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high altitude truly differs from that at sea level. It is pos-
sible that arterial desaturation induced by high altitude
shifts SaO 2 during sleep to the steeper portion of the dis-
sociation curve and thereby amplifies the influence of ven-
tilatory dysrhythmia on SaO 2 .
Ventilatory and SaO 2 oscillations similar to those
observed by Kryger and colleagues 98 have also been
described at high altitude by Lahiri and colleagues 36 in
Sherpas native to high altitude but not in Sherpas native
to low altitude. The potential contribution of ethnic and/
or genetic differences is suggested by a study comparing
Tibetan and Chinese Han residents of 4000 meters. Sleep
was studied in a hypobaric chamber at simulated altitudes
of 2261 and 5000 meters. At the higher altitude, Tibetans
had more periodic breathing, higher SaO 2 , and better sleep
structure than did the Han subjects. 100
Although decreased hypoxic ventilatory response during
wakefulness has been observed in natives of Leadville 101
and in Sherpas native to high altitude, 102 it is unclear
whether this contributes to respiratory dysrhythmia and
hypoxemia in highlanders during sleep at altitude.
However, improvement in hypoxemia during wakefulness
and sleep in long-term residents at high altitude with use
of the ventilatory stimulant medroxyprogesterone acetate
suggests that decreased ventilatory drive may have a per-
missive role. 98 , 103 Similar findings are reported for acetazol-
amide which over a three week's treatment in residents in
the Andes at 4300 m increased oxygen saturation and
markedly reduced the apnea-hypopnea index during
sleep. 104
Natives and long-term residents of high altitude exhibit
chronic mountain sickness or Monge's disease, a syndrome
of excessive polycythemia with headache, dizziness, breath-
lessness, and sleep disturbance. The pathophysiology of
the syndrome is debated, but likely is induced by increased
hypoxemia reflecting the combined effects of altitude,
decreased ventilatory drive and lung dysfunction. Com-
pared to normal subjects, individuals with chronic moun-
tain sickness exhibit exaggerated hypoxemia during sleep
without an increase in RDI. 104-106 These subjects also
exhibit greater daytime hypoxemia and thus the role of
sleep-associated desaturation remains uncertain.
drase, which likely works by reducing alkalotic ventilatory
inhibition. Recent studies suggest that benzodiazepines
and other hypnotic agents may improve sleep quality
without apparent adverse effects. 107
Clinical Pearl
Sleep at altitude is disturbed by the opposing influ-
ences of hypoxic stimulation and alkalotic inhibition
which lead to periodic breathing and frequent associ-
ated arousals. Effective treatments include correction
of alkalosis with acetazolamide or blunting of hypoxic
stimulation with some benzodiazepines.
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CONCLUSIONS
The sensation of disrupted sleep after ascent to high alti-
tude is associated with frequent awakenings, which in part
probably reflect sleep fragmentation by respiratory dys-
rhythmia typically consisting of monotonously repetitive
periodic breathing. This periodicity is produced by venti-
latory inhibition by hypocapnic alkalosis alternating with
stimulation by hypoxia, which terminates apnea and initi-
ates hyperpnea with consequent hypocapnia, leading to
perpetuation of periodicity. Sleep disruption and periodic
breathing decrease with time at moderate altitude and are
also considerably reduced by pretreatment with acetazol-
amide, which reduces alkalosis. In long-term residents of
high altitude, less-distinctive, undulating respiratory dys-
rhythmias are described, with unstable and decreased arte-
rial oxygenation.
The most common treatment is prophylactic adminis-
tration of acetazolamide, an inhibitor of carbonic anhy-
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