M. Ohi et al., OXYGEN DESATURATION FOLLOWING VOLUNTARY HYPERVENTILATION IN NORMAL SUBJECTS, American journal of respiratory and critical care medicine, 149(3), 1994, pp. 731-738
Citations number
40
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
To investigate the severity of oxygen desaturation following voluntary
hyperventilation (VHV) in normal subjects and its possible relation t
o chemoresponsiveness, we examined respiration following VHV in 16 nor
mal male subjects. Monitoring was performed according to the standard
polysomnography protocol including measurements of arterial oxygen sat
uration (Sa(O2)) and transcutaneous PCO2 (PtcCO(2)). This subjects hyp
erventilated voluntarily for 3 min, and were then observed for more th
an 15 min. They hyperventilated again for another 3 min, and were foll
owed again for more than 15 min. Eleven subjects fell into non-REM sle
ep after VHV, and their mean lowest Sa(O2) was 67.6 +/- 13.0% (n = 15
trials in 11 subjects, mean +/- SD). Falling asleep during hypocapnia
caused desaturation, and periodic breathing was invariably observed so
on after. The difference between the Ptc(CO2) during non-REM sleep wit
h stable breathing and the Ptc(CO2) when the Sa(O2) was 90% following
VHV was defined as the Delta Ptc(CO2) (90). The Delta Ptc(CO2) (90) an
d hypoxic ventilatory response (HVR) were positively and significantly
correlated (r = 0.73, p < 0.01). While the subjects were awake, the m
ean lowest Sa(O2) was 73.5 +/- 17.4% (17 trials in 12 subjects). Remai
ning awake induced oxygen desaturation in some subjects but not in oth
ers. In one subject, desaturation during the waking state was caused b
y hypoventilation, not by central apnea. In the seven subjects whose r
espiration following VHV was monitored during the waking state in one
trial and during the sleeping state in another trial, plots of the Ptc
(CO2)-Sa(O2) relationship for the waking state were generally position
ed above those made for the sleeping state. We conclude that during hy
pocapnia after hyperventilation, (1) desaturation invariably occurs du
ring sleep, and may even occur in the waking state, (2) the hypoxic ve
ntilatory drive contributes to an earlier recovery from posthyperventi
lation desaturation during the sleeping state, and (3) behavioral cont
rol of respiration may not fully compensate for the loss of chemical r
espiratory control in some instances in the waking state.