ライフサイエンスコーパス: cerebral perfusion pressure

1 sure deficit (mean Deltaarea under the curve-cerebral perfusion pressure).

2 and vasopressor titration for maintenance of cerebral perfusion pressure.

3 /pyruvate ratio increased with reductions in cerebral perfusion pressure.

4 ely 90 mm Hg using norepinephrine to control cerebral perfusion pressure.

5 cranial pressure, mean arterial pressure, or cerebral perfusion pressure.

6 initial levels of intracranial pressure and cerebral perfusion pressure.

7 e in intracranial pressure and a decrease in cerebral perfusion pressure.

8 ysiology of hypertension and determinants of cerebral perfusion pressure.

9 was unchanged from baseline at any range of cerebral perfusion pressure.

10 animals which showed no changes at the same cerebral perfusion pressure.

11 e and intracranial pressure while decreasing cerebral perfusion pressure.

12 ng intracranial pressure, thereby decreasing cerebral perfusion pressure.

13 nial pressure, pressure reactivity index, or cerebral perfusion pressure.

14 cerebral perfusion pressure, termed optimal cerebral perfusion pressure.

15 inimum interpreted as the value of "optimal" cerebral perfusion pressure.

16 e with maintaining intracranial pressure and cerebral perfusion pressure.

17 and was performed without compromise in the cerebral perfusion pressure.

18 onship between pressure reactivity index and cerebral perfusion pressure.

19 cluded end-tidal CO2 as well as coronary and cerebral perfusion pressure.

20 on pressure (18 +/- 1 to 25 +/- 2; p = .04); cerebral perfusion pressure (16 +/- 3 to 18 +/- 3; p = .

21 epa Wash significantly reduced impairment of cerebral perfusion pressure (23+/-2 vs. 10+/-3 mmHg, p=0

22 t cerebral perfusion pressure 70 compared to cerebral perfusion pressure 40.

23 s in flow velocity for each step increase in cerebral perfusion pressure (57.5+/-19.9 cm x sec, 61.3+

24 sis lactate/pyruvate ratios were improved at cerebral perfusion pressure 70 compared to cerebral perf

25 Cerebral blood flow was higher in the cerebral perfusion pressure 70 group but did not reach s

26 ex (3.4 +/- 0.3 to 1.6 +/- 0.1 L/min/m2) and cerebral perfusion pressure (75.6 +/- 3.6 to 62.0 +/- 6.

27 P within the normal autoregulatory limits of cerebral perfusion pressure, 90 mins after onset, had no

28 ded by controlling intracranial pressure and cerebral perfusion pressure according to a local protoco

29 henylephrine is often used for management of cerebral perfusion pressure after traumatic brain injury

30 ents undergoing monitoring and management of cerebral perfusion pressure alone.

31 in intracranial pressure, an improvement in cerebral perfusion pressure and a decrease in cerebral e

32 Cerebral perfusion pressure and arterial PCO2 were maint

33 intracranial hypertension and assessment of cerebral perfusion pressure and autoregulation is the fo

34 cts of hypothermia on intracranial pressure, cerebral perfusion pressure and brain edema.

35 c and oxygenation monitoring, measurement of cerebral perfusion pressure and intracranial pressure, a

36 n the injured brain, despite improvements in cerebral perfusion pressure and intracranial pressure.

37 d gender to examine the relationship between cerebral perfusion pressure and low, high, or normal mea

38 Most episodes of hypoxia occur while cerebral perfusion pressure and mean arterial pressure a

39 tial confounders of the relationship between cerebral perfusion pressure and mean middle cerebral art

40 tial confounders of the relationship between cerebral perfusion pressure and mean middle cerebral art

41 focus on secondary brain ischemia, in which cerebral perfusion pressure and oxygen delivery have gai

42 The relationship between cerebral perfusion pressure and pressure reactivity inde

43 01 at initial resuscitation rapidly restored cerebral perfusion pressure and stabilized hemodynamics

44 been recently shown to increase coronary and cerebral perfusion pressures and higher rates of return

45 on + an impedance threshold device increased cerebral perfusion pressures and lowered diastolic intra

46 Doppler-derived mean velocity index based on cerebral perfusion pressure, and autoregulation reactivi

47 activity index, mean velocity index based on cerebral perfusion pressure, and autoregulation reactivi

48 Cerebral blood flow, cerebral perfusion pressure, and autoregulatory index de

49 prevented reductions in cerebral blood flow, cerebral perfusion pressure, and autoregulatory index du

50 n pial artery diameter, cerebral blood flow, cerebral perfusion pressure, and elevated intracranial p

51 tid blood flow, coronary perfusion pressure, cerebral perfusion pressure, and end-tidal CO2 were incr

52 tracranial pressure, mean arterial pressure, cerebral perfusion pressure, and fluid volume may be det

53 racranial pressure, arterial blood pressure, cerebral perfusion pressure, and impaired cerebral autor

54 results of this study show that both ICP and cerebral perfusion pressure are increased during ETS.

55 sured by the traditional measures of ICP and cerebral perfusion pressure, as well as middle cerebral

56 Noninvasive technologies for ICP and cerebral perfusion pressure assessment are being tested

57 ebral microdialysis to assess the effects of cerebral perfusion pressure augmentation on regional phy

58 Cerebral perfusion pressure augmentation resulted in a s

59 Cerebral perfusion pressure augmentation significantly i

60 Early aggressive cerebral perfusion pressure augmentation to a cerebral p

61 We investigated whether a cerebral perfusion pressure autoregulation range-which u

62 The percentage of time with cerebral perfusion pressure below (%cerebral perfusion p

63 and current guidelines recommend maintaining cerebral perfusion pressure between 40 mm Hg-60 mm Hg.

64 ceeding the 20 mmHg threshold, and to target cerebral perfusion pressure between 50 and 70 mmHg.

65 artery transcranial Doppler velocity, PaCO2, cerebral perfusion pressure between the different steps.

66 fe-threatening condition due to elevation of cerebral perfusion pressure beyond the limits of autoreg

67 s effective as phenylephrine for maintaining cerebral perfusion pressure, but intracranial pressure a

68 significantly with intracranial pressure and cerebral perfusion pressure, but not with pressure react

69 anisms may underlie the observed increase in cerebral perfusion pressure, carotid blood flow, and sur

70 ed digitally recorded intracranial pressure, cerebral perfusion pressure, cerebrovascular pressure re

71 ins (n = 14), systolic arterial pressure and cerebral perfusion pressure corrected immediately (both

72 Cerebral perfusion pressure (CPP = MAP - ICP) decreased

73 n ICP during the infusion produced a fall in cerebral perfusion pressure (CPP) and a significant decr

74 ted curve-fitting method that determined the cerebral perfusion pressure (CPP) at which the pressure

75 We monitored intracranial pressure (ICP) and cerebral perfusion pressure (CPP) before and during OLT

76 data showing that aggressive maintenance of cerebral perfusion pressure (CPP) can worsen outcome due

77 s in pial artery diameter, cortical CBF, and cerebral perfusion pressure (CPP) concomitant with eleva

78 patients with poor outcome were managed at a cerebral perfusion pressure (CPP) differing more from th

79 erial pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and laser Doppler flo

80 dium concentrations, mean arterial pressure, cerebral perfusion pressure (CPP), central venous pressu

81 We continuously monitored ICP, cerebral perfusion pressure (CPP), mean arterial pressur

82 CBF is related to cerebral perfusion pressure (CPP).

83 P stabilized intracranial pressure (ICP) and cerebral perfusion pressure (CPP).

84 ology for the continuous updating of optimal cerebral perfusion pressure (CPPopt) for patients after

85 lity in time, its ability to give an optimal cerebral perfusion pressure (CPPopt) recommendation, and

86 ) were independently associated with optimal cerebral perfusion pressure curve absence.

87 relation between the absence of the optimal cerebral perfusion pressure curve and physiological vari

88 In 28% of all 1,561 periods, an optimal cerebral perfusion pressure curve was absent.

89 primary outcome being absence of the optimal cerebral perfusion pressure curve.

90 Sequential optimal cerebral perfusion pressure curves were used to create a

91 pendently associated with absence of optimal cerebral perfusion pressure curves.

92 n consumption was unchanged from baseline as cerebral perfusion pressure decreased in either group.

93 e brain and body temperatures increased when cerebral perfusion pressure decreased to between 20 and

94 t thresholds showed no significant impact on cerebral perfusion pressure deficit (mean Deltaarea unde

95 Cerebral perfusion pressure gradually decreased as ICP i

96 ean arterial pressure greater than 70 mm Hg, cerebral perfusion pressure greater than 50 mm Hg, PaO2

97 group (38.2%) was significantly higher than cerebral perfusion pressure group (18.2%; relative risk

98 The cerebral perfusion pressure group in comparison with int

99 essure < lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity)

100 ssure-targeted therapy (n = 55) (maintaining cerebral perfusion pressure >/= 60 mm Hg, using normal s

101 dle cerebral artery flow velocity occur with cerebral perfusion pressure >40 mm Hg in severe pediatri

102 middle cerebral artery flow velocity despite cerebral perfusion pressure >40 mm Hg.

103 ombined with vasopressor therapy to maintain cerebral perfusion pressure >60 mmHg.

104 dministration of hematoma, while maintaining cerebral perfusion pressure >65 mm Hg.

105 rine or arginine vasopressin was titrated to cerebral perfusion pressure >70 mm Hg (randomized and bl

106 , and dextrose were administered to maintain cerebral perfusion pressure >70 mm Hg, filling pressure

107 ns, all received mannitol and the target was cerebral perfusion pressure >or=60 mm Hg.

108 of complications associated with targeting a cerebral perfusion pressure>70, we hypothesize that targ

109 nd after RBCT: Pbto2, intracranial pressure, cerebral perfusion pressure, hemoglobin oxygen saturatio

110 ental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular co

111 ve quantified the response to an increase in cerebral perfusion pressure in a region of interest arou

112 d the relationship of cerebral blood flow to cerebral perfusion pressure in a swine model of pediatri

113 een middle cerebral artery flow velocity and cerebral perfusion pressure in pediatric traumatic brain

114 re observed in intraparenchymal pressure and cerebral perfusion pressure in the perihematoma region a

115 e use of catecholamine infusions to maintain cerebral perfusion pressure in the setting of a high-dos

116 Mean arterial pressure and cerebral perfusion pressure increased significantly, and

117 The cerebral perfusion pressure intervention resulted in a g

118 and tissue compartments were reduced by the cerebral perfusion pressure intervention.

119 This suggests that monitoring and optimizing cerebral perfusion pressure is critical to the managemen

120 pressure result in better outcome than when cerebral perfusion pressure is managed alone.

121 d therapeutic interventions used to optimize cerebral perfusion pressure is unclear and requires furt

122 tracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of rea

123 ranial pressure between the two drugs at any cerebral perfusion pressure level.

124 arterial pressure levels of 70 and 80 mm Hg, cerebral perfusion pressure levels of 50, 60, and 70 mm

125 inuous estimation of the "lower" and "upper" cerebral perfusion pressure limits of cerebrovascular pr

126 enoted automatically the "lower" and "upper" cerebral perfusion pressure limits of reactivity, respec

127 ime with cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity)

128 ciated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity,

129 mm Hg, mean arterial pressure <70 mm Hg, or cerebral perfusion pressure <60 mm Hg and fluid balance

130 ed by cerebral perfusion pressure threshold, cerebral perfusion pressure <60 mm Hg was not associated

131 Cerebral perfusion pressure<40 mm Hg following pediatric

132 In severe traumatic brain injury, cerebral perfusion pressure management based on cerebrov

133 Individualized autoregulation-guided cerebral perfusion pressure management may be a plausibl

134 ne for maintaining tissue oxygenation during cerebral perfusion pressure management.

135 ood pressure control for the optimization of cerebral perfusion pressure may constitute the most impo

136 lic; aortic minus right atrial pressure) and cerebral perfusion pressure (mean arterial minus mean in

137 Cerebral perfusion pressures, measured in nine additiona

138 t was to find a way of improving the optimal cerebral perfusion pressure methodology by introducing a

139 ion in addition to intracranial pressure and cerebral perfusion pressure monitoring leads to better o

140 ge Glasgow Outcome Scale: all operating room cerebral perfusion pressure more than 40 mm Hg (adjusted

141 tive risk, 0.61; 95% CI, 0.58-0.64), all ICU cerebral perfusion pressure more than 40 mm Hg (adjusted

142 he lactate/pyruvate ratio was not related to cerebral perfusion pressure, nor was the percent time-bu

143 A quarter of the units did not aim for a cerebral perfusion pressure of > 60 mm Hg.

144 val revealed that an inability to maintain a cerebral perfusion pressure of > or =50 mm Hg on the fir

145 The ability to maintain a cerebral perfusion pressure of > or =50 mm Hg was the si

146 oring is recommended to maintain an adequate cerebral perfusion pressure of >60 mm Hg.

147 At a cerebral perfusion pressure of < 25 mm Hg, cerebral bloo

148 MO, with cerebral blood flow decreasing at a cerebral perfusion pressure of < 25 mm Hg, compared with

149 perfusion pressure of 39 to 25 mm Hg; and d) cerebral perfusion pressure of < 25 mm Hg.

150 lower in the ECMO group at baseline and at a cerebral perfusion pressure of < 25 mm Hg.

151 mL/100 g/ min to 29 +/- 12 mL/100 g/min at a cerebral perfusion pressure of < 25 mm Hg.

152 ral perfusion pressure of 55 to 40 mm Hg; c) cerebral perfusion pressure of 39 to 25 mm Hg; and d) ce

153 crisis and cell injury volumes compared to a cerebral perfusion pressure of 40 mm Hg in an immature s

154 MO or completion of surgery in controls); b) cerebral perfusion pressure of 55 to 40 mm Hg; c) cerebr

155 e of the vasoactive drug was reduced until a cerebral perfusion pressure of 65 mm Hg was reached and

156 erebral perfusion pressure augmentation to a cerebral perfusion pressure of 70 mm Hg in pediatric tra

157 Targeting a cerebral perfusion pressure of 70 mm Hg resulted in a gr

158 pressure>70, we hypothesize that targeting a cerebral perfusion pressure of 70 mm Hg with the use of

159 mL/100 g/min for 2.0 Hz and increased global cerebral perfusion pressure of 91 mm Hg for 0 Hz, 100.5

160 sured with positron emission tomography at a cerebral perfusion pressure of approximately 70 mm Hg an

161 ients underwent monitoring and management of cerebral perfusion pressure only.

162 d cerebral perfusion pressure target-called "cerebral perfusion pressure optimal".

163 ively constant level despite fluctuations of cerebral perfusion pressure or arterial blood pressure.

164 Hyperventilation resulted in increases in cerebral perfusion pressure (p <.0001) and reductions in

165 There were trends for rising cerebral perfusion pressure (p = 0.03) and intracranial

166 gow Coma Scale score, intracranial pressure, cerebral perfusion pressure, PaCO2, total hemoglobin con

167 METHODS AND MAIN Cerebral perfusion pressure-pressure reactivity index cu

168 an arterial pressure range 80-97, mean 88.6; cerebral perfusion pressure range 62-88, mean 76.5).

169 ours after introduction of the hematoma, the cerebral perfusion pressure recorded in the perihematoma

170 reate a color-coded maps of autoregulation - cerebral perfusion pressure relationship evolution over

171 ral extraction of oxygen in conjunction with cerebral perfusion pressure result in better outcome tha

172 Cerebral perfusion pressure, Sao2, and Fio2 were similar

173 s mean increase appears to be independent of cerebral perfusion pressure, Sao2, and Fio2.

174 y-seven percent of respondents felt that the cerebral perfusion pressure should be maintained at >70

175 and adjusting for intracranial pressure and cerebral perfusion pressure, systemic glucose concentrat

176 After 8 hrs, in both groups, cerebral perfusion pressure, systolic arterial pressure,

177 d on identifying "one" autoregulation-guided cerebral perfusion pressure target-called "cerebral perf

178 We compared cerebral perfusion pressure-targeted approach with the c

179 Patients were randomized to receive either cerebral perfusion pressure-targeted therapy (n = 55) (m

180 Cerebral perfusion pressure-targeted therapy, which reli

181 ated individualized target for management of cerebral perfusion pressure, termed optimal cerebral per

182 of cerebral extraction of oxygen along with cerebral perfusion pressure, than in the control group o

183 concept of an individually targeted level of cerebral perfusion pressure that aims to restore impaire

184 no correlation with intracranial pressure or cerebral perfusion pressure; the correlation with pressu

185 ment may be a plausible alternative to fixed cerebral perfusion pressure threshold management in seve

186 In addition, no single cerebral perfusion pressure threshold was associated wit

187 When examined by cerebral perfusion pressure threshold, cerebral perfusio

188 te ratio related to any particular sustained cerebral perfusion pressure threshold.

189 We hypothesized that increased cerebral perfusion pressure through phenylephrine sex de

190 h albumin dialysis was started after fall of cerebral perfusion pressure to 45 mmHg and continued for

191 ons of pressure reactivity index and optimal cerebral perfusion pressure using ICM+ software (Cambrid

192 The cerebral perfusion pressure values at which this "U-shap

193 e ratio values appear to be elevated despite cerebral perfusion pressure values customarily considere

194 ial pressure was >30 mm Hg (p < .001) or the cerebral perfusion pressure was <40 mm Hg (p < .001).

195 Using an infusion of the allocated drug, cerebral perfusion pressure was adjusted to 65 mm Hg.

196 The corresponding changes for cerebral perfusion pressure was an increase from 45 (37-

197 Hypoxic episodes were more common when cerebral perfusion pressure was below 60 mm Hg (relative

198 Regional cerebral perfusion pressure was calculated for each intr

199 After 20 mins of data collection, cerebral perfusion pressure was increased to 75 mm Hg by

200 After 20 mins of data collection, cerebral perfusion pressure was increased to 85 mm Hg an

201 In the ICP-targeted protocol, cerebral perfusion pressure was kept at >50 mm Hg and hy

202 In the CBF-targeted protocol, cerebral perfusion pressure was kept at >70 mm Hg and Pa

203 One hour after injury, cerebral perfusion pressure was manipulated with the vas

204 es 2, with arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (

205 Cerebral perfusion pressure was not restored until manni

206 heart rate, intracranial pressure (ICP) and cerebral perfusion pressure was recorded during the step

207 ion pressure were similar between groups but cerebral perfusion pressure was significantly higher in

208 Four ranges of cerebral perfusion pressure were evaluated: a) baseline

209 ICP, blood pressure and cerebral perfusion pressure were not significantly diffe

210 agement of cerebral extraction of oxygen and cerebral perfusion pressure, while a control group of 17

211 These data indicate that elevation of cerebral perfusion pressure with phenylephrine sex depen

212 l blood pressure, intracranial pressure, and cerebral perfusion pressure, with real-time calculations

213 tivity), or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity)