Control of Ventilation Flashcards
Which specific nerve stimulates the muscles required for inspiration?
Phrenic nerves
C3-5
Which specific nerve stimulates the muscles required for expiration?
Intercostal nerves
Which type of nerve control ventilation on inspiration?
Somatic motor
What will happen to the heart if its nerve supply were to be cut off?
Would the lungs have the same effect?
It would continue to pump as it has its own intrinsic rhythm.
No, lungs would cease to breathe without nerve supply (i.e. spinal cord severed above C3-5)
Where is the actions of ventilation controlled from?
ill defined respiratory centres in the pons and medulla (brain stem).
What do the DRG and VRG do?
They co-ordinate the firing of the smooth repetitive cyclic activation of neurons responsible for respiratory cycle.
What does the DRG control?
Which nerves does it utilise?
Muscles for inspiration via .the phrenic and intercostal nerves.
What does the VRG control?
Muscles for expiration (some inspiration), tongue, pharynx and larynx muscles.
What is the main function of the VRG, particularly on expiration?
It maintains tone and patency of upper airways, therefore very important during the expiratory phase even during passive expiration as it maintains tone of pharynx, larynx and tongue muscles.
How can emotions have an effect on respiratory rate?
Limbic system is connected to the respiratory system.
Which part of the brain has the ‘final say’ when it comes to ventilation?
The brain stem (pons and medulla)
It’s stimulation can be overridden by voluntary signals from the higher brain centres but not completely (e.g. you cant hold your breath until you die).
What is the purpose of stretch receptors in the thoracic wall?
They are essentially a safety mechanism.
Stretch receptors in the thoracic wall detect stretch at full inspiration (i.e. at threshold) and respond by creating a reflex inhibition of expiration to prevent over-inflation of the alveoli (i.e. prevents rupture).
How does chemical composition of the blood affect respiratory rate?
Chemical chemoreceptors detect changes and subconsciously alter ventilation.
There are central and peripheral chemoreceptors.
Where are central chemoreceptors located?
Medulla
What is meant by the central chemoreceptors respond ‘indirectly’ to changes in CO2?
Central chemoreceptors respond directly to changes in H+ in the CSF, however H+ ions are unable to cross the blood brain barrier.
CO2 (a gas) is able to cross the blood-brain barrier and when it does, it creates more bicarbonate and H+ ions in the CSF. It is these H+ ions that bind to chemoreceptors.
What is the main thing dictating our rate and depth of breathing (essentially our ventilation)?
PaCO2 (not pH, not PaO2)
How does the central chemoreceptors respond to an increase in PaCO2 (i.e. hypercapnea)?
Increased PaCO2 Increased CO2 in CSF Increased H+ in CSF H+ binds to chemoreceptors Causes reflex stimulation of ventilation Hyperventilation kicks in to bring down CO2 levels to normal values.
When would the central chemoreceptors cause reflex inhibition of ventilation?
When CO2 levels fall
Hypoventilation would bring values back to normal.
When you hold your breath for a period of time, what is causing the forced sensation to want to inspire more air?
It is the build up of CO2
In free diving, why is it dangerous to hyperventilate before the dive in order to blow of CO2 levels?
Hyperventilating before going under water to blow of CO2 levels means they can hold their breath for longer as they lose that drive to breathe.
This can be quite dangerous if your O2 levels fall before you feel the drive to breathe again then you lose consciousness under water and drown.
10% increase in PaCO2 leads to a _____% increase in ventilation.
CO2 is extremely ______ to cells.
100%
toxic
What is meant by ‘Hypoxic drive’?
Ventilation is driven by hypoxia, by a fall in O2 rather than an increase in CO2 (which would be by central chemoreceptors).
Why do many people suffering from chronic lung disease rely more on their peripheral chemoreceptors as opposed to their central chemoreceptors?
Because they become desensitised to high levels of CO2 in the body and their central chemoreceptors are less efficient.
Their ventilation is driven by their peripheral chemoreceptors which detect changes in PaO2.
Where are peripheral chemoreceptors found?
Carotid and aortic bodies
What do peripheral chemoreceptors detect?
Mainly, they detect changes in the PaO2, but they also detect changes in pH (H+ ions).
What is different about peripheral and central chemoreceptors in terms of H+ ions and how they interact with receptors?
Only peripheral receptors bind to H+ ions in the plasma, central chemoreceptors can only bind to H+ ions in the CSF as they are unable to cross the blood-brain barrier.
Unlike central chemoreceptors, peripheral chemoreceptors can respond to [H+] ions generated in any metabolic process e.g. lactic acidosis, i.e. any H+ in plasma.
How do peripheral chemoreceptors control ventilation?
Detect changes in O2 H+ binds to chemoreceptor (When O2 is low), K channel closes Cell depolarises Dopamine released Action potential fired Signal to begin hyperventilation
Why are peripheral chemoreceptors less sensitive compared to central chemoreceptors?
It is based on the Hb/O2 binding curve.
There has to be a significant change in PaO2 to invoke the peripheral chemoreceptor to alter ventilation (this is because large changes in PaO2 cause very little change in Hb saturation).
On the other hand, the body is not very tolerable to changes in CO2, a small change would cause a much greater change in Hb binding capacity. Therefore, the central chemoreceptors respond rapidly to changes in CO2.
At what point do peripheral chemoreceptors begin to activate?
When PaO2 falls below 60mm Hg (around 3000m altitude).
What will happen to respiration rate in an anaemic patient with a blood oxygen content half the normal value?
It will increase
It will decrease
It will stay the same
It will stay the same
PaCO2 hasn’t changed which is our primary drive for ventilation (i.e. central chemoreceptors), and we know that the PaO2 in anaemic persons is normal (it is RBC count or binding capacity that affects the total blood O2 content, not the PaO2), there is no problem with ventilation or diffusion so the amount of O2 in solution in the plasma is normal i.e. the PaO2. The amount of O2 in solution in plasma determines the PaO2, if this is normal then the peripheral chemoreceptors think O2 is normal and will not do anything about it, therefore no change in ventilation/respiratory rate.
What is meant by peripheral chemoreceptors responding to PaO2 and not oxygen content.
This means that they only respond to the arterial partial pressure of oxygen, that is the partial pressure of oxygen in solution in the plasma (which would be about 2% of total O2 content).
Total oxygen content includes the O2 bound to Hb in RBC (around 98%), this does not influence the peripheral chemoreceptors.
Peripheral chemoreceptors can also detect changes in pH i.e. H+ in the plasma.
What would be the homeostatic response to a fall in pH (H+ increases)?
Stimulation of ventilation, i.e. hyperventilation
pH decreases
H+ increases
CO2 increases
Hyperventilation decreases CO2
Peripheral chemoreceptors can also detect changes in pH i.e. H+ in the plasma.
What would be the homeostatic response to a rise in pH (H+ decreases)?
Inhibition of ventilation, i.e. hypoventilation
pH rises
H+ decreases
CO2 falls
Hyperventilation increases CO2 levels
Chamber 1
Normal PaO2
High PaCO2
Chamber 2
Low PaO2
No PaCO2
Which chamber is more unpleasant, and why?
Chamber 1
We are wholly programmed to get rid of PaCO2, our primary function in ventilation. Breathing in CO2 (which we don’t normally do), we affect the already small pressure gradient of carbon dioxide (which is only 6mm Hg), this then affects the partial pressure gradient which pulls plasma out of the blood.
Homeostatic mechanism = Central chemoreceptors = Hyperventilation (pulling in more CO2)
Why is it not possible to voluntarily hyperventilate?
Ventilation is reflexly inhibited by an increase in PaO2 or a decrease in PaCO2 or [H+].
Which common drugs affect the respiratory system, and how?
Barbiturates and opiods.
They depress the respiratory centre, which can be fatal.
Why is nitrous oxide, used as an anaesthetic agent, dangerous in sufferers of chronic advanced lung disease?
They have a hypoxic drive and NO blocks the action of the peripheral chemoreceptors so they cannot detect a decrease in PaO2 or an increase in PaCO2. Giving oxygen aggravates the situation.
What is the effect of most gaseous anaesthetic agents?
Most gaseous anaesthetic agents increase respiratory rate but decrease tidal volume so decrease alveolar ventilation.
