ライフサイエンスコーパス: blood gas

1 pressure, heart rate, and systemic arterial blood gas.

2 hange in PFR from baseline to final arterial blood gas.

3 recorded at the time of a clinical arterial blood gas.

4 ce marker, was calculated with each arterial blood gas.

5 y, in lung-function laboratories to estimate blood gases.

6 r measurement of arterial and central venous blood gases.

7 daily digital chest radiographs and arterial blood gases.

8 ios and were used to compute global arterial blood gases.

9 usion ratios (V(A)/Q) predictive of arterial blood gases.

10 ary compliance and deterioration in arterial blood gases.

11 d-base physiology was measured with arterial blood gases.

12 ood flow were measured with pulmonary venous blood gases.

13 n intrapulmonary vasodilatation and arterial blood gases.

14 xchange impairment as determined by arterial blood gases.

15 which helps restore breathing and normalizes blood gases.

16 measured VCO2ML, VCO2NL, lung mechanics, and blood gases.

17 sion did not affect systemic hemodynamics or blood gases.

18 22.7 L. min(-1) under conditions of altered blood gases.

19 lung compliance, inspiratory resistance, and blood gases.

20 collected ventilation variables and arterial blood gases.

21 We conclude that in this range of blood gases: (1) the GG reflex to negative pressure is u

22 catheter (2% to 51%), and determination of a blood gas (24% to 70%).

23 ntion was associated with 128 fewer arterial blood gases, 73 fewer chest radiographs, and 16 fewer RB

24 um erythropoietin levels (76%), and arterial blood gases (75%) were the most frequent tests used in t

25 erature monitoring and intermittent arterial blood gas (ABG) analysis was undertaken.

26 uring multidisciplinary rounds, all arterial blood gas (ABG) results, ventilator settings and ventila

27 crossover format, and the patients' arterial blood gases (ABGs) were measured at baseline and at inte

28 ir pulmonary function tests (PFTs), arterial blood gases (ABGs), and respiratory muscle strength as e

29 The authors explored associations between blood gas abnormalities in more than 1,000 preterm infan

30 of the subjects, with separate analyses for blood gas abnormalities on multiple days and for partial

31 ssels but did not cause alveolar flooding or blood gas abnormalities.

32 hemorrhagic shock, we measured hemodynamics, blood gases, acid-base status, metabolism, organ functio

33 e obtained concerning demographics, arterial blood gas, Acute Physiology and Chronic Health Evaluatio

34 alveolar dead space fraction (first arterial blood gas after intubation) (per 0.1 unit increase: odds

35 ra vigilance should be applied in monitoring blood gases after delayed sternal closure to assess clin

36 phragm energy expenditure (effort), arterial blood gases, airway pressure, tidal volume and its coeff

37 nts, lung injury was assessed by analysis of blood gases, alveolar permeability, lung histology, AFC,

38 The results of arterial blood gas analyses at t = 4 minutes and t = 13 minutes (

39 In total, 295,079 arterial blood gas analyses, including the PaO2, between July 201

40 Arterial blood gas analysis (PaO2, PaCO2), peak airway pressure (

41 Gas exchange was assessed by arterial blood gas analysis after ventilation with each gas mixtu

42 Gas exchange was evaluated by blood gas analysis and multiple inert gas elimination te

43 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following I

44 arrest preceding PICU admission and arterial blood gas analysis taken within 1 hour of PICU admission

45 and compared with PaCO2 values when arterial blood gas analysis was performed.

46 PE underwent perfusion lung scintigraphy and blood gas analysis within 48 h from clinical presentatio

47 ion, pulmonary function testing and arterial blood gas analysis, and echocardiographic, imaging, and

48 tal sinus vein for collection of samples for blood gas analysis.

49 may decrease the need for repeated arterial blood gas analysis.

50 re measured and blood samples were drawn for blood gas analysis.

51 nnula was taken every half-hour for arterial blood gas analysis.

52 e values determined by standard intermittent blood gas analysis.

53 son-Hasselbalch equation and reported on the blood gas analysis.

54 A total of 409 patients with arterial blood gases analyzed at least once and with a complete s

55 validated through concurrent, blind, ex situ blood gas analyzer (BGA) measurements.

56 As Na(+)(direct) measurements on a blood gas analyzer are not influenced by the total prote

57 arterial oxygen levels were measured with a blood gas analyzer.

58 s were analyzed in duplicate on two separate blood gas analyzers and CO-oximeters.

59 Blood gas analyzers and core laboratory chemistry analyz

60 However, as blood gas analyzers are not available at all clinical wa

61 Arterial blood gas and CE are required in LT candidates for diagn

62 The SenDx 100 portable blood gas and electrolyte analyzer is a simple and easy

63 body fluid homeostasis, indicated by similar blood gas and electrolyte concentrations in urine and bl

64 nd corresponding arterial and central venous blood gas and lactate measurements were made.

65 Concurrent arterial blood gas and lactate measurements were taken.

66 t maintain stable haemodynamics, have normal blood gas and oxygenation parameters and maintain patenc

67 ondary outcomes included changes in arterial blood gas and respiratory parameters, weaning duration,

68 Blood gas and tissue pH regulation depend on the ability

69 Rapid decreases in blood gases and a slower reduction in blood glucose sugg

70 Blood gases and biochemistry were monitored to assess or

71 Arterial blood gases and electrolytes were measured before and af

72 for continuous intravascular measurements of blood gases and electrolytes.

73 compared to lowlanders we measured arterial blood gases and global cerebral blood flow (duplex ultra

74 ized carboxyhemoglobin and improved arterial blood gases and intrapulmonary vasodilatation, reflectin

75 ET using cycle ergometry and ramp protocols; blood gases and lactate concentrations were measured eve

76 Consequences of CSA, including altered blood gases and neurohormonal activation, could result i

77 Arterial blood gases and pH were measured every 30 mins for the f

78 axic breathing pattern with markedly altered blood gases and pH, and pathological responses to challe

79 atory center's output to changes in arterial blood gases and pH, is one of the most important determi

80 gy and other aspects of physiology including blood gases and respiration, the physiology and biomecha

81 positive study results with normal arterial blood gases and therefore do not fulfill criteria for HP

82 tter were studied for evaluation of arterial blood gases and validation of the grading method for pre

83 Seven days post-CBD, blood gases and ventilation in 21% O2 were normal, where

84 Arterial blood gases and ventilator settings were monitored every

85 ere not accompanied by marked alterations in blood gases and were abolished by vagotomy or atropine.

86 approximately 85% of maximum while arterial blood gases and work of breathing were assessed.

87 nert gas measurements) and 10 (hemodynamics, blood gases) and 20 (hemodynamics, blood gases, inert ga

88 entral venous pressure, heart rate, arterial blood gas, and pulse oximetric saturation were recorded.

89 y function tests, Brasfield scores, arterial blood gases, and age were correlated with lung pathology

90 scles while monitoring respiration, arterial blood gases, and blood glucose in mice exposed to 8% O2

91 mpared with baseline in heart rate, arterial blood gases, and blood pressure, but serum nitrite conce

92 rial pressure, heart rate, systemic arterial blood gases, and cardiac output and index.

93 sessed by pulmonary function tests, arterial blood gases, and chest X-rays, but the correlation with

94 Data on vital signs, electrolytes, arterial blood gases, and coagulation were collected before and a

95 Ventilator parameters, arterial blood gases, and derived oxygenation and ventilation ind

96 invasive monitoring to measure hemodynamics, blood gases, and gas exchange during exercise.

97 arterial pressure, cardiac output, arterial blood gases, and lactate were measured concurrently with

98 nography, pulmonary function tests, arterial blood gases, and left ventricular ejection fraction were

99 xide concentration in the exhaled gas (ENO), blood gases, and mean arterial pressure were measured ev

100 macrocirculation, echocardiography, arterial blood gases, and microcirculation parameters did not dif

101 Pulmonary hemodynamics, arterial blood gases, and plasma concentrations of arachidonate m

102 Systemic and pulmonary hemodynamics, blood gases, and plasma nitrate were assessed.

103 We measured electrolytes, blood gases, and plasma-free hemoglobin in arterial bloo

104 n systemic and cerebral venous hemodynamics, blood gases, and prostanoid (prostaglandin E2, 6-ketopro

105 ng injury in terms of respiratory mechanics, blood gases, and pulmonary edema.

106 ro-oculography, minute ventilation, arterial blood gases, and serum theophylline levels.

107 therapists recorded demographic information, blood gases, and ventilator type and settings, and they

108 asurements of baseline vital signs, arterial blood gases, and ventilatory settings.

109 Arterial blood gases are critical in regulation of cerebral blood

110 indices of cerebral oxygenation to arterial blood gases are not well defined.

111 or the fetus, although the roles of arterial blood gases are recognized to be critical in the regulat

112 ary vasoconstriction may help to explain why blood gases are within physiologic ranges for a certain

113 Basal and hourly hemodynamics and blood gases (arterial and venous) under steady state res

114 Tonometric Pco2, arterial blood gases, arterial and portal venous lactates, and po

115 ther rat strains.We measured ventilation and blood gases at rest (eupnoea) and during hypoxia (FIO2 =

116 reduced as expected, whereas ventilation and blood gases at rest under normoxia were normal.

117 , excessive lung distension directly affects blood-gas barrier and lung vascular permeability.

118 The blood-gas barrier is able to maintain its extreme thinne

119 How the blood-gas barrier is regulated to be extremely thin but

120 The pulmonary blood-gas barrier needs to satisfy two conflicting requi

121 The strength of the blood-gas barrier on the thin side is attributable to th

122 apillary transfer is sensitive to changes in blood-gas barrier thickness of approximately 5 microm.

123 ibrosis, and edema, which cause an increased blood-gas barrier thickness, impair the efficiency of th

124 ed that active transport of gases across the blood-gas barrier was unnecessary in the lung, capillari

125 lmonary circulation and diffusion across the blood-gas barrier.

126 gs were collected (age, smoking history, and blood gas before lung harvesting).

127 ure, brain temperature, cerebral blood flow, blood gases, blood pressure, and pH.

128 ies have historically focused on normalizing blood gases but new research suggests that a higher PCO2

129 Prostacyclin does not mediate blood gas changes, alterations of pulmonary hemodynamics

130 We assessed the effects of blood gas changes, within the range encountered during m

131 minutes of each phase, we measured arterial blood gases, changes in end-expiratory lung volume of no

132 ith the baseline period, unadjusted arterial blood gas, chest radiograph, and RBC utilization in the

133 ider financial incentives targeting arterial blood gas, chest radiograph, and RBC utilization.

134 designed to decrease the avoidable arterial blood gases, chest radiographs, and RBC utilization on u

135 utcome was the number of orders for arterial blood gases, chest radiographs, and RBCs per patient.

136 ssive cycle exercise test with capillary (c) blood gas collection.

137 ncremental cycle exercise test with arterial blood gas collection.

138 scopy in neonates on intraoperative arterial blood gases, compared with open surgery.

139 measured in 13 subjects for eight different blood gas conditions, with the end-tidal partial pressur

140 Changes in blood gases conformed to predictions of a computer lung

141 well characterized because of challenges in blood gas control and limited availability of validated

142 dynamics, electrocardiography, biochemistry, blood gases, cytokines, and blood cells were collected a

143 tasets comprising hemodynamics, calorimetry, blood gases, cytokines, and cardiac and renal function w

144 We analyzed arterial blood gas data during 0 to 24 hours after the return of

145 r, in some practice settings, daily arterial blood gas data required to calculate the respiratory com

146 blood pressure monitoring and for assessing blood gas data.

147 Every blood gas derangement (hypoxemia, hyperoxemia, hypocapni

148 Findings suggest that individual blood gas derangements do not increase brain damage risk

149 for tracking unanticipated events related to blood gas deterioration.

150 Hemodynamics, arterial blood gas determination, alveolar permeability, wet-to-d

151 ially to 0.4+/-0.1 at the time of the second blood gas determination, thus permitting greater concent

152 A Student's t-test on pre- to post-blood gas differences showed a significantly lower PetCO

153 ratory rate, oxygen saturation, and arterial blood gases do not measure dyspnoea.

154 (2) ), oesophageal temperature, and arterial blood gases during exposure to three commonly experience

155 The effect of thoracoscopy on blood gases during repair of EA/TEF in neonates requires

156 Arterial blood gases, dyspnea, and comfort were recorded.

157 found between NKCC2 +/+ and +/- mice in BP, blood gas, electrolytes, creatinine, plasma renin concen

158 utput by thermodilution, arterial and venous blood gases; electrolytes; lactate; base excess; oxygen

159 Arterial blood gases estimated from the PET-based V(A)/Q distribu

160 o lung epithelial cells is essential for air-blood gas exchange.

161 We studied 1,034 arterial blood gases from 703 patients; 650 arterial blood gases

162 erial blood samples taken for measurement of blood gases, glucose and lactate and plasma adrenaline,

163 en at appropriate intervals for biophysical (blood gases, glucose, lactate) and endocrine (catecholam

164 g m(-2) ), FMD (Duplex ultrasound), arterial blood gases, Hct and [Hb], blood viscosity, and NO metab

165 Blood gas, hemodynamic, and gastric tonometric data were

166 Arterial and venous blood gases, hemodynamics, and pulmonary mechanics were

167 maintained alveolar ventilation and arterial blood gas homeostasis but at the expense of earlier dyna

168 tress in the dental office may help maintain blood gas homeostasis.

169 functional residual capacity increased, and blood gas improved until reaching the flat portion of th

170 Heart and respiratory rates and blood gases improved similarly for patients in both mask

171 formed direct field measurements of arterial blood gases in climbers breathing ambient air on Mount E

172 not very high (<20%) but to measure arterial blood gases in patients strongly suspected of having OHS

173 in MAP increased, despite similar changes in blood gases in response to umbilical cord occlusion, ove

174 e minimal level that would maintain arterial blood gases in the following ranges: pH 7.35-7.45, PaCO2

175 easurements were taken before (hemodynamics, blood gases, inert gas measurements) and 10 (hemodynamic

176 dynamics, blood gases) and 20 (hemodynamics, blood gases, inert gas measurements) minutes after induc

177 We analyzed matched blood samples for blood gas, inflammatory cytokine concentration, cystatin

178 the end of each phase, we measured arterial blood gases, inspiratory effort, and work of breathing b

179 animals in which no significant hemodynamic, blood gas, lactate, microcirculatory, and tissue Pco2 ab

180 is the process whereby the brainstem senses blood gas levels and adjusts homeostatic functions such

181 l and is refractory to modest alterations of blood gas levels of CO2 and O2.

182 es included serial pulmonary function tests, blood gases, lung compliance, computed tomography (CT) i

183 Pulmonary and systemic hemodynamics, blood gases, lung pressures, subpleural blood flow (lase

184 ia after out-of-hospital cardiac arrest, two blood gas management strategies are used regarding the P

185 Measurement of blood gases, mean arterial blood pressure, functional ca

186 oxyglucose, tissue myeloperoxidase, arterial blood gases, mean arterial pressure, and lung tissue pro

187 for CPO, p =.0125), obtained fewer arterial blood gas measurements (2.7 +/- 1.2 for IPO vs. 4.1 +/-

188 ly ventilated patients may not have arterial blood gas measurements available at relevant timepoints.

189 Blood gas measurements were collected on healthy lifetim

190 dings, all values from preoperative arterial blood gas measurements, and BAS procedure data.

191 ion), comorbidities, chest imaging, arterial blood gas measurements, and pulse oximetry.

192 Arterial blood gas measurements, intubation rate, days of mechani

193 Radial artery catheterization, arterial blood gas measurements, mechanical ventilation, vasopres

194 e was assessed from symptom scores, arterial blood gas measurements, pulmonary function testing, and

195 regard to oxygen weaning and use of arterial blood gas measurements.

196 CGRP antagonism did not alter basal arterial blood gas, metabolic, cardiovascular or endocrine status

197 Arterial samples were taken for blood gases, metabolic status and hormone analyses.

198 Perioperative POCT includes arterial blood gas monitoring, chemistry, co-oximetry panels, par

199 ry is increasingly substituting for arterial blood gas monitoring, noninvasive surrogate markers for

200 nitoring was done simultaneous with arterial blood gas monitoring.

201 in 30 minutes from LUS, using transcutaneous blood gas monitoring.

202 ed on the concurrent availability of routine blood gas Na(+)(direct) as well as core laboratory Na(+)

203 isolated remaining CB to maintain normal CB blood gases (normoxic, normocapnic perfusate), to inhibi

204 unit arrival, and postresuscitation arterial blood gas obtained.

205 The CGRP antagonist did not alter basal blood gas or cardiovascular status in the fetus.

206 increases in cerebral blood flow, changes in blood gases or brain temperature, or rat strain; (3) the

207 eractions are mediated either via changes in blood gases or by brainstem neuronal connections, but th

208 sham CBD had no effect on resting breathing, blood gases or chemoreflexes (P >0.05).

209 anges in vital signs, electrolytes, arterial blood gases, or coagulation parameters.

210 sure monitoring, measurement of mixed venous blood gases, or monitoring of cardiac output by oxygen c

211 total of 70 simultaneous pulse oximeter and blood gas pair samples.

212 Each patient's initial pulse oximeter/blood gas pair was used in the statistical analysis.

213 gs, peak inspiratory pressures, and arterial blood gases (Pao2, Paco2, pH, and oxygen saturation).

214 Arterial blood gas parameters, clinical symptoms, health-related

215 Arterial blood gas parameters, serum electrolytes, and urine elec

216 EOV to invasive hemodynamic measurements and blood gases performed during exercise.

217 ated with NIPPV demonstrated higher arterial blood gas pH (p < .001), lower PaCO2 (p < .05), and a lo

218 re monitored continuously and fetal arterial blood gases, pH and metabolites were measured at predete

219 traction ratio, plasma lactate, hemoglobin), blood gases, pH, and hematocrit were made before fractur

220 Arterial blood gases predicted from PET data correlated well with

221 Simultaneous blood gas, pulse oximetry, and ventilator settings were

222 xcluded from comparison, leaving 21 arterial blood gas/pulse oximeter pairs for analysis.

223 in the equations allows better prediction of blood gas reference values at sea level and at altitudes

224 tant role for the carotid bodies in eupnoeic blood gas regulation, (2) suggest that the carotid bodie

225 ion, for each protocol, we recorded arterial blood gas, respiratory mechanics, alveolar recruitment,

226 iratory pressure level, we assessed arterial blood gases, respiratory mechanics, ventilation inhomoge

227 Arterial blood gases, respiratory rate, and patient comfort were

228 Cardiac nerve blockade exaggerated the fetal blood gas response to haemorrhage somewhat but did not s

229 Severity criteria often depend on arterial blood gas results.

230 Blood gas samples from the pulmonary artery and both int

231 Blood gas samples were drawn at 0, 4 and 13 minutes.

232 imultaneous arterial and jugular venous bulb blood gas samples were recorded prospectively.

233 eplaced left carotid artery catheters, acute blood gas samples were taken 1 to 24 hours after gavage

234 However, chest radiography and arterial blood gas sampling seem useful while acute spirometry do

235 ration by pulse oximetry (SpO(2) ), arterial blood gas, spirometry, and contrast-enhanced echocardiog

236 One thousand one hundred ninety blood gas, SpO2, and ventilator settings from 137 patien

237 In one cohort, the maternal arterial blood gas status, the value at which 50% of the maternal

238 In the pilot study, left-over blood gas syringes were collected for further laboratory

239 judged by volume of colloid given, number of blood gases taken, and by measurement taken from cranial

240 dynamic variables, systemic and mixed venous blood gas tensions and oxygenation, arterial lactate con

241 vidence in humans that forcibly altering the blood gas tensions during repeated periods of exercise a

242 minimising any deviations from normal in the blood gas tensions, as sensed by the chemoreceptors.

243 Arterial blood gas tensions, hemodynamic variables, and the oxyge

244 The arterial blood gas test showed partially compensated pulmonary al

245 Arterial blood gas testing, chest radiographs, and RBC transfusio

246 r the maintenance of physiological levels of blood gases through the regulation of breathing.

247 consistently <14 cm H2O with normal arterial blood gases throughout the observation period.

248 blood was removed at 0, 2, 4, and 5 hrs for blood gases, tumor necrosis factor (TNF)-alpha, nitric o

249 distress syndrome survival, laboratory use, blood gases use, radiograph use, and appropriate use of

250 s of variance using these same pre- and post blood gas values confirmed the significant decrease in P

251 The authors compared infants with blood gas values in the highest or lowest quintile for g

252 priori based on PaO(2) on the first arterial blood gas values obtained in the ICU.

253 LD-CBF, cortical tP(O2), and sagittal sinus blood gas values to P(a,O2).

254 After each experiment, blood gas values were measured, and retinas were isolate

255 tory parameters, hemodynamic parameters, and blood gas values were measured.

256 on of extracorporeal carbon dioxide removal, blood gas values were significantly improved at 24 hours

257 eosinophil count on admission with arterial blood gas values, duration of mechanical ventilation, an

258 Arterial and venous blood gas values, glucose, and cardiac output were colle

259 volume aimed in part at normalizing arterial blood gas values.

260 cols designed to optimize lung inflation and blood gas values.

261 globin concentration, oxygen saturation, and blood gas values.

262 O2), heart rate, cardiac output and arterial blood gas variables at peak exercise on a cycle ergomete

263 Arterial blood gas variables included Pa(O(2)), Pa(CO(2)), pH, an

264 Mechanical ventilator settings, arterial blood gases, vital signs, and use of vasopressors were c

265 A baseline arterial blood gas was obtained on noninvasive passive therapy an

266 A baseline arterial blood gas was obtained on noninvasive therapy and 4 mins

267 on pressure support ventilation, an arterial blood gas was obtained, V(D)/V(T) was calculated, and th

268 A normal baseline for arterial blood gases was achieved by adjusting the inspiratory/ex

269 ND INTERVENTIONS: Whole-lung CT and arterial blood gases were acquired simultaneously in 77 patients

270 Before and after arterial blood gases were also obtained.

271 rterial oxygen content, Hb, lactate, pH, and blood gases were analyzed in blood samples.

272 blood gases from 703 patients; 650 arterial blood gases were associated with SpO2 less than or equal

273 phic and clinical data and room-air arterial blood gases were collected and analyzed.

274 -CPR for 15 minutes, and arterial and venous blood gases were collected at baseline and minutes 5, 10

275 Cardiorespiratory and arterial blood gases were collected throughout both exercise test

276 Physiologic parameters and arterial blood gases were continuously monitored.

277 In 5 dogs, blood gases were determined at baseline and at 2 min of

278 Arterial blood gases were drawn at baseline (sea level and at alt

279 were drawn every 6 hrs for 72 hrs, arterial blood gases were drawn every 12 hrs for 72 hrs, and both

280 Arterial blood gases were drawn every 15 mins, and the ventilator

281 Cerebral venous blood gases were drawn from a jugular bulb venous cathet

282 Arterial and deep venous blood gases were measured and oxygen consumption (VO2) w

283 iac outputs, filling pressures, and arterial blood gases were measured at 1-minute intervals during e

284 Arterial and mixed venous blood gases were measured at baseline, 1 min after cardi

285 nerve discharge, end-tidal CO2, and arterial blood gases were measured before during and after hypoxi

286 usion pressure, cardiac output, and arterial blood gases were measured before, 1 min after, and then

287 Oxygen delivery and blood gases were measured during both conditions.

288 Arterial blood gases were measured every 30 minutes intraoperativ

289 Arterial blood gases were measured, and ventilator settings were

290 od flow and radial artery and femoral venous blood gases were measured.

291 Flows in these vessels and arterial blood gases were measured.

292 Radial artery and femoral venous blood gases were measured.

293 Respiratory pattern variables and capillary blood gases were not significantly modified between expe

294 At those settings, blood gases were pH 7.31 +/- 0.06, PaCO2 was 58 +/- 21 m

295 res, mean blood pressure, plasma glucose and blood gases were similar among groups.

296 with the nuclear lumen while respiratory and blood gases were stabilized.

297 rst minute of CPR, arterial and mixed venous blood gases were superior in the 3 experimental groups c

298 Blood gases were within acceptable limits during TLV.

299 Arterial blood gases were within the normal range and effective a

300 of ventilated TBI patients who had arterial blood gases within 24 h of admission to the ICU at 61 US