Breathing and brain blood flow during sleep in patients with
chronic mountain sickness.
Sun, Shinfu, Cheryl Oliver-Pickett, Yang Ping, Alexander J. Micco,
Tarshi Droma, Stacy Zamudio, Jianguo Zhuang, Shao-Yung Huang, Rosann
G. McCullough, Allen Cymerman, Lorna G. Moore.
Tibet Institute of Medical Sciences, Lhasa, Tibet Autonomous
Region, The People's Republic of China 85000, Cardiovascular
Pulmonary Research Laboratory, University of Colorado Health Sciences
Center, Denver, CO 80262, Department of Anesthesiology, University of
Colorado Health Sciences Center, Denver, CO 80262, Altitude
Physiology and Medicine Division, U. S. Army Medical Research and
Development Command, Natick, MA, Department of Anthropology,
University of Colorado at Denver, Denver, CO 80217
APStracts 3:0154A, 1996.
Chronic mountain sickness (CMS) patients have lower arterial O2
saturation (SaO2) during sleep compared with healthy high-altitude
residents but whether nocturnal arterial O2 content (CaO2) and brain
O2 delivery are reduced is unknown. We measured SaO2, CaO2, sleep
-disordered breathing (SDB), and internal carotid artery flow velocity
in 8 CMS patients, 8 age-matched healthy CMS controls, 11 healthy
younger-aged Han, and 11 healthy younger-aged Tibetan male residents
of Lhasa, Tibet (3658 m). CMS patients spent a greater portion of the
night in SDB (total # episodes of apnea, hypopnea, and
hypoventilation) than the CMS controls, young Han or young Tibetans
(15% vs. 5%, 1% and 1% respectively, p < 0.05) due to more
frequent apnea and hypoventilation episodes and longer duration of
all types of episodes. SDB and unexplained arterial O2 desaturation
caused nocturnal SaO2 to be lower and more variable in CMS patients
than CMS controls, younger-aged Han, or Tibetan men. Average CaO2 was
similar but the CMS patients spent 29% whereas the other groups spent
less than 4% of the night at values below 18 ml O2/100 ml whole
blood. Internal carotid artery flow velocity during wakefulness was
similar in CMS patients and controls despite higher end-tidal PCO2
values in the CMS patients. Comparing contiguous sleep stages, flow
velocity rose from stage 2 to REM in both groups. Whereas flow
velocity remained elevated from awake to REM in the CMS controls, it
fell in the CMS patients. During episodes of SDB, internal carotid
flow velocity increased in CMS controls but did not change in the CMS
patients such that values were lower in the patients than controls at
the end and after SDB episodes. We concluded that SDB and episodes of
unexplained desaturation lowered nocturnal SaO2 and CaO2 which,
together with a lack of compensatory increase in internal carotid
artery flow velocity, likely decreased brain O2 delivery in CMS
patients during a considerable portion of the night.
Received 26 April 1995; accepted in final form 27 February 1996.
APS Manuscript Number A456-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96