The pulmonary function in bronchial asthma was analysed from three new viewpoints; 1) arterial-alveolar carbon dioxide tesion difference, 2) expiratory carbon dioxide distribution curve and carbon dioxide (%)-air flow-volume curve, 3) changes of viscous resistance throughout the respiratory cycle, the inspiratory dynamic resistance and the difference of the coefficient of laminar flow resistance (K
1) and the coefficient of turbulant flow resistance (K
2). At the same time the reversibility which is characteristic of bronchial asthma was analysed.
1) Arterial-Alveolar Carbon Dioxide Tension Difference
Expired air was sampled by four different methods consisting of end-tidal method, Haldane-Priestley method, breath-holding method and rebreathing method, and was served for carbon dioxide measurement by means of Capnograph. It was found that end-tidal method was the most adequate for the measurement of P
ACO2 in bronchial asthma. The peak of end-tidal P
CO2 was regarded as the mean alveolar carbon dioxide tension, and this was subtracted from the arterial carbon dioxide tension measured by Combianalyser to obtain arterial-alveolar carbon dioxide tension difference. The mean arterial-alveolar carbon dioxide tension difference in 15 cases of bronchial asthma was 6.5±2.7mmHg, which approached to zero by administering bronchodilators manifesting the presence of reversibility. The difference between arterial and alveolar carbon dioxide tension suggested that the formerly believed evenness of the pulmonary blood distribution in the patients of bronchial asthma was erroneous, and this assumption was proved in one case using the oxgen saturation method of Briscoe, et al.
Further observations on the arterial and alveolar carbon dioxide lead to the conclusion that the estimation of arterial carbon dioxide tension from alveolar carbon dioxide tension is impossible in the cases with bronchial asthma where the wide variation of arterial-alveolar carbon dioxide tension difference is present.
2) Expiratory Carbon Dioxide Distribution Curve and Carbon Dioxide (%)-Air Flow-Volume Curve
The expiratory carbon dioxide distribution curves in the normal and emphysematous individuals assume characteristic patterns, each falling within certain range. In these cases, diagnosis and classification of severity can be carried out by the combined use of FEV
1CO
2 with expiratory carbon dioxide distribution curve, while expiratory carbon dioxide distribution curves in bronchial asthma fall in between those of normal and emphysematous cases with a very wide variation, and the degrees of change of the curve after administering bronchodilators are also variable according to the individual, some approaching to nearly equal to that of the normal and the others only slightly. Consequently, it is assumed that the pathophysiologic mechanism of bronchial asthma is complex.
Observations on carbon dioxde (%)-air flow-volume curves obtained by forced expiration suggested that trapped gas is expelled from relatively upper respiratory tract in some case, so that it was considered that the airway constrictions is induced simultaneously both in the upper and lower respiratory tracts in the early stage of asthmatic attack.
3) Viscous Resistance Throughout The Respiratory Cycle and Inspiratory Dynamic Resistance.
The viscous resistance throughout one respiratory cycle was measured on the curve obtained by the intraesophageal pressure method, and FEV
1/VC based on the spirogram during forced expiration does not necessaaily indicate the elevation of viscous resistance in the attack free state of bronchial asthma. Some cases of bronchial asthma showed elevation in the expiratory resistance more than the inspiratory resistance, as in chronic emphysema, while others showed elevation in the inspiratory resistance more than the exspiratory resistance,
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