Arousal and breathing responses to airway occlusion in healthy sleeping adults.
ABSTRACT The arousal and breathing responses to total airway occlusion during sleep were measured in 12 normal subjects (7 males and 5 females) aged 25-36 yr. Subjects slept while breathing through a specially designed nosemask, which was glued to the nose with medical-grade silicon rubber. The lips were sealed together with a thin layer of Silastic. The nosemask was attached to a wide-bore (20 mm ID) rigid tube to allow a constant-bias flow of room air from a blower. Total airway occlusion was achieved by simultaneously inflating two rubber balloons fixed in the inspiratory and expiratory pipes. A total of 39 tests were done in stage III/IV nonrapid-eye movement (NREM) sleep in 11 subjects and 10 tests in rapid-eye-movement (REM) sleep in 5 subjects. The duration of total occlusion tolerated before arousal from NREM sleep varied widely (range 0.9-67.0 s) with a mean duration of 20.4 +/- 2.3 (SE) s. The breathing response to occlusion in NREM sleep was characterised by a breath-by-breath progressive increase in suction pressure achieved by an increase in the rate of inspiratory pressure generation during inspiration. In contrast, during REM sleep, arousal invariably occurred after a short duration of airway occlusion (mean duration 6.2 +/- 1.2 s, maximum duration 11.8 s), and the occlusion induced a rapid shallow breathing pattern. Our results indicate that total nasal occlusion during sleep causes arousal with the response during REM sleep being more predictable and with a generally shorter latency than that in NREM sleep.
- SourceAvailable from: erj.ersjournals.com[Show abstract] [Hide abstract]
ABSTRACT: The pathophysiology of obstructive sleep apnoea (OSA) is complex and incompletely understood. A narrowed upper airway is very common among OSA patients, and is usually in adults due to nonspecific factors such as fat depo- sition in the neck, or abnormal bony morphology of the upper airway. Functional impairment of the upper airway dilating muscles is particularly impor- tant in the development of OSA, and patients have a reduction both in tonic and phasic contraction of these muscles during sleep when compared to normals. A variety of defective respiratory control mechanisms are found in OSA, including impaired chemical drive, defective inspiratory load responses, and abnormal upper airway protective reflexes. These defects may play an important role in the abnor- mal upper airway muscle responses found among patients with OSA. Local upper airway reflexes mediated by surface receptors sensitive to intrapharyngeal pressure changes appear to be important in this respect. Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea, because of a reduction in respi- ratory drive related to the hypocapnia which results from postapnoeic hyperventi- lation. A cyclical pattern of repetitive obstructive apnoeas may result. A better understanding of the integrated pathophysiology of OSA should help in the development of new therapeutic techniques.
- [Show abstract] [Hide abstract]
ABSTRACT: This review focuses on the adverse effects of sleep derangements on physicians and patients in the intensive care unit. Recent evidence suggests that the complexity and level of care delivered in the intensive care unit (ICU) has outstripped a trainee's ability to forego sleep and is compromising both physician and patient safety and thereby threatens the foundation of the profession. Sleepy physicians are not only more capable of committing medical errors, but are also more likely to suffer motor vehicle crashes, workplace conflicts, and occupational injuries. Moreover, critically ill patients may suffer from sleep derangements due to a host of factors that includes mechanical ventilation, ICU noise levels, and healthcare activities, although a majority of sleep disturbances in this population are as yet unexplained. Besides suffering at the hands of sleepy physicians, critically ill patients may experience adverse outcomes due to severe sleep derangements during their ICU stay. In conclusion, both critically ill patients and intensive care physicians are susceptible to sleep deprivation and derangements that may ultimately adversely influence patient outcomes. Administrators of an ICU need to be cognizant of the effect of sleep, or lack thereof, on patient and physician safety. Researchers in the areas of sleep medicine and critical care need to collaborate on furthering our understanding of this emerging area of study.Clinical Intensive Care 09/2005; 16:129-136.
- [Show abstract] [Hide abstract]
ABSTRACT: In obstructive sleep apnea (OSA), arousals generally occur at apnea termination and help restore airflow. However, timing of arousals in central sleep apnea (CSA) has not been objectively quantified, and since arousals can persist even when CSA is alleviated, may not play the same defensive role as they do in OSA. We hypothesized that arousals following central events would occur longer after event termination than following obstructive events and would be related to circulation time. We examined polysomnograms from 20 patients with heart failure (HF) (left ventricular ejection fraction ≤ 45%): 10 with OSA and 10 with CSA (apneahypopnea index ≥ 15). Twenty central or obstructive apneas or hypopneas were analyzed in each patient. Compared to the OSA group in whom arousals generally occurred at obstructive event termination, in the CSA group they occurred longer after central event termination (0.9 ± 1.1 versus 8.0 ± 4.1 s, p < 0.0001), but before peak hyperpnea. Time from arousal to peak hyperpnea did not differ between groups (4.3 ± 1.1 vs 4.8 ± 1.6 s, p = 0.416). Unlike the OSA group, latency from apnea termination to arousal correlated with circulation time in the CSA group (r = 0.793, p = 0.006). In HF patients with CSA, apnea-to-arousal latency is longer than in those with OSA, and arousals usually follow resumption of airflow. These observations provide evidence that arousals are less likely to act as a protective mechanism to facilitate resumption of airflow following apneas in CSA than in OSA. Simms T; Brijbassi M; Montemurro LT; Bradley TD. Differential timing of arousals in obstructive and central sleep apnea in patients with heart failure. J Clin Sleep Med 2013;9(8):773-779.Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine 01/2013; 9(8):773-9. · 2.93 Impact Factor