Measurement of effective elastance of the total respiratory system in ventilated patients by a computed method. Comparison with the static method.

We have studied 28 patients mechanically ventilated for acute respiratory failure at different levels of externally applied positive end-expiratory pressure (PEEPe). We describe and compare a computed method of measuring "effective" elastance of the total respiratory system (Ers,eff) with the static values of elastance of the total respiratory system (Ers,st), obtained with the end-inflation occlusion technique. Ers,eff was computed by an original device (Heres, R.P.A., Belgium), also the effective resistance of the total respiratory system was calculated. At zero end-expiratory pressure set by the ventilator (ZEEP). Ers,eff averaged 29.5 +/- 13.5 cm H2O x L-1 while Ers,st non-corrected for intrinsic PEEP (PEEPi) averaged 36.4 +/- 15.1 cm H2O x L-1 and Ers,st corrected for PEEPi averaged 28.2 +/- 13.4 cm H2O x L-1. The small difference between Ers,eff and Ers,st corrected for PEEPi was statistically significant and these two values were highly correlated (r = 0.98). This significant difference disappeared rapidly with PEEPe and probably reflects a frequency-dependance due to pendelluft. We also observed that PEEPi was present in 21 of 27 patients at ZEEP. Our results also indicate that low levels of PEEP may improve Ers in hyperinflated COPD patients, without inducing further hyperinflation. In conclusion, values of Ers,eff are very similar to static values corrected for PEEPi and permit an accurate and rapid approach to the management of ventilated patients.

[A new case of hypersensitivity pneumopathy caused by salazopyrine?]. / Un nouveau cas de pneumopathie d'hypersensibilité à la Salazopyrine?

On the basis of a new case of Salazopyrine hypersensitivity pneumonitis, the authors describe the value of bronchoalveolar lavage and of the lymphoblast transformation test. They also describe the difficulties in making the diagnosis of such pathology and review the various possible differential diagnoses in their patient.

Sustained 24-h efficacy of NVA237, a once-daily long-acting muscarinic antagonist, in COPD patients.

NVA237 is a once-daily inhaled long-acting muscarinic antagonist in development for the treatment of COPD. This randomized, double-blind, placebo-controlled, four-period, incomplete block crossover study, with open-label active comparator (tiotropium), assessed the efficacy and safety of NVA237. Patients (>or=40 years; smoking history >or=10 pack-years) with stable moderate-to-severe COPD (post-bronchodilator FEV(1) >or= 30% and <80% predicted, FEV(1)/FVC < 0.7) received NVA237 12.5, 25, 50 or 100 microg, placebo, or tiotropium 18 microg once-daily for 7 days. The primary endpoint was mean trough (23-24 h post-dose) FEV(1) on Day 7. Secondary endpoints included mean trough FEV(1) on Day 1, and FEV(1) and FVC at individual time points post-dose on Days 1 and 7. 83 patients (mean age 64.4 years; male 83.1%; mean COPD duration 6.7 years; mean post-bronchodilator FEV(1) 1.5 L/52.7% predicted) were randomized; 78 completed. Mean trough FEV(1) on Day 7 and Day 1 was significantly higher with all active treatments versus placebo (p < 0.05). NVA237 50 microg, 100 microg and tiotropium showed clinically relevant improvements versus placebo on Day 7 (differences of 131, 142 and 127 mL, respectively; p < 0.0001) and 1 (differences of 121, 135 and 112 mL, respectively; p < 0.0001). On Day 1, but not Day 7, FEV(1) was significantly higher (p < 0.05) with NVA237 50 and 100 microg versus tiotropium from 5 min up to 2 and 4 h post-dose, respectively. All doses of NVA237 and tiotropium were well tolerated. NVA237 once-daily was effective and well tolerated versus placebo, and demonstrated rapid and sustained 24-h bronchodilation. (ClinicalTrials.gov Identifier: NCT00501852).

Comparison of central venous, oesophageal and mouth occlusion pressure with water-filled catheters for estimating pleural pressure changes in healthy adults.

The validity of the central venous and water-filled oesophageal catheter technique as a measure of pleural pressure changes was tested in ten healthy subjects in different body positions during inspiratory efforts with occluded airways, by comparing the simultaneous changes in mouth pressure (delta Pm) taken to represent pleural pressure changes, in central venous pressure (delta Pcv) and in oesophageal pressure (delta Poes). delta Pcv/delta Pm values were close to unity in the sitting and left lateral positions, whereas in the supine and right lateral position, substantial deviations from unity were found in some instances. delta Poes/delta Pm values were close to unity in all positions, except some rare instances. No appreciable phase difference between delta Pm/delta Poes and delta Pm/delta Pcv was found when the amplitude ratios were close to unity. We conclude that valid measurements of pleural pressure changes can be obtained in most instances with the central venous and the water-filled oesophageal catheter system according to the occlusion test procedure.

Coxsackie B3 virus: an unusual cause of unilateral mediastinal nodal enlargement.

We report on a patient with febrile illness, right unilateral paratracheal widening, pulmonary infiltrates, pleural effusions, exanthema and diarrhea. The right paratracheal widening was due to lymph node enlargement confirmed by CT scan. Symptoms disappeared subsequently without specific treatment. On the basis of serological tests, we are able to diagnose a coxsackie B3 virus infection. No previous case report of unilateral mediastinal nodal enlargement contemporary to a coxsackie B3 virus infection was found in our review of the literature.

Pulmonary hypertension associated with portal thrombosis.

Pulmonary hypertension accompanying portal hypertension is a rare cause of plexogenic pulmonary arteriopathy, which etiopathogenesis is still unknown. The case report presented is that of a young man who underwent surgery at age 8 for ruptured esophageal varices associated with portal thrombosis, and who later developed pulmonary hypertension which led to death at age 21. Hepatic filtration shunt and similarity of this syndrome to pulmonary hypertension subsequent to ingestion of the appetite depressant Aminorex suggest the hypothesis that pressor substances, not detoxified by the liver, are released into the pulmonary circulation.