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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.

ABSTRACTExcessive daytime sleepiness (EDS) affects approximately half of patients with obstructive sleep apnea (OSA) and can persist in some despite normalization of breathing, oxygenation, and sleep quality with primary OSA therapy, such as continuous positive airway pressure (CPAP). EDS is often overlooked and under discussed in the primary care setting and in the follow-up of CPAP-treated patients due to difficult assessment of such a multi-dimensional symptom. This review aims to provide suggestions for procedures that can be implemented into routine clinical practice to identify, evaluate, and manage EDS in patients treated for OSA, including how to appropriately use various self-report and objective assessments along the clinical pathway and options for pharmacotherapy. In addition, examples of when it is appropriate to refer a patient to a sleep specialist for evaluation are discussed.

Background: Hypoglossal nerve stimulation (HNS) with Inspire is a novel treatment indicated for moderate or severe obstructive sleep apnoea/hypopnoea syndrome (OSAHS), intolerant to or unable to be treated with continuous positive airway pressure (CPAP). Objective: The aim of this study was to assess the cost effectiveness of treating moderate or severe OSAHS, in patients intolerant to CPAP, with HNS, compared with standard care, from a National Health Service (NHS) perspective. Methods: A cohort state transition model was developed to compare HNS with Inspire with no treatment in UK adult patients with moderate or severe OSAHS who have previously tried and have not responded to CPAP therapy. Published literature was applied in the model to estimate incremental cost-effectiveness ratios (ICERs; 2019 Great British pounds per quality-adjusted life-year [QALY] gained), from an NHS and personal social services (PSS) perspective, over a cohort’s lifetime. Results: The model base-case predicts that patients undergoing HNS will incur lifetime costs of £65,026 compared with £36,727 among untreated patients. The HNS cohort would gain 12.72 QALYs compared with 11.15 QALYs in the no-treatment arm. The ICER of treating severe OSAHS with HNS is therefore estimated to be £17,989 per QALYs gained. Probabilistic sensitivity analysis found that at a threshold of £30,000/QALY, HNS has a 69% probability of being cost effective. Limitations of the model include uncertainty around the utility data that were not sourced directly from HNS clinical trials. There is further uncertainty in the relationship between change in the Apnoea-Hypopnoea Index (AHI) and reduction in ischaemic heart disease and stroke because of difficulty capturing the reduction in risk over a long time horizon in studies. Conclusions: Over a patient’s lifetime, HNS with Inspire is expected to be cost effective when compared with no treatment in patients with severe OSAHS who have tried and have not responded to CPAP, from an NHS perspective.

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.

IntroductionAlthough 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.MethodsCohort analysis including all patients established on home NIV from two European centres between 2008 and 2014.ResultsHome 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).ConclusionThe 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.

BackgroundThe 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 (EMGdi) and ventilation during stage 2 sleep in patients with COPD alone and patients with overlap syndrome.MethodsEMGdiand 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 EMGdiwas measured to indirectly assess upper airway resistance.ResultsThirty-five patients with COPD, 12 healthy subjects and 14 patients with OSA completed the study. Of 35 patients with COPD, 19 had COPD alone (FEV138.5%±16.3%) whereas 16 had an overlap syndrome (FEV147.5±16.2%, AHI 20.5±14.1 events/hour). Ventilation (VE) 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 EMGdiwas 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).ConclusionsStage 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.

Continuous positive airway pressure (CPAP) is an effective treatment for obstructive sleep apnea (OSA). However, long-term compliance with CPAP is limited. We tested the hypothesis that CPAP levels routinely used during sleep increase neural respiratory drive (NRD) and breathlessness, which may discourage compliance.

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.

The evidence of a putative causal effect of sleep apnea-induced intermittent hypoxia on the pathogenesis of gestational hypertension and preeclampsia is mounting. The present review presents the evidence of current literature and questions whether an early diagnosis and treatment of obstructive sleep apnea during pregnancy can reduce the risk of preeclampsia.

The therapeutic value of transcutaneous electrical stimulation of the genioglossus muscle in patients with obstructive sleep apnea (OSA) to reduce sleep-disordered breathing is unclear.

Exercise capacity in chronic obstructive pulmonary disease (COPD) is limited by both breathlessness and leg muscle fatigue. Neural respiratory drive, measured as diaphragm electromyogram (EMGdi) activity expressed as a proportion of maximum (EMGdi%max), quantifies the mechanical load on the respiratory muscles and relates closely to breathlessness. We tested the hypothesis that end-exercise EMGdi%max would be higher in patients stopping because of breathlessness than in those limited by leg fatigue.

Breathlessness is an important cause of exercise limitation and reduced quality of life for patients with chronic obstructive pulmonary disease (COPD). One of the challenges of breathlessness management in COPD is the lack of physiological markers that reliably correlate with patients' symptoms. The aim of this study was to test the hypothesis that neural respiratory drive (NRD), measured with diaphragm electromyogram (EMGdi) activity, is closely related to breathlessness in COPD. We also investigated whether neuroventilatory uncoupling, which is the dissociation of ventilation from NRD as a consequence of abnormal pulmonary mechanics, contributes to breathlessness intensity over an awareness of levels of NRD alone.