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SGUL - Physiology 1 > Neural Control of Breathing > Flashcards

Neural Control of Breathing Flashcards

1
Q

How is breathing initiated?

A

Neural activation of respiratory muscles - this provides the movement required for ventilation.

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2
Q

What causes respiratory muscles to contract?

A

Require neural inputs/ stimulations to contract - because they are skeletal muscle

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3
Q

Which muscles are utilised in quiet inspiration ?

A

Diaphragm

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4
Q

Which muscles are utilised in forced inspiration?

A
  • Contraction of diaphragm and internal intercostal muscles
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5
Q

What is involved in quiet expiration?

A
  • Elastic recoil
  • Relaxation of the diaphragm
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6
Q

What is involved in forced expiration?

A

Elastic recoil and contraction of internal intercostal/abdominal muscles
- Relaxation of diaphragm

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7
Q

How does the central pattern generator (CPG) determine how often and hard to breathe?

A

The CPG integrates data from various neuronal inputs to regulate ventilation.

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8
Q

Give examples of signals that integrate to regulate breathing.

A
  • pH of arterial blood
  • amount of CO2 and O2 in arterial blood
  • current lung volume
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9
Q

List the two main chemoreceptors

A

CENTRAL CHEMORECEPTORS
PERIPHERAL CHEMORECEPTORS

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10
Q

Where are central chemoreceptors located?

A

Ventrolateral surface of the medulla oblongata

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11
Q

What do central chemoreceptors detect?

A

pH changes of the spinal fluid

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12
Q

What can desensitise central chemoreceptors?

A

Chronic hypoxia and increased carbon dioxide

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13
Q

Where are peripheral chemoreceptors located?

A
  • Aortic body
  • Carotid body
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14
Q

What do peripheral chemoreceptors detect?

A

AORTIC BODY - detect changes in blood O2 and CO2
CAROTID BODY - detect changes in blood O2 and CO2, and pH

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15
Q

Do peripheral chemoreceptors desensitise?

A

No

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16
Q

What is hypoxic drive?

A
  • Form of respiratory drive
  • Oxygen chemoreceptors used instead of carbon dioxide receptors to regulate the respiratory cycle
  • Increased ventilation is response to decreased levels of O2 within arterial blood
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17
Q

A swimmer dives into shallow waters. What happens? PART 1

A

HYPERVENTILATION:
- Overbreathing, either consciously or as a results of overexertion, artificially lowers carbon dioxide levels (hypocapnia).

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18
Q

A swimmer dives into shallow waters. What happens? PART 2

A

OXYGEN DROPS:
- As the breath hold begins, oxygen is metabolised and carbon dioxide levels increase.
- As the breath hold continues, the body becomes starved of oxygen.

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19
Q

A swimmer dives into shallow waters. What happens? PART 3

A

UNCONSCIOUSNESS:
- Under normal circumstances, increased carbon dioxide would trigger a breath
- CO2 levels were low upon submersion (due to hyperventilation)
- Not enough CO2 to initiate a breath, and the swimmer loses consciousness.

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20
Q

A swimmer dives into shallow waters. What happens? PART 4

A
  • Once consciousness lost, the body reacts and forces a breath.
  • Lungs to fill with water
  • Death if no immediate rescue
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21
Q

Describe what sleep apnoea is.

A

Temporary cessation of breathing during sleep.

22
Q

What are the health effects of sleep apnoea?

A
  • tiredness (poor sleep quality)
  • cardiovascular complications (due to stress and increased sympathetic nervous system tone)
  • obesity and diabetes (due to inflammation and metabolic disfunction)
23
Q

How can sleep apnoea be investigated?

A

Polysomnography

24
Q

What is obstructive sleep apnoea?

A

Blockage of the upper respiratory tract during sleep

25
Q

What physiological process causes obstructive sleep apnoea?

A

Relaxation of the genioglossus muscle

26
Q

What are the risk factors for obstructive sleep apnoea?

A
  • obesity
  • alcohol/ sedatives
  • smoking
27
Q

What is central sleep apnoea?

A

Dysfunction in the process that initiates breathing

28
Q

What are the causes of central sleep apnoea? PART 1

A

STROKE: damage to the respiratory centres in the brain
DRUGS (EG. OPIODS): suppression of neuronal activity
CENTRAL HYPOVENTILATION SYNDROME: may come about through injury/ trauma to the brain stem, or may be congenital - results in respiratory arrest during sleep

29
Q

What are the causes of central sleep apnoea? PART 2

A

NEONATES: still continuing development of the respiratory centres in the brain
ALTITUDE: eg. Cheyne-Stoke respiration

30
Q

Describe Cheyne-Stokes respiration

A

Oscillating apnoea and hyperpnoea
- Irregular pattern of breathing caused by chemoreceptor dysfunction and heart failure

31
Q

What is the steps behind Cheyne Stokes respiration? PART 1

A
  • Pathological stimulus (such as increased altitude, CR disfunction, heart failure, etc.) that results in hypercapnia and hypoxaemia.
  • To compensate, body starts hyperventilating.
  • Causes hypocapnia, and thus alkalosis.
32
Q

What is the steps behind Cheyne Stokes respiration? PART 2

A
  • Body decreases its respiratory drive, and the body will compensate with hypoventilation.
  • Causes hypercapnia and hypoxaemia, and the cycle continues.
33
Q

Where are contractile signals initiated and where does the pathway follow?

A
  • Initiated in the brain and descend via spinal tracts.
  • Signals then pass from descending upper motor neuron tracts within the spinal cord to lower motor neurons that innervate (respiratory) skeletal muscles causing them to contract.
34
Q

What are peripheral chemoreceptors activated by?

A
  • Low O2, high CO2, and low pH
  • Will signal to medullar centres to increase ventilation.
35
Q

What do stretch receptors do and where are they located?

A

Stretch receptors within the lungs that prevent damage due to over-inflation

36
Q

What do irritant receptors do and where are they located?

A

Irritant receptors within the airways that initiate cough.

37
Q

What is the level of ventilation proportional to?

A

Level of PaCO2

38
Q

What feedback response provides the predominant stimulus for respiration in healthy individuals?

A

Hypercapnic drive
- Increased ventilation in response to increased levels of CO2 within arterial blood

39
Q

When does hypoxic drive become the dominant stimulus for respiration?

A

Low PaO2 levels, or in chronically hypercapnic individuals

40
Q

Describe muscle dystrophy

A
  • Atrophy of respiratory muscles
  • Failure to generate sufficient muscular contractile force to generate the movements required to breathe.
41
Q

Describe motor neuron disease

A
  • Degradation of the motor neurons required to conduct signals from the brainstem to respiratory muscles.
42
Q

Describe spinal cord injury

A
  • Damage to the pathway required to conduct signals from the brainstem to respiratory muscles.
43
Q

How are the right balances in blood gases maintained?

A

By maintaining pressure gradients between alveoli and blood

44
Q

Why does the O2 demand increase in exercise?

A

Increased ATP production, and increased consumption of O2

45
Q

What is the formula linking ventilation, tidal volume and respiratory rate?

A

Ventilation = Tidal volume x respiratory rate

46
Q

Why do central respiratory chemoreceptors not respond to changes in [H+]?

A

H+ doesnt cross the blood brain barrier

47
Q

What happens when you fall asleep (relating to ventilation)?

A
  • decreased metabolic rate (as less respiratory demands)
  • decreased heart rate, blood pressure and cardiac output
  • decreased tidal volume, breathing frequency and minute volume
48
Q

Why is the rate of ventilation being modulated constantly?

A

Adjusted to meet the body’s changing O2 demand and for adequate expulsion of CO2

49
Q

In what circumstances does O2 demand and/or CO2 production increase?

A
  • With increased physical activity
  • During infection
50
Q

How can activation of respiratory muscles be impaired?

A
  • Damage to the pathway of electrical stimuli from the brain to the respiratory muscle can impair activation of respiratory muscles.
  • Damage to the medulla, spinal cord, motor neurones etc.
51
Q

How do central respiratory chemoreceptors indirectly monitor arterial CO2 levels?

A
  • CO2 diffuses and passes through the blood brain barrier into the cerebrospinal fluid
  • In the fluid CO2 reacts with H20 to form H2CO3 (carbonic acid) which ionises into H+
  • So the chemoreceptor detects changes in [H+] which corresponds to changes in CO2.
52
Q

How does a change in [CO2] affect central respiratory chemoreceptors?

A
  • Increase in [CO2] will form more carbonic acid which will dissociate into more [H+]
  • pH will decrease causing activation of chemoreceptors to increase
  • Increased activation of chemoreceptors will cause more stimuli to be sent to the brain stem
  • Ventilation will increase a greater amount
  • More CO2 is expelled from the body

SGUL - Physiology 1 (68 decks)

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