How does experimental pulmonary embolism decrease CO2 elimination?

Abstract

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 (VCO2,br) decreased from 9.3 +/- 2.8 to 7.0 +/- 2.6 ml and end-tidal PCO2 (PETCO2) decreased from 28.7 +/- 4.2 to 21.8 +/- 3.3 Torr. During the ensuing 70 min, VCO2,br increased back to baseline but PETCO2 was still 13% less than baseline. Both PaCO2 (41.5 +/- 1.7 to 55.1 +/- 8.1 Torr) and PvCO2 (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 VCO2,br by 25%, due mostly to increased alveolar VD (VDalv). Then, VCO2,br recovered back to baseline as CO2 accumulated in tissues and lung. In contrast, elevated VDalv caused persistent decreased PETCO2, which did not detect recovery of VCO2,br nor increase in PaCO2 during RPA occlusion.