Healthy Sleep

October 16, 2008 at 11:56 am | In airway, medicine | Leave a Comment
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http://www.umm.edu/patiented/articles/what_sleep_apnea_000065_1.htm

In sleep studies, subjects spend about one-third of their time asleep, suggesting that most people need about 8 hours of sleep each day. Individual adults differ in the amount of sleep they need to feel well rested, however. Infants may sleep up to 16 hours a day.

The daily cycle of sleeping and waking is called the circadian rhythm . It’s commonly referred to as the biologic clock. Circadian means “about a day.” Hundreds of bodily functions follow biologic clocks, but sleeping and waking comprise the most prominent circadian rhythm. The sleeping and waking cycle is approximately 24 hours. (People who are confined to windowless homes, with no clocks or other time cues, sleep and wake on a slightly longer cycle.) The 24-hour circadian rhythm typically adheres to the following factors:

  • Humans are designed for daytime activity and nighttime rest.
  • There is a natural peak in sleepiness at mid-day, the traditional siesta time.

In addition, daily rhythms mix with other factors that may interfere or change individual patterns:

  • The firing of nerve cells in the brain may be faster or slower in different individuals.
  • The monthly menstrual cycle in women can shift the pattern.
  • Light signals coming through the eyes reset the circadian cycles each day, so changes in season or various exposures to light and dark can unsettle the pattern. The importance of sunlight as a cue for circadian rhythms is dramatized by the problems experienced by people who are totally blind. They commonly suffer trouble sleeping and other rhythm disruptions.

The Response in the Brain to Light Signals

The response to light signals in the brain is an important key factor in sleep:

  • Light signals travel to a tiny cluster of nerves in the hypothalamus in the center of the brain, the body’s master clock, which is called the supra chiasmatic nucleus or SCN.
  • This nerve cluster takes its name from its location. It sits just above (supra) the optic chiasm, a major junction for nerves transmitting information about light from the eyes.
  • The approach of dusk each day prompts the SCN to signal the nearby pineal gland to produce the hormone melatonin.
  • Melatonin is thought to act as the body’s time-setting hormone. The longer a person is in darkness the longer the duration of melatonin secretion. Secretion can be diminished by staying in bright light. Melatonin also appears to trigger the need to sleep.

Sleep Cycles

Sleep consists of two distinct states that alternate in cycles and reflect differing levels of brain nerve cell activity:

Non-Rapid Eye Movement Sleep (NonREM). NonREM sleep is also termed quiet sleep. NonREM is further subdivided into three stages of progression:

  • Stage 1 (light sleep)
  • Stage 2 (so-called true sleep)
  • Stage 3 to 4 (deep “slow-wave” or delta sleep)

With each descending stage, awakening becomes more difficult. It is not known what governs NonREM sleep in the brain. A balance between certain hormones, particularly growth and stress hormones, may be important for deep sleep.

Rapid Eye-Movement Sleep (REM). REM sleep is termed active sleep. Most vivid dreams occur in REM sleep. REM-sleep brain activity is comparable to that in waking, but the muscles are virtually paralyzed, possibly preventing people from acting out their dreams. In fact, except for vital organs like lungs and heart, the only muscles not paralyzed during REM are the eye muscles. REM sleep may be critical for learning and for day-to-day mood regulation. When people are sleep-deprived, their brains must work harder than when they are well rested.

The REM/NREM Cycle. The cycle between quiet (NonREM) and active (REM) sleep generally follows this pattern:

  • After about 90 minutes of NonREM sleep, eyes move rapidly behind closed lids, giving rise to REM sleep.
  • As sleep progresses the NonREM/REM cycle repeats.
  • With each cycle, NonREM sleep becomes progressively lighter, and REM sleep becomes progressively longer, lasting from a few minutes early in sleep to perhaps an hour at the end of the sleep episode.

The upper airway resistance syndrome

October 12, 2008 at 11:16 am | In Head & Neck, airway, medicine | Leave a Comment
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Exar EN, Collop NA.

Division of Pulmonary and Critical Care Medicine, Allergy and Clinical Immunology, Medical University of South Carolina, Charleston 29425, USA. exarem@musc.edu

The upper airway resistance syndrome (UARS) is a recently described form of sleep-disordered breathing in which repetitive increases in resistance to airflow within the upper airway lead to brief arousals and daytime somnolence. This review will first describe the chronological progression of our understanding of UARS within the broader context of sleep-disordered breathing. The primary symptom, daytime somnolence, appears to result directly from repetitive EEG arousals. The level of negative intrathoracic pressure is the most likely stimulus for arousal, possibly mediated by mechanoreceptors in the upper airway. A general consensus regarding the exact clinical definitions and the physiologic measurement techniques leading to a diagnosis does not exist, although esophageal manometry and pneumotachographic airflow measurements taken during polysomnography are the “gold standard.” Less invasive diagnostic modalities have been proposed, but none of them have been well-validated. Aside from daytime somnolence, hypertension is an important sequela of this disorder, likely resulting from autonomic and cardiovascular changes induced by increased negative intrathoracic pressure. Nasal continuous positive airway pressure is the most efficacious form of therapy, although low patient compliance may limit its practical application. The safety and efficacy of surgical treatments are poorly documented in the literature. Palatal tissue reduction by radiofrequency ablation and the use of oral appliances hold promise as safe and effective modalities, but these treatments require further study.

stridor in a young child

January 21, 2008 at 1:24 pm | In airway | Leave a Comment
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Stridor in childhood.

McBride JT.

The acute onset of stridor in a young child usually represents viral croup, particularly during the fall and early winter. If the clinical picture is entirely consistent with this diagnosis and gas exchange is maintained, management with cool mist at home is appropriate. Rapid deterioration is unusual in viral croup; however, if obstruction is prolonged or becomes unusually severe, racemic epinephrine aerosols, hospitalization for careful observation, a brief course of corticosteroid therapy, and, rarely, endotracheal intubation may be required. Many of the other causes of acute stridor in childhood represent true pediatric emergencies: epiglottitis, foreign body aspiration, bacterial tracheitis, allergic airway edema, and retropharyngeal abscess, all requiring management with a consultant. Chronic stridor in infancy most often represents laryngomalacia, a developmental abnormality of the laryngeal cartilage which usually resolves by the second year of life and rarely requires specific treatment. Other causes of chronic stridor in childhood include subglottic hemangioma, vocal cord paralysis, and a long list of abnormalities. In the older child with chronic stridor or in the infant whose clinical picture is unusual for laryngomalacia, airway roentgenograms, barium studies, or laryngoscopy/bronchoscopy should be obtained to establish the definitive diagnosis.

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