PULMO-SLEEP APNEA Flashcards
Why do we sleep?
Brain wake and evolved Restoration Conservation of energy Protein Impacts immune system Allow processing of input Memory consolidation depends on sleep
What are the Socioeconomic Consequences?
40 mill Americans suffer from chronic disorders of sleep and wakefulness.
ES ,OSA-93%- W, 82% -M not clinically dx
Excessive daytime sleepiness (EDS) impairs:
Human performance that can lead to accidents home, road, career
31% drivers fall asleep-
Academic performance, learning, and judgment
Increased weight, mood disorders, stress, cardiovascular complications
Inc. infections
Definitions of Sleep
reversible behavioral state of perceptual disengagement from, and unresponsiveness to, the environment.- not aware
very complex amalgam of physiologic and behavior processes.
A process, unlike coma, that is physiologic, recurrent, and reversible.
Where is the body’s master “clock”
suprachiasmatic nucleus (SCN) of the hypothalamus. Behind eyes Crossing some optic chiasm
Light-dark signals reach the SCN via a retinohypothalamic track fibers.
Circardian- about a day
SCN cells are circadian oscillators, exhibiting a stable, biphasic firing cycle. synchronized by exposure of light.
Sleep hygiene
How to keep circadian clock on time?
Regular wake up time-more important than sleep time
Bright light sun exposure helps more
Keep Circadian Clock on Time:
Awaken at approximately the same time each day.
Obtain bright light (e.g. sun) during desired daytime hours.
Maximize Homeostatic Sleep Drive:
Limit napping when insomnia is a problem
“siesta” or afternoon nap is fine if no trouble sleeping at night.
Go to bed only when sleepy.
Reduce Physiological and Psychological Arousal:
Limit or eliminate caffeine, chocolate, nicotine, alcohol.
Exercise long before bedtime (morning exercise works well).
Shut your day down at least 1 hour before bedtime.
Sleep in a comfortable bedroom, especially not too hot.
Agent blocks adenosine
Caffeine
Improve Sleep Hygiene tips
Take hot showers or baths at least 2 hours before bedtime.
Place the alarm clock where it cannot be seen.
Keep the bedroom dark, quiet, and cool, with no pets.
Avoid stressful activities in the evening.
Use the bed only for sleep and intimacy.
Sleep ROS
Do you wake up feeling rested and refreshed?
How long does it take you to fall asleep?
Do you snore, or has your bed partner complained about you snoring?
Do you have any leg discomfort at night?
The alerting effects of the biologic clock:
Oppose the Homeostatic Sleep Drive with its alerting effect.
Allow for a consolidated WAKE during the subjective day.
Initiate a mid-day dip in biologic clock alerting activities.
Homeostatic Sleep Drive:
It is proportional to the amount of previous WAKE and Sleep Debt.
Sleep Debt builds throughout the day.
What’s normal: Adults need 7-8 hours of sleep, Children need 9 or more hours of sleep
DM and HTN
affect sleep
When Patients Say They Are Tired EDS vs. fatigue Sleepiness: able to sleep if given a chance Fatigue: tired but does not fall asleep Body is tired but mind is very active
Ask the patient: If given a chance to stretch out and sleep right now, what would happen?
There is a pos-test question on this. This is a simple but very important concept for primary care providers. The questions from the Epworth should guide them
Epidemiology of Insomnia
Overall prevalence of an insomnia symptom within the last year: ~30%
Risk factors:
Female gender
meta-analysis of 31 studies: relative risk (RR) = 1.41
Medical, psychiatric, and substance abuse issues
Social factors (many co-vary)
Possible genetic factors
Age
You can quickly review some specifics social factors should include: Lower socioeconomic status Unemployment Marital status (divorced or widowed) Lack of education Race, ethnicity, country of origin Shift work Poor sleep hygiene Adverse sleeping environment Far-northern latitudes
Sleep-Related Arousal As a Trait
Primary insomnia
Markers of hyperarousal:
Reduced parasympathetic tone
Increased basal metabolism
Elevated circulating catecholamines
Increased electroencephalogram (EEG) ß activity (cortical activation)
Elevated body temperature
High activity of hypothalamo-pituitary-adrenal axis
Psychophysiologic: Characteristics
Contributed to and reinforced by poor sleep hygiene
Tension, anxiety, arousal in association with efforts to sleep, or in the usual sleeping environment
Negative expectations regarding ability to sleep
Clockwatching
Ability to fall asleep when not trying to
Better sleep away from home
Cognitive-Behavioral Treatment of Insomnia
Counseling in sleep hygiene
Cognitive therapy and stimulus control therapy
Sleep restriction therapy
Improve patient’s understanding of his/her sleep
Establish realistic expectations regarding sleep
Review simple relaxation techniques
Dissuade patient from believing lack of sleep will be harmful
Most Insurance will reimburse PCPs’ for patient education not cognitive therapy
Relaxation techniques could include deep breathing, reduce stimulation, etc
Behavioral Management of Insomnia
Sleep Restriction Therapy
Set the alarm for the same time each morning, regardless of the amount of sleep obtained the night before.
No daytime naps allowed
Keep a sleep diary for at least 7 days and compute the total amount of sleep per night (total sleep time [ TST]) indicated by the diary.
Set up a schedule restricting the time spent in bed to equal the TST.
As sleep efficiency improves, bedtime is advanced (go to bed earlier) by 15- to 20-minute intervals, maintaining the same wake time.
RLS
A distressing need/urge to move the legs, usually accompanied by an uncomfortable, deep-seated sensation in the legs that is:
Brought on by rest
Relieved with moving or walking
Worse in the night or evening (circadian
Primary (idiopathic):
No precipitating factor Younger age onset ("growing pains) Genetic association Autosomal dominant Chromosome 12/14
Secondary:
Iron deficiency (~25%) Pregnancy (~25%) Renal failure (up to 60%) Drugs Antidepressants
RLS is common Prevalence: Etiologies of RLS: Treatment Anticipate augmentation and rebound
3% to 15% of the general population
Up to 25% of primary care patients
Most cases are primary and hereditary
Secondary etiologies: Iron deficiency, end-stage renal disease (ESRD), peripheral neuropathies
Identify and treat precipitants: Drugs, iron deficiency, sleep deprivation, renal failure
Dopamine agonists are first-line pharmacologic agents
Pramipexole and ropinirole are FDA-approved for RLS
Dopaminergic agents
Iron, if ferritin < 50 ng/mL
Anticonvulsants (gabapentin)
Low-potency opiates
Benzodiazepines (clonazepam)
Circadian Rhythm Sleep Disorders
Jet lag Delayed sleep phase (sleep onset insomnia) Advanced sleep phase (sleep maintenance insomnia) Shift work sleep disorder Irregular sleep-wake rhythm Shift workers Adolescents Elderly and chronically hospitalized Travelers Physicians and nurses
REM Behavior Disorder
Normal REM sleep associated with inhibition of skeletal muscles to prevent “acting out” dreams
RBD involves failure of the inhibition
Now shown to be a precursor to certain degenerative neurologic conditions such as Parkinson’s Disease in a significant percent (40%) of these patients
Responds well to clonazepine
Narcolepsy
Excessive Daytime Sleepiness
Cataplexy: brief emotionally triggered episodes of muscle weakness, Laughter trigger muscle weakness- sleep paralysis comes on when wide awake (50%)
Sleep paralysis (40-80%)
Hypnogogic and hypnopompic hallucinations (40-80%)
Fragmented sleep
Mild obesity
Multiple types
DX-sleep study
Parasomnias
Deep sleep Sleep walking- less w/ age, slow wave sleep dec. Night terrors Bed Wetting Nocturnal eating Hypersomnia Nocturnal Seizures
Prevalence of SDB and OSA
sleep disorder breathing
Approximately 42 million American adults have SDB
9% women and 25% men in the middle-aged working population have OSA
OSA defined as AHI > 5
30% a primary care office may have OSA d/t relationship of morbidities
~75% of severe SDB patients are not diagnosed Young Sleep 2008
DM, CA, CVD
OSA
most common/most predominant.
anyone with AHI > 5
Causes airway to narrow = snoring and breathing difficulties
Relaxing too much may become blocked completely = OSA
MC of SDB
Partial or complete collapse of upper airway
Muscles controlling soft palate and tongue relax
Apnea- cessation of airflow for > 10 seconds
obstruction, central, mixed
Hypopnea- A decrease in airflow lasting > 10 seconds with a 30% reduction in airflow and with at least a 4% oxygen desaturation from baseline
Flow limitation
Upper airway narrowing
Earliest sign of impending upper airway closure
RERA
Respiratory Effort Related Arousal, interferes w/ sleep
Flow limitation leading to arousal
Classification of SDB
AHI (Apnea/Hypopnea Index)
Number of apneas
“severity” of the SDB
10 sec of not breathing every 2min
AHI = 0-4 Normal
AHI = 5-14 Mild
AHI =15-30 Moderate
AHI > 30 Severe
Measured by polysogram
Name the effects of transient arousals.
hypoxia hypercapnia Arousal Neurocognitive impairment (memory loss) Daytime sleepiness Impaired quality of life Metabolic effects Cardiovascular effects Cancer
result in activation of sympathetic nervous system___release of norepinephrine with deleterious cardiovascular consequences.
Major factors include:
Obesity Snoring Male gender (until about age 50) Postmenopausal state Overbite Upper airway anatomic obstruction (including nose) AA, Asian, or Hispanic
Signs and Symptoms of OSA: History
Snoring Unrefreshing sleep/daytime sleepiness Witnessed apneas Insomnia Restless sleep Nocturnal heartburn Morning headache- common Nocturia- apnea, will wake then urinate Dry mouth, sore throat, sinus and nasal congestion Mood, memory, and learning problems Parasomnias Impotence Enuresis Many with almost no symptoms-idiopathic
Cardiovascular Effects of OSA
Systemic hypertension
Pulmonary hypertension (with sustained hypoxemia)
atrial fibrillation-OSA trigger
Coronary artery disease
Congestive heart failure
Stroke and transient ischemic attacks (TIA)
Mortality
OSA and Metabolic Dysfunction
glucose intolerance and insulin resistance
50% DM have sleep apnea
independent contributing factor
HCP must screen
Hypoxemia
CPAP improves insulin sensitivity, CVD
10mmHG reduction
Atrial fib- sleeps
Epworth Sleepiness Scale (ESS)
average sleep propensity
> 10 excessive daytime sleepiness
no cause
no apnea related
STOP BANG Obstructive Sleep Apnea
Snore Tired Observed apnea Pressure BMI Age >older Neck circumference Gender 2 out 4 92% apnea sensitive
Positive airway pressure (PAP)
generally accepted as the gold standard
Inc. pressure inc. size of airway
Alternatives: Surgery (UPPP, LAUP, mandibular advancement) Dental appliances-some affect Drug therapies Tracheostomy Pacing (upper airway, cardiac)
Why Treat Sleep Apnea Before Any Surgery?
ss
Sleep apnea and hypertension are the leading independent predictors of complications in bariatric surgery after surgeon’s skill
Decrease complication rate
Decrease impact of comorbidities
Increase adherence to exercise/nutritional/diet guidelines post surgery
37% of patients will continue to need PAP despite surgical succe
OSA: Diagnosis and Management
Recommendations from the American Academy of Pediatrics 2002:
Trouble school underdeveloped Sleeping 30% ADHD Large tonsils and Adenoids-removal Nasal congestion- serious early mouth breathers- high arch narrow jaw Max mandibular expansion referred to a subspecialist.