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 End tidal carbon dioxide concentration, body temperature

21 20 minutes of advanced cardiac life support, end-tidal carbon dioxide (+/-SD) averaged 4.4+/-2.9 mm H

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

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

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

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

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

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

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

29 The end-tidal carbon dioxide detector appropriately detected

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

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

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

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

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

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

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

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

38 End-tidal carbon dioxide levels reflect cardiac output d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 End-tidal carbon dioxide was quantitated with convention

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 End-tidal CO2 was monitored and maintained at isocapnic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 End-tidal PCO2 and PaC02 values were simultaneously obta

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 The end-tidal to arterial PCO2 difference throughout normoca

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

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

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

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

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