Pharyngeal Collapse Research Articles

After-discharge in the upper airway muscle genioglossus following brief hypoxia.

Genioglossus (GG) after-discharge is thought to protect against pharyngeal collapse by minimizing periods of low upper airway muscle activity. How GG after-discharge occurs and which single motor units (SMUs) are responsible for the phenomenon are unknown. The aim of this study was to investigate genioglossal after-discharge. During wakefulness, after-discharge was elicited 8-12 times in healthy individuals with brief isocapnic hypoxia (45-60 s of 10% O2 in N2) terminated by a single breath of 100% O2. GG SMUs were designated as firing solely, or at increased rate, during inspiration (Inspiratory phasic [IP] and inspiratory tonic [IT], respectively); solely, or at increased rate, during expiration (Expiratory phasic [EP] or expiratory tonic [ET], respectively) or firing constantly without respiratory modulation (Tonic). SMUs were quantified at baseline, the end of hypoxia, the hyperoxic breath, and the following eight normoxic breaths. A total of 210 SMUs were identified in 17 participants. GG muscle activity was elevated above baseline for seven breaths after hyperoxia (p < 0.001), indicating a strong after-discharge effect. After-discharge occurred due to persistent firing of IP and IT units that were recruited during hypoxia, with minimal changes in ET, EP, or Tonic SMUs. The firing frequency of units that were already active changed minimally during hypoxia or the afterdischarge period (p > 0.05). That genioglossal after-discharge is almost entirely due to persistent firing of previously silent inspiratory SMUs provides insight into the mechanisms responsible for the phenomenon and supports the hypothesis that the inspiratory and expiratory/tonic motor units within the muscle have idiosyncratic functions.

Orofacial Myofunctional Therapy in Obstructive Sleep Apnea Syndrome: A Pathophysiological Perspective.

Obstructive sleep apnea (OSA) syndrome is a multi-factorial disorder. Recently identified pathophysiological contributing factors include airway collapsibility, poor pharyngeal muscle responsiveness, a low arousal threshold, and a high loop gain. Understanding the pathophysiology is of pivotal importance to select the most effective treatment option. It is well documented that conventional treatments (continuous positive airway pressure (CPAP), upper airway surgery, and dental appliance) may not always be successful in the presence of non-anatomical traits, especially in mild to moderate OSA. Orofacial myofunctional therapy (OMT) consists of isotonic and isometric exercises targeted to oral and oropharyngeal structures, with the aim of increasing muscle tone, endurance, and coordinated movements of pharyngeal and peripharyngeal muscles. Recent studies have demonstrated the efficacy of OMT in reducing snoring, apnea–hypopnea index, and daytime sleepiness, and improving oxygen saturations and sleep quality. Myofunctional therapy helps to reposition the tongue, improve nasal breathing, and increase muscle tone in pediatric and adult OSA patients. Studies have shown that OMT prevents residual OSA in children after adenotonsillectomy and helps adherence in CPAP-treated OSA patients. Randomized multi-institutional studies will be necessary in the future to determine the effectiveness of OMT in a single or combined modality targeted approach in the treatment of OSA. In this narrative review, we present up-to-date literature data, focusing on the role of OSA pathophysiology concepts concerning pharyngeal anatomical collapsibility and muscle responsiveness, underlying the response to OMT in OSA patients.

Upper Oesophageal Sphincter Aplasia in Equids: Observations in Preoperative Patients and a Possible Association with some Cases of Dorsal Pharyngeal Collapse and Paradoxical Sleep Deprivation

Upper Oesophageal Sphincter Aplasia in Equids: Observations in Preoperative Patients and a Possible Association with some Cases of Dorsal Pharyngeal Collapse and Paradoxical Sleep Deprivation

The Effect of Lateral Pharyngeal Collapse Patterns on Therapy Response in Upper Airway Stimulation Surgery.

Obstructive sleep apnea (OSA) is characterized by repeated upper airway collapse while sleeping which leads to intermittent hypoxemia. Upper airway stimulation (UAS) is a commonly practiced modality for treating OSA in patients who cannot tolerate, or do not benefit from, positive airway pressure (PAP). The purpose of this study is to identify the effect of lateral pharyngeal collapse patterns on therapy response in UAS. A retrospective cohort study from a single, tertiary-care academic center was performed. Patients who underwent UAS between October 2016 and July 2019 were identified and analyzed. Drug-induced Sleep Endoscopy (DISE) outcomes between Apnea-Hypopnea Index (AHI) responders and AHI non-responders were compared. Those with complete concentric collapse at the velopharynx were not candidates for UAS. About 95 patients that underwent UAS were included in this study. Pre- to Post-UAS demonstrated significant improvements in Epworth Sleepiness Scale (12.0 vs 4.0, P = .001), AHI (29.8 vs 5.4, P < .001) and minimum oxygen saturation (79% vs 83%, P < .001). No DISE findings significantly predicted AHI response after UAS. Specifically, multiple types of lateral pharyngeal collapse patterns did not adversely effect change in AHI or AHI response rate. Demonstration of lateral pharyngeal collapse on DISE, in the absence of complete concentric velopharyngeal obstruction, does not appear to adversely affect AHI outcomes in UAS patients. VI.

Dynamic computed tomography evaluation of the nasopharynx in normal Beagle dogs.

Pharyngeal collapsibility has been used as diagnostic criteria in dogs, whereas the normal range and quantitative method have not been studied. Dynamic and static computed tomography (CT) was performed in 23 normal Beagle dogs to quantify the nasopharyngeal collapsibility at different locations. Using dynamic CT, maximum and minimum nasopharyngeal cross-sectional areas (CSAs) were measured at the level of the cranial end of the soft palate, pterygoid hamulus, foramen lacerum, bony labyrinth, and caudal end of the soft palate. The ratio of all maximum and minimum CSA to nasopharyngeal CSA at the level of the caudal hard palate (rCSAmax and rCSAmin) and the nasopharyngeal collapsibility were calculated. The differences of rCSAmax, rCSAmin, and nasopharyngeal collapsibility were analyzed at various locations. The nasopharyngeal collapsibility at the level of foramen lacerum, bony labyrinth, and caudal end of soft palate were higher than the others. At the level of the caudal end of the soft palate, rCSAmin was lower than that of the foramen lacerum and bony labyrinth, whereas rCSAmax at foramen lacerum was higher than that of the caudal end of the soft palate. These results indicated that the nasopharynx at the level of foramen lacerum and caudal end of the soft palate were considered notable locations for evaluating collapsibility. Dynamic CT could show the nasopharyngeal dynamic profile and will be an adequate modality for evaluating nasopharynx. Our results will be helpful for further comparative studies in dogs with and without nasopharyngeal collapse.

Pathophysiology of Upper Airway Collapse

Previous pathophysiologic studies have revealed that the upper airway dimension reaches a minimal value at the end of expiration, and pharyngeal negative pressure is not an essential prerequisite for upper airway collapse. Furthermore, pharyngeal collapse occurs in spite of increased activity of upper airway dilator muscles in patients with obstructive sleep apnea (OSA) compared with normal subjects. Pharyngeal sensory threshold is elevated in patients with OSA, which contributes to inadequate activity of upper airway dilator muscles. Pharyngeal narrowing results in several types of airflow limitation, of whom the mechanisms are mainly explained using Starling resistor model and negative effort dependence. Several studies have been conducted over the past years to validate polysomnographic surrogate markers which indicate specific pathophysiologic phenotypes, and such attempts may be able to lead us to personalized treatment for OSA.

Non-REM Apnea and Hypopnea Duration Varies across Population Groups and Physiologic Traits.

Rationale: Symptoms and morbidities associated with obstructive sleep apnea (OSA) vary across individuals and are not predicted by the apnea-hypopnea index (AHI). Respiratory event duration is a heritable trait associated with mortality that may further characterize OSA.Objectives: We evaluated how hypopnea and apnea durations in non-REM (NREM) sleep vary across demographic groups and quantified their associations with physiological traits (loop gain, arousal threshold, circulatory delay, and pharyngeal collapsibility).Methods: Data were analyzed from 1,546 participants from the Multi-Ethnic Study of Atherosclerosis with an AHI ≥5. Physiological traits were derived using a validated model fit to the polysomnographic airflow signal. Multiple linear regression models were used to evaluate associations of event duration with demographic and physiological factors.Measurements and Main Results: Participants had a mean age ± SD of 68.9 ± 9.2 years, mean NREM hypopnea duration of 21.73 ± 5.60, and mean NREM apnea duration of 23.87 ± 7.44 seconds. In adjusted analyses, shorter events were associated with younger age, female sex, higher body mass index (P < 0.01, all), and Black race (P < 0.05). Longer events were associated with Asian race (P < 0.01). Shorter event durations were associated with lower circulatory delay (2.53 ± 0.13 s, P < 0.01), lower arousal threshold (1.39 ± 0.15 s, P < 0.01), reduced collapsibility (-0.71 ± 0.16 s, P < 0.01), and higher loop gain (-0.27 ± 0.11 s, P < 0.05) per SD change. Adjustment for physiological traits attenuated age, sex, and obesity associations and eliminated racial differences in event duration.Conclusions: Average event duration varies across population groups and provides information on ventilatory features and airway collapsibility not captured by the AHI.

Complex sleep‐disordered breathing after vagus nerve stimulation: broadening the spectrum of adverse events of special interest

Two young males with refractory epilepsy of unknown aetiology were referred for vagus nerve stimulation (VNS). Sleep disturbances emerged following VNS parameter changes. In Patient 1, video-polysomnogram (PSG) disclosed snoring and catathrenia in non-REM sleep. Central apnoea also occurred, but more rarely. In Patient 2, video-PSG showed mixed apnoea with desaturation and episodes of stridor followed by a catathrenia-like sound. A drug-induced sleep endoscopy (DISE) revealed, during VNS OFF time, glossoptosis, "trap door" of the epiglottis, and paresis of the left side of the larynx and ipsilateral vocal cords. During ON time, there were periods of pharyngeal collapse, in which video-PSG revealed patterns suggestive of both obstructive and central sleep apnoea. All these sleep-related phenomena were coincident with VNS ON time. In the first patient, VNS parameter adjustment was sufficient to successfully reverse all the symptoms, whereas the other patient required concomitant treatment with continuous positive airway pressure. The data broaden our knowledge about sleep disorders related to VNS, in particular stridor and catathrenia. We suggest that central sleep apnoea may be associated with laryngeal occlusion. DISE may be considered in selected cases as a valuable clinical tool to evaluate, in a single session, the effectiveness of multiple VNS parameter changes on respiration and laryngeal side effects. [Published with video sequences].

Intermittent Hypoxia Mediates Caveolae Disassembly That Parallels Insulin Resistance Development.

Repetitive complete or incomplete pharyngeal collapses are leading to chronic intermittent hypoxia (CIH), a hallmark feature of obstructive sleep apnea (OSA) syndrome responsible for many metabolic disorders. In humans, an association between OSA and insulin resistance has been found independently of the degree of obesity. Based on our previous work showing that hypoxia applied to adipocytes led to cellular insulin resistance associated with caveolae flattening, we have investigated the effects of CIH on caveolae structuration in adipose tissue. Original exploratory experiences demonstrate that 6 weeks-exposure of lean mice to CIH is characterized by systemic insulin resistance and translates into adipocyte insulin signaling alterations. Chronic intermittent hypoxia also induces caveolae disassembly in white adipose tissue (WAT) illustrated by reduced plasma membrane caveolae density and enlarged caveolae width, concomitantly to WAT insulin resistance state. We show that CIH downregulates caveolar gene and protein expressions, including cavin-1, cavin-2, and EHD2, underlying molecular mechanisms responsible for such caveolae flattening. Altogether, we provide evidences for adipose tissue caveolae disassembly following CIH exposure, likely linked to cavin protein downregulation. This event may constitute the molecular basis of insulin resistance development in OSA patients.

Pharyngomalacia in Neonates: The Missed Issue.

Background: Airway malacia (AM) is a weakness of the airway's frameworks making them collapsible during the respiratory phases. Although the larynx, trachea, and bronchus are the usual sites for malacia to occur, there is another important type of malacia that involves the pharynx. Pharyngomalacia (PM) or concentric pharyngeal wall inspiratory collapse (PWIC) is mostly missed during bronchoscopic evaluations in the neonates with noisy breathing because people are not aware of this condition.Methods: This study aimed to evaluate the nasopharyngeal investigation among neonates suffering from noisy breathing. The retrospective study was undertaken to assess the frequency of PM and to propose indications for intervention in 100 neonates with noisy breathing. A thin fiberoptic bronchoscope was used to evaluate the upper airways under conscious status without any sedation in the neonates.Results: A total of 100 neonates with noisy breathing from September 2015 to October 2018 were retrospectively analyzed. The most common presenting symptom was inspiratory stridor which was observed in 35 (92.1%) of cases. PM was diagnosed in 38 neonates (38%) including 27 (71%) males and 13 (29%) females. Seventeen (44.7%) cases had mild, 11 (28.9%) cases had moderate, and 10 (26.4%) cases had a severe type of PM. PM was more prominent at the velopharynx level in 15 (39.4%) cases, and it was accompanied by up to six synchronous airway abnormalities. The most frequent synchronous airway abnormality was laryngomalacia in 13 (34.3%).Conclusion: PM is one of the causes of noisy breathing in infants. Since PM can be accompanied by the presence of other types of airway malacia, the issue becomes more complicated. On the other hand, lack of experience and facilities are two main causes for the accurate diagnosis and effective management among neonates. This study indicates that the investigation of pharynx is a missed part of the many workups that are used to diagnose the site of involvement in neonates with noisy breathing.

Methodology for evaluating effects of mandibular advancement devices in treating OSAS

Obstructive sleep apnoea syndrome is characterized by an obstruction in the upper airway due to the pharyngeal collapse during sleep. Mandibular advancement devices have gained success and large popularity as a non-invasive treatment for OSAS. Nevertheless, the effects of mandibular advancement devices were poorly investigated in literature. To this aim the paper proposes a procedure to achieve a numerical simulation model useful to assess the stress/strain distribution on the temporomandibular joint and periodontal ligaments caused by the mandibular advancement. The findings suggest that the mandibular roto-translation induced by the MAD provoke high stress on the molars and premolar teeth.

Longus capitis and rectus capitis ventralis minor rupture in a horse following general anaesthesia for a laryngeal tie-forward procedure

The authors present a case of a racehorse with acute respiratory distress, bilateral epistaxis and laryngeal swelling following a laryngeal tie-forward procedure. An emergency tracheostomy was performed following brief endoscopic...

A scalable method of determining physiological endotypes of sleep apnea from a polysomnographic sleep study.

Sleep apnea is caused by several endophenotypic traits, namely pharyngeal collapsibility, poor muscle compensation, ventilatory instability (high loop gain), and arousability from sleep (low arousal threshold). Measures of these traits have shown promise for predicting outcomes of therapies (e.g. oral appliances, surgery, hypoglossal nerve stimulation, CPAP, and pharmaceuticals), which may become an integral part of precision sleep medicine. Currently, the methods Sands et al. developed for endotyping sleep apnea from polysomnography (PSG) are embedded in the original authors’ code, which is computationally expensive and requires technological expertise to run. We present a reimplementation and validation of the integrity of the original authors’ code by reproducing the endo-Phenotyping Using Polysomnography (PUP) method of Sands et al. The original MATLAB methods were reprogrammed in Python; efficient algorithms were developed to detect breaths, calculate normalized ventilation (moving time-average), and model ventilatory drive (intended ventilation). The new implementation (PUPpy) was validated by comparing the endotypes from PUPpy with the original PUP results. Both endotyping methods were applied to 38 manually scored polysomnographic studies. Results of the new implementation were strongly correlated with the original (p < 10–6 for all): ventilation at eupnea V̇ passive (ICC = 0.97), ventilation at arousal onset V̇ active (ICC = 0.97), loop gain (ICC = 0.96), and arousal threshold (ICC = 0.90). We successfully implemented the original PUP method by Sands et al. providing further evidence of its integrity. Additionally, we created a cloud-based version for scaling up sleep apnea endotyping that can be used more easily by a wider audience of researchers and clinicians.

Flow-Identified Site of Collapse During Drug-Induced Sleep Endoscopy: Feasibility and Preliminary Results

Flow-Identified Site of Collapse During Drug-Induced Sleep Endoscopy: Feasibility and Preliminary Results

Drug-induced sleep endoscopy: techniques, interpretation and implications.

The purpose of this article is to highlight recent advances in the burgeoning field of drug-induced sleep endoscopy (DISE). One of the first studies to investigate the correlation of DISE findings and natural sleep endoscopy found good agreement in clinically significant obstruction. Previous studies have shown good agreement of DISE findings with the use of different sedative agents implying that the choice of sedative may not be crucial. However, recent studies show variable patterns of collapse, especially at the tongue base, with the use of different sedative agents. A universally accepted classification scheme for drug-induced sleep endoscopy is lacking. A new DISE classification system, termed Palate, Tonsils, Lateral pharyngeal wall, Tongue base, Epiglottis, was introduced this year with the noted advantage of being able to better differentiate between clinically relevant tonsillar and lateral pharyngeal wall collapse. Despite recent advances in the field, there remains no general consensus that DISE findings predict surgical success but may aid in the identification of patients who will respond well to oral appliance therapy. Drug-induced sleep endoscopy is a structure-based evaluation of the upper airway that more closely resembles the natural sleep state compared with awake evaluation.

Manipulation of Lateral Pharyngeal Wall Muscles in Sleep Surgery: A Review of the Literature.

Background: Obstructive sleep apnea syndrome (OSAS) occurs due to upper airway obstruction resulting from anatomical and functional abnormalities. Upper airway collapsibility, particularly those involving the lateral pharyngeal wall (LPW), is known to be one of the main factors contributing to the pathogenesis of OSAS, leading the authors of the present study to propose different strategies in order to stiffen the pharyngeal walls to try to restore normal airflow. Methods: An exhaustive review of the English literature on lateral pharyngeal wall surgery for the treatment of OSAS was performed using the PubMed electronic database. Results: The research was performed in April 2020 and yielded approximately 2000 articles. However, considering the inclusion criteria, only 17 studies were included in the present study. Conclusions: The analyzed surgical techniques propose different parts of LPW on which to focus and a variable degree of invasivity. Despite the very promising results, no gold standard for the treatment of pharyngeal wall collapsibility has been proposed. However, thanks to progressive technological innovations and increasingly precise data analysis, the role of LPW surgery seems to be crucial in the treatment of OSAS patients.

How obesity affects nasal function in obstructive sleep apnea: anatomic and volumetric parameters

IntroductionObstructive sleep apnea is a consequence of upper airway collapse. Any obstructive sector in the upper airway can contribute to pharyngeal collapse. Obesity and obesity-related disorders play an important role in obstructive sleep apnea and its relationship with increased upper airway resistance. ObjectiveThis study was designed to evaluate the relationship between obesity and properties of the nasal cavity in patients with obstructive sleep apnea. MethodsThe study was conducted retrospectively by review of medical records of adult patients. The nasal obstruction symptom evaluation, NOSE instrument, was used to measure nasal obstruction. Sleep breathing disorders were evaluated by polysomnography exams. Nasal volume was obtained by computed tomography scans and volumetric reconstruction of nasal airway. Nasal anatomic alterations were assessed by nasal endoscopy. ResultsAnalysis of 83 patient records, among whom 54 were male and 29 females, found the mean body mass index of 28.69 kg/m2. Obese and non-obese groups were determined by using cut-off 30 kg/m2. In the comparison between groups, the obese group had a positive and significant correlation with apnea/hypopnea index (p = 0.02), NOSE instrument (p = 0.033) and inferior turbinate hypertrophy (p = 0.036), with odds ratio 1.983 (95% IC 1.048 − 3.753). nasal septum deviation (p = 0.126) and nasal airway volume evaluation (p = 0.177) showed no significant results. ConclusionObesity was significantly correlated with subjective nasal obstruction, NOSE scale, and inferior turbinate hypertrophy in patients with obstructive sleep apnea. There was no correlation with the nasal volume evaluation. Level of Evidence3b - Individual case-control study.

Association Between Breathing Route, Oxygen Desaturation, and Upper Airway Morphology.

This study aimed to assess the role of capnography in objectively evaluating breathing routes during drug-induced sleep endoscopy (DISE) and further elucidate the relationship between breathing route, obstructive sleep apnea (OSA) severity, and DISE findings. Prospective observational study. Nighty-five patients with established OSA were recruited for this study from May 2017 to May 2019. DISE was performed in the operating room. Sedation was maintained with propofol using a target-controlled infusion system and the depth of sedation was monitored based on the bispectral index. The breathing routes, which included oral breathing, oronasal breathing, and nasal breathing, were detected using capnography. DISE findings were recorded using the VOTE (velum, oropharynx, base of tongue, and epiglottis) classification. Patients with mouth breathing were associated with increased OSA severity, worse oximetric variables, and higher body mass index in comparison with those with other breathing routes. Mouth breathing was associated with a higher degree and higher prevalence of lateral pharyngeal wall collapse and tongue base collapse during DISE. Mouth breathing was significantly associated with worse oxygen desaturation and increased degree of upper airway collapse. Therefore, patients with mouth breathing during propofol-based intravenous anesthesia should be carefully monitored. 4 Laryngoscope, 131:E659-E664, 2021.

0568 Physiologic OSA Traits and CPAP Adherence Among Patients with Coronary Artery Disease and OSA

Abstract Introduction Obstructive sleep apnea (OSA) is common in patients with coronary artery disease (CAD), but adherence to continuous positive airway pressure (CPAP) in this population is poor. Low arousal threshold (ArTH), a pathophysiologic OSA trait, is associated with low rates of regular CPAP use in sleep clinic populations. We aimed to determine whether ArTH or other physiologic OSA traits (i.e. pharyngeal collapsibility, muscle compensation, loop gain) are associated with CPAP adherence in patients with CAD and OSA. Methods A secondary analysis of a randomized controlled trial of OSA treatment in patients with CAD (RICCADSA) was performed. OSA (apnea hypopnea index, AHI≥5/hour) was assessed by polysomnography. Arousal threshold (% eupneic ventilation, %Ve), loop gain (LG), pharyngeal collapsibility (%Ve) and compensation (%Ve) were estimated from polysomnography using a validated method. Adherence to auto-titrated CPAP (hours/night) was obtained from machine downloads at 1, 3, 6, 12 and 24 months. Mixed modelling was used to assess the association between OSA traits and CPAP adherence. Results Participants (n=262) were 64.1±7.9 years old, with BMI of 29.2±4.2 and 86% were men. The mean AHI was 40.8±23.6 events/hour with oxygen nadir of 81.3±7.1%. The median (IQR) CPAP adherence (hrs/night) was 3.0 (0.9, 5.8) at 1-mo and 3.0 (0.0, 5.6) at 24-mo. Compared to reference studies, the CAD patients exhibited an elevated LG 0.63 (0.53, 0.79), similar ArTH (%Ve) of 117.5% (106.5%, 136.4%), higher collapsibility (%Ve) at 90.1% (82.3%, 94.8%) and lower compensation (%Ve) at 3.7% (-0.7%, 8.7%).Only increasing pharyngeal muscle compensation was associated with lower CPAP adherence (β -0.04, p-value 0.048), effect modified by pharyngeal collapsibility (Compensation x Collapsibility, β &amp;lt;0.01, p-value 0.042). Conclusion In this group of patients with CAD, increasing muscle compensation was associated with lower CPAP adherence. Physiologic OSA traits may provide insight into prediction of CPAP adherence among patients with OSA and CAD. Support Zinchuk: Parker B. Francis Fellowship Program in Clinical Research. Sands: American Heart Association. Peker: Swedish Research Council, Swedish Heart-Lung Foundation.

0448 Scaled-Up Sleep Apnea Endotyping Using Polysomnography for Clinical Use

Abstract Introduction Sleep apnea is caused by several key endophenotypic traits namely pharyngeal collapsibility, poor muscle compensation, ventilatory instability (high loop gain), and arousability from sleep (low arousal threshold). Already, measures of these traits have shown promise for predicting outcomes of therapies (oral appliances, surgery, hypoglossal nerve stimulation, CPAP, or pharmaceuticals) and thus may be an integral part of future precision sleep medicine with treatments administered based on underlying pathophysiology. However, currently, the novel methods developed for endotyping from polysomnography are computationally expensive and can only be performed by the original authors or their collaborators due to the need for technological expertise. Here we present a cloud-based method for endotyping sleep apnea from polysomnography for use in the clinical arena. Methods For cloud-based use, we optimized the Phenotype Using Polysomnography (‘PUP’) method of Sands et.al. (2015-2018) by performing the following: Code was translated from MATLAB to Python; efficient methods were developed to detect breaths, calculate normalized ventilation (moving time-average), and model ventilatory drive (intended ventilation). The new implementation (‘PUP.py’) was validated by comparing the measured traits against the original values. Results 38 manually scored clinical polysomnographic studies were endophenotyped using the two implementations. Results of the new implementation (‘PUP.py’) were strongly correlated with the original (p&amp;lt;10-6 for all): collapsibility and compensation (ventilation at eupneic drive ‘Vpassive’: r=0.98; ventilation at arousal threshold, r=0.97), loop gain (r=0.96), and arousal threshold (r=0.92). Conclusion We successfully implemented the original method by Sands et.al. to scale up sleep apnea endotyping and make it available to a broader audience. Support This work was supported by the Icelandic Centre for Research RANNÍS, the European Union’s Horizon 2020 SME Instrument (733461), and the American Heart Association (15SDG25890059).