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Michael I Polkey - One of the best experts on this subject based on the ideXlab platform.
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effect of ambulatory continuous positive airway pressure on neural Respiratory Drive and functional capacity in excessive dynamic airway collapse
European Respiratory Journal, 2018Co-Authors: Georgios Kaltsakas, Michael I Polkey, Maxime Patou, Gill Arbane, Elodie Lhuillie, Liju Ahmed, David Dcruz, James H Hull, Patrick MurphyAbstract:Excessive dynamic airway collapse (EDAC) and tracheobronchomalacia (TBM) occur due to weakening of the walls of the central airways leading to airway collapse on expiration. The aim of this study was to investigate the effect of ambulatory continuous positive airway pressure (CPAP) on neural Respiratory Drive and exercise capacity. Patients with CT or bronchoscopic evidence of EDAC or TBM underwent baseline testing and 6-minute walk test (6MWT). Physiological testing was performed with patients self-ventilating and on CPAP at 4, 7 and 10 cmH2O to identify optimal ambulatory CPAP pressure. Patients then underwent repeat 6MWT on sham or active CPAP in a random order. Neural Respiratory Drive index (NRDI) was assessed by surface electromyography of the parasternal intercostals (EMGpara%max x Respiratory rate). We studied 19 (8 male), ambulatory adult patients with EDAC and/or TBM: age 60±13years and BMI 34.5±6.5kg/m2. The NRDI was 346±182AU self-ventilating with unloading of the Respiratory muscles with CPAP (delta -125±116AU; p In conclusion, ambulatory CPAP reduces neural Respiratory Drive and increases exercise capacity in patients with EDAC/TBM.
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S134 Effect of continuous positive airway pressure on neural Respiratory Drive and functional capacity in excessive dynamic airway collapse patients
Core outcomes for mechanical ventilation, 2017Co-Authors: Georgios Kaltsakas, Michael I Polkey, Nicholas Hart, Gill Arbane, Liju Ahmed, James H Hull, Maxime Patout, David D'cruz, Patrick B. MurphyAbstract:Excessive dynamic airway collapse (EDAC) and tracheobronchomalacia (TBM) occur due to weakening of the walls of the central airways leading to airway collapse on expiration. Positive airway pressure provides a pneumatic stent maintaining airway patency. CPAP is used to prevent airway collapse during sleep, but could also facilitate improved exercise capacity in this patient group. The aim of this study was to investigate the effect of ambulatory continuous positive airway pressure (CPAP) on neural Respiratory Drive and exercise capacity. Patients with CT or bronchoscopic evidence of EDAC or TBM underwent baseline testing and 6 min walk test (6MWT). Physiological testing was performed with patients self-ventilating and on CPAP at 4, 7 and 10 cm H 2 O to identify optimal ambulatory CPAP pressure. Patients then underwent repeat 6MWT on sham or active CPAP in a random order. Neural Respiratory Drive index (NRDI) was assessed by surface electromyography of the parasternal intercostals (EMG para %max χ Respiratory rate) while self-ventilating and on CPAP. We studied 20 (9 male), ambulatory adult patients with EDAC and/or TBM: mean ±SD age 60±13 years, height 1.67±0.86 m, and BMI 34.1±6.6 kg/m 2 . The NRDI was 356±182 AU while self-ventilating and reduced when CPAP was applied (231±122 AU; p In conclusion, CPAP reduces neural Respiratory Drive and increases exercise capacity in patients with EDAC/TBM. Furthermore, the degree of functional limitation and off-loading of the Respiratory muscles on CPAP can identify those likely to have a reduction in neural Respiratory Drive and enhanced exercise tolerance.
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Neural Respiratory Drive and Arousal in Patients with Obstructive Sleep Apnea Hypopnea.
Sleep, 2015Co-Authors: Sichang Xiao, Baiting He, Joerg Steier, John Moxham, Michael I PolkeyAbstract:STUDY OBJECTIVES: It has been hypothesized that arousals after apnea and hypopnea events in patients with obstructive sleep apnea are triggered when neural Respiratory Drive exceeds a certain level, but this hypothesis is based on esophageal pressure data, which are dependent on flow and lung volume. We aimed to determine whether a fixed threshold of Respiratory Drive is responsible for arousal at the termination of apnea and hypopnea using a flow independent technique (esophageal diaphragm electromyography, EMGdi) in patients with obstructive sleep apnea. SETTING: Sleep center of state Key Laboratory of Respiratory Disease. PATIENTS: Seventeen subjects (two women, mean age 53 ± 11 years) with obstructive sleep apnea/hypopnea syndrome were studied. METHODS: We recorded esophageal pressure and EMGdi simultaneously during overnight full polysomnography in all the subjects. MEASUREMENTS AND RESULTS: A total of 709 hypopnea events and 986 apnea events were analyzed. There was wide variation in both esophageal pressure and EMGdi at the end of both apnea and hypopnea events within a subject and stage 2 sleep. The EMGdi at the end of events that terminated with arousal was similar to those which terminated without arousal for both hypopnea events (27.6% ± 13.9%max vs 29.9% ± 15.9%max, P = ns) and apnea events (22.9% ± 11.5%max vs 22.1% ± 12.6%max, P = ns). The Pes at the end of Respiratory events terminated with arousal was also similar to those terminated without arousal. There was a small but significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea (25.3% ± 14.2%max vs 21.7% ± 13.2%max, P < 0.05]. CONCLUSIONS: Our data do not support the concept that there is threshold of neural Respiratory Drive that is responsible for arousal in patients with obstructive sleep apnea.
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Neural Respiratory Drive and breathlessness in COPD
The European respiratory journal, 2014Co-Authors: Caroline J. Jolley, Joerg Steier, Michael I Polkey, Y M Luo, Gerrard F. Rafferty, John MoxhamAbstract:The aim of this study was to test the hypothesis that neural Respiratory Drive, measured using diaphragm electromyogram (EMG di ) activity expressed as a percentage of maximum (EMG di%max ), is closely related to breathlessness in chronic obstructive pulmonary disease. We also investigated whether neuroventilatory uncoupling contributes significantly to breathlessness intensity over an awareness of levels of neural Respiratory Drive alone. EMGdi and ventilation were measured continuously during incremental cycle and treadmill exercise in 12 chronic obstructive pulmonary disease patients (forced expiratory volume in 1 s±sd was 38.7±14.5 % pred). EMG di was expressed both as EMG di%max and relative to tidal volume expressed as a percentage of predicted vital capacity to quantify neuroventilatory uncoupling. EMG di%max was closely related to Borg breathlessness in both cycle (r=0.98, p=0.0001) and treadmill exercise (r=0.94, p=0.005), this relationship being similar to that between neuroventilatory uncoupling and breathlessness (cycling r=0.94, p=0.005; treadmill r=0.91, p=0.01). The relationship between breathlessness and ventilation was poor when expansion of tidal volume became limited. In chronic obstructive pulmonary disease the intensity of exertional breathlessness is closely related to EMG di%max . These data suggest that breathlessness in chronic obstructive pulmonary disease can be largely explained by an awareness of levels of neural Respiratory Drive, rather than the degree of neuroventilatory uncoupling. EMG di%max could provide a useful physiological biomarker for breathlessness in chronic obstructive pulmonary disease.
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Neural Respiratory Drive and arousal in patients with obstructive sleep apnea–hypopnea
European Respiratory Journal, 2014Co-Authors: Sichang Xiao, Ying-xin Wu, Baiting He, Joerg Steier, John Moxham, Michael I PolkeyAbstract:Background: Repetitive arousals after apnea and hypopnea events in patients with obstructive sleep apnea have been hypothesized to be triggered by Respiratory effort. Objectives: The purpose of the study is to determine whether the threshold of Respiratory Drive responsible for arousal for apnea is the same as that for hypopnea. Methods: Seventeen subjects (two females and fifteen males, mean age 53±11 years) with obstructive sleep apnea and hypopnea were studied by recording diaphragm EMG and esophageal pressure during overnight full polysomnography. Results: A total of 709 hyponea events and 986 apnea events were analyzed. There was wide variation in Pes at the end of both apnea and hypopnea events and the maximal Pes could be four times higher than the minimal Pes at the end of apnea within a subject. 15.5%±14.2% of hypopnea events and 9.5%±11.6% of apnea events during stage 2 were terminated without arousal. There was significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea [(25.3±14.2) % EMGmax. vs (21.7 ±13.2)%EMGmax, p 0.05)] and apnea events [(22.9±11.5) % EMGmax vs (22.1±12.6) % EMGmax, p>0.05]. Conclusions: our data do not support the concept that there is threshold of Respiratory Drive which responsible for arousal to resume airflow.
John Moxham - One of the best experts on this subject based on the ideXlab platform.
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Observational Study of Neural Respiratory Drive During Sleep at High Altitude.
High altitude medicine & biology, 2017Co-Authors: Joerg Steier, John Moxham, Nic Cade, Ben Walker, Caroline J. JolleyAbstract:Steier, Joerg, Nic Cade, Ben Walker, John Moxham, and Caroline Jolley. Observational study of neural Respiratory Drive during sleep at high altitude. High Alt Med Biol. 18:242-248, 2017. AIMS Ventilation at altitude changes due to altered levels of pO2, pCO2 and the effect on blood pH. Nocturnal ventilation is particularly exposed to these changes. We hypothesized that an increasing neural Respiratory Drive (NRD) is associated with the severity of sleep-disordered breathing at altitude. METHODS Mountaineers were studied at sea level (London, United Kingdom), and at altitude at the Aconcagua (Andes, Argentina). NRD was measured as electromyogram of the diaphragm (EMGdi) overnight by a transesophageal multi-electrode catheter; results were reported for sea level, 3,380 m, 4,370 m, and 5,570 m. RESULTS Four healthy subjects (3 men, age 31(3)years, body mass index 23.6(0.9)kg/m2, neck circumference 37.0(2.7)cm, forced expiratory volume in 1 second 111.8(5.1)%predicted, and forced vital capacity 115.5(6.3)%predicted) were studied. No subject had significant sleep abnormalities at sea level. Time to ascent to 3,380 m was 1 day, to 4,370 m was 5 days, and the total nights at altitude were 21 days. The oxygen desaturation index (4% oxygen desaturation index [ODI] 0.8(0.4), 22.0 (7.2), 61.4 (26.9), 144.9/hour, respectively) and the EMGdi (5.2 (1.9), 12.8 (5.1), 14.1 (3.4), 18.5%, respectively) increased with the development of periodic breathing at altitude, whereas the average SpO2 declined (97.5 (1.3), 84.8 (0.5), 81.0 (4.1), 68.5%, respectively). The average EMGdi correlated well with the 4%ODI (r = 0.968, p = 0.032). CONCLUSION NRD sleep increases at altitude in relation to the severity of periodic breathing.
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S23 Neural Respiratory Drive during sleep at high altitude
Thorax, 2016Co-Authors: Joerg Steier, John Moxham, Nic Cade, Ben Walker, Caroline J. JolleyAbstract:Introduction Ventilation at altitude changes due to altered levels of pO2, pCO2 and the effect on blood pH. Nocturnal ventilation is particularly exposed to these changes. We hypothesised that increasing neural Respiratory Drive is associated with the severity of sleep-disordered breathing at altitude. Subjects and methods British mountaineers were studied at sea level (London, UK), and at altitude at the Aconcagua (Andes, Argentina). Neural Respiratory Drive (NRD) was measured as electromyogram of the diaphragm (EMGdi) overnight by a transoesophageal multi-electrode catheter (Yinghui Medical Ltd, Guangzhou, China). Following initial assessment with a polysomnography (London, UK), pulse oximetry measured oxygen concentration and oxygen desaturation indices (4%ODI) at altitude. Results Four healthy subjects (3male, age 31 (3) years, body-mass-index 23.6 (0.9) kg/m 2 , neck circumference 37.0 (2.7) cm, FEV 1 111.8 (5.1)% predicted, FVC 115.5 (6.3)% predicted) were studied. Inspiratory and expiratory muscle strength were normal (PImax 130.7 (29.8) cm H 2 O, PEmax (153.3 (38.4) cm H 2 O). No subject had significant sleep abnormalities at sea level (Total Sleep Time 344.4 (30.5) mins, Sleep Efficiency 86.6 (6.4)%, Respiratory Disturbance Index 0.8 (0.4)/hour, mean SpO 2 97.5 (1.3%). The oxygen desaturation index increased with the development of periodic breathing at altitude (4% ODI 22.0 (7.2)/hour at 3,380m, 61.4 (26.9)/hour at 4,370m). Average nocturnal SpO2 (84.8 (0.5%)) at 3,380m; 81.0 (4.1%) at 4,370m) and nadir oxygenation (68.1 (8.6%) at 3,380m; 67.4 (7.6%) at 4,370m) dropped with altitude. The average EMGdi was 5.2 (19.1%) max at sea level and increased to 14.1 (3.4%) at altitude when falling asleep at 4,370m, and correlated well with the 4%ODI (r = 0.968, p = 0.032). EMGdi during the last inspiratory effort prior to central apnoea was 5.1 (1.5%) max, while the first inspiratory effort following central apnoea was 10.5 (3.2%) max at 4,370m. Conclusion The severity of periodic breathing when asleep deteriorates with an increase in altitude, induced by an elevated neural Respiratory Drive as a response to hypobaric environmental conditions.
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Neural Respiratory Drive and Arousal in Patients with Obstructive Sleep Apnea Hypopnea.
Sleep, 2015Co-Authors: Sichang Xiao, Baiting He, Joerg Steier, John Moxham, Michael I PolkeyAbstract:STUDY OBJECTIVES: It has been hypothesized that arousals after apnea and hypopnea events in patients with obstructive sleep apnea are triggered when neural Respiratory Drive exceeds a certain level, but this hypothesis is based on esophageal pressure data, which are dependent on flow and lung volume. We aimed to determine whether a fixed threshold of Respiratory Drive is responsible for arousal at the termination of apnea and hypopnea using a flow independent technique (esophageal diaphragm electromyography, EMGdi) in patients with obstructive sleep apnea. SETTING: Sleep center of state Key Laboratory of Respiratory Disease. PATIENTS: Seventeen subjects (two women, mean age 53 ± 11 years) with obstructive sleep apnea/hypopnea syndrome were studied. METHODS: We recorded esophageal pressure and EMGdi simultaneously during overnight full polysomnography in all the subjects. MEASUREMENTS AND RESULTS: A total of 709 hypopnea events and 986 apnea events were analyzed. There was wide variation in both esophageal pressure and EMGdi at the end of both apnea and hypopnea events within a subject and stage 2 sleep. The EMGdi at the end of events that terminated with arousal was similar to those which terminated without arousal for both hypopnea events (27.6% ± 13.9%max vs 29.9% ± 15.9%max, P = ns) and apnea events (22.9% ± 11.5%max vs 22.1% ± 12.6%max, P = ns). The Pes at the end of Respiratory events terminated with arousal was also similar to those terminated without arousal. There was a small but significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea (25.3% ± 14.2%max vs 21.7% ± 13.2%max, P < 0.05]. CONCLUSIONS: Our data do not support the concept that there is threshold of neural Respiratory Drive that is responsible for arousal in patients with obstructive sleep apnea.
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Neural Respiratory Drive and breathlessness in COPD
The European respiratory journal, 2014Co-Authors: Caroline J. Jolley, Joerg Steier, Michael I Polkey, Y M Luo, Gerrard F. Rafferty, John MoxhamAbstract:The aim of this study was to test the hypothesis that neural Respiratory Drive, measured using diaphragm electromyogram (EMG di ) activity expressed as a percentage of maximum (EMG di%max ), is closely related to breathlessness in chronic obstructive pulmonary disease. We also investigated whether neuroventilatory uncoupling contributes significantly to breathlessness intensity over an awareness of levels of neural Respiratory Drive alone. EMGdi and ventilation were measured continuously during incremental cycle and treadmill exercise in 12 chronic obstructive pulmonary disease patients (forced expiratory volume in 1 s±sd was 38.7±14.5 % pred). EMG di was expressed both as EMG di%max and relative to tidal volume expressed as a percentage of predicted vital capacity to quantify neuroventilatory uncoupling. EMG di%max was closely related to Borg breathlessness in both cycle (r=0.98, p=0.0001) and treadmill exercise (r=0.94, p=0.005), this relationship being similar to that between neuroventilatory uncoupling and breathlessness (cycling r=0.94, p=0.005; treadmill r=0.91, p=0.01). The relationship between breathlessness and ventilation was poor when expansion of tidal volume became limited. In chronic obstructive pulmonary disease the intensity of exertional breathlessness is closely related to EMG di%max . These data suggest that breathlessness in chronic obstructive pulmonary disease can be largely explained by an awareness of levels of neural Respiratory Drive, rather than the degree of neuroventilatory uncoupling. EMG di%max could provide a useful physiological biomarker for breathlessness in chronic obstructive pulmonary disease.
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Neural Respiratory Drive and arousal in patients with obstructive sleep apnea–hypopnea
European Respiratory Journal, 2014Co-Authors: Sichang Xiao, Ying-xin Wu, Baiting He, Joerg Steier, John Moxham, Michael I PolkeyAbstract:Background: Repetitive arousals after apnea and hypopnea events in patients with obstructive sleep apnea have been hypothesized to be triggered by Respiratory effort. Objectives: The purpose of the study is to determine whether the threshold of Respiratory Drive responsible for arousal for apnea is the same as that for hypopnea. Methods: Seventeen subjects (two females and fifteen males, mean age 53±11 years) with obstructive sleep apnea and hypopnea were studied by recording diaphragm EMG and esophageal pressure during overnight full polysomnography. Results: A total of 709 hyponea events and 986 apnea events were analyzed. There was wide variation in Pes at the end of both apnea and hypopnea events and the maximal Pes could be four times higher than the minimal Pes at the end of apnea within a subject. 15.5%±14.2% of hypopnea events and 9.5%±11.6% of apnea events during stage 2 were terminated without arousal. There was significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea [(25.3±14.2) % EMGmax. vs (21.7 ±13.2)%EMGmax, p 0.05)] and apnea events [(22.9±11.5) % EMGmax vs (22.1±12.6) % EMGmax, p>0.05]. Conclusions: our data do not support the concept that there is threshold of Respiratory Drive which responsible for arousal to resume airflow.
Joerg Steier - One of the best experts on this subject based on the ideXlab platform.
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Observational Study of Neural Respiratory Drive During Sleep at High Altitude.
High altitude medicine & biology, 2017Co-Authors: Joerg Steier, John Moxham, Nic Cade, Ben Walker, Caroline J. JolleyAbstract:Steier, Joerg, Nic Cade, Ben Walker, John Moxham, and Caroline Jolley. Observational study of neural Respiratory Drive during sleep at high altitude. High Alt Med Biol. 18:242-248, 2017. AIMS Ventilation at altitude changes due to altered levels of pO2, pCO2 and the effect on blood pH. Nocturnal ventilation is particularly exposed to these changes. We hypothesized that an increasing neural Respiratory Drive (NRD) is associated with the severity of sleep-disordered breathing at altitude. METHODS Mountaineers were studied at sea level (London, United Kingdom), and at altitude at the Aconcagua (Andes, Argentina). NRD was measured as electromyogram of the diaphragm (EMGdi) overnight by a transesophageal multi-electrode catheter; results were reported for sea level, 3,380 m, 4,370 m, and 5,570 m. RESULTS Four healthy subjects (3 men, age 31(3)years, body mass index 23.6(0.9)kg/m2, neck circumference 37.0(2.7)cm, forced expiratory volume in 1 second 111.8(5.1)%predicted, and forced vital capacity 115.5(6.3)%predicted) were studied. No subject had significant sleep abnormalities at sea level. Time to ascent to 3,380 m was 1 day, to 4,370 m was 5 days, and the total nights at altitude were 21 days. The oxygen desaturation index (4% oxygen desaturation index [ODI] 0.8(0.4), 22.0 (7.2), 61.4 (26.9), 144.9/hour, respectively) and the EMGdi (5.2 (1.9), 12.8 (5.1), 14.1 (3.4), 18.5%, respectively) increased with the development of periodic breathing at altitude, whereas the average SpO2 declined (97.5 (1.3), 84.8 (0.5), 81.0 (4.1), 68.5%, respectively). The average EMGdi correlated well with the 4%ODI (r = 0.968, p = 0.032). CONCLUSION NRD sleep increases at altitude in relation to the severity of periodic breathing.
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S23 Neural Respiratory Drive during sleep at high altitude
Thorax, 2016Co-Authors: Joerg Steier, John Moxham, Nic Cade, Ben Walker, Caroline J. JolleyAbstract:Introduction Ventilation at altitude changes due to altered levels of pO2, pCO2 and the effect on blood pH. Nocturnal ventilation is particularly exposed to these changes. We hypothesised that increasing neural Respiratory Drive is associated with the severity of sleep-disordered breathing at altitude. Subjects and methods British mountaineers were studied at sea level (London, UK), and at altitude at the Aconcagua (Andes, Argentina). Neural Respiratory Drive (NRD) was measured as electromyogram of the diaphragm (EMGdi) overnight by a transoesophageal multi-electrode catheter (Yinghui Medical Ltd, Guangzhou, China). Following initial assessment with a polysomnography (London, UK), pulse oximetry measured oxygen concentration and oxygen desaturation indices (4%ODI) at altitude. Results Four healthy subjects (3male, age 31 (3) years, body-mass-index 23.6 (0.9) kg/m 2 , neck circumference 37.0 (2.7) cm, FEV 1 111.8 (5.1)% predicted, FVC 115.5 (6.3)% predicted) were studied. Inspiratory and expiratory muscle strength were normal (PImax 130.7 (29.8) cm H 2 O, PEmax (153.3 (38.4) cm H 2 O). No subject had significant sleep abnormalities at sea level (Total Sleep Time 344.4 (30.5) mins, Sleep Efficiency 86.6 (6.4)%, Respiratory Disturbance Index 0.8 (0.4)/hour, mean SpO 2 97.5 (1.3%). The oxygen desaturation index increased with the development of periodic breathing at altitude (4% ODI 22.0 (7.2)/hour at 3,380m, 61.4 (26.9)/hour at 4,370m). Average nocturnal SpO2 (84.8 (0.5%)) at 3,380m; 81.0 (4.1%) at 4,370m) and nadir oxygenation (68.1 (8.6%) at 3,380m; 67.4 (7.6%) at 4,370m) dropped with altitude. The average EMGdi was 5.2 (19.1%) max at sea level and increased to 14.1 (3.4%) at altitude when falling asleep at 4,370m, and correlated well with the 4%ODI (r = 0.968, p = 0.032). EMGdi during the last inspiratory effort prior to central apnoea was 5.1 (1.5%) max, while the first inspiratory effort following central apnoea was 10.5 (3.2%) max at 4,370m. Conclusion The severity of periodic breathing when asleep deteriorates with an increase in altitude, induced by an elevated neural Respiratory Drive as a response to hypobaric environmental conditions.
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Neural Respiratory Drive and Arousal in Patients with Obstructive Sleep Apnea Hypopnea.
Sleep, 2015Co-Authors: Sichang Xiao, Baiting He, Joerg Steier, John Moxham, Michael I PolkeyAbstract:STUDY OBJECTIVES: It has been hypothesized that arousals after apnea and hypopnea events in patients with obstructive sleep apnea are triggered when neural Respiratory Drive exceeds a certain level, but this hypothesis is based on esophageal pressure data, which are dependent on flow and lung volume. We aimed to determine whether a fixed threshold of Respiratory Drive is responsible for arousal at the termination of apnea and hypopnea using a flow independent technique (esophageal diaphragm electromyography, EMGdi) in patients with obstructive sleep apnea. SETTING: Sleep center of state Key Laboratory of Respiratory Disease. PATIENTS: Seventeen subjects (two women, mean age 53 ± 11 years) with obstructive sleep apnea/hypopnea syndrome were studied. METHODS: We recorded esophageal pressure and EMGdi simultaneously during overnight full polysomnography in all the subjects. MEASUREMENTS AND RESULTS: A total of 709 hypopnea events and 986 apnea events were analyzed. There was wide variation in both esophageal pressure and EMGdi at the end of both apnea and hypopnea events within a subject and stage 2 sleep. The EMGdi at the end of events that terminated with arousal was similar to those which terminated without arousal for both hypopnea events (27.6% ± 13.9%max vs 29.9% ± 15.9%max, P = ns) and apnea events (22.9% ± 11.5%max vs 22.1% ± 12.6%max, P = ns). The Pes at the end of Respiratory events terminated with arousal was also similar to those terminated without arousal. There was a small but significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea (25.3% ± 14.2%max vs 21.7% ± 13.2%max, P < 0.05]. CONCLUSIONS: Our data do not support the concept that there is threshold of neural Respiratory Drive that is responsible for arousal in patients with obstructive sleep apnea.
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Neural Respiratory Drive and breathlessness in COPD
The European respiratory journal, 2014Co-Authors: Caroline J. Jolley, Joerg Steier, Michael I Polkey, Y M Luo, Gerrard F. Rafferty, John MoxhamAbstract:The aim of this study was to test the hypothesis that neural Respiratory Drive, measured using diaphragm electromyogram (EMG di ) activity expressed as a percentage of maximum (EMG di%max ), is closely related to breathlessness in chronic obstructive pulmonary disease. We also investigated whether neuroventilatory uncoupling contributes significantly to breathlessness intensity over an awareness of levels of neural Respiratory Drive alone. EMGdi and ventilation were measured continuously during incremental cycle and treadmill exercise in 12 chronic obstructive pulmonary disease patients (forced expiratory volume in 1 s±sd was 38.7±14.5 % pred). EMG di was expressed both as EMG di%max and relative to tidal volume expressed as a percentage of predicted vital capacity to quantify neuroventilatory uncoupling. EMG di%max was closely related to Borg breathlessness in both cycle (r=0.98, p=0.0001) and treadmill exercise (r=0.94, p=0.005), this relationship being similar to that between neuroventilatory uncoupling and breathlessness (cycling r=0.94, p=0.005; treadmill r=0.91, p=0.01). The relationship between breathlessness and ventilation was poor when expansion of tidal volume became limited. In chronic obstructive pulmonary disease the intensity of exertional breathlessness is closely related to EMG di%max . These data suggest that breathlessness in chronic obstructive pulmonary disease can be largely explained by an awareness of levels of neural Respiratory Drive, rather than the degree of neuroventilatory uncoupling. EMG di%max could provide a useful physiological biomarker for breathlessness in chronic obstructive pulmonary disease.
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Neural Respiratory Drive and arousal in patients with obstructive sleep apnea–hypopnea
European Respiratory Journal, 2014Co-Authors: Sichang Xiao, Ying-xin Wu, Baiting He, Joerg Steier, John Moxham, Michael I PolkeyAbstract:Background: Repetitive arousals after apnea and hypopnea events in patients with obstructive sleep apnea have been hypothesized to be triggered by Respiratory effort. Objectives: The purpose of the study is to determine whether the threshold of Respiratory Drive responsible for arousal for apnea is the same as that for hypopnea. Methods: Seventeen subjects (two females and fifteen males, mean age 53±11 years) with obstructive sleep apnea and hypopnea were studied by recording diaphragm EMG and esophageal pressure during overnight full polysomnography. Results: A total of 709 hyponea events and 986 apnea events were analyzed. There was wide variation in Pes at the end of both apnea and hypopnea events and the maximal Pes could be four times higher than the minimal Pes at the end of apnea within a subject. 15.5%±14.2% of hypopnea events and 9.5%±11.6% of apnea events during stage 2 were terminated without arousal. There was significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea [(25.3±14.2) % EMGmax. vs (21.7 ±13.2)%EMGmax, p 0.05)] and apnea events [(22.9±11.5) % EMGmax vs (22.1±12.6) % EMGmax, p>0.05]. Conclusions: our data do not support the concept that there is threshold of Respiratory Drive which responsible for arousal to resume airflow.
Yuanming Luo - One of the best experts on this subject based on the ideXlab platform.
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neural Respiratory Drive and arousal in patients with obstructive sleep apnea hypopnea
European Respiratory Journal, 2014Co-Authors: Sichang Xiao, Joerg Steier, John Moxham, Michael I Polkey, Yuanming LuoAbstract:Background: Repetitive arousals after apnea and hypopnea events in patients with obstructive sleep apnea have been hypothesized to be triggered by Respiratory effort. Objectives: The purpose of the study is to determine whether the threshold of Respiratory Drive responsible for arousal for apnea is the same as that for hypopnea. Methods: Seventeen subjects (two females and fifteen males, mean age 53±11 years) with obstructive sleep apnea and hypopnea were studied by recording diaphragm EMG and esophageal pressure during overnight full polysomnography. Results: A total of 709 hyponea events and 986 apnea events were analyzed. There was wide variation in Pes at the end of both apnea and hypopnea events and the maximal Pes could be four times higher than the minimal Pes at the end of apnea within a subject. 15.5%±14.2% of hypopnea events and 9.5%±11.6% of apnea events during stage 2 were terminated without arousal. There was significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea [(25.3±14.2) % EMGmax. vs (21.7 ±13.2)%EMGmax, p 0.05)] and apnea events [(22.9±11.5) % EMGmax vs (22.1±12.6) % EMGmax, p>0.05]. Conclusions: our data do not support the concept that there is threshold of Respiratory Drive which responsible for arousal to resume airflow.
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neural Respiratory Drive and ventilation in patients with chronic obstructive pulmonary disease during sleep
American Journal of Respiratory and Critical Care Medicine, 2014Co-Authors: Yuanming Luo, John Moxham, Hong Yuan, Michael I PolkeyAbstract:To the Editor: Patients with chronic obstructive pulmonary disease (COPD) experience sleep-related hypoventilation (1, 2). However, there is controversy as to whether this occurs due to an increase in upper airway resistance or a reduction in neural Respiratory Drive. Elevated neural Respiratory Drive in wakefulness is well documented in COPD (3). O’Donoghue and coworkers (4) reported in patients with COPD that a sleep-related hypoventilation was due to increased upper airway resistance, and Ballard and coworkers (5) reported an increase in upper airway resistance moving from wakefulness to sleep, although upper airway resistance was not consistently greater during sleep (see Figure 3 of their article [5]). Moreover, in healthy young adults, a poor correlation was observed between changes in ventilation and upper airway resistance (6). Morrell and coworkers (7) addressed the question directly in tracheotomized subjects, confirming hypoventilation during sleep, thus excluding an obligate contribution from upper airway resistance. To further address the question, we performed diaphragm electromyography (EMGdi) using a multipair esophageal electrode as an index of neural Respiratory Drive (8–11). Some of the data have been previously reported in abstract form (12). A total of 17 stable patients with moderate to very severe COPD and 14 age-matched normal subjects participated. All subjects were free from obstructive sleep apnea (OSA; apnea–hypopnea index < 5.0 events/h) and snoring confirmed by prior overnight polysomnography, and were free from clinically significant coexisting diseases, including neuromuscular disorders. The study was approved by the Ethics Committee of the Chinese State Key Laboratory of Respiratory Disease, and all patients gave their informed consent to participate. A multipair esophageal electrode catheter (Yinghui Medical Technology Co., Ltd, Guangzhou, China) was used as previously described (8) to record the EMGdi during overnight polysomnography (9–11). Airflow was recorded with a pneumotachograph connected to a full facemask. Maximal EMGdi was recorded from maximal voluntary inspiratory maneuvers. Polysomnography was manually analyzed based on standard criteria (13). The root mean square (RMS) of the EMGdi (RMSEMGdi) was calculated by computer with a time constant of 100 milliseconds. Efficacy of neural Respiratory Drive was defined as the ratio of minute ventilation to peak RMSEMGdi of each breath. Data were selected during stable breathing without Respiratory events. Data collected for 10 minutes before sleep and for at least 15 minutes during non–rapid eye movement (NREM) and REM in the supine position were selected for analysis. Two-way ANOVA was used to test differences between wakefulness, NREM, and REM sleep; data are presented as means (±SD), and statistical significance was determined as a P value of less than 0.05. Some subjects could not tolerate the full facemask, and satisfactory measurements were therefore obtained in 10 male patients with COPD (age, 59.3 ± 11.5 yr; body mass index, 20.8 ± 3.1 kg/m2; FEV1, 34.2 ± 15.8% predicted; FEV1/FVC, 37.8 ± 11.6%; oxygen saturation <90%, 2.0 ± 4.0% of total sleep time) and 10 control subjects (nine males and one female, age, 58.1 ± 9.0 yr; body mass index, 22.8 ± 2.8 kg/m2; FEV1 97.8 ± 9.5% predicted). The maximal RMSEMGdi measured from patients with COPD was similar to control subjects (180.7 ± 92.0 μV vs. 161.7 ± 53.6 μV). RMSEMGdi, as a percent maximal, in patients with COPD was significantly higher than that in normal subjects during wakefulness, NREM, and REM (Table 1). Compared with wakefulness, the RMSEMGdi decreased by 31 (±12)% in NREM, and further decreased by 49 (±12)% in REM sleep in patients with COPD. Similarly, ventilation decreased by 30 (±14)% in NREM and 44 (±11)% in REM. As shown in Table 1, the reduction in ventilation was principally mediated by tidal volume. The reductions in the RMSEMGdi and ventilation were of smaller magnitude in normal subjects. The efficacy of neural Respiratory Drive in normal subjects was significantly higher than that in patients with COPD during both wakefulness and sleep. However, sleep did not change the efficacy of neural Respiratory Drive in either patients with COPD or normal subjects (Table 1 and Figure 1). Table 1. The Root Mean Square of the Diaphragm Electromyography and Ventilation during Wakefulness and Sleep and Their Change Compared with Wakefulness Figure 1. Polysomnography including five-channel diaphragm electromyography (EMGdi; 1–5) from a multipair esophageal electrode, airflow from pneumotachograph, end-tidal CO2, electroencephalogram (EEG; C3A2 and C4A1), and left and right electrooculograms ... This is the first study to simultaneously accurately record ventilation with a pneumotachograph connected to a full facemask and EMGdi, during wakefulness, NREM, and REM sleep, in patients with COPD without coexisting OSA. The efficacy of neural Respiratory Drive reflects upper airway resistance if lung mechanics and lower airway resistance remain the same. Because this is considered to be the case (4, 5), we speculate that the unchanged efficacy of neural Respiratory Drive between wakefulness and sleep argues against a substantial increase in upper airway resistance during sleep in either nonobese patients with COPD or normal subjects. This result is consistent with the work of Meurice and coworkers (14), who reported that upper airway resistance changed little in some patients with COPD during sleep. Although O’Donoghue and colleagues (4) concluded that sleep-related hypoventilation in patients with COPD was because of a threefold increase in upper airway resistance, the subjects they studied may have had mild OSA, because an apnea–hypopnea index up to 10 events/h was permitted. Our results are consistent with the results reported by Morrell and coworkers (7), who showed that the development of sleep-related hypoventilation is independent of upper airway resistance, because the reduction of ventilation from wakefulness to NREM sleep in subjects who were breathing through the upper airway was similar to that in laryngectomized subjects who were breathing through a tracheal stoma. Our conclusions are also consistent with other data supporting the case that reduction of neural Respiratory Drive is important in sleep-related hypoventilation. For example, when continuous positive airway pressure is applied in patients with COPD to eliminate upper airway resistance (1), or to normalize upper airway resistance to waking levels in normal subjects (15), sleep-related hypoventilation is still evident. Naturally, our study has some limitations. We had a relatively small sample size, and all patients were from one ethnic group and were not in Respiratory failure, which could modify pharyngeal behavior (15). Our data are only representative of those who could sleep while instrumented. Thus, our findings should not be extended uncritically to all patients with COPD. However, in contrast to the previous hypothesis that hypoventilation is principally due to upper airway resistance, our study suggests that sleep-associated hypoventilation in patients with COPD is mainly related to reduction of neural Respiratory Drive. This observation suggests that noninvasive positive-pressure ventilation is a more logical approach than continuous positive airway pressure to the treatment of nocturnal hypoventilation in COPD.
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Neural Respiratory Drive and Ventilation in Patients with Chronic Obstructive Pulmonary Disease during Sleep
American journal of respiratory and critical care medicine, 2014Co-Authors: Yuanming Luo, John Moxham, Hong Yuan, Michael I PolkeyAbstract:To the Editor: Patients with chronic obstructive pulmonary disease (COPD) experience sleep-related hypoventilation (1, 2). However, there is controversy as to whether this occurs due to an increase in upper airway resistance or a reduction in neural Respiratory Drive. Elevated neural Respiratory Drive in wakefulness is well documented in COPD (3). O’Donoghue and coworkers (4) reported in patients with COPD that a sleep-related hypoventilation was due to increased upper airway resistance, and Ballard and coworkers (5) reported an increase in upper airway resistance moving from wakefulness to sleep, although upper airway resistance was not consistently greater during sleep (see Figure 3 of their article [5]). Moreover, in healthy young adults, a poor correlation was observed between changes in ventilation and upper airway resistance (6). Morrell and coworkers (7) addressed the question directly in tracheotomized subjects, confirming hypoventilation during sleep, thus excluding an obligate contribution from upper airway resistance. To further address the question, we performed diaphragm electromyography (EMGdi) using a multipair esophageal electrode as an index of neural Respiratory Drive (8–11). Some of the data have been previously reported in abstract form (12). A total of 17 stable patients with moderate to very severe COPD and 14 age-matched normal subjects participated. All subjects were free from obstructive sleep apnea (OSA; apnea–hypopnea index < 5.0 events/h) and snoring confirmed by prior overnight polysomnography, and were free from clinically significant coexisting diseases, including neuromuscular disorders. The study was approved by the Ethics Committee of the Chinese State Key Laboratory of Respiratory Disease, and all patients gave their informed consent to participate. A multipair esophageal electrode catheter (Yinghui Medical Technology Co., Ltd, Guangzhou, China) was used as previously described (8) to record the EMGdi during overnight polysomnography (9–11). Airflow was recorded with a pneumotachograph connected to a full facemask. Maximal EMGdi was recorded from maximal voluntary inspiratory maneuvers. Polysomnography was manually analyzed based on standard criteria (13). The root mean square (RMS) of the EMGdi (RMSEMGdi) was calculated by computer with a time constant of 100 milliseconds. Efficacy of neural Respiratory Drive was defined as the ratio of minute ventilation to peak RMSEMGdi of each breath. Data were selected during stable breathing without Respiratory events. Data collected for 10 minutes before sleep and for at least 15 minutes during non–rapid eye movement (NREM) and REM in the supine position were selected for analysis. Two-way ANOVA was used to test differences between wakefulness, NREM, and REM sleep; data are presented as means (±SD), and statistical significance was determined as a P value of less than 0.05. Some subjects could not tolerate the full facemask, and satisfactory measurements were therefore obtained in 10 male patients with COPD (age, 59.3 ± 11.5 yr; body mass index, 20.8 ± 3.1 kg/m2; FEV1, 34.2 ± 15.8% predicted; FEV1/FVC, 37.8 ± 11.6%; oxygen saturation
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Assessment of neural Respiratory Drive in humans
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases, 2013Co-Authors: Zhi-da Liu, Sichang Xiao, Zhi-hui Qiu, Kang-xin Tan, Liu Miaofang, Yuanming LuoAbstract:Objective Assessment of neural Respiratory Drive is useful for diagnosis of dyspnea and Respiratory failure with unknown causes. The purpose of the study was to compare the sensitivity of trandiaphragmatic pressure (Pdi) and diaphragm electromyogram (EMGdi) in assessment of neural Respiratory Drive. Methods A combined catheter with 10 electrodes and 2 balloons was used to record EMGdi and Pdi during CO2 rebreathing. Three different inspiratory maneuvers-inspiration from functional residual capacity to total lung capacity (TLC), deep inspiration from functional residual capacity against closed airway (MIP), and short sharp inspiration through the nose (Sniff) were performed. Ten healthy subjects [male 4 and female 6; age (26±4) years] were studied. Results Linear relationship between EMGdi and end-tidal CO2 (r=0.83-0.98, all P
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Neural Respiratory Drive to the diaphragm in patients with COPD during sleep
B70. SLEEP DISORDERED BREATHING: PATHOPHYSIOLOGY, 2012Co-Authors: Zhi-hui Qiu, Hong Yang, Nanshan Zhong, Yuanming LuoAbstract:Patients with COPD may develop hypoxia and hypercapnia during sleep, in particular in REM stage although normal ventilation is usually sustained during daytime. Reduction of neural Respiratory Drive during sleep was hypothesized to be an important mechanism underling hypoxia and hypercapnia. However healthy subjects do not develop hypoxia during sleep. To determine whether change of neural Respiratory Drive in patients with COPD differed from that in normal subjects, we studied nine patients with COPD (age 58.6±11.8 years; FEV1%pred 49±18) and six normal subjects (Age 58.9±10.1 years; FEV 1 %pred 98.0%±10.5%). We recorded the diaphragm EMG from a multipair esophageal electrode during overnight full polysomnography including recording of airflow which was measured by pneumotachograph. Sleep efficiency in both groups was low mainly because of interference of face mask and pneumotachograph. Sleep efficiency in COPD group was worse than that in normal group (52.8 ±16.1 vs 69.5±13.7). Tidal volume (ml/kg) in patients with COPD decreased by 32.2%±21.3% in NREM stages and further decreased by 45.6%±16.6% in REM stage compared with wakefulness. The decrease of tidal volume from wakefulness to sleep in COPD was significantly larger than that in normal subjects. Diaphragm EMG decreased by 30.0%±21.4% and 37.1%±20.0% from wakefulness to NREM and REM respectively in patients with COPD. However, diaphragm EMG in normal subjects remained the same or only slightly decreased during sleep when compared with wakefulness. We conclude that reduction in neural Drive during sleep in patients with COPD is greater than that normal subjects and may be responsible for hypoxia in patients with COPD.
Sichang Xiao - One of the best experts on this subject based on the ideXlab platform.
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Neural Respiratory Drive and Arousal in Patients with Obstructive Sleep Apnea Hypopnea.
Sleep, 2015Co-Authors: Sichang Xiao, Baiting He, Joerg Steier, John Moxham, Michael I PolkeyAbstract:STUDY OBJECTIVES: It has been hypothesized that arousals after apnea and hypopnea events in patients with obstructive sleep apnea are triggered when neural Respiratory Drive exceeds a certain level, but this hypothesis is based on esophageal pressure data, which are dependent on flow and lung volume. We aimed to determine whether a fixed threshold of Respiratory Drive is responsible for arousal at the termination of apnea and hypopnea using a flow independent technique (esophageal diaphragm electromyography, EMGdi) in patients with obstructive sleep apnea. SETTING: Sleep center of state Key Laboratory of Respiratory Disease. PATIENTS: Seventeen subjects (two women, mean age 53 ± 11 years) with obstructive sleep apnea/hypopnea syndrome were studied. METHODS: We recorded esophageal pressure and EMGdi simultaneously during overnight full polysomnography in all the subjects. MEASUREMENTS AND RESULTS: A total of 709 hypopnea events and 986 apnea events were analyzed. There was wide variation in both esophageal pressure and EMGdi at the end of both apnea and hypopnea events within a subject and stage 2 sleep. The EMGdi at the end of events that terminated with arousal was similar to those which terminated without arousal for both hypopnea events (27.6% ± 13.9%max vs 29.9% ± 15.9%max, P = ns) and apnea events (22.9% ± 11.5%max vs 22.1% ± 12.6%max, P = ns). The Pes at the end of Respiratory events terminated with arousal was also similar to those terminated without arousal. There was a small but significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea (25.3% ± 14.2%max vs 21.7% ± 13.2%max, P < 0.05]. CONCLUSIONS: Our data do not support the concept that there is threshold of neural Respiratory Drive that is responsible for arousal in patients with obstructive sleep apnea.
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Neural Respiratory Drive and arousal in patients with obstructive sleep apnea–hypopnea
European Respiratory Journal, 2014Co-Authors: Sichang Xiao, Ying-xin Wu, Baiting He, Joerg Steier, John Moxham, Michael I PolkeyAbstract:Background: Repetitive arousals after apnea and hypopnea events in patients with obstructive sleep apnea have been hypothesized to be triggered by Respiratory effort. Objectives: The purpose of the study is to determine whether the threshold of Respiratory Drive responsible for arousal for apnea is the same as that for hypopnea. Methods: Seventeen subjects (two females and fifteen males, mean age 53±11 years) with obstructive sleep apnea and hypopnea were studied by recording diaphragm EMG and esophageal pressure during overnight full polysomnography. Results: A total of 709 hyponea events and 986 apnea events were analyzed. There was wide variation in Pes at the end of both apnea and hypopnea events and the maximal Pes could be four times higher than the minimal Pes at the end of apnea within a subject. 15.5%±14.2% of hypopnea events and 9.5%±11.6% of apnea events during stage 2 were terminated without arousal. There was significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea [(25.3±14.2) % EMGmax. vs (21.7 ±13.2)%EMGmax, p 0.05)] and apnea events [(22.9±11.5) % EMGmax vs (22.1±12.6) % EMGmax, p>0.05]. Conclusions: our data do not support the concept that there is threshold of Respiratory Drive which responsible for arousal to resume airflow.
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neural Respiratory Drive and arousal in patients with obstructive sleep apnea hypopnea
European Respiratory Journal, 2014Co-Authors: Sichang Xiao, Joerg Steier, John Moxham, Michael I Polkey, Yuanming LuoAbstract:Background: Repetitive arousals after apnea and hypopnea events in patients with obstructive sleep apnea have been hypothesized to be triggered by Respiratory effort. Objectives: The purpose of the study is to determine whether the threshold of Respiratory Drive responsible for arousal for apnea is the same as that for hypopnea. Methods: Seventeen subjects (two females and fifteen males, mean age 53±11 years) with obstructive sleep apnea and hypopnea were studied by recording diaphragm EMG and esophageal pressure during overnight full polysomnography. Results: A total of 709 hyponea events and 986 apnea events were analyzed. There was wide variation in Pes at the end of both apnea and hypopnea events and the maximal Pes could be four times higher than the minimal Pes at the end of apnea within a subject. 15.5%±14.2% of hypopnea events and 9.5%±11.6% of apnea events during stage 2 were terminated without arousal. There was significant difference in EMGdi at the end of Respiratory events between hypopnea and apnea [(25.3±14.2) % EMGmax. vs (21.7 ±13.2)%EMGmax, p 0.05)] and apnea events [(22.9±11.5) % EMGmax vs (22.1±12.6) % EMGmax, p>0.05]. Conclusions: our data do not support the concept that there is threshold of Respiratory Drive which responsible for arousal to resume airflow.
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Assessment of neural Respiratory Drive in humans
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases, 2013Co-Authors: Zhi-da Liu, Sichang Xiao, Zhi-hui Qiu, Kang-xin Tan, Liu Miaofang, Yuanming LuoAbstract:Objective Assessment of neural Respiratory Drive is useful for diagnosis of dyspnea and Respiratory failure with unknown causes. The purpose of the study was to compare the sensitivity of trandiaphragmatic pressure (Pdi) and diaphragm electromyogram (EMGdi) in assessment of neural Respiratory Drive. Methods A combined catheter with 10 electrodes and 2 balloons was used to record EMGdi and Pdi during CO2 rebreathing. Three different inspiratory maneuvers-inspiration from functional residual capacity to total lung capacity (TLC), deep inspiration from functional residual capacity against closed airway (MIP), and short sharp inspiration through the nose (Sniff) were performed. Ten healthy subjects [male 4 and female 6; age (26±4) years] were studied. Results Linear relationship between EMGdi and end-tidal CO2 (r=0.83-0.98, all P
