Nolan Stephen R, Saxena Manox, Burgess Keith R, Simmel Rein, Braude Stanley
Department of Critical Care, Manly Hospital, Manly, New South Wales, Australia.
Respirology. 2004 Jun;9(2):204-10. doi: 10.1111/j.1440-1843.2004.00562.x.
The aim of this study was to investigate the mechanisms of post-hyperventilation hypoxia.
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.
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.
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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