Chronic obstructive pulmonary disease laboratory findings

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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.

Laboratory Findings

The following laboratory findings may be seen in patients suspected to have COPD.[1][2]

Pulse Oximetry

Arterial Blood Gas (ABG)

  • ABG may show changes of hypoxemia and hypercapnia depending on the severity of disease.
  • Milder exacerbation may present only with hypoxemia without accompanied hypercapnia
  • Hypercapnia is usually seen when FEV1 falls below 1 L/s or 30% of the predicted value
  • A pH value below 7.3 usually indicates a severe exacerbation and respiratory compromise.


  • COPD patients may have hypoxemia due to the chronic underlying disease. This chronic hypoxemia may lead to polycythemia(hematocrit > 52% in men or 47% in women is diagnostic of polycythemia.
  • Correction of hypoxemia should reduce secondary polycythemia in patients who have quit smoking.

Blood Test

  • A blood test would indicate inflammation (as indicated by a raised white blood cell count and elevated C-reactive protein).
    • Neutrophils infiltrate the lung tissue, aided by damage to the airways caused by irritation.
    • Damage caused by irritation of the airways leads to inflammation and leads to neutrophils being present
    • Mucosal hypersecretion is promoted by a substance released by neutrophils
    • Further obstruction to the airways is caused by more goblet cells in the small airways. This is typical of chronic bronchitis
    • Although infection is not the reason or cause of chronic bronchitis it is seen to aid in sustaining the bronchitis.

Serum Electrolytes

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.

Sputum Culture

Human B-type Natriuretic Peptide

  • Research are ongoing on Human B-type natriuretic peptide (BNP) and pro-BNP to find if it can help to differentiate between congestive heart failure and COPD. However, no conclusive results are still drawn.

Alpha 1 Antitrypsin Levels

  • Serum alpha1 antitrypsin levels below the protective threshold value (ie, 3-7 mmol/L) lead to severe form of emphysema
  • 95% cases are due to the severe variant the Z allele present in these patients.
  • Specific phenotyping, and genetic counselling is reserved for patients in whom serum levels are 7-11 mmol/L.


  1. Lundgren FL, Cabral MM, Clímaco DC, de Macedo LG, Coelho Mde A, Dias AL (2007). "Determination of the efficacy of FEV6 as a surrogate for FVC in the diagnostic screening for chronic obstructive pulmonary disease through the comparison of FEV1/FVC and FEV1/FEV6 ratios". J Bras Pneumol. 33 (2): 148–51. PMID 17724533.
  2. MacNee W (2008). "Update in chronic obstructive pulmonary disease 2007". Am J Respir Crit Care Med. 177 (8): 820–9. doi:10.1164/rccm.200801-167UP. PMID 18390963.

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