Control of breathing (asleep)

Question 1

What is sleep

Answer 1

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

Question 2

How do we measure electrical activity in sleep

Answer 2

Measurement with Electroencephalogram (EEG)

Question 3

Describe the electrical activity in the brain when awake

Answer 3

alpha and beta activity

Question 4

Describe the electrical activity in the different stages of sleep

Answer 4

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.

Question 5

List some neurotransmitters involved in controlling sleep

Answer 5

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

Question 6

Summarise the control of breathing normally

Answer 6

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.

Question 7

Describe the differences in EEG when asleep and when awake

Answer 7

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

Question 8

What happens to muscle activity during sleep

Answer 8

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.

Question 9

Summarise the control of breathing during sleep

Answer 9

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

Question 10

Describe the voluntary control of breathing when awake

Answer 10

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

Question 11

What are the pathways for the control of breathing during wake

Answer 11

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

Question 12

Describe reflex/autonomic breathing

Answer 12

§ 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.

Question 13

Describe the Pre-Botzinger complex

Answer 13

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

Question 14

Why is the location of the Pre-Botzinger complex important

Answer 14

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

Question 15

Why do we not know much about sleep

Answer 15

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

Question 16

Do we have cortical control of breathing during sleep

Answer 16

no

Question 17

How does sleep affect minute ventilation (l/min)

Answer 17

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

Question 18

How does sleep affect alveolar ventilation (l/min)

Answer 18

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

Question 19

How does sleep affect breathing frequency

Answer 19

15.1 15.2 (¯1) 14.9 (¯1)

Question 20

Describe changes in tidal volume during sleep

Answer 20

420 373 (¯11) 367 (¯13)

Question 21

Describe changes in oxygen saturation during sleep

Answer 21

97.3 96.5 (¯1) 96.2 (¯1)

Question 22

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

Answer 22

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.

Question 23

What happens to PaCO2 during sleep and why is this important

Answer 23

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

Question 24

Why does PaCO2 increase during sleep

Answer 24

§ 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.

Question 25

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

Answer 25

Lower increases in PCO2 with an increase in ventilation

Question 26

What is the current debate regarding sensitivity to PCO2 during sleep

Answer 26

Whether a higher or lower sensitivity is better in athletes.

BUT in patients a lower sensitivity is good

Question 27

Why is hypercapnia mandatory during sleep

Answer 27

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

Question 28

Describe central sleep apnoea

Answer 28

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

Question 29

What is meant by the apnoeic threshold

Answer 29

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

Question 30

Why do we see changes in respiratory parameters during sleep

Answer 30

§ 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.

Question 31

What is meant by apnoea

Answer 31

The cessation of breathing

Question 32

Which part of the airway is affected in obstructive sleep apnoea

Answer 32

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

Question 33

What is meant by ILP and ELP

Answer 33

ILP- pressure inside the airway

ELP- pressure pushing on the airway

Question 34

What happens in obstructive sleep apnoea

Answer 34

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

Question 35

What is key to remember about younger people

Answer 35

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

Question 36

Why do we snore

Answer 36

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

Question 37

Outline the causes of obstructive sleep apnoea

Answer 37

§ 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.

Question 38

Describe the key differences between obstructive and central sleep apnoea

Answer 38

§ 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

Question 39

Describe the cycle seen in obstructive sleep apnoea

Answer 39

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).

Question 40

What are the consequences of obstructive sleep apnoea for patients

Answer 40

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

Question 41

Describe the coneqeunces of COPD on SaO2

Answer 41

§ 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.

Question 42

Describe the impact of heart failure

Answer 42

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.

Question 43

How many people with HF have central sleep apnoea

Answer 43

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