Abstract
Chronic pulmonary emphysema, as one of the chronic obstructive pulmonary diseases, is known to be associated with a severe impairment of gas exchange. In an attempt to clarify the real state of impaired alveolar functions in chronic pulmonary emphysema, particularly from a standpoint of the pulmonary weighting function, the functional residual capacity (FRC) that is here considered as an actual space for gas exchange is presumed to consist of at least three functionally different groups of alveoli: 1) fast ventilated space, 2) normally ventilated space, and 3) poorly ventilated space. Under this assumption, a percentage of each space in the FRC, percent distributions of ventilation and perfusion among spaces, and ventilation-perfusion ratio in each space were measured and/or calculated and, consequently, nonuniform distributions of ventilation and perfusion throughout the lungs were revealed. This, together with a calculated percentage of the anatomic right-to-left shunts, pointed to a possible existence of a conceptional “non-ventilated space” in which the predicted ventilation-perfusion ratio would be zero.
Thus, in view of the functional subdivision of the FRC into the above four spaces, the present study was made on the nonuniform distributions of various functional parameters concerning alveolar gas exchange in case of chronic pulmonary emphysema and the data obtained were compared with those previously reported in case of bronchial asthma.
The results are summarized as follows:
1) The fast ventilated space (fast space) consisting of 7.2±3.2% of the FRC participated in 56.4±7.3% of the total ventilation and was perfused by 9.5±5.1% of the total pulmonary blood flow. The ventilation-perfusion ratio and turn over rate of this space were 5.77±1.88 and 7.74±3.86 respectively and improved only a little following the administration of bronchodilator.
2) The normally ventilated space (normal space) holding 19.9±7.3% of the FRC took part in 29.7±6.5% of the total ventilation and received 31.9±7.4% of the total pulmonary blood flow, the ventilation-perfusion ratio being 0.79±0.08. The administration of bronchodilator did not affect these values.
3) Although the poorly ventilated space (slow space) occupied 72.9±7.5% of the FRC, that is, indeed more than two thirds of the FRC, it was concerned with only 13.9±4.7% of the total ventilation and was perfused by 53.1±9.0% of the total pulmonary blood flow. Consequently, the ventilation-perfusion ratio of this space was as extremely low as 0.21±0.06 and the O2-CO2 diagram also indicated a severe impairment of alveolar gas exchange in this space. The administration of bronchodilator did not affect the volume of this space but improved a little the ventilation-perfusion ratio up to 0.26±0.08. This slight improvement apparently resulted from both a little increase in the absolute ventilation and a slight decrease in the absolute blood flow, though it was far less than the improvement observed in case of bronchial asthma in which a marked increase of the ventilation-perfusion ratio was associated with a decrease in volume of the slow space itself.
4) Presence of the “non-ventilated space” was suggested by an anatomic venous admixture rate of 5.7±2.8%. This space probably represents a group of alveoli in case of atelectasis and bullae associated with emphysema.
5) Fair correlation between the calculated A-aDO2 and a-ADCO2 and those actually measured, as evidenced by the correlation coefficients (r) of 0.876 for A-aDO2 and 0.961 for a-ADCO2, may justify the fast and normal space subdivisions as a way of analysis in evaluating the alveolar functions.
