825 Central Sleep Apnea and Sinus Bradycardia

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A322-A322
Author(s):  
Jared Colvert ◽  
Glen Greenough

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):

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

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.


1995 ◽  
Vol 78 (5) ◽  
pp. 1806-1815 ◽  
Author(s):  
M. S. Badr ◽  
F. Toiber ◽  
J. B. Skatrud ◽  
J. Dempsey

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.


2019 ◽  
pp. 642-653
Author(s):  
Ai Ping Chua ◽  
Loutfi S. Aboussouan

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.


1992 ◽  
Vol 73 (3) ◽  
pp. 1141-1145 ◽  
Author(s):  
K. G. Henke ◽  
C. E. Sullivan

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.


Sleep apnea disease is a disease at the respiration system in a human that dangerous and has a high mortality rate. There is two sleep apnea, the first is central sleep apnea and then obstructive sleep apnea, basically sleep apnea is a condition that somebody stop breathing when they were sleeping for a few second, sleep apnea caused by the relaxation of respiration muscle. When sleep apnea comes back, sleep apnea patients need to wake up from and breathe normally again. This system is made to provide some mechanism outside of the human body to help obstructive sleep apnea patient woke up from their sleep and breathe well. Furthermore, with this system, might patients could be monitored although they were not at a hospital. In its work, the system is using a microcontroller and smartphone that are connected with the MQTT protocol to help patients. The microcontroller is used for sensing patient heart rate by connecting it with the AD8232 module sensor wich then the signal would be classified to determine the condition of sleep apnea using the KNN classification method. The result of classification by the microcontroller be delivered to the user’s smartphone to be the trigger for alarm, patient’s monitoring system, etc. Research result shows that the MQTT protocol 100% successful to transmit the data with 39.74 ms delay. The patient, patient’s family, and medic smartphone’s apps can monitor and successfully show a notification when sleep apnea’s patient recurring. Accurate of the sensor at sensing heart rate is 91.32% and the accuracy of the classification method is 86.6%. Other than that, the average processing speed from the sensing proses to classification is 1273.85 ms, and the time needed for data arrived at the user’s smartphone is 1312.74 ms.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A242-A242
Author(s):  
N Watanabe ◽  
J Levri ◽  
V Peng ◽  
S M Scharf ◽  
M Diaz

Abstract Introduction Obstructive sleep apnea (OSA) is a common disease, often treated using continuous positive airway pressure (CPAP). In many cases, patients fail an attended CPAP titration study, often due to inadequate control of AHI, and treatment-emergent central apneas as CPAP is increased. Here, we report our experience using volume-assured pressure support (VAPS) for these patients. Methods We retrospectively reviewed records of 45 adults who had OSA diagnosed on polysomnography (PSG) in whom CPAP titration had failed. In these patients, VAPS-AE (adjustable expiratory pressure) titrations were performed. Patients with central sleep apnea on baseline PSG were excluded. Results Reasons for CPAP titration failure included: treatment emergent central apneas (25), failure of maximum CPAP pressure to treat OSA (18), and persistent hypoxia (2). Average age was 57.9±13.1, BMI was 40.2±8.7, 26 males, Epworth sleepiness score was 10.7±7.9. The following significant changes from baseline PSG to VAPS titration were observed: AHI: 65.3±29.3 to 22.3 ±16.1 (p&lt;.001) events/hour. Time &lt; 88% saturation: 63.7 (median) to 6.9 (median) min (p&lt;.001). The number of patients with AHI&lt;15 was 0 on PSG and 16 (36%) on VAPS-AE, while the number of patients with AHI&lt;30 was 7 (16%) on PSG and 32 (71%) on VAPS-AE. Improvement in AHI was not related to gender, age, or narcotic use, but was correlated with BMI: ΔAHI = 12.2 - (1.4 * BMI); p=.05. VAPS resulted in improved sleep architecture: slow wave sleep increased (medians: 1.4% to 19.6% total sleep time (TST)) (p&lt;.001), REM sleep increased (medians 6.4% to 13.6% TST) (p&lt;.01). Conclusion For OSA patients for whom CPAP titration failed, titration with VAPS-AE was an effective treatment for many patients. Support N/A


2021 ◽  
pp. 1199-1202
Author(s):  
Vichaya Arunthari ◽  
Brynn K. Dredla

Sleep-related breathing disorders are categorized into obstructive sleep apnea syndromes, central sleep apnea syndrome, and sleep-related hypoventilation or hypoxic syndromes. These disorders can occur in adults and children. Clinical characteristics, diagnosis, and treatment are discussed in this chapter. Sleep apnea occurs when recurrent complete (apnea) or nearly complete (hypopnea) cessation of airflow develops, accompanied by preservation of the respiratory drive manifested as persistent respiratory muscle effort. Apnea is defined as the cessation of airflow for more than 10 seconds, using a valid measure of airflow. Hypopnea is an airflow reduction of at least 30% from baseline that lasts at least 10 seconds and is accompanied by an oxygen desaturation of 4% or more.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A346-A347
Author(s):  
H S Rao

Abstract Introduction Central sleep apneas (CA) are frequently seen on pediatric polysomnograms (PPSG) independently or in conjunction with obstructive sleep apnea (OSA). In the pediatric population, the AASM defines CA as the absence of chest and/or abdominal movement associated with a cessation of airflow of more than 20s or longer than 2 baseline respiratory cycles if associated with an arousal, an awakening or oxygen desaturation ≥ 3%. Scoring CAs on PPSG based on AASM definition can cause confusion among providers as CAs are generally associated with central nervous disorders causing reduced or absent respiratory drive. Methods Retrospective review of 71 consecutive diagnostic PPSGs to analyze patterns of CAs scored per AASM definition was performed. None of the children had a disorder causing reduced respiratory drive. Data on age, obstructive AHI (Apnea Hypopnea Index), CO2, Oxygen saturation, Central AHI and diagnosis were collected. Results 68 of 71 children had varying degree of OSA and CAs. Three main patterns of CAs were observed: occurring in NREM, following sigh breaths or arousals and CAs seen in REM sleep. CO2 and oxygen saturation were in the normal range. Conclusion In our study, CAs were more often seen in young children related to reduced functional residual capacity and immaturity of chest wall. CAs in REM sleep was seen more often in children with lung disorders and gastroesophageal reflux. CAs associated with arousals/awakenings were seen in conjunction with OSA or periodic limb movement disorder (PLMD). Though a finding of CAs &gt;5/hour is considered significant, the minimum number of events required to cause a specific disorder or syndrome remains elusive and may be different in different patient populations. As such, there is no threshold of the number of central apneas associated with disease. CAs associated with disorders causing reduced or absent respiratory drive are mostly seen in NREM sleep and associated with abnormal gas exchange. The context in which the CAs are seen on PPSGs should be clearly described to avoid confusion among ordering providers. In CAs associated with arousals/awakenings, it is important to target the cause of arousals such as OSA or PLMD. Support None


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