Control of breathing during sleep

Question 1

Sleep measured with

Answer 1

Electroencephalogram (EEG)

Question 2

Control of breathing diagram

slide 5, lecture 18

Answer 2

The process of sleep affects many aspects of respiratory control
Resp muscles – upper airway and pump muscles
Direct influence on respiratory control centres
Also influences blood gases and chemosensitivity

Question 3

Control of breathing during sleep

slide 6, lecture 18

Answer 3

▪ During sleep, emotional and voluntary/behavioural
control is eliminated. Only reflex/autonomic control is
dominant.
▪ NO cortical control (motor cortex/ limbic system) when in deep sleep.

Question 4

Voluntary breathing (when awake) comes from the

Answer 4

motor homunculus (located in the brain between
motor areas for the shoulder and the trunk).

Question 5

Reflex/Autonomic Control of Breathing

respiratory neurones are found? Named?

Answer 5

▪ The respiratory neurones are found on the rostralventral-lateral medullary surface.
▪ The cluster of respiratory nuclei is named the PreBotzinger Complex.
o These neurones reciprocally inhibit each other
(when one fires, the other stops) which allows
breathing to take place but if you take them out of the brainstem they will still generate rhythm, on the ventra-lateral surface of the medulla (close to the surface because sensing pH in cerebrospinal fluid)

Question 6

Change in tidal volume+ O2 saturation in sleep

Answer 6

During sleep, only reliant on brainstem cells
When you sleep, breathing goes down= hypoventilate, reduces by about 10% due to change in tidal volume (shallower but rate= same)= doesn’t change O2 saturation at sea level

Question 7

Changes in SaO2 with sleep

graph= slide 12, lecture 18

Answer 7

PaO2 reduces but saturation stays high because you’re on the flat part of the O2 dissociation curve= not usually a problem
Respiratory disease= saturation starts at a lower level= falling asleep is more dangerous because O2 levels falls

Question 8

Change in CO2 with sleep

Importance?

Answer 8

Reducing Tidal volume= PCO2 INCREASES
If it didn’t go up you wouldn’t breathe when you sleep because reduction in Tidal Volume + increase in PCO2 is the mechanism that keeps you breathing when you sleep
Need CO2 to increase above apnoeic threshold otherwise you get central sleep apnoea because switched off motor cortex+ become less sensitive to CO2

Question 9

Ventilatory sensitivity to CO2

graph depicting this (slide 14, lecture 18)

Answer 9

If you plot PCO2 against ventilation, slope= PCO2 sensitivity
Low sensitivity= more likely to retain CO2= more likely to become more hypercapnic
Less sensitive to CO2 when sleeping

Question 10

If the PaCO2 does not to raise above the apnoeic threshold during sleep

Answer 10

breathing will stop: Central Sleep Apnoea

Question 11

The influences of sleep on the upper airway which can lead to obstructive sleep apnoea are
Results in?
Relevant anatomy?
Explanation?

Answer 11

1) a reduced upper airway muscle activity during sleep,
2) extra luminal pressure (ELP) (amount of pressure pushing down on the outside of the airway) and negative intra luminal pressure (ILP) (amount of pressure inside airway)
Results in occlusion of the phalangeal airway during sleep called: Obstructive Sleep Apnoea
The part of the airway in question is above the trachea (upper airway with no cartiledge)

When you sleep you lose muscle tone so the part in the back of the throat behind the small palate becomes relaxed= generate negative pressure downstream from the relaxed airway which sucks it shut. If you add positive pressure onto the top of the airway (e.g. if there is a lot of fat on it)= collapse of airway

Question 12

Change in anatomy of someone with obstructive sleep apnoea

Answer 12

Open space behind the tongue (on epiglottis) in healthy person
Unhealthy: fat on tongue, neck+ jaw is more setback= anatomically disadvantaged

Question 13

Sign of someone with obstructive sleep apnoea

Answer 13

Snoring= turbulent airflow going over the vocal chords because the airway is narrower so its like sucking a drink out of a smaller straw (air around the sides goes slower than in the middle)

Question 14

Difference between obstructive sleep apnoea and central apnoea

Answer 14

In central apnoea= no airflow+ no effort to breath

Obstructive= no airflow+ effort to breath but equal+ opposite= not effective

Question 15

Sleeping pattern in someone with obstructive sleep apnoea diagram (slide 24, lecture 18)

Answer 15

Patients fall asleep= muscle activity reduces= stop breathing= high CO2, low O2= try breathe harder= wake up

Question 16

Disease exacerbated by sleep

Graph depicting this (slide 26, lecture 18)

Answer 16

COPD
Normally decrease in PaO2 doesn’t influence O2 saturation (unless at high altitude)
But patietns with COPD changes O2 saturation significantly= can go to respiratory failure, may need ventilation at night

Question 17

Diseases leading to increased likliehood of central sleep apnoea

Answer 17

Heart failure
because about 50% of patients with heart failure hyperventilate and therefore have a low PaCO2 (below the apnoeic threshold) which means they can experience central sleep apnoea

Heart failure= pulmonary oedema= fluid in lungs irritates receptors in lungs= hyperventilation= low CO2= don’t breathe during sleep
Already got a bad heart so central sleep apnoea= accelerates mortality