Neural Control of Breathing Flashcards
Describe muscle movements when inhaling and when exhaling?
Inhale: The diaphragm and external intercostals contract Exhale: There is lung recoil but also our internal intercostals and abdominals are involved.
What are accessory muscles and give examples?
Muscles with other roles that can help with ventilation. Examples: For inhalation, sternocleidomastoid and scalene muscles.
For exhaling our abdominals.
Describe the neural innervation for the muscles involved in breathing?
Starts in the medulla with our upper motor neurones. These UMN’s project down to the lower motor neurones in the spinal cord. C3-C5 innervates the diaphragm via the phrenic nerve, while T1-T12 innervates the intercostal muscles.
What are respiratory pattern generator (RPG) theories? Give examples.
They are theories on how we produce the breathing that we do. Examples include:
- Network theory
- Conditional network bursting theory
- Pacemaker theory
- Hybrid pacemaker-network model.
* *Important point: We have an oscillator for breathing and that it is very complex.
What are the 2 forms of neurones which are important in RPG?
Ventral respiratory group (VRG) which are involved with finishing inspiration and expiration.
Dorsal respiratory group (DRG) which is involved with inspiration initiation.
Both originate in the medulla oblongata.
Describe the model of interaction and function of the VRG and DRG neurones?
Starts with a nucleus in the DRG telling the UMNs to fire to cause the inspiratory LMNs to fire and initiate inspiration. The nucleus will also be signaling to another nucleus in the DRG, which then signals all the way up to the VRG and stimulates the UMNs here to cause the expiratory LMNs to fire and allow exhalation after the inspiration that has just occurred. There is communication between the two nucleui in the VRG and one of them projects down to tell the DRG that what it is doing is good and to now inhale again.
There is also inhibition from stretch receptors via the vagus nerve, which tells the DRG the lungs are full and to stop firing. Note that in normal quiet breathing, muscles are not required for expiration it is just lung recoil, so to do this the nerves in the DRG simply must switch off, only for more heavy breathing are the VRGs required.
What is the VE equation and describe 2 ways ventilation cane increased.
VE = VT x f
VT is the tidal volume (amount of air expired/inhaled during normal breathing) and f is the frequency that you breathe. VT can be increased by recruiting more muscle fibres and f can be increased by increased alternation of RPG (which increases the rate), these are the two ways which ventilation can be increased.
What is Corticol Control and Corticol override?
Control of breathing by cortical neurones completely bypasses the medulla and go all the way down to the LMNs and can tell the diaphragm and intercostals to contract. This is known as cortical override, as our conscious control of breathing can override our automatic control (allows us to hold our breath).
What would occur if a patient had a stroke in the medulla area (in terms of breathing)?
Patient wouldn’t be able to automatically breathe, you would have to consciously do it (a problem when you fall asleep, as you can only breathe consciously when awake). You can also get vice versa.
**If there was damage to C3-C5 part of the spinal cord it would cause issues with inhalation due to the diaphragm not being innervated properly anymore.
What is Ondine’s curse?
Patient is born in a state where they have to be awake to breathe. It is more properly known as congenital central hypoventilation syndrome, it can also be caused by injury.
The RPG doesn’t work properly and therefore the person relies on cortical control and must be ventilated when asleep. It is a rare condition.
What is obstructive sleep apnoea (OSA)?
*What are the risks?
Caused by the genioglossus muscle (the main muscle of the tongue) being relaxed and hence the tongue obstructs the upper airway. Therefore obstruction when sleeping. The person stops breathing and then wakes up to breathe. Snoring is caused by the tongue flapping at the back of the oropharynx.
*Accidents due to the disturbed sleep making people fatigued, strokes and myocardial infarction (may be due to increased stress).
Repeated cycles of disturbed sleep over a long period appear to be deleterious.
Risk factors of OSA?
Alcohol which causes widespread reduced muscle tone (leading to relaxed genioglossus).
Obesity due to the fat reducing the diameter of the airway and neuromuscular disease where there is poor control of muscles.
What is central sleep apnoea (CSA)?
Caused due to a lack of central control of breathing, not obstruction. It may be seen in neonates due to a poorly developed/experienced central nervous system. It could be a result of stroke that has damaged the respiratory control areas or could be a result of drugs e.g. opioids suppress respiration.
Describe the link between CSA and heart failure?
Could be that a failing heart deprives the brain of blood (i.e. brain hypoperfusion) which leads to CSA due to respiratory centres not working properly or being damaged.
Or it could be that CSA causes periods of severe hypoxaemia (due to not breathing, intaking O2) which damages the heart (cardiac hypoxia).
Where are the peripheral and central chemoreceptors located and what changes do they respond to?
Peripheral chemoreceptors in our carotid body (linked to glossopharyngeal nerve), which responds to high PaCO2, low PaO2 and acidaemia. Only the peripheral chemoreceptors can detect acidaemia.
We also have central chemoreceptors which are located on the ventral surface of the medulla. They respond to changes in CSF pH and have about 75% of control over changing ventilation.
