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Flashcards in Control of breathing (asleep) Deck (43)
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1
Q

What is sleep

A

Sleep on-set is usually within 5-10minutes of lights-out
Sleep cycles of 90 minutes
Rapid Eye Movement (REM) sleep, and Non-REM Sleep
Reticular activating system- low frequency and high voltage activity

2
Q

How do we measure electrical activity in sleep

A

Measurement with Electroencephalogram (EEG)

3
Q

Describe the electrical activity in the brain when awake

A

alpha and beta activity

4
Q

Describe the electrical activity in the different stages of sleep

A
Stage 1- theta activity
Stage 2- spindle and k complex
Stage 3- delta activity
Stage 4- delta activity (less frequent)
REM sleep- beta and theta activity.
5
Q

List some neurotransmitters involved in controlling sleep

A

Histamine: Activates the cortex in wakefulness
Serotonin: Prepares the brain for slow wave sleep & reduces the ‘activating system’
Noradrenaline: Stimulates and promotes wake
Acetylcholine: Activates the cortex and increases vigilance
Orexin/Hypocretin: Promotes wake, prevents sleep, stimulates metabolism and regulates appetite
Glutamate: Stimulates the nervous system and activates the cortex
GABA: Inhibits wake, and causes sleep
Adensoine: Induces sleep

6
Q

Summarise the control of breathing normally

A

Change in PCO2/PO2 is detected by respiratory centre
This communicated with the respiratory muscles to inflate the lungs and ventilate- changing the PCO2 and PO2
Cross talk between respiratory centre, respiratory muscles and inflation of the lung.

7
Q

Describe the differences in EEG when asleep and when awake

A

neurones fire at same time to produce high voltage, low frequency waves in sleep (delta activity), whereas when awake is more random so low voltage, high frequency

8
Q

What happens to muscle activity during sleep

A

functional paralysis of the postural muscles - hence if using accessory muscles (e.g. COPD) to breathe normally, then cannot use these in REM sleep
During REM, only 2 unparalysed muscles are diaphragm and eye muscles.

9
Q

Summarise the control of breathing during sleep

A

three inputs to resp centre (automatic, voluntary and emotional [limbic]), but only reflexive breathing using brainstem active during sleep

10
Q

Describe the voluntary control of breathing when awake

A

Voluntary breathing (when awake) comes from the motor homunculus (located in the brain between motor areas for the shoulder and the trunk).

11
Q

What are the pathways for the control of breathing during wake

A

voluntary is the corticospinal pathway (from the motor cortex), automatic is the bulbospinal pathway (from respiratory neurones in brainstem)

12
Q

Describe reflex/autonomic breathing

A

§ The respiratory neurones are found on the rostral-ventral-lateral medullary surface.
§ The cluster of respiratory nuclei is named the Pre-Botzinger Complex.
o These neurones reciprocally inhibit each other (when one fires, the other stops) which allows breathing to take place.

13
Q

Describe the Pre-Botzinger complex

A

Contains a network of cells (respiratory nuclei) not pacemakers.

14
Q

Why is the location of the Pre-Botzinger complex important

A

present on rostroventrolateral surface of medulla to detect cerebrospinal pH based on CO2 levels - to change ventilation accordingly

15
Q

Why do we not know much about sleep

A

It is hard to measure activity of the brain during sleep.

16
Q

Do we have cortical control of breathing during sleep

A

no

17
Q

How does sleep affect minute ventilation (l/min)

A

Awake - 6.28
Sleep- 5.67 (-10%)
REM- 5.44 (-13%)
Decreases

18
Q

How does sleep affect alveolar ventilation (l/min)

A

Awake- 4.02
Sleep- 3.38 (-16%)
REM- 3.21 (-20%)

19
Q

How does sleep affect breathing frequency

A

15.1 15.2 (¯1) 14.9 (¯1)

20
Q

Describe changes in tidal volume during sleep

A

420 373 (¯11) 367 (¯13)

21
Q

Describe changes in oxygen saturation during sleep

A

97.3 96.5 (¯1) 96.2 (¯1)

22
Q

Despite PaO2 decreasing, why does SaO2 not decrease as much, and how does this differ in patients with COPD

A

PaO2 decreases but saturation barely changes as on flat region of ODC; if have respiratory disease and normally have sats of 80%, then will have a much larger decrease in sats for same decrease in PaO2 - nocturnal respiratory failure
need to monitor respiratory gases morning and night to see what has happened.

23
Q

What happens to PaCO2 during sleep and why is this important

A

will increase when sleeping - if does not go up will not breathe and then will not wake up; vitally important that it goes up - approx 0.5kPa in health people; become less sensitive to CO2 in sleep

24
Q

Why does PaCO2 increase during sleep

A

§ CO2 levels RISE during sleep à this is necessary so that we don’t die.
o The CO2 level required to trigger breathing is lower when awake than when we are asleep.
o PaCO2 increases by 0.5kPa in healthy people.
§ There is a reduced sensitivity of central chemoreceptors to CO2 during sleep.
§ People’s sensitivity to CO2 is variable and determines why some people (elite sportsman) might have steeper slopes.
§ Apnoeic threshold – the threshold over which CO2 level has to be in order to allow us to breathe.

25
Q

What is a consequence of this reduced sensitivity to PaCO2 on a graph of ventilation vs End tidal PCO2

A

Lower increases in PCO2 with an increase in ventilation

26
Q

What is the current debate regarding sensitivity to PCO2 during sleep

A

Whether a higher or lower sensitivity is better in athletes.

BUT in patients a lower sensitivity is good

27
Q

Why is hypercapnia mandatory during sleep

A

If the PaCO2 does not to raise above the apnoeic threshold during sleep, breathing will stop: Central Sleep Apnoea

28
Q

Describe central sleep apnoea

A

if tidal volume does not drop, PaCO2 will not rise and breathing stops - central as controlled by brainstem; may be congenital (CCHS - central congenital hypoventilation syndrome/Ondine’s curse) or arise after stroke
treated by artificial ventilation

29
Q

What is meant by the apnoeic threshold

A

Apnoeic threshold – the threshold over which CO2 level has to be in order to allow us to breathe.

30
Q

Why do we see changes in respiratory parameters during sleep

A

§ During sleep, with less input from the respiratory centres, you have less output to the respiratory muscles so blood gas levels will change (as seen adjacent).
§ A rough ~10% reduction in ventilation with lower TV of ~350ml instead of 500ml.
§ Breathing when awake is more driven by CO2 levels.

31
Q

What is meant by apnoea

A

The cessation of breathing

32
Q

Which part of the airway is affected in obstructive sleep apnoea

A

The upper airway above the trachea that has no cartilage (it is just a muscular tube)

33
Q

What is meant by ILP and ELP

A

ILP- pressure inside the airway

ELP- pressure pushing on the airway

34
Q

What happens in obstructive sleep apnoea

A

Loss of muscle tone- negative pressure generated downstream from loss of tone- causing the airway to get sucked close
Positive pressure added to this (adipose tissue- extra positive pressure on the tube)- can collapse the airway

35
Q

What is key to remember about younger people

A

Their upper airways have a greater muscle tone- OSA- less common

36
Q

Why do we snore

A

Airways not fully occluded- leading to turbulent airflow- over vocal cords- snoring
sleeping on your side may stop snoring- less pressure on airway

37
Q

Outline the causes of obstructive sleep apnoea

A

§ Before the cartilage rings of the trachea, is a muscular tube.
o The muscular tube is distensible so good for swallowing.
§ When you’re asleep, the following happens:
o The muscles relax.
§ Genioglossus and Levator Palatini muscles.
o Positive extra-luminal pressure is present (gravity, adipose weight).
o Negative intra-luminal pressure is present.
§ These can predispose you to airway collapse which is also known as obstructive sleep apnoea (OSA).
§ When a breath is taken in, the uvula blocks the airway.
§ A recessed jaw can also predispose someone to OSA.

38
Q

Describe the key differences between obstructive and central sleep apnoea

A

§ In obstructive sleep apnoea, there may be no airflow but they are still TRYING to breathe so there is thoracic and abdominal effort.
§ Central Sleep Apnoea is due to changes in sensitivity of the chemoreceptors while obstructive sleep apnoea has healthy chemoreceptors.

Central: airflow, thoracic and abdominal effort stops when become apnoeic - no effort to breathe
Obstructive: airflow stops but thoracic/abdominal effort reduces and becomes less frequent - effort to breathe but ineffective - not getting anything in as the airway is blocked

39
Q

Describe the cycle seen in obstructive sleep apnoea

A
  1. Patient falls asleep and lose UA muscle function.
    a. Not to do with respiratory control, there is a mechanical obstruction.
  2. No breathing so O2 levels fall and CO2 levels rise.
  3. Eventually, either the hypoxia or hypercapnia wakes you up (and breathing against an obstruction (chemosensitivity is still normal). Patent airway and increased ventilation (inducing the next apnoea) – sleep
  4. Cycle begins again. Patients may be unaware of this (could happen once per minute).
40
Q

What are the consequences of obstructive sleep apnoea for patients

A

it can be debilliating- lose emotional intelligence when sleepy- can make more negative decisions.

41
Q

Describe the coneqeunces of COPD on SaO2

A

§ The ODC allows breathing rate to change without significant changes in O2 saturation and during REM sleep, SO2 and PaO2 drop a little more.
§ People with lung disease (COPD) however, can fall into the steep part of the ODC which produces problems with SO2. Note: in HEALTHY people, during sleep, ventilation decreases but oxygen saturation stays the same BUT CO2 levels will change.

42
Q

Describe the impact of heart failure

A

Heart failure- pulmonary oedema- this fluid ittirates receptors in the lungs- causing hyperventilation- low PCO2- below apnoeic threshold- don’t breathe- central sleep apnoea- heart already not working well, if you can’t breathe- accelerates mortality of HF.

43
Q

How many people with HF have central sleep apnoea

A

50% of patients with heart failure hyperventilate (and therefore have a LOW PaCO2 à below the apnoeic threshold).