Relationship between airflow limitation in response to upper airway negative pressure during wakefulness and obstructive sleep apnea severity.

PURPOSE: The objective was to determine if alteration in airflow induced by negative pressure (NP) applied to participants' upper airways during wakefulness, is related to obstructive sleep apnea (OSA) severity as determined by the apnea-hypopnea index (AHI). METHODS: Adults 18 years of age or greater were recruited. All participants underwent overnight polysomnography to assess their apnea-hypopnea index (AHI). While awake, participants were twice exposed, orally, to -3 cm H2O of NP for five full breaths. The ratio of the breathing volumes of the last two breaths during NP exposure to the last two breaths prior to NP exposure was deemed the NP ratio (NPR). RESULTS: Eighteen participants were enrolled. A strong relationship between the AHI and the exponentially transformed NPR (ExpNPR) for all participants was observed (R2 = 0.55, p < 0.001). A multivariable model using the independent variable ExpNPR, age, body mass index and sex accounted for 81% of variability in AHI (p = 0.0006). A leave-one-subject-out cross-validation analysis revealed that predicted AHI using the multivariable model, and actual AHI from participants' polysomnograms, were strongly related (R2 = 0.72, p < 0.001). CONCLUSION: We conclude that ExpNPR, was strongly related to the AHI, independently of demographic factors known to be related to the AHI.

Sleep apnoea and heart failure.

Heart failure and sleep disordered breathing (SDB) are two common conditions that frequently overlap and have been studied extensively in the past three decades. Obstructive sleep apnoea (OSA) may result in myocardial damage due to intermittent hypoxia that leads to increased sympathetic activity and transmural pressures, low-grade vascular inflammation, and oxidative stress. On the other hand, central sleep apnoea and Cheyne-Stokes respiration (CSA-CSR) occurs in heart failure, irrespective of ejection fraction, either reduced (HFrEF), preserved (HFpEF) or mildly reduced (HFmrEF). The pathophysiology of CSA-CSR relies on several mechanisms leading to hyperventilation, breathing cessation and periodic breathing. Pharyngeal collapse may result at least in part from fluid accumulation in the neck, owing to daytime fluid retention and overnight rostral fluid shift from the legs. Although both OSA and CSA-CSR occur in heart failure, the symptoms are less suggestive than in typical (non-heart failure-related) OSA. Overnight monitoring is mandatory for a proper diagnosis, with accurate measurement and scoring of central and obstructive events, since the management will be different depending on whether the sleep apnoea in heart failure is predominantly OSA or CSA-CSR. SDB in heart failure is associated with worse prognosis, including higher mortality, than in patients with heart failure but without SDB. However, there is currently no evidence that treating SDB improves clinically important outcomes in patients with heart failure, such as cardiovascular morbidity and mortality.

Effect of Ultrafiltration on Sleep Apnea and Cardiac Function in End-Stage Renal Disease.

RATIONALE: End-stage renal disease (ESRD) patients have high annual mortality mainly due to cardiovascular causes. The acute effects of obstructive and central sleep apnea on cardiac function in ESRD patients have not been determined. We therefore tested, in patients with ESRD, the hypotheses that (1) sleep apnea induces deterioration in cardiac function overnight and (2) attenuation of sleep apnea severity by ultrafiltration (UF) attenuates this deterioration. METHODS: At baseline, ESRD patients, on conventional hemodialysis, with left ventricular ejection fraction (LVEF) >45% had polysomnography (PSG) performed on a non-dialysis day to determine the apnea-hypopnea index (AHI). Echocardiography was performed at the bedside, before and after sleep. Isovolumetric contraction time divided by left ventricular ejection time (IVCT/ET) and isovolumetric relaxation time divided by ET (IVRT/ET) were measured by tissue doppler imaging. The myocardial performance index (MPI), a composite of systolic and diastolic function was also calculated. One week later, subjects with sleep apnea (AHI ≥15) had fluid removed by UF, followed by repeat PSG and echocardiography. -Results: Fifteen subjects had baseline measurements, of which 7 had an AHI <15 (no-sleep-apnea group) and 8 had an AHI ≥15 (sleep-apnea group). At baseline, there was no overnight change in the LVEF in either the no-sleep-apnea group or the sleep-apnea group. In the no-sleep-apnea group, there was also no overnight change in MPI, IVCT/ET and IVRT/ET. However, in the sleep-apnea group there were overnight increases in MPI, IVCT/ET and IVRT/ET (p = 0.008, 0.007 and 0.031, respectively), indicating deterioration in systolic and diastolic function. Following fluid removal by UF in the sleep-apnea group, the AHI decreased by 48.7% (p = 0.012) and overnight increases in MPI, IVCT/ET and IVRT/ET observed at baseline were abolished. CONCLUSIONS: In ESRD, cardiac function deteriorates overnight in those with sleep apnea, but not in those without sleep apnea. This overnight deterioration in the sleep-apnea group may be at least partially due to sleep apnea, since attenuation of sleep apnea by UF was accompanied by elimination of this deleterious overnight effect.

Dissociation between objectively quantified snoring and sleep quality.

BACKGROUND: The impact of simple snoring on sleep structure and sleepiness has not been well described. In several studies, self-reported snoring was associated with increased daytime sleepiness. However, most studies did not distinguish patients with simple snoring from those with coexisting obstructive sleep apnea (OSA) using objective measures. We therefore evaluated the relationship between objectively measured snoring and both sleep structure and daytime sleepiness in patients with no or mild OSA. METHODS: Subjects referred for suspected sleep disorders underwent polysomnography (PSG) during which breath sounds were recorded by a microphone. Those with an apnea-hypopnea index (AHI) <15/h were analyzed. Individual snores were identified by a computer algorithm, from which the snore index (SI) was calculated as the number of snores/h of sleep. Sleep stages and arousals were quantified. Daytime sleepiness was evaluated using the Epworth Sleepiness Scale (ESS) score. RESULTS: 74 (35 males) subjects were included (age, mean ±â€¯SD: 46.4 ±â€¯15.3 years and body mass index: 29.8 ±â€¯7.0 kg/m2). The mean SI was 266 ±â€¯243 snores/h. Subjects were categorized according to their SI into 3 tertiles: SI < 100, between 100-350, and >350. No sleep structure indeces, arousals, or ESS score differed among SI tertiles (p > 0.13). There was no correlation between SI and any of these variables (p > 0.29). In contrast, the AHI was significantly related to frequency of arousals (r = 0.23, p = 0.048). CONCLUSIONS: These findings suggest that simple snoring assessed objectively is not related to indices of sleep structure or subjective sleepiness.

The effect of fluid overload on sleep apnoea severity in haemodialysis patients.

As in heart failure, obstructive and central sleep apnoea (OSA and CSA, respectively) are common in end-stage renal disease. Fluid overload characterises end-stage renal disease and heart failure, and in heart failure plays a role in the pathogenesis of OSA and CSA. We postulated that in end-stage renal disease patients, those with sleep apnoea would have greater fluid volume overload than those without.End-stage renal disease patients on thrice-weekly haemodialysis underwent overnight polysomnography on a nondialysis day to determine their apnoea-hypopnoea index (AHI). Extracellular fluid volume of the total body, neck, thorax and right leg were measured using bioelectrical impedance.28 patients had an AHI ≥15 (sleep apnoea group; OSA:CSA 21:7) and 12 had an AHI <15 (no sleep apnoea group). Total body extracellular fluid volume was 2.6 L greater in the sleep apnoea group than in the no sleep apnoea group (p=0.006). Neck, thorax, and leg fluid volumes were also greater in the sleep apnoea than the no sleep apnoea group (p<0.05), despite no difference in body mass index (p=0.165).These findings support a role for fluid overload in the pathogenesis of both OSA and CSA in end-stage renal disease.

Influence of head position on obstructive sleep apnea severity.

OBJECTIVE: Supine body orientation plays an important role in precipitating upper airway collapse in a significant proportion of obstructive sleep apnea (OSA) patients known to have supine-predominant OSA (OSAsup). Traditionally, trunk position is used to assess OSAsup, but the role of the head position has not been established. We hypothesized that head position influences OSA independently of trunk position. METHODS: Head and trunk positions were determined from subjects undergoing overnight polysomnography. The apnea-hypopnea index (AHI), rapid eye movement (REM), and non-REM sleep time of all trunk and head positions (lateral and supine) were calculated and compared against the complete supine position, i.e., head and trunk supine. RESULTS: In 26 subjects, lateral rotation of the head to the right or left with the trunk supine resulted in a significant reduction in AHI from 36.0 ± 22.5 to 25.8 ± 16.6 (p = 0.008), and an AHI drop <10 in 27% of patients. The "trunk lateral-head lateral" position resulted in a more dramatic reduction in AHI from 31.6 ± 20.2 to 4.1 ± 4.1 (p < 0.0001). The distributions of REM and non-REM sleep were not different among positions. In the subgroup with a body mass index (BMI) <32 kg/m2 (15 subjects), the AHI reduction with lateral head rotation was significant (p = 0.005) but not in remaining 11 obese patient with a BMI ≥32 kg/m2 (p = 0.24). CONCLUSION: OSA severity with the trunk in the supine position decreased significantly when the head rotated from supine to lateral, particularly in non-obese patients. These results demonstrate an important influence of head position on the AHI, independently of trunk position and sleep stage, in patients with OSA.

In-hospital diagnosis of sleep apnea in stroke patients using a portable acoustic device.

PURPOSE: Sleep apnea (SA) is highly prevalent in post-stroke patients. Due to physical disability and relative inaccessibility of polysomnography (PSG) to test for SA, patients with stroke frequently remain undiagnosed and untreated. Portable SA monitoring can facilitate at-home or in-hospital testing for SA. However, portable SA monitoring is not recommended in those with complex medical conditions, such as stroke, due to the lack of validation of portable monitoring in such patients. METHODS: The objective of our study was to test the accuracy and feasibility of a portable single-channel acoustic device, BresoDx™ for quantifying the apnea-hypopnea index (AHI) and diagnosing SA in a post-stroke population. Patients who recently suffered a stroke and were undergoing rehabilitation in a stroke rehabilitation unit (SRU) underwent testing with BresoDx both simultaneously during attended PSG and unattended on the SRU. RESULTS: We studied 23 stroke patients of whom 78% had SA (defined by AHI ≥15) on PSG. All of the patients tolerated the BresoDx. Using cutoff AHI of ≥15 by PSG to diagnose SA, BresoDx had sensitivity of 90.0%, specificity of 84.6%, and overall accuracy of 87.0% in the laboratory. CONCLUSIONS: This study demonstrates that BresoDx is well tolerated and feasible to use in the post-stroke population where it was found to have excellent positive and negative predictive values for the diagnosis of SA.

Association between resting-state brain functional connectivity and muscle sympathetic burst incidence.

The insula (IC) and cingulate are key components of the central autonomic network and central nodes of the salience network (SN), a set of spatially distinct but temporally correlated brain regions identified with resting-state (task free) functional MRI (rsMRI). To examine the SN's involvement in sympathetic outflow, we tested the hypothesis that individual differences in intrinsic connectivity of the SN correlate positively with resting postganglionic muscle sympathetic nerve activity (MSNA) burst incidence (BI) in subjects without and with obstructive sleep apnea (OSA). Overnight polysomnography, 5-min rsMRI, and fibular MSNA recording were performed in 36 subjects (mean age 57 yr; 10 women, 26 men). Independent component analysis (ICA) of the entire cohort identified the SN as including bilateral IC, pregenual anterior cingulate cortex (pgACC), midcingulate cortex (MCC), and the temporoparietal junction (TPJ). There was a positive correlation between BI and the apnea-hypopnea index (AHI) (P < 0.001), but dual-regression analysis identified no differences in SN functional connectivity between subjects with no or mild OSA (n = 17) and moderate or severe (n = 19) OSA. Correlation analysis relating BI to the strength of connectivity within the SN revealed large (i.e., spatial extent) and strong correlations for the left IC (P < 0.001), right pgACC/MCC (P < 0.006), left TPJ (P < 0.004), thalamus (P < 0.035), and cerebellum (P < 0.013). Indexes of sleep apnea were unrelated to BI and the strength of SN connectivity. There were no relationships between BI and default or sensorimotor network connectivity. This study links connectivity within the SN to MSNA, demonstrating several of its nodes to be key sympathoexcitatory regions.

Effects of exercise training on sleep apnoea in patients with coronary artery disease: a randomised trial.

Overnight fluid shift from the legs to the neck and lungs may contribute to the pathogenesis of obstructive sleep apnoea (OSA) and central sleep apnoea (CSA). We hypothesised that exercise training will decrease the severity of OSA and CSA in patients with coronary artery disease (CAD) by decreasing daytime leg fluid accumulation and overnight rostral fluid shift.Patients with CAD and OSA or CSA (apnoea-hypopnoea index >15 events per h) were randomised to 4 weeks of aerobic exercise training or to a control group. Polysomnography, with measurement of leg, thoracic and neck fluid volumes and upper-airway cross-sectional area (UA-XSA) before and after sleep, was performed at baseline and follow-up.17 patients per group completed the study. Apnoea-hypopnoea index decreased significantly more in the exercise group than in the control group (31.1±12.9 to 20.5±9.4 versus 28.1±13.5 to 27.0±15.1 events per h, p=0.047), in association with a greater reduction in the overnight change in leg fluid volume (579±222 to 466±163 versus 453±164 to 434±141 mL, p=0.04) and by a significantly greater increase in the overnight change in UA-XSA in the exercise group (p=0.04).In patients with CAD and sleep apnoea, exercise training decreases sleep apnoea severity via attenuation of overnight fluid shift and an increase in UA-XSA.

Effect of ultrafiltration on sleep apnea and sleep structure in patients with end-stage renal disease.

RATIONALE: In end-stage renal disease (ESRD), a condition characterized by fluid overload, both obstructive and central sleep apnea (OSA and CSA) are common. This observation suggests that fluid overload is involved in the pathogenesis of OSA and CSA in this condition. OBJECTIVES: To test the hypothesis that fluid removal by ultrafiltration (UF) will reduce severity of OSA and CSA in patients with ESRD. METHODS: At baseline, on a nondialysis day, patients with ESRD on thrice-weekly hemodialysis underwent overnight polysomnography along with measurement of total body extracellular fluid volume (ECFV), and ECFV of the neck, thorax, and right leg before and after sleep. The following week, on a nondialysis day, subjects with an apnea-hypopnea index (AHI) greater than or equal to 20 had fluid removed by UF, followed by repeat overnight polysomnography with fluid measurements. MEASUREMENTS AND MAIN RESULTS: Fifteen patients (10 men) with an AHI greater than or equal to 20 (10 OSA; 5 CSA) participated. Mean age was 53.5 ± 10.4 years and mean body mass index was 25.3 ± 4.8 kg/m(2). Following removal of 2.17 ± 0.45 L by UF, the AHI decreased by 36% (43.8 ± 20.3 to 28.0 ± 17.7; P < 0.001) without affecting uremia. The reduction in AHI correlated with the reduction in total body ECFV (r = 0.567; P = 0.027) and was associated with reductions in ECFV of the right leg (P = 0.001), overnight change in ECFV of the right leg (P = 0.044), ECFV of the thorax (P = 0.001), and ECFV of the neck (P = 0.003). CONCLUSIONS: These findings indicate that fluid overload contributes to the pathogenesis of OSA and CSA in ESRD, and that fluid removal by UF attenuates sleep apnea without altering uremic status.

New frontiers in obstructive sleep apnoea.

OSA (obstructive sleep apnoea), the most common respiratory disorder of sleep, is caused by the loss of upper airway dilating muscle activity during sleep superimposed on a narrow upper airway. This results in recurrent nocturnal asphyxia. Termination of these events usually requires arousal from sleep and results in sleep fragmentation and hypoxaemia, which leads to poor quality sleep, excessive daytime sleepiness, reduced quality of life and numerous other serious health consequences. Furthermore, patients with untreated sleep apnoea are at an increased risk of hypertension, stroke, heart failure and atrial fibrillation. Although there are many predisposing risk factors for OSA, including male gender, endocrine disorders, use of muscle relaxants, smoking, fluid retention and increased age, the strongest risk factor is obesity. The aim of the present review is to focus on three cutting-edge topics with respect to OSA. The section on animal models covers various strategies used to simulate the physiology or the effects of OSA in animals, and how these have helped to understand some of the underlying mechanisms of OSA. The section on diabetes discusses current evidence in both humans and animal models demonstrating that intermittent hypoxia and sleep fragmentation has a negative impact on glucose tolerance. Finally, the section on cardiovascular biomarkers reviews the evidence supporting the use of these biomarkers to both measure some of the negative consequences of OSA, as well as the potential benefits of OSA therapies.

Differing effects of obstructive and central sleep apneas on stroke volume in patients with heart failure.

RATIONALE: Obstructive sleep apnea and central sleep apnea increase risk of mortality in patients with heart failure (HF), possibly because of hemodynamic compromise during sleep. However, beat-to-beat stroke volume (SV) has not been assessed in response to obstructive and central events during sleep in patients with HF. Because obstructive events generate negative intrathoracic pressure that reduces left ventricular (LV) preload and increases afterload, but central events do not, obstructive events should lead to greater hemodynamic compromise than central events. OBJECTIVES: To determine the effects of obstructive and central apneas and hypopneas during sleep on SV in patients with HF. METHODS: Patients with systolic HF (LV ejection fraction ≤ 45%) and sleep apnea underwent beat-to-beat measurement of SV by digital photoplethysmography during polysomnography. Change in SV from before to the end of obstructive and central respiratory events was calculated and compared between these types of events. MEASUREMENTS AND MAIN RESULTS: Changes in SV were assessed during 252 obstructive and 148 central respiratory events in 40 patients with HF. Whereas SV decreased by 6.8 (±8.7)% during obstructive events, it increased by 2.6 (±5.4)% during central events (P < 0.001 for difference). For obstructive events, reduction in SV was associated independently with LV ejection fraction, duration of respiratory events, and degree of oxygen desaturation. CONCLUSIONS: In patients with HF, obstructive and central respiratory events have opposite hemodynamic effects: whereas obstructive sleep apnea appears to have an adverse effect on SV, central sleep apnea appears to have little or slightly positive effects on SV. These observations may have implications for therapeutic approaches to these two breathing disturbances.

The Effect of Simulated Obstructive Apneas on Mechanical Characteristics of Lower Airways in Individuals with Asthma.

Increased negative intrathoracic pressure that occurs during pharyngeal obstruction can increase thoracic fluid volume that may contribute to lower airway narrowing in individuals with obstructive sleep apnea (OSA) and asthma. Our previous study showed that fluid accumulation in the thorax induced by simulated OSA can increase total respiratory resistance. However, the effect of fluid shift on lower airway narrowing has not been investigated. To examine the effect of fluid accumulation in the thorax on the resistance of the lower airway. Non-asthma participants and individuals with (un)controlled asthma were recruited and underwent a single-day experiment. A catheter with six pressure sensors was inserted through the nose to continuously measure pressure at different sites of the airway, while a pneumotachograph was attached to a mouthpiece to record airflow. To simulate obstructive apneas, participants performed 25 Mueller maneuvers (MMs) while lying supine. Using the recordings of pressure sensor and airflow, total respiratory (RT), lower respiratory components (RL), and upper airway (RUA) resistances were calculated before and after MMs. Generalized estimation equation method was used to find the predictors of RL among variables including age, sex, body mass index, and the effect of MMs and asthma. Eighteen participants were included. Performing MMs significantly increased RT (2.23 ± 2.08 cmH2O/L/s, p = 0.003) and RL (1.52 ± 2.00 cmH2O/L/s, p = 0.023) in participants with asthma, while only RL was increased in non-asthma group (1.96 ± 1.73 cmH2O/L/s, p = 0.039). We found the model with age, and the effect of MMs and asthma severity generated the highest correlation (R2 = 0.69, p < 0.001). We provide evidence that fluid accumulation in the thorax caused by excessive intrathoracic pressure increases RL in both non-asthma and asthma groups. The changes in RL were related to age, having asthma and the effect of simulated OSA. This can explain the interrelationship between OSA and asthma.

Adaptive servo-ventilation for sleep-disordered breathing in patients with heart failure with reduced ejection fraction (ADVENT-HF): a multicentre, multinational, parallel-group, open-label, phase 3 randomised controlled trial.

BACKGROUND: In patients with heart failure and reduced ejection fraction, sleep-disordered breathing, comprising obstructive sleep apnoea (OSA) and central sleep apnoea (CSA), is associated with increased morbidity, mortality, and sleep disruption. We hypothesised that treating sleep-disordered breathing with a peak-flow triggered adaptive servo-ventilation (ASV) device would improve cardiovascular outcomes in patients with heart failure and reduced ejection fraction. METHODS: We conducted a multicentre, multinational, parallel-group, open-label, phase 3 randomised controlled trial of peak-flow triggered ASV in patients aged 18 years or older with heart failure and reduced ejection fraction (left ventricular ejection fraction ≤45%) who were stabilised on optimal medical therapy with co-existing sleep-disordered breathing (apnoea-hypopnoea index [AHI] ≥15 events/h of sleep), with concealed allocation and blinded outcome assessments. The trial was carried out at 49 hospitals in nine countries. Sleep-disordered breathing was stratified into predominantly OSA with an Epworth Sleepiness Scale score of 10 or lower or predominantly CSA. Participants were randomly assigned to standard optimal treatment alone or standard optimal treatment with the addition of ASV (1:1), stratified by study site and sleep apnoea type (ie, CSA or OSA), with permuted blocks of sizes 4 and 6 in random order. Clinical evaluations were performed and Minnesota Living with Heart Failure Questionnaire, Epworth Sleepiness Scale, and New York Heart Association class were assessed at months 1, 3, and 6 following randomisation and every 6 months thereafter to a maximum of 5 years. The primary endpoint was the cumulative incidence of the composite of all-cause mortality, first admission to hospital for a cardiovascular reason, new onset atrial fibrillation or flutter, and delivery of an appropriate cardioverter-defibrillator shock. All-cause mortality was a secondary endpoint. Analysis for the primary outcome was done in the intention-to-treat population. This trial is registered with ClinicalTrials.gov (NCT01128816) and the International Standard Randomised Controlled Trial Number Register (ISRCTN67500535), and the trial is complete. FINDINGS: The first and last enrolments were Sept 22, 2010, and March 20, 2021. Enrolments terminated prematurely due to COVID-19-related restrictions. 1127 patients were screened, of whom 731 (65%) patients were randomly assigned to receive standard care (n=375; mean AHI 42·8 events per h of sleep [SD 20·9]) or standard care plus ASV (n=356; 43·3 events per h of sleep [20·5]). Follow-up of all patients ended at the latest on June 15, 2021, when the trial was terminated prematurely due to a recall of the ASV device due to potential disintegration of the motor sound-abatement material. Over the course of the trial, 41 (6%) of participants withdrew consent and 34 (5%) were lost to follow-up. In the ASV group, the mean AHI decreased to 2·8-3·7 events per h over the course of the trial, with associated improvements in sleep quality assessed 1 month following randomisation. Over a mean follow-up period of 3·6 years (SD 1·6), ASV had no effect on the primary composite outcome (180 events in the control group vs 166 in the ASV group; hazard ratio [HR] 0·95, 95% CI 0·77-1·18; p=0·67) or the secondary endpoint of all-cause mortality (88 deaths in the control group vs. 76 in the ASV group; 0·89, 0·66-1·21; p=0·47). For patients with OSA, the HR for all-cause mortality was 1·00 (0·68-1·46; p=0·98) and for CSA was 0·74 (0·44-1·23; p=0·25). No safety issue related to ASV use was identified. INTERPRETATION: In patients with heart failure and reduced ejection fraction and sleep-disordered breathing, ASV had no effect on the primary composite outcome or mortality but eliminated sleep-disordered breathing safely. FUNDING: Canadian Institutes of Health Research and Philips RS North America.

Role of nocturnal rostral fluid shift in the pathogenesis of obstructive and central sleep apnoea.

Obstructive sleep apnoea (OSA) is common in the general population and increases the risk of motor vehicle accidents due to hypersomnolence from sleep disruption, and risk of cardiovascular diseases owing to repetitive hypoxia, sympathetic nervous system activation, and systemic inflammation. In contrast, central sleep apnoea (CSA) is rare in the general population. Although their pathogenesis is multifactorial, the prevalence of both OSA and CSA is increased in patients with fluid retaining states, especially heart failure, where they are associated with increased mortality risk. This observation suggests that fluid retention may contribute to the pathogenesis of both OSA and CSA. According to this hypothesis, during the day fluid accumulates in the intravascular and interstitial spaces of the legs due to gravity, and upon lying down at night redistributes rostrally, again owing to gravity. Some of this fluid may accumulate in the neck, increasing tissue pressure and causing the upper airway to narrow, thereby increasing its collapsibility and predisposing to OSA. In heart failure patients, with increased rostral fluid shift, fluid may additionally accumulate in the lungs, provoking hyperventilation and hypocapnia, driving below the apnoea threshold, leading to CSA. This review article will explore mechanisms by which overnight rostral fluid shift, and its prevention, can contribute to the pathogenesis and therapy of sleep apnoea.

A system for portable sleep apnea diagnosis using an embedded data capturing module.

UNLABELLED: Sleep apnea (SA) is a very common disease with serious health consequences, yet is very under-diagnosed, partially because of the high cost and limited accessibility of in-laboratory polysomnography (PSG). The purpose of this work is to introduce a newly developed portable system for the diagnosis of SA at home that is both reliable and easy to use. The system includes personal devices for recording breath sounds and airflow during sleep and diagnostic algorithms to process the recorded data. The data capturing device consists of a wearable face frame with an embedded electronic module featuring a unidirectional microphone, a differential microphone preamplifier, a microcontroller with an onboard differential analogue to digital converter, and a microSD memory card. The device provides continuous data capturing for 8 h. Upon completion of the recording session, the memory card is returned to a location for acoustic analysis. We recruited 49 subjects who used the device independently at home, after which each subject answered a usability questionnaire. Random data samples were selected to measure the signal-to-noise ratio (SNR) as a gauge of hardware functionality. A subset of 11 subjects used the device on 2 different nights and their results were compared to examine diagnostic reproducibility. Independent of those, system's performance was evaluated against PSG in the lab environment in 32 subject. The overall success rate of applying the device in un-attended settings was 94 % and the overall rating for ease-of-use was 'excellent'. Signal examination showed excellent capturing of breath sounds with an average SNR of 31.7 dB. Nine of the 11 (82 %) subjects had equivalent results on both nights, which is consistent with reported inter-night variability. The system showed 96 % correlation with simultaneously performed in-lab PSG. CONCLUSION: Our results suggest excellent usability and performance of this system and provide a strong rationale to further improve it and test its robustness in a larger study.

Sleep Apnea Detection by Tracheal Motion and Sound, and Oximetry via Application of Deep Neural Networks.

Purpose: Sleep apnea (SA) is highly prevalent, but under diagnosed due to inaccessibility of sleep testing. To address this issue, portable devices for home sleep testing have been developed to provide convenience with reasonable accuracy in diagnosing SA. The objective of this study was to test the validity a novel portable sleep apnea testing device, BresoDX1, in SA diagnosis, via recording of trachea-sternal motion, tracheal sound and oximetry. Patients and Methods: Adults with a suspected sleep disorder were recruited to undergo in-laboratory polysomnography (PSG) and a simultaneous BresoDX1 recording. Data from BresoDX1 were collected and features related to breathing sounds, body motions and oximetry were extracted. A deep neural network (DNN) model was trained with 61-second epochs of the extracted features to detect apneas and hypopneas from which an apnea-hypopnea index (AHI) was calculated. The AHI estimated by BresoDX1 (AHIbreso) was compared to the AHI determined from PSG (AHIPSG) and the sensitivity and specificity of SA diagnosis were assessed at an AHIPSG ≥ 15. Results: Two-hundred thirty-three participants (mean ± SD) 50 ± 16 years of age, with BMI of 29.8 ± 6.6 and AHI of 19.5 ± 22.7, were included. There was a strong relationship between AHIbreso and AHIPSG (r = 0.91, p < 0.001). SA detection for an AHIPSG ≥ 15 was highly sensitive (90.0%) and specific (85.9%). Conclusion: We conclude that the DNN model we developed via recording and analyses of trachea-sternal motion and sound along with oximetry provides an accurate estimate of the AHIPSG with high sensitivity and specificity. Therefore, BresoDX1 is a simple, convenient and accurate portable SA monitoring device that could be employed for home SA testing in the future.