special situation- sleep Flashcards
what is NREM sleep?
- Stages 1-4 associated with development of large slow delta waves
- Arousal threshold increases with stage (takes stage 4-3 or 3-2)–> not necessarily awakening the person
- Implications for control for CRS
- Inactive brain in a movable body (muscle tone)-> EMG
- Deeper stages of sleep (stage 4) a lot bigger stimulus needed to wake patient
what is REM sleep?
- Paradoxical sleep as similar to awake
- Dream state
- Active brain in a paralysed body –>: atonia
- No activity on EMG
- EEG similar to one who is awake
- Lost muscle tone (EMG)
Is an active state despite being asleep
what cardiovascular effects are seen in REM?
- increase in HR and BP
- increased SNS activity
- during dreams, very much an active state but muscle tone is lost
what are those involved in non-feedback during wakefulness ?
- behaviour
- reticular formation ( muscular tone of upper airways maintained)
- brainstem aminergic
- during NREM there is a loss of wakefulness drive
feedback mechanisms involved in NREM are?
- 02, co2 and pH
- all responsible for respiratory drive during NREM sleep
what happens to breathing during sleep?
- Tv lost but fr doesn’t change
- shallower breathing
- reduced A ventilation
- fall of VE greater than fall of metabolism
- hypoventilation –> good for feedback mechanisms as co2 levels drive breathing when asleep
during NREM what provides the drive to breathe?
- co2 levels
- hypoventilation induces a fall in Pa02 and rise in paco2
- reduced co2 sensitivity (increase in set point from 5.3kpa –> 6kpa)
- reduced drive to breathe when asleep
- responses to hypoxia and hypercapnia are depressed
what is the apnoeic threshold ?
an threshold in which is c02 levels rise above this then there will be a drive to breathe
- if co2 levels drop below it then the drive to breathe is lost –> apnoea
- During this point co2 levels rise above threshold (time lag) and chemoreceptors are stimulated to increase drive of breathing again
- Time lag between actual co2 levels and chemoreceptor activation
- Is normal
- leads to unstable, periodic breathing
what is sleep apnoea?
- cessation of breathing during sleep
- needs certain length to be defined as apnoea (10s)
- fr varies nightly
- origin can be central or peripheral
what is obstructive SA?
- respiratory efforts are there but there’s no airflow
what is central SA?
- no respiratory efforts
- brain has not told the lungs to breathe (no change in pPL)
what causes OSA?
- Reticular formation activity falls during sleep
- Loss of muscle tone in airways
- Obesity risk factor (flab around neck) –> more likely to induce airway closure
- Associated with development of hypertension / strokes
- Nerve activity to diaphragm –> genioglossus muscle activity lost
- Upper airways collapse and cause obstruction
what are the physiological causes of CSA?
· Sleep-onset – removal of wakefulness drive exposes apneic threshold (change of control-> CO2)
· Post- arousal/sigh – arousal has brief return to wakefulness – hypercapnic response
Phasic REM sleep – pontogeniculo-occiptal (PGO) waves bypass medullary centres and inhibit diaphragm (inhibit inspiratory muscles)
what causes hypocapnic CSA?
- Low paco2 when awake and increased co2 sensitivity
- heart failure -> no rise in paco2 in sleep as no fall in VE
- high alt–> hyperVE induces hypocapnia
what causes hypercapnic CSA?
- hypoVE in wakefulness -> worsens in sleep leafing to a mismatch between co2 and set point with periodic breathing pattern
- CCHS
- brainstem disorders or opioid use (depresses the brainstem)
