Volitional assessment of respiratory muscle strength

Respiratory muscle weakness may induce dyspnoea, secretion retention and respiratory failure. Assessing respiratory muscle strength is mandatory in neuromuscular diseases and in case of unexplained dyspnoea. A step by step approach is recommended, starting with simple volitional tests. Using spirometry, respiratory muscle weakness may be suspected on the basis of an abnormal flowvolume loop or a fall of supine vital capacity. When normal, maximal inspiratory and expiratory pressures against a near complete occlusion exclude significant muscle weakness, but low values are more difficult to interpret. Sniff nasal inspiratory pressure is a useful alternative because it is easy and it eliminates the problem of air leaks around the mouthpiece in patients with neuromuscular disorders. The strength available for coughing is easily assessed by measuring peak cough flow. In most cases, these simple non invasive tests are sufficient to confirm or to eliminate significant respiratory muscle weakness and help the timely introduction of ventilatory support or assisted cough techniques. In a minority of patients, a more complete evaluation is necessary using non volitional tests like cervical magnetic stimulation of phrenic nerves

Does respiratory infection due to Chlamydia pneumoniae still exist?

Does respiratory infection due to Chlamydia pneumoniae still exist

Inter-observer agreement on apnoea hypopnoea index using portable monitoring of respiratory parameters.

Although portable polygraphy or portable monitoring of respiratory parameters (PM) is commonly used to confirm obstructive sleep apnoea syndrome, agreement on apnoea hypopnoea index (AHI), the main measure of disease severity, has not been evaluated. The aim of this study was to assess the agreement on AHI among multiple observers as well as between individual observers and automated analysis. A total of 88 ambulatory sleep recordings ("Embletta") were independently scored by 8 physicians (observers). Agreement on AHI, using intraclass correlation coefficient (ICC), was measured among observers. Bland Altman plots were built to compare individual observers with PM. Among observers, ICCs were .73 for agreement on AHI, .71 for hypopnoea index and .98 for desaturation index. Compared to visual analysis, automated analysis underestimated AHI by 5.1 events on average. When comparing individual observers with automated analysis, systematic bias varied from -1. to +1 .5 events/h on AHI. Among observers who used PM in a clinical setting, agreement on AHI was limited. When automated and individual visual analyses were compared, the systematic bias varied from almost zero to values sufficient to affect clinical diagnosis. Much of the discordance was due to different counts of hypopnoea, whereas agreement on apnoea and desaturation index was better. Efforts should be directed towards standardisation of visual analysis, improvement and quality control of ambulatory sleep studies

GLI 2012 equations define few spirometric anomalies in the general population: the PneumoLaus study.

Reduced lung function predicts increased mortality, but its prevalence may vary depending on definition considered, use of bronchodilation and applied reference values. We aimed to assess lung function abnormalities in Lausanne, Switzerland, and their association with clinical history. In a general population sample, spirometry was performed and bronchodilation applied if the ratio forced expiratory volume in 1 s (FEV1) / forced vital capacity (FVC) or the FVC was below the lower limit of normal (LLN) according to Global Lung Function Initiative 2012 references. Results for FEV1/FVC according to the LLN were compared to the 0.7 fixed ratio. Respiratory risk factors, symptoms and self-reported respiratory diagnoses were recorded through a questionnaire. Out of the 3342 included subjects, 3.8% had chronic obstruction and 2.5% reversible obstruction when using the LLN; possible lung restriction alone was present in 1.8%, and associated with chronic obstruction in 0.4%. Ever smokers had a higher prevalence of abnormal spirometry, chronic obstruction and reversible obstruction; there was no difference with regard to possible restriction. Overall, chronic airway obstruction was found in 8.9% of current smokers, 4.6% of former smokers and 1.5% of never smokers. Only one third of participants with chronic obstruction were aware of a respiratory disease. Prevalence of abnormal lung function in the population of Lausanne is low. This may be due to a low rate of ever-smokers, the application of a full bronchodilation dose, but also to inherent characteristics of this population

Outcome after unilateral lung volume reduction surgery in patients with severe emphysema.

OBJECTIVE: Bilateral lung volume reduction surgery (LVRS) has emerged as a palliative treatment option in patients with severe pulmonary emphysema. However, it is not known if a sustained functional improvement can be obtained using an unilateral approach. METHODS: We hypothesized that a palliative effect can also be obtained by unilateral LVRS and prospectively assessed lung function, walking distance, and dyspnea before and 3, 6, 12, 18, 24 and 36 months after unilateral LVRS. RESULTS: Twenty-eight patients were operated by the use of video-assisted thoracoscopic surgery (VATS) with a mean follow-up of 16.5 months (range 3-36 months). Forced expiratory volume in 1 s (FEV1) was significantly improved up to 3 months (1007+/-432 compared to 1184+/-499 ml, P<0.001), residual volume up to 24 months (4154+/-1126 compared to 3390+/-914 ml, P<0.01), dyspnea up to 12 months (modified Borg dyspnea scale 6.6+/-1.8 compared to 3.9+/-1.8, P=0.01) and walking distance up to 24 months (343+/-107 compared to 467+/-77 m, P<0.05) after unilateral LVRS compared to preoperative values. Overall, 25 of 28 patients reported a subjective benefit after unilateral LVRS. There was no 30-day mortality. Only two patients required surgery on the contralateral side after 4.5 and 6 months, respectively, both suffering from alpha-1-antitrypsin deficiency. CONCLUSIONS: Unilateral LVRS by the use of VATS results in a sustained beneficial effect, improving walking distance and dyspnea for up to 24 months in patients with severe emphysema. The preservation of the contralateral side for future intervention if required renders unilateral LVRS an attractive concept in this difficult palliative situation

Transfer factor for carbon monoxide: a glance behind the scene.

The transfer factor for carbon monoxide (TLCO) is widely used in pulmonary function laboratories because it represents a unique non-invasive window on pulmonary microcirculation. The TLCO is the product of two primary measurements, the alveolar volume (VA) and the CO transfer coefficient (KCO). This test is most informative when VA and KCO are examined, together with their product TLCO. In a normal lung, a low VA due to incomplete expansion is associated with an elevated KCO, resulting in a mildly reduced TLCO. Thus, in case of low VA, a seemingly "normal KCO" must be interpreted as an abnormal gas transfer. The most common clinical conditions associated with an abnormal TLCO are characterised by a limited number of patterns for VA and KCO: incomplete lung expansion, discrete loss of alveolar units, diffuse loss of alveolar units, emphysema, pulmonary vascular disorders, high pulmonary blood volume, alveolar haemorrhage

Techniques d'évaluation de la force des muscles respiratoires. [Techniques for assessing respiratory muscle strength.]

La faiblesse des muscles respiratoires peut entraîner une dyspnée, un encombrement bronchique et une insuffisance respiratoire potentiellement fatale. L'évaluation de la force musculaire respiratoire s'impose donc dans les affections neuro-musculaires, mais également dans les situations de dyspnée inexpliquée par une première évaluation cardiaque et pulmonaire. À la spirométrie, une faiblesse musculaire est suspectée sur la base de la boucle débit-volume montrant un débit de pointe émoussé et une fin prématurée de l'expiration. Une diminution importante de la capacité vitale en position couchée suggère une paralysie diaphragmatique. La force inspiratoire est mesurée par la pression inspiratoire maximale (PImax) contre une quasi-occlusion des voies aériennes. Ce test relativement difficile est d'interprétation délicate en cas de collaboration insuffisante. La mesure de la pression nasale sniff (SNIP) est une alternative utile, car elle élimine le problème des fuites autour de l'embout buccal et la réalisation du reniflement est facile. De même, la pression trans-diaphragmatique sniff mesure la force du diaphragme au moyen de sondes oesophagienne et gastrique. En cas de collaboration insuffisante, on peut recourir à la stimulation magnétique des nerfs phréniques qui induit une contraction non-volontaire du diaphragme. La force expiratoire est mesurée par la pression expiratoire maximale (PEmax) contre une quasi-occlusion. La force disponible pour tousser est mesurée par la pression gastrique à la toux, ou plus simplement par le débit de pointe à la toux. Chez les patients à risque, la mesure de la force des muscles respiratoires permet d'instaurer à temps une assistance ventilatoire ou à la toux

Respiratory muscle fatigue limiting physical exercise?

Inspiratory muscle fatigue has been documented during loaded breathing or acute respiratory failure, but its role in exercise limitation is still undetermined. Electromyographic (EMG) signs of diaphragmatic fatigue develop in normal subjects hyperventilating above 70% of maximal voluntary ventilation (MVV), a ventilatory level commonly attained at peak exercise. EMG signs of diaphragmatic fatigue also occur during high power cycling exercise in normal subjects and chronic obstructive pulmonary disease (COPD) patients. However, a loss of respiratory muscle strength has rarely been documented following strenuous physical exercise with techniques independent of the subjects' collaboration. Prior inspiratory muscle fatigue decreases exercise tolerance in normal subjects but its effect is largely unknown in COPD patients. Respiratory muscle rest by negative pressure ventilation was reported to improve exercise tolerance in COPD, but this beneficial effect was not confirmed by controlled studies. The effect of inspiratory muscle training on exercise tolerance is still undefined by existing data, in part because of differences in methods and selection criteria between studies. Although respiratory muscle fatigue may occur during exercise, it is not clearly established whether interventions directed at respiratory muscles may improve exercise tolerance in COPD