ライフサイエンスコーパス: hypoventilation

1 ied within 5 minutes of seizure onset due to hypoventilation.

2 illator settings that would lead to alveolar hypoventilation.

3 contrast two orphan disorders of late-onset hypoventilation.

4 f patients who had both hyperventilation and hypoventilation.

5 sias, and frequent autonomic instability and hypoventilation.

6 r airway obstruction leading to hypoxemia or hypoventilation.

7 ovements, 86% autonomic instability, and 23% hypoventilation.

8 yskinesias, 69 autonomic instability, and 66 hypoventilation.

9 ctal oxygen desaturation is a consequence of hypoventilation.

10 7-41) with captive bolt guns was followed by hypoventilation.

11 ry severity score was 25-32) was followed by hypoventilation.

12 riers may be at risk for developing alveolar hypoventilation.

13 OX2B gene and evidence of nocturnal alveolar hypoventilation.

14 y Ins, and expire shortly after birth due to hypoventilation.

15 eathing and may possibly improve symptoms of hypoventilation.

16 or control over secretions, airway spasm, or hypoventilation.

17 in a syndrome resembling congenital central hypoventilation.

18 Air breathing in CH rats induced hypoventilation, a 12% increase in ABP, no change in mRA

19 psychiatric symptoms, seizures, and central hypoventilation, a paraneoplastic immune-mediated syndro

20 ificant postventilator apneas and postapneic hypoventilation also occurred even when end-tidal CO(2)

21 e caudal MR simultaneously produces enhanced hypoventilation and a 51% decrease in the CO(2) response

22 Central hypoventilation and apnea accompany generalized status e

23 acking AMPK-alpha1 and AMPK-alpha2 exhibited hypoventilation and apnea during hypoxia, with the prima

24 nd thereby aids the clinician in identifying hypoventilation and apnea in the sedated patient at an e

25 deficiencies in AMPK expression precipitate hypoventilation and apnea, even when carotid body affere

26 rove safety by enabling early recognition of hypoventilation and by reducing the risk of oversedation

27 eous marriage who presented with respiratory hypoventilation and died 10 days and 4 years later, resp

28 Carotid body denervation (CBD) causes hypoventilation and increases the arterial PCO2 set-poin

29 rons accompanies REM sleep and is a cause of hypoventilation and obstructive sleep apnea in humans.

30 m (CNS) leptin levels or activity may induce hypoventilation and the Pickwickian syndrome in some obe

31 ted oxygen desaturation was a consequence of hypoventilation and whether factors such as seizure loca

32 onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD) an

33 The effects of sedation, hypoxia, hypoventilation, and changes in intrathoracic pressure c

34 ilibrium, dysarthria, dysphagia, and central hypoventilation, and died 2 months and 6 months, respect

35 rial carbon dioxide levels (PaCO2), alveolar hypoventilation, and increased cardiorespiratory morbidi

36 lation, leading to hypotension, bradycardia, hypoventilation, and potentially respiratory arrest.

37 erized by weight loss, parkinsonism, central hypoventilation, and psychiatric disturbances.

38 ry stress incontinence, sleep apnea, obesity hypoventilation, and type II diabetes mellitus.

39 hat of the adults, although dysautonomia and hypoventilation are less frequent or severe in children.

40 s, sudden infant death syndrome, and central hypoventilation are relatively frequent conditions in th

41 The mechanisms that link obesity and hypoventilation are unknown, but thought to involve depr

42 sities and durations of exercise a sustained hypoventilation, as well as reduced systemic pressure an

43 ecreased level of consciousness, and central hypoventilation associated with ovarian teratoma (OT) an

44 alysis of ACSF in or near to the RTN, causes hypoventilation but has no significant effect on the CO(

45 o2 - Paco2 remained essentially stable after hypoventilation but increased significantly after induci

46 and CO2 production, indicating a reversal of hypoventilation by stimulation of central respiratory co

47 Hypoventilation can occur in REM sleep and progress into

48 tributions of airway obstruction and central hypoventilation could not be determined because airway f

49 d (ACSF) in or near to the caudal MR, causes hypoventilation (decrease in the ratio of minute ventila

50 The hypoventilation during induction in the control group an

51 We hypothesize that capnography could detect hypoventilation during induction of bronchoscopic sedati

52 Compared to placebo, significant hypoventilation during the fentanyl trial was indicated

53 We also question whether the transient hypoventilation elicited by CB denervation means that th

54 other comorbidities, including sleep apnea, hypoventilation, gastroesophageal reflux, degenerative j

55 re randomized to: starting bronchoscopy when hypoventilation (hypopnea, two successive breaths of at

56 rs and adverse events including hypotension, hypoventilation, ileus, and coma.

57 bserved in 38%, normoventilation in 29%, and hypoventilation in 46%, with a 13% overlap of patients w

58 RATIONALE: Regional hypoventilation in bronchoconstricted patients with asth

59 fy forebrain sites underlying seizure-evoked hypoventilation in humans.

60 at was normal on MRI correlated with central hypoventilation; in another case, hyperactivity in the c

61 The hypoventilation is attributed to reduced CB afferent act

62 In addition, alveolar hypoventilation is discussed in children with congenital

63 e induction and start bronchoscopy following hypoventilation may decrease hypoxemia without compromis

64 Understanding the cause of this peri-ictal hypoventilation may lead to preventative strategies.

65 sedation and starting bronchoscopy following hypoventilation, may decrease hypoxemia.

66 opnea, whereas reduced ventilatory drive and hypoventilation narrowed the DeltaPET(CO2) and increased

67 Significant hypoventilation occurred during the induction and start

68 The magnitude of hypoventilation on return to sleep was not affected by t

69 hyperventilation followed by more prolonged hypoventilation on return to sleep.

70 target range in 91% of cases and because of hypoventilation or hyperventilation in 9%.

71 al recommendations were available in case of hypoventilation or hyperventilation.

72 several hours is necessary for recurrence of hypoventilation or other complications.

73 all three rat strains, CBD elicited eupnoeic hypoventilation (PaCO2 +8.7-11.0 mmHg) 1-2 days post-CBD

74 After 60 mins of hypoventilation, Pico2 - Paco2 decreased to 14.2+/-1.1 a

75 ssive parenchymal derecruitment and alveolar hypoventilation, potentially aggravating systemic hyperc

76 Hypoventilation preceded OAAS < 4 by 96.5 +/- 88.1 secon

77 omboembolism, preoperative vena cava filter, hypoventilation, pulmonary hypertension), and age>or=45

78 geal amyloid included radiculopathy, central hypoventilation, recurrent subarachnoid haemorrhage, dep

79 ened with hyperventilation and narrowed with hypoventilation, regardless of the stimulus and whether

80 We report a patient manifesting severe hypoventilation resulting from diaphragmatic paresis sec

81 however, she became dyspneic and manifested hypoventilation secondary to muscle weakness.

82 ive noninvasive strategies for management of hypoventilation, sleep-disordered breathing, and cough i

83 ts suffering from this syndrome, therapeutic hypoventilation strategy designed to reduce mechanical d

84 f the terminal bowel) and congenital central hypoventilation syndrome (CCHS) (also known as NB-HSCR-C

85 ysregulation (ROHHAD) and congenital central hypoventilation syndrome (CCHS) are distinct in presenta

86 g exercise, children with congenital central hypoventilation syndrome (CCHS) demonstrate coupling of

87 The cause of congenital central hypoventilation syndrome (CCHS) is unknown, but a geneti

88 Congenital Central Hypoventilation Syndrome (CCHS) patients exhibit comprom

89 Congenital central hypoventilation syndrome (CCHS) typically presents in th

90 stem development, lead to congenital central hypoventilation syndrome (CCHS), a neurodevelopmental di

91 Like patients with congenital central hypoventilation syndrome (CCHS), our patient had a relat

92 en found in patients with congenital central hypoventilation syndrome (CCHS), the cardinal feature of

93 A) in awake children with congenital central hypoventilation syndrome (CCHS), who have absent or near

94 cluding neuroblastoma and congenital central hypoventilation syndrome (CCHS).

95 which are associated with congenital central hypoventilation syndrome (CCHS).

96 enital breathing disorder congenital central hypoventilation syndrome (CCHS).

97 utations, which cause the central congenital hypoventilation syndrome (CCHS, also known as Ondine's c

98 cy of NIV during similar episodes in obesity hypoventilation syndrome (OHS).

99 mice provide a model for congenital central hypoventilation syndrome and suggest that Pbx3 mutations

100 Central congenital hypoventilation syndrome is caused by mutations of the g

101 AD with disorders outside congenital central hypoventilation syndrome, further advancement will be ma

102 iscussed in children with congenital central hypoventilation syndrome, myelomeningocele, and Prader-W

103 Patients with obesity hypoventilation syndrome, previous bariatric surgery, co

104 Additional comorbidities included obesity hypoventilation syndrome, sleep apnea syndrome, hyperten

105 ion, diabetes mellitus, sleep apnea, obesity hypoventilation syndrome, venous stasis ulcers, intestin

106 oreflex that characterize congenital central hypoventilation syndrome.

107 obably contributes to the congenital central hypoventilation syndrome.

108 including sleep apnea syndromes and obesity hypoventilation syndrome.

109 in children affected with congenital central hypoventilation syndrome.

110 rmal men are more vulnerable to load-induced hypoventilation than women, due to increased upper airwa

111 The alveolar hypoventilation that occurred during insufflation with v

112 2/6 hypertension, and all with sleep apnea, hypoventilation, type II diabetes mellitus, and urinary

113 Regional hypoperfusion but not hypoventilation typifies lung gas exchange in HF.

114 ze abnormalities, deafness, facial weakness, hypoventilation, vascular malformations of the internal

115 ng permissive hypercapnia, due to controlled hypoventilation, warrants investigation.

116 ndent outcome effect of hyperventilation and hypoventilation was assessed.

117 Hypoventilation was observed in 74.6% of the patients be

118 Both hyperventilation and hypoventilation were associated with worse outcomes in i

119 All 8 animals demonstrated central apnea and hypoventilation, which resulted in the death of 1 and co

120 e involvement of large contiguous regions of hypoventilation with substantial subresolution intraregi

121 insonism, depression, severe weight loss and hypoventilation, with brain pathology characterized by T