ライフサイエンスコーパス: hypercarbia

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1 oxia) and increased inspired carbon dioxide (hypercarbia).

2 nt improvement in oxygenation while limiting hypercarbia.

3 uch as increased intraabdominal pressure and hypercarbia.

4 nchanged during hypoxia and increased during hypercarbia.

5 a reduction in tidal volume with subsequent hypercarbia.

6 and permits identification of the causes for hypercarbia.

7 ion for exacerbation of COPD associated with hypercarbia.

8 -REM sleep, with continuous desaturation and hypercarbia.

9 seline to 1.96 +/- 0.18 muL/mm(2)/min during hypercarbia.

10 er trial comparing hypoxia (17% FIO(2)) with hypercarbia (2.7% FICO(2)).

11 ally detrimental conditions (e.g. hypoxemia, hypercarbia, acidosis, hypothermia, hypervolemia, and in

12 ala as an important chemosensor that detects hypercarbia and acidosis and initiates behavioral respon

13 t was not receiving lorazepam in response to hypercarbia and failed to rise while the patient was rec

14 entilation, potentially aggravating systemic hypercarbia and hypoxemia.

15 ence points to impaired arousal responses to hypercarbia and hypoxia, which ultimately leads to asphy

16 f their jugular veins and aorta in room air, hypercarbia, and 100% O2.

17 equences include increased airway pressures, hypercarbia, and decreased pulmonary compliance.

18 ng resting rCBF or the elevation elicited by hypercarbia (arterial CO2 pressure, Pa,CO2, approximatel

19 ncrease in ventilation due to the O2-induced hypercarbia [calculated as the production (delta VE/delt

20 did not change significantly relative to the hypercarbia condition but remained significantly elevate

21 Hypercarbia decreased SaO(2) (-2.6+/-0.6%, P=0.002) comp

22 Both hypoxia and hypercarbia decreased the balance between pulmonary and

23 deadspace are sufficient to account for the hypercarbia developed by patients with acute exacerbatio

24 anges in PaCO2 and SaO2; and that O2-induced hypercarbia does not indicate a failure of respiratory c

25 Although both groups developed hypercarbia during oleic acid infusion, PaCO2, steadily

26 ventilation-perfusion ratios), adding to the hypercarbia from increased deadspace.

27 luded mucosal laceration in six patients and hypercarbia in one.

28 ole of respiratory control during O2-induced hypercarbia in patients with chronic obstructive pulmona

29 teric perfusion decreased intestinal mucosal hypercarbia, leading to improvement of intramucosal pH.

30 = .014) after adjustment for age, degree of hypercarbia, maximal respiratory rate, use of an arteria

31 To determine whether hypercarbia occurs following the use of open suctioning

32 study compares the impact of hypoxia versus hypercarbia on oxygen delivery, under conditions of fixe

33 did not significantly underestimate arterial hypercarbia or acidosis.

34 compared with cells reperfused with relative hypercarbia (PCO2 of 71 torr, pH 6.8) or hypocarbia (PCO

35 nsion, hypernatremia, acidosis, hypoxia, and hypercarbia predicts hospital mortality, surgical intens

36 Compared with normocarbic reperfusion, hypercarbia significantly reduced cell death from 54.8%

37 hagfish exposed acutely to severe sustained hypercarbia tolerated among the most severe blood acidos

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