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Sleep Research Laboratory, Queen Elizabeth Hospital, and Department of Medicine, Toronto Hospital, University of Toronto, Toronto, Ontario, Canada M5G 2C4
Received 21 February 1996; accepted in final form 3 November 1996.
Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. Douglas
Bradley. Effects of inhaled
CO2 and added dead space on idiopathic central sleep apnea. J. Appl.
Physiol. 82(3): 918-926, 1997.
We hypothesized
that reductions in arterial PCO2 (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
four occasions during which the fraction of end-tidal
CO2 and transcutaneous PCO2 were measured: during room air
breathing (N1), alternating room air
and CO2 breathing
(N2),
CO2 breathing all night
(N3), and addition of dead space via
a face mask all night (N4).
Central apneas were invariably preceded by reductions in
fraction of end-tidal CO2. Both
administration of a CO2-enriched
gas mixture and addition of dead space induced 1- to 3-Torr increases
in transcutaneous PCO2, which
virtually eliminated apneas and hypopneas; they decreased from
43.7 ± 7.3 apneas and hypopneas/h on
N1 to 5.8 ± 0.9 apneas and
hypopneas/h during N3
(P < 0.005), from 43.8 ± 6.9 apneas and hypopneas/h during room air breathing to 5.9 ± 2.5 apneas and hypopneas/h of sleep during
CO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients were
breathing through added dead space during
N4 (P < 0.005). Because 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.
carbon dioxide inhalation; periodic breathing
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