How does experimental pulmonary embolism decrease CO₂ elimination?

To test how large pulmonary embolism changes non-steady state CO₂ kinetics, the right pulmonary artery (RPA) was occluded in 5 anesthetized, ventilated, thoracotomized dogs. By 1 min after RPA occlusion, CO₂ volume exhaled per breath (V(C02,br)) decreased from 9.3 ± 2.8 to 7.0 ± 2.6 ml and end-tidal P(CO2) (PET(CO2)) decreased from 28.7 ± 4.2 to 21.8 ± 3.3 Torr. During the ensuing 70 min, V(CO2,br) increased back to baseline but PET(C02) was still 13% less than baseline. Both Pa(CO2), (41.5 ± 1.7 to 55.1 ± 8.1 Torr) and PV@B(CO2) (48.2 ± 1.9 to 62.8 ± 6.5 Torr) steadily increased and approached equilibrium by 45 min of RPA occlusion. Cardiac output did not significantly change. In summary, RPA occlusion immediately decreased V(CO2,br) by 25%, due mostly to increased alveolar VD(VD(alv)). Then, V(CO2,br) recovered back to baseline as CO₂ accumulated in tissues and lung. In contrast, elevated VD(alv) caused persistent decreased PET(C02), which did not detect recovery of V(C02,br) nor increase in Pa(CO2) during RPA occlusion.