Cardiorespiratory Responses to Voluntary Hyperventilation During Normobaric Hypoxia.

Unexplained physiological events (PE), possibly related to hypoxia and hyperventilation, are a concern for some air forces. Physiological monitoring could aid research into PEs, with measurement of arterial oxygen saturation (So₂) often suggested despite potential limitations in its use. Given similar physiological responses to hypoxia and hyperventilation, the present study characterized the cardiovascular and respiratory responses to each. Ten healthy subjects were exposed to 55 mins of normobaric hypoxia simulating altitudes of 0, 8000, and 12,000 ft (0, 2438, and 3658 m) while breathing normally and voluntarily hyperventilating (doubling minute ventilation). Respiratory gas analysis and spirometry measured end-tidal gases (Po₂ and Pco₂) and minute ventilation. So₂ was assessed using finger pulse oximetry. Mean arterial, systolic, and diastolic blood pressure were measured noninvasively. Cognitive impairment was assessed using the Stroop test. Voluntary hyperventilation resulted in a doubling of minute ventilation and lowered Pco₂, while altitude had no effect on these. Po₂ and So₂ declined with increasing altitude. However, despite a significant drop in Po₂ of 15.2 mmHg from 8000 to 12,000 ft, So₂ was similar when hyperventilating (94.7 ± 2.3% vs. 93.4 ± 4.3%, respectively). The only cardiovascular response was an increase in heart rate while hyperventilating. Altitude had no effect on cognitive impairment, but hyperventilation did. For many cardiovascular and respiratory variables, there is minimal difference in responses to hypoxia and hyperventilation, making these challenging to differentiate. So₂ is not a reliable marker of environmental hypoxia in the presence of hyperventilation and should not be used as such without additional monitoring of minute ventilation and end-tidal gases.