Estimating alveolar dead space from the arterial to end-tidal CO(2) gradient: a modeling analysis.

Abstract

Using an original, validated, high-fidelity model of pulmonary physiology, we compared the arterial to end-tidal CO(2) gradient divided by the arterial CO(2) tension (Pa-E'CO(2)/PaCO(2)) with alveolar dead space expressed as a fraction of alveolar tidal volume, calculated in the conventional manner using Fowler's technique and the Bohr equation: (VDalv/VTalv)(Bohr-Fowler). We examined the variability of Pa-E'CO(2)/PaCO(2) and of (VDalv/VTalv)(Bohr-Fowler) in the presence of three ventilation-perfusion defects while varying CO(2) production (Vdot;CO(2)), venous admixture, and anatomical dead space fraction (VDanat). Pa-E'CO(2)/PaCO(2) was approximately 59.5% of (VDalv/VTalv)(Bohr-Fowler). During constant alveolar configuration, the factors examined (Vdot;CO(2), pulmonary shunt fraction, and VDanat) each caused variation in (VDalv/VTalv)(Bohr-Fowler) and in Pa-E'CO(2)/PaCO(2). Induced variation was slightly larger for Pa-E'CO(2)/PaCO(2) during changes in VDanat, but was similar during variation of venous admixture and Vdot;CO(2). Pa-E'CO(2)/PaCO(2) may be a useful serial measurement in the critically ill patient because all the necessary data are easily obtained and calculation is significantly simpler than for (VDalv/VTalv)(Bohr-Fowler). Using an original, validated, high-fidelity model of pulmonary physiology, we have demonstrated that the arterial to end-tidal carbon dioxide pressure gradient may be used to robustly and accurately quantify alveolar dead space. After clinical validation, its use could replace that of conventionally calculated alveolar dead space fraction, particularly in the critically ill.