Abstract Chronic obstructive pulmonary disease is defined as a situation of progressive airflow limitation, sometimes reversible, whose pathogenetic mechanisms responsible are to be attributed, on the one hand, to the progressive obstruction of the central and peripheral airways, with structural modification of their histological status and, secondly, to a progressive destruction of the elastic component of the parenchymal tissue, with loss of alveoli and pulmonary capillaries. It follows that such a combination of inflammatory insults at the level of the bronchial and bronchiolar airways and loss of alveoli and capillaries, inevitably, leads to a progressive inefficiency of intrapulmonary gas exchange, which may be different if we keep into account the different phenotypic manifestations of the disease, especially in its early onset. In this review, we try to go beyond what it is commonly declared in the GOLD statement thatrather than regular arterial blood gases analysis, it would be more sensible to use pulse oximetry as a screening test since this is a simple, cheap, painless and non-invasive technique which is fairly accurateand perform arterial blood gas analysis only on patients with an arterial saturation of less than 92% and in patients with suspected CO2 retention, although this will rarely be present in the absence of arterial hypoxaemia and desaturation and in stable patients with FEV1< 50% predicted or with clinical signs of right heart failure. Since this statement seems to minimize the issue of gas exchange in COPD, with this review, which deals with all the aspects of gas exchange impairment and all the tests it is possible to execute, we would like to refresh

Pulmonary Gas Exchange in Chronic Obstructive Lung Disease

Renato Prediletto
2014

Abstract

Abstract Chronic obstructive pulmonary disease is defined as a situation of progressive airflow limitation, sometimes reversible, whose pathogenetic mechanisms responsible are to be attributed, on the one hand, to the progressive obstruction of the central and peripheral airways, with structural modification of their histological status and, secondly, to a progressive destruction of the elastic component of the parenchymal tissue, with loss of alveoli and pulmonary capillaries. It follows that such a combination of inflammatory insults at the level of the bronchial and bronchiolar airways and loss of alveoli and capillaries, inevitably, leads to a progressive inefficiency of intrapulmonary gas exchange, which may be different if we keep into account the different phenotypic manifestations of the disease, especially in its early onset. In this review, we try to go beyond what it is commonly declared in the GOLD statement thatrather than regular arterial blood gases analysis, it would be more sensible to use pulse oximetry as a screening test since this is a simple, cheap, painless and non-invasive technique which is fairly accurateand perform arterial blood gas analysis only on patients with an arterial saturation of less than 92% and in patients with suspected CO2 retention, although this will rarely be present in the absence of arterial hypoxaemia and desaturation and in stable patients with FEV1< 50% predicted or with clinical signs of right heart failure. Since this statement seems to minimize the issue of gas exchange in COPD, with this review, which deals with all the aspects of gas exchange impairment and all the tests it is possible to execute, we would like to refresh
2014
Gas exchange
COPD
Hypoxemia
Hypocapnia
VA/Q relationships
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/277859
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