1. The extent of the reflex hypoxic respiratory drive was investigated in a group of patients who were hypoxaemic because of chronic bronchitis.
2. Oxygen was substituted for the inspired air for periods of 1–2 min. This produced a rise in arterial Po2 (Pa,o2) which varied considerably from patient to patient, but in each case the rate of rise was effectively linear with time. The resulting fall in ventilation, measured over 15 s periods, was compared with the Pa,o2 achieved.
3. In most patients the Pa,o2 did not reach hyperoxic levels. The total contribution of their peripheral chemoreceptor reflexes to their resting ventilation could not therefore be measured. The fraction of the ventilation abolished when the Pa,o2 was corrected to near-normal levels was measured instead. In two patients whose Pa,o2 on air was 6·0 and 6·5 kPa (45 and 49 torr) this fraction was 25 and 27%. In three patients whose initial Pa,o2 was 8·0–8·8 kPa (60–66 torr), it was 18–21%. In three patients with an initial Pa,o2 of more than 9·3 kPa (70 torr), it was 5–16%.
4. Each of these patients therefore had a reflex hypoxic respiratory drive. In the more severely hypoxaemic patients the fraction measured was an important part of the overall efferent drive to the respiratory muscles.