Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease

To compare data derived from a computer model of the pulmonary circulation with data from a case series of patients with chronic obstructive pulmonary disease (COPD). To evaluate the specific factors contributing to CO2 retention due to oxygen therapy in patients with acute exacerbations of COPD. Da...

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Vydané v:Critical care medicine Ročník 24; číslo 1; s. 23
Hlavní autori: Hanson, 3rd, C W, Marshall, B E, Frasch, H F, Marshall, C
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 01.01.1996
Predmet:
Blood Pressure
Carbon Dioxide - blood
Computer Simulation
Humans
Hypercapnia - etiology
Hypercapnia - physiopathology
Lung Diseases, Obstructive - blood
Lung Diseases, Obstructive - physiopathology
Lung Diseases, Obstructive - therapy
Oxygen - blood
Oxygen Inhalation Therapy - adverse effects
Pulmonary Artery - physiopathology
Pulmonary Circulation
Vasoconstriction
Ventilation-Perfusion Ratio
ISSN:0090-3493
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Popis
Shrnutí:To compare data derived from a computer model of the pulmonary circulation with data from a case series of patients with chronic obstructive pulmonary disease (COPD). To evaluate the specific factors contributing to CO2 retention due to oxygen therapy in patients with acute exacerbations of COPD. Data from a computer model of the pulmonary circulation were compared with a previous case series. Patient data were derived from previous case series. Simulated application of oxygen therapy. The computer model of the pulmonary circulation generates data comparable with those data from a series of patients with COPD treated with supplemental oxygen and permits identification of the causes for hypercarbia. Therapy with supplemental oxygen alters hypoxic pulmonary vasoconstriction and modulates the Haldane effect, resulting in changes in physiologic deadspace. Changes in physiologic deadspace are sufficient to account for the hypercarbia developed by patients with acute exacerbations of COPD when treated with supplemental oxygen.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0090-3493
DOI:10.1097/00003246-199601000-00007