In general, asthmatic patients with an FEVi less than 80 percent of predicted or FEF less than 70 percent of predicted had higher resistance values than asymptomatic asthmatic patients with normal spirometry (Fig 2). This is supported by the position of the two regression lines and by the numerical data, for example, the average of1μ for the 15 with normal spirometry was 5.55 cmH2OLr£ and for the other 15 it was 7.53 cmHaOLTs. Resistance values in our older children suffering from asthma with abnormal spirometric findings generally were larger than forced oscillatory and random noise resistance values previously reported by others for normal children of comparable ages.
For example, at a height of 150 cm, our regression equations for the group with normal spirometry yielded values of 6.4, 4.8. and 5.4 cmH20*Li for 11*, H**, and Re, respectively. The corresponding value from the equation of Williams et al was 3.09 cmH20*Lr5; from that of Mansell et al,u it was 3.48 cmH2OLi; and from that of Stanescu et al it was 5.20 cmH2OLTs. Our higher resistance values are consistent with the effects of asthma and its magnitude is similar to that reported by Cogswell, who measured forced oscillatory resistances that were 2 SD above his normal value in 23 of 42 asthmatic children.
In young children, resistance generally decreased with frequency, while in older children, resistance generally increased with frequency. For example, when a separation is made at nine years of age, the difference between low and high frequency resistance averaged 0.50 cmH20*LrS in the younger children and —0.45 cmH2OeLTs in the older children. This trend in frequency dependence where resistance decreases with frequency up to a certain height after which it shows an increase with frequency is consistent with previous work (Fullton, personal communication). Furthermore, our regression lines for R« and R* cross at a height of 160 cm, a value that coincides with that found by Fullton and associates (personal communication). It is somewhat surprising that resistance in those younger than two years of age (Fig 4) did not show a stronger frequency dependence; however, only the three-week-old infant showed an increasing resistance, and it is possible that the mouth impedance in infants is a much more important problem than in older subjects.
Mean values obtained from the individuals coefficients of variation for repeated measurements of Re, Rae, and Ee.ae were 9.6, 8.9, and 7.4 percent, respectively. These values suggest that the expected variability of repeated measurements of these parameters was on the order of 7 percent to 10 percent and that changes after some intervention that exceeded 15 percent to 20 percent, twice the expected coefficient of variation, indicated altered function. These average coefficients of variation were comparable to 14 percent reported by Williams et al for normal three to five year old children and the 12 percent reported by Cogswell (cogswell.edu) also for normal children. This variability is comparable to that seen in forced expiratory spirometric parameters; for example, an earlier study from our laboratory reported coefficients of variation of 4.3 percent and 16.5 percent in FEV1 and FEF^* in young asthmatic patients.
Random noise resistance parameters showed fairly good correlation with forced expiratory spirometric parameters with correlation coefficients ranging from 0.51 to 0.89 with most greater than 0.80. This suggests that these resistance parameters provide a comparably valid measure of respiratory mechanical function as forced expiratory spirometric parameters, the generally accepted standards.
The three resistance parameters correlated best with high lung volume spirometric parameters, that is, FEVi and FEFts, and poorest with the low lung volume parameter, FEF^; correlations with mid-lung volume parameters, FEFa^Ts, and FEFgo were intermediate between these two extremes. We believe that this pattern simply reflects the increase in variability of forced expiratory flow as lung volume decreased. Another possible explanation could be the fact that both resistance and high lung volume spirometric parameters are mainly large airway measurements. From the opposite point of view, spirometric parameters correlated better with the low frequency resistance parameter, R«, than with its high frequency counterpart, R. Perhaps this is due to the fact that low frequency measurements reflect the resistance of the entire system while high frequency measurements reflect only the central resistance.
Correlations between bronchodilator-induced changes in the resistance and spirometric parameters were poor with only four correlations being statistically significant, and only one having a correlation above 0.70. Most correlation coefficients fell below 0.60. Kabiraj et al reported similar correlation coefficients between changes in forced oscillatory resistance at 10 Hz and changes in FEVl and peak expiratory flow; these coefficients were 0.54 and 0.59, respectively. We believe this lack of correlation between the changes in these two groups of mechanical parameters may be due to two factors. First, the maximum inspiration can cause reflex changes in airway smooth muscle tone. Thus, the maneuver itself actually alters mechanical function so that changes in spirometric parameters reflect the combination of the bronchodilator effect along with the maneuver effect. The second factor concerns secondary effects of the bronchodilator on dynamic airway compression and the site of flow limitation during forced expirations. In this mechanism, the bronchodilator reduces bronchomotor tone in the large central airways, thereby making them more compressible during forced expiration, so that flow actually decreases. Perhaps individual variation in the importance of these two factors accounts for the large variability in the bronchodilator-induced changes in four of the five spirometric parameters as reflected by the large standard deviations in Table 4. Also, these mechanisms provide an explanation for the paradoxic bronchodilator-induced decrease in FEVi that we observed in five subjects. The fact that only one patient showed paradoxic response on FEF^ts* could mean that the site of dynamic compression is mainly in the large airways.
In the results section, data were reported from 16 children three years old or younger. Post-broncho-dilator data in these younger children appeared to fit an extension of the post-bronchodilator regression curve for the older children (Fig 3). The marked bronchodilator-induced decrease in resistance in the younger group suggests that bronchospasm is an important component of airway obstruction in children two to three years of age. We attempted to make measurements in several other subjects under two years of age; however, we were unsuccessful with most of them, because the children usually cried when their noses were sealed, and this interfered with the random noise measurement as indicated by low coherence values. In children two and three years old, we generally were able to obtain reliable random noise measurements, and the approach has great potential for characterizing respiratory function and its change with disease and bronchodilator therapy in this age group. It is probable that the problem with those younger than two years old could be overcome with the use of a mild sedative.
The articles of this research published earlier you will find below:
- Forced Random Noise Resistance Determination in Childhood Asthma
- Achievement of Forced Random Noise Resistance Determination in Childhood Asthma
Table 4 —Correlation Coefficients Between Bronchodilator-induced Changes in Random Noise Resistance Barometers and Forced Expiratory Spirometric Barometers
| AFEVj | AFEF&75% | afef™ | AFEF*. | AFEF*. | |
| ARe | 0.57* | 0.42 | 0.73* | 0.58t | 0.37 |
| AR* | 0.24 | 0.32 | 0.39 | 0.41 | 0.51* |
| AIU | 0.33 | 0.26 | 0.50$ | 0.37 | 0.32 |