mechanisms of breathing (W3) - part 1 Flashcards

1
Q

when is atmospheric and alveolar pressure equal

A

at the end of a normal breath

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2
Q

how do we get balance at the end of a normal breath?

A

elastic recoil

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3
Q

where does the chest wall and lung want to recoil

A

chest wall - outward
lungs - inward

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4
Q

how to move gas into lungs?

A

pressure greater outside lungs than inside

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5
Q

which intercostal muscles are involved in inspiring

A

external

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6
Q

why is expiration a passive process

A

lung elastic recoil is inward, alveolar pressure higher than atmospheric

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7
Q

which is quicker - inspiration or expiration - and why

A

inspiration because it is an active process

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8
Q

which muscles take part in forced expiration (active process)

A

abdominal muscles, internal intercostal muscles

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9
Q

what is tidal volume

A

difference in volume between inspiration and expiration

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10
Q

what is respiratory frequency/rate

A

breaths per minute

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11
Q

what condition does dynamic hyperinflation occur in

A

COPD

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12
Q

what causes SOBOE in COPD

A

decreased lung elastic recoil
obstructive airways disease
static and dynamic hyperinflation
inability to efficiently increase tidal volume

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13
Q

what does SOBOE stand for

A

shortness of breath on exertion

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14
Q

what is static and dynamic hyperinflation

A

?

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15
Q

how may inspiration and expiration be disrupted

A

airflow obstruction (eg COPD, asthma)
weakness of respiratory muscles
lung tissue damage
thoracic cage disorders (AS, kyphoscoliosis)

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16
Q

which part of the brain causes a complete stop in breathing if removed

A

medulla

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17
Q

which part of the brain controls voluntary breathing

A

cortex

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18
Q

which part of the brain controls automatic breathing

A

brainstem

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19
Q

what do inspiratory neurones cause

A

contraction of inspiratory muscles
activation of expiratory neurones

20
Q

effect of expiratory neurones on inspiratory neurones

A

inhibiting

21
Q

effect of large inspiration on expiratory neurons

A

larger activation expiratory neurons cause contraction of expiratory muscles (active process)

22
Q

breath stacking in COPD

A

more inspiration than expiration, leads to inability to get more air into lungs

23
Q

environmental factors that change basic breathing pattern

A

inhaled noxious substances
speech/volition
sleep
exercise

24
Q

lung receptors?

A

slowly adapting receptors
rapidly adapting receptors
C-fibre endings

25
Q

2 types of chemoreceptors that input to the respiratory rhythm - what do they sense

A

peripheral chemoreceptors - sense changes in arterial blood
central chemoreceptors - sense changes in cerebrospinal fluid

26
Q

which nerve carries afferent nerve fibres from lung receptors

A

vagus nerve (CN10)

27
Q

what happens if the nerve containing afferent nerve fibres is cut or stimulated

A

cut - breathing pattern has greater amplitude, smaller frequency
stimulated - breathing pattern has smaller amplitude and greater frequency

28
Q

another name for slowly adapting receptors

A

stretch receptors

29
Q

what type of receptors are SARs (slowly adapting receptors

A

mechanoreceptors

30
Q

where are SARs situated

A

close to airway smooth muscle

31
Q

what are SARs stimulated by

A

stretching of airway walls during respiration

32
Q

what do SARs help do?

A

initiate expiration and prevent overinflation of the lungs

33
Q

which reflex does SARs initiate? what is this?

A

Hering-Breuer inflation reflex
prolonged inspiration produces prolonged expiration

34
Q

another name for RARs

A

irritant receptors

35
Q

where are RARs located

A

airway epithelium

36
Q

what type of receptors are RARs

A

mechanoreceptors

37
Q

what do RARs respond to

A

rapid lung inflation, chemicals, smoke, dust

38
Q

where are RARs most useful and why

A

trachea and large bronchi - if something hits your large airway its your first opportunity to expel it

39
Q

what can RARs initiate

A

cough, mucus production, bronchoconstriction (stops anything getting further in)

40
Q

why do RARs initiate bronchoconstriction and why can this be bad?

A

stops anything from getting further in, but can be pathologically activated eg in COPD

41
Q

what are C fibres

A

unmyelinated nerve fibres

42
Q

what can C fibres be stimulated by

A

increased interstitial fluid (oedema) and various inflammatory mediators (histamine, prostaglandins, bradykinins)

43
Q

where are C fibres found

A

further out in alveoli and bronchioles

44
Q

2 types of C fibre endings

A

bronchial (in airway epithelium)
pulmonary (close to pulmonary capillaries)

45
Q

what do peripheral chemoreceptors respond to and is it fast or slow

A

fast response to arterial pO2, pCO2, H+

46
Q

what do central chemoreceptors respond to and is it fast or slow

A

slow response to arterial pCO2