RESP: Neural control of breathing

Question 1

Why must rate of ventilation be modulated?

Answer 1

To match body’s demand for O2 and production of CO2. Adequate absorption of O2 + expulsion of CO2 achieved by maintaining pressure gradients b/w alveoli + blood

Question 2

In what circumstances does O2 demand/CO2 production increase?

Answer 2

• During physical activity
  
  • Infection, injury or metabolic dysfunction

Question 3

How does breathing change to modulate ventilation?

Answer 3

As O2 consumption increases, breathing frequency increases, as does ventilation

Question 4

What does ventilation increases alongside with to increase total O2 transported?

Answer 4

Cardiac output - More blood pumped out = greater perfusion of blood at alveoli, greater V/Q coupling.

Question 5

What physiological processes initiate breathing?

Answer 5

Respiratory muscles:

• Provide movement required for ventilation
• Consist of skeletal muscle, therefore require neural inputs/stimulation to contract

Innervation:

• Motor neurones synapsing from descending spinal tracts provide the contractile signal

Question 6

Which muscles are utilised in quiet/forced inspiration/expiration?

Answer 6

Quiet breathing:

• Inspiration - Diaphragm
• Expiration - Elastic recoil

Increased/ forced ventilation:

• Inspiration
  
  • Respiratory - External intercostals
  • Accessory - Sternomastoid, Pectorals, scalene
• Expiration
  
  • Respiratory - Elastic recoil, Internal intercostals
  • Accessory - Abdominals

Question 7

What are the neuronal systems within the brainstem that generate basic breathing pattern?

Answer 7

PRG - Potine respiratory group

DRG - Dorsal respiratory group

VRG - Ventral respiratory group

Question 8

How does the CPG determine rate + depth of breathing?

Answer 8

Receives inputs from central and peripheral chemoreceptors

Inputs from higher somatic and emotional centres also feed into CPG, hence breathing subject to voluntary control

Central pattern generator consists of:

• Pons
• Medulla oblongata, which divides into:
  
  • Dorsal respiratory group - Responsible for somatic motor neurones (inspiration), acts on:
    
    • Scalene and sternocleidomastoid muscles
    • External intercostals
    • Diaphragm
  • Ventral respiratory group - Responsible for somatic motor neurones (expiration), acts on:
    
    • Internal intercostals
    • Abdominal muscles

Sensory receptors:

• Medullary chemoreceptors (detect CO2 level changes), acts directly on CPG, stimulates somatic motor neurones
• Carotid and aortic chemoreceptors (detect changes in O2 and pH levels), send impulse to afferent sensory neurones, which then send impulse to CPG stimulates somatic motor neurones

Question 9

How do central chemoreceptors respond to changes in arterial PCO2?

Answer 9

• Present in medulla
• Indirectly monitor changes in arterial CO2
• Respond to changes in H+ within CSF, though as H+ cannot cross blood brain barrier, they don’t respond directly to changes in blood pH (except via PaCO2 as CO2 can diffuses across the blood brain barrier)
• Chemoreceptors are activated when they detect high H+ levels (Low pH)

Question 10

How do peripheral chemoreceptors respond to changes in arterial O2, CO2 and pH?

Answer 10

• Peripheral chemoreceptors consist of type-I glomus cells present within carotid and aortic bodies, detect levels of O2, CO2 and pH within arterial blood
• Activated by ⬇️PaO2, ⬆️PaCO2 and acidaemia (Low pH)
• Signal to respiratory centres in medulla (via sensory nerves) to ⬆️ventilation (negative feedback)

Question 11

What is the relationship between ventilation and PaCO2?

Answer 11

Generally proportional to one another - This is hypercapnic drive and this is the predominant stimulus for respiration in humans.

Question 12

How does hypoxaemia affect ventilation?

Answer 12

Stimulates increased ventilation - Hypoxic drive

Question 13

What happens during the transition from wakefulness to sleep?

Answer 13

• ⬇️metabolic rate = ⬇️respiratory demands
• Postural changes alters mechanics of breathing
• ⬇️tidal volume, ⬇️breathing frequency, ⬇️minute volume
• ⬇️SaO2 (approx 96%), ⬆️PaCO2 (approx 7kPa)
• ⬇️Upper airway calibre

Question 14

What pathologies are associated with dysfunction in central processes that initiate breathing?

Answer 14

• Trauma - Damage to respiratory centres in brainstem
• Stroke - Ischaemia-induced brainstem tissue injury
• Drugs (opioids etc.) - Suppression of neuronal activity
• Congenital central hypoventilation syndrome
• Neonates - Incomplete development of respiratory centres prior to birth
• Altitude - Control systems unable to cope with abnormal atmospheric environment (low O2 + low CO2). e.g. Cheyne-Stokes respiration

Extent of impact can vary from mild to severe

Question 15

Describe sleep apnoea

Answer 15

Characterised by >5 episodes per hour lasting >10 seconds

It’s when breathing stops and starts during sleep, and can be due to obstructive issues, or central issues.

Durations of apnoeas may be as long as 90 seconds and frequency of episodes as high as 160 per hour

Effect on health:

• Tiredness (poor sleep quality)
• CVS complications (stress + ⬆️SNS tone)
• Obesity/ Diabetes (inflammation + metabolic dysfunction)

Question 16

What causes obstructive sleep apnoea?

Answer 16

Caused by temporary blockade of upper respiratory tract. This narrowing and obstruction can be caused by a combination of:

• Increased pressure on neck due to increased, obesity- related, fat deposition
• Individual variation in facial structures displacing the genioglossus (1 of the tongue muscles) into airway
• Fluid moving from legs to head and neck due to recumbent position adopted during sleep, swelling pharyngeal tissues

Question 17

What causes central sleep apnoea?

Answer 17

Dysfunction in CNS processes that initiate breathing, causing cessation of automated breathing during sleeping (temp or permanently), as pathways initiating breathing no longer function. Examples include:

• Inhibition to the brainstem caused by drugs such as opioids and barbiturates
• Injury to brainstem caused by stroke or trauma
• Congenital defects in brainstem signalling processes (central hypoventilation syndrome, in which individuals lack the capacity to breath whilst asleep)
• Insufficient development of relevant structures and pathways in neonates (infantile central sleep apnoea)
• Hypocapnia (and reduced ventilation) associated with altitude and hypobaric oxygen pressure

Question 18

How can you differentiate between obstructive and central sleep apnoeas?

Answer 18

Polysomnography by whether diaphragmatic contractions continue during the apnoea.

Obstructive sleep apnoeas are associated with increasing diaphragmatic effort as it tries to overcome the upper respiratory blockade.

In central sleep apnoea, the diaphragm usually fails to respond during periods of apnoea (as there’s temporary cessation of CNS-resp muscle pathway that initiates breathing)

Question 19

Describe Cheyne-Stokes respiration

Answer 19

It’s a particular abnormal breathing pattern and central sleep apnoea involving oscillating apnoea and hyperpnoea. Periods of apnoea (with resulting hypercapnia and hypoxaemia) stimulate compensatory hyperventilation. However, due to underlying pathological circumastances (e.g. heart failure, brain injury, chemoreceptor dysfunction), the hyperventilatory response overcompensates, producing hypocapnia, respiratory alkalosis and a loss of respiratory drive resulting in a subsequent period of apnoea (and the cycle begins again until it resolves or the individual wakes)