How does experimental pulmonary embolism decrease CO2 elimination?

Peter H. Breen, Bhaskar Mazumdar, Sean C. Skinner

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


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.

Original languageEnglish
Pages (from-to)217-224
Number of pages8
JournalRespiration Physiology
Issue number3
StatePublished - Sep 1996


  • Dead space
  • Embolism, pulmonary, CO kinetics
  • Gas exchange
  • Mammals, dog
  • Perfusion, lung, embolism

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine


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