PHYSIOLOGY OF SLEEP & BREATHING. John KOLBE Respiratory Services Green Lane Hospital, & Faculty of Health Science University of Auckland. .
PHYSIOLOGY OF SLEEP & BREATHING.
Green Lane Hospital, &
Faculty of Health Science
University of Auckland.
“Bodily function such as that which normally recurs for several hours per night in which the nervous system is inactive, eyes closed, postural muscles relaxed and consciousness nearly suspended.”
Sustained quiescence in a species, specific state accompanied by reduced responsiveness to external stimuli.
Additionally in mammals;
- quick reversibility to the wakeful condition
- characteristic EEG changes
- ?spontaneous occurrence with endogenous
WHY DO WE SLEEP?
So we ain’t knackered, guv?
STAGES OF SLEEP
- Stage 1
- Stage 2
- Stage 3} Slow Wave Sleep
- Stage 4}
REM Sleep (motor activity is inhibited)
burst activity ( delta waves)
Fall in ventilation, CO, heart rate, blood pressure.
REM and non-REM sleep alternate cyclically
- 20-30min every 90-120 min
- increases later in night
SLEEP IN NEWBORN & INFANTS
Enter sleep through REM (active sleep)
NREM-REM cycle, 50-60 min from birth
REM may be up to 50% of total
ECG patterns on non-REM emerge between 2-6 months and consolidate into sleep cycle
SWS becomes prominent when brain structure and function develop.
Sleep Architecture in Young Adults
Sleep is entered through non-REM
NREM and REM sleep alternate within period of 90-120 mins
SWS predominate in the first third of the night and linked to sleep initiation - approx 20 % of total
REM sleep predominates in the last third of the night and is linked to circadian temperature rhythms - 20-25% of total.
SLEEP ARCHITECTURE IN YOUNG ADULTS
Wakefulness in sleep, <5% of night
Stage I2 - 5%
Stage II45 - 55%
Stage III3 - 8%
Stage IV10 - 15%
NREM 75 - 80%
REM 20 - 25% in 4-6 episodes
Effect of Age on Sleep
SWS fades with age (halves cf adolescents)
By 60 years no SWS in some men (loss of cortical synaptic density)
REM % of sleep is maintained in health old age (?relates to intellectual functioning)
Arousals increase with age
STRUCTURE OF HUMAN SLEEP
Amount favoured by an individual is highly variable (4-10 hours)
Amount needed is unclear, performance falls off <5-5.5 hours for most
Sleep deprivation leads to a “sleep debt” of SWS and REM
Proportions of each stage vary with age - significance unclear
Structure of Human Sleep Cont.
Sleep patterns are very much habit and humans can adapt to bizarre sleep patterns and appear to function effectively
Shift workers have increased physical and psychological morbidity
Lack of SWS postulated to lead to loss of psychomotor performance
Lack of REM postulated to lead to irritability, mood swings etc.
NON-REM SLEEP & BREATHING
- stim effect of wakefulness
Fluctuations in respiratory drive (in stage 1&2)
Non-chemical respiratory inputs are minimised.
Breathing regulated by metabolic respiratory control (in deeper stages, stable)
VE and slight PaCO2
REM SLEEP & BREATHING
Irregular respiratory drive
Ventilatory response to chemical and mechanical stimuli may be transiently reduced or abolished
Short periods of (central) apnoea occur
Intercostal and accessory muscle activity
Generalised inhibition of skeletal muscle tone (including pharyngeal muscles)
disturbances of respiratory structure or function
-intercostal and accessory muscle function activity ( imp in those with structurally small oropharynx)
•principally pharyngeal dilators/stabilisers
-genioglossus is predominantly an inspiratory phasic muscle
-tensor palatonic is a tonic postural muscle
•are “respiratory” muscles (output from CNS)
•respond to standard respiratory stimuli viz CO2, O2
•respond to negative pressure via superior laryngeal nerve
Sleep and Pharyngeal Muscle
•Inspiratory phasic muscles eg genioglossus, have near normal activity during sleep
•Tonic postural muscles (tensor palatini) activity
•Upper airway resistance increases during sleep in normals (x = 3) as a result of tonic muscle relaxation snoring
•Risk factors include males gender, obesity, alcohol /sedatives
•Not necessarily benign; associated with
- CAD risk
- cerebrovascular risk
•In isolation is a poor marker for OSA (<50% of snorers suspected of OSA have AHI >10)
Not indication in itself to progress to sleep study unless other features present (eg witnessed apnoeas, hypersomnolence)
•UAW obstruction at level of tongue/palate
•Size of UAW lumen is a balance between
-tendency of pharynx to collapse during inspiration
-dilating forces (pharyngeal muscles)
Mechanisms of Obstruction.