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Year 1 - BRS > 6.15 - Control of Lung Function > Flashcards

6.15 - Control of Lung Function Flashcards

1
Q

What nuclei in the medulla oblongata and pons control breathing?

A
  • dorsal respiratory group
  • ventral respiratory group
  • apneustic centre
  • pneumotaxic centre
  • pneumonic: DIVE (dorsal inspiration ventral expiration)
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2
Q

What does the dorsal respiratory group do?

A
  • inspiratory centre
  • main ‘controller’ of inspiration
  • sets the ‘rate’
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3
Q

What does the ventral respiratory group do?

A
  • expiratory centre
  • inactive during quiet breathing
  • inhibit apneustic centre
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4
Q

What does the apneustic centre do?

A
  • associated with inspiration
  • stimulates activity in the dorsal respiratory group (DRG)
  • inhibited by pulmonary afferents
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5
Q

What does the pneumotaxic centre do?

A
  • associated with expiration - the ‘inspiratory off switch’
  • regulates depth and frequency
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6
Q

Which of the medulla oblongata nuclei inhibit/activate the others?

A
  • dorsal and ventral respiratory groups inhibit each other
  • pneumotaxic centre inhibits DRG
  • apneustic centre activates DRG
  • VRG inhibits apneustic centre
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7
Q

Explain the graph of respiratory pacemaker during quiet breathing.

A
  • APs increase in frequency (apneustic centre) until pneumotaxic centre is activated, which stops inspiration - called ramp potential patterns
  • after period of latency, apneustic centre helps program rhythm into dorsal respiratory group
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8
Q

What is the innervation of respiratory muscles like?

A
  • phrenic nerve (motor) key player in innervating diaphragm
  • vagus nerve (parasympathetic)
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9
Q

In normal circulation, what are the capillaries like in terms of gaps between the cells?

A

H2O filled gap junctions but capillaries are thought to be continuous

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10
Q

What are the capillaries like in the blood-brain barrier?

A
  • BBB has tight junctions due to nerve cells which help even more tightly pack endothelial cells together, which restricts what can cross it
  • BBB a lot less leaky
  • does not allow H+ ions through the membrane
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11
Q

How does CO2 and H2O affect our drive to breathe?

A
  • in capillary: CO2 + H2O –> H2CO3 –> H+ + HCO3-
  • the H+ and HCO3- cannot cross the lipid bilayer of endothelial cells (and therefore BBB) as they are charged, but CO2 can
  • CO2 crosses into CSF where it reacts with H2O to form carbonic acid, dissociating into H+ + HCO3-
  • the H+ interact with afferent fibres in the medulla which send signals to DRG to determine rate and rhythm of breathing
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12
Q

What are the three types of receptors in the airways that affect ventilation?

A
  • irritant receptors
  • stretch receptors
  • J receptors
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13
Q

What are irritant receptors?

A
  • afferent receptors embedded within and beneath airway epithelium
  • cough receptors - detect foreign matter and leads to cough to get rid of it
  • leads to cough - involves forceful expiration against a closed glottis with sudden glottal opening and high velocity expulsion of air
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14
Q

What are stretch receptors?

A
  • further down airways down secondary bronchi in tubes that can change size depending on pressure
  • excessive inflation of lungs activates pulmonary stretch receptors
  • afferent signals to respiratory centres inhibit DRG and apneustic centre and stimulate pneumotaxic VRG
  • this inhibits inspiration and stimulates expiration
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15
Q

What are J receptors?

A
  • located next to alveoli
  • sensitive to oedema and pulmonary capillary engorgement (leads to high pressure)
  • increases breathing frequency after this as the above impede ability of lungs to ventilate and exchange gas e.g. oedema is thick
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16
Q

Describe the graph of volitional apnoea.

A
  • when ventilating, arterial O2 and CO2 remain stable
  • when holding breath, arterial O2 decreases and CO2 increases - accumulation of H+ beyond BBB stimulates medulla to breathe in
  • CO2 threshold for breathing - once CO2 passes that we start struggling for breath (but can be overcome)
  • O2 threshold for blackout - once O2 passes below this, we blackout
17
Q

How does hyperventilating affect the graph of volitional apnoea?

A
  • increasing ventilation increases arterial O2 and decreases CO2
  • once breath is held, CO2 threshold for breathing (struggle phase) is now much closer to O2 threshold for blackout so once you start struggling you may blackout soon after
  • using motor cortex going through to control inspiratory muscles to keep them contracted and inhibit/overcome effect of expiratory muscles
18
Q

What is an acid?

A

A molecule with a loosely bound H+ ion that it can donate

19
Q

What is the paradox with acids?

A

A greater H+ concentration refers to a lower pH

20
Q

Why must acidity of blood be tightly regulated?

A

Changes in acidity will alter the 3D structure of proteins (enzymes, hormones, protein channels) which may mean they become less efficient/do not work

21
Q

What is a base?

A
  • an anionic (negatively charged ion) molecule capable of reversibly binding protons (to reduce the amount that are ‘free’)
  • H+A- <–> H+ + A-
  • this relationship is an equilibrium - increasing something on one side will push the equation in the opposite direction
22
Q

How was the buffering capacity of blood discovered?

A
  • by Pitts and Swan who injected a dog with 14M acid that they thought would kill him
  • but his blood pH changed very little
  • blood has enormous buffering capacity that can react almost immediately to imbalances
23
Q

How was pH figured out from H+ concentration?

A
  • orders of magnitude difference between H+, Na+, K+: H+ = 0.00000004Eq/L, Na+ = 140Eq/L, K+ = 4Eq/L
  • these relatively tiny numbers for [H+] are inconvenient to use
  • Sorensen scaled the data using a log10 transformation: log10[H+] = -7.4
  • made numbers much more manageable, although negative
  • -log10[H+] = 7.4
  • the inverse function of log is (10^x), using this we can calculate [H+] from pH
  • [H+] = 10^(-pH)
24
Q

What is alkalaemia?

A

Higher than normal blood pH

25
Q

What is acidaemia?

A

Lower than normal blood pH

26
Q

What is alkalosis?

A

Circumstances that decrease H+ concentration and increase pH

27
Q

What is acidosis?

A

Circumstances that increase H+ concentration and decrease pH

28
Q

How is alkalaemia and acidaemia corrected by the body?

A
  • an acidosis causes acidaemia and will need an alkalosis to correct
  • an alkalosis causes alkalaemia and will need an acidosis to correct
  • changes in ventilation can stimulate a rapid compensatory response to change CO2 elimination and alter pH
  • changes in HCO3- and H+ retention/secretion in kidneys can stimulate a slow compensatory response to alter pH
29
Q

Where are peripheral chemoreceptors located?

A
  • chemoreceptors that sample blood and assess for H+ and CO2 concentration are at bifurcation of carotid arteries in structures called carotid bodies and aortic bodies in aortic arch
  • positioned near the carotid baroreceptors (sensitive to changes in blood pressure)
30
Q

Describe the emotional change to ventilation.

A
  • special senses (taste/smell/hear/sight) and higher brain centres like limbic system elicit emotional response
  • this can affect the respiratory control centre in brainstem
  • affects breathing rate
  • normal situation: motor control > medulla reactivity
31
Q

How are nerves distributed so that exercise can affect breathing?

A
  • a branch of the efferents from the primary motor cortex that go to skeletal musculature also innervate medulla (to tell brain to start breathing since we are exercising)
  • proprioceptive afferents from muscle spindles and Golgi tendons innervate the medulla on the way to the brain - can be shown by cycling someone else’s legs - changes their ventilation as brain recognises big muscles moving = should probably breathe faster
32
Q

What is the cold shock ventilatory response?

A

Immersion in cold water (<10oC) results in inspiratory gasp and hyperventilation due to superficial sensory nerve endings in skin –> can lead to death

Year 1 - BRS (73 decks)

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