Surface EMG-based quantification of inspiratory effort: a quantitative comparison with Pes.

BACKGROUND: Inspiratory patient effort under assisted mechanical ventilation is an important quantity for assessing patient-ventilator interaction and recognizing over and under assistance. An established clinical standard is respiratory muscle pressure [Formula: see text], derived from esophageal pressure ([Formula: see text]), which requires the correct placement and calibration of an esophageal balloon catheter. Surface electromyography (sEMG) of the respiratory muscles represents a promising and straightforward alternative technique, enabling non-invasive monitoring of patient activity. METHODS: A prospective observational study was conducted with patients under assisted mechanical ventilation, who were scheduled for elective bronchoscopy. Airway flow and pressure, esophageal/gastric pressures and sEMG of the diaphragm and intercostal muscles were recorded at four levels of pressure support ventilation. Patient efforts were quantified via the [Formula: see text]-time product ([Formula: see text]), the transdiaphragmatic pressure-time product ([Formula: see text]) and the EMG-time products (ETP) of the two sEMG channels. To improve the signal-to-noise ratio, a method for automatically selecting the more informative of the sEMG channels was investigated. Correlation between ETP and [Formula: see text] was assessed by determining a neuromechanical conversion factor [Formula: see text] between the two quantities. Moreover, it was investigated whether this scalar can be reliably determined from airway pressure during occlusion maneuvers, thus allowing to quantify inspiratory effort based solely on sEMG measurements. RESULTS: In total, 62 patients with heterogeneous pulmonary diseases were enrolled in the study, 43 of which were included in the data analysis. The ETP of the two sEMG channels was well correlated with [Formula: see text] ([Formula: see text] and [Formula: see text] for diaphragm and intercostal recordings, respectively). The proposed automatic channel selection method improved correlation with [Formula: see text] ([Formula: see text]). The neuromechanical conversion factor obtained by fitting ETP to [Formula: see text] varied widely between patients ([Formula: see text]) and was highly correlated with the scalar determined during occlusions ([Formula: see text], [Formula: see text]). The occlusion-based method for deriving [Formula: see text] from ETP showed a breath-wise deviation to [Formula: see text] of [Formula: see text] across all datasets. CONCLUSION: These results support the use of surface electromyography as a non-invasive alternative for monitoring breath-by-breath inspiratory effort of patients under assisted mechanical ventilation.

Resting limb muscle perfusion during inspiratory muscle loading in hypoxia and normoxia.

INTRODUCTION: Fatiguing of respiratory muscles reduces peripheral muscle perfusion. Further, acute hypoxia enhances respiratory muscle fatigue. This study investigated the effects of inspiratory muscle loading (IML) on resting locomotor muscle perfusion in hypoxia compared to normoxia. METHODS: Ten subjects completed two study days of fatiguing IML (blinded, randomized) in normobaric hypoxia (targeted oxygen saturation 80%) and normoxia, respectively. Contrast-enhanced ultrasound (CEUS) of the gastrocnemius muscle and popliteal doppler ultrasonography were used to monitor muscle perfusion. Based on CEUS and monitored cardiac output, perfusion surrogate parameters (CLPaer and CLPap) were established. RESULTS: Muscle perfusion declines early during IML in normoxia (CLPaer: -54±25%, p<0.01; CLPap: -58±32%, p<0.01) and hypoxia (CLPaer: -43±23%, p<0.01; CLPap: -41±20%, p<0.01). Hypoxia compared to normoxia increased cardiac output before (+23±19%, p<0.01 ANOVA) and during (+22±20%, p<0.01 ANOVA) IML, while local muscle perfusion during IML remained unchanged (CLPaer: p=0.41 ANOVA; CLPap: p=0.29 ANOVA). CONCLUSION: Acute hypoxia compared to normoxia does not affect locomotor muscle perfusion during fatiguing IML.

Diaphragmatic fatigue during inspiratory muscle loading in normoxia and hypoxia.

INTRODUCTION: Diaphragmatic fatigue (DF) occurs during strenuous loading of respiratory muscles (e.g., heavy-intensity whole-body exercise, normocapnic hyperpnea, inspiratory resistive breathing). DF develops early on during normoxia, without further decline toward task failure; however, its progression during inspiratory muscle loading in during hypoxia remains unclear. Therefore, the present study used volume-corrected transdiaphragmatic pressures during supramaximal magnetic phrenic nerve stimulation (Pdi,twc) to investigate the effect of hypoxia on the progression of diaphragmatic fatigue during inspiratory muscle loading. METHODS: Seventeen subjects completed two standardized rounds of inspiratory muscle loading (blinded, randomized) under the following conditions: (i) normoxia, and (ii) normobaric hypoxia (SpO2 80%), with Pdi,twc assessment every 45 s. RESULTS: In fatiguers (i.e., Pdi,twc reduction >10%, n=10), biometric approximation during normoxia is best represented by Pdi,twc=4.06+0.83 exp(-0.19 × x), in contrast to Pdi,twc=4.38-(0.05 × x) during hypoxia. CONCLUSION: Progression of diaphragmatic fatigue during inspiratory muscle loading assessed by Pdi,tw differs between normoxia and normobaric hypoxia: in the former, Pdi,tw follows an exponential decay, whereas during hypoxia, Pdi,tw follows a linear decline.