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LSS: respiratory > lecture 8: breathlessness and control of breathing > Flashcards

lecture 8: breathlessness and control of breathing Flashcards

1
Q

what are the functions of the respiratory muscles?

A
  • maintaining PO2, PCo2,PH
  • defence of the airways and the lungs
  • exercise
  • speech
  • control of intra thoracic and infra abdominal pressures
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2
Q

what controls breathing?

A

breathing is controlled by the medulla, the cortex and the reflexes

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3
Q

show a graph of tidal breathing :

what does it show?

A
  • the graph shows a single resp cycle
  • VT (tidal volume)
  • TTHOT (total time for resp cycle)
    -VE (minute ventilation)
    (tidal volume x frequency
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4
Q

***how to work out the frequency?

A

1/ TTOT

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5
Q

what does V.E = VT/T1 X T1/TOTT show?

A
  • minute ventilation = tidal volume x frequency
    can also be seen as
    VE = VT x 60/TTOT

TTOT can be split into inspiratory TI and expiratory TE

VT/T1 = mean inspiratory flow
how powerfully the muscles contract
T1/TOTT = inspiratory duty cycle
the proportion of time actually inspiring

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6
Q

how to calculate inspiratory duty cycle?

A

T1/TTOT

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7
Q

what is minute ventilation in normal subjects?

A

normal VE - 6L/min
normal tidal volume - ).5 L
normal inspiratory duty cycle - 40%

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8
Q

how does use of nose clip affect breathing rate

A
  • reduces breathing rate while VE remains roughly the same but VT increases as breathing is deeper.
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9
Q

how does use of a tube affect breathing rate?

A

increases dead space which increases VE, VT and frequency to clear dead space.

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10
Q

what happens to tidal breathing in disease?

A
  • Intrathoracic airways are narrowed so difficulty ventilating lungs MORE on expiration.
  • Lower TV as less air can fill the lungs but compensated by a faster breathing rate (equal TI/TTOT).
  • People with COPD breathe much shallower and faster but NOT harder.
  • REMEMBER: people with obstructive lung disease have difficulty expiring.
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11
Q

where does involuntary control of breathing happen?

A
  • the medulla
  • this always overrides the behavioural centre
  • responds to the metabolic demands for and producing CO2
    determines a set point for Co2

The Limbic System (survival responses), frontal cortex (emotions), sensory inputs (pain, startle) and sleep (reticular formation) may influence the metabolic centre.

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12
Q

where does voluntary control of breathing happen?

A

The motor area of cerebral cortex.

Can control acts such as breath holding and singing.

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13
Q

***show a diagram of the organisation of breathing control: ›

A
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14
Q

what is present in the metabolic controller?

A

H ion receptors

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15
Q

what nerves are the respiratory spinal motor neurones?

A

the phrenic nerves

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16
Q

what are the 2 main feedbacks in the metabolic controller?

A
  1. Chemoreceptors in the carotid bodies sense hydrogen ion levels in the blood from levels of O2 and CO2. This feeds back to the metabolic controller and has a DOMINANT influence.
    a. Removal of carotid bodies reduces response to CO2 levels by up to 40%.
  2. The stretch and irritant receptors on the lungs can influence the metabolic control of breathing.
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17
Q

what is the peripheral chemoreceptor ?

A
  • This carotid body chemoreceptor is a well vascularised bundle of cells at the junction of the internal and external carotid arteries in the neck
  • This serves as the rapid response system for detecting changes in arterial PO2 and PCO2
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18
Q

where does the pacemaker of breathing come from?

A
  • 10 groups of neurones in the medulla

-

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19
Q

what is the pre botzinger complex?

A

in ventro-cranial medulla, seems essential for generating the respiratory rhythm and is known as the ‘gasping centre’

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20
Q

what re the 6 groups of neurones which control the phases of the resp cycle?

A

o Early inspiratory – initiates inspiratory flow via respiratory muscles.
o Inspiratory augmenting – may dilate pharynx, larynx and airways.
o Late inspiratory – signals the end of inspiration.
o Expiratory decrementing – may brake passive expiration by abducting larynx and pharynx.
o Expiratory augmenting – activate expiratory muscles when ventilation increases UPON EXERCISE.
o Late expiratory – signal the end of expiration, may dilate the pharynx in preparation for inspiration.

21
Q

what nerve afferents from nose and face?

A

5th nerve

22
Q

what nerve afferents from from pharynx and larynx ?

A

9th nerve

23
Q

what nerve afferents from bronchi and bronchioles?

A

10th nerve

24
Q

what is the hering breuer reflex?

A

o Hering-Breuer reflex from pulmonary stretch receptors in the lungs, terminates inspiration/expiration but this is weak in humans.

25
Q

** explain this graph

A

♣ The slope (S) is an index of chemo-sensitivity.
♣ B is the apnoeic threshold, sensitive to acid-base status (only operates in sleep).
♣ This measures the sensitivity of the metabolic respiratory centre to hydrogen ions by use of a carbon dioxide challenge – breathing into a CO2 primed bag.
♣ The respiration into a closed bag maintains rising CO2 levels which raises the minute ventilation in response.
o NOTE: A 30Lmin-1 rise in VE for every 1kPa rise in PaCO2.
♣ Green = normoxia while orange = hypoxia (which increases sensitivity of acute CO2 response – mediated by the carotid body).

26
Q

what is Chronic Metabolic Acidosis ?

A

increases the threshold (x-axis intercept -> left) but does NOT alter sensitivity (gradient).

27
Q

what is Chronic Metabolic Alkalosis ?

A

decreases the threshold and again does not alter the gradient.

28
Q

explain the graph some more ***

A

♣ The black line represents the VE at which PCO2 is below normal resting level.
o During sleep, ventilation would drop to zero but due to continual CO2 production, after 10-60 seconds, PaCO2 has risen enough (threshold) to restart breathing.
♣ A depressed ventilatory response to PCO2 means a flattening of the slope (decreased sensitivity) and a rise in set point (resting PaCO2 threshold).
o This could be the result of a disease affecting metabolic control or suppressive drugs (anaesthetics).
♣ An important peripheral cause of a reduction in sensitivity would be respiratory muscle weakness which usually progresses to a raised PaCO2.

29
Q

is the system more sensitive to CO2 or O2

A

CO2

30
Q

what happens to minute ventilation when there is a decrease in arterial PO2?

A

it increases

31
Q

what does a fall in ventilation result in?

A
  • causes fall in PaO2
  • rise in PaCO2
  • the fall in Po2 increases the sensitivity of the carotid body to PaCo2 and H+
  • this means ventilation increases
  • PaO2 increases
32
Q

why is the body not well adapted to altitude?

A

hypoxic hyperventilation lowers to PCO2 and inhibits the ventilatory response

33
Q

what happens to the tidal volume graph for a patient with emphysema or bronchitis?

A
  • their breathing is more shallow and frequent
  • so it looks like a normal ventilation
  • their more or less normal inspiratory flow suggests their neural drive or force is normal
  • however, this is not the case
  • looking at the nervous action of the diaphragm
  • the diaphragm is working more harder to achieve the same VT/TI
  • the minute ventilation is normal
  • but breathing is shallow
34
Q

what happens in response to respiratory acidosis?

A
  • a fall in ventilation leads to a rise in CO2 and hydrogen ions
  • this stimulates the metabolic controller to increase breathing
  • this is a rapid response system
  • there is also a renal system
  • this is renal excretion and retention of weak acids
  • renal compensation however takes a much longer time
35
Q

what happens in response to metabolic acidosis ?

A
  • this is when there is an excess of H+ ions in response to metabolism
  • the compensatory mechanisms are
  • renal excretion
  • ventilation stimulation to decrease CO2
36
Q

what happens in response to metabolic alkalosis?

A
  • hypoventilation increases the CO2 and the H+
  • renal retention of weak acids
  • renal excretion of chloride ions
  • ## may happen in acute asthmatic attacks
37
Q

what are the types of hypoventilation?

A
  • central
  • peripheral

within each section is = acute and chronic

38
Q

what is central acute hypoventilation?

A
  • metabolic center poisoning
39
Q

what is central chronic hypoventilation?

A
  • metabolic center congenital issue
  • obesity
  • chronic mountain sickness
40
Q

what is peripheral acute hypoventilation?

A
  • muscle relaxant drugs

- myasthenia gravis

41
Q

what is peripheral chronic hypoventilation?

A
  • resp muscle weakness of neuromuscular
42
Q

what is COPD in terms of hypoventilation?

A
  • mix of central hypoventilation and peripheral
  • caused by lung inefficiency
  • the metabolic controller is insensitive
43
Q

what are the conditions for hyperventilation?

A
  • chronic hypoxemia
  • excess H +
  • chronic anxiety
  • pulmonary vascular disease
44
Q

what is breathlessness

A
  • subjective so hard to define
  • breathlessness at rest = difficulty inspiring
  • breathlessness at exercise= cardiac or resp disease
45
Q

what are the types of breathlessness?

A
  • tightness - difficulty in inspiring
  • increased work and effort - high lung volume means high resistance against breathing
  • air hunger - powerful urge to breathe
46
Q

what is air hunger like?

A
  • like suffocation
  • ## difference between VE demand and VE achieved
47
Q

what is a scale for measuring breathlessness?

A
  • borg scale

10 points

48
Q

what is breath holding time?

A
  • test of behaviour vs metabolic demand

- the break point is the expression of air hunger

LSS: respiratory (17 decks)

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