Tidal volume dependency of gas exchange in bronchoconstricted pig lungs.
Independent of airway pressure, pulmonary resistance is known to fall with increasing tidal volumes, traditionally thought to result from radial traction on the airways. R. C. Anafi and T. A. Wilson (J Appl Physiol 91: 1185-1192, 2001) recently presented a model of a single terminal airway that explains the tidal volume-associated fall in resistance with an additional mechanism pertinent to narrow airways: a stable, nearly closed airway that is challenged with an increase in tidal volume "pops open" to become a stable, well-opened airway, and thus resistance drops suddenly. To test this model in vivo, the effects of high (24 ml/kg) and low (9 ml/kg) tidal volume in bronchoconstricted lungs were assessed using 1) the multiple inert gas elimination technique (MIGET) and 2) a 15-breath multiple breath inert gas washout (MBW) technique in anesthetized pigs. With high tidal volume, ventilation/perfusion (Va/Q) mismatch was reduced (log SD Q from 1.30 +/- 0.11 to 1.09 +/- 0.12, P < 0.05), and blood flow to lung units with Va/Q ratios < 0.1 was significantly reduced (37 +/- 4% of cardiac output to 7 +/- 4%, P < 0.05). Dynamic compliance was twice as high during high-tidal-volume ventilation (P = 0.002). MBW analysis revealed that, while heterogeneity of ventilation during bronchoconstriction was not significantly different between either low or high tidal volume (log SD Vmbw = 1.39 +/- 0.09 and 1.34 +/- 0.02, respectively), preinspiratory lung volume (PILV) decreased by 42% with low-tidal-volume ventilation (P < 0.05), whereas it did not change with high-tidal-volume ventilation. The higher PILV during high tidal volume is also consistent with Anafi and Wilson's model. In summary, the outcomes from MIGET, and to some extent the MBW, in our anesthetized and mechanically ventilated pigs are consistent with a bistable terminal airway model as proposed by Anafi and Wilson. However, our data do not allow exclusion of other mechanisms that may lead to improved ventilatory distribution when tidal volume is increased.
Kleinsasser
Axel
A
Department of Medicine, Division of Physiology, University of California-San Diego, La Jolla, California 92093-0623, USA.
Olfert
I Mark
IM
Loeckinger
Alex
A
Prisk
G Kim
GK
Hopkins
Susan R
SR
Wagner
Peter D
PD
D000280:Administration, Inhalation; D000403:Airway Resistance; D000818:Animals; D001985:Bronchial Provocation Tests; D016084:Bronchoconstriction / Q000187:drug effects; D016085:Bronchoconstrictor Agents / Q000008:administration & dosage; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D008168:Lung / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D016210:Methacholine Chloride / Q000008:administration & dosage; D008954:Models, Biological; D010100:Oxygen / Q000097:blood; D011652:Pulmonary Circulation / Q000187:drug effects; D011659:Pulmonary Gas Exchange / Q000187:drug effects; D012123:Pulmonary Ventilation / Q000187:drug effects; D015203:Reproducibility of Results; D034421:Sus scrofa; D013990:Tidal Volume / Q000187:drug effects; D014692:Ventilation-Perfusion Ratio
D016085:Bronchoconstrictor Agents; D016210:Methacholine Chloride; D002245:Carbon Dioxide; D010100:Oxygen