ライフサイエンスコーパス: central venous pressure

1 hrough the pulmonary circulation at a normal central venous pressure.

2 nd autotransfusion in patients with elevated central venous pressure.

3 ogressive fibrosis due to prolonged elevated central venous pressure.

4 by mean aortic pressure, both subtracted by central venous pressure.

5 s with congenital heart disease and elevated central venous pressure.

6 istress syndrome patients with a low initial central venous pressure.

7 gement may differ based on patients' initial central venous pressure.

8 outcome when compared to guiding therapy on central venous pressure.

9 mean aortic pressure both subtracted by mean central venous pressure.

10 decreasing lung compliance without impacting central venous pressure.

11 documentation and manifestations of elevated central venous pressures.

12 h govern the static and dynamic arterial and central venous pressures.

13 86, respectively, compared with 0.55 for the central venous pressure, 0.56 for the global end-diastol

14 iving LVAD support for >/=30 days had higher central venous pressures (11+/-6 versus 8+/-5 mm Hg, P=0

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

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

17 +/- 12 mm Hg vs. 33 +/- 8 mm Hg, p = 0.002, central venous pressure: 20 +/- 6 mm Hg vs. 16 +/- 8 mm

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

19 pulmonary capillary wedge pressure 33%, and central venous pressure 27% while increasing cardiac out

20 2 to 93 +/- 4 beats min(-1)), while reducing central venous pressure (5.5 +/- 07 to 0.2 +/- 0.6 mmHg)

21 ure (9.0 +/- 0.6 to 14.3 +/- 0.8 mm Hg), and central venous pressure (6.6 +/- 0.7 to 10.7 +/- 0.9 mm

22 velocity pressure gradient added to invasive central venous pressure accurately estimates systolic pu

23 f exogenous ANP and observations of elevated central venous pressure after a similar volume expansion

24 ty index was not an independent predictor of central venous pressure after adjusting for inferior ven

25 Central venous pressure, airway pressure, pericardial pr

26 ermine whether static and dynamic changes in central venous pressure alter cerebral venous pressure.

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

28 correlation coefficient between the baseline central venous pressure and change in stroke volume inde

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

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

31 oth outcomes included greater intraoperative central venous pressure and greater transfusion volumes.

32 effusion was associated with higher PCWP and central venous pressure and lower serum albumin.

33 en saturation remains low, despite achieving central venous pressure and mean arterial pressure targe

34 F, and systemic and leg oxygen delivery, but central venous pressure and muscle metabolism remained u

35 nificantly with respect to the monitoring of central venous pressure and oxygen and the use of intrav

36 an-adrenergic receptor inhibition normalized central venous pressure and partly restored glymphatic a

37 robserver variability in the measurements of central venous pressure and pulmonary artery occlusion p

38 ressure signal (Paw) to pressure tracings of central venous pressure and pulmonary artery occlusion p

39 m pulmonary capillary wedge pressure (PCWP), central venous pressure and SV (via thermodilution) were

40 demonstrated an interaction between initial central venous pressure and the effect of fluid strategy

41 lthough the mean systemic filling pressure - central venous pressure and the number of cardiac index-

42 PICCs can be used to measure central venous pressure and to follow trends in a clinic

43 Central venous pressure and velocity-time integral were

44 ols(n=9), both toxins decreased arterial and central venous pressures and systemic vascular resistanc

45 reload (pulmonary artery occlusion pressure, central venous pressure) and end-diastolic ventricular v

46 0 g of liver tissue, mean arterial pressure, central venous pressure, and CI were analyzed.

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

48 index correlated with cool extremities, high central venous pressure, and low 24-hr fluid output; and

49 ng age, elevated serum creatinine, increased central venous pressure, and red blood cell transfusion

50 pressure, cerebral perfusion pressure (CPP), central venous pressure, and urine output before and aft

51 Aortic pressures, central venous pressures, and heart rates were not diffe

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

53 ar clamping techniques supplemented with low central venous pressure anesthesia, availability of nove

54 Low central venous pressure anesthetic technique was used in

55 dex (CFIp, calculated as (occlusive pressure-central venous pressure)/(aortic pressure-central venous

56 enous-return (mean systemic filling pressure-central venous pressure), arterial load properties (syst

57 espiratory distress syndrome patients with a central venous pressure available at enrollment, 609 wit

58 sites in 10 eyes, was associated with higher central venous pressure before treatment (P = 0.03), pro

59 d markers of intravascular volume, including central venous pressure, brain-natriuretic-peptide conce

60 pulmonary artery pressure (sPAP) and higher central venous pressure, but not with other clinical or

61 ation correlated with knee mottling and high central venous pressure, but these correlations were not

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

63 with significant increase in cardiac index), central venous pressure by 21% (7-54%), (mean systemic p

64 ased mean systemic pressure by 82% (76-95%), central venous pressure by 33% (21-59%), (mean systemic

65 s no carcinine-induced effect on heart rate, central venous pressure, cardiac index, or stroke index.

66 al-venous equilibrium pressure, arterial and central venous pressure, cardiac output (LiDCOplus; LiDC

67 measured mean arterial pressure, heart rate, central venous pressure, cardiac output, stroke volume v

68 d continuous aortic, pulmonary arterial, and central venous pressures, cardiac output by thermodiluti

69 ring, including intra-arterial catheters and central venous pressure catheters, and more technologica

70 nal tube from previously placed arterial and central venous pressure catheters.

71 n saturation, intra-arterial blood pressure, central venous pressure, chest wall movement, electrocar

72 n and congenital heart disease with elevated central venous pressure complicated by PLE.

73 inical decisions regarding fluid management, central venous pressure continues to be recommended for

74 A low central venous pressure (CVP) (mean threshold <8 mm Hg)

75 gical signal used to detect right atrial and central venous pressure (CVP) abnormalities in cardio-va

76 Patients who developed WRF had a greater central venous pressure (CVP) on admission (18 +/- 7 mm

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

78 Central venous pressure (CVP) provides information regar

79 Efferent postganglionic muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patien

80 ysiological study, SNA, blood pressure (BP), central venous pressure (CVP), and heart rate were recor

81 rs, intra-arterial blood pressure (BP), ECG, central venous pressure (CVP), and muscle sympathetic ne

82 Arterial blood pressure (BP), central venous pressure (CVP), and peripheral muscle sym

83 LV) dilation, mitral regurgitation, elevated central venous pressure (CVP), and preserved right ventr

84 Arterial blood pressure (BP), central venous pressure (CVP), and SNA were recorded dur

85 ompare peripheral venous pressure (PVP) with central venous pressure (CVP), as well as other invasive

86 terial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve

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

88 ent in the emergency department: a) initiate central venous pressure (CVP)/central venous oxygen satu

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

90 rived maximal pressure gradient added to the central venous pressure demonstrated the best correlatio

91 tial pulmonary artery occlusion pressure and central venous pressure did not correlate significantly

92 Marked increase in central venous pressure during passive leg raising canno

93 The changes in central venous pressure during passive leg raising did n

94 ual care, including arterial blood pressure, central venous pressure, electrocardiography, and transo

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

96 2 secs, knee mottling, or cool extremities), central venous pressure, fluid output, and central venou

97 We examined the relationship between initial central venous pressure, fluid strategy, and 60-day mort

98 s in pulmonary artery occlusion pressure and central venous pressure following saline infusion also d

99 us in MacTel2 combined with an acute rise in central venous pressure, for which the right side may be

100 Mean central venous pressure from the CICCs was 11 + 7 mm Hg,

101 RV function improved as measured by central venous pressure (from 23.4 +/- 4.9 to 10.5 +/- 3

102 the receiver operating characteristic of the central venous pressure, global end-diastolic volume ind

103 e by 33% (21-59%), (mean systemic pressure - central venous pressure) gradient by 144% (83-215)%, whi

104 re by 21% (7-54%), (mean systemic pressure - central venous pressure) gradient by 28% (23-86%), and v

105 ent of increase in (mean systemic pressure - central venous pressure) gradient, of preload responsive

106 the increase in the (mean systemic pressure -central venous pressure) gradient.

107 s without baseline shock, those with initial central venous pressure greater than 8 mm Hg experienced

108 Taking an increase in central venous pressure greater than or equal to 3 or gr

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

110 allenge, we hypothesized that an increase in central venous pressure greater than or equal to 5 cm H2

111 RV dysfunction was defined as central venous pressure >15 mmHg and consistent echocard

112 ean arterial pressure >70 mm Hg; ScvO2 <70%; central venous pressure >8 mm Hg.

113 Pulmonary artery occlusion pressure and central venous pressure have been considered to be relia

114 Additionally, central arterial pressure, central venous pressure, heart rate, arterial blood gas,

115 form the procedure, the inability to monitor central venous pressure in the emergency department, and

116 lure after enalaprilat despite reductions in central venous pressure in this group.

117 Central venous pressure increased from the seated to sup

118 re, pulmonary artery occlusion pressure, and central venous pressure, increased and SVR decreased in

119 ules: laparoscopy with pneumoperitoneum, low central venous pressure, intermittent pedicle clamping,

120 Clinical evaluation of central venous pressure is difficult, depends on experie

121 The global effect of the fluid challenge on central venous pressure is greater in nonresponders, but

122 Central venous pressure is only weakly supported as a to

123 erial pressure, pulmonary arterial pressure, central venous pressure, kaolin and celite activated clo

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

125 ferior vena cava diameter < 2 cm predicted a central venous pressure < 10 mm Hg with a sensitivity of

126 a ramp test, targeting the following goals: central venous pressure <12 mm Hg, pulmonary capillary w

127 (area under the curve) to discriminate a low central venous pressure (< 10 mm Hg) was 0.91 for inferi

128 n in the remaining 14 patients who all had a central venous pressure<12 mm Hg.

129 LBNP caused a sustained reduction in supine central venous pressure (mean [SD], 5.7 [2.2] mm Hg to 1

130 ent targeting three physiological variables: central venous pressure, mean arterial pressure, and eit

131 learance group was resuscitated to normalize central venous pressure, mean arterial pressure, and lac

132 he ScvO2 group was resuscitated to normalize central venous pressure, mean arterial pressure, and Scv

133 is-induced hypoperfusion, specific levels of central venous pressure, mean arterial pressure, urine o

134 view of widening the range of cardiac index:central venous pressure measurements and increasing the

135 IRV significantly increased central venous pressure measurements from both catheter

136 of the trauma patient, or FAST, is replacing central venous pressure measurements to detect hemoperic

137 clinical study, three to 12 paired, digital, central venous pressure measurements were recorded from

138 Paired central venous pressure measurements were taken from 19-

139 After TIPS, central venous pressure (median, 11 vs 15 cm H(2)O; P <

140 tage of nursing staff, problems in obtaining central venous pressure monitoring, and challenges in id

141 Analysis by repeated measures showed PICC central venous pressure more than CICC central venous pr

142 ristics, heart rate, mean arterial pressure, central venous pressure, near-infrared spectroscopy, blo

143 Neither central venous pressure nor left ventricular end diastol

144 Neither central venous pressure nor pulmonary artery occlusion p

145 of <60 mm Hg, heart rate of >120 beats/min, central venous pressure of >15 mm Hg, stroke volume inde

146 hange in pericardial pressure, and change in central venous pressure of 1.1 +/- 0.7, 1.1 +/- 0.8, 0.7

147 A central venous pressure of 10 mm Hg was chosen a priori

148 Mean arterial pressure >/=65 mm Hg and central venous pressure of 10 to 15 mm Hg were hemodynam

149 (18% vs 18%; p = 0.928), whereas those with central venous pressure of 8 mm Hg or less experienced l

150 rapy administering fluid boluses to attain a central venous pressure of 8 to 12 mm Hg, vasopressors t

151 disorders, and disorders involving increased central venous pressure or mesenteric lymphatic obstruct

152 Pullers reduce central venous pressures or renal venous pressures to in

153 PCWP (odds ratio [OR], 1.06 [1.03-1.10]) and central venous pressure (OR, 1.09 [1.05-1.15]) were asso

154 data, PCWP (OR, 1.06 [1.01-1.11]; P=0.032), central venous pressure (OR, 1.14 [1.06-1.23]; P<0.001)

155 ) higher PCWP and 2.4 mm Hg (1.2-3.6) higher central venous pressure (P<0.001 for both).

156 g total GLP-1 concentrations correlated with central venous pressure (P=0.025).

157 val (p = .05); fluid requirements (p = .05); central venous pressures (p </= .007); indicators of hem

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

159 which were separately analyzed were elevated central venous pressure, peripheral edema, ascites, and

160 re-central venous pressure)/(aortic pressure-central venous pressure); pressure values in mm Hg) of t

161 Prior intravenous protamine, central venous pressure prior to protamine, preoperative

162 High baseline central venous pressure, prolonged fluorescein transit t

163 rterial pressure (invasive and noninvasive), central venous pressure, pulmonary arterial pressure, le

164 MAP, heart rate, central venous pressure, pulmonary artery occlusion pres

165 of intracranial pressure, pleural pressure, central venous pressure, pulmonary artery occlusion pres

166 ences in heart rate, mean arterial pressure, central venous pressure, pulmonary artery occlusion pres

167 RV recovery was defined as improvements in central venous pressure, pulmonary artery systolic press

168 did not affect ejection fraction or increase central venous pressure, pulmonary pressures, or left at

169 strate a lack of correlation between initial central venous pressure/pulmonary artery occlusion press

170 rterial pressure, pulmonary artery pressure, central venous pressure, pulse oximetry, and end-tidal C

171 ena cava diameter correlated moderately with central venous pressure (R = 0.58), whereas the inferior

172 Central venous pressure recorded via PICCs is slightly h

173 The slope of the multipoint cardiac index:central venous pressure relationship increased (p = .02)

174 pleural pressure, pericardial pressure, and central venous pressure, respectively.

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

176 By analogy with the classical central venous pressure rules to assess a fluid challeng

177 sion pressure (CPP), mean arterial pressure, central venous pressure, serum sodium concentrations, se

178 a previous meta-analysis that concluded that central venous pressure should not be used to make clini

179 2 mm Hg between two measurements was 79% for central venous pressure strips without Paw vs. 86% with

180 not obligatory for sustaining venous return, central venous pressure,stroke volume and (.)Q or mainta

181 Whilst lying in the supine posture, central venous pressure (supine, 7 +/- 3 vs. microgravit

182 ith LeTx, as reflected by greater or earlier central venous pressures, systemic vascular resistance,

183 on and pulmonary regurgitation) and invasive central venous pressure, systolic pulmonary artery press

184 a cava diameter is a more robust estimate of central venous pressure than the inferior vena cava coll

185 haracteristics, patient population, baseline central venous pressure, the correlation coefficient, an

186 At lower initial central venous pressures, the difference between arms wa

187 At higher initial central venous pressures, the difference in treatment be

188 to support the widespread practice of using central venous pressure to guide fluid therapy.

189 y infused prior to LBNP sufficient to return central venous pressure to pre-heat stress values.

190 rial lactate upon clamping as well as in the central venous pressure upon unclamping.

191 The range of central venous pressure values was 1-23 mm Hg with a med

192 f cardiac index (pulse contour analysis) and central venous pressure values.

193 Median central venous pressure was 15.5 mm Hg (range, 12-28), a

194 In 5 (62.5%) patients, central venous pressure was elevated secondary to congen

195 Central venous pressure was kept constant by colloid/cry

196 y that the estimated area under the curve of central venous pressure was smaller in nonresponders was

197 arterial blood pressure, both subtracted by central venous pressure, was determined for CFI during r

198 erial blood pressure, electrocardiogram, and central venous pressure were also recorded continuously.

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

200 cle sympathetic nerve activity and estimated central venous pressure were recorded during nonhypotens

201 Measurements of central venous pressure were recorded from both sites by

202 During the clinical study, measurements of central venous pressure were recorded from patients who

203 Although blood and central venous pressures were invasively monitored in >

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