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

3 and vasopressor titration for maintenance of cerebral perfusion pressure.

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

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

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

7 initial levels of intracranial pressure and cerebral perfusion pressure.

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

9 ysiology of hypertension and determinants of cerebral perfusion pressure.

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

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

12 e and intracranial pressure while decreasing cerebral perfusion pressure.

13 ng intracranial pressure, thereby decreasing cerebral perfusion pressure.

14 cing pressure in the brain without impairing cerebral perfusion pressure.

15 onship between pressure reactivity index and cerebral perfusion pressure.

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

17 cerebral perfusion pressure, termed optimal cerebral perfusion pressure.

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

19 e with maintaining intracranial pressure and cerebral perfusion pressure.

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

21 adient, which is not modulated by changes in cerebral perfusion pressure.

22 a cerebral perfusion pressure above optimal cerebral perfusion pressure (+12.4 +/- 8.3 mm Hg; p < 0.

23 05 [72%]), nutrition (162 of 199 [81%]), and cerebral perfusion pressure (128 of 199 [64%]).

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

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

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

27 e of cerebral perfusion pressure and optimal cerebral perfusion pressure 48 hours before delayed cere

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

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

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

31 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.

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

33 Inducing hypertension resulted in a cerebral perfusion pressure above optimal cerebral perfu

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

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

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

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

38 Here we show that astrocytes detect falling cerebral perfusion pressure and activate CNS autonomic s

39 Cerebral perfusion pressure and arterial PCO2 were maint

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

41 iority is focused on maintenance of adequate cerebral perfusion pressure and avoidance of secondary b

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

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

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

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

46 ocytes are acutely sensitive to decreases in cerebral perfusion pressure and may function as intracra

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

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

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

50 , there is a significant discrepancy between cerebral perfusion pressure and optimal cerebral perfusi

51 al perfusion pressure, and the difference of cerebral perfusion pressure and optimal cerebral perfusi

52 ngepoint was also found in the difference of cerebral perfusion pressure and optimal cerebral perfusi

53 n pressure [p = 0.97]; and the difference of cerebral perfusion pressure and optimal cerebral perfusi

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

55 The relationship between cerebral perfusion pressure and pressure reactivity inde

56 01 at initial resuscitation rapidly restored cerebral perfusion pressure and stabilized hemodynamics

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

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

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

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

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

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

63 In cases where intracranial pressure, cerebral perfusion pressure, and brain tissue oxygenatio

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

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

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

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

68 nges in cerebral perfusion pressure, optimal cerebral perfusion pressure, and the difference of cereb

69 at occur as a result of chronically elevated cerebral perfusion pressure are hypothesized to precede

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

71 levated intracranial pressure and inadequate cerebral perfusion pressure are not infrequent during ex

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

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

74 Cerebral perfusion pressure at time of delayed cerebral

75 We characterized optimal cerebral perfusion pressure at time of delayed cerebral

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

77 Cerebral perfusion pressure augmentation resulted in a s

78 Cerebral perfusion pressure augmentation significantly i

79 Early aggressive cerebral perfusion pressure augmentation to a cerebral p

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

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

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

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

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

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

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

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

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

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

90 ates characterized by intracranial pressure, cerebral perfusion pressure, compensatory reserve index,

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

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

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

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

95 anial compartment (SPP), which is lower than cerebral perfusion pressure (CPP) because of extracrania

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

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

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

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

100 ketamine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in children with sever

101 a MAP increase of 25.7% resulted in a 34.2% cerebral perfusion pressure (CPP) increase and 16.3% Pbt

102 an epidural balloon catheter until negative cerebral perfusion pressure (CPP) was obtained.

103 iations between PRx, age, GCS, ICP, MAP, and cerebral perfusion pressure (CPP) were examined with sum

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

105 Cerebral perfusion pressure (CPP), calculated as mean ar

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

107 ntracranial fluid dynamic parameters such as cerebral perfusion pressure (CPP), cerebral blood flow (

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

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

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

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

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

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

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

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

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

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

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

119 e of cerebral perfusion pressure and optimal cerebral perfusion pressure (decrease from -0.2 +/- 11.2

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

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

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

123 erebral ischemia in a comparable time frame (cerebral perfusion pressure delayed cerebral ischemia 81

124 s in intracranial pressure and reductions in cerebral perfusion pressure do occur during proning, the

125 Cerebral perfusion pressure gradually decreased as ICP i

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

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

128 The cerebral perfusion pressure group in comparison with int

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

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

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

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

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

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

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

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

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

138 without brain herniation; and maintenance of cerebral perfusion pressure (>40 mm Hg) for 72 h after t

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

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

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

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

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

144 n pressures that exceeded individual optimal cerebral perfusion pressure in delayed cerebral ischemia

145 ce of elevated intracranial pressure and low cerebral perfusion pressure in obstructive intraventricu

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

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

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

149 Optimal cerebral perfusion pressure increased 30 hours before th

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

151 The cerebral perfusion pressure intervention resulted in a g

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

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

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

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

156 Adherence to the cerebral perfusion pressure key performance indicator wa

157 Each 1 mm Hg increase in cerebral perfusion pressure led to a decrease in the jug

158 d intracranial pressure greater than 20 plus cerebral perfusion pressure less than 60 mm Hg were asso

159 h poor day-30 modified Rankin Scale, whereas cerebral perfusion pressure less than 65 and less than 7

160 d intracranial pressure greater than 20 plus cerebral perfusion pressure less than 70 mm Hg were asso

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

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

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

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

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

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

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

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

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

170 Cerebral perfusion pressure<40 mm Hg following pediatric

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

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

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

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

175 levated intracranial pressure and inadequate cerebral perfusion pressure may contribute to poor outco

176 reased intracranial pressure and compromised cerebral perfusion pressure may occur with prone positio

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

178 brain oxygen tension, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and

179 Cerebral perfusion pressures, measured in nine additiona

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

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

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

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

184 es of cerebral perfusion pressure or optimal cerebral perfusion pressure, nor the resulting differenc

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

186 Cerebral perfusion pressure, nutrition, and hypocarbia t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 This appears necessary to establish a cerebral perfusion pressure on the order of 100 mm Hg at

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

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

208 was used to calculate significant changes in cerebral perfusion pressure, optimal cerebral perfusion

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

210 d not correlate to either absolute values of cerebral perfusion pressure or optimal cerebral perfusio

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

212 gen tension-brain oxygen tension gradient to cerebral perfusion pressure (p = 0.004) when comparing n

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

214 e of cerebral perfusion pressure and optimal cerebral perfusion pressure [p = 0.51]).

215 sion pressure, nor the resulting difference (cerebral perfusion pressure [p = 0.69]; optimal cerebral

216 ebral perfusion pressure [p = 0.69]; optimal cerebral perfusion pressure [p = 0.97]; and the differen

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

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

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

220 Proportion of cerebral perfusion pressure readings from less than 65 t

221 Proportion of cerebral perfusion pressure readings from less than 65 t

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

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

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

225 Cerebral perfusion pressure, Sao2, and Fio2 were similar

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

227 ement guided by autoregulation-based optimal cerebral perfusion pressure should be explored in future

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

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

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

231 (PRx) and deviation from the autoregulatory cerebral perfusion pressure target (DeltaCPPopt = actual

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

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

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

235 Cerebral perfusion pressure-targeted therapy, which reli

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

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

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

239 rdized induction of hypertension resulted in cerebral perfusion pressures that exceeded individual op

240 ng of hourly values of intracranial pressure/cerebral perfusion pressure, the compensatory reserve in

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

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

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

244 When examined by cerebral perfusion pressure threshold, cerebral perfusio

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

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

247 ces of intracranial pressure-time burden and cerebral perfusion pressure-time burden should be tested

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

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

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

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

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

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

254 Burden of low cerebral perfusion pressure was also associated with poo

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

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

257 Regional cerebral perfusion pressure was calculated for each intr

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

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

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

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

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

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

264 Cerebral perfusion pressure was not restored until manni

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

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

267 to brain tissue oxygen tension gradient, and cerebral perfusion pressure were 14 mm Hg (SD, 4), 53 mm

268 ion, jugular venous bulb oxygen tension, and cerebral perfusion pressure were 29 mm Hg (SD, 9), 45 mm

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

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

271 Intracranial pressure and cerebral perfusion pressure were recorded every 4 hours,

272 A new concept advocates an individual cerebral perfusion pressure where cerebral autoregulatio

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

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

275 ween cerebral perfusion pressure and optimal cerebral perfusion pressure with worsening of autoregula

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

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