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I've got hypertension > Lecture 18 > Flashcards

Lecture 18 Flashcards

1
Q

The Bohr effect is characterised by a right shift in the lungs BECAUSE Hb has a high affinity for oxygen at low PCO2

A

False (in the lungs, it is characterised by a left shift), true

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2
Q

Why do we need to maintain normal levels of O2 and CO2?

A

for metabolic and biochemical stability

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3
Q

What are the three basic elements of the control of breathing?

A
  • central controller
  • effectors
  • sensors
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4
Q

Describe the central controller

A

This receives information from the sensors in the periphery. It is made up of the pons, medullar and other parts of the brain and it sets the pattern of breathing and coordinates the sensors and effectors to maintain the respiratory homeostasis

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5
Q

Describe the effectors

A

These are the respiratory muscles which adjust ventilation in response to receiving information from the central controller eg. to push out CO2 by muscles

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6
Q

Describe the sensors

A

These are the chemoreceptors, lung and other receptors. They receive a variety of neural and chemical inputs from central and peripheral receptors

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7
Q

What are the three levels of respiratory control?

A
  • respiratory rhythmicity centres
  • apneustic and pneumotaxis centres
  • higher centres
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8
Q

What is the purpose of the respiratory rhythmicity centre?

A

This is to generate cycles of contraction and relaxation in the diaphragm, establishing pace and respiration. It modifies its activity in response to chemical and pressure changes

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9
Q

What are the three neurons of the respiratory rhythmicity centre?

A
  • Pre-Botzinger complex
  • Ventral respiratory group (VRG)
  • inspiratory centre of the dorsal respiratory group (DRG)
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10
Q

Where is the respiratory rhythmicity complex located?

A

This is in the mid-brain area (medulla oblongata)

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11
Q

One of the neurons of the respiratory rhythmicity complex is the dorsal respiratory group. What is the purpose of these neurons?

A

These send signals to the diaphragm and external intercostals to initiate inspiration. They have no effect on the expiratory muscles

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12
Q

One of the neurons of the respiratory rhythmicity complex is the ventral respiratory group. What is the purpose of these neurons?

A

They don’t have any function during restful breathing but if you are exercising, we need to use accessory expiratory and inspiratory muscles so the VRG signals these

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13
Q

One of the neurons of the respiratory rhythmicity complex is the pre-Botzinger complex. What is the purpose of these neurons?

A

This is the rhythm generator which control accessory inspiratory muscles and accessory expiratory muscles.

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14
Q

Any change in the level of ________, ________ or ________ will be relayed to the respiratory centres

A

O2
CO2
H+

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15
Q

What is the part of the respiratory control that is at the level of the pons?

A

The anpeustic and pneumotaxic centres

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16
Q

What is the purpose of the the anpeustic and pneumotaxic centres?

A

This adjusts the output of the respiratory rhythmicity centre

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17
Q

What is another name for the pneumotaxic centre also known as?

A

the pontine respiratory group

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18
Q

What does the anpeustic do?

A

This sends inspiratory signals to the DRG which send signals to the inspiratory muscles

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19
Q

What is the purpose of the pneumotaxic centre?

A

This inhibits the apneustic centre so it stops inspiratory signals sent by the apneustic centre (to DRG) and initiates active exhalation as you also want to push out CO2 during exercise to stop inspiration and start exhalation

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20
Q

Where are the higher centres located?

A
  • cerebral cortex
  • limbic system
  • hypothalamus
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21
Q

What is the purpose of the higher centres?

A

when you alter the activity of the pneumotaxic centre, the HC can override everything

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22
Q

What happens if there is damage above the medulla oblongata?

A

Nothing because the medulla oblongata (respiratory rhythmicity centre) takes care of everything do damage above it means we can still generate signals

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23
Q

What happens if there is damage below the medulla oblongata?

A

This has an effect as the signals can’t go to the respiratory muscles

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24
Q

What do the sensors sense the change in?

A

chemicals such as CO2, O2, H+ and HCO3-

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25
Q

What are the two types of chemoreceptors that are sensors?

A

central chemoreceptors

peripheral chemoreceptors

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26
Q

What do the central chemoreceptors (eg. those in the respiratory centre) sense changes in?

A

CO2 and H+ in response to changes in CO2

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27
Q

What do the peripheral chemoreceptors sense changes in?

A

O2 and H+ (not from CO2)

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28
Q

Where are the central chemoreceptors located?

A

they are on the ventrolateral surface of the medulla

29
Q

What are the central chemoreceptors sensitive to, and why is this?

A

They are sensitive to PCO2 by not PO2 of the blood because CO2 can diffuse quickly across the blood brain barrier

30
Q

What is the blood-brain barrier permeable to and what is it relatively impermeable to?

A

It is permeable to CO2 but relatively impermeable to H+ and HCO3-

31
Q

Explain what happens when CO2 diffuses cross the blood brain barrier in the medulla into the cerebro-spinal fluid?

A

CO2 diffuses quickly into the CSF. It combines with H2O to form carbonic acid which dissociates to form H+ and HCO3-. The H+ is sensed by the central chemoreceptor and then this sends information to the respiratory centre (DRG) which sends signals to the respiratory muscles

32
Q

Because CO2 diffuses quickly into the CSF, what does mean in terms of small changes in CO2?

A

small changes in the concentration of CO2 is immediately detected

33
Q

What is the name for increased concentration of CO2?

A

hypercapnia

34
Q

Central chemoreceptors cause ______% of the increased ventilation in response to __________

A

70

hypercapnia

35
Q

Central chemoreceptors are sensitive to the _______ of the surrounding ___________ fluid

A

pH

extracellular

36
Q

Central chemoreceptors are insensitive to ________ acidity

A

arterial

37
Q

Where are the peripheral chemoreceptors located?

A

They are quite close to the arterial baroreceptors

There are in the aortic and carotid bodies

38
Q

What stimulates the peripheral chemoreceptors?

A

arterial H+ and PO2

39
Q

What is the predominant peripheral chemreceptor?

A

carotid body

40
Q

What three things are the major stimuli for the central and peripheral chemoreceptors?

A
  1. significantly decreased PO2 (hypoxia)
  2. increased H+ concentration (metabolic acidosis)
  3. increased PCO2 (respiratory acidosis)

in the arterial blood

41
Q

What is the major stimuli for the central and peripheral chemoreceptors?

A

Central: These respond to changes in the brain extracellular fluid. They are stimulated by increased PCO2 via associated changes in the H+ concentration

Peripheral: Stimulated mainly by a decrease in PO2 and an increase in arterial H+ concentration.

42
Q

Which one of the following is NOT correct regarding the respiratory control centre?
A. It is located in the medulla.
B. Dorsal respiratory group (DRG) consists of only inspiratory
neurons and produce only inspiratory stimulus
C. Pre-Botzinger complex is the respiratory rhythm generator.
D. Sectioning the brain stem at the level of low medulla leads
to respiratory arrest.
E. Ventral respiratory group (VRG) neurons produce inspiratory
and expiratory stimulus at rest.

A

E. Ventral respiratory group (VRG) neurons produce inspiratory
and expiratory stimulus at rest.

They don’t play a role during rest, only when required

43
Q

What is the minimal ventilation?

A

How much air we are taking in at the level of the mouth or the nose.

44
Q

What is the breathing responses to hypoxia?

A

As the PO2 decreases, there is increased ventilation assuming there is no change in the CO2

45
Q

What is the normal resting level of arterial PO2?

A

100mmHg

46
Q

What can cause a decrease in the inspired PO2?

A

going up a mountain

47
Q

What could cause a decrease in the alveolar PO2?

A

a disease like fibrosis or due to a decrease in inspired PO2

48
Q

Describe the negative feedback in response to a decrease in inspired PO2?

A

This causes a decrease in alveolar PO2 and therefore a decrease in arterial PO2. This is detected by the peripheral chemoreceptors (mainly the carotid body). This increases its firing which stimulates the respiratory neurons in the medulla oblongata (DRG) to cause the increase of contractions of the respiratory muscles (diaphragm). This increases ventilation. We return the alveolar and arterial PO2 toward normal which acts as negative feedback to stop the increased firing of the peripheral chemoreceptors

49
Q

Why are we insensitive to smaller reductions in arterial partial pressure of O2?

A

There is not much change in ventilation until we drop below 60 mmHg which related to the Hb saturation. The flat top part of the Hb saturation curve gives us flexibility in delivering O2 without any problems, even if there is a small drop in O2 pressure.
This means that Hb is pretty much fully saturated so there is no point in bringing more O2 in (therefore it is insensitive to small decreases in PO2)

50
Q

Explain the acclimatisation to high altitude

A

In the short term, we increase the ventilation by sending signals to the DRG which sends signals to the respiratory muscles. In the long term, there are some chronic changes

51
Q

What are 4 chronic changes made when you acclimatise to high altitude?

A
  1. peripheral chemoreceptors which stimulate ventilation
  2. EPO secreted by the kidneys increases the erythrocyte and Hb conc in the blood
  3. increases skeletal muscle capillary density which increases the mitochondria and muscle myoglobin
  4. plasma volume decreases, resulting in an increases conc of the erythrocytes and Hb in the blood
52
Q

What are the breathing responses to hypercapnia?

A

The concentration of CO2 has an effect of pH. Small increases in CO2 have large effects on ventilation.

53
Q

What is the normal PCO2 in the arteries?

A

40mmHg

54
Q

When is the hypercapnia response commonly seen?

A

in emphysema as there is increased compliance so you have to work harder to push the CO2 out which leads to retention of CO2 leading to respiratory acidosis

55
Q

When do we see respiratory alkalosis?

A

When there is reduced CO2 in psychiatric disorders

56
Q

Explain what happens when you breathe in gas mixture containing CO2?

A

PCO2 increases which increases the alveolar PCO2 and this increases the arterial PCO2.
This increases arterial [H+] which is detected by the peripheral chemoreceptors and they increase their firing/ This makes up 30% of the response. 70% of the response comes from the increase arterial PCO2 causing an increase PCO2 in the brain extracellular fluid which leads to an increase in the [H+] of the brain ECF. This causes the central chemoreceptors to increase their firing via reflex to cause increased contractions of the respiratory muscles.
Both of these lead to increased ventilation and then there is return of alveolar and arterial PCO2 back to normal, as well as ECF PCO2 back to normal and ECF and arterial [H+] toward normal

57
Q

Describe the breathing responses to arterial acidity

A

As the plasma [H+] increases, the minimum ventilation increases

58
Q

What is the normal resting level of plasma H+?

A

40 nmol/L

59
Q

Explain the steps to restore arterial [H+] back to normal after it increases

A

There is increased arterial [H+] which causes increased firing of peripheral chemoreceptors and in reflex via medullary neurons, increases contractions of theses muscles. This increases ventilation which decreases alveolar PCO2. This decreases arterial PCO2 and restores [H+] back to normal

60
Q

How is ventilation controlled during exercise?

A

During exercise, we are consuming more O2 and producing more venous CO2. This increases [H+] which is sensed by the central and peripheral chemoreceptors. They send signals to the respiratory muscles to increase ventilation to bring in more O2 and push out more CO2.

61
Q

The major stimuli for the increased ventilation at moderate exercise is not only due to increased ______ production. Explain this

A

CO2
Exercising muscles produce more CO2 which increases only venous PCO2 and not arterial PCO2. This is because
a. the level of arterial PCO2 is determined by alveolar PCO2
b. alveolar pCO2 is determined by the ratio of CO2 production to alveolar ventilation.
As the alveolar ventilation also increases in exact proportion to the CO2, there is no change in the arterial PCO2

62
Q

What happens to the arterial PCO2 during exercise?

A

The ventilation increases as you do exercise which means that you are pushing out more CO2 than you are producing so there is less CO2 in the arteries

63
Q

What happens to the venous PCO2 during exercise?

A

It increases but this has no effect on our breathing as CO2 is pushed to the lungs so there is no effect on vetilation

64
Q

What is the equation for the alveolar PCO2?

A

CO2 production/alveolar ventilation

65
Q

What happens to the minute ventilation (in L/min) when we go from rest to maximal exercise?

A

It increases as we consume more oxygen

66
Q

What happens to the arterial PO2 when we go from rest to maximal exercise?

A

It remains constant because you are consuming and producing more oxygen

67
Q

What happens to arterial [H+] when we go from rest to maximal exercise?

A

it increases due to the production of lactic acid which decreases the pH

68
Q

As well as increasing ventilation due to increased Co2 production, what are four things that also increase ventilation?

A
  • increased temperature
  • increased plasma epinephrine and potassium concentrations
  • motor centre (higher centres)
  • mechanoreceptors in skeletal muscles sensing changes and sending them to the respiratory centre to stimulate ventilation

I've got hypertension (47 decks)

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