleral venous pressure, or uveoscleral flow at night could acco

225 TS group was divided into patients with high venous pressure (P(v)>20 mm Hg) and normal P(v) on the b

226 .05); fluid requirements (p = .05); central venous pressures (p </= .007); indicators of hemoconcent

227 with increases in mean pulmonary and central venous pressures (P<0.05).

228 y multiple flow-rate infusion and episcleral venous pressure (Pe) measured by manometry.

229 ity, 82%; 95% CI, 72%-92%), elevated jugular venous pressure (pooled sensitivity, 76%; 95% CI, 62%-90

230 the nos3 gene (eNOS), was ligated and portal venous pressure (Ppv), abdominal aortic blood flow (Qao)

231 al venous pressure)/(aortic pressure-central venous pressure); pressure values in mm Hg) of the left

232 Prior intravenous protamine, central venous pressure prior to protamine, preoperative ejectio

233 Elevated venous pressure produces congestion in the orbit with re

234 High baseline central venous pressure, prolonged fluorescein transit time, and

235 pressure (invasive and noninvasive), central venous pressure, pulmonary arterial pressure, left and r

236 acranial pressure, pleural pressure, central venous pressure, pulmonary artery occlusion pressure, an

237 MAP, heart rate, central venous pressure, pulmonary artery occlusion pressure, me

238 heart rate, mean arterial pressure, central venous pressure, pulmonary artery occlusion pressure, or

239 overy was defined as improvements in central venous pressure, pulmonary artery systolic pressure, RV/

240 affect ejection fraction or increase central venous pressure, pulmonary pressures, or left atrial fil

241 lack of correlation between initial central venous pressure/pulmonary artery occlusion pressure and

242 pressure, pulmonary artery pressure, central venous pressure, pulse oximetry, and end-tidal CO(2) wer

243 strain-gauge plethysmography used to measure venous pressure (Pv), forearm and calf blood flow, vascu

244 his protocol we have non-invasively assessed venous pressure (Pv,est), isovolumetric cuff pressure (P

245 re and heart rate were unchanged, peripheral venous pressure (PVP) increased (P < 0.05), MSNA total a

246 We sought to compare peripheral venous pressure (PVP) with central venous pressure (CVP)

247 Portal venous pressure (PVP), IHR, plasma and hepatic levels of

248 Portal venous pressure (PVP), portal venous flow (PVF), and hep

249 diameter correlated moderately with central venous pressure (R = 0.58), whereas the inferior vena ca

250 r diastolic blood pressure, elevated jugular venous pressure, recent weight gain, and lower blood ure

251 Central venous pressure recorded via PICCs is slightly higher, b

252 lope of the multipoint cardiac index:central venous pressure relationship increased (p = .02).

253 and 0.53+/-0.20; P=0.0004), higher pulmonary venous pressure relative to left ventricular transmural

254 occur in iloprost-treated animals, as portal venous pressure remained within baseline range (P < 0.05

255 pressure, pericardial pressure, and central venous pressure, respectively.

256 us administration with monitoring of jugular venous pressure, respiratory rate, and arterial oxygen s

257 in the peak splanchnic blood flow or portal venous pressure response following ET-A receptor blockad

258 In addition, initial central venous pressure, right ventricular end-diastolic volume

259 By analogy with the classical central venous pressure rules to assess a fluid challenge, we hy

260 pose of the study was to measure the retinal venous pressure (RVP) in the eyes of primary open-angle

261 Increased pulmonary venous pressure secondary to left heart disease is the m

262 ssure (CPP), mean arterial pressure, central venous pressure, serum sodium concentrations, serum osmo

263 us meta-analysis that concluded that central venous pressure should not be used to make clinical deci

264 Portal venous pressure showed 16% and 56% increases after burn

265 between two measurements was 79% for central venous pressure strips without Paw vs. 86% with Paw.

266 gatory for sustaining venous return, central venous pressure,stroke volume and (.)Q or maintaining mu

267 Whilst lying in the supine posture, central venous pressure (supine, 7 +/- 3 vs. microgravity, 4 +/-

268 , as reflected by greater or earlier central venous pressures, systemic vascular resistance, and chan

269 ulmonary regurgitation) and invasive central venous pressure, systolic pulmonary artery pressure, dia

270 iameter is a more robust estimate of central venous pressure than the inferior vena cava collapsibili

271 istics, patient population, baseline central venous pressure, the correlation coefficient, and/or the

272 At lower initial central venous pressures, the difference between arms was predom

273 At higher initial central venous pressures, the difference in treatment between ar

274 ort the widespread practice of using central venous pressure to guide fluid therapy.

275 d prior to LBNP sufficient to return central venous pressure to pre-heat stress values.

276 ers reduce central venous pressures or renal venous pressures to increase renal perfusion.

277 culation is critically dependent on elevated venous pressures to sustain effective venous return.

278 tate upon clamping as well as in the central venous pressure upon unclamping.

279 The range of central venous pressure values was 1-23 mm Hg with a median valu

280 c index (pulse contour analysis) and central venous pressure values.

281 Portal venous pressure was assessed after minor (30%), standard

282 severity of heart failure, elevated jugular venous pressure was associated with an increased risk of

283 Her venous pressure was elevated, but the liver was not enla

284 5.5 mL/100 mL tissue; P=0.005), and resting venous pressure was higher (13.0 versus 10.5 mm Hg; P=0.

285 Central venous pressure was kept constant by colloid/crystalloid

286 ary vein ostia were cannulated and pulmonary venous pressure was measured before RF energy applicatio

287 Portal venous pressure was significantly elevated post-PH in mi

288 he estimated area under the curve of central venous pressure was smaller in nonresponders was 0.12.

289 The mean reduction of portal venous pressures was 43.7%, with a mean decrease of 73%

290 l blood pressure, both subtracted by central venous pressure, was determined for CFI during radial ar

291 ood pressure, electrocardiogram, and central venous pressure were also recorded continuously.

292 Heart rate, blood pressure and central venous pressure were measured.

293 athetic nerve activity and estimated central venous pressure were recorded during nonhypotensive lowe

294 Measurements of central venous pressure were recorded from both sites by using t

295 the clinical study, measurements of central venous pressure were recorded from patients who had an i

296 the ileum remained unchanged even when ileal venous pressures were increased to 15 mm Hg.

297 Although blood and central venous pressures were invasively monitored in > 50% of t

298 nous pressure (FHVP) from the wedged hepatic venous pressure (WHVP).

299 at could be used to accurately assess portal venous pressure would be valuable when diagnosing portal

300 We hypothesized that initial central venous pressure would modify the effect of fluid managem