Fig. 4.

The PvCO₂ decreases to PcCO₂ (the capillary PCO₂ pressure) after releasing CO₂ in the alveolar space. The partial pressure of CO₂ in the alveoli (PACO₂) which are perfused is equal to PcCO₂. This pressure represents the “ideal” alveolar gas, as it derives from pulmonary units which are both perfused and ventilated. This model ignores other factors possibly affecting the CO₂ dynamics, such as the CO₂ production from the inflammatory cells residing in the inflamed lung. Actually, this ideal PACO₂ may be “diluted” by the gas coming from unperfused but ventilated alveoli (alveolar dead space). The PACO₂ then becomes P_ETCO₂. In turn, the P_ETCO₂ may be diluted into the gas ventilating the airways and the apparatus (anatomical dead space) becoming P_ETCO₂. It must be realized that the number of molecules of CO₂ involved are exactly the same, but their concentration (and partial pressure) depends on the progressive dilution with alveolar gases and “anatomical” gases. In normal individual, PACO₂ and P_ETCO₂ differ only of 1–2 mmHg, being the alveolar dead space negligible. The PvCO₂ may also reach the arterial circulation without any modification in presence of venous admixture. In this case, PaCO₂ is the result of mixing between PcCO₂ and PvCO₂. Greater is the venous admixture, greater is the difference between PaCO₂ (higher) and PcCO₂. In the perfect gas exchanger, P_ETCO₂ equals the PACO₂ (no alveolar dead space) and PACO₂ equals PaCO2 (no venous admixture). Therefore P_ETCO₂/PaCO₂ equals 1