ライフサイエンスコーパス: minute ventilation

1 10 with 15% arteriovenous shunt and baseline minute ventilation.

2 n oxygen delivery, under conditions of fixed minute ventilation.

3 changes in body temperature, heart rate, and minute ventilation.

4 O2, PaO2, respiratory system compliance, and minute ventilation.

5 al and its association with nitric oxide and minute ventilation.

6 posure in a manner inversely proportional to minute ventilation.

7 augmented hypoxic sensitivity and increased minute ventilation.

8 to -0.13; I = 84.0%), but not heart rate or minute ventilation.

9 ncreased after AIHH, but not tidal volume or minute ventilation.

10 SCH, but there was no significant effect on minute ventilation.

11 on (MV) strategies that intentionally reduce minute ventilation.

12 patients with CHF to markedly increase their minute ventilation.

13 es included compliance, Pao2:Fio2 ratio, and minute ventilation.

14 adjusting the frequency to maintain constant minute ventilation.

15 4.3 to 1.3 hours; P = .36), daily changes of minute-ventilation (-0.0 L/min; 95% CI, -0.2 to 0.2 L/mi

16 improvement of 21.6 mm Hg (CO2), 168 mL/sec (minute ventilation), 0.25 mL/kg (airway opening tidal vo

17 on III (APACHE III; 104 [SD 31] vs 89 [33]), minute ventilation (11.1 [3.2] vs 9.6 [2.4] L/min), and

18 y pressure, 24.8+/-2.4 to 13.7+/-0.7 cm H2O; minute ventilation, 12.7+/-1.4 to 6.2+/-0.8 L/min; respi

19 Hypoglycaemia significantly augmented minute ventilation (123 +/- 4 to 143 +/- 7 ml min(-1) )

20 ) had higher FIO2 (0.65 vs. 0.44, p = .006), minute ventilation (14.6 vs. 9.9 L/min, p = .005), posit

21 adrenaline (1 mug kg(-1) min(-1) ) increased minute ventilation (145 +/- 4 to 173 +/- 5 ml min(-1) )

22 Minute ventilation (29 +/- 8 versus 21 +/- 6 L/min, p <

23 , patients with OSA had greater increases in minute ventilation (5.8+/-0.8 versus 3.2+/-0.7 L/min; P=

24 s 20.5+/-7 mL x min[-1] x kg[-1] [placebo]), minute ventilation (57.5+/-17 [enalapril] versus 55.4+/-

25 .3 kPa]; p = .005) without affecting expired minute ventilation (6.2 +/- 0.4 to 6.5 +/- 0.4 L/min; p

26 , patients with CHF had greater increases in minute ventilation (6.7+/-1.4 versus 2.7+/-0.9 L/min, P=

27 /-16 yr vs. 54+/-17 yr, p<0.01) with a lower minute ventilation (8.8+/-2.2 L/min vs. 10.1+/-2.9 L/min

28 , respiratory rate was elevated with reduced minute ventilation, a result of lung compliance below de

29 Unlike naloxone, rescue agent 9 increases minute ventilation above normal in fentanyl- or carfenta

30 Both healthy and injured sheep reduced minute ventilation according to the amount of extracorpo

31 Breathing abnormalities include decreased minute ventilation and a specific loss of sighs, which w

32 e magnitude of adenosine evoked responses in minute ventilation and blood pressure was analogous to t

33 d artery causes a dose-dependent increase in minute ventilation and blood pressure with a concomitant

34 Minute ventilation and body temperature were unchanged d

35 epinephrine was significantly lower, whereas minute ventilation and exhaled CO2 were significantly in

36 While monitoring minute ventilation and heart rate, exercise challenge wa

37 Minute ventilation and mechanical power were lower in th

38 reathing during CPAP with the helmet; and c) minute ventilation and Pco2 should be monitored during C

39 riables that affect CO2 elimination, such as minute ventilation and peak airway pressure (peak Paw) a

40 ses in frequency of breathing, tidal volume, minute ventilation and peak inspiratory and expiratory f

41 venous shunt allows significant reduction in minute ventilation and peak inspiratory pressure without

42 Once a panic attack is triggered, minute ventilation and respiratory rate increase regardl

43 dioxide challenge, probands exhibited larger minute ventilation and respiratory rate responses relati

44 le BDNF was also correlated with lactate and minute ventilation and selected WAnT parameters.

45 7 ppm) concentration was found at the lowest minute ventilation and the largest inspiratory circuit v

46 VE (minute ventilation) and the ratio VE/VCO2 (ventilation r

47 robust and enduring changes in tidal volume, minute ventilation, and combined respiratory responses o

48 lood flow (FBF), heart rate, blood pressure, minute ventilation, and end-tidal CO(2) were determined.

49 nd it increased fractional inspiratory time, minute ventilation, and mean inspiratory flow (all p < o

50 d respiratory variables (i.e., tidal volume, minute ventilation, and respiratory rate).

51 Still, overall mean respiratory rate, minute ventilation, and sleep architecture were equivale

52 ) and placebo infusion on oxygen saturation, minute ventilation, and sympathetic nerve activity durin

53 , peak inspiratory flow rate demand, exhaled minute ventilation, and the duration of respiratory musc

54 ship between lung volume and carbon dioxide, minute ventilation, and tidal volume (both at airway ope

55 electroencephalography, electro-oculography, minute ventilation, arterial blood gases, and serum theo

56 pecific to acute lung injury, and identified minute ventilation as a potential novel predictor of dea

57 p were induced to hyperventilate to the same minute ventilation as during exercise, using modest CO2

58 Low end-tidal CO2 and high variance in minute ventilation at baseline predicted panic attacks d

59 tly decreased respiratory rate and decreased minute ventilation at peak exercise.

60 xide was considered to be the point at which minute ventilation began to rise in a linear fashion as

61 p62 levels were inversely associated with minute ventilation (beta -16.18 [-28.44; -3.91], p(adj)

62 rate (beta = 0.28; P = 0.01), and increased minute ventilation (beta = 7.21; P = 0.05), considered s

63 05; respiratory rate: beta = 0.36, P = 0.01; minute ventilation: beta = 11.25, P = 0.01; passive resp

64 ences in arterial CO2 tension or in tidal or minute ventilation between the groups.

65 eous measurements of pulmonary gas exchange, minute ventilation, blood lactate, and quadriceps muscle

66 N and C lambs had similar minute ventilation but a markedly different breathing pa

67 pared with baseline, R-ED and ECCO2R reduced minute ventilation by 50% and 27%, respectively.

68 ve to saline, SCH-treated hamsters decreased minute ventilation by decreasing tidal volume and oxygen

69 0 breaths/min, compared with CMV at the same minute ventilation, can improve CO2 exchange.

70 n 62% (IQR, 45-77%) of predicted, and median minute ventilation/carbon dioxide production slope 34.9

71 strate that baseline peak VO(2) and baseline minute ventilation/carbon dioxide production slope predi

72 aseline peak VO(2)>14 mL/(kg.min) as well as minute ventilation/carbon dioxide production slope<=34 w

73 eak oxygen consumption predicted, and higher minute ventilation/carbon dioxide production slope.

74 entilatory efficiency (slope of the ratio of minute ventilation/carbon dioxide production) were 15.7

75 ues of predicted peak oxygen consumption and minute-ventilation/carbon dioxide production slope, whic

76 In contrast, at isotime, minute ventilation, cardiac output and systemic oxygen d

77 Minute ventilation/CO(2) production (VE/Vco(2)) slope is

78 clonidine, 2.6 +/- 0.2 mEq/L), and decreased minute ventilation (control, 39.7 +/- 2.1 versus clonidi

79 Minute ventilation decreased accordingly from 6.5 +/- 0.

80 matched control subjects, dopamine decreased minute ventilation despite decreased oxygen saturation a

81 Asthma mice showed significant impairment in minute ventilation despite increased peak expiratory flo

82 Minute ventilation determined CO2 clearance during perfl

83 Compensatory increases in minute ventilation during exercise maintained alveolar v

84 Dopamine did not decrease minute ventilation during normoxia in normal subjects.

85 gated the effects of dopamine and placebo on minute ventilation during normoxic breathing in 8 patien

86 ulted in consistently lower tidal volume and minute ventilation during test circuit activities.

87 ng 8% CO2 elicited a moderate hyperpnea, and minute ventilation during the final minute of CO2 breath

88 Baseline measures of minute ventilation during the placebo and antioxidant tr

89 ia (calculated as the difference between the minute ventilation during the second full minute of hypo

90 Peak oxygen uptake increased and heart rate, minute ventilation, dyspnea, and leg fatigue decreased a

91 of HFNC on gas exchange, inspiratory effort, minute ventilation, end-expiratory lung volume, dynamic

92 ses, as well as with levels of tidal volume, minute ventilation, end-tidal CO(2), and irregularity in

93 8 to 14.2 +/- 3.5 (p < 0.01) breaths/min and minute ventilation from 10.4 +/- 1.6 to 4.9 +/- 1.7 L/mi

94 Lowering tidal volume to 4 mL/kg reduced minute ventilation from 7.8 +/- 1.5 to 5.2 +/- 1.1 L/min

95 es) on MSNA, heart rate, blood pressure, and minute ventilation in 14 untreated patients with OSA and

96 HeO2 resulted in the greatest maximum minute ventilation in both bike and KE (p < 0.05) but ha

97 ed expiratory flow, breathing frequency, and minute ventilation in both groups (p < 0.05).

98 exercise is associated with abnormally high minute ventilation in patients with CHF and with a limit

99 reathing frequency, tidal volume, and, thus, minute ventilation in response to a respiratory challeng

100 emicircular canals by yaw rotation increased minute ventilation in young but not older subjects.

101 tion in patients with CHF and with a limited minute ventilation increase in patients with COPD, funct

102 his apnea suppression normalized inspiratory minute ventilation increased during all wake/sleep state

103 m 7.04+/-0.07 to 7.31+/-0.15 (p = .0012) and minute ventilation increased from 0.66+/-0.40 to 4.00+/-

104 Normalized inspiratory minute ventilation increased significantly during wakefu

105 Minute ventilation increased significantly for 30 minute

106 he respiratory stimulating effect of 7% CO2; minute ventilation increased to 250 +/- 17 ml/min before

107 Minute ventilation influences clearance of CO2.

108 or induced acute cerebral hypoxia-ischemia, minute ventilation initially increased, and then hypopne

109 atory times), and increases in tidal volume, minute ventilation, inspiratory drive (i.e., tidal volum

110 is effect is relatively modest when baseline minute ventilation is < or = 10 L/min, because of the lo

111 ethysmography; polymorphonuclear leukocytes; minute ventilation; knockout mice; methacholine

112 breathing, probands had significantly larger minute ventilation, larger tidal volumes, and more varia

113 The breathing reserve index (BRI = minute ventilation/maximal voluntary ventilation) at the

114 scutaneous carbon dioxide, tidal volume, and minute ventilation may assist in refining strategies to

115 via mouth occlusion pressure (P(0.1) ), and minute ventilation measured at rest.

116 Ventilatory ratio is defined as [minute ventilation (ml/min) x Pa(CO(2)) (mm Hg)]/(predic

117 in Heart Failure) trial investigated whether minute ventilation (MV) adaptive servo-ventilation (ASV)

118 f four levels of spontaneous breath in total minute ventilation (n = 9 per group, 6 hr each): 1) biph

119 respiratory rate often sufficient to sustain minute ventilation near baseline levels, without arousal

120 At a constant minute ventilation, nitric oxide inhalation caused dose-

121 (FIO2, positive end-expiratory pressure, and minute ventilation) occurred in patients fed EPA+GLA com

122 taneous breathing, these data were observed: minute ventilation of < 10 L/min; resting respiratory ra

123 with and without the mixing chambers, with a minute ventilation of 14 L/min and a nitric oxide concen

124 piratory fluctuations and was highest with a minute ventilation of 21 L/min and higher during pressur

125 In each mode, minute ventilation of 7, 14, and 21 L/min and installati

126 ng exercise at a given absolute intensity or minute ventilation, older women have a greater degree of

127 , p < .05) despite a lack of any increase in minute ventilation or respiratory rate.

128 s no difference in oxygenation, ventilation, minute ventilation, or pH after tracheostomy.

129 However, ventilatory equivalents (minute ventilation/oxygen consumption) revealed signific

130 Hypoxia increased heart rate (P < 0.05) and minute ventilation (P < 0.05) at rest and exercise under

131 0.001), mean blood pressure (P = 0.009) and minute ventilation (P = 0.002); any effect of hyperoxia

132 Significant differences were found in minute ventilation (p = 0.006), temperature-corrected Pa

133 logy score, age, comorbidities, arterial pH, minute ventilation, PaCO2, PaO2/FiO2 ratio, intensive ca

134 atory times), and increases in tidal volume, minute ventilation, peak inspiratory and expiratory flow

135 eNOS-/- male mice had smaller increases in minute ventilation, peak inspiratory flow and inspirator

136 breathing (e.g., depression of tidal volume, minute ventilation, peak inspiratory flow, and inspirato

137 Different methods for estimating minute ventilation performed well in relative terms with

138 t of a spontaneous breath, fraction of total minute ventilation provided by the ventilator, and mean

139 genation index, increasing fraction of total minute ventilation provided by the ventilator, increasin

140 essure, oxygenation index, fraction of total minute ventilation provided by the ventilator, peak vent

141 oxygenation index, and the fraction of total minute ventilation provided by the ventilator.

142 oxygenation index, and the fraction of total minute ventilation provided by the ventilator.

143 /- 4 vs. He 18 +/- 5 ml/kg per min) and peak minute ventilation (RA 53 +/- 12 vs. He 53 +/- 15 liters

144 RA 724 +/- 163 vs. He 762 +/- 123 s) or peak minute ventilation (RA 97 +/- 27 vs. He 97 +/- 28 liters

145 al practice, that is, more than 30% of total minute ventilation, reduced lung injury with improved re

146 effectiveness of TGI, provided that inspired minute ventilation remains unchanged and end-expiration

147 Ventilatory efficiency (minute ventilation required to eliminate carbon dioxide,

148 espiratory parameters (ventilatory settings, minute ventilation, respiratory rate, airway pressures)

149 Men and women had near identical minute ventilation responses to total load (applied extr

150 ); however, because the males had 45% higher minute ventilations than the females, the deposition rat

151 Minute ventilation, tidal volume, and breathing frequenc

152 EE, substrate utilization, minute ventilation, tidal volume, and respiratory rate w

153 gnals, namely, heart rate, respiratory rate, minute ventilation, tidal volume, capillary oxygen satur

154 /min (96% of total CO2 production), allowing minute ventilation to be reduced from 10.3 +/- 1.4 L/min

155 Peak Vo(2), E/CO2 slope (ratio of minute ventilation to carbon dioxide production), and he

156 es hypoventilation (decrease in the ratio of minute ventilation to oxygen consumption, V(E)/V(O2)) an

157 erence can be corrected easily by increasing minute ventilation until expired tidal volume equals des

158 Minute ventilation ( V E) increased following all trials

159 in infusion (30 microg/d) markedly increased minute ventilation (V E) across all sleep/wake states, b

160 correlation between the increase in baseline minute ventilation (V E) and hyperleptinemia (r = 0.77,

161 We assessed minute ventilation (V E) at rest and during hypercapnic

162 Ro 32-0432 decreased minute ventilation (V E) by 51.0 +/- 5.5% (mean +/- SEM)

163 During O(3) exposure (1 pm, 3 h), minute ventilation (V E) decreased by 64 +/- 4% in wild-

164 DA receptors during development, we measured minute ventilation (V E) in 5-d, 10-d, and 15-d-old inta

165 We previously observed an increase in minute ventilation (V E) with resistive unloading (He-O2

166 O(2)), carbon dioxide production (V CO(2)), minute ventilation (V E), and tidal volume (VT) between

167 the selective MOR agonist DAMGO, analgesia, minute ventilation (V E), heart rate (HR) and mean arter

168 Minute ventilation (V E), lung volume, and expiratory ai

169 eathing pattern at maximal exercise: maximal minute ventilation (V Emax) (r = -0.47; p = 0.009), and

170 aximal oxygen consumption (V O2max), maximal minute ventilation (V Emax), and maximum voluntary venti

171 upward shift in the CO2-response curves for minute ventilation (V I) and frequency (f ), and a signi

172 c hypoxia increased the gross variability of minute ventilation (V I), tidal volume (VT), inspiratory

173 ational activity of expiratory time (TE) and minute ventilation (V I), whereas a load of 6 cm H2O/L/s

174 he effect of subcutaneous leptin infusion on minute ventilation (V(E) ) and the hypoxic ventilatory r

175 However, the effect of leptin on minute ventilation (V(E) ) and the hypoxic ventilatory r

176 Minute ventilation (V(E)) in 2, 4, and 6% CO(2) was meas

177 ography, BP), oxygen saturation (SpO(2)) and minute ventilation (V(E)) were measured continuously.

178 Inspired minute ventilation (V(I)), R(UA) and end-tidal CO(2) pre

179 ecline, whereas both tidal volume (V(T)) and minute ventilation (.V(E) ) significantly increased in t

180 Ten male subjects were asked to breathe at minute ventilation (V1) equal or slightly greater than 6

181 Here we define a pathway in which increased minute ventilation (&Vdot;E ) is signalled by deoxyhaemo

182 ivity was indexed by the two-breath nadir in minute ventilation ( VE ) during 1 min of hyperoxia (100

183 Measurements included minute ventilation ( VE ), end-tidal partial pressures o

184 tion (EOV) refers to regular oscillations in minute ventilation (VE) during exercise.

185 ed by correlating CO2 production (V(CO2)) to minute ventilation (VE) in each test.

186 ller, the regression line for the P(a,CO(2))-minute ventilation (VE) relation shifted to higher VE an

187 Post-C5 SCI rats demonstrated deficits in minute ventilation (Ve) responses to a 7% CO2 challenge

188 Minute ventilation (VE) was measured using whole-body pl

189 f exhaled carbon dioxide volume (VCO(2)) and minute ventilation (VE), along with exhaled respiratory

190 f humans as a function of concentration (C), minute ventilation (VE), duration of exposure (T), and a

191 achieved by generating significantly larger minute ventilation (VE), from 24 +/- 11 to 29 +/- 10 L/m

192 We determined minute ventilation (VE), oxygen consumption (VO2), carbo

193 e and week 30: carbon dioxide output (VCO2), minute ventilation (VE), peak VE/VCO2 ratio, ventilatory

194 ilatory efficiency, commonly assessed by the minute ventilation (VE)-carbon dioxide production (VCO2)

195 is predominantly reported as an increase in minute ventilation (VE).

196 -0.5 to 1.0] mL/kg/min; P = .46), peak Vo2, minute ventilation (Ve)/carbon dioxide production (Vco2)

197 % versus 71% +/- 19%; P = 0.007), and higher minute ventilation (VE)/carbon dioxide production (VCO2)

198 abnormal, characterized by elevation of the minute ventilation (VE)/CO(2) elimination slope (VE/VCO(

199 , range 6 to 44 watts, p < 0.05) and maximal minute ventilation (VEmax) increased by a median of 22%

200 d signaling is involved in the regulation of minute ventilation, ventilation-perfusion matching, pulm

201 ting in a NREM sleep-associated decrement in minute ventilation (VI = 11.10 +/- 0.67, 9.32 +/- 0.91,

202 air, CO2 increased the gross variability of minute ventilation (VI) and tidal volume (VT), and decre

203 CO2 response slopes were increased 303% for minute ventilation (VI)(P </= 0.01) and 251% for mean in

204 ptors by acute hypoxia causes an increase in minute ventilation (VI), heart rate (HR) and arterial bl

205 arterial blood oxygen stimulate increases in minute ventilation via activation of peripheral and cent

206 In the morbidly obese, at high minute ventilations, VO(2RESP) is greater than in normal

207 CH rats breathing 12% O2 had greater minute ventilation (VP) than N rats breathing air, but t

208 vel bicycle and treadmill exercise such that minute ventilation was <25 l/min.

209 During hypoxia, minute ventilation was 12.9+/-1.3 L/min on dopamine and

210 Minute ventilation was determined during each minute of

211 In all 3 periods, minute ventilation was higher in the CF and CFDM groups

212 ere were no differences in hemodynamics, but minute ventilation was lower in the AVCO2R group and Pac

213 Minute ventilation was lowered to less than half of its

214 Minute ventilation was maintained constant at each tidal

215 Minute ventilation was recorded during infusion of insul

216 During HFNC, minute ventilation was reduced (P < 0.001) at constant a

217 To maintain normocapnia, minute ventilation was reduced from 3.8 +/- 0.1 L/min to

218 Minute ventilation was reduced from 5.6 L/min at baselin

219 Minute ventilation was reduced to induce hypercapnia wit

220 Minute ventilation was reduced, and normocarbia (Paco2 3

221 Minute ventilation was smaller with the impedance system

222 Minute ventilation was then altered by adjusting tidal v

223 r study, ITPV, compared with CMV at the same minute ventilation, was associated with a significantly

224 Inspiratory time (0.75 sec), FIO2 (0.3), and minute ventilation were held constant.

225 Inspiratory tidal volume and minute ventilation were increased in AAV-GAA-treated vs.

226 Resting heart rate, blood pressure and minute ventilation were measured when breathing normoxic

227 Respiratory frequency and minute ventilation were significantly increased when CEE

228 Respiratory rate, tidal volume, and minute ventilation were studied to determine their effec

229 gh arousal threshold, may be able to sustain minute ventilation when challenged with negative airway

230 Dex-Asthma mice compensated to maintain high minute ventilation, whereas Asthma mice showed significa

231 enous CO2 removal enabled a 50% reduction in minute ventilation while maintaining normocarbia and may

232 real venovenous CO2 removal device to reduce minute ventilation while maintaining normocarbia.

233 rious effects of opioids such as fentanyl on minute ventilation while, if possible, preserving the an

234 nerated airway pressures, tidal volumes, and minute ventilation within the targeted range for the sta