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Flashcards in Control of breathing Deck (59)
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1
Q

When are you aware of breathing?

A

When something goes wrong, when scuba diving, when sleeping next to a snorer

2
Q

What is dyspnoea?

A

Shortness of breath

3
Q

What are the two key tasks with the control of breathing?

A
  • Establish automatic rhythm
  • Adjust the rhythm to accommodate
     Metabolic (arterial blood gases + pH changes)
     Mechanical (postural changes – e.g. muscles of respiration could have an impact on postural changes)
     Episodic non-ventilatory behaviours e.g. speaking, sniffing, eating
4
Q

Under normal breathing conditions what is matched with O2 and CO2?

A
  • O2: rate of absorption is matched to delivery

- CO2: rate of generation is matched to removal

5
Q

What is balance in ventilation achieved by?

A
  • Changes in blood flow and oxygen delivery -> local control

- Changes in depth and rate of respiration -> central control

6
Q

What are the complexities to do with the respiratory system as opposed to the cardiovascular system?

A
  • No single pacemaker generating basic rhythm of breathing

- No single muscle devoted to the pumping of air

7
Q

In an active tissue what will there be higher levels of and what do we want to do?

A
  • because it’s active there will be more CO2 so a higher PCO2
  • we want to increase blood flow
  • we want to increase O2 delivery to that tissue
8
Q

How does CO2 lead to increased blood flow in an active tissue?

A
  • CO2 is a dilator

- higher PCO2 -> vasodilation of vessel -> blood flow increased -> increased O2 delivery -> increased CO2 removal

9
Q

What is lung perfusion and how does that help with the local control of gas transport?

A
  • lung perfusion is How well blood is flowing within the pulmonary circuit
  • An area of the lung with decreased partial pressure of oxygen will lead to vasoconstriction which will lead to decreased blood flow
  • This allows the redirection of blood to areas of higher PO2 so that that can be picked up by red blood cells
10
Q

What is alveolar ventilation and how does that help with local gas transport?

A

If we have increased PCO2 detected in alveoli it will lead to bronchodilation which will lead to increased air flow to areas of lower Pco2 which will lead to more removal of CO2

11
Q

What are the three mechanisms of local control of gas transport?

A
  1. partial pressures of oxygen and carbon dioxide in active tissue
  2. lung perfusion
  3. alveolar ventilation
12
Q

How does the central control of ventilation work?

A

Sensors (chemical and peripheral chemoreceptors and mechanoreceptors) -> Central controller (Respiratory centres in the pons and medulla) -> effectors (muscles of ventilation)

13
Q

Where are central chemoreceptors found and what do they detect?

A
  • found in medulla
  • detect:
     Change in pH
     Hypercapnia (too much CO2)
14
Q

Where are peripheral chemoreceptors found and what do they detect?

A
  • found in aortic and carotid bodies
  • detect:
     Hypoxia
     Hypercapnia
     Change in pH
15
Q

what are mechanoreceptors, what do they do and what are the different types?

A
  • they are lung receptors that respond to stretch
  • different types are:
     Rapidly adapting receptors
     Slowly adapting receptors
     C-fibres receptors
16
Q

What are the factors influencing rate and depth of breathing?

A
  • Changing body demands, e.g. exercise
  • Altitude – acute mountain sickness
  • Disease
  • Changing levels of … in arterial blood
     CO2
     H+
     O2 – only a problem when Po2 of alveolar gas and arterial blood falls below 60 mmHg
17
Q

Where are the central chemoreceptors found?

A
  • Just beneath the ventral surface of the medulla

- Close to entry of VIII & XI cranial nerves (if they were damaged it may damage the chemoreceptors)

18
Q

What are the central chemoreceptors stimulated by?

A
  • Stimulated by acidic or high Pco2 in the CSF (cerebral spinal fluid)
     Diffusion of ions across the blood brain barrier can affect acidity – CSF is only weakly buffered
     CO2 can easily pass across the blood brain barrier into the CSF as it is lipid soluble
19
Q

What effect do the central chemoreceptors have?

A

With an increase in PCO2 and H+ ions in the CSF the pH would be decreased and so the chemoreceptors would bring about increased ventilation which would lead to more removal of CO2 and so then there would be a lower PCO2 and less H+ ions in the spinal cerebral fluid

20
Q

Where are the two different types of peripheral chemoreceptors located and what nerve are each of them innervated by?

A
  • Located in carotid body at bifurcation of carotid arteries
     Innervated by carotid sinus nerve (CNS) which is innervated by glossopharyngeal
  • Located in aortic bodies above and below aortic arch
     Innervated by the vagus nerve
21
Q

What is the stimuli of peripheral chemoreceptors?

A

Decrease in Po2, increase in PCO2 and decrease in pH in arterial blood

22
Q

What happens in PO2 decreases below 60 mmHg?

A

 Central chemoreceptors switch off

 Peripheral chemoreceptors increase breathing rate

23
Q

What responds to respiratory acidosis and respiratory alkalosis?

A

Peripheral chemoreceptors

24
Q

What is respiratory acidosis?

A

 If CO2 increases (for example limited gas exchange in emphysema -> increased pCO2 (lose gas exchange surface)
 Leads to retention of CO2 increased above our expected partial pressure
 We see a shift in: (CO2 + H2 HxCO3 H+ + HCO3-) to the right due to chateliers principle:
 Therefore there are more H+ ions and so the pH drops respiratory acidosis (pH<7.35)

25
Q

What is respiratory alkalosis?

A

 If PCO2 decreases. For example, hyperventilation such as a panic attack (leads to decreased PCO2)
 We see a shift in: (CO2 + H2 HxCO3 H+ + HCO3-) to the left:
 Therefore there are less H+ ions, the pH increases (become more alkaline) respiratory alkalosis (pH>7.45)
 However after a while the person will tire themselves out and stop breathing as much so the PCO2 will return back to normal

26
Q

Where are mechanoreceptors found, what do they all respond to and what are they innervated by?

A
  • found in lung tissue and airways
  • characterised by their response to lung inflation
  • all innervated by fibres of the vagus nerve
27
Q

What are slowly adapting mechanoreceptors also called and where are they found?

A
  • Also known as bronchopulmonary stretch receptors

- Stretch receptors in the visceral pleura, bronchioles and alveoli

28
Q

What do slowly adapting mechanoreceptors do?

A
  • Linked with reflex called Hering Breuer reflex
  • Stimulated by inflation
  • Over-inflation leads to increased discharge of signals from receptors (hering-breuer reflex/ inflation reflex) -> inhibition of respiratory centres -> deflation
  • Sustained response
29
Q

What are rapidly adapting mechanoreceptors also called and where are they found?

A
  • known as Irritant receptors

- In airway epithelia (close to mucosa)

30
Q

What are rapidly adapting mechanoreceptors involved in and what do they respond to?

A
  • Involved in defence and cough reflex
  • Respond to
     Noxious gases
     Smoke dust/ cold air
31
Q

What do rapidly adapting mechanoreceptors do?

A
  • Noxious substances leads to discharge of signals from receptors which leads to bronchoconstriction and cough reflex to try and get rid of noxious substance
  • Shape the ventilatory pattern and protecting the airway
  • Initially fire rapidly but then soon decrease their firing rate
32
Q

What are C fibres mechanical receptors also known as and what are they part of?

A
  • Part of defence system

- Also known as J receptors

33
Q

Where are mechanoreceptors found?

A

Found in alveoli wall (close to capillaries) and conducting airways (bronchial mucosa)

34
Q

What do C fibres mechanoreceptors do?

A

Respond to chemical/ mechanical stimuli (e.g. histamine and oedema) -> increased discharge of signals from receptors -> bronchoconstriction (leads to rapid shallow breathing) and mucus secretion (which can also cause vessels to become constricted and limit airflow)

35
Q

Give an example of how C fibres respond to left heart failure

A

Left heart failure can cause engorgement of the pulmonary capillaries, this innervates the C-fibres receptors causing rapid shallow breathing

36
Q

What centres are there in the central control of ventilation?

A
  • respiratory centres in the pons and medulla
37
Q

What centre is found in the medulla?

A

Rhythmicity centre

38
Q

What two centres are found in the pons?

A

Pneumotaxic and Apneustic centres

39
Q

What does the rhythmicity centre do?

A
  • Controls automatic breathing
  • Interacting neurones that fire either during:
  • Inspiration (I neurons) or
  • Expiration (E neurones)
40
Q

What do the Pneumotaxic and Apneustic centres do?

A
  • Modify the firing pattern of medullary centres

- Regulate respiratory rate and depth of respiration

41
Q

What two respiratory groups are found in the respiratory centre?

A
  • Dorsal respiratory group (DRG) – I neurones inspiratory centre
  • Ventral Respiratory group (VRG) – E and I neurones Expiratory centre
42
Q

What do I neurones in the DRG do and what do E neurones in the VRG do?

A
  • ‘I’ neurones in DRG regulate the activity of phrenic nerve (regulates diaphragm)
     Allows us to set rhythm and stimulate muscles of quiet inspiration
  • ‘E’ neurones in VRG -> passive process
     Activity of E neurones inhibit I neurones leading to passive exhalation
43
Q

What does the apneustic centre do?

A

 Promotes inspiration, stimulates the I neurones

 Increased intensity of inhalation during respiratory cycle

44
Q

What does the pneumotaxic centre do?

A

 Inhibits apneustic centre

 Stops inhalation and promotes exhalation

45
Q

When are the centres in the pons needed?

A

In forced breathing

46
Q

How do central neurones determine ventilation rate?

A

by regulating tidal volume (TV) and respiratory rate (f)

- VR = TV x f

47
Q

What are the key regulators of breathing?

A

CO2 and H+

48
Q

What increases when CO2 increases?

A

ventilation rate and depth

49
Q

If there is decreased interstitial PO2 why will diffusion in gas exchange take place quicker?

A

There is a greater pressure difference

50
Q

What is alveolar ventilation also called?

A

ventilation-to-perfusion ratio or V/Q ratio

51
Q

How does the brain’s involuntary respiratory centres set and adjust the respiratory rhythm?

A

By regulating the activities of the respiratory muscles

52
Q

What leads to the voluntary control of respiration?

A
  • Action in the cerebral cortex
  • This affects the output of either the respiratory centres or motor neurones in the spinal cord that control respiratory muscles
53
Q

What happens during quiet breathing?

A
  • Activity in the DRG increases over a period of about 2 seconds stimulating the inspiratory muscles
  • After 2 seconds the DRG neurones become inactive for the next 3 seconds (inhibited by ‘E’ neurones in VRG). This allows the inspiratory muscles to relax and passive exhalation takes place
54
Q

What happens during forced breathing?

A
  • Increases in the level of activity in the DRG stimulate neurones of the VRG that activate the accessory muscles involved in inhalation
  • After each inhalation active exhalation take place as the neurones of the expiratory centre stimulate the appropriate accessory muscles
55
Q

How do CNS stimulants such as amphetamine or caffeine increase the respiratory rate?

A

They facilitate the respiratory centres

56
Q

What is hypercapnia and what is hypocapnia?

A

Hypercapnia is an increased Pco2 and hypocapnia is a decreased pCO2

57
Q

How does the Hering-Bruer reflex work during deflation?

A

The deflation reflex normally functions during forced exhalation when both the inspiratory and expiratory centres are active. The reflex inhibits the expiratory centres and stimulates the inspiratory centres when the lungs are deflating. These receptors are located in the alveolar wall near the alveolar capillary network.

58
Q

What is apnea?

A
  • a period where respiration is suspended
59
Q

How do coughing and sneezing work?

A

Coughing and sneezing both involve apnea (a period where respiration is suspended). A forceful expulsion of air is used to remove the offending stimulus. The glottis is forcibly closed while the lungs are still relatively full. The abdominal and internal intercostal muscles then contract suddenly creating pressure that blast the air out of the respiratory passageways carrying foreign particles when the glottis reopens