ライフサイエンスコーパス: ventilatory

1 activation of HIF-2alpha strikingly impaired ventilatory acclimatisation to chronic hypoxia (HVRs: 4.

2 the initial G(pCO2) is a modest predictor of ventilatory acclimatization.

3 correlated well with most other measures of ventilatory acclimatization.

4 Of note, maintaining ventilatory activity at low carbon dioxide levels is amo

5 Human ventilatory activity persists, during wakefulness, even

6 lop pulmonary edema as a consequence of poor ventilatory adaptation to hypobaric hypoxia.

7 ycardia, reduction in PCA and an increase in ventilatory amplitude (VAMP) without any changes in vent

8 ted HR 1.10, 95% CI 1.00-1.22, P=0.049), and ventilatory anaerobic threshold (adjusted HR 0.82, 95% C

9 They reached the ventilatory anaerobic threshold earlier (81.4 +/- 9.5 vs

10 , early diagnosis and utilizing ARDS Network ventilatory and conservative fluid management recommenda

11 Ventilatory and electroencephalographic recordings were

12 The magnitude of the ventilatory and haemodynamic responses depended on both

13 Separately, ventilatory and haemodynamic responses to systemic hypox

14 pothesized that alveolar mechanics vary with ventilatory and lung conditions.

15 lopmental nicotine exposure (DNE) alters the ventilatory and metabolic response to hyperthermia in ne

16 alyses to study the association of PPCs with ventilatory and other perioperative variables.

17 Demographic, disease factor, and ventilatory and outcome data were collected, and 328 pat

18 We conclude that the magnitudes of the ventilatory and pulmonary vascular responses to sustaine

19 as found between the magnitudes of pulmonary ventilatory and pulmonary vascular responses.

20 tion, and opens new avenues to study certain ventilatory and speech disorders.

21 Potentiation of the ventilatory and sympathetic drive in response to CC acti

22 f peripheral neuropathy and abnormalities of ventilatory and upper airway neural control.

23 ppreciation of the interplay of hemodynamic, ventilatory, and skeletal myopathic processes in this co

24 turtles have a unique abdominal-muscle-based ventilatory apparatus whose evolutionary origins have re

25 arget Vt of 6 ml/kg during neurally adjusted ventilatory assist (NAVA).

26 Both neurally adjusted ventilatory assist and a noninvasive mechanical ventilat

27 iability was higher during neurally adjusted ventilatory assist and ineffective efforts appeared only

28 e in excess was shorter in neurally adjusted ventilatory assist and PSV-NIV+ than in PSV-NIV- (p < .0

29 aks was insignificant with neurally adjusted ventilatory assist and significantly lower than in press

30 anical ventilation such as neurally adjusted ventilatory assist are feasible and improve patient phys

31 iratory failure, levels of neurally adjusted ventilatory assist between 0.5 and 2.5 cm H2O/muvolt are

32 re support ventilation and neurally adjusted ventilatory assist during wakefulness and with two doses

33 ential clinical benefit of neurally adjusted ventilatory assist in patients receiving noninvasive mec

34 nloading were observed for neurally adjusted ventilatory assist levels from 0.5 cm H2O/muvolt (46% [4

35 applied in a random order: neurally adjusted ventilatory assist levels: 0.5, 1, 1.5, 2, 2.5, 3, 4, 5,

36 Neurally adjusted ventilatory assist provides better patient-ventilator in

37 gorithm but was shorter in neurally adjusted ventilatory assist than in pressure support ventilation

38 was significantly lower in neurally adjusted ventilatory assist than in pressure support ventilation

39 algorithm (NAVA-NIV-), and neurally adjusted ventilatory assist with a noninvasive mechanical ventila

40 tion algorithm (PSV-NIV+), neurally adjusted ventilatory assist without a noninvasive mechanical vent

41 In neurally adjusted ventilatory assist, double triggering occurred sometimes

42 With neurally adjusted ventilatory assist, ineffective triggering index fell to

43 re support ventilation and neurally adjusted ventilatory assist, the noninvasive mechanical ventilati

44 re support ventilation and neurally adjusted ventilatory assist.

45 eous breathing on a T-piece or low levels of ventilatory assist.

46 ore double triggering with neurally adjusted ventilatory assist.

47 r assist delivered, each, at three levels of ventilatory assistance.

48 e time until death or the need for permanent ventilatory assistance.

49 a Novalung R100 ventilator (Metran) or usual ventilatory care.

50 sion, D1 receptor-modulated ventilation, and ventilatory chemoreflex activation by hypoxia or hyperca

51 rtantly, TAL also effectively normalized the ventilatory CO2 chemoreflex in BN rats, but TAL did not

52 stems such as breathing and specifically the ventilatory CO2 chemoreflex.

53 without altering P aC O2 or pH and enhanced ventilatory CO2 sensitivity (3.4 +/- 0.4 to 5.1 +/- 0.8

54 ely 22, 41 and 68 mmHg, respectively) on the ventilatory CO2 sensitivity of central chemoreceptors wa

55 ely disordered breathing pattern and reduced ventilatory CO2 sensitivity.

56 by an augmented carotid body and whole body ventilatory CO2 sensitivity.

57 he tidal volume signal (related to medullary ventilatory command), (3) autonomic function, and (4) co

58 ulating spinal cord functions, on descending ventilatory commands in healthy humans.

59 analysis, we provide the first evidence of a ventilatory component in HRV similar to mammalian respir

60 However, it should be expected that the ventilatory condition (quasi-static vs. dynamic) and lun

61 reload and decreased cardiac output, whereas ventilatory consequences include increased airway pressu

62 tion may produce significant hemodynamic and ventilatory consequences such as increased intraabdomina

63 at patients limited by breathlessness due to ventilatory constraints can be identified as those reach

64 ent of novel therapeutic strategies to treat ventilatory control disorders associated with respirator

65 ance, ventilation-perfusion mismatching, and ventilatory control instability.

66 d prolonged circulation time, implicates the ventilatory control system and suggests feedback instabi

67 due to reductions in the sensitivity of the ventilatory control system.

68 associated pneumonia rates were 9.6 of 1,000 ventilatory days and 19.8 of 1,000 ventilatory days, res

69 of 1,000 ventilatory days and 19.8 of 1,000 ventilatory days, respectively (p = 0.0076).

70 In terms of ventilatory days, ventilator-associated pneumonia rates

71 versus 2.2 mm Hg/L; P<0.001), and increased ventilatory dead-space fraction (17+/-1 versus 12+/-2%;

72 nary function testing reveals an obstructive ventilatory defect that is typically not reversed by inh

73 nfections 16%), pulmonary (diffusion 79% and ventilatory defects 63%, pulmonary alveolar proteinosis

74 of HIV-infected individuals have obstructive ventilatory defects and reduced diffusing capacity is se

75 Hypoxemia and enhanced ventilatory demands result, although both are usually as

76 lished the hypoxic ventilatory response, and ventilatory depression during hypoxia was exacerbated un

77 e increase in ventilation to the increase in ventilatory drive across the drop.

78 e increase in ventilation to the increase in ventilatory drive across the drop.

79 ion, pneumonia and hypoxia, impaired hypoxic ventilatory drive and decreased patient satisfaction.

80 usal threshold was estimated as the level of ventilatory drive associated with arousal.

81 sal threshold was quantified as the level of ventilatory drive associated with arousal.

82 This fuels the notion that the human ventilatory drive during wakefulness often results from

83 n which spontaneous biological variations in ventilatory drive repeatedly induce temporary and irregu

84 We measured locomotor-ventilatory dynamics in 14 subjects running at a self-se

85 respiratory muscle atrophy and weakness and ventilatory dysfunction.

86 ic ventilatory response and the mechanism of ventilatory dysfunctions arising from AMPK deficiency.

87 onfidence interval [CI] 0.77-0.88, P<0.001), ventilatory efficiency (adjusted HR 1.10, 95% CI 1.00-1.

88 gen consumption (Vo2 [mL/kg per minute]) and ventilatory efficiency (the VE/Vco2 slope).

89 14 versus </=14 mL O(2).kg(-1).min(-1)]) and ventilatory efficiency (VE/Vco(2) slope [<34 versus >/=3

90 hs and assessed changes in lung function and ventilatory efficiency (Ve/Vco(2)).

91 Submaximal exercise parameters, such as ventilatory efficiency and anaerobic threshold, measured

92 points under the fentanyl condition, whereas ventilatory efficiency and dead space ventilation were i

93 take, anaerobic threshold, oxygen pulse, and ventilatory efficiency appropriately focus upon the card

94 These patients had particularly poor ventilatory efficiency compared with patients without hy

95 tilation led to hypocapnia and poor exercise ventilatory efficiency in chronic obstructive pulmonary

96 =0.977; confidence interval [CI]=0.97-0.98), ventilatory efficiency slope (P=0.01; HR=1.02; CI=1.01-1

97 ptake (VO(2)) was 67+/-22% of predicted; and ventilatory efficiency was 32+/-8.

98 ration, percent predicted peak Vo2 [%ppVo2], ventilatory efficiency) were examined.

99 e capacity, respiratory muscle strength, and ventilatory efficiency.

100 t improve RV function, exercise capacity, or ventilatory efficiency.

101 ed peak oxygen consumption >15 ml/min/kg and ventilatory equivalent for carbon dioxide <45 l/min/l/mi

102 levels, whereas peak respiratory frequency, ventilatory equivalent for CO2, and IL-6 and IL-1beta le

103 indices (peak oxygen consumption [VO(2)] and ventilatory equivalents for exhaled carbon dioxide [VE/V

104 tion (OR, 11.3; 95% CI, 7.4-17.1; P < .001), ventilatory failure (OR, 12.4; 95% CI, 8.2-18.8; P < .00

105 io [OR], 17.1; 95% CI, 13.8-21.3; P < .001), ventilatory failure (OR, 15.9; 95% CI, 12.8-19.8; P < .0

106 nant myopathy characterized by neuromuscular ventilatory failure in ambulant patients.

107 ve pressure modes and their role in managing ventilatory failure in neuromuscular diseases and other

108 outbreaks had a higher proportion of patient ventilatory failure.

109 developed progressive muscular hypotonia and ventilatory failure.

110 recordings were analyzed with respect to the ventilatory flow signal to detect preinspiratory potenti

111 are brief, they cause large fluctuations in ventilatory flow.

112 y insignificant because 'step-driven flows' (ventilatory flows attributable to step-induced forces) c

113 tory amplitude (VAMP) without any changes in ventilatory frequency (fV).

114 ntrol respiration, yet mechanisms regulating ventilatory frequency are poorly understood.

115 ontrols were assessed for postbronchodilator ventilatory function, smoking history, atopy, and treatm

116 ch the abdominal muscles took on the primary ventilatory function, whereas the broadened ribs became

117 ostic group on decline in postbronchodilator ventilatory function.

118 d with an increased risk of COPD and reduced ventilatory function.

119 y (CB) chemoreceptor stimulus influenced the ventilatory gain of the central chemoreceptors to CO2 .

120 that adrenaline release can account for the ventilatory hyperpnoea observed during hypoglycaemia by

121 ssociated condition had significantly longer ventilatory, ICU, and hospital days compared with those

122 al lung fields in a chest CT scan, and mixed ventilatory impairment in a spirometric test were reveal

123 We found that the normal ventilatory increase in response to elevated tissue CO(2

124 Peak oxygen consumption decreased and ventilatory inefficiency (VE/VCO2 slope) increased with

125 Formula: see text]e/[Formula: see text]co2), ventilatory inefficiency was closely related to PcCO2 (r

126 way (BN) rats exhibit an inherent and severe ventilatory insensitivity to hypercapnia but also exhibi

127 Herein, we tested the hypothesis that the ventilatory insensitivity to hypercapnia in BN rats is d

128 ress the potential consequences of locomotor-ventilatory interactions for elite endurance athletes an

129 he rationale for recommendations on selected ventilatory interventions for adult patients with ARDS.

130 Ventilatory limitation and gas exchange impairment are i

131 ubgroup, the patients who developed DH had a ventilatory limitation contributing to exercise cessatio

132 loading during exercise would indicate true ventilatory limitation to exercise in mild COPD.

133 formance was reduced and was associated with ventilatory limitation, greater desaturation, and dyspne

134 Ventilatory long-term facilitation can be evoked by brie

135 However, the magnitude of ventilatory long-term facilitation was not enhanced over

136 Secondary outcomes included ventilatory management (including tidal volume [VT] expr

137 Ventilatory management changed over time (P < 0.001), wi

138 Despite advances in ventilatory management, FC remains associated with signi

139 Data on ventilatory management, gas exchange, hemodynamics, and

140 cian recognition of ARDS, the application of ventilatory management, the use of adjunctive interventi

141 a peak pressure of 40 cm H(2)O) and dynamic ventilatory maneuvers (increase and decrease in positive

142 ar mechanics during quasi-static and dynamic ventilatory maneuvers in noninjured and injured lungs.

143 w affected the stability of upper airway and ventilatory mechanics.

144 nts under mechanical ventilation in the ICU, ventilatory mode or settings may influence sleep quality

145 ding, the types of anesthetic techniques and ventilatory modes are varying to fit the procedural requ

146 ng 15-sec end-inspiratory and end-expiratory ventilatory occlusions performed at two levels of positi

147 We propose that daytime ventilatory oscillations generally result from a chemore

148 elucidates the mechanism underlying daytime ventilatory oscillations in heart failure and provides a

149 LG was defined as the ratio of the ventilatory overshoot to the preceding reduction in vent

150 LG was defined as the ratio of the ventilatory overshoot to the preceding reduction in vent

151 nder normoxia had resting cardiovascular and ventilatory parameters similar to controls.

152 taneously assessed hemodynamic measurements, ventilatory parameters, and peripheral oxygen usage duri

153 Were this true, modifications of ventilatory pattern and positioning aimed at geographic

154 dent RTN neuronal activation and rescued the ventilatory phenotype.

155 The ventilatory phenotypes associated with both inducible an

156 Ventilatory power links the combined physiology inherent

157 to predict prognosis among patients with HF, ventilatory power provides relatively greater prognostic

158 Multivariate analysis demonstrated that ventilatory power was the strongest indicator of prognos

159 ion, VE/Vco(2) slope, circulatory power, and ventilatory power were all predictive of cardiac events

160 as a prognostic index, we hypothesized that ventilatory power would provide greater prognostic discr

161 sure, creating a novel index that we labeled ventilatory power.

162 are not well-known, especially under current ventilatory practices.

163 Both injurious ventilatory protocols developed comparable levels of phy

164 erfused lungs were allocated to one of three ventilatory protocols for 3 hours: control group receive

165 omly allocated to one of the three following ventilatory protocols for 4 hours: spontaneous breathing

166 cycling with isocapnic hyperpnea (muscle and ventilatory pump), during Ex plus an inspiratory load of

167 with a small additional contribution by the ventilatory pump.

168 the relative contribution of the muscle and ventilatory pumps to stroke volume in patients without a

169 d hypercapnic ventilatory responses (HCVRs), ventilatory recruitment threshold (VRT-CO2), baroreflex

170 ores the state dependence of the hypercapnic ventilatory reflex (HCVR).

171 One week after CB excision, the hypoxic ventilatory reflex was greatly reduced as expected, wher

172 n in 21% O2 were normal, whereas the hypoxic ventilatory reflex was still depressed (95.3%) and hypox

173 mediates a large portion of the hypercapnic ventilatory reflex, regulates breathing differently duri

174 (CCs) are considered a dominant mechanism in ventilatory regulation.

175 control subjects in association with higher ventilatory requirements.

176 ation, rate of oxygen consumption (VO2), and ventilatory reserve (ventilation/maximum ventilatory vol

177 circulatory reserve rather than an exhausted ventilatory reserve underlying the limitation of exercis

178 in vivo significantly decreased the hypoxic ventilatory response (Delta VE control 74 +/- 6%, Delta

179 a for 7 days manifest an exaggerated hypoxic ventilatory response (HVR) (10.8 +/- 0.3 versus 4.1 +/-

180 phy, SH attenuated the acute (5 min) hypoxic ventilatory response (HVR) and caused a high incidence o

181 ABSTRACT: The hypoxic ventilatory response (HVR) is biphasic, consisting of a

182 increase in ventilation, termed the hypoxic ventilatory response (HVR).

183 ce in patients with COPD, mostly by reducing ventilatory response and dyspnea during exercise; these

184 ing of the mechanisms underlying the hypoxic ventilatory response and highlight the significance of p

185 /or AMPK-alpha2 are required for the hypoxic ventilatory response and the mechanism of ventilatory dy

186 Heightened neural drive promoting a ventilatory response beyond that required to overcome an

187 s exhibited a significantly enhanced hypoxic ventilatory response compared to AV-CHF rats.

188 tivation of the muscle metaboreflex causes a ventilatory response in COPD patients but not in healthy

189 Excessive ventilatory response in this group was associated with h

190 ignificant differences in any of the central ventilatory response indices were found between CB normo

191 P) 12-13, a critical period when the hypoxic ventilatory response is at its weakest.

192 poxia, contrary to the view that the hypoxic ventilatory response is determined solely by increased c

193 ene (c-fos) expression to assess the hypoxic ventilatory response of mice with conditional deletion o

194 ion of Tac1-Pet1 neuron activity blunted the ventilatory response of the respiratory CO2 chemoreflex,

195 k oxygen consumption/kg (r=-0.479; P=0.024), ventilatory response to carbon dioxide production at ana

196 uced thermogenic response, and (3) a reduced ventilatory response to CO(2) after postnatal day 12 (P1

197 n in cold stress (4 degrees C) and a reduced ventilatory response to CO(2), we hypothesized that neon

198 (PPADS, a P2 receptor blocker) decreased the ventilatory response to CO2 by 30%.

199 ed in RTN neurons, essentially abolished the ventilatory response to CO2.

200 The ventilatory response to exercise requires substantial ch

201 cle afferents in reflex control of the human ventilatory response to exercise.

202 RATIONALE: An increased ventilatory response to exertional metabolic demand (hig

203 instem 5-HT is sufficient for an appropriate ventilatory response to hypercapnia up until P15.

204 monstrate that the EP3R is important for the ventilatory response to hypercapnia.

205 th subtle but significant alterations in the ventilatory response to hyperthermia in neonatal rats.

206 e (aOR, 2.28; 95% CI, 1.28-4.07; P = 0.005), ventilatory response to hypoxia at exercise less than 0.

207 tivity parameters (high desaturation and low ventilatory response to hypoxia at exercise) were indepe

208 -carboxamido) acetic acid) did not mimic the ventilatory response to hypoxia.

209 ed an interference in the cardiovascular and ventilatory response to hypoxia.

210 vel of chemosensitivity as determined by the ventilatory response to hypoxia.

211 and, when silenced, observed blunting of the ventilatory response to inhaled CO2Tac1-Pet1 neurons thu

212 In wakefulness, the ventilatory response to normoxic hypercapnia is higher i

213 KEY POINTS: The ventilatory response to reduced oxygen (hypoxia) is biph

214 harge in anesthetized rats and decreased the ventilatory response to serotonin in awake and anestheti

215 The ventilatory response was abolished and the haemodynamic

216 gene, erythrocytosis, and augmented hypoxic ventilatory response, all hallmarks of Egln1 loss of fun

217 ha2 deletion virtually abolished the hypoxic ventilatory response, and ventilatory depression during

218 bition of CD73 in vivo decreased the hypoxic ventilatory response, reduced the hypoxia-induced heart

219 en sensing and the initiation of the hypoxic ventilatory response, yet the gene expression profile of

220 CSE using morpholinos attenuated the hypoxic ventilatory response.

221 play a pivotal role in promoting the hypoxic ventilatory response.

222 nt the hyperventilation nor abnormal hypoxic ventilatory response.

223 iabetes, we measured hypoxic and hypercapnic ventilatory responses (HCVRs), ventilatory recruitment t

224 terozygous PHD2 deficiency, enhances hypoxic ventilatory responses (HVRs: 7.2 +/- 0.6 vs. 4.4 +/- 0.4

225 ted to CSN neural activity combined with the ventilatory responses indicate that caffeine alters cent

226 oxygen detection and the cardiovascular and ventilatory responses of fish to hypoxia, we hypothesize

227 m neurochemistry is associated with impaired ventilatory responses to acute hypoxia and mortality.

228 Caffeine ameliorated ventilatory responses to acute hypoxia in normoxic anima

229 rterial blood pressure (MAP), heart rate and ventilatory responses to all steady state exercise inten

230 xygen sensing, and impaired carotid body and ventilatory responses to chronic hypoxia, which were cor

231 Experimental evidence, including exaggerated ventilatory responses to CO2 and prolonged circulation t

232 rons, increased apnea frequency, and blunted ventilatory responses to CO2.

233 nary vascular resistance and more pronounced ventilatory responses to exercise, lower pulmonary arter

234 1-2 days post-CBD (P <0.05), and attenuated ventilatory responses to hypoxia (P <0.05) and venous so

235 g, intracellular signalling and promotion of ventilatory responses to hypoxia in adult and larval zeb

236 The cardioaccelerator and ventilatory responses to rhythmic exercise in the human

237 receptor antagonist, alters CB function and ventilatory responses when administered acutely.

238 be capable of eliciting exercise-like cardio-ventilatory responses, but their relative contributions

239 ibution of the carotid body (CB) in observed ventilatory responses, CB afferent discharge before and

240 the exposure, measurements were made of the ventilatory sensitivities to acute isocapnic hypoxia (G(

241 gether with the evidence of severely blunted ventilatory sensitivity to CO2 in mice with conditional

242 HIF prolyl hydroxylase, PHD2, show enhanced ventilatory sensitivity to hypoxia and carotid body hype

243 ndings demonstrate that PHD enzymes modulate ventilatory sensitivity to hypoxia and identify PHD2 as

244 Ventilatory sensitivity to hypoxia increases in response

245 2alpha enzyme-substrate couple in modulating ventilatory sensitivity to hypoxia.

246 nt-ventilator interaction suggested that the ventilatory settings were suboptimal and could have been

247 the assessment of oxygenation under standard ventilatory settings, 118 (80.8%) patients continued to

248 cruitment and may be useful to individualize ventilatory settings.

249 Step-driven flows varied depending on ventilatory state (high versus low lung volume), suggest

250 ation of tension pneumothorax depends on the ventilatory status of the patient.

251 ns of tension pneumothorax differ by subject ventilatory status.

252 Biotrauma due to injurious ventilatory strategies can lead to the release of mediat

253 has been the development of lung-protective ventilatory strategies, based on our understanding of th

254 bjective was to review the impact of initial ventilatory strategy on mortality and the risks related

255 We compared the preventive effects of a ventilatory strategy, aimed at decreasing pulmonary aspi

256 % of infants vs. 48.7%, P=0.04), less use of ventilatory support (in 4.0% vs. 10.8%, P=0.01), and few

257 o had advanced respiratory failure requiring ventilatory support at the time of oseltamivir initiatio

258 Adult patients with ventilatory support for more than 60 days.

259 Among ICU patients receiving acute ventilatory support for respiratory failure, PDM resulte

260 ht (OR, 3.41; 95% CI, 1.61-7.26), and use of ventilatory support for the newborn (OR, 2.85; 95% CI, 1

261 ions of domiciliary medical technology, home ventilatory support has either led or run in parallel wi

262 maternal benzodiazepine treatment, rates of ventilatory support increased by 61 of 1000 neonates and

263 spiratory distress should be considered when ventilatory support is not readily available.

264 ffect of prone positioning during mechanical ventilatory support on outcomes.

265 zes the trends and growing evidence base for ventilatory support outside the hospital.

266 One of the great advances in ventilatory support over the past few decades has been t

267 urs), broad-spectrum antibiotic therapy, and ventilatory support resulted in full recovery without th

268 ciated with a shorter duration of mechanical ventilatory support than was early parenteral nutrition

269 Titrating ventilatory support to maintain normal levels of inspira

270 nd with an increased frequency of oxygen and ventilatory support use.

271 , comorbidities, hemodynamic parameters, and ventilatory support used before ECLS.

272 to predict which patients required extended ventilatory support was limited.

273 oxygen therapy, nasogastric-tube feeding, or ventilatory support was recorded.

274 h confirmed H1N1 pneumonia and on mechanical ventilatory support were randomized to receive adjuvant

275 Supplemental oxygen and ventilatory support were required in 67.9% and 11.1%, re

276 days alive and breathing without mechanical ventilatory support within the first 28 days after rando

277 l-cause death, respiratory failure requiring ventilatory support, and hospitalization duration.

278 Organ Failure Assessment score, duration of ventilatory support, and mortality.

279 n supplementation, nasogastric-tube feeding, ventilatory support, and relative improvement in the cli

280 associated with an increase in intensity of ventilatory support, NIV failure, and intensive care uni

281 c therapist whenever desired while receiving ventilatory support, self-initiated use of noise-canceli

282 e care unit admission, the need for invasive ventilatory support, the length of hospital stay, or the

283 if they met eligibility criteria for partial ventilatory support, tolerated pressure support ventilat

284 evious myocardial infarction, renal disease, ventilatory support, use of circulatory support, glycopr

285 s lung-protective ventilation during partial ventilatory support, while maintaining diaphragm activit

286 , broad-spectrum antibiotics, and mechanical ventilatory support.

287 maintaining diaphragm activity under partial ventilatory support.

288 blood products, fluid balance, and modes of ventilatory support.

289 c, may alleviate the anxiety associated with ventilatory support.

290 spiratory failure to insure need for ongoing ventilatory support.

291 ostomy to patients with a need for continued ventilatory support.

292 minor respiratory interventions, and use of ventilatory support.

293 creasing the risk for failed liberation from ventilatory support.

294 ic strain imposed on the circulatory and the ventilatory systems, resulting in an apparent matching b

295 of knee extensor muscles (P=0.008), and the ventilatory threshold power (P=0.02) were also significa

296 ify the application of oxygen consumption at ventilatory threshold, to describe CPX variables with an

297 Ventilatory transitions initiated in 'preferred' phases

298 imized antagonistic interactions and aligned ventilatory transitions with assistive phases of the ste

299 sitivity was measured as the RSNA and minute ventilatory (VE) responses to hypoxia and hypercapnia.

300 and ventilatory reserve (ventilation/maximum ventilatory volume ratio [VE/MVV]) were measured continu