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

Abstract

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

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.…”

Pulmonary blood transit time and impaired arterial oxygenation in patients with chronic liver disease

“…This suggested that hyperperfused lung regions (probably the bases) allowed rapid transit of the albumin-air microbubble complexes in patients with an abnormal A-aDO 2 in the supine position, and that an increased CO was partially responsible. 16,18,22,23,25 In this situation (rapid transit of erythrocytes and pulmonary vasodilatation), even though capillary dilatation is not sufficient to impede the diffusion of oxygen, the time available for blood to take up oxygen molecules is reduced, and this leads to alveolocapillary oxygen disequilibrium (so-called "diffusion-perfusion" imbalance). 1,16,18 It has been reported that a considerable number of patients have mild IPVD, which can only be demonstrated by transesophageal echocardiography using agitated saline, and not by the transthoracic route that we employed.…”

Pulmonary vascular disorders in portal hypertension

“…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.…”