P (a-ET)CO 2 and VDalv frac were closely associated with the alveolar part of V/Q Eng and as such, were also influenced by variables representing a dysfunctional pulmonary perfusion. No “real” dead space variables from Bohr’s equation contributed to the explanation of the variance of the two CO 2 indices. Adding MPP (P (a-ET)CO 2) and airway dead space (VDalv frac) to the models improved them only marginally. The highest correlation was found with the alveolar part of V/Q Eng to alveolar tidal volume ratio for both, P (a-ET)CO 2 ( r = 0.899) and VDalv frac ( r = 0.938). The R 2 of the selected model, representing how much of the variance in the response could be explained by the selected variables, was reported. The simplest, best-fit model was selected based on the maximum adjusted R 2 and smallest Mallow’s p (C p). Multiple linear regression analysis was performed on P (a-ET)CO 2 and VDalv frac assessing which explanatory variables best explained the variance in each response. Univariate Pearson correlation was first explored for both CO 2 indices before V/Q Eng and the explanatory variables with rho were reported.

Bohr’s physiological and alveolar dead space variables, cardiac output (CO), mean pulmonary pressure (MPP), venous admixture ( Q ˙ s / Q ˙ t ), airway dead space, tidal volume, oxygen consumption, and slope III of the volumetric capnogram were evaluated (explanatory variables). Data to calculate the CO 2 indices (response variables) and dead space variables were measured every 30 min. Six healthy adult horses were anesthetized in dorsal recumbency breathing spontaneously for 3 h.

The aim of this experimental study was to evaluate which factors influence these CO 2 indices in anesthetized spontaneously breathing horses.

The arterial to end-tidal CO 2 difference (P (a-ET)CO 2) and alveolar dead space fraction (VDalv frac = P (a-ET)CO 2/PaCO 2), are used to estimate Enghoff’s “pulmonary dead space” (V/Q Eng), a factor which is also influenced by venous admixture and other pulmonary perfusion abnormalities and thus is not just a measure of dead space as the name suggests.

Typical physiologic dead space