36 th Annual Educational Conference. Sleep Physiology. Wakefulness 9/4/2013

Transcription

1 36 th Annual Educational Conference Understanding Sleep study Results Dainis Irbe MD Emerald Sleep Disorders Center October 5, 2013 Sleep Physiology Wakefulness REM Indeterminate NREM Wakefulness 1

2 Stage 1 NREM θ Waves Stage 2 NREM Sleep Spindles K-Complexes Stage 3 NREM % δ Waves Stage 4 NREM > 50 % δ Waves Stage REM Alpha Waves Conjugate Eye Movements 2

3 Sleep Stages Overnight NREM is more common in the first part of sleep. REM is more common in the latter half of sleep Parasomnias Impressive Phenomena Positive Family History Usually Deep NREM Sleep (Stages 3/4) Common in childhood, decrease with age Persistence into adulthood NOT a sign of psychopathology Can be induced or precipitated by fever, sleep deprivation, and certain medications Parasomnias Parasomnias are disruptive sleep-related disorders that can occur during arousals from REM sleep or partial arousals from Non-REM sleep. Parasomnias include nightmares, night terrors, sleepwalking, confusional arousals and many others. 3

4 Nightmares Night Terrors Age 3-6 yrs 4-8 yrs Sleep Stage REM NREM (3/4) Time of Night Late Early State on waking Upset / Scared Disoriented Response to parents Consolable Unaware of Parents Return to Sleep Difficult Easy / Rapid Memory of Event Vivid None Nightmare or Night Terror? (American Academy of Pediatrics, 1998) Nightmare Night Terror Scary dream awakens child. Child awakes only partially, if at all. Occurs in last hours of the night. Occurs one to four hours after child falls asleep. Child cries and is afraid. Child is aware of caregiver. Child sits up, thrashes, and may struggle with caregiver. Child may scream, cry or talk aloud. Eyes may be staring ahead, with heart racing. Child is not very aware of caregiver. Child may have trouble going back to sleep. Child often remembers dream and may want to talk about it. Child often goes back to sleep without fully awakening. Child has no memory of a dream, or of waking up, screaming, or thrashing. Night terrors A person experiencing a night terror or sleep terror abruptly awakes from sleep in a terrified state. The person may appear to be awake, but is confused and unable to communicate. They do not respond to voices and are difficult to fully awaken. Night terrors last anywhere from a few seconds up to 30 minutes, after which time the person usually lies down and appears to fall back asleep. People who have sleep terrors usually don't remember the events the next morning. 4

5 Night Terrors 5 % of pre-schoolers. Starts between ages 4-12 and resolves spontaneously Increased FHx of enuresis / sleepwalking in 1 st degree relatives During Stage 3-4 during 1 st third of night. Sits upright, stares, appears frightened, screams, cries, autonomic arousal, unresponsiveness Lasts ~ 10 minutes then child returns to undisturbed sleep. No recall. SLEEP TERRORS 'Parvor Nocturnus' Extreme ANXIETY with consistent behavior & autonomic signs (tachycardia, flushing, sweating). Unresponsive to consolation or external stimuli. Confused, disoriented, amnestic Night Terrors Not associated with psych problems in childhood; although in adults, associated with PTSD, panic disorders If disruptive or occur daily, can try Benzo qhs. Sometimes can be manifestation of seizures 5

6 Onset of Night Terror - EEG Spontaneous attack during stage 3 of NREM sleep 2 s of diffuse hypersynchronous high voltage delta wave arousal Brief EEG delta discharge immediately preceding the clinical episode Increased heart rate (shown from EKG) N-REM vs. REM Non-REM Slow EEG REM (paradoxical) EEG similar to awake person Muscular activity Dreaming rare 80% of sleep time No movement Dreaming common Hard to arouse easily 20% of sleep time Causes of Night Terrors Genetic Factors Sleep Disordered Breathing (SDB) Acute Triggers 6

7 Genetic Factors Guilleminault et. al % of children with both NT and SDB have at least 1 immediate relative with parasomnia. Kales et. al % had 1 or more relatives in the pedigree with NT or Sleepwalking. Owens et. al % risk if both parents were affected. LEG CRAMPS Triggered by movement or muscle contraction. Predisposing: pregnancy, diabetes, exercise (poor conditioning), medications Exclude:RLS, PLM, OSA, focal seizures, lo calcium, neuropathy Sleep Motor Phenomena Hypnic Jerks Body Rocking Restless Legs Syndrome Periodic Limb Movement Disorder Parathesias and desire to move the legs Stage 1-2 NREM Sleep More common in children than recognized 40% start in childhood 7

8 Restless Legs Syndrome Periodic Limb Movement Disorder Stage 1-2 NREM Sleep More common in children than recognized 40% start in childhood Secondary Causes Anemia, Pregnancy, Uremia, Neuropathy Periodic Limb Movement Disorder Periodic leg movements causing artifacts in the respiratory channels 8

9 Sleep stage analysis - stage 3 sleep Arousal (EEG activation) 9

10 Arousal with stage change Chin EMG activation NREM sleep snoring pattern in chin EMG 10

11 Evidence of upper airway resistance with arousal (RERA) Cyclic obstructive hypopneas with arousals, but without O2 desaturations Non-obstructive (central) hypopneas without arousal. Note exaggerated waveforms in abdominal channel, possibly caused by over tightened belt or increased channel sensitivity 11

12 Irregular breathing pattern and movement artifact during wakefulness Obstructive apneas with arousals and O2 desaturations Obstructive apneas with minimal chest and abdomen movement 12

13 Sleep onset central apneas Post-arousal central apnea (normal response) Normal respiratory fluctuations in REM sleep (no arousals and no oxygen desaturations) 13

14 83% Snoring with changes in respiratory pattern and reduced O2 saturation levels Snoring with irregular breathing pattern and O2 desaturations Patient on CPAP with residual upper airway resistance and arousal 14

15 Symptoms of OSA Snoring Witnessed Apneas Daytime Sleepiness/fatigue AHI >30, 54% are not sleepy!! Kapur et al. Sleep 2005;28: Nocturia Nighttime Heartburn Night sweats AM Headaches, dry mouth, sore throat Depression/Personality Changes Altered Cognition (memory, learning) Signs of OSA Shallow/narrow posterior oropharynx Large or very small neck Retrognathia, micrognathia Obesity HBP CVA MI GERD Diagnosis of OSA Oximetry Negative does not exclude OSA! Positive doesn t diagnose OSA! Portable Screening Usually some measure of respiratory effort, oximetry, and heart rate Negative doesn t exclude OSA. Positive does Dx OSA. Polysomnography Gold Standard 15

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17 Fairly normal overnight pulse oximetry. Some fluttering noted between 2-3 am and 4-5 am. 3 minute snapshot of the PSG for the patient with the normal pulse oximetry. Ten obstructive events noted in these 3 minutes. Arousals and PLM s associated with each apneic event. Abnormal pulse oximetry showing frequent severe desaturations. 17

18 4 minute screenshot of patient with abnormal pulse oximetry. Patient is actually having very frequent central apneas and very fragmented sleep pattern. Pathophysiology Small posterior oropharynx Obesity Jaw structure Tonsils/adenoids Muscle relaxation at sleep onset Paralysis during REM sleep Partial/complete collapse posterior oropharynx during sleep Hypopneas/Apneas Increased negative intrathoracic pressures Increase GERD in susceptible persons Increased R heart blood return (Apnea =>Mueller Maneuver alternating with Valsalva) Increased release of atrial-naturetic peptide => increased urine production => nocturia Umlaf et al. Sleep 2004;27: Increased R sided pressures (cross-over through patent foramen ovale =>?paradoxical emboli) Beelke et al. Sleep 2002;25:21-27 May result in decrease LVEF by 25% Decreased Vt May decrease O2 saturation 18

19 Sedative Hypnotics and Apnea Use of hypnotics/sedatives in patients with sleep apnea has been discouraged Arousals from sleep necessary to resume breathing after apneas Hypnotics suppress brain arousal and reduce airway tone Adapt Servo Ventilation Variable bi-level device Base pressure 9/5 Adjusts IPAP to supplement ventilation when < 90% of average ventilation Initiates breath if no effort Airflow VPAP Adapt SV (ASV on) RESMED Cardiopulmonary Consequences Vagal during respiratory event: BP falls, Heart rate falls Sympathetic during arousal: BP suddenly rises, heart rate rises. Oxygen falls during event, several second delay before return to normal after arousal In patients with ASCVD: good model for V. Tach (dog studies). 19

20 Consequences to sleep The combination of events leads to distress signals sent to brain. Sensory blockade at reticular nucleus of thalamus Arousal if sensory stimulus strong and repetitive. Breathing restored => sleep returns => the process starts all over again. Gender differences in normal sleep: Increase in subjective sleep complaints Relatively few differences in sleep architecture Women have more preserved deep sleep with aging Gender difference Insomnia: women 17%, men 5% Depression: women 21%, men 7% Hypothyroid.: women 22%, men 4% Ankle edema: 55%, men 35% Apneas: women 52%, men 63% Cardiac palpitation: women 39%, men 21% 20

21 Gender difference Women consume less coffee and ETOH Smaller face, Shorter mandibule Lower hyoid bone Weight gain: usually lower body Postmenopausal weight gain: usually neck and upper body Hormonal effect on sleep Estrogen: increases total sleep time and REM sleep Progesterone: increases NREM sleep, BDZ like sedation, dose dependent Sleep and menstrual cycle Late luteal phase: increased excessive daytime sleepiness, decreased sleep efficiency, increased wake after sleep onset PMS: excessive daytime sleepiness, insomnia, decreased deep sleep and sleep efficiency 21

22 Sleep and pregnancy Daytime sleepiness, fatigue, increased body temp., SOB Insomnia from abdominal mass, bladder distention, fetal movements, leg cramps, backache, GER High progesterone Decreased O2 supine Sleep in pregnancy 1 st trimester: increased total sleep time, decreased deep sleep 2d trimester: total sleep - normal, decreased deep sleep 3d trimester: decreased total sleep, decreased deep and REM sleep, decreased sleep efficiency, increased awakenings/arousals Pregnancy and snoring 30% women report onset of snoring in pregnancy /third trimester/ 14% reported snoring always, /4% of non pregnant/ OSAS, 43% snorers vs.22% of non snorers with fetal complications hypoxemia associated with IUGR and decreased Apgars 22

23 Periodic leg movements Periodic leg movements and/or restless legs syndrome /RLS/ may be associated with Fe deficiency anemia, type 2 diabetes, uremia, Symptoms subside postpartum 20% develop RLS in 3d trimester Avoid caffeine Sleep in postpartum 30% of new mothers report disturbed sleep and average 2 hours of wakefulness after sleep onset First time mothers sleep most disturbed, alterations of melatonin, cortisol Women with premature infants have decreased sleep time Postpartum depression Nighttime labor and major sleep disruption in 3d trimester associated with depressed mood after childbirth Decreased REM sleep latencies associated with depressed mood Sleepwalking/terror and nightmares decline in pregnancy Migraine and seizures tend to remit 23

24 FDA classification of drug safety A: controlled human studies-little risk to fetuses in 1 st trimester B: animal studies-little fetal risk with no controlled human studies, no later trimester risk C:teratogenic in animal and human studies D: acceptable fetal-risk in life threatening cases X: contraindicated FDA classification Acetominophen:B/B/B Aspirin: D/D/D NSAID s: B/B/D Zolpidem: B Zaleplon: C TCI s: C/D Trazadone: C, nursing caution Most of new antidepressants: class C Most of stimulants: C, including Modafinil Sleep and menopause OSA: increase prevalence and severity of post-menopausal symptoms, HRT may improve sleep efficiency and OSA symptoms Insomnia may persist despite HRT HRT does not improve the quality of life 24

25 Women and shift work Increased risk for cancer Decreased melatonin production Increased estrogen production Tendency eating more fat food More smokers 24% versus daytime job of 17% smokers 25