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
