PULMONARY VASCULAR DILATATION AND DIFFUSION-DEPENDENT IMPAIRMENT OF GAS-EXCHANGE IN LIVER-CIRRHOSIS

Citation
Abh. Crawford et al., PULMONARY VASCULAR DILATATION AND DIFFUSION-DEPENDENT IMPAIRMENT OF GAS-EXCHANGE IN LIVER-CIRRHOSIS, The European respiratory journal, 8(12), 1995, pp. 2015-2021
Citations number
29
Categorie Soggetti
Respiratory System
ISSN journal
09031936
Volume
8
Issue
12
Year of publication
1995
Pages
2015 - 2021
Database
ISI
SICI code
0903-1936(1995)8:12<2015:PVDADI>2.0.ZU;2-#
Abstract
To test the hypothesis that diffusion-limitation for oxygen is due to abnormal vascular dilatation and significantly contributes to the arte rial hyperaemia of liver cirrhosis requires an experimental approach t hat detects both diffusion-limitation for oxygen and the presence of a bnormal dilatation of pulmonary vessels exposed to alveolar gas. We th erefore studied the gas exchange of a 64 year old man with alcoholic l iver cirrhosis and severe resting arterial hypoxaemia (arterial oxygen tension (Pa,O-2) 7.5 kPa) whilst breathing air and 100% O-2 using con ventional blood gas (CBG) analysis, the multiple inert gas elimination technique (MIGET) and whole body seintigraphy (WBS) following the i.v . administration of radiolabelled boli of macroaggregates with a minim um diameter of 15 mu M. During air breathing, there was a consistently positive difference between the arterial oxygen tension predicted by MIGET and that actually measured (P-M Pa,O-2, average 0.9 kPa). During O-2 breathing, P-M Pa,O-2 became negative, (average -12.2 kPa), and s hunt estimated by the O-2 method (% of Q') was consistently less than that measured by MIGET. Whereas both O-2 method and MIGET estimates of shunt never exceeded 25%, the WBS shunt was 40%, indicating that a su bstantial fraction of cardiac output flowed through abnormally dilated pulmonary vessels, some of which were exposed to alveolar gas and, he nce, participated in gas exchange. Although our observations pertain t o one subject, we believe they provide the most convincing in vivo evi dence to date that abnormal dilatation of interalveolar vessels may, p er se, result in a significant diffusion impairment for O-2. Furthermo re, in view of the consistently negative P-M Pa,O-2 observed during ox ygen breathing, we speculate that such abnormal vascular dilatation ma y also have produced a significant diffusive impairment of one or more of the less soluble inert gases used in the MIGET analysis.