Post-hyperventilation hypoxaemia is due to alteration of ventilation and perfusion matching.
OBJECTIVE
The aim of this study was to investigate the mechanisms of post-hyperventilation hypoxia.


METHODS
Seven healthy male volunteers, aged 29.1 +/- 1.4 years, underwent two 10-min periods of voluntary hyperventilation to pulmonary end tidal CO2 values of 20 mmHg (severe hyperventilation), or 30 mmHg (moderate hyperventilation). Post-hyperventilation, the arterial oxygen saturation, VE and arterial blood gas values were measured. Sleep was excluded by EEG monitoring.


RESULTS
Maximal hypoxaemia occurred in proportion to severity of hyperventilation; at approximately 5 min post-hyperventilation Pao2 fell to 64 +/- 7 mmHg (severe hyperventilation) and 72 +/- 6 mmHg (moderate hyperventilation) from 97 +/- 3 mmHg at baseline. Hypoxaemia persisted beyond the time of normalization of Paco2 and HCO3. On another occasion, a N2 washout test was performed after severe hyperventilation, which excluded bronchoconstriction.


CONCLUSIONS
Relative hypoventilation may partly explain post-hyperventilation hypoxaemia, but by excluding bronchoconstriction and periodic breathing, we have demonstrated that most of the hypoxaemia must have been due to alteration of pulmonary blood flow distribution causing a fall in V/Q ratio.
Nolan
Stephen R
SR
Department of Critical Care, Manly Hospital, Manly, New South Wales, Australia.
Saxena
Manox
M
Burgess
Keith R
KR
Simmel
Rein
R
Braude
Stanley
S
D000328:Adult; D001784:Blood Gas Analysis; D002153:Calorimetry, Indirect; D006801:Humans; D006985:Hyperventilation / Q000503:physiopathology*; D000860:Hypoxia / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D011652:Pulmonary Circulation / Q000502:physiology; D014692:Ventilation-Perfusion Ratio / Q000502:physiology*