Am. J. Respir. Crit. Care Med., Vol 152, No. 6, Dec 1995, 1950-1955.
Hypocapnia and increased ventilatory responsiveness in patients with idiopathic central sleep apnea
A Xie, R Rutherford, F Rankin, B Wong and TD Bradley
Sleep Research Laboratory, Queen Elizabeth Hospital, Toronto, Ontario, Canada.
We previously demonstrated that central apneas during sleep in patients
with idiopathic central sleep apnea (ICSA) are triggered by abrupt
hyperventilation. In addition, baseline PCO2 at the time of augmented
breaths which triggered central apneas was lower than for augmented breaths
which did not trigger apneas. These observations led us to hypothesize that
patients with ICSA chronically hyperventilate maintaining their PCO2 close
to the threshold for apnea during sleep owing to increased chemical
respiratory drive. To test these hypotheses, we recorded transcutaneous
PCO2 (PtcCO2) during overnight sleep studies on nine consecutive patients
with ICSA and nine sex-, age- , and body-mass-index-matched control
subjects. Daytime PaCO2 as well as rebreathing and single breath
ventilatory responses to CO2 were also measured. Compared with the control
subjects, the patients had significantly lower mean PtcCO2 during sleep
(37.8 +/- 1.2 versus 42.7 +/- 10.9 mm Hg, p < 0.01) and lower PaCO2
while awake (35.1 +/- 1.3 versus 38.8 +/- 0.9 mm Hg, p < 0.05).
Furthermore, patients with ICSA had significantly higher ventilatory
responses to CO2 for both the rebreathing (3.14 +/- 0.34 versus 1.60 +/-
0.32 L/min/mm Hg, p < 0.005) and single breath methods (0.51 +/- 0.10
versus 0.25 +/- 0.04 L/min/mm Hg, p < 0.05). We conclude that: (1)
patients with ICSA chronically hyperventilate awake and asleep and (2)
chronic hyperventilation is probably related to augmented central and
peripheral respiratory drive which predisposes to respiratory control
system instability.
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Copyright © 1995 American Thoracic Society
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