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Transition Block 1 > Resp Physiology > Flashcards

Resp Physiology Flashcards

1
Q

what are the resp centres in the brain?

A

pons
medulla
resp rate generated in medulla and modified in the pons

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2
Q

resp centres are mainly influenced by stimuli received from where?

A

mainly central chemoreceptors and peripheral chemoreceptors

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3
Q

resp centres are also influenced by stimuli received from where?

A 
higher brain centres (cerebral cortex, limbic system, hypothalamus)
stretch receptors
juxtapulmonary (J) receptors
joint receptors
baroreceptors
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4
Q

how do stretch receptors work?

A

found in the walls of bronchi and bronchioles

inflation triggers hering-breur reflex which guards against hyperinflation

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5
Q

how do J receptors work?

A

stimulated by pulmonary capillary congestion and pulmonary oedema (also pulmonary emboli) and cause rapid shallow breathing

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6
Q

baroreceptor function?

A

increased ventilatory rate in response to decreased BP

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7
Q

factors which stimulate the resp centres cause what?

A

increased awareness of breathing discomfort - shortness of breath

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8
Q

what factors can stimulate resp centres?

A 
hypoxia
hypercapnia
acidosis
central arousal (anxiety etc)
increased body temp
pain
joint movement during exercise
drugs (amphetamines etc)
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9
Q

what do peripheral chemoreceptors do?

A

sense tension of oxygen and carbon dioxide and H+ concentration in the blood

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10
Q

what do central chemoreceptors respond to?

A

concentration of H+ in CSF

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11
Q

where are central chemoreceptors found?

A

near the surface of the medulla

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12
Q

where are peripheral chemoreceptors found?

A

carotid bodies

aortic bodies

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13
Q

describe the BBB

A

separates CSF from blood
relatively impermeable to H+ and HCO3
CO2 diffuses readily

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14
Q

why is CSF less buffered than blood?

A

contains less protein

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15
Q

buffer equation

A

CO2 + H2O <> H2CO3 <> H+ + HCO3

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16
Q

how does hypercapnia influence ventilation?

A

CO2 generates H+ in CSF which stimulate central chemoreceptors
increased CO2 = increased ventilation
(most potent stimulation of respiration in normal people)

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17
Q

how does hypoxia influence respiration?

A

ventilation increases as oxygen levels drop
peripheral chemoreceptors are stimulated first as oxygen levels drop
once oxygen levels drop below a certain level neurons are depressed and ventilation decreases again

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18
Q

how does hypoxia drive respiration?

A

effect is all via peripheral chemoreceptors
- only stimulated when pO2 <8 kPa
not important in normal respiration but becomes important in chronic CO2 retention (COPD) and at high altitudes

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19
Q

how does H+ drives respiration?

A

effect is via peripheral chemoreceptors as H+ doesn’t cross BBB
peripheral chemoreceptors help adjust for acidosis caused by addition of non-carbonic acid H+ to the blood (lactic acid from exercise, DKA etc)
their stimulation by H+ causes hyperventilation and increases elimination of CO2 from the body
(CO2 helps generate H+ so elimination of CO2 reduces load of H+)

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20
Q

effect of increased CO2 in arterial blood and increased H+ in CSF?

A

strongly stimulates central chemoreceptors
dominant control of ventilation
weakly stimulates peripheral chemoreceptors

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21
Q

effect of increased H+ in arterial blood?

A

stimulates peripheral chemoreceptors
important in acid base balance
doesn’t affect central chemoreceptors as arterial H+ cant penetrate BBB

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22
Q

what does the ventilatory pump consist of?

A 
resp muscles
peripheral nerves
chest wall
pleura (transmural pressure gradient)
airways
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23
Q

what factors affect the ventilatory pump?

A

neuromuscular weakness
decreased compliance of chest wall
loss of transmural pressure gradient across lungs (pneumothorax)
increased airway resistance

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24
Q

inspiration is active or passive?

A

active (depends on active process)

expiration is passive

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25
Q

how is the volume of the thorax increased?

A

increased vertically by contraction of diaphragm (major resp muscle)
external intercostal muscle contraction lifts ribs and moves out sternum (bucket handle mechanism)

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26
Q

accessory muscles of inspiration?

A 
sternocleidomastoid
scalenus (only contract during forceful inspiration)
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27
Q

muscles of active expiration?

A 
internal intercostal muscles
abdominal muscles
(contract only during active expiration)
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28
Q

major muscles of inspiration?

A

diaphragm

external intercostal

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29
Q

what 3 pressures are important in ventilation?

A 
atmospheric pressure (760mmHg)
intra-alveolar pressure (760mmHg when equilibrated with atmospheric pressure)
intrapleural pressure (usually less than atmospheric at 756mmHg)
30
Q

what is intrapleural pressure

A

pressure within pleural sac - pressure exerted outside the lungs

31
Q

how does intra-alveolar pressure change during respiratory cycle?

A

starts at atmospheric pressure > drops a bit then returns to normal during inspiration > increases then returns to normal during expiration

32
Q

how does intra-pleural pressure change during respiratory cycle?

A

starts below atmospheric pressure (756) > drops further during inspiration > increases back to 756 during expiration

33
Q

what is transmural pressure gradient?

A

pressure difference across lung wall (between intra-alveolar and intra-pleural pressures)

34
Q

what can abolish transmural pressure gradient?

A

pneumothorax (equalises pressure between pleural space and alveoli)

35
Q

what forces keep the alveoli open?

A 
transmural pressure gradient
pulmonary surfactant (opposes alveolar surface tension)
alveolar interdependence
36
Q

what forces promote alveolar collapse?

A

elasticity of stretched pulmonary connective tissue fibres

alveolar surface tension

37
Q

how is airway resistance calculated?

A

flow = change in pressure/resistance

38
Q

primary determinant of airway resistance?

A

radius of conducting airway

39
Q

sympathetic vs parasympathetic stimulation of airway?

A 
sympathetic = bronchodilation
parasympathetic = bronchoconstriction
40
Q

chest during inspiration vs expiration?

A 
inspiration = airways are pulled open by expanding thorax, intrapleural pressure falls
expiration = chest recoils, intrapleural pressure rises
41
Q

describe dynamic air compression during active expiration

A

makes active expiration to be more difficult in patients with airway obstruction
rising pleural pressure during active expiration compresses the alveoli and airway
pressure applied to alveolus helps push air out of lungs
pressure on airway tends to compress it

42
Q

dynamic airway compression doesn’t cause problems in normal people, why?

A

increased airway resistance causes an increase in airway pressure upstream
this helps open the airways by increasing the driving pressure between the alveolus and airway (ie the pressure downstream)

43
Q

why does dynamic airway compression cause problems in patients with airway obstruction?

A

if there is an obstruction, the driving pressure between the alveolus and airway is lost over the obstructed segment
this causes a fall in airway pressure along the airway downstream resulting in airway compression by the rising pleural pressure during active inspiration
problem can become worse if the patient also has loss of decreased elastic recoil of lungs

44
Q

what is compliance?

A

effort that has to go into stretching or distending the lungs
(volume change per unit of pressure change across lungs)
decreased by factors such as pulmonary fibrosis

45
Q

work of breathing normally requires how much energy?

A 
3% total energy for quiet breathing (operating at half full)
increases in following situations
- decreased compliance
- restricted chest expansion
- increased resistance
- elastic recoil is decreased
- need for increased ventilation
46
Q

gas exchanger (exchange of O2 and CO2 between blood and lungs) consists of what?

A

alveoli
pulmonary capillaries
interstitial space between these

47
Q

alveolar walls consist of what?

A

single layer of flattened type 1 alveolar cells

each alveolus encircled by pulmonary capillaries

48
Q

partial pressure gradients across pulmonary capillaries?

A

O2 partial pressure gradient = 60mmHg

CO2 partial pressure = 6mmHg (diffusion coefficient for CO2 is 20 times that of O2)

49
Q

what 4 factors influence rate of gas transfer across alveolar membrane?

A

partial pressure gradient
surface area
thickness of barrier
diffusion coefficient (solubility of gas in the membrane)

50
Q

what can affect the gas exchanger?

A 
emphysema 
lung collapse
pulmonary fibrosis/oedema
pneumonia
PE
(some of these also decrease compliance)
51
Q

CO and how is it calculated?

A

volume of blood pumped by each ventricle per min

CO = SVR X HR

52
Q

normal CO?

A

5L per min (increases in exercise)

53
Q

SV and how is it measured?

A

volume ejected by each ventricle per heart beat

SV = EDV - ESV

54
Q

what regulates SV?

A

intrinsic factors = within heart muscle

extrinsic = nervous and hormonal control

55
Q

intrinsic control of SV?

A

change in SV due to change in diastolic length of myocardial fibres which is determined by end diastolic volume and determines preload (EDV is determined by venous return to the heart)

56
Q

what does frank starling curve describe?

A

relationship between venous return, EDV and SV
“ higher EDV = higher SV”
matches SV of right and left ventricle

57
Q

how does heart failure shift frank starling curve?

A

to the right

58
Q

leading cause of heart failure?

A

coronary artery disease

59
Q

what does left sided heart failure cause?

A

pulmonary capillary congestion and pulmonary oedema

leads to shortness of breath, orthopnoea and paroxysmal nocturnal dyspnoea

60
Q

how many O2 can each haemoglobin hold?

A

each Hb holds 4 haem

each haem holds 1 O2 (reversibly)

61
Q

primary factor which determines percent saturation of Hb with O2?

A

pO2

62
Q

what is the significance of the sigmoid curve in oxygen dissociation curve?

A

flat upper portion means when O2 levels are above a certain level a moderate fall in O2 levels wont really affect oxygen loading
steep lower part means that when O2 levels are lower, a small drop in O2 causes a large drop in % Hb saturation (peripheral tissues get a lot of O2 for a small drop in O2)

63
Q

Hb saturation in anaemia?

A

slightly lower in anaemia

64
Q

how does anaemia affect O2 content of the blood?

A

lower Hb = lower O2 content of blood
anaemia impairs the O2 carrying capacity of the blood > cells unable to sustain aerobic metabolism > anaerobic metabolism > increased H+ concentration in metabolically active tissues
also leads to increased CO

65
Q

how is arterial pO2 affected in anaemia?

A

normal (sensed by peripheral chemoreceptors)

66
Q

investigations in shortness of breath?

A 
CXR
ECG
FBC
ABGs
troponin T
67
Q

lung volumes?

A

tidal volume = 500ml
inspiratory reserve volume = 3L
expiratory reserve volume = 1L
residual volume = 1200ml

68
Q

lung capacities?

A

inspiratory capacity = 3.5L
functional residual capacity = 2200ml
vital capacity = 4500ml
total lung capacity = 5700ml

69
Q

normal FEV1/FVC?

A

> 75%

70
Q

spirometry in obstructive lung disease?

A 
FEV1/FVC = reduced
FEV1 = low
FVC = normal or a bit low
71
Q

spirometry in restrictive lung disease?

A 
FEV1/FVC = normal
FEV1 = low
FVC = equally low
72
Q

GOLD classification of airflow limitation in COPD?

A

GOLD 1 = FEV1 > 80% predicted
GOLD 2 = FEV1 50-79%
GOLD 3 = FEV1 30-49%
GOLD 4 = FEV1 < 30%

Transition Block 1 (14 decks)

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