Control of breathing Flashcards

1
Q

What are the two types of control of breathing?

A

Involuntary (metabolic)

Voluntary (behavioural)

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2
Q

Describe involuntary control:

A

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

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3
Q

Describe voluntary control:

A

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

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4
Q

What is the role of the medulla in control of breathing?

A

Primary respiratory control centre, with a ventral respiratory group to stimulate expiration and dorsal respiratory group to stimulate inspiration (also controls other reflexes)

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5
Q

What is the role of the pons in control of breathing?

A

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

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6
Q

What is the role of the hypothalamus in control of breathing?

A

It can override signals to increase resp rate in flight or fight

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7
Q

What are the nerves involved in control of breathing?

A

Phrenic nerve supplies the diaphragm (autonomic), Vagus nerve innervates diaphragm, larynx and pharynx (autonomic) and posterior thoracic nerves innervate the intercostals (somatic)

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8
Q

What are chemoreceptors?

A

Sensory receptors that transduce chemical signals to action potentials; respiratory chemoreceptors sense pH of environment because most CO2 converted to carbonic acid so pH proportional to CO2

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9
Q

What are the three main sensory receptors used in resp?

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

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10
Q

Describe chemoreceptor negative feedback:

A

Alkalosis will result from a decreased level of CO2, suggesting hyperventilation, causing the chemoreceptors to signal the medulla to decrease ventilation rate; conversely, acidosis will result from increased CO2, increasing the rate of firing to increase ventilation rate

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11
Q

What are the contrasting response speeds of chemoreceptors?

A

Hyperperfused carotid bodies can rapidly detect change, where as perfusion of ECF bathing medulla is slow, so central responses are slower

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12
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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13
Q

Describe control of breathing whilst asleep:

A

Only reflexive breathing during brainstem occurs, using the bulbospinal pathway from the respiratory neurones of the medulla

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14
Q

What is the PreBotzinger complex?

A

A 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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15
Q

What are the changes in breathing whist asleep?

A

Voluntary control stops and minute ventilation decreases, causing hypoventilation (same rate but shallower as tidal volume decreases)

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16
Q

What are the changes in blood gases whilst asleep?

A

PaO2: decreases

SaO2: barely changes as are on the flat region of the ODC (if have normally lower sats, then much larger decrease [nocturnal respiratory failure])

PaCO2: increases when sleeping (approx 0.5kPa)

17
Q

What are the two types of sleep apnoea?

A

Central Sleep Apnoea: no effort to breathe

Obstructive Sleep Apnoea: effort to breathe but ineffective

18
Q

What is hypercapnia?

A

Abnormally high CO2 levels

mandatory for sleep breathing

19
Q

What is the Apnoeic sleep threshold?

A

PaCO2 needed for breathing to occur during sleep - if tidal volume does not decrease, then PaCO2 will not increase and will not breathe

20
Q

What is central sleep apnoea?

A

Failure of tidal volume to decrease due to stroke or central congenital hypoventilation syndrome that means PaCO2 does not increase, and no effort is made to breathe

21
Q

What are the only muscles not paralysed during sleep?

A

Diaphragm and eye muscles

22
Q

What is obstructive sleep apnoea?

A

Negative pressure generated during inhalation acts on floppy airways, can force shut rather than allow air to enter - exacerbated by excess adipose tissue because this applies external positive pressure that increases the problem

23
Q

What is the Obstructive sleep apnoeic cycle?

A

Apnoea leads to arousal and patent airway, increasing ventilation that causes sleep to restart, but decreased accessory muscle function leads to hypercapnia and return of apnoea, again woken by effort of breathing against closed airway - stops deep sleep and can be debilitating

24
Q

How might pulmonary oedema effect breathing control during sleep?

A

(Fluid in the lungs) irritates receptors that causes hyperventilation, lowering PaCO2, hence causing cessation of breathing due to central sleep apnoea; affects 50% of heart failure patients and accelerates mortality (fluid results from pulmonary hypertension 2/2 heart failure)