Ventilatory response to transient hyperoxia in head injury hyperventilation.
We have measured breath-by-breath instantaneous minute ventilation (VIinst) before, during, and after the administration of 10 breaths of 100% oxygen to seven male patients with head injury hyperventilation. The patients were hypoxemic (PaO2 61.2 +/- 6.3) and hypocapnic (PaCO2 26.6 +/- 5.9) with a respiratory alkalosis (pH 7.53 +/- 0.06) while breathing air. Following the oxygen VIinst fell on the average by 40 +/- 12.7% from 16.06 +/- 3.75 1.min-1 to a minimum of 9.73 +/- 3.20 1.min-1 at 20.4 +/- 2.9 s after the first breath of oxygen. In the majority of our hyperventilating patients, almost all of the resting hyperventilation could be abolished transiently by 100% oxygen. This fall in ventilation represents the peripheral chemoreceptor contribution to resting ventilation and is increased in the head injury patients in comparison with normal subjects breathing air or hypoxic gas mixtures, altitude-acclimatized subjects and patients who are hypoxic because of chronic bronchitis or interstitial lung disease. We suggest that the increased reflex hypoxic drive to ventilation found in our patients is secondary to their cerebral injury, resulting in a reduction of descending cortical inhibitory influences on the medullary respiratory control centers.
D000293:Adolescent; D000328:Adult; D000368:Aged; D001930:Brain Injuries / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000097:blood; D002628:Chemoreceptor Cells / Q000503:physiopathology; D006801:Humans; D006985:Hyperventilation / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood*; D010102:Oxygen Inhalation Therapy
D002245:Carbon Dioxide; D010100:Oxygen