Control of Breathing

Question 1

Which area of the brain is responsible for autonomic breathing?

Answer 1

ponsomedullary areas

Pons and medulla

Question 2

Which area of the brain is responsible for manual control of breathing via control of the respiratory muscles?

Answer 2

Cortical area
(double check this)

Question 3

What is the role of the Pneumotaxic centre centre in control of ventilation?

Answer 3

It inhibits inspiratory phase, prevents apneusis.

Describes the breathing pattern when there is a long inspiration then a short quick expiration

Question 4

What is the role of the apneustic centre in control of ventilation?

Answer 4

Prolongs inspiration.

prevents gasping breathing

Question 5

What are the 4 main respiratory nuclei(groups of cells) that control the pattern of breathing?

Answer 5

• Dorsal respiratory group (DRG)
• Ventral respiratory group (VRG)
• Pre-Bötzinger complex (PBC) important as its thought to be the pacemaker for breathing
• Bötzinger complex (BC)

Question 6

Reminder

Answer 6

LC 21:00 turn this slide into a poster at some point.

Question 7

What is the role of the Dorsal respiratory group (DRG) in breathing control?

Answer 7

• Located within the medulla.
• Contains only inspiratory neurons that fire immediately prior to and during inspiration to the principal inspiratory muscles.
• It receives input from chemoreceptors and lung mechanoreceptors as well as higher brain centres which influence, so they can alter the rate they fire at depending on the feedback they receive.

Question 8

What is the pathway for voluntary breathing control?

Answer 8

Voluntary breathing control comes from the cortex, signals are sent down the pyramidal tracts to the respiratory muscles (e.g. intercostals, diaphragm, abdominals etc.)

Question 9

What else influences the central pattern generator for breathing?
(ponsomedullary/ pacemaker for breathing)

Answer 9

Higher centres = Temperature and emotion.

Question 10

What else influences the central pattern generator for breathing?
(ponsomedullary/ pacemaker for breathing)

Answer 10

The respiratory muscles then feedback information via other control centres such as:

The efficiency of ventilation is detected by chemoreceptors in the CNS and PNS. Which detect changed in PCO₂, PO₂, PH etc. this info is sent to the medulla (part of the central pattern generator)

Information about lung volume, muscle load and irritants is detected by lung receptors such as; Stretch, irritant, juxtapulmonary and proprioceptors. And also sent to the medulla/ central pattern generator.

Both of these alongside Higher centres (Temperature and emotion) (this influences the pons part of the CPG) influence the central pattern generator and so affects the pattern of breathing.

Question 11

Stretch receptors;

• What are they?
• Where are they found?
• What’s their role?

Answer 11

An example of mechanical receptors.
Site: Smooth muscle of the bronchial walls.
Roles; Makes inspiration shorter/shallower and delays the next inspiratory cycle.

Question 12

What is the Hering-Breuer inflation reflex?

Answer 12

When you take a deep breath in you activate all the mechanoreceptors in your bronchial walls, which stops you breathing in more, so then your respiratory muscles switch off then you can breath out.

So essentially it inhibits inspiration / stops you breathing in too much.

Question 13

What is the deflation reflex?

Answer 13

Where breathing out, squishing your lungs augments inspiration.
= so breathing out induces breathing in.

(Kind of the opposite of the Hering-Breuer inflation reflex).

Question 14

Juxtapulmonary receptors (aka “J” receptors)

• What do they cause/ their effect?
• Where are they found?
• What stimulates them?

Answer 14

Site: Alveolar/bronchial walls, close to capillaries

Cause: Apnoea or rapid shallow breathing breathing, fall in heart rate and blood pressure, laryngeal constriction, relaxation of skeletal muscles.

Stimulated by: Increased alveolar wall fluid, oedema, pulmonary congestion, microembolisms, inflammatory mediators e.g. histamine.

Their specific role is unknown. we need to know all of the above, so if still unsure do more research so its easier to remember.

Question 15

Irritant receptors.

• Where are they found?
• What’s their role?
• What are they stimulated by?

Answer 15

Site: Found throughout the airways between epithelial cells.

Role: Depends on their location;

• Receptors in trachea: lead to cough.
• Receptors in lower airways: lead to hyperpnoea also reflex bronchial and laryngeal constriction.

Stimulated by; irritant gases, smoke and dust, inflammation, rapid large inflations and deflations, pulmonary congestion.

Question 16

Why do we take a deep augmented breath every 5-20mins at rest?

Answer 16

This is as a result of irritant receptors, the purpose is these reverse the slow collapse of lungs in quiet breathing, so restore you to normal lung volume.

Question 17

Proprioceptive afferents.

• Where are they found?
• What are they stimulated by?
• What are they important for?

Answer 17

Site: Respiratory muscles (and others)

Stimulated by: shortening and load of respiratory muscles (but not diaphragm)

They are definitely stimulated in diseases such as; COPD asthma, fibrosis, restrictive disorders which increase the load on respiratory muscles.

They’re also important for: Coping with increased load, and achieving optimal tidal volume and frequency.

Question 18

What are the roles of pain receptors in the airways?

Answer 18

When triggered they often cause brief apnoea, followed by increased breathing.

Question 19

What is the role of receptors in trigeminal region and larynx?

Answer 19

Can causes: apnoea (slow your breathing down) or spasm, alter heart rate.

Also if nasal trigeminal nerve ending are activated they’ll make you sneeze.

Question 20

What is the role of arterial baroreceptors?

Answer 20

When they’re stimulated they inhibit breathing.

Question 21

Why do some patient find that sitting near an open window / using a hand held fan on their face helps their breathing?

Answer 21

Because the airflow over the nose/ mouth aka TRIGEMINAL REGION triggers the receptors in the trigeminal region and larynx, which fools their brain into thinking they’re breathing more than they actually are bc their activated, and will slow their breathing to a certain extent.

Question 22

Why must ventilation and metabolism be closely matched.

Answer 22

If you’re breathing too much in relation to how much CO₂ you’re producing, you’ll make yourself hypocapnic. and vice versa you’ll make yourself hypercapnic.

Question 23

Alveolar PCO₂ and ventilation at inversely proportional, so if one increases so will the other.

But when alveolar PCO₂ goes above 11kPa (extremely hypercapnic) this changes, but how does it change and why?

Answer 23

It has a depressant effect on the brain, so you breath less as your brain is going to sleep (not a good thing btw).

This decreases ventilation rate, so its no longer inversely proportional.

Question 24

Alveolar PCO₂ and ventilation at inversely proportional, so if one increases so will the other.

But when alveolar PCO₂ goes below 5 kPa (extremely hypocapnic) this changes, but how and why does it change?

Answer 24

The ventilation rate plateaus which is good bc otherwise your ventilation rate would drop to 0.

So this happens because it stops you from dying.

Question 25

What is the effect of a high PH on ventilation rate, and why?

Answer 25

Causes metabolic alkalosis, so at any given PCO₂ your ventilation rate is lower than normal, which is beneficial as you’re breathing less you’re accumulating PCO₂ which increases the acidity helps restore PH.

Question 26

What is the effect of a low PH on ventilation rate and why?

Answer 26

Causes metabolic acidosis, so at any given PCO₂ you’re breathing more than normal which is beneficial as you’re expelling more CO₂ than you’re producing this helps restore PH to normal.

Question 27

What is the effect of low arterial PO₂ on ventilation?

Answer 27

Normally we operate around 12-16 PO₂ kPa, so when it drops below 8 PO₂ kPa = hypoxia, ventilation massively increases, until PO₂ Drops below 4 PO₂ kPa
(extreme hypoxia) there is a depression of the respiratory centre as your brain goes to sleep (NOT GOOD) because your cells are dying.

Question 28

What can effect the effect of arterial PO₂ on ventilation.

And what does this tell us about what is the principle chemoreceptor that has the biggest effect on ventilation.

Answer 28

Arterial PCO₂ as there is a synergistic relationship between hypoxia and hypercapnia.
(I.E. The combined effect is greater than the sum of the individualistic effects).

If PCO₂ is too high e.g. 6 kPa, then respiration increases even more than you’d expect if PCO₂ was normal.

So, this tells us that under normal circumstances for a healthy adult, its actually CO₂ that is the principle chemoreceptor responsible for your breathing, as if there is little change in O₂ there isn’t much of an effect on ventilation compared to the effect of changing CO₂.

Question 29

Central chemoreceptors, where are located?

Answer 29

Location of chemosensitive areas; Ventrolateral surfaces of the medulla near the exit of cranial nerves C9 &10.

(note: chemoreceptors are separate from respiratory neurones such as DRG, VRG etc)

Question 30

Where are central chemoreceptors / neurons found?

Answer 30

In between Glial cells in the brain, near CSF and a capillary.

Question 31

What is the role of the blood brain barrier in the brain?

Answer 31

It controls what goes in and out of the interstitium, regulates the chemical fluid/environment around the neurone.

Question 32

What is the pH in the interstitial fluid around the chemoreceptors governed by?

Answer 32

(The blood brain barrier is impermeable to H+ and HCO₃-, this means that those things from the blood cant influence the chemoreceptor.)

But O₂ and CO₂ can diffuse, so the interstitial pH is governed by diffusion of CO₂ from the blood and HCO₃- & H+ from CSF

Question 33

Why is it that a rise in PCO₂ in the blood decreases the pH in the interstitial fluid (IF) around the chemoreceptors?

Answer 33

When PCO₂ goes up, it diffuses in, reacts with the H₂O, and then produce H+, which makes the IF more acidic.

Question 34

What are central chemoreceptors primarily affected by?

A - Changes in arterial PCO₂
or
B - Changes in arterial pH

and why?

Answer 34

A

Bc CSF has little protein, so little buffering of pH. I.E. small change in PCO₂ = Large change in pH.

Central chemoreceptors do not respond to O₂.

80 of response to raised PCO₂ remains after removal of peripheral chemoreceptors.

Response slow, about 20 secs.