Pharyngeal narrowing/occlusion during central sleep apnea

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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825 Central Sleep Apnea and Sinus Bradycardia

SLEEP ◽

10.1093/sleep/zsab072.822 ◽

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):

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.00330.2013 ◽

2013 ◽

Vol 115 (4) ◽

pp. 474-482 ◽

Cited By ~ 8

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.

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Help, I Can’t Breathe!

Sleep Disorders ◽

10.1093/med/9780190671099.003.0037 ◽

2019 ◽

pp. 642-653

Author(s):

Ai Ping Chua ◽

Loutfi S. Aboussouan

Keyword(s):

Sleep Apnea ◽

Sleep Apnea Syndrome ◽

Central Sleep Apnea ◽

Apnea Hypopnea Index ◽

Central Apnea ◽

Arousal Index ◽

Cpap Titration ◽

Obstructive Sleep ◽

Apnea Syndrome ◽

Complex Sleep Apnea

This chapter presents a case of treatment-emergent central sleep apnea (TECSA), which is also known as complex sleep apnea syndrome or continuous positive airway pressure (CPAP)–emergent central sleep apnea. In this disorder, central apnea events emerge in patients with obstructive sleep apnea (OSA) after initiation of CPAP treatment. This phenomenon has been identified in up to 20% of patients with OSA who undergo CPAP titration. Polysomnography in those with TECSA usually shows an elevated residual Apnea–Hypopnea Index and arousal index after PAP initiation and occurs primarily during non–rapid-eye-movement sleep. Several mechanisms that have been postulated will be reviewed. The phenomenon is usually self-limiting, and recommended management includes applying the lowest PAP pressure needed to achieve reasonable control and avoiding modalities that exacerbate hypocapnia.

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Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.3.918 ◽

1997 ◽

Vol 82 (3) ◽

pp. 918-926 ◽

Cited By ~ 77

Author(s):

Ailiang Xie ◽

Fiona Rankin ◽

Ruth Rutherford ◽

T. Douglas Bradley

Keyword(s):

Sleep Apnea ◽

Dead Space ◽

Sleep Apnea Syndrome ◽

Central Sleep Apnea ◽

Face Mask ◽

Air Breathing ◽

Central Sleep Apnea Syndrome ◽

Apnea Threshold ◽

Central Apneas ◽

End Tidal

Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. Douglas Bradley. Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea. J. Appl. Physiol. 82(3): 918–926, 1997.—We hypothesized that reductions in arterial [Formula: see text]([Formula: see text]) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising[Formula: see text] would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous[Formula: see text] were measured: during room air breathing ( N1), alternating room air and CO2 breathing ( N2), CO2 breathing all night ( N3), and addition of dead space via a face mask all night ( N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous [Formula: see text], which virtually eliminated apneas and hypopneas; they decreased from 43.7 ± 7.3 apneas and hypopneas/h on N1 to 5.8 ± 0.9 apneas and hypopneas/h during N3( P < 0.005), from 43.8 ± 6.9 apneas and hypopneas/h during room air breathing to 5.9 ± 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 ( P< 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 ( P< 0.005). Because raising[Formula: see text] through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in[Formula: see text] below the apnea threshold.

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

Journal of Applied Physiology ◽

10.1152/jappl.1992.73.3.1141 ◽

1992 ◽

Vol 73 (3) ◽

pp. 1141-1145 ◽

Cited By ~ 17

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.

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Chiari malformation and central sleep apnea syndrome: efficacy of treatment with adaptive servo-ventilation

Jornal Brasileiro de Pneumologia ◽

10.1590/s1806-37132014000500014 ◽

2014 ◽

Vol 40 (5) ◽

pp. 574-578 ◽

Cited By ~ 1

Author(s):

Jorge Marques do Vale ◽

Eloísa Silva ◽

Isabel Gil Pereira ◽

Catarina Marques ◽

Amparo Sanchez-Serrano ◽

...

Keyword(s):

Sleep Apnea ◽

Chiari Malformation ◽

Sleep Apnea Syndrome ◽

Central Sleep Apnea ◽

Decompressive Surgery ◽

Type I ◽

Central Apnea ◽

Adaptive Servo Ventilation ◽

Central Sleep Apnea Syndrome ◽

Apnea Syndrome

The Chiari malformation type I (CM-I) has been associated with sleep-disordered breathing, especially central sleep apnea syndrome. We report the case of a 44-year-old female with CM-I who was referred to our sleep laboratory for suspected sleep apnea. The patient had undergone decompressive surgery 3 years prior. An arterial blood gas analysis showed hypercapnia. Polysomnography showed a respiratory disturbance index of 108 events/h, and all were central apnea events. Treatment with adaptive servo-ventilation was initiated, and central apnea was resolved. This report demonstrates the efficacy of servo-ventilation in the treatment of central sleep apnea syndrome associated with alveolar hypoventilation in a CM-I patient with a history of decompressive surgery.

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Use of average volume-assured pressure support as a therapeutic option in patients with central sleep apnea syndrome

Sleep And Breathing ◽

10.1007/s11325-021-02379-z ◽

2021 ◽

Author(s):

John Mario Levri ◽

Naomitsu Watanabe ◽

Victor T. Peng ◽

Steven M. Scharf ◽

Montserrat Diaz-Abad

Keyword(s):

Sleep Apnea ◽

Pressure Support ◽

Therapeutic Option ◽

Sleep Apnea Syndrome ◽

Central Sleep Apnea ◽

Average Volume ◽

Central Sleep Apnea Syndrome ◽

Apnea Syndrome

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Aging is associated with increased propensity for central apnea during NREM sleep

Journal of Applied Physiology ◽

10.1152/japplphysiol.00125.2017 ◽

2018 ◽

Vol 124 (1) ◽

pp. 83-90 ◽

Cited By ~ 2

Author(s):

Susmita Chowdhuri ◽

Sukanya Pranathiageswaran ◽

Hillary Loomis-King ◽

Anan Salloum ◽

M. Safwan Badr

Keyword(s):

Carbon Dioxide ◽

Older Adults ◽

Young Adults ◽

Nrem Sleep ◽

The Elderly ◽

Central Apnea ◽

Elderly Adults ◽

Rapid Eye Movement Sleep ◽

Controller Gain ◽

Central Apneas

The reason for increased sleep-disordered breathing with predominance of central apneas in the elderly is unknown. We hypothesized that the propensity to central apneas is increased in older adults, manifested by a reduced carbon-dioxide (CO2) reserve in older compared with young adults during non-rapid eye movement sleep. Ten elderly and 15 young healthy adults underwent multiple brief trials of nasal noninvasive positive pressure ventilation during stable NREM sleep. Cessation of mechanical ventilation (MV) resulted in hypocapnic central apnea or hypopnea. The CO2 reserve was defined as the difference in end-tidal CO2 ([Formula: see text]) between eupnea and the apneic threshold, where the apneic threshold was [Formula: see text] that demarcated the central apnea closest to the eupneic [Formula: see text]. For each MV trial, the hypocapnic ventilatory response (controller gain) was measured as the change in minute ventilation (V̇e) during the MV trial for a corresponding change in [Formula: see text]. The eupneic [Formula: see text] was significantly lower in elderly vs. young adults. Compared with young adults, the elderly had a significantly reduced CO2 reserve (−2.6 ± 0.4 vs. −4.1 ± 0.4 mmHg, P = 0.01) and a higher controller gain (2.3 ± 0.2 vs. 1.4 ± 0.2 l·min−1·mmHg−1, P = 0.007), indicating increased chemoresponsiveness in the elderly. Thus elderly adults are more prone to hypocapnic central apneas owing to increased hypocapnic chemoresponsiveness during NREM sleep. NEW & NOTEWORTHY The study describes an original finding where healthy older adults compared with healthy young adults demonstrated increased breathing instability during non-rapid eye movement sleep, as suggested by a smaller carbon dioxide reserve and a higher controller gain. The findings may explain the increased propensity for central apneas in elderly adults during sleep and potentially guide the development of pathophysiology-defined personalized therapies for sleep apnea in the elderly.

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1266 Primary Central apnea and loss of muscle atonia during REM

SLEEP ◽

10.1093/sleep/zsaa056.1260 ◽

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.

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