Assessing respiratory mechanics and muscle function is critical for both clinical practice and research purposes. Several methodological developments over the past two decades have enhanced our understanding of respiratory muscle function and responses to interventions across the spectrum of health and disease. They are especially useful in diagnosing, phenotyping and assessing treatment efficacy in patients with respiratory symptoms and neuromuscular diseases. Considerable research has been undertaken over the past 17 years, since the publication of the previous American Thoracic Society (ATS)/European Respiratory Society (ERS) statement on respiratory muscle testing in 2002. Key advances have been made in the field of mechanics of breathing, respiratory muscle neurophysiology (electromyography, electroencephalography and transcranial magnetic stimulation) and on respiratory muscle imaging (ultrasound, optoelectronic plethysmography and structured light plethysmography). Accordingly, this ERS task force reviewed the field of respiratory muscle testing in health and disease, with particular reference to data obtained since the previous ATS/ERS statement. It summarises the most recent scientific and methodological developments regarding respiratory mechanics and respiratory muscle assessment by addressing the validity, precision, reproducibility, prognostic value and responsiveness to interventions of various methods. A particular emphasis is placed on assessment during exercise, which is a useful condition to stress the respiratory system.

Estimation of chest wall motion by surface measurements only allows one-dimensional measurements of the chest wall. We have assessed on optical reflectance system (OR), which tracks reflective markers in three dimensions (3-D) for respiratory use. We used 86 (6-mm-diameter) hemispherical reflective markers arranged circumferentially on the chest wall in seven rows between the sternal notch and the anterior superior iliac crest in two normal standing subjects. We calculated the volume of the entire chest wall and compared inspired and expired volumes with volumes obtained by spirometry. Marker positions were recorded by four TV cameras; two were 4 m in front of and two were 4 m behind the subject. The TV signals were sampled at 100 Hz and combined with grid calibration parameters on a personal computer to obtain the 3-D coordinates of the markers. Chest wall surfaces were reconstructed by triangulation through the point data, and chest wall volume was calculated. During tidal breathing and vital capacity maneuvers and during CO2-stimulated hyperpnea, there was a very close correlation of the lung volumes (VL) estimated by spirometry [VL(SP)] and OR [VL(OR)]. Regression equations of VL(OR) (y) vs. VL(SP) (x, BTPS in liters) for the two subjects were given by y = 1.01x-0.01 (r = 0.996) and y = 0.96x + 0.03 (r = 0.997), and by y = 1.04x + 0.25 (r = 0.97) and y = 0.98x + 0.14 (r = 0.95) for the two maneuvers, respectively. We conclude spirometric volumes can be estimated very accurately and directly from chest wall surface markers, and we speculate that OR may be usefully applied to calculations of chest wall shape, regional volumes, and motion analysis.

We measured pressures and power of diaphragm, rib cage, and abdominal muscles during quiet breathing (QB) and exercise at 0, 30, 50, and 70% maximum workload (Wmax) in five men. By three-dimensional tracking of 86 chest wall markers, we calculated the volumes of lung- and diaphragm-apposed rib cage compartments (Vrc,p and Vrc,a, respectively) and the abdomen (Vab). End-inspiratory lung volume increased with percentage of Wmax as a result of an increase in Vrc,p and Vrc,a. End-expiratory lung volume decreased as a result of a decrease in Vab. DeltaVrc,a/DeltaVab was constant and independent of Wmax. Thus we used DeltaVab/time as an index of diaphragm velocity of shortening. From QB to 70% Wmax, diaphragmatic pressure (Pdi) increased approximately 2-fold, diaphragm velocity of shortening 6.5-fold, and diaphragm workload 13-fold. Abdominal muscle pressure was approximately 0 during QB but was equal to and 180 degrees out of phase with rib cage muscle pressure at all percent Wmax. Rib cage muscle pressure and abdominal muscle pressure were greater than Pdi, but the ratios of these pressures were constant. There was a gradual inspiratory relaxation of abdominal muscles, causing abdominal pressure to fall, which minimized Pdi and decreased the expiratory action of the abdominal muscles on Vrc,a gradually, minimizing rib cage distortions. We conclude that from QB to 0% Wmax there is a switch in respiratory muscle control, with immediate recruitment of rib cage and abdominal muscles. Thereafter, a simple mechanism that increases drive equally to all three muscle groups, with drive to abdominal and rib cage muscles 180 degrees out of phase, allows the diaphragm to contract quasi-isotonically and act as a flow generator, while rib cage and abdominal muscles develop the pressures to displace the rib cage and abdomen, respectively. This acts to equalize the pressures acting on both rib cage compartments, minimizing rib cage distortion.

Expiratory flow limitation (EFL) during tidal breathing is a major determinant of dynamic hyperinflation and exercise limitation in chronic obstructive pulmonary disease (COPD). Current methods of detecting this are either invasive or unsuited to following changes breath-by-breath. It was hypothesised that tidal flow limitation would substantially reduce the total respiratory system reactance (Xrs) during expiration, and that this reduction could be used to reliably detect if EFL was present.To test this, 5-Hz forced oscillations were applied at the mouth in seven healthy subjects and 15 COPD patients (mean¡SD forced expiratory volume in one second was 36.8¡11.5 % predicted) during quiet breathing. COPD breaths were analysed (n=206) and classified as flow-limited if flow decreased as alveolar pressure increased, indeterminate if flow decreased at constant alveolar pressure, or nonflow-limited.Of these, 85 breaths were flow-limited, 80 were not and 41 were indeterminate. Among other indices, mean inspiratory minus mean expiratory Xrs (DXrs) and minimum expiratory Xrs (Xexp,min) identified flow-limited breaths with 100% specificity and sensitivity using a threshold between 2. Unlike healthy subjects who do not develop expiratory flow limitation (EFL) even during exhaustive exercise [1], many chronic obstructive pulmonary disease (COPD) patients are flow-limited (FL) at rest [2]. These patients can only increase their expiratory flow rate during exercise by allowing their end-expiratory lung volume (VL) to rise, an energetically inefficient strategy that is accompanied by severe dyspnoea that reduces exercise duration [3,4]. The severity of dyspnoea in COPD is better predicted by the presence of EFL during tidal breathing than by the forced expiratory volume in one second (FEV1) [5,6]. Thus, a simple method of detecting EFL during tidal breathing would be a potentially useful clinical tool. Several noninvasive methods have been proposed to detect tidal EFL in COPD patients, but each has its limitations and, to the best of the authors9 knowledge, to date none has been tested against any form of "gold standard" in spontaneously breathing patients.In 1993, PESLIN et al. [7] reported that some COPD patients during mechanical ventilation developed large negative swings in the respiratory system input reactance (Xrs, i.e. the imaginary part of total input impedance) measured by a forced oscillation technique (FOT). Similar behaviour was observed in a simplified mechanical model of the respiratory system when a flow-limiting segment was included [8] and in mechanically ventilated rabbits [9] after intravenous methacholine infusion. This phenomenon occurs because the linear velocity of gas passing through flow-limiting segments (choke points) equals the local speed of wave propagation [10]. Normally the reactance reflects the elastic and inertial properties of the respiratory system but when flow limitation is present, the oscillatory signal cannot pass through the choke points and reach the alveoli, producing a ...

BackgroundAppropriate interpretation of pulmonary function tests (PFTs) involves the classification of observed values as within/outside the normal range based on a reference population of healthy individuals, integrating knowledge of physiologic determinants of test results into functional classifications, and integrating patterns with other clinical data to estimate prognosis. In 2005, the American Thoracic Society and the European Respiratory Society jointly adopted technical standards for the interpretation of PFTs. We aimed to update the 2005 recommendations and incorporate evidence from recent literature to establish new standard for PFT interpretation.MethodsThis technical standards document was developed by an international joint task force, appointed by the European Respiratory Society and the American Thoracic Society with multidisciplinary expertise in conducting and interpreting pulmonary function tests, and developing international standards. A comprehensive literature review was conducted, and published evidence was reviewed.ResultsRecommendations for the choice of reference equations and limits of normal of the healthy population to identify individuals with unusually low or high results, respectively are discussed. Interpretation strategies for bronchodilator responsiveness testing, limits of natural changes over time and severity are also updated. Interpretation of measurements made by spirometry, lung volumes and gas transfer are described as they relate to underlying pathophysiology with updated classification protocols of common impairments.ConclusionsPFTs interpretation must be complemented with clinical expertise and consider the inherent biological variability of the test and the uncertainty of the test result to ensure appropriate interpretation of an individual's lung function measurements.

Background: Dynamic hyperinflation of the lungs impairs exercise performance in chronic obstructive pulmonary disease (COPD). However, it is unclear which patients are affected by dynamic hyperinflation and how the respiratory muscles respond to the change in lung volume. Methods: Using optoelectronic plethysmography, total and regional chest wall volumes were measured non-invasively in 20 stable patients with COPD (mean (SD) forced expiratory volume in 1 second 43.6 (11.6)% predicted) and dynamic hyperinflation was tracked breath by breath to test if this was the mechanism of exercise limitation. Resting ventilation, breathing pattern, symptoms, rib cage and abdominal volumes were recorded at rest and during symptom limited cycle ergometry. Pleural, abdominal, and transdiaphragmatic pressures were measured in eight patients. Results: End expiratory chest wall volume increased by a mean (SE) of 592 (80) ml in 12 patients (hyperinflators) but decreased by 462 (103) ml in eight (euvolumics). During exercise, tidal volume increased in euvolumic patients by reducing end expiratory abdominal volume while in hyperinflators tidal volume increased by increasing end inspiratory abdominal and rib cage volumes. The maximal abdominal pressure was 22.1 (9.0) cm H 2 O in euvolumic patients and 7.6 (2.6) cm H 2 O in hyperinflators. Euvolumic patients were as breathless as hyperinflators but exercised for less time and reached lower maximum workloads (p,0.05) despite having better spirometric parameters and a greater expiratory flow reserve. Conclusions: Dynamic hyperinflation is not the only mechanism limiting exercise performance in patients with stable COPD. Accurate measurement of chest wall volume can identify the different patterns of respiratory muscle activation during exercise.

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During healthy pregnancy, pulmonary function, ventilatory pattern and gas exchange are affected through both biochemical and mechanical pathways, as summarised in figure 1.