Pulmonary Division and Sleep Disorders Centre, University Hospital Zurich, Zurich, Switzerland.
Pulmonary Division and Sleep Disorders Centre, University Hospital Zurich, Zurich, Switzerland; Zurich Centre for Human Integrative Physiology and Zurich Centre for Interdisciplinary Sleep Research, University of Zurich, Zurich, Switzerland.
Chest. 2014 Aug;146(2):299-308. doi: 10.1378/chest.13-2967.
Sleep-disordered breathing may impair cerebral oxygenation in patients with OSA syndrome, in particular during altitude travel. We studied cerebral tissue oxygenation (CTO) at low and moderate altitude in patients with OSA and evaluated whether acetazolamide improved CTO.
Eighteen patients with OSA living at < 600 m discontinued CPAP therapy during studies in Zurich (490 m) and during two sojourns of 3 days in the Swiss Alps (2 days at 1,860 m and 1 day at 2,590 m) separated by a 2-week washout period at < 600 m. Patients received acetazolamide (2 × 250 mg/d) or placebo at altitude in a randomized, double-blind, crossover design. Nocturnal polysomnography, including CTO monitoring by near-infrared spectroscopy (NIRS), was performed.
At 490 m, medians of CTO, peripheral oxygen saturation as measured by pulse oximetry (Spo2), and apnea/hypopnea index were 65%, 93%, and 57.3/h, respectively. At 2,590 m, on placebo, the corresponding values were 59%, 86%, and 86.4/h, respectively (P < .05, all corresponding comparisons). Acetazolamide increased CTO and Spo2 at 2,590 m by mean values of 2% (95% CI, 0%-4%) and 2% (95% CI, 1%-3%), respectively, and reduced the apnea/hypopnea index by 23.4/h (95% CI, 14.0-32.8/h) (P < .05, all changes). Cerebral total hemoglobin concentration, a NIRS-derived surrogate reflecting regional cerebral blood volume, increased by a similar degree in response to apneas at 490 m and 2,590 m and during acetazolamide and placebo treatment.
In patients with OSA staying at altitude, nocturnal cerebral and arterial oxygenation were reduced in association with exacerbated sleep apnea. Acetazolamide partially improved CTO, Spo2, and sleep apnea without impairing the cerebral blood flow response to apneas.
ClinicalTrials.gov; No.: NCT00714740; URL: www.clinicaltrials.gov.
睡眠呼吸障碍可能会损害阻塞性睡眠呼吸暂停低通气综合征(OSA)患者的大脑氧合,尤其是在高原旅行期间。我们研究了 OSA 患者在低海拔和中海拔时的脑组织氧合(CTO),并评估了乙酰唑胺是否能改善 CTO。
18 名居住在<600 米处的 OSA 患者在苏黎世(490 米)进行研究期间以及在瑞士阿尔卑斯山停留 3 天的两次旅行期间(2 天在 1860 米,1 天在 2590 米)中断 CPAP 治疗,两次旅行之间有 2 周的洗脱期,<600 米。患者以随机、双盲、交叉设计的方式接受乙酰唑胺(2×250 mg/d)或安慰剂治疗。进行了夜间多导睡眠图监测,包括近红外光谱(NIRS)监测 CTO。
在 490 米时,CTO、脉搏血氧饱和度(SpO2)测量的外周氧饱和度和呼吸暂停/低通气指数的中位数分别为 65%、93%和 57.3/小时。在 2590 米时,服用安慰剂时,相应值分别为 59%、86%和 86.4/小时(均 P<.05,所有相应比较)。乙酰唑胺平均使 CTO 和 SpO2 在 2590 米时增加 2%(95%CI,0%-4%)和 2%(95%CI,1%-3%),并使呼吸暂停/低通气指数减少 23.4/小时(95%CI,14.0-32.8/小时)(均 P<.05,所有变化)。作为反映区域性脑血流的近红外光谱衍生替代物的脑总血红蛋白浓度,在 490 米和 2590 米时以及乙酰唑胺和安慰剂治疗期间,对呼吸暂停的反应也以相似的程度增加。
在居住在高原的 OSA 患者中,夜间大脑和动脉氧合降低与睡眠呼吸暂停加重有关。乙酰唑胺部分改善了 CTO、SpO2 和睡眠呼吸暂停,而没有损害对呼吸暂停的脑血流反应。
ClinicalTrials.gov;编号:NCT00714740;网址:www.clinicaltrials.gov。