Control of Ventilation

Question 1

Which specific nerve stimulates the muscles required for inspiration?

Answer 1

Phrenic nerves

C3-5

Question 2

Which specific nerve stimulates the muscles required for expiration?

Answer 2

Intercostal nerves

Question 3

Which type of nerve control ventilation on inspiration?

Answer 3

Somatic motor

Question 4

What will happen to the heart if its nerve supply were to be cut off?

Would the lungs have the same effect?

Answer 4

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)

Question 5

Where is the actions of ventilation controlled from?

Answer 5

ill defined respiratory centres in the pons and medulla (brain stem).

Question 6

What do the DRG and VRG do?

Answer 6

They co-ordinate the firing of the smooth repetitive cyclic activation of neurons responsible for respiratory cycle.

Question 7

What does the DRG control?

Which nerves does it utilise?

Answer 7

Muscles for inspiration via .the phrenic and intercostal nerves.

Question 8

What does the VRG control?

Answer 8

Muscles for expiration (some inspiration), tongue, pharynx and larynx muscles.

Question 9

What is the main function of the VRG, particularly on expiration?

Answer 9

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.

Question 10

How can emotions have an effect on respiratory rate?

Answer 10

Limbic system is connected to the respiratory system.

Question 11

Which part of the brain has the ‘final say’ when it comes to ventilation?

Answer 11

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).

Question 12

What is the purpose of stretch receptors in the thoracic wall?

Answer 12

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).

Question 13

How does chemical composition of the blood affect respiratory rate?

Answer 13

Chemical chemoreceptors detect changes and subconsciously alter ventilation.

There are central and peripheral chemoreceptors.

Question 14

Where are central chemoreceptors located?

Answer 14

Medulla

Question 15

What is meant by the central chemoreceptors respond ‘indirectly’ to changes in CO2?

Answer 15

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.

Question 16

What is the main thing dictating our rate and depth of breathing (essentially our ventilation)?

Answer 16

PaCO2 (not pH, not PaO2)

Question 17

How does the central chemoreceptors respond to an increase in PaCO2 (i.e. hypercapnea)?

Answer 17

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.

Question 18

When would the central chemoreceptors cause reflex inhibition of ventilation?

Answer 18

When CO2 levels fall

Hypoventilation would bring values back to normal.

Question 19

When you hold your breath for a period of time, what is causing the forced sensation to want to inspire more air?

Answer 19

It is the build up of CO2

Question 20

In free diving, why is it dangerous to hyperventilate before the dive in order to blow of CO2 levels?

Answer 20

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.

Question 21

10% increase in PaCO2 leads to a _____% increase in ventilation.

CO2 is extremely ______ to cells.

Answer 21

100%

toxic

Question 22

What is meant by ‘Hypoxic drive’?

Answer 22

Ventilation is driven by hypoxia, by a fall in O2 rather than an increase in CO2 (which would be by central chemoreceptors).

Question 23

Why do many people suffering from chronic lung disease rely more on their peripheral chemoreceptors as opposed to their central chemoreceptors?

Answer 23

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.

Question 24

Where are peripheral chemoreceptors found?

Answer 24

Carotid and aortic bodies

Question 25

What do peripheral chemoreceptors detect?

Answer 25

Mainly, they detect changes in the PaO2, but they also detect changes in pH (H+ ions).

Question 26

What is different about peripheral and central chemoreceptors in terms of H+ ions and how they interact with receptors?

Answer 26

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.

Question 27

How do peripheral chemoreceptors control ventilation?

Answer 27

``` 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 ```

Question 28

Why are peripheral chemoreceptors less sensitive compared to central chemoreceptors?

Answer 28

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.

Question 29

At what point do peripheral chemoreceptors begin to activate?

Answer 29

When PaO2 falls below 60mm Hg (around 3000m altitude).

Question 30

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

Answer 30

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.

Question 31

What is meant by peripheral chemoreceptors responding to PaO2 and not oxygen content.

Answer 31

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.

Question 32

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)?

Answer 32

Stimulation of ventilation, i.e. hyperventilation pH decreases H+ increases CO2 increases Hyperventilation decreases CO2

Question 33

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)?

Answer 33

Inhibition of ventilation, i.e. hypoventilation pH rises H+ decreases CO2 falls Hyperventilation increases CO2 levels

Question 34

Chamber 1 Normal PaO2 High PaCO2 Chamber 2 Low PaO2 No PaCO2 Which chamber is more unpleasant, and why?

Answer 34

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)

Question 35

Why is it not possible to voluntarily hyperventilate?

Answer 35

Ventilation is reflexly inhibited by an increase in PaO2 or a decrease in PaCO2 or [H+].

Question 36

Which common drugs affect the respiratory system, and how?

Answer 36

Barbiturates and opiods. They depress the respiratory centre, which can be fatal.

Question 37

Why is nitrous oxide, used as an anaesthetic agent, dangerous in sufferers of chronic advanced lung disease?

Answer 37

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.

Question 38

What is the effect of most gaseous anaesthetic agents?

Answer 38

Most gaseous anaesthetic agents increase respiratory rate but decrease tidal volume so decrease alveolar ventilation.