Neural Control of Breathing

Question 1

How is breathing initiated?

Answer 1

→ Neural activation of respiratory muscles which provide the movement required for ventilation

Question 2

What do respiratory muscles consist of?

Answer 2

→ Skeletal muscle

Question 3

What do respiratory muscles require to contract?

Answer 3

→Neural inputs/stimulation to contract

Question 4

What provides the contractile signal?

Answer 4

→ Innervation from motor neurons synapsing from descending spinal tracts

Question 5

Which muscles (including accessory muscles) are utilised in quiet/ forced inspiration and expiration?

Answer 5

INSPIRATION:
→quiet breathing: diaphragm

→increased/ forced ventilation: external intercostal muscles (pectorals, sternomastoid and scalene muscles as accessories)

EXPIRATION:
→quiet breathing: elastic recoil

→increased/ forced ventilation: elastic recoil and internal intercostal muscles (abdominal muscles as accessories)

Question 6

How are basic breathing patterns generated?

Answer 6

→ By neuronal systems within the brainstem

Question 7

What is the PRG?

Answer 7

→ Pontine respiratory group

→modulate response to hypercapnia, and hypoxia

Question 8

What is the DRG?

Answer 8

→ Dorsal respiratory group

→stimulates inspiratory movements.

Question 9

What is the VRG?

Answer 9

→ Ventral respiratory group

→stimulates expiratory movements.

Question 10

What are the signals that the CPG receives?

Answer 10

→ pH of arterial blood
→ Amount of CO2 and O2 in arterial blood
→Current lung volume
→ How stretched the lungs are
→ The CPG(central pattern generator (CPG) integrates data from these various neuronal inputs to regulate ventilation

Question 11

What does the CPG do with these signals?

Answer 11

→ Integrates data from these neuronal inputs to regulate ventilation

Question 12

Where are the CRC (central chemoreceptors) found?

Answer 12

→ In the medulla

Question 13

What do CRC do?

Answer 13

→ Indirectly monitors changes in arterial CO2

Question 14

Why doesn’t the CRC directly respond to changes in blood pH?

Answer 14

→ Responds to changes in H+ within the cerebrospinal fluid

→ H+ cannot cross the blood brain barrier so CRC cannot directly respond to changes in pH

Question 15

Where are peripheral chemoreceptors found?

Answer 15

→ In the aortic body and carotid

Question 16

What do peripheral chemoreceptors detect?

Answer 16

→ Changes in blood oxygen and CO2, but not pH
→ Activated by ↓PaO2, ↑PaCO2 and acidaemia
→ Signal to respiratory centres in medulla (via sensory nerves) to increase ventilation (negative feedback).

Question 17

What is the hypoxic drive?

Answer 17

→Increased ventilation in response to decreased PaO2

Question 18

What is sleep apnoea?

Answer 18

→ temporary cessation of breathing during sleep

→ Characterised by >5 episodes per hour lasting >10 seconds.

Question 19

What are 4 causes of sleep apnoea?

Answer 19

→ Stroke
→ Drugs- suppression of neuronal activity- brainstem function is inhibited
→ Central hypoventilation syndrome
→ Altitude- control systems unable to cope with abnormal atmospheric environment (i.e. low O2 and low CO2), e.g. Cheyne-Stokes respiration

Question 20

What are the 3 categories of sleep apnoea?

Answer 20

→ Central- when the brain temporarily stops sending signals to the muscles that control breathing
→ Obstructive- muscles that support the soft tissues in the upper airway relax during sleep and block the normal flow of air in and out of the nose and mouth.
→ Mixed

Question 21

What is Cheyne- stokes respiration?

Answer 21

→ Oscillating hyperpnoea and apnoea

→ Hypercapnia→ Compensatory hyperventilation→ Hypocapnia + alkalosis→ ↓respiratory drive→ Compensatory hypoventilation→
Hypoxaemia

Question 22

How does Cheyne-stokes respiration occur?

Answer 22

→ Apnoea causes compensatory hyperventilation
→ Hyperventilation overcompensates producing hypocapnia
→the hyperventilatory response overcompensates, producing hypocapnia, respiratory alkalosis and a loss of respiratory drive

Question 23

Why is it impossible to asphyxiate yourself?

Answer 23

→ Urge to breathe caused by excess CO2 will be overpowering

→ Acute hypoxaemia results in loss of consciousness ( involuntary breathing begings)

Question 24

Why is there a need to modulate the rate of ventilation?

Answer 24

→ rate of ventilation is constantly adjusted to meet the body’s demand for O2 and production of CO2

Question 25

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

Answer 25

→ Demand for O2 (and CO2 production) increases during physical activity….. → …..and during infection, injury or metabolic dysfunction. → VO2 in healthy rats < rats subjected to burns < rats subjected to burns + infection.

Question 26

How does breathing change to modulate the rate of ventilation?

Answer 26

Increases tidal volume → breathing frequency → increased minute ventilation

Question 27

How is total O2 transported increased?

Answer 27

→ Ventilation increases alongside cardiac output → increased O2 delivery achieved by increasing cardiac output, not PaO2 → A unit volume of blood can contain finite O2 so just increasing breathing does not increase O2 supply so you need to increase ventilation and cardiac output

Question 28

What happens to metabolic rate, SNS, PNS tone during sleep?

Answer 28

↓metabolic rate = ↓respiratory demands | → ↓SNS & ↑PNS tone = ↓HR, BP & CO

Question 29

What happens to tidal volume, breathing frequency, and minute volume during sleep?

Answer 29

↓tidal volume, ↓breathing frequency, ↓minute volume

Question 30

What happens to SaO2 and PaCO2 and upper airway calibre during sleep?

Answer 30

↓SaO2 (≈96%), ↑PaCO2 (≈7kPa) | ↓upper airway calibre

Question 31

What are the effects of apnoea on heath?

Answer 31

→ Tiredness (poor sleep quality) → Cardiovascular complications (stress + ↑SNS tone) → Obesity/Diabetes (inflammation + metabolic dysfunction)- feedback loop

Question 32

How does the Central Pattern Generator determine the rate & depth of breathing in hyperventilation?

Answer 32

→ increased ventilation rate will remove too much carbon dioxide from their body →chemoreceptors detect this change, →send a signal to the medulla, which signals the respiratory muscles →to decrease the ventilation rate so carbon dioxide levels and pH can return to normal levels.

Question 33

What happens to regulate breathing in someone with diarrhoea and hence acidosis?

Answer 33

→loses a lot of bicarbonate in the intestinal tract, →decreases bicarbonate levels in the plasma. →while hydrogen ion concentrations stays the same, blood pH will decrease →increase ventilation to remove more carbon dioxide to reduce the hydrogen ion concentration

Question 34

Why do respiratory muscle tissues require nervous stimulation?

Answer 34

All respiratory muscle tissues are of the skeletal type, and so require nervous stimulation in order to contract

Question 35

How are contractile signals initiated?

Answer 35

→Contractile signals are initiated within the brain | →descend via spinal tracts, which synapse with the lower motor neurons that innervate the respiratory muscle tissue

Question 36

Which types of responses provides predominant signals involved in regulating ventilation?

Answer 36

CRC response to PaCO2 provides the predominant

Question 37

Where are type-I glomus cells found?

Answer 37

→Peripheral chemoreceptors consist of type-I glomus cells present with carotid and aortic bodies, which detect levels of O2, CO2 and pH within arterial blood

Question 38

In what situations does hypoxic drive take on a greater role?

Answer 38

→individuals with severe chronic lung pathology (e.g. COPD) that are unable to ventilate respiratory structures sufficiently →results in chronic hypercapnia and hypoxia (type II respiratory failure).

Question 39

Why is central respiratory chemoreceptor responses reduced in chronic hypercapnia?

Answer 39

→due to homeostatic mechanisms that compensate for chronic acidification of the CSF and increase CSF pH back to normal levels

Question 40

Potential causes of central breathing dysfunction...

Answer 40

* Inhibition the brainstem caused by drugs such as opioids and barbiturates * Injury to the brainstem caused by stroke or trauma * Congenital defects in brainstem signalling processes (congenital central hypoventilation syndrome) * Insufficient development of the relevant structures and pathways in neonates * Hypocapnia (and reduced ventilation) associated with altitude and hypobaric oxygen pressure.

Question 41

Limbic system inputs...

Answer 41

``` Emotional stimuli (e.g. anxiety) acting through the hypothalamus to the medulla and pons ```

Question 42

What do central and peripheral chemoreceptors have in common?

Answer 42

Both central and peripheral chemoreceptors function via negative feedback.