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
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.