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Non-invasive mechanical ventilation
  1. D VANPEE,
  2. D CLAUSE,
  1. Université Catholique de Louvain
  2. Mont-Godinne Hospital
  3. 5530 Yvoir
  4. Belgium
  1. S NAVA
  1. Respiratory Intensive Care Unit
  2. Centro Medico di Pavia
  3. Via Ferrata 8
  4. 27100 Pavia, Italy
  5. snava{at}

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We read with interest the study by Morettiet al concerning the incidence and causes of failure of non-invasive mechanical ventilation (NIV) after initial success.1 It is an interesting study, but some important factors associated with the initial treatment of chronic obstructive pulmonary disease (COPD) which could influence the results of the study are not addressed. The aim of NIV includes not only the correction of alveolar hypoventilation, but also the unloading of inspiratory muscles. NIV reduces the work of breathing, allowing resting of respiratory muscles and recovery of muscle function. How long had the patients in the two groups been in an acute state before admission to the intensive care units? Where were they before being enrolled in the study—in an emergency unit or in a pneumology ward? Was it the same for the two groups? Perhaps the patients in group 2 had suffered from respiratory muscle overload for longer. Earlier NIV treatment may avoid late failure.2

Another factor not known in the study is the dose of corticosteroids used in the two groups during the time in the intensive care unit. Was the dose of corticosteroids higher in group 2? Corticosteroids are probably not good for recovery of muscle function in these cases and there is no consensus for the use of systemic steroids in the treatment of patients with acute exacerbations of COPD. The ATS and ERS guidelines acknowledge the lack of supporting evidence for the use of steroids in patients with hypercapnic exacerbations of COPD.3 ,4 These patients should be checked for possible deleterious effects of high doses of steroids.


authors' reply We thank Dr Vanpee and colleagues for the comments about our paper on the incidence and causes of failure of non-invasive mechanical ventilation after initial success1-1 and welcome the opportunity to clarify some important issues. They ask, firstly, whether the duration of the respiratory muscle fatigue may have influenced our results. The diagnosis of respiratory muscle fatigue is very complex and is difficult to perform in the clinical setting. To our knowledge, the loss of force induced by “acute fatigue” can only be identified by the electrical or magnetic stimulation of the phrenic nerve, but only if this is compared with the pressures obtained in a previously fresh muscle.1-2 In the clinical setting the occurrence of acute alveolar hypoventilation (hypercapnic respiratory failure) associated with, for example, abdominal paradoxical movements, tachypnoea, or recruitment of accessory muscles may suggest failure of the respiratory pump. At admission the two groups of patients showed some or all these signs and the same degree of decompensation of arterial blood gas tensions (pH 7.25 v 7.22; Paco 2 87 mm Hg v83 mm Hg for the successful and late respiratory failure groups, respectively), so that the “theoretical degree” of pump failure, if any, was likely to be similar in the two groups. Concerning the timing of the occurrence of acute respiratory failure, it should be pointed out that one of the two respiratory intensive care units (RICU), which is part of a rehabilitation centre, does not have an emergency room, so all the patients were transferred to the unit from the pneumological ward as soon as their condition deteriorated. The other RICU is part of a regional general hospital but, again, more than 50% of the patients enrolled in the study came from the pneumological ward, not from the ICU. This latter subset of patients was, however, equally distributed between the successful and late failure groups.

Finally, Dr Vanpee and colleagues are concerned about the possible differences between the two groups in the dosage of steroids used in the acute phase. We did not analyse the daily doses of steroids in the two groups of patients. It is our practice, however, to use systemic methylprednisone (40–80 mg) in acute exacerbations of COPD because it has been shown that it may improve respiratory mechanics1-3and also pulmonary function,1-4 and the British Thoracic Society recommends at least a brief trial of steroids in this situation.1-5 However, these doses are not likely to affect the short term function of the respiratory muscles since the only “acute” study performed in rats showed a relatively small effect on diaphragmatic fibres with doses at least 10 times higher.1-6


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