Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • In Bogot a city situated at a high altitude

    2018-11-05

    In Bogotá, a city situated at a high altitude (2640m above sea level), the normal SpO2 during wakefulness is found between 90 and 92% [8–12]. Unlike the observed sea level, a decrease of 3% or higher from this point, which is the criterion to define the presence of hypopnea, necessarily implicates the appearance of desaturation and its possible consequences. It is, therefore, very important to know the SpO2 behavior during sleep at Bogota׳s altitude as an initial step to investigate the role of altitude and the possible clinical repercussions of oxygen desaturation in patients with SAHS and if these findings justify a redefinition of this syndrome at this altitude. The objective of this study was to describe the oxygen saturation during wakefulness sleep and apneas–hypopneas in adults at an altitude of 2640m.
    Materials and methods Patients of 18 years or more, sent for basal polysomnogram at the Laboratory of Sleep of Fundación Neumológica Colombiana in Bogota, city situated 2640m above sea level, between the years of January 2004 and December 2005, were included. Nocturnal polysomnogram were performed for a minimum of 4h, with Alice 3 and 4 from Respironics®, following international recommendations: 3 electroencephalogram axl inhibitor (C3M2, C4M1, O1M2), 2 electro-oculography channels and electromyography (mandible and legs), electrocardiogram, air flow by pressure cannula and thermistor, respiratory effort with thoracic and abdominal belts, finger pulse oxymetry, snoring and position. The SpO2 was measured by MARS Model 2001 oxymeters with the following technical specifications: Measurement amplitude of 0–100%, precision: 70–100%±25 and a resolution of 1%. The value of oxygen saturation and the pulse frequency were determined by an average of a 2s sample. Manual scoring of the records was performed. The sleep stages were classified according to international criteria during the years of study (Reschtchaffen and Kales) [13]. Apnea was defined as the complete cessation of air flow during 10s or more and hypopnea as the reduction of, at least, 30% of the flow for 10s, associated to a arousal or a oxygen desaturation of axl inhibitor 3% or more. The apnea–hypopnea index (AHI) was defined as the total number of apneas and hypopneas per hour of sleep. The severity of OSA was determined according to AHI: Mild: 5–15/h; moderate: 16 to 30/h; and severe: more than 30/h [14]. Oxygen desaturation was defined by a SpO2 lower than 90%. Patients who received oxygen during the study, the studies for CPAP titration, and those with less than 4h, were excluded. We used averages and standard deviations for the quantitative variables and the proportions for qualitative variables. To establish differences between the SpO2 during the different stages of sleep for each group according to AHI, we used the test for independent samples and the ANOVA test. To establish the degree of statistical significance of the different proportions, we used the square test. We used Pearson׳s coefficient to establish the correlation between AHI with age and IMC. We considered it significant when p<0.05. We used the statistical programs SPSS 10.0.
    Discussion The main finding of this study was that patients with OSA at an altitude of 2640m above sea level showed a significant oxygen desaturation during sleep, which decreases even more with the increased severity of OSA especially during REM sleep and during the events of apnea and hypopnea, reaching values as low as 78% during REM sleep and 75% during the above mentioned events. The worst desaturation during REM sleep in patients with sleep apnea has been described and has been related with the duration of apneas during this sleep stage [15]. Patz et al., have studied the effect of altitude upon AHI and did not find important differences between the minimal saturation in three different altitudes (0m, 1370m and 2423m) [16]. Some studies have described the behavior of oxygen saturation during sleep. Gries et al. found that the average saturation in 350 normal subjects during sleep, in Cleveland, Ohio (173m above sea level), was of 96.5%. The saturation decreased mildly with age, ranging from 96.8% in the group of 1–10 years of age, to 95.1 in the group of 60 years of age [17].