Effects of inhaled co2 and added deadspace on idiopathic central
sleep apnea.
Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. Douglas Bradley.
Sleep Research Laboratory, Queen Elizabeth Hospital and the
Department of Medicine, The Toronto Hospital, University of Toronto,
Toronto, Ontario, Canada
APStracts 3:0530A, 1996.
We hypothesized that reductions in PaCO2 below the apnea threshold
play a key role in the pathogenesis of idiopathic central sleep apnea
syndrome (ICSAS). If so, we reasoned that raising PaCO2 would abolish
apneas in these patients. Accordingly, patients with ICSAS were
studied overnight on 4 occasions: on room air (N1); alternating room
air and CO2 breathing (N2); CO2 breathing all night (N3), and
addition of deadspace via a facemask all night (N4) during which
fraction of end tidal CO2 (FETCO2) and transcutaneous PCO2 (PtcCO2)
were measured. Central apneas were invariably preceded by reductions
in FETCO2. Both administration of a CO2 enriched gas mixture and
addition of deadspace induced 1-3 mm Hg increases in PtcCO2, which
virtually eliminated apneas and hypopneas; they decreased from
43.7&7.3 per hr on N1 to 5.8&0.9 per hr on N3 (p<0.005);
from 43.8&6.9 per hr on room air to 5.9&2.5 per hr of sleep
on inhaled CO2 during N2 (p<0.01); and to 11.6% of the room air
level while breathing through added deadspace during N4 (p<0.005).
Since raising PaCO2 through two different means virtually eliminated
central sleep apneas, we conclude that central apneas during sleep in
ICSA are due to reductions in PaCO2 below the apnea threshold.
Received 21 February 1996; accepted in final form 3 November
1996.
APS Manuscript Number A172-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996