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Oxygen desaturation following voluntary hyperventilation in normal subjects.
Am J Respir Crit Care Med. 1994 Mar;149(3 Pt 1):731-8.

Ohi M, Chin K, Hirai M, Kuriyama T, Fukui M, Sagawa Y, Kuno K.

Department of Clinical Physiology, Kyoto University, Japan.
Abstract

To investigate the severity of oxygen desaturation following voluntary hyperventilation (VHV) in normal subjects and its possible relation to chemoresponsiveness, we examined respiration following VHV in 16 normal male subjects. Monitoring was performed according to the standard polysomnography protocol including measurements of arterial oxygen saturation (SaO2) and transcutaneous PCO2 (PtcCO2). The subjects hyperventilated voluntarily for 3 min, and were then observed for more than 15 min. They hyperventilated again for another 3 min, and were followed again for more than 15 min. Eleven subjects fell into non-REM sleep after VHV, and their mean lowest SaO2 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 soon after. The difference between the PtcCO2 during non-REM sleep with stable breathing and the PtcCO2 when the SaO2 was 90% following VHV was defined as the delta PtcCO2 (90). The delta PtcCO2 (90) and hypoxic ventilatory response (HVR) were positively and significantly correlated (r = 0.73, p < 0.01). While the subjects were awake, the mean lowest SaO2 was 73.5 +/- 17.4% (17 trials in 12 subjects). Remaining awake induced oxygen desaturation in some subjects but not in others. In one subject, desaturation during the waking state was caused by hypoventilation, not by central apnea. In the seven subjects whose respiration following VHV was monitored during the waking state in one trial and during the sleeping state in another trial, plots of the PtcCO2-SaO2 relationship for the waking state were generally positioned above those made for the sleeping state.(ABSTRACT TRUNCATED AT 250 WORDS)

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