Central control of breathing and breathlessness Flashcards

1
Q

What variables can be calculated from a volume time graph

A
  1. Minute ventilation: Tidal volume (on expiration) x frequency
  2. mean inspiratory flow: gradient
    • How rapidly diaphragm is contracting
  3. Ti/Ttotal = inspiratory duty cycle - proportion of time spend inhaling
  4. Minute ventilation: inspiratory duty cycle x mean inspiratory flow
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2
Q

What are the determinants of a tidal breath

A
  • Neural drive

- Timing

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3
Q

How does chronic bronchitis and emphysema affect minute ventilation?

A
  • groups with airways obstruction breath quicker and more shallow
  • Proportion spent on inspiration same
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4
Q

What does the metabolic breathing centre respond to?

A
  • Metabolic demands for and production if CO2
    • Determines set point
    • Monitored as PaCO2
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5
Q

How does the metabolic controller determine minute ventilation?

A

programmes mean inspiratory flow rate and inspiratory and expiratory times separetly
adjusted to maintain primarily a constant blood and tissue H+ concentration, and secondarily a constant SaO2 (but not PaO2)

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6
Q

How does central breathing signalling occur?

A
  1. Metabolic controller sends specific frequency to spinal motoneurons via phrenic nerves
  2. Diaphragm contract and chest expands
  3. Switches off inspiration and switch on expiration alternatingly
  4. Upper airway muscles also under MC control
    • dilate on inspiration and narrow on expiration to allow for smooth airflow
  5. Carotid bodies feedback chemical and mechanoreceptors in stretch, irritant receptors in lung and respiratory muscles also feedback to MC
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7
Q

Where does feedback for breathing control come from?

A
  1. Higher brain centres
  2. Mechanoreceptors in lung and upper airway
  3. Peripheral chemoreceptors in carotid bodies
  4. Central chemoreceptor on ventral medullary surface

see notes

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8
Q

How is the rate of breathing controlled neurally?

A

PreBotzinger Complex; contains network of cells (not a pacemaker) that reciprocally inhibit each other to generate rhythm; present on rostroventrolateral surface of medulla to detect cerebrospinal pH based on CO2 levels

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9
Q

At what phases of breathing do the neurons of the Pre botzinger complex depolarise?

A

Early inspiratory: initiates inspiratory flow via respiratory muscles
- May dilate pharynx, larynx, airwas
Late inspiratory: signals end of inspiration and stop start of expiration
Expiratory decrementing: stop passive expiration by adducting larynx and pharynx
Expiratory augmenting: activate expiratory muscles when ventilation inc e.g exercise
Late expiratory: signal end of expiration and onset of inspiration
- May dilate pharynx

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10
Q

What is the Hering Breuer reflex?

A

mechanoreceptors present in the bronchi and pleura detect stretch, so that upon maximal lung expansion these signal to the medulla/pons via the Vagus nerve to prevent overinflation; pneumotaxic centre of the pons inhibits apneustic centre to stop inspiration

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11
Q

What are the parts of the metabolic controller?

A
  • central part in medulla responding to H+ ion of ECF

- peripheral part at carotid bifurcation, the H+ receptors of the carotid body

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12
Q

What is the minute ventilation relationship in PaCO2 and Pa02

A
  • Body more sensitive to changes in PaCO2 and H+

- PaO2 not as tightly controlled, SaO2 is important

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13
Q

What determines the concentration of hydrogen ions?

A

[H+] = constant x PaCO2/HCO3-

Strong ion difference: [Na+ + H+] – Cl-

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14
Q

What parts of the body regulate pH?

A
  • Lung: fast

- Kidney: slow

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15
Q

What are compensatory mechanisms for acidosis?

A

Ventilatory stimulation lowers PaCO2 and H+
Renal excretion of weak (lactate and keto) acids
Renal retention of chloride to reduce strong ion difference

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16
Q

What are compensatory mechanisms for alkalosis?

A

Hypoventilation raises PaCO2 and H+

  • Renal retention of weak (lactate and keto) acids
  • Renal excretion of chloride to increase strong ion difference
17
Q

What are the types of respiratory acidosis?

A
  • Acute: hypoventilation causes PaO2 ↓, PaCO2 and H+ ↑ which stimulates metabolic centre (and carotid body) to increase minute ventilation and restore blood gas and H+ levels.
  • Chronic: ventilatory compensation may be inadequate for PaCO2 homeostasis but a) renal excretion of weak acids (lactate and keto), b) renal retention of chloride to reduce strong ion difference, returns H+ to normal, even though PaCO2 remains high and PaO2 low.
18
Q

What is the mechanisms behind respiratory alkalosis?

A

ventilation in excess of metabolic needs

19
Q

What are causes of alkalosis?

A
  • Chronic hypoxaemia
  • Excess H+ (metabolic causes)
  • Pulmonary vascular disease
  • Chronic anxiety (psychogenic)
20
Q

What are the types of breathlessness?

A
  • Tightness: difficulty in inspiring due to airway narrowing; a feeling that the chest is not expanding normally.
  • Increased work and effort: breathing at a high minute ventilation, or at a normal minute ventilation but at a high lung volume, or against an inspiratory or expiratory resistance
  • Air hunger: sensation of a powerful urge to breath, e.g a breath hold during exercise
    Mismatch between VE demand and output
21
Q

How is respiratory demand coordinated?

A

Metabolic controller sends signal to spinal motoneurons

22
Q

How is respiratory output coordinated?

A

Afferents from lung, chest wall and chemoreceptors

23
Q

Where does voluntary breath control occur?

A

motor cortex, and controls breath holding, singing, talking etc - can be overridden by involuntary

24
Q

Where does involuntary breath control occur?

A

brainstem, and adjusts ventilation rate in response to pH levels in the blood

25
Q

What are the parts of the metabolic centre?

A
  • Medulla (Muscles): primary respiratory control centre, with a ventral respiratory group to stimulate expiration and dorsal respiratory group to stimulate inspiration (also controls other reflexes)
  • Pons (VT): located under medulla to control rate of breathing, with an apneustic centre that stimulates long, deep breathing and increases tidal volume (inhibited by stretch receptors), as well as a pneumotaxic centre that inhibits inspiration by limiting phrenic nerve activity and inhibiting the apneustic centre to lower tidal volume
26
Q

What are the parts of the behavioural centre?

A
  • Motor Cortex: neural centre for voluntary respiratory control, with different regions that control different muscles
  • Hypothalamus: can override signals to increase respiratory rate for fight or flight
  • Nerves involved: phrenic nerve supplies the diaphragm (autonomic), Vagus nerve innervates diaphragm, larynx and pharynx (autonomic) and posterior thoracic nerves innervate the intercostals (somatic)
27
Q

Where are respiratory chemoreceptors found and what do they detect?

A
  • Central chemoreceptors: located on ventrolateral surface of medulla to detect CSF pH (can be desensitised by chronic hypoxia/hypercapnia)
  • Aortic chemoreceptors: detect oxygen and CO2
  • Carotid chemoreceptors: detect oxygen, pH and CO2