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RESP > Neural control of breathing > Flashcards

Neural control of breathing Flashcards

1
Q

Which muscle involved in inspiration?

A

diaphragm

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2
Q

Which muscles are involved in forced inspiration?

A

Respiratory : external intercotsals

Accessory : pectroals, sternomastoid, scalene

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3
Q

Which muscle involved in expiration?

A

elastic recoil of lung

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4
Q

Which muscles involved in forced expiration?

A

Respiratory : elastic recoil, internal intercostals

Accessory : abdominals

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5
Q

What causes respiratory muscles to contract?

A
  • Contractile signals initiated within medulla upper motor neurons
  • descend via spinal tracts
  • synapses w lower motor neurons that innervate the respiratory muscle tissue
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6
Q

What’s the basic pattern of ventilation determined by?

A

complex system of neurons within brainstem : medulla+ pons -central pattern generator (CPG) /respiratory pattern generator (RPG)

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7
Q

What innervates the diaphragm?

A

C3-5 via phrenic nerve

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8
Q

What innervates the intercostal muscles?

A

T1-12

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9
Q

Role of ventral respiratory group (VRG)?

A

expiratory output + innervation of URT (in medulla)

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10
Q

Role of dorsal respiratory group (DRG)?

A 
inspiratory output (in medulla)
receives input from chemoreceptors + sensory
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11
Q

What’s pre-Bötzinger complex?

A

cluster of interneurons in VRG (in medulla)

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12
Q

What’s the higher centre in pons?

A

pontine respiratory group (PRG)

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13
Q

Why’s breathing a subject to voluntary control + emotional states

A

inputs from higher somatic + emotional centres feed into CPG

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14
Q

Why’s it impossible to voluntarily self asphyxiate?

A

urge to breath due to excess CO2

acute hypoxaemia –>unconsciousness

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15
Q

What’s reciprocal inhibition?

A

inspiratory neuronal activation signals via interneurons to inhibit expiratory neurons

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16
Q

What initiates compensatory changes in ventilation?

A

CPG receives inputs from central + peripheral chemoreceptors

17
Q

How does the central respiratory chemoreceptors (CRC) monitor changes in PaCO2 eg increase?

A

responding to changes in pH of the CSF

  • arterial CO2 passes via BBB into CSF
  • reacts ->carbonic acid
  • H+ activates CRCs
18
Q

Why doesn’t CRC respond to blood pH directly?

A
  • increase PaCO2 decreases pH

- H+ in arterial blood cannot pass via BBB

19
Q

What’s the predominant signal regulating ventilation?

A

CRC response to PaCO2

70%

20
Q

What do peripheral chemoreceptors consist of + location?

A

type-I glomus cells in carotid +aortic bodies

21
Q

Role of peripheral chemoreceptors

A

activated by low O2, high CO2,low pH,

signal to medullar centres to increase ventilation

22
Q

Eg of CPG integrating info from other inputs

A

stretch receptors within lungs that prevent damage due to over-inflation
irritant receptors within airways that initiate cough

23
Q

Define hypercapnic drive

A

ventilation proportional to PaCO2 due to dominant CRC

24
Q

Define hypoxic drive

A

low PaO2 stimulates increased ventlation

25
Q

Define type II respiratory failure

A

COPD - chronic hypercapnia + hypoxia

26
Q

Why are CRC responses reduced when chronic hypercapnia?

A

due to homeostatic mechanisms that compensate for chronic acidification of CSF + increase CSF pH back to normal levels, even in high PaCO2

27
Q

If chronic hypercapnia how to initiate ventilation?

A

PO2

28
Q

Define sleep apnoea + durations?

A

temporary cessation of breathing during sleep
>5 episodes per hour lasting >10 s
may be as long as 90s and 160 episodes per hour

29
Q

Effects of sleep apnoea on health?

A 
Tiredness 
Cardiovascular complications (stress + ↑SNS tone)
Obesity/Diabetes (inflammation + metabolic dysfunction)
30
Q

Define obstructive sleep apnoea

A

temporary blockade of URT

31
Q

What causes obstructive sleep apnoea?

A

-Increased p on the neck =obesity, fat deposition
-Variation in facial structures= displacing genioglossus (tongue muscle) into airway
-Fluid moving legs to head + neck =recumbent position
during sleep, swelling pharyngeal tissues
-Relaxation of pharyngeal dilator muscles

32
Q

Risk factors of obstructive sleep apnea?

A
  • obesity- fat deposition/neck circumference
  • alcohol/sedatives -decrease in muscle tone
  • smoking -irritation/inflammation
33
Q

Define central sleep apnoea

A

dysfunction in CNS processes that initiate breathing

34
Q

What causes central sleep apnoea?

A
  • opioids + barbiturates = inhibiton of brainstem
  • stroke/trauma = injury to brainstem
  • central hypoventilation syndrome = congenital defects in brainstem signalling processes
  • insufficient development of respiratory centres in neonates (infantile central sleep apnoea)
  • hypocapnia = altitude, hypobaric oxygen p, Cheyne-Stokes respiration
35
Q

How to differentiate obstructive + central sleep apnoeas?

A

polysomnography -whether diaphragmatic contractions continue during apnoea

36
Q

Diff between obstructive vs central diaphragmatic contractions?

A 
Obstructive = increasing diaphragmatic effort as it tries to overcome URT blockage
Central = no diaphragm response as temporary cessation of the CNS respiratory muscle pathway that initiates breathing
37
Q

Define Cheyne-Stokes respiration

A

oscillating apnoea + hyperpnoea

38
Q

Describe Cheyne-Stokes respiration

A
  • apnoea –>hypercapnia + hypoxaemia
  • stimulate compensatory hyperventilation
  • However due to pathology (heart failure, brain injury, chemoreceptor dysfunction) –>
  • compensatory hyperventilation –>
  • hypocapnia, respiratory alkalosis
  • loss of respiratory drive
  • subsequent period of apnoea

RESP (11 decks)

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