Sleep



Sleep





I. Basic Science



  • Sleep homeostasis



    • Sleep need gradually increases during wakefulness and decreases with sleep.


    • Sleep need has a similar temporal pattern as slow wave sleep.


    • Non rapid eye movement (REM) sleep may be the most restful and needed sleep.


  • Neural models of sleep regulation



    • Two-process model: homeostatic and circadian processes; process S rises during waking and declines in sleep, interacting with circadian process C that is independent of sleep and waking. A separate model proposes that process S varies between an upper and a lower threshold that are both modulated by a single circadian process; does not address REM.


  • REM sleep generated by the pons


II. Circadian Control of Sleep-Wakefulness



  • Both circadian and homeostatic processes control physiologic sleepiness and alertness.


  • The suprachiasmatic nuclei =the mammalian biologic clock


  • The suprachiasmatic nuclei is necessary and sufficient for the generation of circadian rhythms in both sleep-wakefulness and body temperature.


  • Delayed sleep phase



    • Most common in teenagers


    • Sleep onset usually after 2:00 AM


    • Normal sleep architecture and total sleep time if allowed to sleep


    • Chronotherapy: 3-hour delays until reach new time to sleep


    • Light therapy: bright light in morning (minimum of 2,500 lux) and minimize light around CT15


  • Advanced sleep phase



    • More common in older persons


    • Sleep onset usually 6 to 8:00 PM and awaken at 1 to 3:00 AM


    • Treat with late evening light therapy


  • Non-24 hour sleep wake cycle



    • Usually maintain steady pattern of 1 to 2 hours of delay each day in normal light and socialization.


    • More common in blind patients



  • Irregular Sleep-Wake Schedule



    • Disorganization of sleep-wake schedule


    • Normal 24-hour total sleep time but sleep periods fragmented


    • Treatment usually with strict socialization; benzodiazepine nominally useful


III. Sleep-Disordered Breathing



  • Respiratory events



    • Hypopnea: The American Academy of Sleep Medicine Task Force had defined a hypopnea as a decrease in airflow for >10 seconds by more than 50% or a decrease in airflow of <50% but with an arousal or a 3% desaturation.


    • Apnea: An apnea is a reduction of airflow of ≥80% for at least 10 seconds. There are three types:



      • Obstructive apnea: absence or decrease in airflow with a continuation of respiratory effort with any of the following:



        • a decrease in effort, but still visible, followed by a marked increase in effort at the resumption of airflow with a decrease in the amplitude of the airflow channel at the nostrils to <20% of the baseline with continued effort (Aldrich).


        • a cessation of effort, of <10 seconds, with a progressive increase in effort up to the resumption of airflow with a cessation of airflow at the level of the nostrils and mouth lasting at least 10 seconds (Dement)


        • associated with desaturation of 4% or more, arousal, or change to a lighter stage of sleep


    • Central: a parallel cessation of respiratory effort and airflow that begins and ends simultaneously and lasts at least 10 seconds. Central apneas may or may not be associated with a desaturation or arousal.


    • Mixed apneas have both central and obstructive components and a complete cessation of effort for at least 10 seconds any time during the event.


    • Cheyne-Stokes breathing is irregular breathing characterized by a series of shallow breaths that increase in depth and rate, followed by breaths that decrease in depth and rate. It may have an apnea component and/or desaturation.


    • Hypoventilation is a reduced amount of air entering the pulmonary alveoli indicated by an increased PaCO2. The duration is longer than an apnea or hypopnea and often lasts several minutes. It is associated with a gradual decrease in SaO2 and may not be an event but must be reported.


    • Obstructive sleep apnea syndrome: five or more hypopneas or apneas per hour with some associated symptom of hypersomnolence


  • Cardiovascular effects of sleep apnea



    • Impact of sleep on blood pressure



      • Systemic blood pressure during apnea increases with a maximum at the arousal.


      • Nocturnal blood pressure in patients with obstructive sleep apnea (OSA) do not have normal nocturnal blood pressure dip.


      • Continuous positive airway pressure (CPAP) decreases systolic and diastolic blood pressure in OSA patients.


      • Pulmonary hypertension is more common in OSA patients.


    • Cardiac rhythm in OSA patients:



      • Most commonly seen pattern is bradycardia-tachycardia


      • Severe arrhythmias uncommon (venticular tachcardia prevalence increases with SaO2 <65%)



    • Cardiac ischemia in OSA patients results from



      • Hypoxia-reoxygenation


      • Vascular pressure fluctuations


      • Increased sympathetic activation


      • Increased platelet activation


      • Hypertension


    • Left ventricular failure and OSA



      • OSA may contribute to ventricular failure.


      • Positive pressure therapy is an effective treatment.


  • Positive pressure treatment of sleep apnea



    • CPAP—action



      • Pneumatic splinting of upper airway


      • Tries to normalize upper airway resistance


    • CPAP—compliance



      • 8% to 16% of OSA patients will not accept nasal CPAP


    • CPAP—side effects



      • Skin abrasion, allergic reaction, air leak in eyes, congestion, rhinorrhea, dryness, sinusitis, epistaxis, claustrophobia, pneumocephalus, atrial arrhythmia, chest discomfort


    • Bilevel PAP


  • Surgical Management of sleep apnea

Tags:
Sep 8, 2016 | Posted by in NEUROLOGY | Comments Off on Sleep

Full access? Get Clinical Tree
Get Clinical Tree app for offline access