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PHSL232 > Lecture 18 - Control of breathing > Flashcards

Lecture 18 - Control of breathing Flashcards

1
Q

What elements are involved in the control of breathing?

A

For the control of breathing we have three basic elements, the central controller, the sensors, and the effectors.

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2
Q

What is the central controller made up of?

A

The central controller is made up of the pons, medulla, and other parts of the brain.

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3
Q

What do the central controllers do in the control of breathing?

A

Its role is to set the pattern/rhythm of breathing by coordinating sensors and effectors to maintain respiratory homeostasis

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4
Q

What do the sensors in the control of breathing consist of?

A

Our sensors are comprised of chemoreceptors, lung and other receptors

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5
Q

What do the sensors in the control of breathing do?

A

receive a variety of neural and chemical inputs from central and peripheral receptors and relays information to the central controller

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6
Q

Where are the effectors of the control of breathing located?

A

In respiratory muscles

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7
Q

What are the role of effectors in the control of breathing?

A

Adjust ventilation

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8
Q

What does the Apneustic centre do?

A

The apneustic centre fine tunes the inspiratory region going out of DRG.
fail safe, can come in and reinforce signal for breathing

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9
Q

Where is the important centre in terms of controlling respiratory system located?

A

In the medulla

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10
Q

What are our respiratory rhythmicity centres?

A

Dorsal respiratory group (DRG)
Ventral respiratory group (VRG)
Pre-Bötzinger complex

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11
Q

What is the role of the DRG?

A

The DRG is our inspiratory centre. The DRG send inspiratory signals to the diaphragm and to external intercostal muscles (only to external intercostal muscles during forced breathing).

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12
Q

What is the role of the VRG?

A

During quiet breathing the VRG does not send any signals , but during excercise and other events that require heavier breathing, the VRG sends signals to our accessory inspiratory and expiratory muscles.

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13
Q

What is the role of the Pre-Bötzinger
complex?

A

The Pre-Botzinger complex which acts as our respiratory rhythm generator (similar to pacemaker cells in heart). The Pre-Botzinger complex initiates signals and sends it to DRG to induce inspiration.

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14
Q

Relating to the control of breathing, what is found in the pons?

A

In the pons we have the apneustic and pneumotaxic centres (together call pontine respiratory group - PRG)

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15
Q

What is the role of the pneumotaxic centre?

A

The pneumotaxic centre is located above the apneustic centre and it sends inhibitory signals to it. Fine tube how much signal has to go from DRG to VRG.

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16
Q

What is the role of chemoreceptors?

A

Respond to a change in the chemical composition of blood or other fluid surrounding it

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17
Q

What chemicals in the respiratory system do the chemoreceptors respond to?

A

CO2, O2, H+ and HCO3-

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18
Q

What are our two types of chemoreceptors in the respiratory system?

A
  • Central chemoreceptors
  • Peripheral chemoreceptors
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19
Q

What does CO2 and H+ mainly act on?

A

Respiratory system

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20
Q

What receptor does O2 mainly act on? (O2 levels)

A

O2 acts mainly through peripheral chemoreceptor

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21
Q

What are the central chemoreceptors?

A

Specialized cells that are sensitive to the PCO2 but not PO2 of blood in the arteries
- Associated with VRG

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22
Q

What is the effect of CO2 in the brain and central chemoreceptors?

A

CO2 once reaching brain capillary, can easily diffuse past bbb, medulla, and enter the CSF. CO2 once in the CSF combines with water to form H2CO2 which immediately dissociates into the H+ and bicarbonate. This means increased H+ makes the CSF more acidic (drop in pH). Any small change in pH is detected by central chemoreceptors which send signals to inspiratory neurons (DRG)

23
Q

Where are the peripheral chemoreceptors located?

A

The peripheral chemoreceptors are located in the carotid bodies and aortic bodies.

24
Q

What is the role of peripheral chemoreceptors?

A

They are stimulated by any changes in PO2 or increase in H+ concentration in the blood. The carotid body plays an important predominant role of identifying any changes in O2 or H+ levels.

25
Q

What are peripheral chemoreceptors stimulated by?

A

Significantly decreased PO2 - Hypoxia
Increased H+ concentration - metabolic acidosis
Increased PCO2 - respiratory acidosis

26
Q

What are central chemoreceptors stimulated by?

A

Increased PCO2 via associated changes in H+ concentration

27
Q

What are the central chemoreceptors insensitive to?

A

Hypoxia - Oxygen no main signal as not as dissolved as CO2
Arterial acidity

28
Q

What are central chemoreceptors sensitive to?

A

Hypercapnia and hypocapnia as CO2 is easily diffused across blood brain barrier
pH of surrounding extracellular fluid due to H+ signalling

29
Q

What % does central chemoreceptors increase ventilation and why?

A

approx 70%, in response to hypercapnia (excess CO2)

30
Q

Where are the central chemoreceptors located?

A

On the ventrolateral surface of the medulla.

31
Q

How much can exercise increase alveolar ventilation (VA)?

A

20 fold

32
Q

What is the major factor for increased ventilation at moderate exercise?

A

Increased H+ ion concentration
Lactic acid increase from exercising which then increases H+ ion concentration which stimulates further ventilation.
- Not increased CO2 production

33
Q

What can cause our breathing to change? - breathing response

A

Our breathing can change in repsonse to hypoxia, hypercapnia, and arterial acidity concentration

34
Q

What is our breathing response to hypoxia?

A

Peripheral chemoreceptors detect decreased PO2
Respiratory muscle contraction increase (via medullary respiratory neurons)
Increase in ventilation until normal PO2

35
Q

Why is increased ventilation at moderate exercise is not due to increased CO2 production

A

Increased CO2 due to exercise increases only venous PCO2 and not arterial PCO2
As the alveolar ventilation also increases in exact proportion to the CO2 increase, there is no change.

36
Q

What Alveolar PCO2 determined by? (equation)

A

Alveolar PCO2 =
CO2 production/Alveolar ventilation

37
Q

What can stimulate increased ventilation?

A

Increased temperature
Increased plasma epinephrine and K+
Motor cortex
Mechanoreceptors in skeletal muscle

38
Q

Why we are insensitive to smaller reduction in arterial partial pressure of oxygen (PaO2)? - not hypoxia

A

Total oxygen transport by the blood is not reduced very much until the PaO2 falls below 60mmHg.
Increased ventilation would not result in more oxygen added to the blood until that point is reached.
- sigmoidal curve

39
Q

What is little a in cardiorespiratory physiology?

A

arterial/arteries

40
Q

What is big A in cardiorespiratory physiology?

A

Alveolar/alveoli

41
Q

What is the immediate response to PO2 decrease due to high altitude?

A

Hypoxia

42
Q

What is the long term/chronic response to lower PO2 due to high altitude?

A

Acclimatisation:
- Peripheral chemoreceptors stimulate ventilation
- EPO secretion, increase RBC, reduction plasma volume
- Increase skeletal muscle capillary density

43
Q

What is our breathing response to hypercapnia?

A

Our breathing response to hypercapnia (increase CO2) uses both central and peripheral receptors
Reflex mechanisms controlling ventilation prevent even small increase in arterial PCO2 - PaCO2 kept constant

44
Q

Where is our breathing reflex to hypercapnia commonly seen in?

A

emphysema – retention of CO2 – respiratory acidosis (increased CO2 increases H+ concentration)

45
Q

Where is our breathing reflex to hypocapnia commonly seen in?

A

Reduced CO2 – respiratory alkalosis – psychiatric disorders

46
Q

What is the % for the utilisation of peripheral or central chemoreceptors in response to hypercapnia? and why?

A

Peripheral - 30%
Central - 70%
Both change pH, more central chemoreceptor route due to favoured CO2 tranpsort

47
Q

What is the central chemoreceptor pathway in response to hypercapnia?

A

Increased PCO2 in alveoli and arteries
Increased PCO2 in brain ECF (H+)
Increased central chemoreceptor firing
Increased contraction of respiratory muscles
Increased ventilation

48
Q

What is the peripheral chemoreceptor pathway in response to hypercapnia?

A

Increased PCO2 in alveoli and arteries
Increased H+ in arteries
Increased peripheral chemoreceptor firing
Increased contraction of respiratory muscles
Increased ventilation

49
Q

How do chemoreceptors communicate with respiratory muscles?

A

Medullary respiratory neurons

50
Q

What is our breathing response to increased arterial acidity?

A

Increased production of non-CO2 acid
Increased arterial H+
Increased peripheral chemoreceptor firing
Increased respiratory muscle contractions
Increased ventilation
Decrease in PCO2
Return to normal arterial H+

51
Q

What is metabolic acidosis?

A

Increased lactic acid during exercise

52
Q

What is metabolic alkalosis?

A

Metabolic alkalosis – loss of H+ by vomiting

53
Q

What is avg pH of blood at rest?

A

7.4

54
Q

Why does our breathing response to arterial acidity only utilise peripheral chemoreceptors?

A

Arterial acidity affected by pH (H+)
H+ itself can not diffuse accross bbb (CO2 does which can then turn to pH)

PHSL232 (31 decks)

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