| Abstrakt: |
Post-hyperventilation hypoxaemia is due to alteration of ventilation and perfusion matching NOLAN SR, SAXENA M, BURGESS KR, SIMMEL R, BRAUDE S. Respirology 2004; 9: 204–210 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 Pa o2 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 Pa co2 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. [ABSTRACT FROM AUTHOR] |
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