11 Control of Breathing- Asleep Flashcards
Q: What is apnoea?
A: cessation of breathing
Q: What is the apnoeic threshold?
A: the threshold over which CO2 level has to be to make sure we breathe
Q: What’s the difference between other states where you’re also not normally responsive and sleep? Example?
A: (e.g. coma) is that it is REVERSIBLE
Q: Normally, how is sleep measured? What does it show when you’re wide awake?
A: electroencephalogram (EEG)
When you’re wide awake and paying attention, there is high frequency, low voltage activity
Q: What occurs muscularly when you are asleep? (2)
A: postural muscle activity falls and ocular muscle activity falls
Q: At what stage of sleep do you dream? What does brain activity show during this? but?
A: REM sleep
looks like you’re wide awake- However, you are functionally paralysed during REM sleep (this has probably evolved to stop you acting out your dreams)
Q: Summarise the stages of sleep.
A: You go through a period of light sleep and then into Stage 4 which is deep sleep - this is what makes you feel better and restored (in between is a semi-sleep stage)
Q: When you are functionally paralysed, what can be difficult? why?
A: breathing
If a patient breathes a lot with the accessory muscles (e.g. intercostals) then they have more difficulty using these muscles as they are functionally paralysed
Q: Which 2 muscles are spared the functional paralysis?
- Eye Muscles (this is what causes the rapid eye movements)
- Diaphragm (to allow you to breathe)
Q: What does a hypogram show during a night of sleeping? (3) If you have a patient who has difficulty breathing, what is different at the start of the night compared to the end?
A: -Usually, you fall asleep very quickly and then you stay in deep sleep
- After around 90 mins, you have a period of REM sleep
- As you go through the night, the amount of deep sleep decreases and the amount of REM sleep increases
their blood gases
Q: Draw a flow diagram that stems from sleep. (ventilation etc)
A: SLEEP at top (points at 1, 2 and 4
Respiratory centres (arrows from 1 and 2 point to it) right below then clockwise... -1. respiratory muscles -2. lung inflation -3. ventilation -4. change in PCO2/PO2
Q: What is sleep used as a model for?
A: to teach how breathing is controlled
Q: What is breathing controlled by? Describe the 4 steps.
A: by the respiratory centre which sends information to the respiratory muscles
muscle activity causes -> lung inflation -> ventilation -> changes in PCO2 and PO2
Q: Explain how there are inputs to the respiratory centre directly from the respiratory muscle.
A: If you suddenly breathe in deeply - there will be stretch receptor activity coming directly from the lungs as well as the change in chemosensitivity that the deep breath causes - these two inputs influence the respiratory centre
Q: What are the 2 ways in which breathing is controlled? Name another? Why is it different?
A: - Brainstem - reflex/automatic
- Cortex - voluntary/behavioural
Emotional Control of breathing comes from the limbic system which is a separate respiratory input
override the chemosensitivity to behaviourally control your breathing
Q: What does not control breathing when you’re asleep? What controls it?
A: cortical control (no motor cortex control or limbic system control)
brainstem (reflex/automatic)
Q: If you look at the motor homunculus, which area controls voluntary breathing?
What is shown on a PET scan specific to controlling breathing? (Draw)
A: area between the shoulder and the trunk
The hot spots seen on a PET scan tell us that there are some neurons in that region that are controlling breathing
Q: Why are brainstem respiratory neurones vital? Abundance? Where?
A: keep you alive (without you’d be unable to breathe)
relatively small number of these neurones on either side of the brainstem
found on the rostral-ventral-lateral medullary surface
Q: What’s the name given to the cluster of respiratory nuclei? What do these neurones also have? where?
A: Pre-Botzinger Complex
early firing and late firing neurones
As some neurones fire and stop firing, the other neurones start firing - they reciprocally inhibit each other (when one set fires, the other doesn’t)
(we don’t know where these neurones exist in humans)
Q: Name one way in which we measure breathing in humans. What is this? How is it useful?
A: lesion deficit models: using patients who’ve had bleeds in different parts of the brain ->
diagram shows a neural pathway going from the motor cortex, through the brainstem and the spinal cord and to the respiratory muscles
We don’t know if it goes directly through the brainstem neurones or whether there is a separate pathway coming from the brainstem or whether the two pathways (voluntary and involuntary) are connected -> If we study patients with various brain lesions, we can understand more about how it is all connected
Q: What do patients with locked in syndrome have? (2)
A: bleeds high up in the brainstem
They have fully preserved sensory input but they have no motor output (except to the eye muscles)
Q: What’s the effect of sleep on blood gases? eg Oxygen?
A: During sleep you have less input from the respiratory centres and so you have less output to the respiratory muscles
As a result of this, blood gases change when you go to sleep
goes from 97.3 saturation to 96.5 (-1%) = very little change
Q: How does ventilation change when normal peopel are asleep? What won’t it affect? Carbon dioxide?
A: 10% reduction
oxygen saturation
increase
Q: How does breathing change when sleeping?
A: shallower - 350 mL rather than 500 mL
Q: What is breathing driven by when you’re awake?
A: NOT driven by your oxygen levels, it’s more driven by your carbon dioxide levels
Q: Where do most people live on the ODC? What does this allow?
A: most normal people are living on the FLAT part of the ODC
can change your breathing and hence change the partial pressure of oxygen in your blood without changing your oxygen saturation
Q: What drops during REM sleep?
A: SO2 and PaO2 drop slightly
Q: If you have lung disease and you’re living on the steep part of the ODC, what will be a challenge? why? (3) What is recommended?
A: going to sleep will be a challenge because it is going to decrease ventilation, decrease oxygen levels and increase carbon dioxide levels
To compensate, it is sometimes recommended to increase oxygen levels at night
Q: Draw the ODC.
A: PaO2 (KPa) on X and O2 saturation (5) on Y
shape is half a bump
corner is Lung disease (COPD) and after REM sleep point and Awake point
Q: How do carbon dioxide levels change when you’re asleep? Why? (2)
A: rise (CO2 has to increase when you go to sleep or else you will die)
The CO2 level required to trigger breathing when you’re awake is lower than the CO2 required to trigger breathing when you’re asleep
If CO2 didn’t increase when you go to sleep, it will not be sufficient to trigger breathing
Q: What happens in terms of carbon dioxide sensitivity when you’re asleep? why? As a result?
A: become LESS SENSITIVE TO CARBON DIOXIDE because we have less cortical input going to the respiratory centres to make us breathe
As we are less sensitive to carbon dioxide when we breathe, we allow our carbon dioxide levels to rise when we sleep
Q: Why do we think carbon dioxide sensitivity changes as we sleep?
A: because we know that sleep is important for the brain so by allowing ourselves to be less sensitive to carbon dioxide when we’re asleep, it gives us more blood gas range before we wake ourselves up
Q: What happens if we are extremely sensitive to carbon dioxide? Therefore?
A: every time there is a slight change in carbon dioxide level our body would wake us up
Therefore, it could be an adaptive system that allows us to maintain our brain in the sleeping state
Q: How does sleep apnoea affect the heart?
A: Patients with sleep apnoea generate massive pressures in the chest when they are trying to breathe which can exacerbate cardiac conditions
Q: How does heart failure affect the lungs? What is the result? (2)
A: If you have heart failure and hence the blood is not circulating properly through the lungs then you will get more pulmonary oedema
which exacerbates:
- hyperventilation
- difficulty breathing
Q: What are the classifications of sleep apnoea?
A: -obstructive
-central
Q: What occurs in obstructive sleep apnoea? How are patients throughout the day?
A: there may not be any airflow but they are still trying to breathe
These patients will be tired throughout the day because they have disrupted sleep
Q: What is central sleep apnoea also called? Why does central sleep apnoea occur? Problem?
A: Congenital Central Hypoventilation Syndrome (CCHS)
because of the chemosensitivity changing when you go to sleep
Central sleep apnoea is a chemosensitivity problem and it is very rare
Q: Draw the cycle of obstructive sleep apnoea. Describe.
A: continuous cycle of breathing and then not breathing and then breathing again (they wake up to clear their airway)
12= arousal (termination of apnoea)
2= patent airway
4= increased ventilation (induces next apnoea)
DOTTED ARROW
6= sleep
8= decreased upper airway muscle function
10= apnoea (hypoxia/ hypercapnia/ increased effort)
Patients fall asleep and they lose muscle function (particularly in the upper airway) -> lose this muscle function -> you stop breathing
don’t breathe -> oxygen levels fall + carbon dioxide levels increase
Eventually, either the hypoxia or hypercapnia will wake you up -> Waking up allows them to clear their airways and the cycle starts again
Q: What does obstructive apnoea have nothing to do with? rather?
A: nothing to do with RESPIRATORY CONTROL - the blood gases are stimulating breathing but there is a mechanical obstruction preventing breathing
Q: If you block off your nose and mouth and you try to breathe, what happens?
A: increasing the pressure in your thorax
Q: What is the structure of the upper airway? (3)
A: bit at the back of the throat is a muscular tube
At the front you have the tongue and you have the pharyngeal constrictor muscles around the back - the airway at this point is a muscular tube
You do NOT get cartilage rings until you get to the larynx
Q: What is the muscular tube at the back of your mouth good for? bad for?
A: muscular tube is distensible so it is good for swallowing but it is bad to breathe through
Q: What happens to your muscles when you’re asleep?
A: your muscles relax and this applies to the muscles at the back of your throat as well - instead of being open and rigid, the are floppy
Q: What happens if we produce negative pressure at the back of the throat when sleeping?
A: makes the floppy airway get sucked closed during inspiration
Q: What are the pressures when you’re asleep? (2) How can having a fat neck affect them? What is the difficulty?
A: there is negative intraluminal pressure (ILP) and positive extraluminal pressure (ELP) pressing down on the muscular tube
If you are FAT around the neck, then you have even more extraluminal pressure
difficulty is in trying to maintain the airway while sucking air into the lungs
Q: If someone has a recessed jaw, what is their airway like? If they are fat too?
A: already quite small
if you have a narrow tube to begin with and you start putting on fat then you’re going to have problems -> higher chance of suffering from obstructive sleep apnoea
Q: Draw an illustration of the apnoeic threshold. What has happened in this experiment? Condition?
A: REFER
you have stopped the carbon dioxide from exceeding the apnoeic threshold so when the person is asleep they are not breathing
a condition in which this happens - Central Sleep Apnoea
Q: How can you treat central sleep apnoea?
A: artificially ventilating the patients when they are asleep
Q: What occurs in a Ventilatory Sensitivity to CO2 experiment?
A: In this experiment you get people to keep breathing in their own air (You expire more carbon dioxide than you inspire)
Q: What happens if you breathe in your own air (and therefore carbon dioxide)? For a prolonged period?
A: blood carbon dioxide levels will increase and you will try to breathe more to get rid of the carbon dioxide - and by breathing more you breathe in more carbon dioxide and carbon dioxide levels continue to rise
If you keep doing this you will eventually pass our or asphyxiate
Q: How can people’s sensitivity to CO2 slopes vary? (2) Difference? But, in terms of sport?
A: Some people’s slopes are flat whilst others are steep
For people with steep slopes, if they get sick they will try to blow the carbon dioxide off whereas people with flatter slopes will retain carbon dioxide more and slip in to respiratory failure quicker
On the other hand, if you are doing elite performance sport, there is evidence to suggest that a steeper slope (hence brisk CO2 response) favours certain exercises compared to a flatter slope
