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Updated: Aug 24, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Post-hyperventilation hypoxaemia is due to alteration of ventilation and perfusion matching
Stephen R Nolan1, Manox Saxena, Keith R Burgess
1Department of Critical Care, Manly Hospital, Manly, New South Wales, Australia.
Objective:
The aim of this study was to investigate the mechanisms of post-hyperventilation hypoxia.
Methodology:
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.
Conclusion:
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.
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