Mechanisms of worsening gas exchange during acute exacerbations of chronic obstructive pulmonary disease
Author
dc.contributor.author
Barberà, J. A.
Author
dc.contributor.author
Roca, J.
Author
dc.contributor.author
Ferrer, A.
Author
dc.contributor.author
Félez, M. A.
Author
dc.contributor.author
Díaz, O.
Author
dc.contributor.author
Roger, N.
Author
dc.contributor.author
Rodriguez-Roisin, R.
Admission date
dc.date.accessioned
2019-01-29T15:55:05Z
Available date
dc.date.available
2019-01-29T15:55:05Z
Publication date
dc.date.issued
1997
Cita de ítem
dc.identifier.citation
European Respiratory Journal, Volumen 10, Issue 6, 2018, Pages 1285-1291
Identifier
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09031936
Identifier
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10.1183/09031936.97.10061285
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/162777
Abstract
dc.description.abstract
This study was undertaken to investigate the mechanisms that determine abnormal gas exchange during acute exacerbations of chronic obstructive pulmonary disease (COPD). Thirteen COPD patients, hospitalized because of an exacerbation, were studied after admission and 38±10(±SD) days after discharge, once they were clinically stable. Measurements included forced spirometry, arterial blood gas values, minute ventilation (V'E), cardiac output (Q̄'), oxygen consumption (V'O2), and ventilation/perfusion (V'A/Q') relationships, assessed by the inert gas technique. Exacerbations were characterized by very severe airflow obstruction (forced expiratory volume in one second (FEV1) 0.74±0.17 vs 0.91±0.19 L, during exacerbation and stable conditions, respectively; p=.0.01), severe hypoxaemia (ratio between arterial oxygen tension and inspired oxygen fraction (Pa,O2/F(I,O2) 32.7±7.7 vs 37.6±6.9 kPa (245±58 vs 282±52 mmHg); p=0.01) and hypercapnia (arterial carbon dioxide tension (Pa,(CO2)) 6.8±1.6 v