Sleep Flashcards
Definition of OHS
BMI >30
daytime PaCO2 >45
all other causes ruled out
Pathophysiology of OHS
-Decreased respiratory system compliance and increased resistance
-Respiratory muscle fatigue
-impaired response to elevated pCO2 due to decreased ventilatory drive and increased leptin
- impaired response to hypoxia - sustained hypoxia on sleep study during REM highly suggestive
-OSA as well
Parasomnia treatment
- REM and NREM
Melatonin
Clonazapam
Safety
Trial of sleep deprivation (sleep extension)
Nacrolepsy type 1
Possible autoimmune cause of hypersomnia.
- Autoimmune destruction of hypothalamic hypocretin neurons.
—- causes deficient cholinergic system at regulating sleep
—- impaired norepi and dopamine systems
- Pathonomognic : Cataplexy
C- Cataplexy
H- hypono/hyponogonmic
I- insomnia at night
P- sleep paralysis
S- sleepiness
symptoms x 3 months
Diagnoses:
- Can be without any tests if cataplexy present
- SOL <8MINS x2
- SOREM x2
- and/or CSF hypocretin/orexin <110
Narcolepsy type 2
H- hypogognic
I- insomnia
P- paralysis
S- sleepiness
NO cataplexy
Dx:
- same as type 1 however
—- CSF hypocretin >110
—- likely not autoimmune process
Narcolepsy treatment
DAYTIME SLEEPINESS:
Salfiamterol:
– DOP/NE reuptake inhibitor
– approved for osa as well
Pitolisant
- ant/inverse agonist of h3 receptor
Modafinil
meds for adhd
CATAPLEXY
- Sodium oxybate
- pitoliasant
- ssri
Idiopathic hypersomnia
Diagnostic
- Irrepressible need to sleep during the day due to sleepiness x3m
- no cataplexy
- MLST:
—– SOREMS 0-1
- One of the following:
—– 2 SOL <8MINS or total 24 hours sleep time of 660mins
—– insufficient sleep ruled out
Treatment:
- Modafinil
possible:
- Pitolisant
- sodium oxybate
Modafinal/armodafinil
Can be used for EDS after OSA treated and pt still has residual sleepiness.
** patients needs to find alternative BC. Decreases effectiveness of OCPs.
CPAP-
— benefits
HTN only - even if people arent hypertensive
The presence of OSA associated with increased CV events (stroke, MI, sudden death, heart failure) also neurocognitive issues (depression etc.)
— treatement does not change any of that.
— only benefit is to decrease blood pressure by 2-4pts.
Acute mountain sickness
Cerebral edema and/or pulmonary edema
Cerebral edema:
- Hypoxic vasoconstriction causes
Pulmonary edema: pulmonary hypoxic vasoconstriction causes rupture of capillaries and causes edema
Increased cerebral edema
- Management:
—- ascend
- pre-treatment:
—- Acetazolamide (causes a metabolic acidosis therefore minimizes the respiratory alkalosis (maintains ph) caused when at altitude and continues to breath
—- Dexamethasone (decrease cerebral edema)
—- Pulmonary edema: nifedipine or silfenafil
High altitude periodic breathing
Enhanced ventilatory response to hypoxia
– increased to decrease respirations.
– abnormal breathing pattern while at altitude.
Central sleep Apnea
Primary
- idiopathic
Secondary
- Heart failure (cheyne stokes breathing)
- opioids
- Stroke
- PAP emergent
Central Sleep Apnea
- due to opioids
Opioids:
— long acting
— dose dependent
— BIOT, disorganized pattern of breathing
— Ataxic breathing
Treatment:
- decrease opioid dose
- ASV
Central sleep apnea definition
AHI > 5
At least 5 CSA in 1 hour
At least 50% of apneas are related to CSA
Symptoms of sleepiness and fatigue
Central sleep apnea treatment in heart failure
NIPVV
— CPAP
— ASV (if EF >45%)
- trial CPAP - Goal AHI <15
- if not then if EF >45% trial ASV
- otherwise may need CPAP with O2 or bilevel with PAP.
- NO autotitrating devices.
Oxygen
— May decrease AHI and improve SaO2
Heart transplant
Phrenic nerve stimulator
** associated with increased mortality in CHF
Treatment emergent CSA
- May resolved within 3months of OSA treatment with CPAP
- If not then bilevel ST or ASV (check EF)
Physiologic changes during sleep
N1-N3 (75%)
REM sleep (25%)
- most time spent in N2
— K complexes, spindles
During NREM Sleep:
— decreased RR, decreased TV
— Decreased metabolic rate
— decreased SaO2
— Decreased responsiveness to hypoxemia
— Increased PaCO2
* regular breathing
During REM Sleep:
— Further decraeses responsiveness to hypoxemia
— Decreased TV (no accessory muscles- just diaphragm)
* irregular breathing
* increased vulnerability if disordered breathing due to decrease response to ventilation/hypoxemia
Sleep -
Driven by homestatic process C and circadian rhythm.
As awake longer- sleep drive increases however alert signals from the circadian rhythm increase to keep you awake. At night- increased sleep drive, and circadian signalling is decreased – sleep.
Circadian rhythm dicated by light
Light – eye – Reticulohypothalamic tract – SCN – Superior Cervical ganglion – pineal gland (releases melatonin)
Process C (circadian)
Process S
Determine how when and how long we sleep
Advanced sleep cycle
Bed early- awake early
Circadian rhythm <24 hours
Dictated by Per2 gene
Treatment:
- bright light therapy in the evening
- melatonin early evening
Ramelton
Melatonin receptor agonist
Short half life
Used for insomnia
CI: hepatic impairment, use of fluvoxamine
Surorexant/Lemborexant
Orexin Antagonist
Recommended for sleep maintenence in treatment of insomnia
CI:
- Can cause sedation, respiratory depression, SI/depression
Parasomnias
REM and NREM
REM:
- REM SBD:
—- dementia/parkinsons
NREM:
- mostly in N3
—- need to r/o seizure disorder
TreatmentL
- melatonin (RBD only)
- safety
- clonazapam
PLMD
> 15 PLMD Index (# movements/TST)
movements criteria:
- 4 in a row
- Between 5-90s
- each movement 0.5-10sec
- both or single legs
Treatment: same as RLS
— as in RLS- worry about augmentation (get used to the dose) and use in impulse disorders)
