Abstract
The pattern of breathing during the approach to the steady state following step changes of end-tidal P[partial pressure]CO2 and PO2 was determined in normal conscious human subjects. Three types of step were studied as follows: steps of PA[arterial]CO2 against a constant background of hyperoxia (PAO2 .apprx. 200), an almost pure intracranial chemoreceptor stimulus, steps of PAO2 between .apprx. 50 and 80 torr against a background of constant mild hypercapnia, an arterial chemoreceptor stimulus and steps of PACO2 against a background of constant hypoxia (PAO2 .apprx. 50), a mixed stimulus. Steps were small and the responses barely detectable by the subjects. Steps of CO2 in hyperoxia produced the slowest approach to the steady state. A single exponential fitted the ventilation response up to about 4 min (mean half time 83 s for the up and 69 s for the down transients). During the transient the pattern of change of tidal volume (VT) and expiratory time (TE) was the same as in the steady state. Inspiratory time (TI) in the early part of the transient changed in the opposite direction to TE, returning to its steady value after 1.5-3 min. This effect occurred in up and down transients and resulted in a smaller change of respiratory frequency than predicted from the steady-state response. Hypoxic steps produced the fastest approach to the steady state with mean half-times for ventilation of 10.9 s for the up transients and 6.6 for the down. TI followed the same pattern during the transient as in the steady state; TE, following the step out of hypoxia, lengthened to far beyond its final steady value within 5 breaths of the step, only returning to its steady-state value 3-4 min after the step. This resulted in an exaggerated change of frequency during the early part of the transient. Steps of CO2 in hypoxia, a mixed peripheral and central chemoreceptor stimulus, showed a ventilation response which was best fitted by 2 exponentials, the half-times of which were consistent with those obtained for the separate responses. The patterning was also consistent with a mixed response, more so for TI than for TE. The steady-state pattern derived from the pre-switch means was consistent with the pattern previously described. Possible mechanisms are discussed. These results could explain the different patterns seen using re-breathing and steady-state techniques. The validity of using 1 or 2 breath O2 of N2 tests (or other similar tests) as a quantitative measure of the hypoxic response in man is questioned.