Functional recovery of diaphragm paralysis: a long-term follow-up study.

BACKGROUND: Long-term functional outcome of diaphragm paralysis is largely unknown. METHODS: A retrospective study was conducted in 23 consecutive patients (21 males, 56+/-9 years) with uni- or bilateral diaphragm paralysis to examine whether functional respiratory recovery can be predicted from the compound motor action potential (CMAP) of the diaphragm at the time of diagnosis. Pulmonary function and CMAP were evaluated at baseline and at follow-up. CMAP amplitude and latency were recorded by surface electromyography with percutaneous electrical stimulation of the phrenic nerve. Patients were followed for (median) 15 months up to 131 months (range 5-131). Functional respiratory recovery was defined as an increase in forced vital capacity > 400 ml. RESULTS: Functional recovery occurred in 43% of the patients after 12 months (10 out of 23) and in 52% after 24 months (12 out of 23). Type and etiology of paralysis did not influence recovery. CMAP, anthropometric characteristics and baseline pulmonary function did not predict functional respiratory recovery. Whether respiratory muscle training improved pulmonary function is uncertain. Moreover, it did not result in a greater percentage functional respiratory recovery. Relapse after an initial improvement was observed in 26% of the patients. CONCLUSIONS: The present study indicates that functional recovery of diaphragm paralysis is difficult to predict and may occur years after the onset of the paralysis.

Rocuronium exacerbates mechanical ventilation-induced diaphragm dysfunction in rats.

OBJECTIVE: Nondepolarizing neuromuscular blocking agents are commonly used in the intensive care setting, but they have occasionally been associated with development of myopathy. In addition, diaphragmatic atrophy and a reduction in diaphragmatic force were reported after short-term controlled mechanical ventilation in animal models. We hypothesized that infusion of rocuronium, an aminosteroidal neuromuscular blocking agent, during 24 hrs of controlled mechanical ventilation would further alter diaphragm function and would enhance activation of the ubiquitin- proteasome pathway. DESIGN: Randomized, controlled experiment. SETTING: Basic animal science laboratory. SUBJECTS: Male Wistar rats, 14 wks old. INTERVENTIONS: Rats were divided into four groups: a control group, a group of anesthetized rats breathing spontaneously for 24 hrs, and two groups submitted to mechanical ventilation for 24 hrs, receiving a continuous infusion of either 0.9% NaCl or rocuronium. MEASUREMENTS AND MAIN RESULTS: In vitro diaphragm force was decreased more significantly after 24 hrs of mechanical ventilation combined with rocuronium infusion than after mechanical ventilation alone (e.g., tetanic force, -27%; p < .001 vs. mechanical ventilation). Similarly, the decrease in diaphragm type IIx/b fiber dimensions was more pronounced after mechanical ventilation with rocuronium treatment than with saline treatment (-38% and -29%, respectively; p < .001 vs. control). Diaphragm hydroperoxide levels increased similarly in both mechanically ventilated groups. Diaphragm muscle RING-finger protein-1 (MURF-1) messenger RNA expression, an E3 ligase of the ubiquitin-proteasome pathway, increased after mechanical ventilation (+212%, p < .001 vs. control) and increased further with combination of rocuronium (+320%, p < .001 vs. control). Significant correlations were found between expression of MURF-1 messenger RNA, diaphragm force, and type IIx/b fiber dimensions. CONCLUSIONS: Infusion of rocuronium during controlled mechanical ventilation leads to further deterioration of diaphragm function, additional atrophy of type IIx/b fibers, and an increase in MURF-1 messenger RNA in the diaphragm, which suggests an activation of the ubiquitin-proteasome pathway. These findings could be important with regard to weaning failure in patients receiving this drug for prolonged periods in the intensive care unit setting.

Endurance training improves skeletal muscle electrical activity in active COPD patients.

The effect of endurance training on muscle electrical activity during general exercise testing was investigated in physically active patients with chronic obstructive pulmonary disease (COPD). Before and after rehabilitation, patients performed identical incremental exercise tests. Pulmonary gas exchange, venous lactate and pyruvate concentrations, and the quadriceps electromyographic signal were sampled every minute throughout exercise testing. Three weeks of rehabilitation increased exercise capacity without modifying pulmonary function. M-wave amplitude, root mean square (RMS) of electromyographic activity, and RMS/oxygen uptake were increased significantly during post-rehabilitation testing at the same exercise intensity compared to pre-rehabilitation. Median frequency was significantly lower after training. These modifications reflect greater muscle excitability, greater muscle activation for the same level of exercise, and higher recruitment of slow-twitch fibers. Pulmonary rehabilitation in active COPD patients may normalize the electrical activity of skeletal muscles during incremental dynamic exercise. The electromyographic signal confirms neuromuscular changes after endurance training.

Electrophysiologic changes during exercise testing in patients with chronic obstructive pulmonary disease.

To determine whether skeletal muscle is involved in the exercise limitation of chronic obstructive pulmonary disease (COPD), we investigated electrical adaptations in muscle during incremental cycling exercise testing. Changes in quadriceps activity were compared using surface electromyography (SEMG) and motor point stimulation in ten COPD patients and ten healthy subjects. Patients showed significantly lower exercise capacity, and M-wave duration was increased from exercise onset (P < 0.05) with a parallel decrease in amplitude (P < 0.05). The SEMG power spectrum median frequency was always higher (P < 0.04) in patients and its decline was earlier (P < 0.01). The ratio of the root mean square of the SEMG to oxygen uptake was decreased (P < 0.001) during exercise in patients, although it remained constant in controls. Electromyographic parameters were significantly more involved in the exercise limitation than ventilatory factors. Thus, modified electrical activity in muscle appeared in COPD patients from exercise onset, indicating that skeletal muscle function is clearly implicated in the exercise intolerance of these patients.