Hypoxemia of cirrhosis

Wolfe, James; Tashkin, Donald P.; Holly, F. Eugene; Brachman, Michael B.; Genovesi, Michael G.

doi:10.1016/0002-9343(77)90161-9

Cited by 140 publications

(8 citation statements)

References 36 publications

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“…As observed in our current subject, these patients typically show a substantial increase in Pa,O 2 on breathing 100% oxygen, and measurements of intrapulmonary "anatomical" shunt using the radionuclide macroaggregate technique substantially exceed functional estimates of shunt as measured by the O 2 method [2,7,8]. Taken together, these observations have been interpreted as convincing evidence that diffusion-limitation of O 2 due to alveolar vascular dilatation is a significant contributory mechanism to the arterial hypoxaemia associated with liver disease [2,5,7].…”

Section: Discussionsupporting

confidence: 64%

“…Both in vivo angiography and postmortem studies of patients with liver disease and arterial hypoxaemia have consistently documented the presence of extensive pulmonary vascular dilatation, which is limited mainly to those vessels exposed to alveolar gas [1][2][3]7]. As observed in our current subject, these patients typically show a substantial increase in Pa,O 2 on breathing 100% oxygen, and measurements of intrapulmonary "anatomical" shunt using the radionuclide macroaggregate technique substantially exceed functional estimates of shunt as measured by the O 2 method [2,7,8].…”

Section: Discussionmentioning

confidence: 99%

“…Patients with significant arterial hypoxaemia and liver cirrhosis are known to have extensive pulmonary vascular dilatation, which is largely interalveolar in location [1][2][3]. It has been postulated that blood flowing through such dilated interalveolar vessels may not fully equilibrate with alveolar gas because of the increased distance between the alveolar-capillary membrane and red blood cells, resulting in a diffusive impairment to oxygen uptake [4,5].…”

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confidence: 99%

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Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

Crawford¹,

Regnis²,

Laks³

et al. 1995

Eur Respir J

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the actual presence of diffusion-limitation for oxygen. Thus, significant inequality of alveolar ventilationperfusion ratios (V'A/Q') could equally explain a marked improvement in arterial Pa,O 2 with 100% oxygen breathing. Indeed, recent studies using the multiple inert gas elimination technique (MIGET), an analysis which can indirectly detect oxygen diffusion-limitation, have attributed the arterial hypoxaemia in patients with liver cirrhosis to V'A/Q' inequality and intrapulmonary shunting [9][10][11]. However, none of these MIGET studies has providedany direct evidence of actual pulmonary vascular dilatation; and, hence, they do not, by themselves, invalidate the specific hypothesis that diffusionlimitation for oxygen can occur as a direct consequence of abnormal dilatation of interalveolar vessels.To adequately test the above hypothesis requires an experimental approach that has the power to simultaneously Eur Respir J, 1995, 8, 2015-2021 DOI: 10.1183 ABSTRACT: To test the hypothesis that diffusion-limitation for oxygen is due to abnormal vascular dilatation and significantly contributes to the arterial hypoxaemia of liver cirrhosis requires an experimental approach that detects both diffusion-limitation for oxygen and the presence of abnormal dilatation of pulmonary vessels exposed to alveolar gas. We therefore studied the gas exchange of a 64 year old man with alcoholic liver cirrhosis and severe resting arterial hypoxaemia (arterial oxygen tension (Pa,O 2 ) 7.5 kPa) whilst breathing air and 100% O 2 using conventional blood gas (CBG) analysis, the multiple inert gas elimination technique (MIGET) and whole body scintigraphy (WBS) following the i.v. administration of radiolabelled boli of macroaggregates with a minimum diameter of 15 µM.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 shunt 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 substantial fraction of cardiac output flowed through abnormally dilated pulmonary vessels, some of which were exposed to alveolar gas and, hence, participated in gas exchange.Although our observations pertain to one subject, we believe they provide the most convincing in vivo evidence to date that abnormal dilatation of interalveolar vessels may, per se, result in a significant diffusion impairment for O 2 . Furthermore, in view of the consistently negative P-M Pa,O 2 observed during oxygen breathing, we speculate that such abnormal vascular dilatation may also have produced a significant diffusive impairment of one or more of the less soluble inert gases used in the MIGET analysis. Eur Respir J., 1995Respir J., , 8, 2015Respir J., -2021

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Pulmonary vascular dilatation and diffusion-dependent impairment of gas exchange in liver cirrhosis

Crawford¹,

Regnis²,

Laks³

et al. 1995

Eur Respir J

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“…The development of a neovascularization is well known in the liver, the lungs and the skin of cirrhotic patients [Dal Palu et al, 1968;Hut chinson et al. 1968;Wolfe et al, 1977], In order to support this hypothesis in the brain an heterogeneity index was computed for each alcoholic group. The statistical study evidences a significant difference between the control subjects and groups F and C (tableVIIl).…”

Section: Discussionmentioning

confidence: 99%

“…In fact, several authors have shown that a development of arteriove nous shunts at the peripheral organ level fol lows hepatic histological alteration (cirrhosis) [Dal Palu et al, 1968;Hutchinson et al. 1968: Wolfe et al, 1977, Stanley and Cherniack [1976] have discussed, in goats, a func tional impairment in the encephalic vascu larisation following liver failure. Docs a such phenomenon also take place in the brain of human alcoholics?…”

Section: Introductionmentioning

confidence: 99%

Correlations between Cerebral Grey Matter Flow and Hepatic Histology in Alcoholism

et al. 1986

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Thirty alcoholic with a mean age of 44.8 years were examined with the intravenous 133-Xenon method for measurements of regional cerebral flow (rCBF). The results were related to liver histology and hepatic function tests. While there exists no correlation between the rCBF values and hepatic function tests, an important connection between rCBF decrease and the severity of the histological liver analysis is shown. It is suggested that the hepatic biopsy is a good criterion for the long-term evaluation of alcohol impact upon the brain of a given individual and some physiopathological mechanism are discussed.

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