Sleep and related disorders Oct13 M1 Flashcards
electrodes placement for sleep graphs
electro oculography, (eye mvmt)
electro myography (muscles)
electroencephalography (EEG)
stages of sleep (4)
non-REM (N1,N2,N3), REM
N1 sleep
alpha wave activity
N2 sleep
spindles and K complexes
N3 sleep
delta wave activity
REM sleep
bursts of eye activity, change in breathing patterns, muscle inhibition
how sleep cycles vary as night goes
more REM sleep.
more N2
less N3
where more N2 and where more N3 in night
more N2 in end
more N3 in beginning
micro-arousal def
transient disruption in sleep (increase in EMG, EEG)
ascending arousal system location
midbrain and basal forebrain
ascending arousal system ntr types (2)
monoaminergic
orexinergic (hypocretin)
main ntr involved in arousal
orexin (hypocretin)
inhibition of arousal system location
ventrolateral preoptic nucleus (VLPO) (two nuclei ventrally and laterally to optic chiasm)
inhibition of arousal system promotes what type of sleep
non REM
inhibition of arousal system what it does
inhibits arousal areas
nucleus of the circadian rhythm
superchiasmatic nucleus
what generates REM sleep
midbrain and pontine areas
why sleep related to breathing
wakefulness and sleep areas project to resp control areas
how breathing changes during sleep and during transition to sleep
decreased minute ventilation, increased PaCO2.
transition to sleep: periods of instable breathing
3 sleep disordered breathings
- obstructive apnea-hypopnea
- central apnea-hypopnea
- sleep-associated hypoventilation
OSA vs CSA
OSA has resp drive
hypopnea def
20-30 s of reduction in breathing
broad cause of OSA
upper airway closing
symptoms of OSA
heavy snoring, nocturia, excessive daytime sleepiness
important complication of OSA
cardiovascular problems
3 causes of CV problems in OSA
- arousals-sleep fragmentation
- hypoxia-reoxygenation
- negative intrathoracic pressures
how arousals-sleep fragmentation in OSa cause CV disease
lead to SS activation and higher HR following apnea
how hypoxia-reoxygenation in OSA causes CV disease
induces oxidative stress, decreases O2 delivery
how negative intrathoracic pressures generated in OSA
during obstructed inspiratory efforts
how negative intrathoracic pressures generated in OSA cause CV disease
increase left ventricle transmural P, hypertrophy
CV symptoms of cardiovascular complications of OSA
hypertension, arrhythmias, acute coronary events, ischemic attacks, pulm hypertension, CHF
treatment to OSA
weight loss, no alcohol, CPAP
apnea def
cessation of breathing for 10s or more
CSA: why central
absence of airflow is due to absence of resp effort
characteristic breathing seen in CSA
Cheyne-Stokes: increeasing and decreasing pattern, apnea alternating with hyperpnea
treatment for Cheyne-Stokes breathing
bi-level non-invasive ventilation with adapting variation of inspiratory positive airway pressure
IPAP
causes of CSA
hypercapnic, idiopathic, CNS lesions, congestive heart failure
Loop gain def
relationship between magnitude of ventilatory disturbance and ventilatory reponse
high loop gain def
response much more important than ventilatory disturbance
high loop gain consequence
resp instability: promotes hyperventilation and the decrease in PCO2 prevents respiratory drive
SAH (sleep associated hypoventilation) causes
CNS disease, drugs, metabolism, neuromuscular disease, chest wall deformities, COPD, obesity
treatment to sleep associated hypoventilation
treat underlying cause. Also:
- ventilatory stimulant medication
- O2
- non invasive ventilation
