Brian Locke

Sleep Disordered Breathing

CPAP invented in 1980 (prior to that, OSA treated with tracheostomy)

Note: symptoms... Sleepiness = a nap is restful vs Fatigue = a nap is not necessarily restful vs Alertness = ability to respond quickly

Few snippets from Janet's talk

Sleep reasons for BiPAP- higher pressures, pressure intolerance, aerophagia (=no titration study, just good documentation)

Auto-anything = EPAP adjusts

CSA shouldn’t be directly treated with aCPAP

ASV, VAPS = titrating bilevel support (iPAP) Auto+ASV = both ePAP and iPAP can titrate.

ASV = contraindicated in HFrEF and Chronic hypoventilation Targets PS to achieve 90% of calculated volume

VAPs (same as PRVC): iVAPS (rested) = aVAPS = respironics Adjusted the PS to target a tidal volume or minute ventilation

##Sleep disorders

Categories

  • sleep disordered breathing
  • disorders initiation of sleep (e.g. insomnia, social))
  • disorders of duration of sleep (e.g. hypersonic)
  • disorders of movement (e.g. parasomnias)
  • circadian rhythm disorders (e.g. shift-word)

Stages of Sleep

Delta Waves aka slow wave sleep: NREM (n1-3) = restorative sleep. Generally, body tries to get there as quick as possible. Then subsequently cycles through REM sleep = memory consolidation, mood regulation.

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Anatomy

Why do we get sleep apnea?

Upper airway has to be skeletal muscle to allow swallowing / speaking, whereas lower airway is rigid. Downside to that is that it will collapse if the muscle relaxes.

Evolution to allow for speaking predisposes us to sleep apnea

(Also predisposes to aspiration - because the nasopharynx is smaller and less direct pathway to airway = more goes through mouth and epiglottis is way far in the back)

Things that enlarge this tissue = tongue fat.

Will lead to collapse => either snoring or obstructive apnea

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Equipment

Measure apneas and hypopnea with a thermistor (measure temperature - often labeled airflow) and/or pressure transducer. Measure respiratory effort by a belt. Can also measure this with an esophageal pressure tracing, though this is less commonly done due to invasiveness.

  • Apnea = cessation of flow (more than 90% drop) for at least 10 seconds- don't need an arousal or drop in saturation, necessarily

  • Hypopnea = reduction in amount of flow (30%+) and either desaturation (3-4%) OR arousal event. Keep in mind, there will be a circulatory lag (3-4 seconds) before the drop.

  • RERA = drop in the pressure signal followed by an arousal, but no drop in saturation. RDI (instead of AHI) summarizes this. Medicare does not recognize it.

Of note: in a HST where we don't the neurologic correlate of sleep (no EEG surrogate) so you don't know the time denominator precisely. REI = summarizes the events over the total time.

####Subcategorization

Obstructive = if there is activity in the belt channel, indicating respiratory efforts (= discordant with the flow channel). Only way that the body has to abort is by waking up and increasing respiratory tone = an arousal

Central = no activity in the belt channel, indicating lack of respiratory effort. Caused by a change in respiratory drive. Can be due to high altitude, opiates, Cheyne-stokes (cycle length corresponds to circulation cycle time).

Respiratory Drive

Sleep unmasks an apnea threshold where if your CO2 drops below a certain level, it will cause an apnea.

Mechanisms:

When you go up in elevation => increased hypoxic drive to breath => takes a while for CO2 threshold to re-equilibrate => will lead to altitude related periodic breathing). This is reproducible in NREM sleep.

If they were to breath CO2, they would abolish the apnea.

Another mechanism = arousal will occur and change the threshold -> ??? -> leads to a central apnea.

Treatment - emergent = put someone on CPAP and this occurs via ?mechanism. [ ] look in to this. If this persists, it is called complex sleep apnea.