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 thatratherthan regular arterialbloodgasesanalysis, itwould be more sensible to use pulseoximetryas a screening test sincethisis a simple, cheap, painless and noninvasive techniquewhichisfairly accurateand performarterialblood gas analysisonly on patients with an arterialsaturation of lessthan 92% and in patients with suspected CO2retention, althoughthiswillrarely be present in the absence of arterialhypoxaemia and desaturation and in stablepatients with FEV1< 50% predicted or with clinicalsigns of right heartfailure.Sincethis statement seems to minimize the issue of gas exchange in COPD, with thisreview, whichdeals with all the aspects of gas exchangeimpairment and all the testsitispossible to execute, wewouldlike to refresh the information on an issueas the complexity of gas exchange scenario in COPD.
Pulmonary Gas Exchange in Chronic Obstructive Lung Diseases
Renato Prediletto
2014
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 thatratherthan regular arterialbloodgasesanalysis, itwould be more sensible to use pulseoximetryas a screening test sincethisis a simple, cheap, painless and noninvasive techniquewhichisfairly accurateand performarterialblood gas analysisonly on patients with an arterialsaturation of lessthan 92% and in patients with suspected CO2retention, althoughthiswillrarely be present in the absence of arterialhypoxaemia and desaturation and in stablepatients with FEV1< 50% predicted or with clinicalsigns of right heartfailure.Sincethis statement seems to minimize the issue of gas exchange in COPD, with thisreview, whichdeals with all the aspects of gas exchangeimpairment and all the testsitispossible to execute, wewouldlike to refresh the information on an issueas the complexity of gas exchange scenario in COPD.File | Dimensione | Formato | |
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