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Sniff nasal inspiratory pressure (SNIP) is used to assess respiratory muscle strength in neuromuscular diseases like amyotrophic lateral sclerosis (ALS). The effect of contralateral nostril occlusion and mouth sealing on SNIP measurement are unclear. 81 participants were included (16 healthy, 39 patients with limb-onset ALS and 26 patients with bulbar-onset ALS). SNIP was obtained with combinations of mouth open/sealed and contralateral nostril open/occluded. Occluding the contralateral nostril (with mouth closed) increased SNIP by 12 cmH 2 O (95% CI 4, 20; p=0.003) in the healthy participants, by 9 cmH 2 O (95% CI 5, 12; p<0.001) in the limb-onset cohort and by 10 cmH 2 O (95% CI 5, 14; p<0.001) in the bulbar-onset cohort. Opening the mouth decreased SNIP by 19 cmH 2 O (95% CI 5, 34; p<0.009) in healthy participants, by 8 cmH 2 O (95% CI 4, 13; p<0.001) in the limb-onset cohort and by 13 cmH 2 O (95% CI 7, 19; p<0.001) in the bulbar-onset cohort. With contralateral nostril occlusion, 11% fewer individuals would have qualified for non-invasive ventilation. In conclusion, contralateral nostril occlusion increased SNIP compared with standard technique, likely reflecting true strength. Opening the mouth reduced SNIP, emphasising the need for good mouth sealing. Documenting SNIP technique is important for longitudinal assessments and clinical decision-making., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

Chronic respiratory disease can exacerbate the normal physiological changes in ventilation observed in healthy individuals during sleep, leading to sleep-disordered breathing, nocturnal hypoventilation, sleep disruption and chronic respiratory failure. Therefore, patients with obesity, slowly and rapidly progressive neuromuscular disease and chronic obstructive airways disease report poor sleep quality. Non-invasive ventilation (NIV) is a complex intervention used to treat sleep-disordered breathing and nocturnal hypoventilation with overnight physiological studies demonstrating improvement in sleep-disordered breathing and nocturnal hypoventilation, and clinical trials demonstrating improved outcomes for patients. However, the impact on subjective and objective sleep quality is dependent on the tools used to measure sleep quality and the patient population. As home NIV becomes more commonly used, there is a need to conduct studies focused on sleep quality, and the relationship between sleep quality and health-related quality of life, in all patient groups, in order to allow the clinician to provide clear patient-centred information., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

The COVID-19 pandemic changed continuous positive airway pressure (CPAP) setup pathways. We evaluated patients commenced on CPAP in 2019 (prepandemic) and 2020 (post-first UK wave). Face-to-face (F2F) setup numbers, with CPAP turned on, decreased from 613 patients (98.9%) in 2019, to 6 (1.1%) in 2020. In 2020, setups were F2F without CPAP turned on (403 (71.1%)), or remote (158 (27.9%)). Prepandemic median CPAP usage at first follow-up was 5.4 (2.7-6.9) hours/night and fell by 0.9 hours/night (95% CI 0.5 to 1.2, p<0.0001) in 2020. We found clinically relevant reductions in CPAP usage with pathway changes post-COVID-19., Competing Interests: Competing interests: CDT declares consulting fees from Bayer, outside the scope of this work. GG declares grant funding from ResMed UK and travel expenses from Wychwood Communications Limited, both outside the scope of this work. There are no other relevant conflicts of interest., (© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

Introduction: Although home non-invasive ventilation (NIV) is increasingly used to manage patients with chronic ventilatory failure, there are limited data on the long-term outcome of these patients. Our aim was to report on home NIV populations and the long-term outcome from two European centres., Methods: Cohort analysis including all patients established on home NIV from two European centres between 2008 and 2014., Results: Home NIV was initiated in 1746 patients to treat chronic ventilatory failure caused by (1) obesity hypoventilation syndrome±obstructive sleep apnoea (OHS±OSA) (29.5%); (2) neuromuscular disease (NMD) (22.7%); and (3) obstructive airway diseases (OAD) (19.1%). Overall cohort median survival following NIV initiation was 6.6 years. Median survival varied by underlying aetiology of respiratory failure: rapidly progressive NMD 1.1 years, OAD 2.7 years, OHS±OSA >7 years and slowly progressive NMD >7 years. Multivariate analysis demonstrated higher mortality in patients with rapidly progressive NMD (HR 4.78, 95% CI 3.38 to 6.75), COPD (HR 2.25, 95% CI 1.64 to 3.10), age >60 years at initiation of home NIV (HR 2.41, 95% CI 1.92 to 3.02) and NIV initiation following an acute admission (HR 1.38, 95% CI 1.13 to 1.68). Factors associated with lower mortality were NIV adherence >4 hours per day (HR 0.64, 95% CI 0.51 to 0.79), OSA (HR 0.51, 95% CI 0.31 to 0.84) and female gender (HR 0.79, 95% CI 0.65 to 0.96)., Conclusion: The mortality rate following initiation of home NIV is high but varies significantly according to underlying aetiology of respiratory failure. In patients with chronic respiratory failure, initiation of home NIV following an acute admission and low levels of NIV adherence are poor prognostic features and may be amenable to intervention., Competing Interests: Competing interests: MP reports personal fees from ResMed, grants and non-financial support from Fisher & Paykel, non-financial support from MSD, non-financial support and personal fees from Asten, grants from ADIR Association, grants from B&D Electromedical, personal fees from Philips Respironics, and personal fees and non-financial support from Chiesi, outside the submitted work. EL reports non-financial support from Asten, outside the submitted work. JD is an employee of Asten. AD reports grants from Philips Respironics, outside the submitted work. NH reports grants from Guy’s and St Thomas’ Charity, during the conduct of the study, grants from Philips Respironics, non-financial support from Philips Respironics RT Meeting (MYOTRACE), personal fees from Fisher & Paykel, grants from ResMed, grants from B&D Electromedical, and grants from Fisher & Paykel, outside the submitted work. In addition, NH has a patent MYOTRACE pending and is on the Pulmonary Research Advisory Board for Philips. NH’s research group has received unrestricted grants (managed by Guy’s and St Thomas’ Foundation Trust) from Philips Respironics, Philips, ResMed, Fisher & Paykel and B&D Electromedical. Philips Respironics is contributing to the development of the MYOTRACE technology. PBM reports grants and personal fees from Philips Respironics, grants and personal fees from ResMed, and grants and personal fees from B&D Electromedical, outside the submitted work. GK, PL-D, AB, MR, GA, PM, L-CM, CV, JS, JFM and AC have nothing to disclose., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: The mechanisms underlying sleep-related hypoventilation in patients with coexisting COPD and obstructive sleep apnoea (OSA), an overlap syndrome, are incompletely understood. We compared neural respiratory drive expressed as diaphragm electromyogram (EMG di ) and ventilation during stage 2 sleep in patients with COPD alone and patients with overlap syndrome., Methods: EMG di and airflow were recorded during full polysomnography in 14 healthy subjects, 14 patients with OSA and 39 consecutive patients with COPD. The ratio of tidal volume to EMG di was measured to indirectly assess upper airway resistance., Results: Thirty-five patients with COPD, 12 healthy subjects and 14 patients with OSA completed the study. Of 35 patients with COPD, 19 had COPD alone (FEV 1 38.5%±16.3%) whereas 16 had an overlap syndrome (FEV 1 47.5±16.2%, AHI 20.5±14.1 events/hour). Ventilation (V E ) was lower during stage 2 sleep than wakefulness in both patients with COPD alone (8.6±2.0 to 6.5±1.5 L/min, p<0.001) and those with overlap syndrome (8.3±2.0 to 6.1±1.8 L/min). Neural respiratory drive from wakefulness to sleep decreased significantly for patients with COPD alone (29.5±13.3% to 23.0±8.9% of maximal, p<0.01) but it changed little in those with overlap syndrome. The ratio of tidal volume to EMG di was unchanged from wakefulness to sleep in patients with COPD alone and healthy subjects but was significantly reduced in patients with OSA or overlap syndrome (p<0.05)., Conclusions: Stage 2 sleep-related hypoventilation in COPD alone is due to reduction of neural respiratory drive, but in overlap syndrome it is due to increased upper airway resistance., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Introduction: Obstructive sleep apnoea (OSA) is characterised by a loss of neuromuscular tone of the upper airway dilator muscles while asleep. This study investigated the effectiveness of transcutaneous electrical stimulation in patients with OSA., Patients and Methods: This was a randomised, sham-controlled crossover trial using transcutaneous electrical stimulation of the upper airway dilator muscles in patients with confirmed OSA. Patients were randomly assigned to one night of sham stimulation and one night of active treatment. The primary outcome was the 4% oxygen desaturation index, responders were defined as patients with a reduction >25% in the oxygen desaturation index when compared with sham stimulation and/or with an index <5/hour in the active treatment night., Results: In 36 patients (age mean 50.8 (SD 11.2) years, male/female 30/6, body mass index median 29.6 (IQR 26.9-34.9) kg/m(2), Epworth Sleepiness Scale 10.5 (4.6) points, oxygen desaturation index median 25.7 (16.0-49.1)/hour, apnoea-hypopnoea index median 28.1 (19.0-57.0)/hour) the primary outcome measure improved when comparing sham stimulation (median 26.9 (17.5-39.5)/hour) with active treatment (median 19.5 (11.6-40.0)/hour; p=0.026), a modest reduction of the mean by 4.1 (95% CI -0.6 to 8.9)/hour. Secondary outcome parameters of patients' perception indicated that stimulation was well tolerated. Responders (47.2%) were predominantly from the mild-to-moderate OSA category. In this subgroup, the oxygen desaturation index was reduced by 10.0 (95% CI 3.9 to 16.0)/hour (p<0.001) and the apnoea-hypopnoea index was reduced by 9.1 (95% CI 2.0 to 16.2)/hour (p=0.004)., Conclusion: Transcutaneous electrical stimulation of the pharyngeal dilators during a single night in patients with OSA improves upper airway obstruction and is well tolerated., Trial Registration Number: NCT01661712., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)

Introduction: Patient-ventilator asynchrony (PVA) can adversely affect the successful initiation of non-invasive home mechanical ventilation (HMV). The aim of this observational study was to quantify the prevalence of PVA during initiation of HMV and to determine the relationship between PVA and nocturnal gas exchange., Method: Type and frequency of PVA were measured by surface parasternal intercostal muscle electromyography, thoracoabdominal plethysmography and mask pressure during initiation of HMV. Severe PVA was defined, as previously, as asynchrony affecting ≥10% of breaths., Results: 28 patients (18 male) were enrolled aged 61±15 years and with a body mass index of 35±9 kg/m(2). Underlying diagnoses were neuromuscular disease with or without chest wall disease (n=6), obesity related chronic respiratory failure (n=12) and COPD (n=10). PVA was observed in all patients with 79% of patients demonstrating severe PVA. Triggering asynchrony was most frequent, observed in 24% (IQR: 11-36%) of breaths, with ineffective efforts accounting for 16% (IQR: 4-24%). PVA types were similar between disease groups, with the exception of auto-triggering, which was higher in patients with COPD (12% (IQR: 6-26%)). There was no correlation observed between PVA and time spent with oxygen saturations ≤90%, mean oxygen saturations or transcutaneous carbon dioxide levels during overnight ventilation., Conclusions: Severe PVA was identified in the majority of patients, irrespective of pathophysiological disease state. This was not associated with ineffective ventilation as evidenced by gas exchange., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Background: Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood., Patients and Methods: We undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (PL) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory PL volume curves were measured., Results: The obese group had a body mass index (BMI) of 46.8 (17.2) kg/m(2), and the normal group had a BMI of 23.2 (1.6) kg/m(2) (p=0.001). Obese and normals were matched for age (p=0.233), gender (p=0.637) and height (p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) %predicted, p=0.033; FEV1/FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cm H2O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cm H2O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs -2.0 (3.5) cm H2O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cm H2O, p=0.008). BMI correlated with end-expiratory gastric (seated R(2)=0.43, supine R(2)=0.66, p<0.01) and oesophageal pressures (seated R(2)=0.51, supine R(2)=0.62, p<0.01)., Conclusions: Obese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

We surveyed the UK distribution of five factors commonly associated with obstructive sleep apnoea (OSA) to produce an overall risk map that could be used to predict relative prevalence estimates. The weighting and mapping of selected risk factors associated with OSA highlighted significant regional variation in predicted prevalence estimates. These data provide the first attempt to systematically map the UK for OSA and identify areas where the condition is likely to be more prevalent. The data show a significant mismatch between areas identified as having a high predicted prevalence estimate and the distribution of existing sleep centres.

Rationale: Patients with suboptimal asthma control often have nocturnal symptoms which wake them, causing sleep fragmentation., Objectives: It was hypothesised that symptomatic patients were more accurately identified by measuring respiratory effort using chest wall electromyography than by pulmonary function testing., Methods: Nocturnal electrical activity of the parasternal intercostal muscles (EMG(para)) in the second intercostal space was measured in subjects with controlled (diurnal peak expiratory flow (PEF) variability <20%, n=12) and uncontrolled (diurnal PEF variability >20%, n=12) asthma, and it was compared with that in normal subjects (n=12)., Results: Subjects with controlled and uncontrolled asthma did not differ significantly in age (mean (SD) 42 (17) vs 46 (17) years, p=0.64), body mass index (BMI; 26.6 (2.9) vs 27.5 (3.5) kg/m(2), p=0.48) or gender distribution (males:females, 6:6 vs 7:5, p=0.68); the normal subject group was younger (27 (11) years, p=0.011) and slimmer (BMI 21.1 (2.9) kg/m(2), p<0.001). An elevated respiratory disturbance index (RDI) was associated with poor asthma control (RDI in normals 0.5 (0.9), in controlled asthma 4.0 (1.9), p<0.001, and in poorly controlled asthma 7.4 (4.3) h(-1); p<0.021). Similarly, EMG(para)%max (normals 4.9 (3.2)%max evening, 4.9 (3.5)%max morning) was higher in controlled asthma (7.2 (2.3)%max evening, 8.1 (4.0)%max morning, p=0.049) and higher still in uncontrolled asthma (16.8 (14.2)%max in the evening, 18.4 (11.6)%max in the morning, p<0.008)., Conclusions: Nocturnal respiratory effort is increased in those with asthma and neural respiratory drive is more variable in patients with poorly controlled asthma. Changes in the EMG(para) inversely reflect changes in pulmonary function tests. Measuring the EMG(para) offers a method to monitor asthma breath-by-breath while subjects are asleep, which could be adapted for home use.

Background: Neural respiratory drive (NRD) measured from the diaphragm electromyogram (EMGdi) reflects the load/capacity balance of the respiratory muscle pump and is a marker of lung disease severity. EMGdi measurement is invasive, but recording the EMG from the parasternal intercostal muscles using surface electrodes (sEMGpara) could provide a non-invasive method of assessing NRD and disease severity. Objectives To test the hypothesis that NRD measured by sEMGpara correlates with EMGdi, to provide an index of disease severity in cystic fibrosis (CF) and to relate to exercise-induced breathlessness., Methods: 15 patients with CF (mean forced expiratory volume in 1&emsp14;s (FEV(1)) 53.5% predicted) and 15 age-matched healthy controls were studied. sEMGpara and EMGdi were recorded at rest and during exercise. sEMGpara was recorded using surface electrodes and EMGdi using a multipair oesophageal electrode catheter. Signals were normalised using the peak EMG recorded during maximum respiratory manoeuvres and expressed as EMG%max. The respiratory pattern, metabolic data, oesophageal and gastric pressures and Borg scores were also recorded., Results: Mean (SD) resting sEMGpara%max and EMGdi%max were higher in patients with CF than in controls (13.1 (7)% and 18.5 (7.5)% vs 5.8 (3)% and 7.5 (2)%, respectively, p<0.001). In the patients with CF, resting sEMGpara%max and EMGdi%max were related to the degree of airways obstruction (FEV(1)) (r = -0.91 and r = -0.82, both p<0.001), hyperinflation (r = 0.63 and r = 0.56, both p<0.001) and dynamic lung compliance (r = -0.53 and r = -0.59, both p<0.001). During exercise, sEMGpara%max and EMGdi%max were strongly correlated with breathlessness in the patients with CF before (r = 0.906, p<0.001) and after (r = 0.975, p<0.001) the onset of neuromechanical dissociation., Conclusion: sEMGpara%max provides a non-invasive marker of neural drive, which reflects disease severity and exercise-induced breathlessness in CF.

BACKGROUND Exacerbations of chronic obstructive pulmonary disease (COPD) are characterised by increased dyspnoea, reduced quality of life and muscle weakness. Re-exacerbation and hospital admission are common. Pulmonary rehabilitation (PR) administered after hospital admission for an exacerbation can improve quality of life and exercise capacity. OBJECTIVE To determine whether outpatient post-exacerbation PR (PEPR) could reduce subsequent hospital admission episodes. METHODS Patients admitted to hospital for an exacerbation of COPD were randomised to receive either usual follow-up care (UC) or PEPR after discharge. Hospital admission and emergency department attendances for COPD exacerbations were recorded over a 3-month period and analysed on an intention-to-treat basis. Secondary outcomes included exercise capacity and quadriceps strength. RESULTS 60 patients underwent concealed randomisation at the time of their hospital discharge (UC: n=30, mean (SD) age 65 (10) years, forced expiratory volume in 1 s (FEV(1)) 52 (22)% predicted; PEPR: n=30, 67(10) years, 52 (20)% predicted). The proportion of patients re-admitted to hospital with an exacerbation was 33% in the UC group compared with 7% in those receiving PEPR (OR 0.15, 95% CI 0.03 to 0.72, p=0.02). The proportion of patients that experienced an exacerbation resulting in an unplanned hospital attendance (either admission or review and discharge from the emergency department) was 57% in the UC group and 27% in those receiving PEPR (OR 0.28, 95% CI 0.10 to 0.82, p=0.02). CONCLUSIONS Post-exacerbation rehabilitation in COPD can reduce re-exacerbation events that require admission or hospital attendance over a 3-month period. Clinical Trials Registration Number NCT00557115.

Background: Respiratory muscle weakness is an important clinical problem. Tests of varying complexity and invasiveness are available to assess respiratory muscle strength. The relative precision of different tests in the detection of weakness is less clear, as is the value of multiple tests., Methods: The respiratory muscle function tests of clinical referrals who had multiple tests assessed in our laboratories over a 6-year period were analysed. Thresholds for weakness for each test were determined from published and in-house laboratory data. The patients were divided into three groups: those who had all relevant measurements of global inspiratory muscle strength (group A, n = 182), those with full assessment of diaphragm strength (group B, n = 264) and those for whom expiratory muscle strength was fully evaluated (group C, n = 60). The diagnostic outcome of each inspiratory, diaphragm and expiratory muscle test, both singly and in combination, was studied and the impact of using more than one test to detect weakness was calculated., Results: The clinical referrals were primarily for the evaluation of neuromuscular diseases and dyspnoea of unknown cause. A low maximal inspiratory mouth pressure (Pimax) was recorded in 40.1% of referrals in group A, while a low sniff nasal pressure (Sniff Pnasal) was recorded in 41.8% and a low sniff oesophageal pressure (Sniff Poes) in 37.9%. When assessing inspiratory strength with the combination of all three tests, 29.6% of patients had weakness. Using the two non-invasive tests (Pimax and Sniff Pnasal) in combination, a similar result was obtained (low in 32.4%). Combining Sniff Pdi (low in 68.2%) and Twitch Pdi (low in 67.4%) reduced the diagnoses of patients with diaphragm weakness to 55.3% in group B. 38.3% of the patients in group C had expiratory muscle weakness as measured by maximum expiratory pressure (Pemax) compared with 36.7% when weakness was diagnosed by cough gastric pressure (Pgas), and 28.3% when assessed by Twitch T10. Combining all three expiratory muscle tests reduced the number of patients diagnosed as having expiratory muscle weakness to 16.7%., Conclusion: The use of single tests such as Pimax, Pemax and other available individual tests of inspiratory, diaphragm and expiratory muscle strength tends to overdiagnose weakness. Combinations of tests increase diagnostic precision and, in the population studied, they reduced the diagnosis of inspiratory, specific diaphragm and expiratory muscle weakness by 19-56%. Measuring both Pimax and Sniff Pnasal resulted in a relative reduction of 19.2% of patients falsely diagnosed with inspiratory muscle weakness. The addition of Twitch Pdi to Sniff Pdi increased diagnostic precision by a smaller amount (18.9%). Having multiple tests of respiratory muscle function available both increases diagnostic precision and makes assessment possible in a range of clinical circumstances.