Sheng Yan

Contractile Properties of the Human Diaphragm during Chronic Hyperinflation

BACKGROUND In patients with chronic obstructive pulmonary disease (COPD) and hyperinflation of the lungs, dysfunction of the diaphragm may contribute to respiratory decompensation. We evaluated the contractile function of the diaphragm in well-nourished patients with stable COPD, using supramaximal, bilateral phrenic-nerve stimulation, which provides information about the strength and inspiratory action of the diaphragm. METHODS In eight patients with COPD and five control subjects of similar age, the transdiaphragmatic pressure generated by the twitch response to phrenic-nerve stimulation was recorded at various base-line lung volumes, from functional residual capacity to total lung capacity, and during relaxation and graded voluntary efforts at functional residual capacity (twitch occlusion). RESULTS At functional residual capacity, the twitch transdiaphragmatic pressure ranged from 10.9 to 26.6 cm of water (1.07 to 2.60 kPa) in the patients and from 19.8 to 37.1 cm of water (1.94 to 3.64 kPa) in the controls, indicating considerable overlap between the two groups. The ratio of esophageal pressure to twitch transdiaphragmatic pressure, an index of the inspiratory action of the diaphragm, was -0.50 +/- 0.05 in the patients, as compared with -0.43 +/- 0.02 in the controls (indicating more efficient inspiratory action in the patients than in the controls). At comparable volumes, the twitch transdiaphragmatic pressure and esophageal-to-transdiaphragmatic pressure ratio were higher in the patients than in normal subjects, indicating that the strength and inspiratory action of the diaphragm in the patients were actually better than in the controls. Twitch occlusion (a measure of the maximal activation of the diaphragm) indicated near-maximal activation in the patients with COPD, and the maximal transdiaphragmatic pressure was 106.9 +/- 13.8 cm of water (10.48 +/- 1.35 kPa). CONCLUSIONS The functioning of the diaphragms of the patients with stable COPD is as good as in normal subjects at the same lung volume. Compensatory phenomena appear to counterbalance the deleterious effects of hyperinflation on the contractility and inspiratory action of the diaphragm in patients with COPD. Our findings cast doubt on the existence of chronic fatigue of the diaphragm in such patients and therefore on the need for therapeutic interventions aimed at improving diaphragm function.

Association of chest wall motion and tidal volume responses during CO2 rebreathing

The purpose of this study is to investigate the effect of chest wall configuration at end expiration on tidal volume (VT) response during CO2 rebreathing. In a group of 11 healthy male subjects, the changes in end-expiratory and end-inspiratory volume of the rib cage (delta Vrc,E and delta Vrc,I, respectively) and abdomen (delta Vab,E and delta Vab,I, respectively) measured by linearized magnetometers were expressed as a function of end-tidal PCO2 (PETCO2. The changes in end-expiratory and end-inspiratory volumes of the chest wall (delta Vcw,E and delta Vcw,I, respectively) were calculated as the sum of the respective rib cage and abdominal volumes. The magnetometer coils were placed at the level of the nipples and 1-2 cm above the umbilicus and calibrated during quiet breathing against the VT measured from a pneumotachograph. The delta Vrc,E/delta PETCO2 slope was quite variable among subjects. It was significantly positive (P < 0.05) in five subjects, significantly negative in four subjects (P < 0.05), and not different from zero in the remaining two subjects. The delta Vab,E/delta PETCO2 slope was significantly negative in all subjects (P < 0.05) with a much smaller intersubject variation, probably suggesting a relatively more uniform recruitment of abdominal expiratory muscles and a variable recruitment of rib cage muscles during CO2 rebreathing in different subjects. As a group, the mean delta Vrc,E/delta PETCO2, delta Vab,E/delta PETCO2, and delta Vcw,E/delta PETCO2, slopes were 0.010 +/- 0.034, -0.030 +/- 0.007, and -0.020 +/- 0.032 1/Torr, respectively; only the delta Vab,E/delta PETCO2, slope was significantly different from zero. More interestingly, the individual delta VT/delta PETCO2 slope was negatively associated with the delta Vcr,E/delta PETCO2 (r = 0.68, P = 0.021) and delta Vcw,E/delta PETCO2 slopes (r = 0.63, P = 0.037) but was not associated with the delta Vab,E/delta PETCO2 slope (r = 0.40, P = 0.223). There was no correlation of the delta Vrc,E/delta PETCO2 and delta Vcw,E/delta PETCO2 slopes with age, body size, forced expiratory volume in 1 s, or expiratory time. The group delta Vab,I/delta PETCO2 slope (0.004 +/- 0.014 1/Torr) was not significantly different from zero despite the VT nearly being tripled at the end of CO2 rebreathing. In conclusion, the individual VT response to CO2, although independent of delta Vab,E, is a function of delta Vrc,E to the extent that as the delta Vrc,E/delta PETCO2 slope increases (more positive) among subjects, the VT response to CO2 decreases. These results may be explained on the basis of the respiratory muscle actions and interactions on the rib cage.

Modified Campbell diagram to assess respiratory muscle action in speech

Ten normal and four moderate to severe stutterers participated in the study. Pleural (Ppl) and abdominal (Pab) pressure was studied using oesophageal and gastric balloon catheter systems and VL (VL) was studied using magnetometry. The classical Campbell diagram was modified by plotting Pab versus VL. In a preliminary study we determined whether a surrogate curve could be substituted for the true curve in the Campbell diagram. We obtained true relaxation curves in six subjects. We obtained surrogate chest wall relaxation curves by joining the Pab value at functional residual capacity (FRC) to a point on the dynamic expiratory Pab,VL curve where Pab had decreased to half its maximum inspiratory excursion. In order to obtain the mirror image of the elastic recoil curve of the lung subjects breathed slowly from FRC to total lung capacity. Dynamic Pab,VL and Ppl,VL measurements during quiet breathing and speech were superimposed on static lung and chest wall curves. The simultaneous plot of Ppl and Pab provided a continuous measure of transdiaphragmatic pressure as a function of VL. We inferred non‐diaphragmatic muscle recruitment vis‐à‐vis the diaphragm by the relationship of Pab to Ppl and Pab to the relaxation curve. We compared dynamic Ppl during phonation with that during breath‐holding with the glottis open at the same VL, as an estimate of subglottic pressure (Psg). Analysis of variance testing showed that the true, surrogate and predicted relaxation slopes were not significantly different. The strategies that stutterers used to speak were either higher or lower VL than normal subjects and they had a different pattern of respiratory muscle recruitment. Stutterers were unable to achieve the appropriate degree of recruitment to develop and maintain a normal Psg for conversational speech and this contributed to dysfluency. We conclude that the quiet breathing loops can provide a reasonable approximation to the relaxation curve in normal healthy subjects and that modifications to the Campbell diagram provide useful means of measuring Psg and assessing respiratory muscle recruitment patterns.