Chest wall stiffness in patients with chronic respiratory muscle weakness.

Using the weighted spirometer technique we studied chest wall compliance (Cw) in 16 nonobese patients with chronic weakness of the respiratory muscles and 20 healthy control subjects. In order to evaluate the validity of the technique, while Cw was being measured, we monitored thoracoabdominal configuration with 2 pairs of linearized magnetometers and electrical activity of the external oblique with a concentric needle electrode in 3 healthy subjects and 4 patients; in addition, we recorded in 3 subjects the electrical activity from the intercostal muscles and diaphragm throughout the procedure. The method was reproducible within 5.8% and provided Cw values that compared well with those yielded by the relaxation technique. In each subject, the weight-induced shifts in end-expiratory lung volume showed a very good linear correlation with the changes in transrespiratory pressure at end-expiration (r greater than or equal to 0.91). In addition, in none of the subjects tested did the electromyograms reveal any intercostal, diaphragmatic, or abdominal muscle activity at end-expiration, nor did the end-expiratory level ever show a significant departure from the relaxed thoracoabdominal configuration, thus suggesting adequate respiratory muscle relaxation. The reduction in inspiratory muscle force in the patients ranged from 17 to 94% of predicted (mean +/- SE, 43 +/- 6). The decrease in vital capacity, total lung capacity, and functional residual capacity averaged 59, 34, and 15% of predicted, respectively. Both the patient and the control groups showed a large interindividual variability regarding Cw. It varied from 0.117 to 0.258 L/cm H2O (mean +/- SE, 0.162 +/- 0.012) in the patients and from 0.163 to 0.366 L/cm H2O (mean +/- SE, 0.248 +/- 0.013) in the healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Function of respiratory muscles during partial curarization in humans.

The effects of submaximal neuromuscular blockade (SMNB) on the recruitment (or derecruitment) of the respiratory muscles during different types of respiratory maneuvers were studied in four healthy males infused slowly with pancuronium. The effects on lung mechanics were similar to those observed previously in that lung recoil pressure during inspiration did not change while the chest wall pressure-volume (PV) curve was shifted to the right (Rahn diagram). In each subject, SMNB produced a large increase in abdominal (gastric) and transdiaphragmatic pressures at any given lung volume during inspiration, reflecting greater diaphragmatic contribution to respiratory pressure swings. In addition, using concentric needle electrodes, we observed a marked fall in electrical (tonic and phasic) activity in the abdominal and in the intercostal/accessory muscles during SMNB but a slight increase in diaphragmatic activity. This pattern of changes was accentuated as ventilation increased. These findings indicate that the diaphragm is more resistant to curare than the other respiratory muscles in humans and that the transposition of the chest wall PV curve during SMNB is related to a loss of tonic activity in the intercostal musculature. The difference in sensitivity toward curare between the diaphragm and the other respiratory muscles is probably related to a difference in the safety margin at the neuromuscular synapses.

The interaction between the diaphragm, intercostal/accessory muscles of inspiration and the rib cage.

During Mueller maneuvers (MM), the volume change of rib cage, delta Vrc, and abdomen, delta Vab, are equal and opposite. Thus delta Vrc = -delta Vab. Substituting delta Prc.Crc for delta Vrc and delta Pab.Cab for delta Vab yields: delta Prc = - delta Pab.Cab/Crc, where delta Prc, delta Pab, Crc and Cab are applied pressures and compliances of rib cage and abdomen respectively. MM performed solely with the diaphragm permits calculations of Prc in terms of observed changes in Pab and pleural pressure, Ppl. Three trained subjects performed MM with no evidence of inspiratory intercostal or abdominal muscle contraction. During the diaphragmatic MM delta Pab was positive and delta Prc negative. The magnitude of delta Prc/delta Pab was 2-6 times greater than that of delta Ppl/delta Pab. We conclude that neither Pab nor Ppl by themselves displace the relaxed rib cage during Mueller maneuvers. A model in which the diaphragm acts both in parallel and in series with the rib cage, and in which Prc is the sum of Pab and a pressure lying between Pab and Ppl explains these results as well as the hypothesis that Pab displaces the relaxed rib cage during quiet breathing.

[Significance of electromyography of the diaphragm in respiratory physiopathology]. / Intérêt de l'électromyographie du diaphragme en physiopathologie respiratoire.

Adequate electromyographic method are available in order to record the electrical activity of the vertebral (oesophageal surface electrodes) and the right or left costal (concentric needle electrodes) parts of the diaphragm and in order to stabilize the EMG's base line (rejection of the electrical movement's artefacts by means of RC filters). The electromyographic patterns of the agonistic and antagonistic activity of the diaphragm in normal subjects have been clearly defined in different circumstances such as quiet ventilation and hyperventilation. Disturbances of the ventilatory diaphragmatic activity have been demonstrated by electromyography in different diseases: broncho-pneumopathies; supraspinal disorders, myopathies. In normal subjects, global motor responses of the diaphragm to the electrical stimulation of each phrenic nerve can be easily recorded with surface electrodes located in the oesophageal hiatus or placed over the lower intercostal spaces. The phrenic nerve conduction times was measured in 30 normal adults. The average value of this parameter was 7,5 +/- 0,53 msec for excitation on the right side and 8,2 +/- 0,71 on the left. The measurement of the phrenic nerve conduction time seems to provide a sensitive index of involvement of the nerve in diaphragmatic dyskinesias. Prolongation of conduction time was demonstrated in phrenic lesions of various aetiologies such as: peripheral polyneuropathies, traumatic sequelae, mediastinal tumors, phrenic neuritis or idiopathic diaphragmatic paresis. Electrical phrenic stimulation and prostigmin have permitted to establish the diagnosis of myasthenic bloc of the phrenodiaphragmatic transmission.