To test how large pulmonary embolism changes non-steady state CO2 kine
tics, the right pulmonary artery (RPA) was occluded in 5 anesthetized,
ventilated, thoracotomized dogs, By 1 min after RPA occlusion, CO2 Vo
lume exhaled per breath (V-CO2,V-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,V-br increased
back to baseline but PET(CO2) was still 13% less than baseline. Both
Pa-CO2 (41.5 +/- 1.7 to 55.1 +/- 8.1 Torr) and P (V) over bar(CO2) (48
.2 +/- 1.9 to 62.8 +/- 6.5 Torr) steadily increased and approached equ
ilibrium by 45 min of RPA occlusion. Cardiac output did not significan
tly change. in summary, RPA occlusion immediately decreased V-CO2,V-br
by 25%, due mostly to increased alveolar VD (VDalv). Then, V-CO2,V-br
recovered back to baseline as CO2 accumulated in tissues and lung. In
contrast, elevated VDalv caused persistent decreased PET(CO2). which
did not detect recovery of V-CO2,V-br nor increase in Pa-CO2 during RP
A occlusion.