Impairment of gas exchange in liver cirrhosis

Abstract

even at rest when TL,CO falls below about 50% of predicted, and Agustí's patients did not have pulmonary vascular malformations. Perhaps the subject of Crawford's study has lung disease in addition to vascular malformations, and both contribute to the hypoxaemia. Interpretation of radiolabelled particle distributionThe authors used albumin aggregates whose diameters were stated to range from 15 µm to 50 µm. Assuming radioactivity relates to particle mass, not diameter, 50 µm particles would be 37 times hotter than 15 µm particles ((50/15) 3 = 37). If the abnormal vascular channels at their narrowest exceeded 50 µm diameter, this inhomogeneity of size may have posed no problem. If any were less than 50 µm but greater than 15 µm, the hottest particles would have been preferentially caught in the lungs. Thus, without knowing the anatomy of the abnormal vessels or the distribution of particle sizes between 15 and 50 µm, there is a potential interpretative limitation on using the radioactive particle data to quantitatively assess the vascular shunts. Of interest, this would if anything underestimate the shunt, already computed to be about 40%. Interpretation of inert gas (MIGET) dataSeveral issues arise. The authors argue that the room air data suggest diffusion limitation for O 2 because the inert gases, generally considered to be invulnerable to diffusion limitation, predict a higher arterial oxygen tension (Pa,O 2 ) than was measured [13]. This result agrees with EDELL et al. [8] and CASTAING and MANIER [14] (and many other MIGET-based studies in other settings). The low TL,CO is consistent with this. However, whether the dilated vascular channels are the site of this limitation is uncertain. It is hard to imagine how these channels reduce total lung TL,CO to 34% of predicted if indeed the alveolar parenchyma is otherwise normal. Thus, hypothetically abnormal parenchyma could explain the observations rather than limited O 2 exchange across the abnormal vessels. There are thus two competing hypotheses and it would seem that they cannot be distinguished from the present data.The 100% O 2 breathing data are particularly intriguing and the higher measured-than-MIGET-predicted Pa,O 2 is used by the authors as evidence of diffusion limitation of the inert gases, especially the least soluble gas, sulphur hexafluoride (SF6). However, while the diffusion Eur Respir J, 1995, 8, 1993 DOI: 10.1183 ISSN 0903 -1936 The paper in this issue by CRAWFORD et al..08121993 Printed in UK -all rights reserved Copyright ©ERS Journals Ltd 1995 European Respiratory Journal[1] addresses a problem that has vexed clinicians and physiologists for many years: In cirrhosis, the presence and mechanisms of hypoxaemia, usually more severe in the upright posture, and without evidence of classical lung disease, such as obstructive or restrictive syndromes. Ever since abnormally dilated pulmonary blood vessels were first identified in such patients [2], studies have focused on the obvious potential connection between such functional shunts and hy...

Pulmonary–Hepatic vascular Disorders (PHD)

“…Pa,O 2 w40 kPa (w300 mmHg)) observed in many patients. Diffusion impairment to oxygen, as shown by a greater predicted (according to the multiple inert gas elimination technique) [42] than measured Pa,O 2 [40,41] while breathing room air, is also present in advanced HPS, a mechanism also consistent, in part, with the common finding of a low diffusing capacity of the lung for carbon monoxide (DL,CO). It is of note that the presence of an elevated Q9 facilitates, in part, this favourable Pa,O 2 response to breathing 100% oxygen, other things being equal.…”

“…However, the relative contributions of the former three determinants appear to vary. Although it is agreed that V9A/Q9 mismatching is the pivotal mechanism for arterial deoxygenation since it fits well with the presence of lung regions in which alveoli are normally ventilated but overperfused, the relevance of the other two factors remains somewhat speculative [41]. An added conceptual difficulty is the reconciliation of the presence of elevated levels of increased intrapulmonary shunt (i.e.…”

Pulmonary vascular disorders in portal hypertension

“…The magnitude of the shunt can be estimated by calculating the ratio of systemic to total body radioactivity. Estimations obtained using this method exceed by far the functional estimates provided by the oxygen method [64,66,76]. This may be because dilated intrapulmonary vessels may continue to participate in gas exchange, especially when the driving pressure is increased by the administration of pure oxygen.…”

“…Other mechanisms, such as decrease in the affinity of haemoglobin for oxygen and portopulmonary shunt, have been essentially dismissed as causes of severe hypoxaemia in HPS [63]. However, CRAWFORD et al [65] and WAGNER [66] have recently highlighted the complexity of hypoxaemia caused by cirrhosis and suggested that we still do not have the tools to understand fully its mechanism.…”

The hepatopulmonary syndrome: NO way out?: Fig. 1.—

“…As with other lung disorders, hypoxaemia results from impaired gas exchange, which, in HPS, is particularly perturbed by excessive and widespread dilatation of intrapulmonary vessels. After decades of careful investigations, the underlying mechanisms linking altered gas exchange and pulmonary vasodilatation are now well delineated [2][3][4]. Reduced tone causing vascular relaxation occurs at both ends of the capillary bed, i.e.…”