Journal of Applied Physiology, Vol 72, Issue 3 1057-1063, Copyright © 1992 by American Physiological Society
Effects of inspired CO2, hyperventilation, and time on VA/Q inequality in the dog
K. Tsukimoto, J. P. Arcos, W. Schaffartzik, P. D. Wagner and J. B. West
Department of Medicine, University of California, San Diego, La Jolla 92093-0623.
In a recent study by Tsukimoto et al. (J. Appl. Physiol. 68: 2488-2493,
1990), CO2 inhalation appeared to reduce the size of the high
ventilation-perfusion ratio (VA/Q) mode commonly observed in anesthetized
mechanically air-ventilated dogs. In that study, large tidal volumes (VT)
were used during CO2 inhalation to preserve normocapnia. To separate the
influences of CO2 and high VT on the VA/Q distribution in the present
study, we examined the effect of inspired CO2 on the high VA/Q mode using
eight mechanically ventilated dogs (4 given CO2, 4 controls). The VA/Q
distribution was measured first with normal VT and then with increased VT.
In the CO2 group at high VT, data were collected before, during, and after
CO2 inhalation. With normal VT, there was no difference in the size of the
high VA/Q mode between groups [10.5 +/- 3.5% (SE) of ventilation in the CO2
group, 11.8 +/- 5.2% in the control group]. Unexpectedly, the size of the
high VA/Q mode decreased similarly in both groups over time, independently
of the inspired PCO2, at a rate similar to the fall in cardiac output over
time. The reduction in the high VA/Q mode together with a simultaneous
increase in alveolar dead space (estimated by the difference between inert
gas dead space and Fowler dead space) suggests that poorly perfused high
VA/Q areas became unperfused over time. A possible mechanism is that
elevated alveolar pressure and decreased cardiac output eliminate blood
flow from corner vessels in nondependent high VA/Q regions.
