Effects of high-frequency pressure waves applied to upper airway on respiration in central apnea

1992 ◽  
Vol 73 (3) ◽  
pp. 1141-1145 ◽  
Author(s):  
K. G. Henke ◽  
C. E. Sullivan
Keyword(s):  
Sleep Apnea ◽  
High Frequency ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
High Frequency Oscillation ◽  
Central Apnea ◽  
Pressure Oscillations ◽  
Central Apneas ◽  
Airway Defense ◽  
High Frequency Oscillatory

We examined the effects of high-frequency (30-Hz) low-pressure oscillations on respiration in nine patients with central sleep apnea. All patients were studied during sleep and wore a nasal mask through which the oscillations were applied. All tests were performed during periods of repetitive central apneas. Respiratory efforts were monitored from the airflow and calibrated Respitrace signals. After several cycles of apnea were monitored, the oscillatory pressures were applied for brief periods (less than 5 s) at the midpoint of the central apneas. All trials in which arousal occurred were discarded, leaving a total of 106 trials in the nine patients. High-frequency oscillation of the upper airway stimulated respiratory effort(s) in 68% of all trials (72 of 106). Apnea length was significantly shortened in four of the nine patients. In one patient with a tracheostomy, the stimulus applied to his isolated upper airway evoked respiratory efforts during central apnea in 13 of 15 trials. We conclude that high-frequency oscillatory pressures applied to the upper airway can stimulate respiratory efforts during central apnea. This response may be mediated by upper airway receptors involved in nonrespiratory airway defense reflexes and may have implications in the treatment of patients with central sleep apnea.

825 Central Sleep Apnea and Sinus Bradycardia

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A322-A322
Author(s):  
Jared Colvert ◽  
Glen Greenough
Keyword(s):  
Heart Rate ◽  
Sleep Apnea ◽  
Sinus Bradycardia ◽  
Central Sleep Apnea ◽  
Respiratory Drive ◽  
Central Apnea ◽  
Opioid Use ◽  
Significant Past Medical History ◽  
Obstructive Sleep ◽  
Central Apneas

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):

Pharyngeal narrowing/occlusion during central sleep apnea

1995 ◽  
Vol 78 (5) ◽  
pp. 1806-1815 ◽  
Author(s):  
M. S. Badr ◽  
F. Toiber ◽  
J. B. Skatrud ◽  
J. Dempsey
Keyword(s):  
Sleep Apnea ◽  
Sleep Apnea Syndrome ◽  
Central Sleep Apnea ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Intraluminal Pressure ◽  
Central Apnea ◽  
Rapid Eye Movement Sleep ◽  
Cross Sectional ◽  
Central Apneas

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.

scholarly journals Obesity accentuates circadian variability in breathing during sleep in mice but does not predispose to apnea

2013 ◽  
Vol 115 (4) ◽  
pp. 474-482 ◽  
Author(s):  
Eric M. Davis ◽  
Landon W. Locke ◽  
Angela L. McDowell ◽  
Patrick J. Strollo ◽  
Christopher P. O'Donnell
Keyword(s):  
Sleep Apnea ◽  
Rem Sleep ◽  
Central Sleep Apnea ◽  
Diaphragm Muscle ◽  
Emg Activity ◽  
Central Apnea ◽  
Obese Mice ◽  
Obstructive Sleep ◽  
Central Apneas ◽  
The Impact

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.

Effects of high-frequency oscillating pressures on upper airway muscles in humans

1993 ◽  
Vol 75 (2) ◽  
pp. 856-862 ◽  
Author(s):  
K. G. Henke ◽  
C. E. Sullivan
Keyword(s):  
Sleep Apnea ◽  
Eye Movement ◽  
Rem Sleep ◽  
High Frequency ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Low Pressure ◽  
Rapid Eye Movement ◽  
Pressure Oscillations

We examined the effects of high-frequency- (30-Hz) low-pressure oscillations (< 1 cmH2O) applied to the upper airway, via a nose mask, on genioglossus (EMGgg), sternomastoid (EMGsm), and diaphragm electromyogram (EMGdia) activity in sleeping humans. Ten patients with sleep apnea and six normal subjects were studied. The pressure oscillations were applied through the mask for a single breath. The subjects were studied in non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. In the normal subjects, during NREM sleep, peak EMGgg, EMGsm, and EMGdia activity increased significantly in response to the oscillations in 63, 51, and 46%, respectively, of all trials. During REM sleep, significant increases occurred in 73, 88, and 13%, respectively, of all trials. Similar responses were observed in the patients with obstructive sleep apnea. Peak EMGgg, EMGsm, and EMGdia activity increased significantly in 74, 50, and 67%, respectively, of all NREM sleep trials and in 55, 81, and 76%, respectively, of all REM sleep trials. An important finding was that in 46% of the trials in the patients with sleep apnea the oscillation-induced increase in EMGgg activity was associated with a partial or complete reversal of the upper airway obstruction with an increase in tidal volume. This was observed in NREM and REM sleep. We conclude that there are upper airway receptors that respond to low-pressure-high-frequency oscillations applied to the upper airway that have input to the genioglossus and other muscles of respiration. These responses may be utilized in future treatment for sleep apnea.

Sleep and Violence*

1984 ◽  
Vol 29 (2) ◽  
pp. 132-134 ◽  
Author(s):  
L.B. Raschka
Keyword(s):  
Differential Diagnosis ◽  
Sleep Apnea ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Violent Behaviour ◽  
Car Accidents ◽  
Prevention And Treatment ◽  
Respiratory Pathology ◽  
The Brain

Most violence connected with sleep disorder is assumed to be related to sleep walking. It is less well known that other sleep disorders can also give rise to violence. The role of narcolepsy in car accidents is mentioned. Sleep drunkenness can lead to confusion resulting in violent behaviour especially on forced awakening. This condition is associated to sleep apnea. Primary or central sleep apnea is caused by disorders of the brain stem affecting the respiratory center. Secondary or upper airway sleep apnea can be caused by virtually any condition that results in cessation of the airflow due to occlusion of the upper airway. The author describes one patient who engaged in assaultive behaviour on forced awakening following earlier alcohol consumption. The pathomechanism of violent behaviour generated by a combination of sleep apnea and respiratory pathology is described. The differential diagnosis, prevention and treatment is outlined. The use of polysomnography in diagnosis and the potentially dangerous effects of drugs with respiratory depressing effects is highlighted.

scholarly journals 1266 Primary Central apnea and loss of muscle atonia during REM

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A481-A482
Author(s):  
M Elizabeth C Hernandez ◽  
Kanta Velamuri
Keyword(s):  
Sleep Apnea ◽  
Rem Sleep ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Central Apnea ◽  
Muscle Atonia ◽  
Arterial Blood ◽  
Respiratory Events ◽  
History Of ◽  
Central Apneas

Abstract Introduction Central sleep apnea (CSA) syndrome is defined when five or more central apneas and/or hypopneas are present per hour of sleep, more than 50% of all respiratory events. CSA usually occur during NREM stage and rarely during REM. CSA is important to recognize because of complications ranging from frequent nighttime awakenings,sleepiness to adverse cardiovascular outcomes. We present a 40 year old female patient with rare CSA during REM sleep and dream enactment. Report of Case 40yo African American female with history of loud snoring, witnessed sleep apnea, and daytime fatigue. She reported nightmares, sleep talking, and acting out her dreams without injury. Epworth sleepiness score was 5 /24. Her past medical history is significant for depression and anxiety. She has no history of head trauma, no neurologic or cardiovascular disorders. Her medications include fluoxetine and,quetiapine. She denied substance use, narcotic use, or alcohol use. Her level 1 sleep study showed predominantly REM-associated central sleep apneas which is rare. She also was observed to have loss of REM sleep muscle atonia suggestive of REM Behavior disorder. Her sleep architecture was atypical with decreased N3 sleep stage. REM sleep duration was adequate. She was noted to have loss of REM muscle atonia based on AASM guidelins elevated chin EMG, excessive transient muscle activity, and witnessed movement during REM stage via video monitoring. During the study, she had an apnea/hypopnea index (AHI) of 13.1 per hour of sleep, Central apneas were predominantly noted during REM stage, 10 per hour, comprised of 50% of her respiratory events. The minimum SpO2 value with CSA was 94%. She had normal sinus rhythm. Her sleep was fragmented. A total arousals were 28.4/hour,and 7.9/hour were respiratory arousals, and the rest were spontaneous arousals. An echocardiogram showed normal left ventricular ejection fraction of 55 to 60 %. Her room air arterial blood gas was normal with PaC02 of 37 mmHg. MRI of the brain/brainstem was ordered given her atypical REM sleep. She had no acute intracranial abnormalities. There is a non specific finding of a low lying cerebellar tonsils without evidence of Chiari I malformation. Conclusion Our patient has rare idiopathic central apnea in REM stage and is third case reported. She also has loss of muscle atonia during REM with dream enactment which is also rare in her age group. Injury precaution advised.

scholarly journals 1244 A Curious Case of ASV Failure

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A474-A474
Author(s):  
Nishant Chaudhary ◽  
Mirna Ayache ◽  
John Carter
Keyword(s):  
Sleep Apnea ◽  
Airway Obstruction ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Upper Airway Obstruction ◽  
Neck Extension ◽  
Sleep Study ◽  
Obstructive Sleep

Abstract Introduction Positive airway pressure-induced upper airway obstruction has been reported with the treatment of obstructive sleep apnea (OSA) using continuous positive airway pressure (CPAP) along with an oronasal interface. Here we describe a case of persistent treatment emergent central sleep apnea (TECSA) inadequately treated with adaptive servo ventilation (ASV), with an airflow pattern suggestive of ASV-induced upper airway obstruction. Report of Case A 32-year-old male, with severe OSA (apnea hypopnea index: 52.4) and no other significant past medical history, was treated with CPAP and required higher pressures during titration sleep studies to alleviate obstructive events, despite a Mallampati Class II airway and a normal body mass index. Drug-Induced Sleep Endoscopy (DISE) showed a complete velopharynx and oropharynx anterior posterior (AP) collapse, long soft palate, which improved with neck extension. CPAP therapy, however, did not result in any symptomatic benefit and compliance reports revealed high residual AHI and persistent TECSA. He underwent an ASV titration sleep study up to a final setting of expiratory positive airway pressure 9 cm H2O, pressure support 6-15 cm H2O (auto-rate), with a full-face mask due to high oral leak associated with the nasal interface. The ASV device detected central apneas and provided mandatory breaths, but did not capture the thorax or abdomen, despite normal mask pressure tracings. Several such apneas occurred, with significant oxyhemoglobin desaturation. Conclusion We postulate that the ASV failure to correct central sleep apnea as evidenced by the absence of thoracoabdominal inspiratory effort, occurred due to ASV-induced upper airway obstruction. Further treatment options for this ASV phenomenon are to pursue an ASV-assisted DISE and determine the effectiveness of adjunctive therapy including neck extension, nasal mask with a mouth closing device and a mandibular assist device.

Treatment of opioid-related central sleep apnea with positive airway pressure: A systematic review

2014 ◽  
Vol 10 (1) ◽  
pp. 57 ◽  
Author(s):  
Roopika Reddy, MD ◽  
David Adamo, RPSGT ◽  
Thomas Kufel, MD ◽  
Jahan Porhomayon, MD ◽  
Ali A. El-Solh, MD, MPH
Keyword(s):  
Sleep Apnea ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Central Sleep Apnea ◽  
Poor Response ◽  
Supplemental Oxygen ◽  
Cochrane Library ◽  
Adaptive Servo Ventilation ◽  
Bilevel Positive Airway Pressure ◽  
Central Apneas

Objective: To systematically review the various modalities of positive airway pressure (PAP) in the treatment of opioid-related central sleep apnea (CSA).Design: Systematic review.Interventions: MEDLINE, the Cochrane Library, and EMBASE were screened through March 2013 to identify articles which investigated treatment of opioid-related CSA with PAP. Eligible articles were identified in a staged process and were assessed by two investigators independently. The methodological quality of the reporting of eligible articles was assessed using a set of questions addressing both general and statistical methodologies.Results: Five articles met the inclusion criteria for a total of 127 patients. All patients had been on opioids for at least 6 months. The dose ranged from 10 mg to 450 mg daily of morphine equivalent dose. Continuous positive airway pressure (CPAP) was proven mostly ineffective in reducing central apneic events. Bilevel positive airway pressure (BiPAP) with and without supplemental oxygen achieved elimination of central apneas in 62 percent of patients. Adaptive servo ventilation (ASV) yielded conflicting results with 58 percent of participants attaining a central apnea index <10 per hour. The presence of ataxic breathing predicted poor response to PAP.Conclusions: The available evidence on the efficacy of PAP in opioid-related CSA is inconclusive. With the increasing use of opioids, further studies are needed to assess optimal PAP therapy and predictors of success in this group of patients.

Positive airway pressure therapy

2017 ◽  
Author(s):  
Dirk Pevernagie
Keyword(s):  
Sleep Apnea ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Therapeutic Success ◽  
Pressure Therapy ◽  
Cardiovascular Comorbidity ◽  
Adaptive Servo Ventilation ◽  
Obstructive Sleep

This chapter describes positive airway pressure (PAP) therapy for sleep disordered breathing. Continuous PAP (CPAP) acts as a mechanical splint on the upper airway and is the treatment of choice for moderate to severe obstructive sleep apnea (OSA). Autotitrating CPAP may be used when the pressure demand for stabilizing the upper airway is quite variable. In other cases, fixed CPAP is sufficient. There is robust evidence that CPAP reduces the symptomatic burden and risk of cardiovascular comorbidity in patients with moderate to severe OSA. Bilevel PAP is indicated for treatment of respiratory diseases characterized by chronic alveolar hypoventilation, which typically deteriorates during sleep. Adaptive servo-ventilation is a mode of bilevel PAP used to treat Cheyne–Stokes respiration with central sleep apnea . It is crucial that caregivers help patients get used to and be compliant with PAP therapy. Education, support, and resolution of adverse effects are mandatory for therapeutic success.

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