Diffusing Capacity for Nitric Oxide and Carbon Monoxide in Patients With Diffuse Parenchymal Lung Disease and Pulmonary Arterial Hypertension: Recommendation
An interesting study was performed by Bonay et al, who investigated whether the Vcap (determined with the single-breath high/low oxygen method) would be lower in subjects with DPLD and associated PAH than in subjects with DPLD without PAH. This appeared not to be the case, thus excluding the Vcap measurement as a screening test for PAH in subjects with DPLD. In this study, the Dlno/Dlco ratios differ between the different diseases, but the overlap is great. canadian health & care mall
The equation of Roughton and Forster assumes that Dmco and Vcap are independent components by assuming that the 1/Dlco resistance is the sum of two resistances. The question is whether this is correct. Hypoxemia due to thickened membranes can lead to pulmonary vasoconstriction. Capillary flow is a prerequisite to measuring the Dmco. Some investigations in patients with IPF show that capillary density is significantly decreased in diseased areas, leading to a decrease in the Vcap component of the Dlco in addition to the already lowered Dmco component as a consequence of the diseased-thickened membranes, thus making the Vcap component dependent on the Dmco component.
This is of course difficult to assess in vivo, although some research has pointed to the dependency of the Dmco on Hb concentration, and to a relationship between Dmco and Vcap. If the Dmco and Vcap components are dependent, the separation of the Dlco in these two components becomes clinically irrelevant. In other words, the lung is defined as a monoalveolar object, with a relative contribution by the Vcap and the Dmco components. The Dlco measurement is not only a function of membrane thickness and surface area, but also (and not in the least) a function of the ventilation and perfusion inhomogeneity. In 1960, Johnson et al showed that the increase of the Dlco from rest to exercise is partly based on an increase in the Dmco. This is mainly based on improved matching of ventilation and perfusion than on the recruitment of alveoli. Furthermore, ventilation and perfusion inhomogeneity is the main determinant of the Dlco in patients with asthma.
If indeed the Dlno is more sensitive than the Dlco in detecting specific disturbances of the alveolocapillary membrane, then the decreased Dlco in patients with PAH and DPLD is probably due to ventilation and perfusion inhomogeneity instead of to decreased passage through the alveolocapillary membrane. In conclusion, although the overlap is large, we observed a statistically significant difference in Dlno/Dlco ratios between patients with PAH and patients with DPLD. The Dlno/Dlco ratio in patients with PAH was significantly higher than that of healthy volunteers.