ライフサイエンスコーパス: tidal volume

1 ceiving mechanical ventilation with very low tidal volume.

2 by titration of the respiratory rate and/or tidal volume.

3 Mechanical ventilation with low tidal volume.

4 ty index and the coefficient of variation of tidal volume.

5 odal, tsDCS induced a persistent increase in tidal volume.

6 currents by hypoxia were unaffected by high tidal volume.

7 forces) contribute a negligible fraction of tidal volume.

8 chanically ventilated swine by adjusting the tidal volume.

9 anical power led to significant increases in tidal volume.

10 eased despite unchanged respiratory rate and tidal volume.

11 ventilatory rate rather than an increase in tidal volume.

12 sk of ICU mortality compared with subsequent tidal volumes.

13 with saline lavage and augmented using large tidal volumes.

14 ot demonstrate improvements in postoperative tidal volumes.

15 All participants received low tidal volumes.

16 001), whereas we detected no association for tidal volume (1.05, 0.98-1.13; p=0.179).

17 3%; 95% CI, 1.01-1.05; P = 0.004), decreased tidal volume (-1.7 ml; 95% CI, -3.3 to -0.2; P = 0.03),

18 rtery disease, or acute hemorrhage (1B); low tidal volume (1A) and limitation of inspiratory plateau

19 Low tidal volume (2.9-4 ml/kg ideal body weight) and poor co

20 identified by prior work: 1) lung-protective tidal volume, 2) appropriate setting of positive end-exp

21 mL/kg), and mechanical ventilation with high tidal volume (20 mL/kg).

22 inflation; high-stretch group received high tidal volume (30-32 mL/kg) with positive end-expiratory

23 With increasing tidal volume (4, 6, 8, and 10 mL/kg), the change in intr

24 trong for mechanical ventilation using lower tidal volumes (4-8 ml/kg predicted body weight) and lowe

25 Adding extracorporeal CO2 removal at tidal volume 6 mL/kg decreased PaCO2 by 21% (95% CI, 17-

26 Baseline corresponded to tidal volume 6 mL/kg of predicted body weight without ex

27 ariation, and cardiac index were recorded at tidal volume 6 mL/kg predicted body weight and 1 minute

28 nd-expiratory occlusion test obtained during tidal volume 6 mL/kg predicted body weight did not predi

29 d-expiratory occlusion test was performed at tidal volumes 6 and 8 mL/kg predicted body weight and af

30 trol group), mechanical ventilation with low tidal volume (6 mL/kg), and mechanical ventilation with

31 generated tidal volume values (n = 600; mean tidal volume = 6 mL/kg), with a 30% coefficient of varia

32 ally ventilated in pressure-controlled mode (tidal volume, 6 mL/kg; respiratory rate, 40; FIO2, 0.6;

33 d ventilation (control group) with identical tidal volume (7 mL/kg) and positive end-expiratory press

34 cols for 3 hours: control group received low tidal volume (7 mL/kg) with positive end-expiratory pres

35 p < 0.01), possibly as a result of a higher tidal volume (7.2 mL/kg [6.7-8.8] vs. 5.8 [5.1-6.8]; p =

36 two-thirds of patients with ARDS received a tidal volume 8 of mL/kg or less of predicted body weight

37 th moderate-to-severe hypoxemia, the expired tidal volume above 9.5 mL/kg predicted body weight accur

38 In these patients, the expired tidal volume above 9.5 mL/kg predicted body weight predi

39 health record data, we examined patterns of tidal volume administration, the effect on clinical outc

40 ure levels (until day 7) and lower delivered tidal volume after 3 days on extracorporeal membrane oxy

41 Increased tidal volume after cathodal tsDCS opens up the perspecti

42 The fraction of the total tidal volume allocated for alveolar inflation is 34 +/-

43 ventilation may be associated with increased tidal volume and alveolar pressure that could contribute

44 riability index, coefficient of variation of tidal volume and apnoea-hypopnoea index were increased i

45 High tidal volume and cecal ligation and perforation increase

46 sure distribution, how this is influenced by tidal volume and chest compliance, and its interaction w

47 m H2O) were noted, with significantly higher tidal volume and compliance at PEEP10 and PEEP5 than PEE

48 Furthermore, increased tidal volume and decreased chest compliance decreased st

49 Increased tidal volume and decreased chest wall compliance both in

50 mechanical power was achieved by increasing tidal volume and decreasing respiratory rate.

51 ECCO2R enables reductions in tidal volume and driving pressure, key determinants of v

52 ecruitment maneuvers (a stepwise increase of tidal volume and eventually PEEP) or to the low level of

53 urs with matched lung strains (ratio between tidal volume and functional residual capacity) but diffe

54 um driving pressure was achieved by reducing tidal volume and increasing respiratory rate and positiv

55 We assessed expired tidal volume and its association with noninvasive ventil

56 ort), arterial blood gases, airway pressure, tidal volume and its coefficient of variation, respirato

57 ammation than atelectrauma at comparable low tidal volume and lower driving pressure, suggesting that

58 A relationship between tidal volume and mortality in mechanically ventilated ch

59 There was no association between tidal volume and mortality when tidal volume was dichoto

60 12 mL/kg also showed no association between tidal volume and mortality.

61 pressure, respiratory carbon dioxide levels, tidal volume and peroneal nerve muscle sympathetic activ

62 yndrome Network protocol recommends limiting tidal volume and plateau pressure; it also recommends in

63 breath, bins them according to frequency or tidal volume and plots the results against bin means.

64 Tidal volume and positive end-expiratory pressure had no

65 was a 43.8% and 55.3% increase for left lung tidal volume and right lung tidal volume (P < .001 for b

66 itude of the peak coherence function between tidal volume and RSNA frequency spectra.

67 sis was to determine the association between tidal volume and the occurrence of pulmonary complicatio

68 ect harmful forms of OTV including excessive tidal volumes and common forms of patient-ventilator asy

69 rgeting lung recruitment with the use of low tidal volumes and high positive end-expiratory pressure.

70 Protective mechanical ventilation with lower tidal volumes and PEEP reduces compounded postoperative

71 g-protective ventilation with the use of low tidal volumes and positive end-expiratory pressure is co

72 igh respiratory drive and breathe with large tidal volumes and potentially injurious transpulmonary p

73 ute ventilation), 0.25 mL/kg (airway opening tidal volume), and 13.7% (plethysmography tidal volume)

74 Minute ventilation, tidal volume, and breathing frequency were measured befo

75 e positive end-expiratory pressure, baseline tidal volume, and hospital site.

76 Transcutaneous carbon dioxide, tidal volume, and minute ventilation may assist in refin

77 ventilation settings (i.e. plateau pressure, tidal volume, and positive end-expiratory pressure) on I

78 n inability to increase breathing frequency, tidal volume, and, thus, minute ventilation in response

79 ediator-but not functional-responses to high tidal volume are augmented by subthreshold sepsis primin

80 al of Philadelphia (n = 77) and from the low tidal volume arm of the Acute Respiratory Distress Syndr

81 ion; and atelectasis group received the same tidal volume as control but neither positive end-expirat

82 2 patients with ARDS with 11,558 twice-daily tidal volume assessments (evaluated in milliliter per ki

83 The median (interquartile range) expired tidal volume averaged over all noninvasive ventilation s

84 proved in the intervention group (use of low tidal volumes, avoidance of heavy sedation, use of centr

85 /kg predicted body weight and after reducing tidal volume back to 6 mL/kg predicted body weight.

86 ing a simple algorithm targeting the expired tidal volume between 6 and 8 mL/kg of predicted body wei

87 and carbon dioxide, minute ventilation, and tidal volume (both at airway opening and by inductive pl

88 hoalveolar lavage and plasma mediators; high tidal volume but not cecal ligation and perforation impa

89 taset had limited scope for further reducing tidal volume, but driving pressure was still significant

90 Priming of high tidal volume by cecal ligation and perforation intensifi

91 A low or moderate expired tidal volume can be difficult to achieve during noninvas

92 r mechanical ventilation, which, with higher tidal volume, can cause ventilator-associated lung injur

93 e, positive end-expiratory pressure, DeltaP, tidal volume, Cdyn, and PaO2/FIO2 were collected at acut

94 ined by transiently increasing tidal volume (tidal volume challenge) are superior to pulse pressure v

95 to 8 mL/kg predicted body weight, that is, "tidal volume challenge," the changes in pulse pressure v

96 redicted body weight and 1 minute after the "tidal volume challenge." The tidal volume was reduced ba

97 Tidal volume changes (DeltaV(T)) followed the same trend

98 ptor activity (major breathing frequency and tidal volume changes did not alter vagal tone or sympath

99 In addition, oscillatory tidal volume changes were assessed at each pressure step

100 umbar Cobb angle were poor predictors of MRI tidal volumes (chest wall, diaphragm, and left and right

101 l capacity showed moderate correlations with tidal volumes (chest wall, diaphragm, and left and right

102 ed that C-26 mice have a significantly lower tidal volume compared to controls under basal conditions

103 surgery, intraoperative ventilation with low tidal volume compared with conventional tidal volume, wi

104 reover, a 1 ml/kg PBW increase in subsequent tidal volumes compared with the initial tidal volume was

105 ng tidal volume), and 13.7% (plethysmography tidal volume) compared with total lung capacity levels.

106 es, and alternate metrics for evaluating low tidal volume compliance in clinical practice.

107 gnificant dynamic hyperinflation and greater tidal volume constraints (P<0.05).

108 d provide a unique window for evaluating low tidal volume delivery and targets for improvement.

109 idal volume with alternative measures of low tidal volume delivery ranged from 0.38 to 0.66.

110 ; or 7) cecal ligation and perforation, high tidal volume, dexamethasone.

111 am, high tidal volume, saline; 5) sham, high tidal volume, dexamethasone; 6) cecal ligation and perfo

112 atory lung volume increased (P < 0.001), and tidal volume did not change (P = 0.44); the ratio of tid

113 The theoretical basis for minimizing tidal volume during high-frequency oscillatory ventilati

114 rable changes in response to the increase in tidal volume during mechanical ventilation.

115 decrease in the rib cage contribution to the tidal volume during phasic REM sleep becomes a critical

116 8 mL/kg predicted body weight, and the mean tidal volume during the first 72 hours after acute respi

117 xpiratory pressure, DeltaP [PIP minus PEEP], tidal volume, dynamic compliance [Cdyn]) or oxygenation

118 quency or resonant frequency despite reduced tidal volumes, especially in adults, due to regional amp

119 atio, 1.82; 95% CI, 1.20-2.78), whereas mean tidal volume exposure was not (odds ratio, 0.87/1 mL/kg

120 Sixty tidal volumes for each ventilator settings were analyzed

121 and stroke volume variation after increasing tidal volume from 6 to 8 mL/kg predicted body weight pre

122 and stroke volume variation after increasing tidal volume from 6 to 8 mL/kg predicted body weight wer

123 hypothesized that with transient increase in tidal volume from 6 to 8 mL/kg predicted body weight, th

124 here was a reduction in emergency department tidal volume from 8.1 mL/kg predicted body weight (7.0-9

125 patient level, exposure to 24 total hours of tidal volumes greater than 8 mL/kg predicted body weight

126 body weight, 40% of patients were exposed to tidal volumes greater than 8 mL/kg predicted body weight

127 roup, and in 31% of the patients in the high tidal volume group (adjusted odds ratio [low vs high tid

128 32 of 590 patients (39%) in the conventional tidal volume group (difference, -1.3% [95% CI, -6.8% to

129 rred in 231 of 608 patients (38%) in the low tidal volume group compared with 232 of 590 patients (39

130 /kg predicted body weight), an "intermediate tidal volume group" (> 7 and < 10 mL/kg predicted body w

131 10 mL/kg predicted body weight), and a "high tidal volume group" (>/= 10 mL/kg predicted body weight)

132 entilation, patients were assigned to a "low tidal volume group" (tidal volumes </= 7 mL/kg predicted

133 6 mL/kg predicted body weight (n = 614; low tidal volume group) or a tidal volume of 10 mL/kg predic

134 predicted body weight (n = 592; conventional tidal volume group).

135 roup, in 28% of patients in the intermediate tidal volume group, and in 31% of the patients in the hi

136 monia occurred in 23% of patients in the low tidal volume group, in 28% of patients in the intermedia

137 lume group (adjusted odds ratio [low vs high tidal volume group], 0.72; 95% CI, 0.52-0.98; p = 0.042)

138 With tidal volume held constant, negligible changes occurred

139 erapy, mechanical ventilation with injurious tidal volumes, hospital-acquired aspiration, and volume

140 in the KF reduced respiratory frequency and tidal volume in anaesthetized rats.

141 distress syndrome was associated with lower tidal volume in multivariate analysis.

142 Despite low mean tidal volume in the cohort, a significant percentage of

143 aphragmatic stimulation generated sufficient tidal volumes in all STIM animals.

144 n minutes]: OR, 1.14, 95% CI, 1.05-1.24; and tidal volume [in milliliters per kilogram of predicted b

145 The average lung tidal volumes increased after operation for TIS; there w

146 bution due to the change in lung height with tidal volume inflation are probably bigger contributors

147 A low expired tidal volume is almost impossible to achieve in the majo

148 emic respiratory failure, and a high expired tidal volume is independently associated with noninvasiv

149 anical ventilation during surgery, the ideal tidal volume is unclear.

150 Ventilation with low tidal volumes is associated with a lower risk of develop

151 Mechanical ventilation with low tidal volumes is recommended for all patients with acute

152 Protective mechanical ventilation with low tidal volumes is standard of care for patients with acut

153 postoperative increases in all components of tidal volume (left and right chest wall and diaphragm, a

154 Comparing patients ventilated with tidal volume less than 7 mL/kg and greater than 10 mL/kg

155 r than 10 mL/kg or greater than 12 mL/kg and tidal volume less than 8 mL/kg and greater than 10 mL/kg

156 In total, 54.4% of patients received a tidal volume less than 8 mL/kg predicted body weight, an

157 differential diagnosis were associated with tidal volumes less than 6.5 mL/kg (51% use of tidal volu

158 Use of tidal volumes less than 6.5 mL/kg also increased (p < 0.

159 urgery, and received ventilation with higher tidal volumes, lower positive end-expiratory pressure le

160 e treated with low tidal volume ventilation (tidal volume < 6.5 mL/kg predicted body weight) at some

161 idal volumes less than 6.5 mL/kg (51% use of tidal volume <= 6.5 mL/kg if acute respiratory distress

162 were assigned to a "low tidal volume group" (tidal volumes </= 7 mL/kg predicted body weight), an "in

163 The current study elucidated the effects of tidal volume lung inflation [functional residual capacit

164 Tidal volume lung inflation results in structural change

165 hesion molecule-1 protein levels in the high-tidal volume lungs (p < 0.0001).

166 High stress despite low tidal volumes may worsen lung injury and increase risk o

167 wall and diaphragm, and left and right lung tidal volumes) measured at MRI.

168 High tidal volume mechanical ventilation and the resultant ex

169 When compared with low-tidal volume mechanical ventilation, high-tidal volume v

170 n commonly used respiratory variables (i.e., tidal volume, minute ventilation, and respiratory rate).

171 eight (n = 614; low tidal volume group) or a tidal volume of 10 mL/kg predicted body weight (n = 592;

172 during controlled mechanical ventilation at tidal volume of 4, 6, 8, and 10 mL/kg with normal and de

173 DS with lung-protective ventilation, using a tidal volume of 6 mL per kg of predicted bodyweight and

174 lavage, the LTVV group was ventilated with a tidal volume of 6 mL/kg and progressively higher positiv

175 prototypical patient receiving 8 days with a tidal volume of 6 ml/kg PBW, the absolute increase in IC

176 Patients were randomized to receive a tidal volume of 6 mL/kg predicted body weight (n = 614;

177 eceived volume-controlled ventilation with a tidal volume of 7 mL/kg of predicted body weight.

178 t (ventilator-induced lung injury) lung with tidal volume of approximately 3 mL/kg and 1) high positi

179 rpin RNA (shRNA) progressively decreased the tidal volume of breaths yet surprisingly increased breat

180 during controlled mechanical ventilation at tidal volumes of 4, 6, 8, and 10 mL/kg with normal and d

181 ent populations to understand the effects of tidal volume on patient outcome.

182 mechanical ventilation strategies using low tidal volume or high levels of positive end-expiratory p

183 g for PaO2/FIO2 and either driving pressure, tidal volume, or plateau pressure and positive end-expir

184 In scenarios with variation in tidal volume over the 8-day period, mortality was higher

185 se for left lung tidal volume and right lung tidal volume (P < .001 for both), respectively.

186 intervention phase was associated with lower tidal volume (P < 0.01), higher positive end-expiratory

187 risk of hospital death based on quantiles of tidal volume, positive end-expiratory pressure, plateau

188 th significant changes (p < 0.01 for all) in tidal volume, positive end-expiratory pressure, respirat

189 airway pressure release ventilation with low tidal volumes, positive end-expiratory pressure was set

190 also correlated significantly on oscillatory tidal volume/pressure relationships (mean r = 0.81 +/- 0

191 entilator-induced lung injury, including low tidal volume, prone position, and neuromuscular blockers

192 e, but it was stable on the average: average tidal volume ranged between 524.8 and 607.0 mL (p = 0.33

193 text]e/[Formula: see text]co2, dead space to tidal volume ratio (Vd/Vt), and arterial to end-tidal CO

194 0.80 to -0.84; P < 0.001) but not dead space/tidal volume ratio.

195 olume of nondependent and dependent regions, tidal volume reaching nondependent and dependent lung (V

196 ger photoplethysmographic arterial pressure, tidal volume, respiratory carbon dioxide concentrations

197 ot only accurately measure respiratory rate, tidal volume, respiratory minute volume, and peak flow r

198 istance and elastance as a function of time, tidal volume, respiratory rate, and positive end-expirat

199 Secondary outcomes included tidal volume, respiratory rate, minute volume, dynamic l

200 nonventilated, dexamethasone; 4) sham, high tidal volume, saline; 5) sham, high tidal volume, dexame

201 one; 6) cecal ligation and perforation, high tidal volume, saline; or 7) cecal ligation and perforati

202 Initial tidal volume settings strongly predicted exposure to vol

203 Higher tidal volumes shortly after ARDS onset were associated w

204 inhibition, (2) nonlinear complexity of the tidal volume signal (related to medullary ventilatory co

205 Based on the tertiles of tidal volume size in the first 2 days of ventilation, pa

206 Tidal volume, static compliance, tidal impedance variati

207 ol ventilation with only 50% achieving a low tidal volume strategy (plateau pressure <= 30 cm H2O) wi

208 ed with mechanical ventilation using the low tidal volume strategy as per the Acute Respiratory Distr

209 Even when not increasing tidal volume, strong spontaneous effort may potentially

210 -expiratory pressure to avoid atelectasis, a tidal volume that is limited to less than 5-7 cc/kg per

211 ndent to dependent regions without change in tidal volume) that was caused by spontaneous breathing d

212 We investigated the association of tidal volume, the level of PEEP, and driving pressure du

213 variation obtained by transiently increasing tidal volume (tidal volume challenge) are superior to pu

214 Lowering tidal volume to 4 mL/kg reduced minute ventilation from

215 Inspiratory pressure was adjusted to control tidal volume to 5-7 mL/kg, maintaining a plateau pressur

216 lume did not change (P = 0.44); the ratio of tidal volume to DeltaPes (an estimate of dynamic lung co

217 elluft, which occurred despite limitation of tidal volume to less than 6 ml/kg.

218 Acute Respiratory Distress Syndrome Network tidal volume trial (n = 100).

219 , and estimate the respiration rate (RR) and tidal volume (TV) from analysis of electrocardiographic

220 d Hering-Breuer mechanoreflex, and increased tidal volume under normal conditions.

221 utamate (10 mm/100 nL) in the PPTg decreased tidal volume (V(T) ) but otherwise increased respiratory

222 y driving pressure (DP(AW)), the quotient of tidal volume (V(T)), and respiratory system compliance (

223 th basis as a sequence of randomly generated tidal volume values (n = 600; mean tidal volume = 6 mL/k

224 ble Ventilation (VV), in which frequency and tidal volume vary from breath-to-breath.

225 venty patients (19.3%) were treated with low tidal volume ventilation (tidal volume < 6.5 mL/kg predi

226 The entire cohort received low tidal volume ventilation 11.4% of the time patients had

227 , we found that the protective effect of low tidal volume ventilation against lung injury caused by l

228 examining this association in the era of low tidal volume ventilation and a fluid conservative strate

229 y distress syndrome patients receiving lower tidal volume ventilation and to determine the factors th

230 Interventions that improve adoption of low tidal volume ventilation are needed.

231 her evidence for early implementation of low tidal volume ventilation as well as new insights into th

232 bal lung stress varies considerably with low tidal volume ventilation for acute respiratory distress

233 zed mice were ventilated with injurious high tidal volume ventilation for periods up to 180 minutes.

234 Although low tidal volume ventilation has been shown to reduce mortal

235 High tidal volume ventilation impaired phenylephrine- and ace

236 Previous studies reported poor low tidal volume ventilation implementation.

237 sociated with a high mortality rate, and low tidal volume ventilation improves mortality.

238 ow-tidal volume mechanical ventilation, high-tidal volume ventilation increased lung edema score and

239 d 34% waited more than 72 hours prior to low tidal volume ventilation initiation.

240 ely recognition of ARDS and adherence to low tidal volume ventilation is important for reducing morta

241 However, the effect of the timing of low tidal volume ventilation is not well understood.

242 Low tidal volume ventilation lowers mortality in the acute r

243 acute lung injury patients receiving lower tidal volume ventilation often have a plateau pressure t

244 years after publication of the landmark low tidal volume ventilation study, use remains poor.

245 ratory distress syndrome recognition and low tidal volume ventilation use have increased over time, t

246 % were associated with increased odds of low tidal volume ventilation use.

247 ine the rate, quality, and predictors of low tidal volume ventilation use.

248 In unadjusted analysis, high tidal volume ventilation was associated with an increase

249 In multivariable modeling, high tidal volume ventilation was the strongest risk factor f

250 tilation) group and ventilated with 4-hr low tidal volume ventilation with spontaneous breathing or w

251 ur attending physicians (6.2%) initiated low tidal volume ventilation within 1 day of acute respirato

252 as 34 physicians (52.3%) never initiated low tidal volume ventilation within 1 day of acute respirato

253 that compared low with high PEEP during low tidal volume ventilation, an increase in the level of PE

254 Modifiable risk factors, including high tidal volume ventilation, are associated with its develo

255 The main management strategy, low tidal volume ventilation, can be associated with the dev

256 ing trials, early exercise and mobility, low tidal volume ventilation, conservative fluid management,

257 Among patients who received low tidal volume ventilation, the mean (SD) percentage of ac

258 nificant improvement include use of targeted tidal volume ventilation, use of caffeine therapy, oxyge

259 Women were less likely to receive low tidal volume ventilation, whereas sepsis and FIO2 greate

260 High tidal volume ventilation-induced pulmonary vascular dysf

261 lness and is also associated with use of low tidal volume ventilation.

262 n predicting fluid responsiveness during low tidal volume ventilation.

263 ably predict fluid responsiveness during low tidal volume ventilation.

264 pressure greater than 30 cm H2O received low tidal volume ventilation.

265 differential diagnosis, or treated with low tidal volume ventilation.

266 We assumed patients received low tidal volume ventilation.

267 put monitoring, and receiving controlled low tidal volume ventilation.

268 most threefold greater driving pressure (and tidal volume) versus spontaneous breathing (28.0 +/- 0.5

269 ion of the RTN to breathing frequency (FR ), tidal volume (VT ) and minute volume (VE ) by inhibiting

270 od pressure, respiratory frequency (fR ) and tidal volume (VT ) were recorded in 28 conscious adult m

271 increased both breathing frequency (fR ) and tidal volume (VT ) whereas, in REM sleep, hypercapnia in

272 hypocapnic; central CO2 response slopes for tidal volume (VT ), breathing frequency (fb ) and rate o

273 Tidal volume (VT) and volume of gas caused by positive e

274 The protective role of a small tidal volume (VT) has been established, whereas the adde

275 stress Syndrome (ARMA) trial in 2000, use of tidal volume (VT) less than or equal to 6 mL/kg predicte

276 nspiratory (plateau) airway pressures, lower tidal volumes (VT), and higher positive end-expiratory p

277 s included ventilatory management (including tidal volume [VT] expressed as mL/kg predicted bodyweigh

278 d by a wide variety of changes in the depth (tidal volume, VT ) and number of breaths (respiratory fr

279 Lower tidal volumes (Vts) attenuate extrapulmonary organ injur

280 Tidal volume was 6 mL/kg in both groups.

281 Although mean tidal volume was 6.8 mL/kg predicted body weight, 40% of

282 uent tidal volumes compared with the initial tidal volume was associated with a 15% increase in morta

283 An increase of 1 ml/kg PBW in initial tidal volume was associated with a 23% increase in ICU m

284 Expired tidal volume was averaged and respiratory and hemodynami

285 tion between tidal volume and mortality when tidal volume was dichotomized at 7, 8, 10, or 12 mL/kg.

286 y weight [7.6-10.2]; p = 0.001), and expired tidal volume was independently associated with noninvasi

287 nute after the "tidal volume challenge." The tidal volume was reduced back to 6 mL/kg predicted body

288 Tidal volume was set at 8 ml/kg, and respiratory rate wa

289 At the end of recruitment, tidal volume was significantly higher (p = 0.002) and ox

290 The mean expired tidal volume was significantly higher in patients who fa

291 Tidal volume was subsequently reduced to 4 mL/kg for the

292 lipopolysaccharides and ventilation at high tidal volume was suppressed in Rap1 knockout mice.

293 ninvasive ventilation sessions (mean expired tidal volume) was 9.8 mL/kg predicted body weight (8.1-1

294 nation, heart rate, transcutaneous PCO2, and tidal volume were simultaneously recorded at each airway

295 Tidal volumes were analyzed across 1,905 hospitalization

296 were exposed to a prolonged duration of high tidal volumes which was correlated with higher mortality

297 Across ICUs, correlation of mean tidal volume with alternative measures of low tidal volu

298 We tested a strategy that combines the low tidal volume with lower respiratory rates and minimally

299 low tidal volume compared with conventional tidal volume, with PEEP applied equally between groups,

300 ransfected mice during inspiration increased tidal volume without altering inspiratory duration, wher