Impairment of (inspiratory and expiratory) respiratory muscles is a common clinical finding, not only in patients with neuromuscular disease but also in patients with primary disease of the lung parenchyma or airways. Although such impairment is common, its recognition is usually delayed because its signs and symptoms are nonspecific and late. This delayed recognition, or even the lack thereof, occurs because the diagnostic tests used in the assessment of respiratory muscle strength are not widely known and available. There are various methods of assessing respiratory muscle strength during the inspiratory and expiratory phases. These methods are divided into two categories: volitional tests (which require patient understanding and cooperation); and non-volitional tests. Volitional tests, such as those that measure maximal inspiratory and expiratory pressures, are the most commonly used because they are readily available. Non-volitional tests depend on magnetic stimulation of the phrenic nerve accompanied by the measurement of inspiratory mouth pressure, inspiratory esophageal pressure, or inspiratory transdiaphragmatic pressure. Another method that has come to be widely used is ultrasound imaging of the diaphragm. We believe that pulmonologists involved in the care of patients with respiratory diseases should be familiar with the tests used in order to assess respiratory muscle function.Therefore, the aim of the present article is to describe the advantages, disadvantages, procedures, and clinical applicability of the main tests used in the assessment of respiratory muscle strength.

BackgroundMost patients with unilateral diaphragm paralysis (UDP) have unexplained dyspnea, exercise limitations, and reduction in inspiratory muscle capacity. We aimed to evaluate the generation of pressure in each hemidiaphragm separately and its contribution to overall inspiratory strength.MethodsTwenty-seven patients, 9 in right paralysis group (RP) and 18 in left paralysis group (LP), with forced vital capacity (FVC) < 80% pred, and 20 healthy controls (CG), with forced expiratory volume in 1 s (FEV1) > 80% pred and FVC > 80% pred, were evaluated for lung function, maximal inspiratory (MIP) and expiratory (MEP) pressure measurements, diaphragm ultrasound, and transdiaphragmatic pressure during magnetic phrenic nerve stimulation (PdiTw).ResultsRP and LP had significant inspiratory muscle weakness compared to controls, detected by MIP (− 57.4 ± 16.9 for RP; − 67.1 ± 28.5 for LP and − 103.1 ± 30.4 cmH2O for CG) and also by PdiTW (5.7 ± 4 for RP; 4.8 ± 2.3 for LP and 15.3 ± 5.7 cmH2O for CG). The PdiTw was reduced even when the non-paralyzed hemidiaphragm was stimulated, mainly due to the low contribution of gastric pressure (around 30%), regardless of whether the paralysis was in the right or left hemidiaphragm. On the other hand, in CG, esophagic and gastric pressures had similar contribution to the overall Pdi (around 50%). Comparing both paralyzed and non-paralyzed hemidiaphragms, the mobility during quiet and deep breathing, and thickness at functional residual capacity (FRC) and total lung capacity (TLC), were significantly reduced in paralyzed hemidiaphragm. In addition, thickness fraction was extremely diminished when contrasted with the non-paralyzed hemidiaphragm.ConclusionsIn symptomatic patients with UDP, global inspiratory strength is reduced not only due to weakness in the paralyzed hemidiaphragm but also to impairment in the pressure generated by the non-paralyzed hemidiaphragm.

A respiratory rate of 17 breaths/min is the parameter with the greatest accuracy for diagnosing overassistance. Respiratory rates of less than or equal to 12 or greater than or equal to 30 are useful clinical references to confirm or exclude pressure support overassistance.

BackgroundThoracoabdominal asynchrony is the nonparallel motion of the ribcage and abdomen. It is estimated by using respiratory inductive plethysmography and, recently, using optoelectronic plethysmography; however the agreement of measurements between these 2 techniques is unknown. Therefore, the present study compared respiratory inductive plethysmography with optoelectronic plethysmography for measuring thoracoabdominal asynchrony to see if the measurements were similar or different.Methods27 individuals (9 healthy subjects, 9 patients with interstitial lung disease, and 9 with chronic obstructive pulmonary disease performed 2 cycle ergometer tests with respiratory inductive plethysmography or optoelectronic plethysmography in a random order. Thoracoabdominal asynchrony was evaluated at rest, and at 50% and 75% of maximal workload between the superior ribcage and abdomen using a phase angle.ResultsThoracoabdominal asynchrony values were very similar in both approaches not only at rest but also with exercise, with no statistical difference. There was a good correlation between the methods and the Phase angle values were within the limits of agreement in the Bland-Altman analysis.ConclusionThoracoabdominal asynchrony measured by optoelectronic plethysmography and respiratory inductive plethysmography results in similar values and has a satisfactory agreement at rest and even for different exercise intensities in these groups.

Small airway and interstitial pulmonary involvements are prominent in chronic hypersensitivity pneumonitis (cHP). However, their roles on exercise limitation and the relationship with functional lung tests have not been studied in detail.Our aim was to evaluate exercise performance and its determinants in cHP. We evaluated maximal cardiopulmonary exercise testing performance in 28 cHP patients (forced vital capacity 57±17% pred) and 18 healthy controls during cycling.Patients had reduced exercise performance with lower peak oxygen production (16.6 (12.3–19.98) mL·kg−1·min−1 versus 25.1 (16.9–32.0), p=0.003), diminished breathing reserve (% maximal voluntary ventilation) (12 (6.4–34.8)% versus 41 (32.7–50.8)%, p<0.001) and hyperventilation (minute ventilation/carbon dioxide production slope 37±5 versus 31±4, p<0.001). All patients presented oxygen desaturation and augmented Borg dyspnoea scores (8 (5–10) versus 4 (1–7), p=0.004). The prevalence of dynamic hyperinflation was found in only 18% of patients. When comparing cHP patients with normal and low peak oxygen production (<84% pred, lower limit of normal), the latter exhibited a higher minute ventilation/carbon dioxide production slope (39±5.0 versus 34±3.6, p=0.004), lower tidal volume (0.84 (0.78–0.90) L versus 1.15 (0.97–1.67) L, p=0.002), and poorer physical functioning score on the Short form-36 health survey. Receiver operating characteristic curve analysis showed that reduced lung volumes (forced vital capacity %, total lung capacity % and diffusing capacity of the lung for carbon dioxide %) were high predictors of poor exercise capacity.Reduced exercise capacity was prevalent in patients because of ventilatory limitation and not due to dynamic hyperinflation. Reduced lung volumes were reliable predictors of lower performance during exercise.

BackgroundPatients with unilateral diaphragmatic paralysis (UDP) may present with dyspnoea without specific cause and limited ability to exercise. We aimed to investigate the diaphragm contraction mechanisms and nondiaphragmatic inspiratory muscle activation during exercise in patients with UDP, compared with healthy individuals.MethodsPulmonary function, as well as volitional and nonvolitional inspiratory muscle strength were evaluated in 35 patients and in 20 healthy subjects. Respiratory pressures and electromyography of scalene and sternocleidomastoid muscles were continuously recorded during incremental maximal cardiopulmonary exercise testing until symptom limitation. Dyspnoea was assessed at rest, every 2 min during exercise and at the end of exercise with a modified Borg scale.Main resultsInspiratory muscle strength measurements were significantly lower for patients in comparison to controls (all p<0.05). Patients achieved lower peak of exercise (lower oxygen consumption) compared to controls, with both gastric (−9.8±4.6 cmH2O versus 8.9±6.0 cmH2O) and transdiaphragmatic (6.5±5.5 cmH2O versus 26.9±10.9 cmH2O) pressures significantly lower, along with larger activation of both scalene (40±22% EMGmax versus 18±14% EMGmax) and sternocleidomastoid (34±22% EMGmax versus 14±8% EMGmax). In addition, the paralysis group presented significant differences in breathing pattern during exercise (lower tidal volume and higher respiratory rate) with more dyspnoea symptoms compared to the control group.ConclusionThe paralysis group presented with exercise limitation accompanied by impairment in transdiaphragmatic pressure generation and larger accessory inspiratory muscles activation compared to controls, thereby contributing to a neuromechanical dissociation and increased dyspnoea perception.

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Background and objective: The precise coordination of respiratory muscles during exercise minimizes work of breathing and avoids exercise intolerance. Fibrotic interstitial lung disease (f-ILD) patients are exercise-intolerant. We assessed whether respiratory muscle incoordination and thoracoabdominal asynchrony (TAA) occur in f-ILD during exercise, and their relationship with pulmonary function and exercise performance. Methods: We compared breathing pattern, respiratory mechanics, TAA and respiratory muscle recruitment in 31 f-ILD patients and 31 healthy subjects at rest and during incremental cycle exercise. TAA was defined as phase angle (PhAng) >20 . Results: During exercise, when compared with controls, f-ILD patients presented increased and early recruitment of inspiratory rib cage muscle (p < 0.05), and an increase in PhAng, indicating TAA. TAA was more frequent in f-ILD patients than in controls, both at 50% of the maximum workload (42.3% vs. 10.7%, p = 0.01) and at the peak (53.8% vs. 23%, p = 0.02). Compared with f-ILD patients without TAA, f-ILD patients with TAA had lower lung volumes (forced vital capacity, p < 0.01), greater dyspnoea (Medical Research Council > 2 in 64.3%, p = 0.02), worse exercise performance (lower maximal work rate % predicted, p = 0.03; lower tidal volume, p = 0.03; greater desaturation and dyspnoea, p < 0.01) and presented higher oesophageal inspiratory pressures with lower gastric inspiratory pressures and higher recruitment of scalene (p < 0.05). Conclusion: Exercise induces TAA and higher recruitment of inspiratory accessory muscle in ILD patients. TAA during exercise occurred in more severely restricted ILD patients and was associated with exertional dyspnoea, desaturation and limited exercise performance.