The Diffusing Capacity of the Lung for Carbon Monoxide (DLCO) test measures the efficiency of gas transfer from the air sacs of the lungs into the bloodstream. Asthma is a chronic inflammatory condition primarily affecting the airways, leading to obstruction and hyper-responsiveness. While most severe lung diseases significantly reduce the DLCO, asthma often presents a counter-intuitive finding: the DLCO remains normal or is subtly increased. This unexpected result provides a crucial diagnostic clue and highlights unique physiological changes in the asthmatic lung.
Understanding the DLCO Measurement
The DLCO test is a standard component of pulmonary function testing, designed to assess the functional integrity of the alveolar-capillary membrane. During the test, a patient inhales a gas mixture containing a small amount of carbon monoxide (CO) and holds their breath for approximately ten seconds. Because CO binds to hemoglobin much more readily than oxygen, it serves as an excellent tracer gas to measure how quickly gas moves from the alveoli into the red blood cells within the pulmonary capillaries.
The final DLCO result is a calculated value influenced by three primary physiological factors that determine gas transfer. The first is the total alveolar surface area available for gas exchange, which represents the expansive interface between air and blood. The second factor is the thickness of the alveolar-capillary membrane, as scarring or fluid buildup increases the distance the gas must travel.
The third and most variable factor is the pulmonary capillary blood volume, which represents the amount of blood in the capillaries available to take up the test gas. The capacity of the blood to absorb CO depends directly on the total amount of hemoglobin present in the capillaries during the test. Changes in this vascular component can profoundly affect the overall DLCO measurement, even if the alveolar structure remains intact.
The Primary Mechanism: Increased Pulmonary Capillary Blood Volume
The observation of a normal or elevated DLCO in asthma is largely attributed to an increase in the volume of blood within the pulmonary capillaries. This change is directly related to the chronic inflammatory processes occurring in the asthmatic airway. Chronic inflammation involves the release of various chemical mediators and immune cells that directly affect the surrounding blood vessels.
These inflammatory mediators, such as histamine and nitric oxide, cause vasodilation, or the widening of local blood vessels, particularly in the bronchial circulation. This increased blood flow within the lung tissue means more hemoglobin is present to rapidly bind the inhaled carbon monoxide. The greater availability of hemoglobin increases the measured rate of CO uptake, leading to a higher calculated DLCO value.
The body’s response to airway obstruction also contributes to increased blood volume through blood flow redistribution. In asthma, airways narrow due to bronchoconstriction, causing poor ventilation in certain lung regions. When alveoli are poorly ventilated, the body initiates a protective reflex called hypoxic vasoconstriction, causing blood vessels supplying those areas to constrict.
This constriction diverts blood away from poorly ventilated areas toward lung regions that are better ventilated. This shunting action increases the blood flow and volume in the capillaries surrounding the healthy, open alveoli. The resulting increase in effective surface area and blood volume available for gas exchange contributes significantly to the elevated overall DLCO measurement.
DLCO Findings in Asthma Versus Other Lung Conditions
The preserved or elevated DLCO in asthma serves as a crucial differentiating factor when diagnosing obstructive lung diseases. Other common conditions that cause shortness of breath often show a characteristically low DLCO, which helps clinicians distinguish between diagnoses. The structural integrity of the alveoli remains largely intact in asthma, which is why the gas exchange capacity is maintained or enhanced.
In contrast, patients with emphysema, a form of Chronic Obstructive Pulmonary Disease (COPD), typically exhibit a significantly decreased DLCO. Emphysema involves the physical destruction of the alveolar walls, permanently reducing the surface area available for gas transfer. This loss of gas exchange architecture directly lowers the diffusing capacity, providing a clear distinction from asthma.
Similarly, restrictive lung diseases such as pulmonary fibrosis and Interstitial Lung Disease (ILD) cause a reduction in DLCO through a different mechanism. These conditions involve thickening and scarring of the alveolar-capillary membrane, which creates a physical barrier that gases must struggle to cross. The increased thickness of this membrane directly impedes the diffusion process, leading to a low DLCO reading that contrasts with the findings in asthma.