Breathing During Sleep

Upper Airway Closure and Reopening

reopening pressures are consistently higher: less negative than closing pressure

airway reopening occurs rapidly and at a certain pressure difference

3 general mechanisms that produce apneas are

size of the upper airway (dependent on anatomic features of the bony and soft tissues)

compliance of the airway channel (dependent on the elasticity of the airway walls)

stiffer wall, harder to close

degree of neuromuscular activation (dependent on nerual control)

muscle activity keeps airway open

respiratory rhythm can lead to phasic Ý or ß in activity of upper airway muscles

chemical stimuli (CO₂ and hypoxia) can effect the amplitude of these changes
Sleep and drugs/alcohol depress the sensitivity of upper airway muscles to chemical stimulation

Factors propagating apneas over years

weight/body fat distribution

alcohol/drugs

sleep deprivation

upper airway inflammation and narrowing

metabolic factors (cortisol, insulin, growth factors)

age

Other factors

downstream pressure

upstream pressure

blood volume: Ý bv, airway closes

stickiness of airway fluid

Sleep state

waking: muscle tone high
light sleep: muscle tone low
slow-wave sleep: muscle tone low
REM sleep: muscle tone high (variations) then low

Body position

standing to supine: airway gets smaller due to gravity effects on the tissue

Circulation time and cardiac output

Sleep Apnea Syndrome

sleep apnea is the cessation of airflow through nose or mouth, lasting > 10s, during sleep

produces interrupted sleep, daytime sleepiness, and asphyxia (hypoxia and hypercapnia during sleep), leading to hypertension and perhaps other cardiovascular effects

muscle activity is reduced during these intervals leading to noise, or can collapse

apneas can be central (stop breathing, uncommon), obstructive (most common), or mixed

Heavy snorer’s disease: 2-4% of population

Respiratory control system of muscles of upper resp muscles are not working properly during sleep

Mandibles big, tonsils small, don’t drink Þ works fine

Don’t breathe well, CO₂ levels rise Þ sleep apnea

What happens in airway to produce event?

closure: several sites, Pcrit (+ Þ apneic), fall in EMG activity (hypothyroidism), airway anatomy

Due to sedatives (alcohol), Cranio-facial features (tonsils), men > women, age

failure to open: surface tension, etc.

Surfactant can ß length of apnea

Obstructive Sleep Apnea Hypopnea Syndrome (OSAHs)

site of obstruction is in the oropharynx or nasopharynx

snoring and apneas are produced by the reduction in neural drive to muscles that accompanies both non-REM and REM sleep

diagnostic criteria

daytime tiredness, sleepiness, or fatigue
loud snoring, snorts, and restlessness
>5 apneas or hypopneas per hour of sleep

Spectrum of disease severity with OSAHs

asymptomatic: observed apneas
moderate: active sleepiness- disturbed sleep
severe: disabling sleepiness and cardiopulmonary failure

so as you Ý hypoxia and sleepiness, you Ý in severity of the disease

auto accidents Ý with severity of apnea Þ how sleepy are you

negative Pcrit Þ normal

positive Pcrit Þ apneic; will collapse easily

obstructive apnea Pcrit 5 to 0
obstructive hypopnea Pcrit 0 to –5
snoring Pcrit – 5 to –10
normal Pcrit –10 to –15

OSAHs treatment classes

CPAP (continuous positive airway pressure): mechanical device applied to nose

Tracheostamy (bypass obstruction)

either Ý Pn (nasal pressure: 80% effectiveness) or ß Pcrit (surgical approaches: 50% effectiveness)

ß Pcrit: structural approach

weight loss, body position, Hyoid and mandibular repositioning, Adenotonsillar repositioning

ß Pcrit:Ý neuromuscular activity

protriptyline, direct electrical hypoglossal stimulation