Journal articles on the topic 'Sleep apnea'
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1
Khan, Muhammad Talha, and Rose Amy Franco. "Complex Sleep Apnea Syndrome." Sleep Disorders 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/798487.
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Complex sleep apnea is the term used to describe a form of sleep disordered breathing in which repeated central apneas (>5/hour) persist or emerge when obstructive events are extinguished with positive airway pressure (PAP) and for which there is not a clear cause for the central apneas such as narcotics or systolic heart failure. The driving forces in the pathophysiology are felt to be ventilator instability associated oscillation in PaCO2arterial partial pressure of Carbon Dioxide, continuous cositive airway pressure (CPAP) related increased CO2carbon dioxide elimination, and activation of airway and pulmonary stretch receptors triggering these central apneas. The prevalence ranges from 0.56% to 18% with no clear predictive characteristics as compared to simple obstructive sleep apnea. Prognosis is similar to obstructive sleep apnea. The central apnea component in most patients on followup using CPAP therap, has resolved. For those with continued central apneas on simple CPAP therapy, other treatment options include bilevel PAP, adaptive servoventilation, permissive flow limitation and/or drugs.
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Suto, Y., and Y. Inoue. "Sleep Apnea Syndrome." Acta Radiologica 37, no. 1P1 (January 1996): 315–20. http://dx.doi.org/10.1177/02841851960371p166.
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Purpose: We attempted to determine the usefulness of high-speed MR imaging for evaluating the severity of sleep apnea syndrome (SAS) by comparing findings of pharyngeal obstruction obtained with high-speed MR with those of all-night polysomnography (PSG). Subjects and Methods: A total of 33 patients with SAS underwent turbo-FLASH MR examination, while awake and after i.v. injection of hydroxyzine hydrochloride. Serial images were examined by cinemode. Pharyngeal findings on MR were divided into single-site obstruction (SO) at the velopharynx, multiple-site obstruction (MO), and no obstruction (NO). PSG findings were analyzed to determine the predominant type of apnea, severity as evaluated by an apnea index (AI), and the lowest SaO2 value during sleep. Results: Seventy-five percent of the central apnea group had SO, and 70% of the mixed apneas had MO, while only 15% of the obstructed apneas had MO. The percentage of patients with severe SAS (AI of 20% or higher) was 48% for the SO, and 70% for the MO. The lowest SaO2 value tended to be low in the mixed apnea in the case of PSG, and tended to be low in the MO at MR examination. Conclusion: Analysis of pharyngeal dynamics using high-speed MR may provide some useful information for evaluating the severity of SAS.
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Peng, Ying-Jie, Xiuli Zhang, Anna Gridina, Irina Chupikova, David L. McCormick, Robert J. Thomas, Thomas E. Scammell, et al. "Complementary roles of gasotransmitters CO and H2S in sleep apnea." Proceedings of the National Academy of Sciences 114, no. 6 (January 23, 2017): 1413–18. http://dx.doi.org/10.1073/pnas.1620717114.
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Sleep apnea, which is the periodic cessation of breathing during sleep, is a major health problem affecting over 10 million people in the United States and is associated with several sequelae, including hypertension and stroke. Clinical studies suggest that abnormal carotid body (CB) activity may be a driver of sleep apnea. Because gaseous molecules are important determinants of CB activity, aberrations in their signaling could lead to sleep apnea. Here, we report that mice deficient in heme oxygenase-2 (HO-2), which generates the gaseous molecule carbon monoxide (CO), exhibit sleep apnea characterized by high apnea and hypopnea indices during rapid eye movement (REM) sleep. Similar high apnea and hypopnea indices were also noted in prehypertensive spontaneously hypertensive (SH) rats, which are known to exhibit CB hyperactivity. We identified the gaseous molecule hydrogen sulfide (H2S) as the major effector molecule driving apneas. Genetic ablation of the H2S-synthesizing enzyme cystathionine-γ-lyase (CSE) normalized breathing inHO-2−/−mice. Pharmacologic inhibition of CSE withl-propargyl glycine prevented apneas in bothHO-2−/−mice and SH rats. These observations demonstrate that dysregulated CO and H2S signaling in the CB leads to apneas and suggest that CSE inhibition may be a useful therapeutic intervention for preventing CB-driven sleep apnea.
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Basner, R. C., E. Onal, D. W. Carley, E. J. Stepanski, and M. Lopata. "Effect of induced transient arousal on obstructive apnea duration." Journal of Applied Physiology 78, no. 4 (April 1, 1995): 1469–76. http://dx.doi.org/10.1152/jappl.1995.78.4.1469.
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Six untreated male patients (age 19–55 yr) with obstructive sleep apnea underwent nocturnal polysomnography with acoustic stimulation to determine the effect of transient arousal on obstructive apneas during sleep. Binaural tone bursts (25–95 dB) were delivered in late expiration during the second obstructive apnea of a cycle consisting of four consecutive apneas. For the group, stimulated apneas were significantly shorter (P < 0.05, Fisher's protected least significant difference test) than were the unstimulated apneas when transient electrocortical arousal was elicited in both non-rapid-eye-movement (non-REM) sleep [mean 17 +/- 7 (SD) vs. 26 +/- 9, 23 +/- 10, and 26 +/- 12 s for 2nd vs. 1st, 3rd, and 4th apnea, respectively, of each cycle] and REM sleep (mean 19 +/- 10 vs. 35 +/- 15, 45 +/- 18, and 39 +/- 20 s). Without electrocortical arousal, the stimulated apnea was significantly shortened in non-REM (23 +/- 9 vs. 25 +/- 7, 24 +/- 8, and 26 +/- 8 s) but not in REM (32 +/- 16 vs. 37 +/- 12, 32 +/- 15, and 30 +/- 16 s). Tones delivered relatively early and late in the apnea were equally likely to be associated with resolution of the apnea. The nadir of arterial oxygen saturation of hemoglobin was inversely proportional to apnea length, with higher saturation nadirs associated with the stimulated apneas. These data indicate that transient arousal, induced by nonrespiratory stimulation, influences the resolution of obstructive apneas during sleep.
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Anne, Pratibha, Rupa Koothirezhi, Ugorji Okorie, Minh Tam Ho, Brittany Monceaux, Cesar Liendo, Sheila Asghar, and Oleg Chernyshev. "833 Evolution of sleep disordered breathing types in heart failure." Sleep 44, Supplement_2 (May 1, 2021): A324—A325. http://dx.doi.org/10.1093/sleep/zsab072.830.
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Abstract Introduction Central sleep apnea is commonly seen in patients with heart failure. Here we present a case demonstrating shifting of predominant apneic events from central to obstructive type after placement of left ventricular assist device (LVAD) in end stage heart failure patient. Report of case(s) Case Presentation: 66 year-old African American male has past medical history of chronic congestive heart failure diabetes, hypertension, paroxysmal atrial fibrillation, anemia, hypothyroidism, chronic kidney disease and sleep apnea. Prior to his LVAD placement, his left ventricular ejection fraction (EF) was <10%. Patient was diagnosed with central sleep apnea with AHI of 58 (with 92% of apneic events being central events), oxygen nadir of 74%. Subsequently, patient had LVAD placed for symptomatic heart failure and repeat polysomnogram repeated at six month demonstrated an improved AHI of 45.8 with predominantly obstructive and mixed apneic events, with only 12.5% being central events. Conclusion This case report highlights not only the improvement of the sleep apnea in CHF treated with LVAD but also shows the shift of apneic events from predominantly central to obstructive type post LVAD. Support (if any) 1. Henein MY, Westaby S, Poole-Wilson PA, Cowie MR, Simonds AK. Resolution of central sleep apnoea following implantation of a left ventricular assist device. Int J Cardiol. 2010 Feb 4;138(3):317–9. PMID: 18752859. 2. Köhnlein T, Welte T, Tan LB, Elliott MW. Central sleep apnoea syndrome in patients with chronic heart disease: a critical review of the current literature. Thorax. 2002 Jun;57(6):547–54. PMID: 12037232 3. Monda C, Scala O, Paolillo S, Savarese G, Cecere M, D’Amore C, Parente A, Musella F, Mosca S, Filardi PP. Apnee notturne e scompenso cardiaco: fisiopatologia, diagnosi e terapia [Sleep apnea and heart failure: pathophysiology, diagnosis and therapy]. G Ital Cardiol (Rome). 2010 Nov;11(11):815–22. Italian. PMID: 21348318.
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Badr, M. S., F. Toiber, J. B. Skatrud, and J. Dempsey. "Pharyngeal narrowing/occlusion during central sleep apnea." Journal of Applied Physiology 78, no. 5 (May 1, 1995): 1806–15. http://dx.doi.org/10.1152/jappl.1995.78.5.1806.
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We hypothesized that subatmospheric intraluminal pressure is not required for pharyngeal occlusion during sleep. Six normal subjects and six subjects with sleep apnea or hypopnea (SAH) were studied during non-rapid-eye-movement sleep. Pharyngeal patency was determined by using fiber-optic nasopharyngoscopy during spontaneous central sleep apnea (n = 4) and induced hypocapnic central apnea via nasal mechanical ventilation (n = 10). Complete pharyngeal occlusion occurred in 146 of 160 spontaneously occurring central apneas in patients with central sleep apnea syndrome. During induced hypocapnic central apnea, gradual progressive pharyngeal narrowing occurred. More pronounced narrowing was noted at the velopharynx relative to the oropharynx and in subjects with SAH relative to normals. Complete pharyngeal occlusion frequently occurred in subjects with SAH (31 of 44 apneas) but rarely occurred in normals (3 of 25 apneas). Resumption of inspiratory effort was associated with persistent narrowing or complete occlusion unless electroencephalogram signs of arousal were noted. Thus pharyngeal cross-sectional area is reduced during central apnea in the absence of inspiratory effort. Velopharyngeal narrowing consistently occurs during induced hypocapnic central apnea even in normal subjects. Complete pharyngeal occlusion occurs during spontaneous or induced central apnea in patients with SAH. We conclude that subatmospheric intraluminal pressure is not required for pharyngeal occlusion to occur. Pharyngeal narrowing or occlusion during central apnea may be due to passive collapse or active constriction.
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Davis, Eric M., Landon W. Locke, Angela L. McDowell, Patrick J. Strollo, and Christopher P. O'Donnell. "Obesity accentuates circadian variability in breathing during sleep in mice but does not predispose to apnea." Journal of Applied Physiology 115, no. 4 (August 15, 2013): 474–82. http://dx.doi.org/10.1152/japplphysiol.00330.2013.
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Obesity is a primary risk factor for the development of obstructive sleep apnea in humans, but the impact of obesity on central sleep apnea is less clear. Given the comorbidities associated with obesity in humans, we developed techniques for long-term recording of diaphragmatic EMG activity and polysomnography in obese mice to assess breathing patterns during sleep and to determine the effect of obesity on apnea generation. We hypothesized that genetically obese ob/ob mice would exhibit less variability in breathing across the 24-h circadian cycle, be more prone to central apneas, and be more likely to exhibit patterns of increased diaphragm muscle activity consistent with obstructive apneas compared with lean mice. Unexpectedly, we found that obese mice exhibited a greater circadian impact on respiratory rate and diaphragmatic burst amplitude than lean mice, particularly during rapid eye movement (REM) sleep. Central apneas were more common in REM sleep (42 ± 17 h−1) than non-REM (NREM) sleep (14 ± 5 h−1) in obese mice ( P < 0.05), but rates were not different between lean and obese mice in either sleep state. Even after experimentally enhancing central apnea generation by acute withdrawal of hypoxic chemoreceptor activation during sleep, central apnea rates remained comparable between lean and obese mice. Last, we were unable to detect patterns of diaphragmatic burst activity suggestive of obstructive apnea events in obese mice. In summary, obesity does not predispose mice to increased occurrence of central or obstructive apneas during sleep, but does lead to a more pronounced circadian variability in respiration.
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Ringler, J., R. C. Basner, R. Shannon, R. Schwartzstein, H. Manning, S. E. Weinberger, and J. W. Weiss. "Hypoxemia alone does not explain blood pressure elevations after obstructive apneas." Journal of Applied Physiology 69, no. 6 (December 1, 1990): 2143–48. http://dx.doi.org/10.1152/jappl.1990.69.6.2143.
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In patients with obstructive sleep apnea (OSA), substantial elevations of systemic blood pressure (BP) and depressions of oxyhemoglobin saturation (SaO2) accompany apnea termination. The causes of the BP elevations, which contribute significantly to nocturnal hypertension in OSA, have not been defined precisely. To assess the relative contribution of arterial hypoxemia, we observed mean arterial pressure (MAP) changes following obstructive apneas in 11 OSA patients during non-rapid-eye-movement (NREM) sleep and then under three experimental conditions: 1) apnea with O2 supplementation; 2) hypoxemia (SaO2 80%) without apnea; and 3) arousal from sleep with neither hypoxemia nor apnea. We found that apneas recorded during O2 supplementation (SaO2 nadir 93.6% +/- 2.4; mean +/- SD) in six subjects were associated with equivalent postapneic MAP elevations compared with unsupplemented apneas (SaO2 nadir 79-82%): 18.8 +/- 7.1 vs. 21.3 +/- 9.2 mmHg (mean change MAP +/- SD); in the absence of respiratory and sleep disruption in eight subjects, hypoxemia was not associated with the BP elevations observed following apneas: -5.4 +/- 19 vs. 19.1 +/- 7.8 mmHg (P less than 0.01); and in five subjects, auditory arousal alone was associated with MAP elevation similar to that observed following apneas: 24.0 +/- 8.1 vs. 22.0 +/- 6.9 mmHg. We conclude that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia. Other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.
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Nakamura, Akira, Yasuichiro Fukuda, and Tomoyuki Kuwaki. "Sleep apnea and effect of chemostimulation on breathing instability in mice." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 525–32. http://dx.doi.org/10.1152/japplphysiol.00226.2002.
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Sleep apnea occurs in humans and experimental animals. We examined whether it also arises in adult mice. Ventilation in male adult 129/Sv mice was recorded concomitantly by electroencephalograms and electromyograms for 6 h by use of body plethysmography. Apnea was defined as cessation of plethysmographic signals for longer than two respiratory cycles. While mice breathed room air, 32.3 ± 6.9 (mean ± SE, n = 5) apneas were observed during sleep but not in quiet awake periods. Sleep apneas were further classified into two types. Postsigh apneas occurred exclusively during slow-wave sleep (SWS), whereas spontaneous apneas arose during both SWS and rapid eye movement sleep. Compared with room air (9.1 ± 1.4/h of SWS), postsigh apneas were more frequent in hypoxia (13.7 ± 2.1) and less frequent in hyperoxia (3.6 ± 1.7) and hypercapnia (2.8 ± 2.1). Our data indicated that significant sleep apnea occurs in normal adult mice and suggested that the mouse could be a promising experimental model with which to study the genetic and molecular basis of respiratory regulation during sleep.
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Cherniack, Neil S. "Sleep Apnea and Insomnia: Sleep Apnea Plus or Sleep Apnea Minus." Respiration 72, no. 5 (2005): 458–59. http://dx.doi.org/10.1159/000087667.
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Vaartjes, Martin, Rob L. M. Strijers, and Nico de Vries. "Posterior Nasal Packing and Sleep Apnea." American Journal of Rhinology 6, no. 2 (March 1992): 71–74. http://dx.doi.org/10.2500/105065892781874784.
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Posterior nasal packing has been reported to be associated with cardiorespiratory complications and, occasionally, with sudden death. To study the rate and incidence of sleep apnea, between October 1989 and September 1990 polysomnography (PSG) was performed in 10 patients who were treated for severe epistaxis with posterior nasal packing. Of these 10 patients, three had obstructive apneas, one had central apneas, and four had a combination of central and/or obstructive and mixed apneas. One patient had no apneas, and one was unable to sleep during PSG. In six patients, PSG was repeated a few months after removal of the packs. Four of these six patients no longer had apneas; one patient had a considerable decrease in number of apneas. One patient did not sleep during the second PSG, however, he had no apneas during the first PSG. This study demonstrates that posterior nasal packing can induce sleep apneas or enhance the severity of an apnea syndrome when present. This may contribute to the cardiorespiratory morbidity and sudden death that has been reported in epistaxis patients treated with posterior packing.
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Don, Garrick W., and Karen A. Waters. "Influence of sleep state on frequency of swallowing, apnea, and arousal in human infants." Journal of Applied Physiology 94, no. 6 (June 1, 2003): 2456–64. http://dx.doi.org/10.1152/japplphysiol.00361.2002.
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Apnea and arousal are modulated with sleep stage, and swallowing may interfere with respiratory rhythm in infants. We hypothesized that swallowing itself would display interaction with sleep state. Concurrent polysomnography and measurement of swallowing allowed time-matched analysis of 3,092 swallows, 482 apneas, and 771 arousals in 17 infants aged 1–34 wk. The mean rates of swallowing, apnea, and arousal were significantly different, being 23.3 ± 8.5, 9.4 ± 8.8, and 15.5 ± 10.6 h−1, respectively ( P < 0.001 ANOVA). Swallows occurred before 25.2 ± 7.9% and during 74.8 ± 6.3% of apneas and before 39.8 ± 6.0% and during 60.2 ± 6.0% of arousals. The frequencies of apneas and arousals were both strongly influenced by sleep state (active sleep > indeterminate > quiet sleep, P < 0.001), whether or not the events coincided with swallowing, but swallowing rate showed minimal independent interaction with sleep state. Interactions between swallowing and sleep state were predominantly influenced by the coincidence of swallowing with apnea or arousal.
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Findley, L. J., M. Boykin, T. Fallon, and L. Belardinelli. "Plasma adenosine and hypoxemia in patients with sleep apnea." Journal of Applied Physiology 64, no. 2 (February 1, 1988): 556–61. http://dx.doi.org/10.1152/jappl.1988.64.2.556.
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Severe hypoxemia causes ATP depletion and increased adenosine production in many body tissues. Therefore we hypothesized that patients with sleep apnea and severe hypoxemia during sleep have higher adenosine production and higher plasma adenosine levels than patients without hypoxemia. Twelve patients with sleep apnea and six normal volunteers had plasma adenosine levels measured by high-performance liquid chromatography. Each patient with sleep apnea had a polysomnograph sleep study with oxyhemoglobin saturation continuously recorded. Five of 12 patients with sleep apnea had both sleep apnea and severe hypoxemia during sleep. These patients with severe nocturnal hypoxemia had significantly higher plasma adenosine levels (means +/- SD 9.7 +/- 5.5 X 10(-8) M) than either a group of six normal volunteers (3.5 +/- 0.7 X 10(-8) M) or a group of seven patients with sleep apnea without hypoxemia at night (3.1 +/- 1.5 X 10(-8) M) (P less than 0.01). In addition plasma adenosine levels were significantly correlated with two indexes of nocturnal hypoxemia (desaturation index rs = 0.79, and median oxyhemoglobin saturation during sleep rs = -0.75, P less than 0.01). Plasma adenosine markedly fell to a normal level in the only two patients with sleep apnea who had successful treatment of their multiple apneas and accompanying severe hypoxemia during sleep.
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Delgado Juan, Ivonne, and Lic Isvel Perón Carmenates. "Obstructive sleep apnea syndrome." Journal of Otolaryngology-ENT Research 15, no. 2 (2023): 81–85. http://dx.doi.org/10.15406/joentr.2023.15.00533.
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Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS) is a frequent, chronic and progressive disorder. It is associated with increased cardiovascular, neurocognitive, and metabolic morbidity, risk of accidents, poor quality of life, and increased mortality. It affects 5% of the adult population, mainly men, and 2% of children between 4 and 5 years of age. Diagnosis is based on suspicion and joint evaluation of the clinical picture with appropriate confirmatory nocturnal studies such as polysomnography. The treatment has two fundamental objectives: to eliminate the respiratory obstruction and, therefore, the breathing stops (apneas) or the hypoventilations (hypopneas) and the drops in oxygen in the blood (desaturations) in any body position or phase of sleep and ensure that the subject sleeps well, improving their sleep quality and reducing or eliminating awakenings and micro-awakenings, which are the main causes of the symptoms.
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Mattiuzzi, Camilla, Massimo Franchini, and Giuseppe Lippi. "Sleep apnea and venous thromboembolism." Thrombosis and Haemostasis 114, no. 11 (2015): 958–63. http://dx.doi.org/10.1160/th15-03-0188.
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SummaryRecent evidence suggests that obstructive sleep apnea is a significant and independent risk factor for a number of cardiovascular disorders. Since the association between obstructive sleep apnea and cardiovascular disease is mediated by endothelial dysfunction, hypercoagulability and platelet abnormalities, we sought to investigate whether sleep apnea may also be considered a risk factor for venous thromboembolism (VTE). We carried out an electronic search in Medline and Scopus using the keywords “apnea” OR “apnoea” AND “venous thromboembolism” OR “deep vein thrombosis” OR “pulmonary embolism” in “Title/Abstract/Keywords”, with no language or date restriction. Fifteen studies (8 case-control, 4 retrospective observational, 2 prospective case-control and 1 prospective observational) were finally selected for this systematic review. In all studies except one (14/15; 93%), obstructive sleep apnea was found to be an independent risk factor for VTE, either deep-vein thrombosis (DVT) or pulmonary embolism (PE). In the two prospective case-control studies the risk of DVT or PE was found to be two-to three-fold higher in patients with obstructive sleep apnea than in those without. In conclusion, the current epidemiological evidence supports the hypothesis that obstructive sleep apnea may be an independent risk factor for VTE.
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Fairbanks, David W., and David N. F. Fairbanks. "Neurostimulation for Obstructive Sleep Apnea: Investigations." Ear, Nose & Throat Journal 72, no. 1 (January 1993): 52–57. http://dx.doi.org/10.1177/014556139307200111.
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Neurostimulation of the upper airway muscles (accessory muscles of respiration) was accomplished in anesthetized dogs and sleeping humans by electrical stimulation of the hypoglossal nerves. Such stimulations relieved partial airway obstructions in dogs. They also aborted (shortened) obstructive sleep apnea events in humans who suffer with obstructive sleep apnea syndrome. In one subject, stimulations delivered in advance of apneic events (by automatic cycling) prevented apneas. Neurostimulation for obstructive sleep apnea may be an important concept for future research and development.
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Dempsey, Jerome A. "Central sleep apnea: misunderstood and mistreated!" F1000Research 8 (June 28, 2019): 981. http://dx.doi.org/10.12688/f1000research.18358.1.
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Central sleep apnea is prevalent in patients with heart failure, healthy individuals at high altitudes, and chronic opiate users and in the initiation of “mixed” (that is, central plus obstructive apneas). This brief review focuses on (a) the causes of repetitive, cyclical central apneas as mediated primarily through enhanced sensitivities in the respiratory control system and (b) treatment of central sleep apnea through modification of key components of neurochemical control as opposed to the current universal use of positive airway pressure.
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Milsom, W., M. Castellini, M. Harris, J. Castellini, D. Jones, R. Berger, S. Bahrma, L. Rea, and D. Costa. "Effects of hypoxia and hypercapnia on patterns of sleep-associated apnea in elephant seal pups." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 4 (October 1, 1996): R1017—R1024. http://dx.doi.org/10.1152/ajpregu.1996.271.4.r1017.
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This project examined the effects of alterations in respiratory drive on the occurrence of sleep apnea in Northern elephant seal pups (Mirounga angustirostris). Sleep pattern was unaffected by levels of hypoxia (approximately 13%) or hypercapnia (approximately 6%) that doubled respiratory frequency during slow-wave sleep (SWS). During sleep in air, short periods of continuous breathing (mean length = approximately 2.6 min) alternated with periods of apnea (mean length = approximately 6.1 min). Under hypoxic or hypercapnic conditions, the frequency of occurrence of apneas was reduced primarily due to the occurrence of some sleep episodes without periods of apnea. In episodes in which apneas did occur, they began later in the sleep episodes, but their length and the length of the periods of eupnea were not significantly altered. During each period of eupnea, however, the instantaneous respiratory rate and the total number of breaths increased. Breathing during sleep was restricted to SWS, never occurring during rapid eye movement (REM) sleep, regardless of the respired gas mixture. If the levels of hypoxia and hypercapnia were raised further, all episodes of apnea during sleep could be eliminated together with all episodes of REM sleep. One interpretation of the data is that the threshold for altering breathing during eupnea (instantaneous breathing frequency and number of breaths per episode of eupnea) is lower than that for altering the lengths of the periods of apnea and eupnea and that the muscle atonia associated with REM sleep extends to all respiratory muscles.
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Insalaco, G., S. T. Kuna, G. Catania, O. Marrone, B. M. Costanza, V. Bellia, and G. Bonsignore. "Thyroarytenoid muscle activity in sleep apneas." Journal of Applied Physiology 74, no. 2 (February 1, 1993): 704–9. http://dx.doi.org/10.1152/jappl.1993.74.2.704.
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In normal subjects the thyroarytenoid muscle (TA), a vocal cord adductor, has phasic expiratory activity during wakefulness that disappears during non-rapid-eye-movement (NREM) sleep. Fiber-optic studies have reported absent or irregular vocal cord movements during obstructive apneas and vocal cord adduction during central apneas. This study was designed to investigate TA activity during NREM sleep in 14 subjects with sleep apnea by means of intramuscular wire electrodes. During central apneas, which were recorded in three subjects, continuous TA activity was observed. During obstructive apneas, which were recorded in all subjects, two different patterns of TA activity were observed: 1) absence of any activity until arousal and 2) phasic activity throughout the apnea. The first pattern was detected in six subjects, whereas both patterns were observed in the remaining eight subjects. No correlation was found between obstructive apnea characteristics and presence or absence of TA activity. In all subjects TA underwent a marked activation during arousal. While nasal continuous positive airway pressure was applied during NREM sleep TA activity was always absent. The persistence of TA activity during central apneas suggests that they may represent an extreme prolongation of neural expiratory discharge. We speculate that a variable interaction of different stimuli acting during obstructive apnea may activate TA, which, in turn, may contribute to glottic narrowing.
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Durgan, David J., Randy F. Crossland, and Robert M. Bryan. "The rat cerebral vasculature exhibits time-of-day-dependent oscillations in circadian clock genes and vascular function that are attenuated following obstructive sleep apnea." Journal of Cerebral Blood Flow & Metabolism 37, no. 8 (January 1, 2016): 2806–19. http://dx.doi.org/10.1177/0271678x16675879.
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Circadian clock components oscillate in cells of the cardiovascular system. Disruption of these oscillations has been observed in cardiovascular diseases. We hypothesized that obstructive sleep apnea, which is associated with cerebrovascular diseases, disrupts the cerebrovascular circadian clock and rhythms in vascular function. Apneas were produced in rats during sleep. Following two weeks of sham or obstructive sleep apnea, cerebral arteries were isolated over 24 h for mRNA and functional analysis. mRNA expression of clock genes exhibited 24-h rhythms in cerebral arteries of sham rats (p < 0.05). Interestingly, peak expression of clock genes was significantly lower following obstructive sleep apnea (p < 0.05). Obstructive sleep apnea did not alter clock genes in the heart, or rhythms in locomotor activity. Isolated posterior cerebral arteries from sham rats exhibited a diurnal rhythm in sensitivity to luminally applied ATP, being most responsive at the beginning of the active phase (p < 0.05). This rhythm was absent in arteries from obstructive sleep apnea rats (p < 0.05). Rhythms in ATP sensitivity in sham vessels were absent, and not different from obstructive sleep apnea, following treatment with L-NAME and indomethacin. We conclude that cerebral arteries possess a functional circadian clock and exhibit a diurnal rhythm in vasoreactivity to ATP. Obstructive sleep apnea attenuates these rhythms in cerebral arteries, potentially contributing to obstructive sleep apnea-associated cerebrovascular disease.
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Wetmore, Stephen J., Lawrence Scrima, and F. Charles Hiller. "Sleep Apnea in Epistaxis Patients Treated with Nasal Packs." Otolaryngology–Head and Neck Surgery 98, no. 6 (June 1988): 596–99. http://dx.doi.org/10.1177/019459988809800611.
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The presence of anterior and posterior nasal packs in patients with epistaxis is known to be associated with cardiorespiratory problems and sometimes death, although the mechanism has not been well understood. To determine the incidence and severity of obstructive sleep apnea in patients with epistaxis treated with both anterior and posterior nasal packs, we obtained polysomnograms on twelve patients while the packs were in place. Ten of these patients demonstrated obstructive sleep apnea. The apnea index (apneas/hour sleep) ranged from 1 to 83, with a mean of 29; the hypopnea index (hypopneas/hour sleep) ranged from 9 to 33, with a mean of 20; and the lowest oxygen saturation (SaO2) ranged from 17% to 91%, with a mean of 77%. Ten patients returned for another polysomnogram after removal of the packs. These baseline studies showed improvement in the apnea index and in the lowest SaO2 in all patients, although four patients still demonstrated at least mild obstructive sleep apnea. This study demonstrates that nasal packs used for the treatment of epistaxis may induce obstructive sleep apnea or markedly exacerbate underlying obstructive sleep apnea and, therefore, contribute to the sudden deaths that have been reported in epistaxis patients.
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Colvert, Jared, and Glen Greenough. "825 Central Sleep Apnea and Sinus Bradycardia." Sleep 44, Supplement_2 (May 1, 2021): A322. http://dx.doi.org/10.1093/sleep/zsab072.822.
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Abstract Introduction Central sleep apnea (CSA) is characterized by a lack of respiratory drive during sleep resulting in repetitive periods of apneas. There are multiple manifestations of CSA as defined by the ICSD3. CSA with Cheyne-Stokes Breathing (CSB) is characterized by a series of crescendo-decrescendo pattern of ventilation followed by central apnea and is often associated with heart failure. Bradyarrythmias have been associated with obstructive sleep apnea (OSA), but an association with central sleep apnea is less clear. Report of case(s) A 76 y/o male with no significant past medical history but with multiple instances of sinus bradycardia on previous EKGs, was referred to sleep medicine for evaluation of snoring, witnessed apneas, and daytime sleepiness. He had no history of CVA, CHF, atrial fibrillation, renal disease, or opioid use. PSG was completed for suspected OSA, and revealed moderate CSA (AHI 10.9 using hypopnea type 1B criteria, CAI 6.1). Central apneas at the latter portion of the study were consistent with a CSA-CSB. Awake heart rate at time of study was 44 bpm. During sleep, his heart rate ranged from 39–89 with a mean of 57 bpm. Due to this unexpected central apnea finding, cardiac evaluation was recommended and echocardiogram revealed a LVEF of 51%, a dilated left atrium, normal left ventricle chamber size, no wall motion abnormalities, and an inability to assess left sided filling pressures. EKG was consistent with sinus bradycardia without AV blocks. Holter monitor revealed sinus rhythm with moderate burden of ectopy. He underwent CPAP titration which revealed an effective CPAP pressure to control obstructive events, but central apneas persisted without CSB pattern. Conclusion In this patient, CSA/CSA-CSB was found in the absence of known risk factors for CSA. Although potentially an early sign of HFpEF related to his longstanding sinus bradycardia, this case raises the question as to whether sinus bradycardia in isolation could decrease cardiac output enough to destabilize ventilation and promote this finding of CSA/CSA-CSB. Support (if any):
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Punjabi, Naresh M., and Vsevolod Y. Polotsky. "Disorders of glucose metabolism in sleep apnea." Journal of Applied Physiology 99, no. 5 (November 2005): 1998–2007. http://dx.doi.org/10.1152/japplphysiol.00695.2005.
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Sleep is a complex behavioral state that occupies one-third of the human life span. Although viewed as a passive condition, sleep is a highly active and dynamic process. The sleep-related decrease in muscle tone is associated with an increase in resistance to airflow through the upper airway. Partial or complete collapse of the airway during sleep can lead to the occurrence of apneas and hypopneas during sleep that define the syndrome of sleep apnea. Sleep apnea has become pervasive in Western society, affecting ∼5% of adults in industrialized countries. Given the pandemic of obesity, the prevalence of Type 2 diabetes mellitus and metabolic syndrome has also increased dramatically over the last decade. Although the role of sleep apnea in cardiovascular disease is uncertain, there is a growing body of literature that implicates sleep apnea in the pathogenesis of altered glucose metabolism. Intermittent hypoxemia and sleep fragmentation in sleep apnea can trigger a cascade of pathophysiological events, including autonomic activation, alterations in neuroendocrine function, and release of potent proinflammatory mediators such as tumor necrosis factor-α and interleukin-6. Epidemiologic and experimental evidence linking sleep apnea and disorders of glucose metabolism is reviewed and discussed here. Although the cause-and-effect relationship remains to be determined, the available data suggest that sleep apnea is independently associated with altered glucose metabolism and may predispose to the eventual development of Type 2 diabetes mellitus.
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Botelho, Ricardo Vieira, Lia Rita Azeredo Bittencourt, José Marcus Rotta, and Sérgio Tufik. "The effects of posterior fossa decompressive surgery in adult patients with Chiari malformation and sleep apnea." Journal of Neurosurgery 112, no. 4 (April 2010): 800–807. http://dx.doi.org/10.3171/2009.7.jns09174.
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Object One of the feared consequences of craniovertebral junction diseases is apnea. Although several cases of patients with central apnea have been described, obstructive sleep apnea has been identified as the most frequent manifestation of sleep respiratory disorder. Neuronal involvement may be responsible for both central and obstructive apneas. The objective of this work was to study the effect of posterior fossa decompressive surgery on respiratory parameters during sleep in patients with craniovertebral junction malformations and breathing-related sleep disorders. Methods In this study, prospectively enrolled consecutive symptomatic adult patients were monitored with full-night polysomnography before and after surgical decompression of the cranial posterior fossa. Results Of the 25 patients who were evaluated, 68% received a diagnosis of sleep apnea. After surgery, the mean number of respiratory events decreased from 180.70 to 69.29 (p = 0.005); the mean number of obstructive events decreased from 107.37 to 60.58 (p = 0.01); and the mean number of central events decreased from 38.45 to 8.05 (p = 0.01). The mean preoperative apnea/hypopnea index decreased from 26.68 to 12.98 (p = 0.06), and the mean central apnea index decreased from 13.81 to 1.68 (p = 0.01). Conclusions Decompressive surgery in patients with craniovertebral junction malformations resulted in decreased respiratory events during sleep, lowered sleep fragmentation, and enhanced the sleep apnea index in a significant number of patients. The effect was more pronounced in patients with central apnea.
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Bernards, Christopher M., Susan L. Knowlton, Douglas F. Schmidt, William J. DePaso, Matthias K. Lee, Susan B. McDonald, and Oneil S. Bains. "Respiratory and Sleep Effects of Remifentanil in Volunteers with Moderate Obstructive Sleep Apnea." Anesthesiology 110, no. 1 (January 1, 2009): 41–49. http://dx.doi.org/10.1097/aln.0b013e318190b501.
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Background There is concern that opioid-based analgesia will worsen sleep-related respiratory insufficiency in patients with obstructive sleep apnea (OSA), resulting in serious morbidity or mortality. However, there are no studies that directly address the merit of this concern. Consequently, the authors designed this study as the first prospective, double-blind, placebo-controlled investigation of opioid pharmacology in patients with documented OSA. Methods Patients (n = 19) with moderate OSA documented by polysomnography (sleep study) were randomized to undergo an additional sleep study while receiving either a saline infusion or a remifentanil infusion (0.075 microg x kg x h). Sleep stages, apneas, hypopneas, and arterial hemoglobin oxygen saturation were continually recorded during saline or remifentanil infusion, and were compared with values obtained during the patients' earlier sleep study. Results Saline infusion had no effect on sleep or respiratory variables. In contrast, remifentanil increased Stage 1 sleep, markedly decreased rapid eye movement sleep, increased arousals from sleep, and decreased sleep efficiency. Remifentanil actually decreased the number of obstructive apneas, but markedly increased the number of central apneas. Arterial hemoglobin oxygen saturation was also significantly lower in OSA patients receiving remifentanil. Conclusions The decrease in obstructive apneas likely resulted from the marked decrease in rapid eye movement sleep caused by remifentanil. Despite fewer obstructions, OSA was worse during remifentanil infusion because of a marked increase in the number of central apneas. These data suggest that caution is warranted when administering opioids to subjects with moderate OSA, but that the primary risk may be central apnea, not obstructive apnea.
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Brown, Devin L., Valerie Durkalski, Jeffrey S. Durmer, Joseph P. Broderick, Darin B. Zahuranec, Deborah A. Levine, Craig S. Anderson, et al. "Sleep for Stroke Management and Recovery Trial (Sleep SMART): Rationale and methods." International Journal of Stroke 15, no. 8 (February 4, 2020): 923–29. http://dx.doi.org/10.1177/1747493020903979.
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Rationale Obstructive sleep apnea is common among patients with acute ischemic stroke and is associated with reduced functional recovery and an increased risk for recurrent vascular events. Aims and/or hypothesis The Sleep for Stroke Management and Recovery Trial (Sleep SMART) aims to determine whether automatically adjusting continuous positive airway pressure (aCPAP) treatment for obstructive sleep apnea improves clinical outcomes after acute ischemic stroke or high-risk transient ischemic attack. Sample size estimate A total of 3062 randomized subjects for the prevention of recurrent serious vascular events, and among these, 1362 stroke survivors for the recovery outcome. Methods and design Sleep SMART is a phase III, multicenter, prospective randomized, open, blinded outcome event assessed controlled trial. Adults with recent acute ischemic stroke/transient ischemic attack and no contraindication to aCPAP are screened for obstructive sleep apnea with a portable sleep apnea test. Subjects with confirmed obstructive sleep apnea but without predominant central sleep apnea proceed to a run-in night of aCPAP. Subjects with use (≥4 h) of aCPAP and without development of significant central apneas are randomized to aCPAP plus usual care or care-as-usual for six months. Telemedicine is used to monitor and facilitate aCPAP adherence remotely. Study outcomes Two separate primary outcomes: (1) the composite of recurrent acute ischemic stroke, acute coronary syndrome, and all-cause mortality (prevention) and (2) the modified Rankin scale scores (recovery) at six- and three-month post-randomization, respectively. Discussion Sleep SMART represents the first large trial to test whether aCPAP for obstructive sleep apnea after stroke/transient ischemic attack reduces recurrent vascular events or death, and improves functional recovery.
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Finlay, M., M. Wilson, J. A. Erwin, D. A. Hansen, M. E. Layton, R. M. Quock, and H. Van Dongen. "0730 Individuals Receiving Methadone For Medication-Assisted Treatment Of Opioid Use Disorder Show Evidence Of Respiratory Depression." Sleep 43, Supplement_1 (April 2020): A278. http://dx.doi.org/10.1093/sleep/zsaa056.726.
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Abstract Introduction A well-established consequence of opiate use is respiratory depression during sleep, with a high prevalence of central sleep apneas. Medication-assisted treatment (MAT) is a widely used therapy for opioid use disorder (OUD) designed to reduce withdrawal symptoms and drug cravings. We investigated the presence of respiratory depression during sleep in patients receiving methadone-based opioid replacement treatment as part of a MAT program for OUD. Methods N=6 individuals (5 females, ages 43.8±12.8y, BMI 27.2±4.1kg/m2), who were within 90 days of methadone initiation, underwent in-laboratory overnight polysomnography (8h TIB, 22:00-06:00). Apneaic and hypopneic events were determined using AASM criteria. Results The average Apnea-Hypopnea Index (AHI) was 16.5±9.0 events/h, with 2 individuals exceeding the threshold of moderate sleep apnea (>15 events/h). 89.5% of the observed apnea-hypopnea events occurred during NREM sleep. Of all events, 57.1±16.3% were central apneas; and of all obstructive, central, and mixed apnea events, 93.0±14.3% were central apneas. Conclusion Individuals with OUD receiving methadone-based MAT may be at risk of respiratory depression during sleep, as evidenced by the frequent occurrence of central sleep apneas. Such risk could be a contributing factor in opioid overdose deaths. Currently, performing respiratory assessments during sleep is not considered standard of care in MAT programs. Our preliminary data suggest that monitoring and treatment of respiratory depression during sleep may be indicated in OUD patients on methadone-based MAT. Support Supported in part by a seed grant from the Washington State University Office of Research Advancement and Partnerships.
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Omran, Amal M., Salah E. Aboubakr, Loutfi S. Aboussouan, Lisa Pierchala, and M. Safwan Badr. "Posthypoxic ventilatory decline during NREM sleep: influence of sleep apnea." Journal of Applied Physiology 96, no. 6 (June 2004): 2220–25. http://dx.doi.org/10.1152/japplphysiol.01120.2003.
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We wished to determine the severity of posthypoxic ventilatory decline in patients with sleep apnea relative to normal subjects during sleep. We studied 11 men with sleep apnea/hypopnea syndrome and 11 normal men during non-rapid eye movement sleep. We measured EEG, electrooculogram, arterial O2 saturation, and end-tidal Pco2. To maintain upper airway patency in patients with sleep apnea, nasal continuous positive pressure was applied at a level sufficient to eliminate apneas and hypopneas. We compared the prehypoxic control (C) with posthypoxic recovery breaths. Nadir minute ventilation in normal subjects was 6.3 ± 0.5 l/min (83.8 ± 5.7% of room air control) vs. 6.7 ± 0.9 l/min, 69.1 ± 8.5% of room air control in obstructive sleep apnea (OSA) patients; nadir minute ventilation (% of control) was lower in patients with OSA relative to normal subjects ( P < 0.05). Nadir tidal volume was 0.55 ± 0.05 liter (80.0 ± 6.6% of room air control) in OSA patients vs. 0.42 ± 0.03 liter, 86.5 ± 5.2% of room air control in normal subjects. In addition, prolongation of expiratory time (Te) occurred in the recovery period. There was a significant difference in Te prolongation between normal subjects (2.61 ± 0.3 s, 120 ± 11.2% of C) and OSA patients (5.6 ± 1.5 s, 292 ± 127.6% of C) ( P < 0.006). In conclusion, 1) posthypoxic ventilatory decline occurred after termination of hypocapnic hypoxia in normal subjects and patients with sleep apnea and manifested as decreased tidal volume and prolongation of Te; and 2) posthypoxic ventilatory prolongation of Te was more pronounced in patients with sleep apnea relative to normal subjects.
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Jain, Vivek, Joseph Marbach, Shawn Kimbro, David C. Andrade, Arad Jain, Eleanor Capozzi, Kyle Mele, Rodrigo Del Rio, Matthew W. Kay, and David Mendelowitz. "Benefits of oxytocin administration in obstructive sleep apnea." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 5 (November 1, 2017): L825—L833. http://dx.doi.org/10.1152/ajplung.00206.2017.
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Activation of oxytocin receptors has shown benefits in animal models of obstructive sleep apnea (OSA). We tested if nocturnal oxytocin administration could have beneficial effects in OSA patients. Eight patients diagnosed with OSA were administered intranasal oxytocin (40 IU). Changes in cardiorespiratory events during sleep, including apnea and hypopnea durations and frequency, risk of event-associated arousals, and heart rate variability, were assessed. Oxytocin significantly increased indexes of parasympathetic activity, including heart rate variability, total sleep time, and the postpolysommogram sleep assessment score, an index of self-reported sleep satisfaction. Although the apnea-hypopnea index was not significantly changed with oxytocin administration, when apnea and hypopnea events were compared independently, the frequency of hypopneas, but not apneas, was significantly ( P ≤ 0.005) decreased with oxytocin treatment. Both apneas and hypopneas were significantly shortened in duration with oxytocin treatment. Oxytocin treatment significantly decreased the percent of apnea and hypopnea events that were accompanied with an arousal. Oxytocin administration has the potential to restore cardiorespiratory homeostasis and reduce some clinically important (objective and patient-reported) adverse events that occur with OSA. Additional studies are needed to further understand the mechanisms by which oxytocin promotes these changes in cardiorespiratory and autonomic function in OSA patients.
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Kishimoto, Masaru, Hiroshi Mori, Hiroshi Iritani, Hiroshi Ogasawara, and Takeo Kumoi. "Two Children with Sleep Apnea." Practica oto-rhino-laryngologica. Suppl. 1986, Supplement4 (1986): 143–49. http://dx.doi.org/10.5631/jibirinsuppl1986.1986.supplement4_143.
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Schneider, H., C. D. Schaub, C. A. Chen, K. A. Andreoni, A. R. Schwartz, P. L. Smith, J. L. Robotham, and C. P. O'Donnell. "Effects of arousal and sleep state on systemic and pulmonary hemodynamics in obstructive apnea." Journal of Applied Physiology 88, no. 3 (March 1, 2000): 1084–92. http://dx.doi.org/10.1152/jappl.2000.88.3.1084.
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During obstructive sleep apnea (OSA), systemic (Psa) and pulmonary (Ppa) arterial pressures acutely increase after apnea termination, whereas left and right ventricular stroke volumes (SV) reach a nadir. In a canine model ( n = 6), we examined the effects of arousal, parasympathetic blockade (atropine 1 mg/kg iv), and sleep state on cardiovascular responses to OSA. In the absence of arousal, SV remained constant after apnea termination, compared with a 4.4 ± 1.7% decrease after apnea with arousal ( P < 0.025). The rise in transmural Ppa was independent of arousal (4.5 ± 1.0 vs. 4.1 ± 1.2 mmHg with and without arousal, respectively), whereas Psa increased more after apnea termination in apneas with arousal compared with apneas without arousal. Parasympathetic blockade abolished the arousal-induced increase in Psa, indicating that arousal is associated with a vagal withdrawal of the parasympathetic tone to the heart. Rapid-eye-movement (REM) sleep blunted the increase in Psa (pre- to end-apnea: 5.6 ± 2.3 mmHg vs. 10.3 ± 1.6 mmHg, REM vs. non-REM, respectively, P< 0.025), but not transmural Ppa, during an obstructive apnea. We conclude that arousal and sleep state both have differential effects on the systemic and pulmonary circulation in OSA, indicating that, in patients with underlying cardiovascular disease, the hemodynamic consequences of OSA may be different for the right or the left side of the circulation.
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Anilkumar, T. V., Sajeesh Parameswaran, Anupama Kurup, M. Aswin Ganesh, V. S. Abhishek, and A. Marthanda Pillai. "Idiopathic central sleep apnea with periodicity presenting as Cheyne-Stokes breathing – Case report." Romanian Journal of Neurology 21, no. 2 (June 30, 2022): 183–85. http://dx.doi.org/10.37897/rjn.2022.2.15.
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Cheyne-Stokes breathing (CSB) is described by a cyclic variation in breathing with periods of central apneas or hypopneas alternating with periods of hypopneas in a gradual waxing and waning manner. It is usually seen in patients with congestive cardiac failure or neurologic disorders. We describe this rare case of idiopathic central sleep apnea coming in a periodic fashion presenting as CSB pattern without specific causes. Overnight polysomnography test showed central sleep apnea; but cardiac evaluation and magnetic resonance imaging of the brain could not find any cause of this sleep-disordered breathing. Idiopathic central sleep apnea usually presents with poor quality of sleep, but many of them easily misdiagnosed and do not get any proper treatment.
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Rani, Seema, Alexandra Cohen, Abigail Strang, and Aaron Chidekel. "1220 Polysomnography in Children with Joubert Syndrome." SLEEP 47, Supplement_1 (April 20, 2024): A520. http://dx.doi.org/10.1093/sleep/zsae067.01220.
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Abstract Introduction Joubert syndrome is autosomal recessive, clinically and genetically heterogeneous with multiorgan involvement. Classic breathing symptoms include episodes of hyperpnea followed by apnea and periodic breathing. Gas exchange abnormalities include hyperventilation with low CO2s and intermittent desaturations. Purpose of this abstract is to report prolonged survival, describe the PSG findings and treatment modalities in 2 cases. Report of case(s) 8-year-old female with Joubert syndrome, global developmental delay, hydrocephalus, hypotonia, cortical blindness presented for initial evaluation of sleep apnea. PSG revealed primarily central sleep apnea with upper airway resistance with snoring with arousal and few episodes of obstructive and mixed apnea and hypopnea. Gas exchange demonstrated episodic, brief desaturations, associated with central apneas. Repeat PSG at 13 years showed intermittent hyperpnea followed by apnea, low ETCO2s with self-limiting desaturations and periodic breathing. Gas exchange revealed low ETCO2 and desaturations. She was treated with clinical observation. PSG at age 20 year demonstrated intermittent hyperpnea followed by episodes of prolonged central apneas, with low ETCO2s and desaturations, and few obstructive hypopneas. Most central apneas associated with self-limiting desaturations, with significant number associated with oxygen saturation below 90%. Gas exchange demonstrated low ETCO2s and episodic desaturations. Supplemental oxygen was prescribed. 20-month-old female with diagnosed Joubert syndrome, cleft lip, polydactyly, hypotonia, dysphagia, and developmental delay presented for loud snoring and gasping during sleep and apneas while awake. Sibling with Joubert Syndrome and a tracheostomy had died. Presented for a second opinion for tracheostomy due to PSG at OSH demonstrating OSAHS with AHI of 18.2, OAI of 3.9 and CAI of 14.3, minimal hypoxemia, normal ETCO2 and SaO2 nadir was 75%. Repeat sleep study done at our center; AHI of 27.7 and OAI of 0.83. ETCO2 was normal, SpO2 nadir was 75% and minimal hypoxemia. Overall PSG demonstrated primarily central apneas with a few obstructive apneas and hypopneas and minimal O2 desaturations. Subsequently underwent BLPAP titration study and treated with non-invasive modality. Conclusion PSG in Joubert syndrome demonstrated intermittent hyperpnea and prolonged central apneas with low ETCO2's and brief desaturations. All events were predominantly present in REM sleep. Patients did well with low respiratory support and did not require tracheostomy. Support (if any)
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Akbarian, Sina, Nasim Montazeri Ghahjaverestan, Azadeh Yadollahi, and Babak Taati. "Distinguishing Obstructive Versus Central Apneas in Infrared Video of Sleep Using Deep Learning: Validation Study." Journal of Medical Internet Research 22, no. 5 (May 22, 2020): e17252. http://dx.doi.org/10.2196/17252.
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Background Sleep apnea is a respiratory disorder characterized by an intermittent reduction (hypopnea) or cessation (apnea) of breathing during sleep. Depending on the presence of a breathing effort, sleep apnea is divided into obstructive sleep apnea (OSA) and central sleep apnea (CSA) based on the different pathologies involved. If the majority of apneas in a person are obstructive, they will be diagnosed as OSA or otherwise as CSA. In addition, as it is challenging and highly controversial to divide hypopneas into central or obstructive, the decision about sleep apnea type (OSA vs CSA) is made based on apneas only. Choosing the appropriate treatment relies on distinguishing between obstructive apnea (OA) and central apnea (CA). Objective The objective of this study was to develop a noncontact method to distinguish between OAs and CAs. Methods Five different computer vision-based algorithms were used to process infrared (IR) video data to track and analyze body movements to differentiate different types of apnea (OA vs CA). In the first two methods, supervised classifiers were trained to process optical flow information. In the remaining three methods, a convolutional neural network (CNN) was designed to extract distinctive features from optical flow and to distinguish OA from CA. Results Overnight sleeping data of 42 participants (mean age 53, SD 15 years; mean BMI 30, SD 7 kg/m2; 27 men and 15 women; mean number of OA 16, SD 30; mean number of CA 3, SD 7; mean apnea-hypopnea index 27, SD 31 events/hour; mean sleep duration 5 hours, SD 1 hour) were collected for this study. The test and train data were recorded in two separate laboratory rooms. The best-performing model (3D-CNN) obtained 95% accuracy and an F1 score of 89% in differentiating OA vs CA. Conclusions In this study, the first vision-based method was developed that differentiates apnea types (OA vs CA). The developed algorithm tracks and analyses chest and abdominal movements captured via an IR video camera. Unlike previously developed approaches, this method does not require any attachment to a user that could potentially alter the sleeping condition.
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Dominici, Michele, Fernando Pompeu Filho, and Marleide da Mota Gomes. "Probable causal link between epilepsy and sleep apnea: case report." Arquivos de Neuro-Psiquiatria 65, no. 1 (March 2007): 164–66. http://dx.doi.org/10.1590/s0004-282x2007000100034.
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Patients with epilepsy were reported to have concomitant sleep apnea, but it has been rarely linked to the epilepsy itself. We present a case of a 28-year-old, obese man with secondary medically resistant partial complex epilepsy due to a brain trauma, with progressive snoring, and sleep agitation, apneas, and important daytime somnolence. It was noticed in the polysomnographic study that he had several sleep respiratory events, probably due both to the epileptic seizures and the sleep apnea syndrome as a co-morbidity. Apnea and epilepsy will be discussed. A careful video-EEG-polysomnography study is important in evaluating refractory epileptic patients and/or epileptic patients with snoring.
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Uzma, Nazia, and VD Reddy. "Sleep Apnea." Journal of Gandaki Medical College-Nepal 9, no. 2 (July 31, 2017): 29–37. http://dx.doi.org/10.3126/jgmcn.v9i2.17863.
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Background: Sleep apnea is a condition that interrupts breathing while sleeping, usually caused by an obstruction blocking the back of the throat so that the air cannot reach the lungs. The brief cessation in breath automatically forces individuals to wake up and restart breathing. This can happen many times during the night, making it hard for the body to get enough oxygen, and impacts the sleep quality. It is the most common type of sleep disorder breathing.Objectives: The present study was designed to investigate the effects of obstructive sleep apnea (OSA) on different mental, physical and nervous disorders which are manifested in such patients. This study would not only benefit in ascertaining the causes of OSA through assessment of higher mental functions of autonomic and peripheral nervous systems but also in the development of algorithm for estimation of degree of damage to the nervous system with severity of OSA.Methods: A total of 1365 consecutive participants participated in this study at the Department of Pulmonary Medicine, Deccan College of Medical Sciences, Hyderabad, Telangana State, India for suspected sleep disordered breathing (SDB) between October 2012 and February 2016. In this cohort, 1140 participants were deemed ineligible, as per the inclusion criteria. Therefore, 225 patients were considered in the study along with 75 control subjects, who were healthy individuals. The cohort was diagnosed by an experienced pulmonologist for the symptoms of snoring and daytime somnolence. The data included documentation of age, gender, weight, height, BMI, waist and neck circumference, and clinical data such as history of apnea, insomnia, dyslipidemia, hypertension, and coronary heart disease. All participants underwent overnight polysomnography (PSG) in sleep laboratory. The cognitive function tests consisted of mini-mental state examination and by employing the depression questionnaire (Using Zung self report depression scale). The autonomic function tests were performed. Variabilities in heart rate were determined. Brain natriuretic peptide (BNP) levels in the blood were measured.Results: The study group had an AHI ≥5 per hour of sleep while the control group had AHI <5 per hour of sleep. Overall, patients in the OSA cohort were older compared to those in the Control cohort. The overnight polysomnography values indicated distinct differences among the parameters of the analysis depending upon the category of the patient (i.e., mild, moderate and severe). Oxygen saturation in blood during both REM and NREM sleep stages clearly indicated lower oxygen in patient cohort than the control group. The cognitive function tests revealed that in comparison to the control group, OSA patients had significantly impaired cognition. OSA patients had significantly higher (p ≤0.05) depression. Motor action, muscle action potential and nerve action potential was significantly lower (p ≤0.05) than that of the control group of healthy patients. The plasma BNP in OSA patients was significantly higher (p ≤0.05) than control subjects. RR intervals in the patient group were significantly shorter than in the control group. The blood pressure of the OSA patients in general was relatively higher than the control group, both during the postural response and in handgrip test.Conclusions: Among the enrolled individuals, those with severe OSA were affected in all faculties, namely, cognitive abilities and health attributes; and had high BNP levels in their blood. In aggregate, OSA patients can be alleviated from the syndrome, if accurate diagnosis is made on time. This study developed an algorithm which would aid the clinicians in early detection of OSA symptoms and mitigate the prognosis of the syndrome. Journal of Gandaki Medical CollegeVolume, 09, Number 2, July December 2016, 29-37
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HARMON, J. DOUGLAS, WARREN MORGAN, and BASHIR CHAUDHARY. "Sleep Apnea." Southern Medical Journal 82, no. 2 (February 1989): 161–64. http://dx.doi.org/10.1097/00007611-198902000-00004.
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QUILLEN, TERRILYNN M. "Sleep Apnea." Nursing 17, no. 12 (December 1987): 5. http://dx.doi.org/10.1097/00152193-198712000-00002.
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Nordstrom, Darick. "SLEEP APNEA." Journal of the American Dental Association 126, no. 7 (July 1995): 828. http://dx.doi.org/10.14219/jada.archive.1995.0294.
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Keys, Karen. "Sleep Apnea." Neurology Now 10, no. 3 (2014): 7. http://dx.doi.org/10.1097/01.nnn.0000451310.93217.72.
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YANTIS, MARY ANN. "Sleep Apnea." American Journal of Nursing 99, no. 9 (September 1999): 24AA—24BB. http://dx.doi.org/10.1097/00000446-199909000-00024.
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Masood, Ahmed, and Barbara Phillips. "Sleep apnea." Current Opinion in Pulmonary Medicine 6, no. 6 (November 2000): 479–84. http://dx.doi.org/10.1097/00063198-200011000-00003.
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Alchanatis, Manos, James MacFarlane, and Sofia Schiza. "Sleep Apnea." Sleep Disorders 2012 (2012): 1. http://dx.doi.org/10.1155/2012/308978.
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Kuipers, Albertus F., and L. Wilbert Bartels. "Sleep Apnea." New England Journal of Medicine 367, no. 22 (November 29, 2012): e33. http://dx.doi.org/10.1056/nejmicm1212352.
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PHILLIPS, BARBARA, YVETTE COOK, FREDERICK SCHMITT, and DAVID BERRY. "Sleep Apnea." Southern Medical Journal 82, no. 9 (September 1989): 1090–92. http://dx.doi.org/10.1097/00007611-198909000-00007.
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Loube, Daniel. "Sleep Apnea." Chest 119, no. 1 (January 2001): 4–5. http://dx.doi.org/10.1378/chest.119.1.4.
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Lomangino, Kevin. "Sleep Apnea." Clinical Nutrition INSIGHT 34, no. 11 (November 2008): 8–9. http://dx.doi.org/10.1097/01.nmd.0000339445.12111.fc.
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Cutler, Andrew J. "Sleep apnea." Medical Update for Psychiatrists 1, no. 4 (July 1996): 127–30. http://dx.doi.org/10.1016/s1082-7579(96)80021-5.
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Suurna, Maria V., and Ofer Jacobowitz. "Sleep Apnea." Otolaryngologic Clinics of North America 53, no. 3 (June 2020): i. http://dx.doi.org/10.1016/s0030-6665(20)30059-1.
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Javaheri, Shahrokh, Ferran Barbe, Francisco Campos-Rodriguez, Jerome A. Dempsey, Rami Khayat, Sogol Javaheri, Atul Malhotra, et al. "Sleep Apnea." Journal of the American College of Cardiology 69, no. 7 (February 2017): 841–58. http://dx.doi.org/10.1016/j.jacc.2016.11.069.
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