Peak inspiratory flow rate after methacholine challenge in asthmatic patients and its impact on the effect of formoterol via different inhalers.

The goal of the present study was to investigate the bronchodilating effects of 6 and 12 microg formoterol delivered by the Turbuhaler, in comparison to salbutamol 200 microg (metered dose inhaler) and to controls without treatment. After inducing acute and severe bronchial obstruction by means of methacholine challenge, peak inspiratory mouth flow (PIMF) was measured through a stenosis, simulating the internal resistance of the Turbuhaler, with the in-check device. In addition the relationship was studied between PIMF and clinical response in the 3 treatment groups. In the 176 patients methacholine caused a mean fall in FEV(1) of 37.1 +/- 6.9% compared to baseline. Ten minutes after bronchodilator inhalation, FEV(1) improved significantly in all three treatment groups. At 30 minutes after bronchodilator administration, only the salbutamol 200 microg and the formoterol 12 microg groups had a significantly greater increase in FEV1 than controls (0.69 +/- 0.43 l and 0.66 +/- 0.37 l vs 0.38 +/- 0.32 l, p < 0.0005), whereas the formoterol 6 microg group showed no significant improvement (0.41 +/- 0.38 l, p = 0.74). Thirteen patients (7.4%) did not reach a minimal PIMF of 30 l/min through the in-check device after challenge. In the four patients in the formoterol 6 microg group with a PIMF below 30 l/min inhalation did not cause bronchodilation. In conclusion, the results demonstrate that 6 microg formoterol via Turbuhaler leads to less and slower onset of bronchodilation compared to the other groups in our setting. If patients fail to generate a PIMF of 30 l/min, 6 microg formoterol via Turbuhaler may provide inadequate relief in a severe asthma attack.

Influence of immersion in water on muscle function and breathing pattern in patients with severe diaphragm weakness.

STUDY OBJECTIVE: Dyspnea is a common symptom in patients with diaphragm weakness or paralysis. In particular, dyspnea may be aggravated by immersion. We hypothesized that immersion to the neck in water would decrease vital capacity and consequently increase the demand/capacity ratio of the respiratory muscles. DESIGN: Case series study. SUBJECTS: Seven patients with profound diaphragm weakness or paralysis proven by phrenic nerve stimulation, and seven normal control subjects. INTERVENTION AND MEASUREMENTS: We measured land-based and water-based spirometry, breathing pattern, and mouth occlusion pressures. RESULTS: We found that the patients could preserve minute ventilation despite a fall in vital capacity from a mean of 2.3 to 1.3 L, but this required an increased respiratory rate (RR) [21.4 to 26.7 breaths/min, p = 0.018]. We used mouth occlusion pressure 100 ms after the start of inspiration (P(0.1)) as an estimation of the drive to breath; P(0.1) increased from 1.4 to 3.9 cm H(2)O (p = 0.018) without significant change in tidal volume. CONCLUSIONS: Relative to control subjects, patients with diaphragm weakness have augmented drive to breathe in order to attempt to defend gas exchange. This conclusion is implied by the presevered minute ventilation with immersion, the augmented RR, and elevated P(0.1) relative to maximum static inspiratory pressure.