Chronic obstructive pulmonary disease Microchapters |
Differentiating Chronic obstructive pulmonary disease from other Diseases |
---|
Diagnosis |
Treatment |
Case Studies |
Chronic obstructive pulmonary disease laboratory findings On the Web |
American Roentgen Ray Society Images of Chronic obstructive pulmonary disease laboratory findings |
FDA on Chronic obstructive pulmonary disease laboratory findings |
CDC on Chronic obstructive pulmonary disease laboratory findings |
Chronic obstructive pulmonary disease laboratory findings in the news |
Blogs on Chronic obstructive pulmonary disease laboratory findings |
Directions to Hospitals Treating Chronic obstructive pulmonary disease |
Risk calculators and risk factors for Chronic obstructive pulmonary disease laboratory findings |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Philip Marcus, M.D., M.P.H. [2]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [3]
Chronic obstructive pulmonary disease has irreversible airflow limitation specially during forced expiration. This is due to the destruction of lung tissue and increase in resistance to flow in the conducting airways. Thus, it doesn't show an improvement in FEV1 post bronchodilator administration (unlike asthma). This characteristic feature is used as an diagnostic criteria for COPD, i.e. a COPD is diagnosed by spirometry if FEV1/FVC < 70% for a matched control. Arterial blood gas may show hypoxemia with or without hypercapnia depending on the disease severity. pH may be normal due to renal compensation. A pH less than 7.3 usually indicate severe respiratory compromise. A blood sample taken from an artery, i.e. Arterial Blood Gas (ABG), can be tested for blood gas levels which may show low oxygen (hypoxaemia) and/or high carbon dioxide (respiratory acidosis if pH is also decreased). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia.
The following laboratory findings may be seen in patients suspected to have COPD.[1][2]
COPD patients have irreversible obstruction of airway that causes retention of carbon-dioxide. This in turn causes them to develop chronic respiratory acidosis. To compensate for this the body may develop metabolic alkalosis that leads to increased bicarbonate production. Bicarbonate levels act as useful indicator of disease progression.