ライフサイエンスコーパス: end-tidal

1 Total halothane dose, measured by cumulative end-tidal (3.8 SE 0.1 minimum alveolar concentration hou

2 eceived standard halothane anaesthesia (1.0% end-tidal, 3 h).

3 The end-tidal alveolar dead space fraction ((PaCO2-PETCO2)/P

4 The initial end-tidal alveolar dead space fraction (first arterial b

5 tio, 1.59; 95% CI, 1.40-1.81) and day 1 mean end-tidal alveolar dead space fraction (odds ratio, 1.95

6 acute hypoxemic respiratory failure, initial end-tidal alveolar dead space fraction (per 0.1 unit inc

7 tio, 1.38; 95% CI, 1.14-1.67) and day 1 mean end-tidal alveolar dead space fraction (per 0.1 unit inc

8 tionship between both initial and day 1 mean end-tidal alveolar dead space fraction and mortality hel

9 However, because end-tidal alveolar dead space fraction is easy to calcul

10 Day 1 mean end-tidal alveolar dead space fraction remained associat

11 maximal inotrope score (p</=0.02), although end-tidal alveolar dead space fraction was no longer sig

12 Risk of Mortality III (all p<0.01), although end-tidal alveolar dead space fraction was no longer sig

13 than titration of inhalational agents using end tidal anesthetic concentration to monitor depth of a

14 er than a protocol based on a measurement of end-tidal anesthetic gas (ETAG) for decreasing anesthesi

15 rotocol incorporating standard monitoring of end-tidal anesthetic-agent concentration (ETAC) for the

16 nd that anesthetic management directed by an end-tidal anesthetic-agent concentration protocol is equ

17 Electrocardiogram and end-tidal capnography waveform capture were initiated fr

18 ects were monitored by pulse oximetry, nasal end-tidal capnography, and serial blood pressure measure

19 Sleep state, ventilation, end tidal carbon dioxide (PET,CO2), arterial oxygen satu

20 aturation, inspired oxygen concentration and end tidal carbon dioxide concentration was 85.2%.

21 End tidal carbon dioxide concentration, body temperature

22 Ventilation (V(E)), end-tidal carbon dioxide ( PETCO2 ) and pulse oximetry e

23 20 minutes of advanced cardiac life support, end-tidal carbon dioxide (+/-SD) averaged 4.4+/-2.9 mm H

24 ovascular control by monitoring ventilation, end-tidal carbon dioxide (CO2-et), oxygen saturation, RR

25 The average end-tidal carbon dioxide (ETCO 2 ) increase of 5.9% was

26 esuscitation guidelines recommend monitoring end-tidal carbon dioxide (ETCO(2)) as an indicator of ca

27 the time-varying association between exhaled end-tidal carbon dioxide (EtCO2) and out-of-hospital car

28 End-tidal carbon dioxide (ETCO2) was recorded in seven p

29 orded in real time during the PPV, including end-tidal carbon dioxide (ETCO2), oxygen saturation (SaO

30 negative pressure (LBNP) until pre-syncope; end-tidal carbon dioxide (P ET , CO 2) was clamped at ba

31 mm Hg with PMLE (n = 58; p < 0.001), whereas end-tidal carbon dioxide (PET(CO(2))) increased in C (n

32 breathing across the physiological range of end-tidal carbon dioxide (PET,CO2; 32-45 mmHg).

33 Ts), peak exercise time, partial pressure of end-tidal carbon dioxide (PETCO2), and VO2/workload slop

34 group A in median (IQR) partial pressure of end-tidal carbon dioxide (Petco2; 33.0 [32.0-34.0] mm Hg

35 Left uterine displacement, maintaining end-tidal carbon dioxide between 32-34 mmHg and maternal

36 Although end-tidal carbon dioxide detection is considered an effe

37 The end-tidal carbon dioxide detector appropriately detected

38 If the end-tidal carbon dioxide detector remained purple, it wa

39 the first chest roentgenogram was taken, the end-tidal carbon dioxide detector was attached to the pr

40 taken to confirm observations made with the end-tidal carbon dioxide detector.

41 Real-time monitoring of end-tidal carbon dioxide during anaesthesia aids in the

42 ether death could be predicted by monitoring end-tidal carbon dioxide during resuscitation after card

43 was no difference in the mean age or initial end-tidal carbon dioxide level between patients who surv

44 3/4 increased tidal volume and decreased the end-tidal carbon dioxide level compared to pre-stimulati

45 Our hypothesis was that an end-tidal carbon dioxide level of 10 mm Hg or less after

46 An end-tidal carbon dioxide level of 10 mm Hg or less measu

47 End-tidal carbon dioxide levels reflect cardiac output d

48 During all exposures, end-tidal carbon dioxide levels were maintained, on aver

49 Among patients with PD, baseline end-tidal carbon dioxide levels were significantly lower

50 d HR as R-R interval (RRI), BP, respiration, end-tidal carbon dioxide levels, and oxygen saturation a

51 Capnography via an end-tidal carbon dioxide monitor measures carbon dioxide

52 s were intubated and evaluated by mainstream end-tidal carbon dioxide monitoring.

53 Ventilation at end-tidal carbon dioxide of 55 mm Hg (hypercapnic ventil

54 omparisons, but the groups did not differ in end-tidal carbon dioxide or respiratory rate.

55 gestive heart failure (CHF), we measured the end-tidal carbon dioxide pressure (PET(CO2)) during spon

56 End-tidal carbon dioxide pressure (PET(CO2)) was gradual

57 middle cerebral artery during variations in end-tidal carbon dioxide pressure (PET,CO2) of +10, +5,

58 )) as reflected by 3 to 5 Torr reductions in end-tidal carbon dioxide tension (P(ETCO2)).

59 Increases in end-tidal carbon dioxide tension coincident with each ga

60 ygen saturation decreased from 98 to 79% and end-tidal carbon dioxide tension was kept constant.

61 A 20-minute end-tidal carbon dioxide value of 10 mm Hg or less succe

62 When a 20-minute end-tidal carbon dioxide value of 10 mm Hg or less was u

63 maintained under experimental suppression of end-tidal carbon dioxide variations, suggesting that res

64 The end-tidal carbon dioxide was highly predictive of stroke

65 End-tidal carbon dioxide was maintained 2 mm Hg above ba

66 End-tidal carbon dioxide was quantitated with convention

67 ulmonary resuscitation and demonstrated that end-tidal carbon dioxide was quantitatively predictive o

68 he ventilatory response to arousal and nadir end-tidal carbon dioxide were determinants of the apnea-

69 ia and the occurrence of a rapid increase in end-tidal carbon dioxide, associated with unexplained pe

70 hypercapnic CBF normalized by the change in end-tidal carbon dioxide, which was recorded during both

71 ionships of stroke volume to measurements of end-tidal carbon dioxide.

72 tact vagus nerves that were hyperventilated (end tidal CO(2), 1.6 +/- 0.4%) to phrenic nerve quiescen

73 End-tidal CO(2) ( PETCO2 ) was measured using a gas anal

74 nial Doppler ultrasound), BP (Finometer) and end-tidal CO(2) ( PETCO2 , capnography) were performed d

75 ity (CBFV; transcranial Doppler ultrasound), end-tidal CO(2) (capnography) and heart rate (ECG) were

76 Blood pressure, end-tidal CO(2) (EtCO(2) ), heart rate (HR), and respira

77 End-tidal CO(2) (EtCO(2)) is used to monitor cardiopulmo

78 d irregularity in her breathing pattern; her end-tidal CO(2) (FET(CO(2))) ranged from 5.3 to 10.9%.

79 findings of excess brain lactate and delayed end-tidal CO(2) (pCO(2)) recovery in subjects with panic

80 usly recorded polysomnography-acquired nasal end-tidal CO(2) (PET(CO(2))) and nasal/oral thermistor i

81 used two gas densities at several levels of end-tidal CO(2) and a number of intrapharyngeal negative

82 doses (Low-KME and High-KME) on resting CBF, end-tidal CO(2) and systemic haemodynamics over a 2 h pe

83 ure (BP), heart rate, and transcutaneous and end-tidal CO(2) concentrations.

84 ygen saturation ( SpO2 ), end-tidal O(2) and end-tidal CO(2) concentrations.

85 d delay (delta), alveolar volume (V(L)), and end-tidal CO(2) fraction (C), were applied to the stabil

86 CBFV and transcutaneous and end-tidal CO(2) levels declined significantly during hea

87 eaths/min, and VT was adjusted to achieve an end-tidal CO(2) of 30 to 35 mm Hg.

88 End-tidal CO(2) partial pressure (P(ET)CO(2)) was increa

89 nspired minute ventilation (V(I)), R(UA) and end-tidal CO(2) pressure (P(ET,CO(2))) were measured in

90 neic hypoventilation also occurred even when end-tidal CO(2) pressure (PET(CO(2))) was raised 3-5 mm

91 central venous pressure, pulse oximetry, and end-tidal CO(2) were continuously monitored and download

92 ate, blood pressure, minute ventilation, and end-tidal CO(2) were determined.

93 sed c-Fos under hypocapnia (approximately 3% end-tidal CO(2)) after PeF stimulation.

94 First, in five normocapnic cats (end-tidal CO(2), 4.3 +/- 0.2%) with intact vagus nerves

95 ionship between ccRTN neuron firing rate and end-tidal CO(2), and a similar shift of the relationship

96 )/CO(2) elimination slope (VE/VCO(2)), a low end-tidal CO(2), and high end-tidal O(2) at the ventilat

97 levels of tidal volume, minute ventilation, end-tidal CO(2), and irregularity in respiratory rate du

98 Respiratory rate, oxygen saturation, end-tidal CO(2), and recovery from sedation were unchang

99 tched tidal volume, breathing frequency, and end-tidal CO(2), but varying respiratory motor output as

100 Under baseline conditions (approximately 3% end-tidal CO(2), hyperoxia, no PeF stimulation) few (11%

101 rresponded with dose-dependent reductions in end-tidal CO(2).

102 ar shift of the relationship between PND and end-tidal CO(2).

103 fter exposure to hypercapnic hyperoxia (6-7% end-tidal CO(2); 3.5 h; no hypothalamic stimulation) and

104 jective breathlessness was manipulated while end-tidal CO(2-) was held constant.

105 alveolar deadspace (p <.01), and arterial-to-end tidal CO2 partial pressure differences (p <.01).

106 Estimates of arterial-to-end tidal CO2 partial pressure differences are reliable

107 We found that estimates of arterial-to-end tidal CO2 partial pressure differences may be used t

108 f alveolar deadspace volumes and arterial-to-end tidal CO2 partial pressure differences were used as

109 in respiratory rate and resulting changes in end-tidal cO2 ( big up tri, openPetCO2) as well as betwe

110 coronary perfusion pressure (>15 mm Hg) and end-tidal CO2 (>10 mm Hg) for successful defibrillation

111 low (48 +/- 5 to 82 +/- 5 mL/min; p < .001); end-tidal CO2 (7.7 +/- 0.9 to 15.7 +/- 2.4; p < .0001);

112 The secondary outcomes included end-tidal co2 (Et co2 ) during CPR, any ROSC, survival t

113 ed with patient data showed correlations for end-tidal CO2 (EtCO 2 ), area under the CO2 curve, and P

114 asma catecholamine levels (P = 0.020), lower end-tidal CO2 (P = 0.005) and reduced middle cerebral ar

115 easured ventilation, arterial O2 saturation, end-tidal CO2 (PET,CO2), blood pressure (intra-arterial

116 Peak end-tidal CO2 (PETCO2) values were significantly higher

117 End-tidal CO2 (r2 = .22; p < .001) correlated better wit

118 The Vt and PDR necessary to decrease end-tidal CO2 20% (from 75 to 60 mm Hg) was different am

119 The correlation between end-tidal CO2 and capillary PCO2 was significant (r2 = .

120 End-tidal CO2 and coronary perfusion pressure were not p

121 Low end-tidal CO2 and high variance in minute ventilation at

122 Secondary end points included end-tidal CO2 as well as coronary and cerebral perfusion

123 tidal volume ratio (Vd/Vt), and arterial to end-tidal CO2 difference were all higher (P<0.05) in pat

124 d reductions in mean cerebral blood flow and end-tidal CO2 during OLBNP.

125 sed greater changes in breath components and end-tidal CO2 during pressure support than during assist

126 se data do not support routine monitoring of end-tidal CO2 during short transport times in adult pati

127 ty was measured by producing alternations in end-tidal CO2 levels (etCO2) (alternation amplitude, 1.2

128 activity developed corresponded to eupnoeic end-tidal CO2 levels in REM sleep.

129 ve average bias of 0.33 torr (0.04 kPa) with end-tidal CO2 lower than capillary PCO2 was established

130 ntubation, time to glottis passage and first end-tidal CO2 measurement, degree of glottis visualizati

131 Continuous end-tidal CO2 monitoring provides the clinician with a r

132 at Paco2 would be more tightly controlled if end-tidal CO2 monitoring was used during hand ventilatio

133 active seizures, 61 post ictal patients) had end-tidal CO2 obtained by oral/nasal sidestream capnomet

134 e activity was raised significantly (from an end-tidal CO2 of 2.5 % to 4.5 %, n = 9).

135 Hypercapnic respiratory failure (end-tidal CO2 of 75 mm Hg) and obstructive lung disease

136 d continued rise in end-tidal CO2, while the end-tidal CO2 of the comparison groups stabilized.

137 In two of the studies, end-tidal CO2 pressure (Pco2) was maintained throughout

138 1) passive hypocapnic hyperventilation, with end-tidal CO2 pressure (PET,CO2) held 10 Torr below the

139 te recovery, oxygen uptake efficiency slope, end-tidal CO2 pressure, and peak VO2 having scores of 5,

140 The mean end-tidal CO2 reading was 43.0 +/- 11.8 torr [5.7 +/- 1.

141 monitor group (ventilation controlled using end-tidal CO2 value from monitor).

142 Dependable end-tidal CO2 values can be obtained in pediatric seizur

143 ntly greater coronary perfusion pressure and end-tidal CO2 values were achieved with the miniaturized

144 End-tidal CO2 values were compared with a capillary PCO2

145 racheal pressure, intracranial pressure, and end-tidal CO2 values were measured (mm Hg); common carot

146 Arterial blood gases and end-tidal CO2 values were measured before and after tran

147 t but only the investigator was aware of the end-tidal CO2 values).

148 End-tidal CO2 was monitored and maintained at isocapnic

149 r variability for Paco2 after transport when end-tidal CO2 was not used for control of ventilation du

150 n pressure, cerebral perfusion pressure, and end-tidal CO2 were increased with sodium nitroprusside-e

151 Arterial and right atrial pressures and end-tidal CO2 were measured.

152 d pressure, right atrial blood pressure, and end-tidal CO2 were monitored continuously until the inte

153 Vital organ perfusion pressures and end-tidal CO2 were significantly improved with ITPR-CPR

154 Phrenic nerve discharge, end-tidal CO2, and arterial blood gases were measured be

155 FM group exhibited lower ventilation, lower end-tidal CO2, and higher ventilatory equivalent of carb

156 ocular pressure, arterial oxygen saturation, end-tidal CO2, and respiration rate (P>0.05).

157 ditionally collected mean arterial pressure, end-tidal CO2, and temperature.

158 st compression is independently predicted by end-tidal CO2, coronary perfusion pressure, and ventricu

159 End-tidal CO2, coronary perfusion pressure, and ventricu

160 Physiologic (peripheral oxygen saturation, end-tidal CO2, heart rate, and respiratory rate) and com

161 ion rates, as well as carotid blood flow and end-tidal CO2, when compared to standard cardiopulmonary

162 nse to 5% CO2 demonstrated continued rise in end-tidal CO2, while the end-tidal CO2 of the comparison

163 hanged significantly during the wean but not end-tidal CO2.

164 condary end points included hemodynamics and end-tidal CO2.

165 O2 with a simultaneous sustained decrease in end-tidal CO2; (2) an abrupt and sustained increase in t

166 domized to receive either inhaled xenon (40% end-tidal concentration) combined with hypothermia (33 d

167 ce of sevoflurane anesthesia (0%, 2%, and 1% end-tidal concentration, respectively) administered to h

168 edation in pediatric patients, and also with end-tidal concentrations of inhalation agents in childre

169 The partial pressure of oxygen during end-tidal expiration (P(ET)o(2)) was kept between 50 and

170 spiratory illness, more atopy, lower flow at end-tidal expiration (V'maxFRC), and greater declines in

171 O2 was restored to normothermic values using end-tidal forcing.

172 n NH and HH were found in oxygen saturation, end tidal gases, breathing rate, middle cerebral artery

173 SNA, fibular microneurography) when clamping end-tidal gases at baseline levels.

174 te (ECG), blood pressure (BP; Finometer) and end-tidal gases were obtained continuously.

175 End-tidal H(2) sampling is a simple method of measuring

176 End-tidal H(2) was measured in the morning (baseline) an

177 nesthetics during surgery (derived from mean end-tidal inhalational anesthetic concentrations).

178 n levels were less than 0.5 % below eupnoeic end-tidal levels in NREM sleep.

179 relationship was found between arterial and end-tidal measures (range r2 = .09 to r2 = .11).

180 arget-controlled infusions or vaporizer with end-tidal monitoring.

181 ber of lung turnovers required to reduce the end tidal N(2) concentration to 2.5% of its starting val

182 idine (1.5 ng/ml; n = 40), sevoflurane (0.9% end-tidal; n = 40), S-ketamine (0.75 mug/ml; n = 20), or

183 h-by-breath ventilation, partial pressure of end-tidal O(2) and CO(2) in 21 healthy lowlanders were r

184 olume, capillary oxygen saturation ( SpO2 ), end-tidal O(2) and end-tidal CO(2) concentrations.

185 (VE/VCO(2)), a low end-tidal CO(2), and high end-tidal O(2) at the ventilatory anaerobic threshold.

186 Three levels of end-tidal O2 pressure (Po2) were employed.

187 were (1) an abrupt and sustained increase in end-tidal O2 with a simultaneous sustained decrease in e

188 This review will present views on end-tidal or arterial carbon dioxide tension management

189 ual loading of the chest wall, suggestive of end-tidal overdistension in the upright position.

190 sed or paradoxically declined, suggestive of end-tidal overdistension.

191 End-tidal P(CO(2)) (P(ET,CO(2))) was held constant throu

192 eroxic hyperpnoea and hyperoxic hypercapnia (end-tidal P(CO(2)) + 5 mmHg above eucapnia).

193 V(E)/V(CO(2)), causing a 5 mmHg increase in end-tidal P(CO(2)) and a 3% lower haemoglobin saturation

194 End-tidal P(CO2) was maintained by increasing the inspir

195 erwent an 8-h isocapnic exposure to hypoxia (end-tidal P(O2)=55 Torr) in a purpose-built chamber.

196 End-tidal partial carbon dioxide pressure (Pet(CO(2)))/P

197 Eighteen subjects had end-tidal partial pressure of carbon dioxide (PetCO2) in

198 oxygen (P(ET,O2)) from 100 to 50 mmHg, with end-tidal partial pressure of carbon dioxide clamped.

199 esponse to a standardized step change in the end-tidal partial pressure of carbon dioxide.

200 The effect of hypoxia on eupnoeic end-tidal partial pressure of CO(2) (P(ET,CO2)) and hypo

201 Elevated end-tidal partial pressure of CO2 (PET(CO2)) causes air

202 Elevation of the end-tidal partial pressure of CO2 (PETco2) increases cer

203 onses to hypoxia were determined by changing end-tidal partial pressure of oxygen (P(ET,O2)) from 100

204 ght different blood gas conditions, with the end-tidal partial pressure of oxygen (PETCO2) ranging fr

205 poxia during hypercapnic breathing (targeted end-tidal partial pressures of expired oxygen and carbon

206 urements included minute ventilation ( VE ), end-tidal partial pressures of oxygen ( PETO2 ) and carb

207 o VT and the difference between arterial and end tidal PCO2 at peak VO2 also increased inversely with

208 No differences in cardiac output, end tidal Pco2, arterial Po2 and Pco2, and brain tempera

209 leads, like coronary perfusion pressure and end tidal PCO2, were predictive of outcomes.

210 s (P = 0.665), consistent with the unchanged end-tidal PCO2 (P = 0.327); whereas, Q(VA) was higher th

211 f a multi-frequency binary sequence input in end-tidal PCO2 (PET,CO2) that included 13 steps into and

212 During ACMV, end-tidal PCO2 (PET,CO2) was either held at normocapnic

213 End-tidal Pco2 (PET,CO2) was increased by altering the l

214 small but significant circadian variation in end-tidal PCO2 (PET,CO2; +/-0.6 mmHg; +/-1.5 % of 24 h m

215 efore training (mean +/- S.E.M. reduction in end-tidal PCO2 = 1.32 +/- 0.36 Torr, ANOVA, P < 0.05).

216 artery blood flow, independent of changes in end-tidal PCO2 and blood pressure External carotid arter

217 nt linear correlations were observed between end-tidal PCO2 and cardiac index and between sublingual

218 End-tidal PCO2 and PaC02 values were simultaneously obta

219 repeated-measures study was used to compare end-tidal PCO2 and PaCO2 at two time points: before and

220 End-tidal PCO2 and PO2 were effectively clamped to resti

221 ical ventilation was established to maintain end-tidal PCO2 approximately 35 torr (-4.7 kPa).

222 eration of a coronary perfusion pressure and end-tidal Pco2 comparable with control rats but with sig

223 rial pressure declined from 138 to 49 mm Hg, end-tidal PCO2 decreased from 35 to 13 mm Hg, and cardia

224 er the addition of expiratory muscle pacing, end-tidal PCO2 fell to 36.3 +/- 1.2 mm Hg.

225 the PPE protocol compared with the constant end-tidal Pco2 in the IPE and control protocols.

226 ence may be due to the progressive change in end-tidal Pco2 in the PPE protocol compared with the con

227 As anticipated, end-tidal PCO2 increased after bicarbonate and decreased

228 e in patients who have the greatest need for end-tidal PCO2 monitoring (i.e., patients who have respi

229 This study indicated that end-tidal PCO2 monitoring correlated well with PaCO2 in

230 to provide suboptimal levels of ventilation (end-tidal PCO2 of 55 to 60 mm Hg).

231 tercostal muscle pacing alone resulted in an end-tidal PCO2 of 57.1 +/- 1.1 mm Hg.

232 The end-tidal PCO2 of each subject was varied according to a

233 inspiratory and expiratory muscle pacing and end-tidal PCO2 remained stable throughout the study peri

234 In the other two studies, end-tidal Pco2 was allowed to vary (poikilocapnic post-e

235 A multifrequency binary sequence in end-tidal PCO2 was employed to stimulate ventilation dyn

236 d passive heat stress during isocapnia (i.e. end-tidal PCO2 was held constant) Submaximal cycling exe

237 End-tidal PCO2 was measured, using a sidestream sensor p

238 s following training with protocol EX + CO2, end-tidal PCO2 was regulated at a lower level during ste

239 t ventricular pressure decline (-dP/dt), and end-tidal PCO2 were continuously measured for 240 mins a

240 Ventilation and end-tidal PCO2 were similar between tasks.

241 lobin oxygen saturation (by pulse oximetry), end-tidal PCO2, and carotid artery blood flow rate, for

242 End-tidal PCO2, CO2 production, and ventilatory variable

243 Vital capacity (VC), oxygen saturation, end-tidal PCO2, maximal inspiratory pressure (MIP), and

244 r CO2 levels (less than 0.5 % below eupnoeic end-tidal percentage CO2 levels in non-REM (NREM) sleep)

245 ntial in the solution and whether changes in end-tidal pH(2) could be measured using a portable breat

246 These data suggested that changes in end-tidal pH(2) indicate the variation of electrode pote

247 We measured the end-tidal plateau in exhaled NO concentration (CETNO) by

248 acute ventilatory response to a reduction in end-tidal PO2 (PET,O2) from 100 to 50 Torr (at a PET, CO

249 ents would be expected, and under hyperoxic (end-tidal PO2 = 200 Torr) conditions, when the presence

250 Data were collected under both hypoxic (end-tidal PO2 = 50 Torr) conditions, when two components

251 latory measurements were made during euoxia (end-tidal Po2, 100 Torr), hypoxia (end-tidal Po2, 50 Tor

252 oxia (end-tidal Po2, 50 Torr) and hyperoxia (end-tidal Po2, 300 Torr).

253 g euoxia (end-tidal Po2, 100 Torr), hypoxia (end-tidal Po2, 50 Torr) and hyperoxia (end-tidal Po2, 30

254 In all trials end-tidal pressure of CO2 was elevated 4-5 mmHg above no

255 tural sleep within <= 2 h prior to EUA under end-tidal sevoflurane 2-3%.

256 acodynamics of CO2 for MBF using prospective end-tidal targeting to precisely control arterial Pco2 a

257 The end-tidal to arterial PCO2 difference throughout normoca

258 Median end-tidal volatile anesthetic concentration was signific

259 ire heart, obtained during breath holding at end-tidal volume (baseline), deep inspiration, and force

260 of the heart within the radiation portals at end-tidal volume (median, 20.9 cm3; range, 1.3 to 88.4 c

261 an change: -10.7 cm3 [-40.2%], P<.001 versus end-tidal volume), whereas expiration increased the card

262 edian change: 4.0 cm3 [21.5%]; P<.001 versus end-tidal volume).

263 The median end-tidal xenon concentration was 47% and duration of th