scholarly journals Combining Bioimpedance and Myographic Signals for the Assessment of COPD During Loaded Breathing

2021 ◽  
Vol 68 (1) ◽  
pp. 298-307
Author(s):  
Dolores Blanco-Almazan ◽  
Willemijn Groenendaal ◽  
Manuel Lozano-Garcia ◽  
Luis Estrada-Petrocelli ◽  
Lien Lijnen ◽  
...  
Keyword(s):  

1997 ◽  
Vol 82 (4) ◽  
pp. 1119-1125 ◽  
Author(s):  
G. S. Supinski ◽  
D. Stofan ◽  
R. Ciufo ◽  
A. Dimarco

Supinski, G. S., D. Stofan, R. Ciufo, and A. DiMarco. N-acetylcysteine administration alters the response to inspiratory loading in oxygen-supplemented rats. J. Appl. Physiol. 82(4): 1119–1125, 1997.—Based on recent studies, it has been suggested that free radicals are elaborated in the respiratory muscles during strenuous contractions and contribute to the development of muscle fatigue. If this theory is correct, then it should be possible to attenuate the development of diaphragm fatigue and/or delay the onset of respiratory failure during loaded breathing by administering a free radical scavenger. The purpose of the present experiment was, therefore, to examine the effect of N-acetylcysteine (NAC), a free radical scavenger and glutathione precursor, on the evolution of respiratory failure in decerebrate unanesthetized rats breathing against a large inspiratory resistive load. We compared the inspiratory volume and pressure generation over time in animals pretreated with either saline or NAC (150 mg/kg) and then loaded until respiratory arrest. After arrest, the diaphragm was excised, and samples were assayed for reduced (GSH) and oxidized glutathione. As a control, we also assessed respiratory function and glutathione concentrations in groups of nonloaded saline- and NAC-treated animals. We found that NAC-treated animals were able to tolerate loading better than the saline-treated group, maintaining higher inspiratory pressures and sustaining higher inspired volumes. Administration of NAC also increased the time that animals could tolerate loading before the development of respiratory arrest. In addition, although saline-treated loaded animals had significant reductions in diaphragmatic GSH levels compared with unloaded controls, the magnitude of this reduction was blunted by NAC administration (i.e., GSH averaged 965 ± 113, 568 ± 83, 907 ± 39, and 784 ± 61 nmol/g for unloaded-saline, loaded-saline, unloaded-NAC, and loaded-NAC groups, P< 0.05, with the value for the loaded-saline group lower than the values for the two unloaded groups; GSH for the loaded-NAC group was not different, however, from unloaded controls). These data demonstrate that administration of NAC, a free radical scavenger, slows the rate of development of respiratory failure during inspiratory resistive loading.



1990 ◽  
Vol 78 (2) ◽  
pp. 149-153 ◽  
Author(s):  
Rachel C. Wilson ◽  
P. W. Jones

1. The intensity of breathlessness was measured during exercise in nine normal subjects using a modified Borg scale to examine the effect of prior experience of breathlessness on subsequent estimates of breathlessness. 2. Each subject performed four exercise tests, each of which consisted of two identical runs of workload incrementation (run 1 and run 2). An inspiratory resistive load of 3.8 cmH2O s−1 l−1 was applied during the appropriate run of the exercise test to examine the effect of (a) prior experience of ‘loaded’ breathing on breathlessness estimation during ‘unloaded’ breathing, and (b) prior experience of ‘unloaded’ breathing on breathlessness estimation during ‘loaded’ breathing. Run 1 was the conditioning run; run 2 was the run in which the effect of conditioning was measured. 3. There was a good correlation between breathlessness and minute ventilation during both unloaded’ breathing (median r = 0.93) and ‘loaded’ breathing (median r = 0.95). 4. The slope of the Borg score/minute ventilation relationship was greater during ‘loaded’ breathing than during ‘unloaded’ breathing (P < 0.01). There was no difference in mean Borg score between ‘unloaded’ and ‘loaded’ breathing. 5. After a period of ‘loaded’ breathing during run 1, estimated breathlessness was significantly reduced during ensuing ‘unloaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which ‘unloaded’ breathing was experienced throughout both run 1 and run 2. 6. After a period of ‘unloaded’ breathing in run 1, estimated breathlessness was significantly increased during ensuing ‘loaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which the inspiratory load had already been experienced in run 1. 7. Changes in the pattern of breathing (inspiratory time, expiratory time, total breath duration, inspiration time/total breath duration ratio and tidal volume) were not consistent with the changes in breathlessness. 8. We suggest that perception of breathlessness may be influenced by a subject's immediate prior experience of an altered relationship between breathlessness and ventilation.



2003 ◽  
Vol 90 (3-4) ◽  
pp. 405-410 ◽  
Author(s):  
Markus Rohrbach ◽  
Claudio Perret ◽  
Bengt Kayser ◽  
Urs Boutellier ◽  
Christina M. Spengler


Author(s):  
Y. Kikuchi ◽  
M. Sakurai ◽  
W. Hida ◽  
S. Okabe ◽  
Y. Chung ◽  
...  


1999 ◽  
Vol 87 (3) ◽  
pp. 1123-1131 ◽  
Author(s):  
G. Supinski ◽  
D. Nethery ◽  
D. Stofan ◽  
L. Szweda ◽  
A. DiMarco

The purpose of the present study was to determine whether it is possible to alter the development of fatigue and ablate free radical-mediated lipid peroxidation of the diaphragm during loaded breathing by administering oxypurinol, a xanthine oxidase inhibitor. We studied 1) room-air-breathing decerebrate, unanesthetized rats given either saline or oxypurinol (50 mg/kg) and loaded with a large inspiratory resistance until airway pressure had fallen by 50% and 2) unloaded saline- and oxypurinol-treated room-air-breathing control animals. Additional sets of studies were performed with animals breathing 100% oxygen. Animals were killed at the conclusion of loading, and diaphragmatic samples were obtained for determination of thiobarbituric acid-reactive substances and assessment of in vitro force generation. We found that loading of saline-treated animals resulted in significant diaphragmatic fatigue and thiobarbituric acid-reactive substances formation ( P < 0.01). Oxypurinol administration, however, failed to increase load trial time, reduce fatigue development, or prevent lipid peroxidation in either room-air-breathing or oxygen-breathing animals. These data suggest that xanthine oxidase-dependent pathways do not generate physiologically significant levels of free radicals during the type of inspiratory resistive loading examined in this study.



1992 ◽  
Vol 73 (5) ◽  
pp. 1720-1727 ◽  
Author(s):  
S. J. Cala ◽  
J. Edyvean ◽  
M. Rynn ◽  
L. A. Engel

We compared the O2 cost of breathing (VO2resp) at high levels of ventilation (HV) with that against high inspiratory pressure loads (HP) using an external elastance when end-expiratory volume, work rate (W), and pressure-time product (P) were matched at two levels of ventilation and elastic loading. Each of five normal subjects performed three pairs of loaded runs (one HV and one HP) bracketed by two resting runs. Mean O2 consumption from the pairs of resting runs was subtracted from that of each of the loaded runs to give VO2resp during loaded breathing. Matching for W and P was within 15% in all 15 pairs of runs. During HV runs, ventilation was 398 +/- 24% of corresponding values during HP runs (P < 0.01). Although there was no difference in W (P > 0.05), the VO2resp during HV runs was 237 +/- 33% of that during HP (P < 0.01) and efficiency of HV was 51 +/- 5% of that during HP (P < 0.01). When W was normalized for the decrease in maximum inspiratory pressure with increased mean lung volume, efficiency during HV and HP runs did not differ (P > 0.05). In the second series of experiments, when both HV and HP runs were matched for W but P was allowed to vary, efficiency increased by 1.42 +/- 0.42% (P < 0.05) for each percent decrease in P during HV runs but was unchanged (P > 0.05) during HP runs despite a 193 +/- 10% increase in P.(ABSTRACT TRUNCATED AT 250 WORDS)



1988 ◽  
Vol 65 (1) ◽  
pp. 249-255 ◽  
Author(s):  
J. F. Watchko ◽  
T. A. Standaert ◽  
D. E. Mayock ◽  
G. Twiggs ◽  
D. E. Woodrum

Minute ventilation (VE), arterial blood gases, diaphragmatic electromyogram (EMG) activity, centroid frequency (Fc) and peak inspiratory airway pressures (Paw) were measured in five unanesthetized tracheostomized infant monkeys during various intensities of inspiratory resistive loaded breathing (IRL) until either 1) ventilatory failure occurred (failed trial) or 2) normocapnia was sustained for 1 h (successful trial). During successful trials VE and arterial PCO2 (PaCO2) were sustained at base-line levels, and an increase in peak integrated diaphragmatic EMG activity and peak inspiratory Paw occurred. In contrast, during ventilatory failure runs, VE decreased and PaCO2 rose compared with their respective base-line values. The fall in VE occurred secondary to a significant decline in breathing frequency. Tidal volume was sustained at base-line levels during all trials (both successful and failed groups). Inspiratory Paw's and peak moving time average EMG were sustained at elevated levels during ventilatory failure runs, suggesting that the respiratory muscles did not fail as pressure generators. Furthermore, the EMG Fc did not change from base line during either successful or failed trials. These data suggest that peripheral muscle fatigue did not occur, although in the absence of a more direct test of muscle performance, i.e., a force-frequency curve, we cannot rule out the possibility that a component of peripheral failure contributed to our results. Ventilatory failure during severe IRL in the infant monkey was most clearly associated with an alteration in the respiratory center timing mechanism, i.e., such failure was a function of a decline in respiratory frequency.



2017 ◽  
Vol 38 (4) ◽  
pp. 554-565 ◽  
Author(s):  
Takako Tanaka ◽  
Nada Basoudan ◽  
Luana T. Melo ◽  
Lisa Wickerson ◽  
Laurent J. Brochard ◽  
...  


1985 ◽  
Vol 19 (4) ◽  
pp. 420A-420A
Author(s):  
Jon F Watchko ◽  
Thomas A Standaert ◽  
David E Woodrum
Keyword(s):  


1999 ◽  
Vol 91 (6) ◽  
pp. 1633-1633 ◽  
Author(s):  
Takashi Nishino ◽  
Naohito Shimoyama ◽  
Tohru Ide ◽  
Shiroh Isono

Background Pain and dyspnea frequently coexist in many clinical situations. However, whether the two different symptoms interact with each other has not been elucidated. To elucidate the interaction between pain and dyspneic sensations, the authors investigated separately the effects of pain on dyspnea and the effects of dyspnea on pain in 15 healthy subjects. Methods Subjects were asked to rate their sensation of pain or dyspnea using a visual analog scale (VAS) during pain stimulation produced by tourniquet inflation (inflation cuff pressure: 350 mmHg) around the calf, and/or the respiratory loading consisted of a combination of resistive load (77 cm H2O x l(-1) x s(-1)) and hypercapnia induced by extra mechanical dead space (255 ml). In addition to changes in VAS scores, changes in ventilatory airflow and airway pressure were continuously measured. Results Pain stimulation and loaded breathing increased VAS scores, ventilation, and occlusion pressure (P0.1). The addition of a pain stimulus during loaded breathing increased the dyspneic VAS score (median 56 [interquartile range 50-62] vs. 64 [55-77]: before vs. after addition of pain stimulus, P &lt; 0.05) with concomitant increases in minute ventilation (10.8 [10.1-13.3] vs. 12.4 [11.0-14.8] l/min, P &lt; 0.05) and P0.1 (5.5 [4.9-7.2] vs. 6.8 [5.8-9.0] cm H2O, P &lt; 0.05). The addition of respiratory loading during pain stimulation did not cause a significant change in pain VAS score (40 [33-55] vs. 31 [30-44]: before vs. after addition of respiratory loading), although both additional burdens increased further minute ventilation (10.0 [8.8-10.9] vs. 12.0 [10.6-13.2] l/min, P &lt; 0.05) and P0.1 (2.5 [2.0-3.0] vs. 6.2 [4.9-7.0] cm H2O, P &lt; 0.05). Conclusion The authors' findings suggest that pain intensifies the dyspneic sensation, presumably by increasing the respiratory drive, whereas dyspnea may not intensify the pain sensation.



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