Journal of Applied Physiology, Vol 62, Issue 3 880-891, Copyright © 1987 by American Physiological Society
Derivation of CO2 output from oscillations in arterial pH
B. A. Cross, R. P. Stidwill, K. D. Leaver and S. J. Semple
Theory predicts that the rate of rise of the oscillation in arterial CO2
partial pressure (PaCO2) is linearly dependent on CO2 flux from venous
blood to alveolar gas. We have measured, in the anesthetized cat, CO2
output (VCO2) and oscillations in arterial pH. The pH signal was
differentiated to give the maximum rate of fall of pH on the downstroke of
the oscillation (dpH/dt decreases max). Since oscillations in pH are due to
oscillations in arterial PCO2, dpH/dt decreases max was considered to be
equivalent to the maximum rate of rise of the PCO2 oscillation. VCO2 was
increased by ventilating the intestines with CO2 and by the intra-arterial
infusion of 2,4-dinitrophenol. VCO2 was decreased by filling the intestines
with isotonic tris(hydroxymethyl)methylamine buffer. The maximum range of
VCO2 covered was 7.8-51 ml/min, and the mean range was from 13.6 +/- 1.3 to
29.7 +/- 1.6 (SE) ml/min. Although CO2 loading produced a small rise and
CO2 unloading a small fall in mean PaCO2, the changes were not
statistically significant, so that overall the response was close to
isocapnia. Over the limited range of VCO2 studied there was a highly
significant linear association between dpH/dt decreases max and VCO2 which
supports the contention that the slope of the upstroke of the PaCO2
oscillation is determined by the CO2 flux from mixed venous blood to
alveolar gas. As such this slope is a potential chemical signal linking
ventilation to CO2 production.
