Ventilation-perfusion inequality in chronic obstructive pulmonary disease.

Wagner, Peter D.; Dantzker, David R.; Dueck, Ronald; Clausen, John A.; West, John B.

doi:10.1172/jci108630

Cited by 389 publications

(218 citation statements)

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“…Similarly, in two of the three patients with liver disease and arterial hypoxaemia recently reported by EDELL et al [10], the measured Pa,O 2 values were greater than those predicted by MIGET during O 2 breathing. These findings contrast with previously published studies using the MIGET analysis in both normal and patient groups breathing 100% O 2 , in whom the measured Pa,O 2 values were invariably substantially less than those predicted by MIGET [14,21,22]. In our own laboratory, using essentially the same experimental protocol and technical equipment as in the current study, we have never previously observed the measured Pa,O 2 to exceed that predicted by MIGET in a large number of both normal subjects and patients with varying lung disorders when breathing 100% O 2 [23].…”

Section: Discussioncontrasting

confidence: 99%

“…In our own laboratory, using essentially the same experimental protocol and technical equipment as in the current study, we have never previously observed the measured Pa,O 2 to exceed that predicted by MIGET in a large number of both normal subjects and patients with varying lung disorders when breathing 100% O 2 [23]. Indeed, inevitable leaks in the O 2 delivery system, deterioration of the arterial blood samples prior to analysis, and insensitivity of the MIGET analysis to detect physiological postpulmonary shunt should all conspire to produce a positive P-M Pa,O 2 during 100% O 2 breathing [14,21]. Particularly in view of our limited data base, experimental error could explain our observation, the most likely sources being in the actual measurement of Pa,O 2 and/or in the MIGET analysis.…”

Section: Discussionmentioning

confidence: 84%

“…Nevertheless, it has frequently been proposed that both in health and disease, diffusion-limitation of individual MIGET gases should be readily detectable by consideration of the respective retentions (R) and blood:gas partition coefficents (i.e. l) of all six gases [14,21,27]. The theoretical basis for such an approach is that, in a homogeneous gas-exchanging lung in which there is complete alveolo-capillary inert gas equilibration, the inverse of individual gas R and l values (and corresponding logarithmic transformations ln (1-R/R) and In l) are linearly related [14,26].…”

Section: Discussionmentioning

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: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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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“…They are mostly related to ventilation±perfusion mismatching [34]. However, during exercise, other mechanisms also add to the alterations in the blood gases, i.e.…”

Section: Pathophysiological Basis Of Functional Impairment In Emphysemamentioning

confidence: 99%

Physiological basis of improvement after lung volume reduction surgery for severe emphysema: where are we?

Marchand¹,

Gayan‐Ramirez²,

Leyn³

et al. 1999

Eur Respir J

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Physiological basis of improvement after lung volume reduction surgery for severe emphysema: where are we? E. Marchand, G. Gayan-Ramirez, P. De Leyn, M. Decramer. #ERJ Journals Ltd 1999. ABSTRACT: Lung volume reduction surgery has become an accepted therapeutic option to relieve the symptoms of selected patients with severe emphysema. In a majority of these patients, it causes objective as well as subjective functional improvement. A proper understanding of the physiological determinants underlying these beneficial effects appears very important in order to better select patients for the procedure that is currently largely carried out on an empirical basis.Lung volume reduction surgery has two distinct effects. Firstly, it causes an increased elastic recoil, which at least partially explains the enhanced maximal expiratory flow. Secondly, it is associated with a reduction of hyperinflation which allows for an increase in global inspiratory muscle strength and in diaphragmatic contribution to tidal volume as well as a decrease in the inspiratory elastic load imposed by the chest wall. Taken together, these effects result in a reduced work of breathing and in an enhanced maximal ventilation which both contribute to the increased exercise capacity and reduced dyspnoea after surgery. The improved lung recoil and the reduced hyperinflation after volume reduction surgery were the primary postulates upon which the usual selection criteria for the procedure were based. It is now likely that these are correct. Nevertheless, some patients do not benefit from lung volume reduction surgery and the current literature does not allow for a refinement of the selection process from a physiological point of view.The exact mechanisms underlying the improvement in lung recoil, lung mechanics, and respiratory muscle function remain incompletely understood. Moreover, the effects of lung volume reduction surgery on gas exchange and pulmonary haemodynamics still need to be more fully investigated. An analysis of the characteristics of patients who do not benefit from the procedure and the development of an animal model for lung volume reduction surgery would probably help address these important issues. Eur Respir J 1999; 13: 686±696.

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“…This gas-exchange impairment leads to a decrease in arterial oxygen partial pressure (paO 2 ), arterial oxygen saturation of hemoglobin (SaO 2 ; hypoxemia) with decreased tissue O 2 delivery. In patients with pneumonia, acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD), VQM is most relevant for the respective degree of impaired gas exchange and resulting hypoxemia (Figure 2; Wagner et al, 1974Wagner et al, , 1977West, 1995West, , 1996Preston, 2007;Tunnicliffe and Shah, 2008;Blanco et al, 2010;Cornet et al, 2010).These lung diseases have in common that in certain regions of the lung Q′ will be higher compared with V′ (V′/Q′ < 1) because…”

Section: Introductionmentioning

confidence: 99%