Sleep apneas in high altitude residents (3,800 m).

The question is: to what extent periodic breathing usually observed in translocated subjects at high altitude affects normal and polycythemic residents of high altitude? Standard sleep parameters, chest wall movements, temperature of ventilated gas and arterial O2 saturation (SaO2) were continuously recorded in 7 normal highlanders (mean hematocrit: 51%) and 14 polycythemic highlanders (mean hematocrit: 68%) during one night in La Paz, 3,850 m, Bolivia. The patterns of breathing instability were analysed by two ways: measuring duration of apneas and counting all the oscillations of SaO2 greater than 1%. Normal and polycythemic highlanders displayed a wide intersubject variability with regard to breathing instability, hence no significant difference in the total number of apneas and oscillations of SaO2 could be evidenced between the 2 groups. However, the longest apneas and the highest number of oscillations of SaO2 were found in the polycythemic highlanders.

Periodic breathing and O2 saturation in relation to sleep stages at high altitude.

This study was designed to compare sleep organization at high altitude (HA) and sea level (SL) and to estimate the extent periodic breathing (PB) negatively influences arterial O2 saturation (SaO2). Six lowlanders were studied at SL and after 3 weeks spent at 3,800 m (La Paz, Bolivia). Three EEG leads, EOG, submental EMG, chest and abdominal motion, temperature of ventilated gas, and SaO2 were polygraphically recorded. Comparison of HA and SL data disclosed that: 1) Sleep organization was identical, with the same percentage of REM and stage 4. 2) PB (cycle length: 20 s; central apnea: 9 s) occurred in three subjects during all stages of sleep except REM (43-60% of total sleep). A periodic lowering in heart rate occurred during ventilatory oscillation. 3) During PB, SaO2 oscillated very regularly from 78-90%, which resulted in a mean SaO2 value calculated during oscillations similar to that of the non-periodic breathers. We conclude that lung O2 uptake during PB is preserved.