Comparison of respiratory and circulatory human responses to progressive hypoxia and hypercapnia

The effects of acute, progressive isocapnic hypoxia and hyperoxic hypercapnia on lung ventilation, heart rate, cardiac output and arterial blood pressure were determined simultaneously in 32 normal individuals. All subjects were exposed to hypoxia and hypercapnia in an entire range of individual tolerance. The piecewise linear approximation technique was used for analysis of the ventilatory and circulatory response curves. In all subjects, the changes in hemodynamics in the response to hypoxia paralleled those occurring in ventilation, during both the first phase of slow increase and the second phase of sharp increase. Fracture point coordinates for ventilation and circulation coincided, with the fracture being registered at an end-tidal PO2 of 79.7 +/- 3.8 mm Hg for ventilation and 79.0 +/- 4.5 mm Hg (p greater than 0.1) for cardiac output. This may give evidence of analogous entries from the peripheral O2-sensitive receptors to the respiratory and vascular motor bulbar centers. By contrast, a more significant rise in ventilation observed during the hypercapnic versus hypoxic drive was not accompanied by any change in the heart rate, cardiac output and arterial blood pressure until the end-tidal PCO2 (PETCO2) had reached a critical level. Fracture point coordinates for ventilation and circulation did not coincide, with the fracture being registered at a PETCO2 of 51.1 +/- 1.9 mm Hg for the former and 57.0 +/- 2.2 mm Hg (p less than 0.01) for the latter. Such differences in the response to hypoxia and hypercapnia were repeatedly observed during 5 test days. The data do not seem to show evidence in favor of an involvement of the hypercapnic challenge in the central regulation of the circulation.