ライフサイエンスコーパス: venous pressure

1 ng lung compliance without impacting central venous pressure.

2 ongenital heart disease and elevated central venous pressure.

3 he pulmonary circulation at a normal central venous pressure.

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

5 syndrome patients with a low initial central venous pressure.

6 d tonographic outflow facility or episcleral venous pressure.

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

8 when compared to guiding therapy on central venous pressure.

9 tic pressure both subtracted by mean central venous pressure.

10 aortic pressure, both subtracted by central venous pressure.

11 coupled with elevated systemic and pulmonary venous pressures.

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

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

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

15 12 mm Hg (median = 8, p = .005); and central venous pressure -2 mm Hg (median = -1, p = .04).

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

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

18 +/- 4 beats min(-1)), while reducing central venous pressure (5.5 +/- 07 to 0.2 +/- 0.6 mmHg) accompa

19 +/- 0.6 to 14.3 +/- 0.8 mm Hg), and central venous pressure (6.6 +/- 0.7 to 10.7 +/- 0.9 mm Hg).

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

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

22 Central venous pressure, airway pressure, pericardial pressure,

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

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

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

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

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

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

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

30 Portal venous pressure and intrahepatic endothelial dysfunction

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 Low central venous pressure anesthetic technique was used intraopera

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

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

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

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

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

61 10 eyes, was associated with higher central venous pressure before treatment (P = 0.03), prolonged f

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

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

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

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

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

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

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

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

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

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

72 from previously placed arterial and central venous pressure catheters.

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

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

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

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

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

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

79 Central venous pressure (CVP) provides information regarding rig

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Hepatic venous pressure gradient (HVPG) and systemic hemodynamic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Hepatic venous pressure gradient measurements, when properly per

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 ption for patients undergoing serial hepatic venous pressure measurements.

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

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

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

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

180 Neither central venous pressure nor left ventricular end diastolic press

181 Neither central venous pressure nor pulmonary artery occlusion pressure

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

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

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

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

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

187 18%; p = 0.928), whereas those with central venous pressure of 8 mm Hg or less experienced lower mor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 Elevated venous pressure produces congestion in the orbit with re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 5.5 mL/100 mL tissue; P=0.005), and resting venous pressure was higher (13.0 versus 10.5 mm Hg; P=0.

250 Central venous pressure was kept constant by colloid/crystalloid

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

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

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

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

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

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

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

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

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

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

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

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

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

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