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Respiratory System > Lungs > Flashcards

Lungs Flashcards

1
Q

what is Boyles law?

A

at a constant pressure and number of gas molecules the pressure is inversely proportional to the size of the container

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2
Q

what is Daltons law?

A

in a dry mixture each gas exerts a partial pressure equal to it fractional share of the volume

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3
Q

why does the P02 decrease at higher altitudes?

A

although it is still 21% of the composition of air, the pressure of the air has decreased so its 21% of a smaller pressure

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4
Q

at body temperature what is the PH20?

A

6KPa

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5
Q

what is the intrapleural pressure at FRC?

A

-0.5Kpa

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6
Q

what is the equation for distending pressure?

A

Pdist = Pin -P out

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7
Q

how is thoracic volume increased?

A

diaphragm contracts
external intercostal muscle contract pushing the rib cage up and out
sternocleidomastoid muscle contract moving the sternum up an out

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8
Q

how is thoracic volume actively decreased?

A

internal intercostal muscles pull the rib cage down and in
abdominal muscles contract forcing the diaphragm up

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9
Q

what areas consist of anatomic dead space?

A

conducting zones

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10
Q

how much alveoli dead space do healthy individuals have?

A

zero

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11
Q

what is the average size of anatomic dead space?

A

150ml

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12
Q

what is physiological dead space?

A

anatomic plus alveoli dead space

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13
Q

what 2 components are needed for gas exchange?

A

ventilation and perfusion

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14
Q

what is the equation for flow in relation to the lungs?

A

flow = area x velocity

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15
Q

why does velocity decrease down the airway generation?

A

total cross sectional area increases (also resistance)

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16
Q

why do alveoli only appear from generation 17?

A

because velocity has slowed to the rate of diffusion therefore gas exchange

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17
Q

what is the average tidal volume?

A

500ml

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18
Q

what ventilation needs to be matched to meet metabolic demand?

A

Alveoli ventilation

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19
Q

how must alveoli gas composition be maintained?

A

by matching ventilation to rate of blood flow which is determined by metabolism

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20
Q

why is the lung distending pressure +5KPa in terms of lung compliance?

A

this lung volume is when lungs are most compliant and easiest to distend

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21
Q

how would you measure lung distending pressure?

A

take oesophageal pressure which is the same as pleural pressure
assume alveoli pressure is 0
then take oesophageal pressure from alveoli pressure

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22
Q

what 2 factors determine compliance?

A

stretchiness of the tissue e.g. elastin and collagen ratio
surface tension at air water interfaces (force trying to collapse the alveoli)

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23
Q

what is the equation for pressure involving surface tension?

A

P=2T (surface T) / radius

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24
Q

what driving force does surface tension contribute to?

A

Lung elastic recoil provides 2/3 which allows passive expiration

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25
Q

what would loss on surface tension do to compliance?

A

increase compliance

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26
Q

what are the functions of surfactant?

A

detergent (phospholipid) that reduces surface tension of alveoli preventing their collapse
and increasing their compliance allowing lung expansion
also keeps lungs dry and prevents oedema from sucking fluid out of the capillaries

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27
Q

how does surfactant exhibit an area dependant effect on alveoli?

A

the same amount of surfactant is present on each alveoli
this results in them being closer together on smaller alveoli exhibiting a larger effect and overcoming the greater pressure on these smaller alveoli

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28
Q

why do premature babies suffer alveoli collapse?

A

their type II pneumocytes have not matured enough to produce surfactant
this increases surface tension, decreasing compliance = alveoli collapse / poor lung expansion

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29
Q

how can premature babies surfactant production be promoted?

A

steroids promote it, baby can be put on a ventilator

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30
Q

what determines FRC?

A

Compliance of Lungs and Chest wall

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31
Q

how and why does intrapleural pressure change from the top to the bottom of the lungs?

A

at the top of the lungs intrapleural pressure is the most negative because the force of the lungs being pulled down from gravity creates extra tension
the bottom of the lungs gravity is acting less, less tension = more positive intrapleural pressure

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32
Q

how and why does distending pressure change from the top to the bottom of the lungs?

A

because of the more negative intrapleural pressure at the top of the lungs, distending pressure is higher at FRC
meaning the alveoli have less compliance to expand further
hence the alveoli at the bottom of the lungs will expand more as they have a lower resting distending pressure and therefore more ability to comply

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33
Q

what is the transit time in the lungs?

A

the time where the blood is available for gas exchange

34
Q

what happens to transit time during exercise?

A

it decreases

35
Q

what are the 4 zones of blood flow in the lungs?

A

zone 1 no flow (dosent occur naturally only in the case of very low BP e.g. haemorrhage
zone 2 intermittent
zone 3 continuous
zone 4 distended

36
Q

where is blood pressure and therefore flow highest in the lungs?

A

the bottom

37
Q

why is blood flow intermittent in higher areas of the lungs?

A

blood pressure decreases can become less than external pressure of the alveoli hence capillaries are compressed

38
Q

when is the VQ ratio at the top of the lungs reduced?

A

during exercise increased metabolic demand = increased blood pressure and blood flow
= less ventilation wasted

39
Q

what is the VQ of dead space?

A

infinity

40
Q

what is the VQ if the alveoli is bypassed by a capillary shunt?

A

zero

41
Q

what does a VQ of less than 1 mean?

A

over perfused
or under ventilated

42
Q

what does a VQ of more than 1 indicated?

A

under perfused
over ventilated

43
Q

what mechanisms try to maintain an optimum VQ?

A

vasodilatation / constriction
bronchi dilation / constriction

44
Q

what is henrys law?

A

the amount of gas dissolved in a solution is proportional to the partial pressure

45
Q

what is the equation for amount of gas dissolved?

A

partial pressure x solubility coefficient

46
Q

what components of haemoglobin bind to which molecules ?

A

4 haem groups (each will bind 1 O2) and 4 globin chains (2α, 2β) which can bind H+ and CO2
Β chains can also bind 2,3 DPG (a byproduct of gylcoltyic metabolism)

47
Q

what does the P50 mean?

A

PO2 when haemoglobin is 50% saturated

48
Q

what happens to the affinity of haemoglobin for O2 as O2 binds?

A

As more O2 binds the shape of haemoglobin changes making it easier for oxygen to bind
this is positive cooperativity

49
Q

what happens towards the end of O2 binding to haemoglobin?

A

affinity for O2 decreases

50
Q

the binding of what substances decrease the haemoglobins affinity for oxygen? what does this cause?

A

H+, CO2, and 2,3DPG
Bohr shift

51
Q

In what tissues in 2,3 DPG levels high?

A

metabolically active tissues as it is a by-product of glycolytic metabolism

51
Q

where is carbonic anhydrase present?

A

Inside erythrocytes

52
Q

how does HCO3 diffuse out of the erythrocyte?

A

Chloride shift
Cl moves in, exchange for the HCO3

53
Q

list the ways CO2 can be transported in the blood

A

HCO3 / H+ in the plasma
bound to Hb (usually deoxy Hb)
dissolved in rbc / plasma
A small amount can be bound to plasma proteins

54
Q

how much of CO2 is transported as HCO3 in the rbc/ plasma?

A

85%

55
Q

explain the Haldane effect

A

deoxy haemoglobin has a higher affinity for CO2 than oxy haemoglobin
this means that in tissues with high metabolism (therefore hypoxic), blood will form more carbaminohaemoglobin for the same PCO2 compared to non metabolically active tissues
this ensures CO2 is removed from tissues it needs to quicker

56
Q

how are the Bohr and Haldane effects complementary in tissues?

A

unloading O2 in tissues helps bind CO2 (Haldane)
the binding of CO2 helps unload O2 (Bohr)

57
Q

how are bohr and Haldane complementary in the lungs?

A

loading O2 in the lungs helps dissociate CO2 (Haldane)
dissociating CO2 helps bind O2 (Bohr)

58
Q

how many ml of oxygen can 1 g of Hb bind?

A

1.39

59
Q

what is the equation for the oxygen capacity of blood?

A

Hb conc x O2 binding capacity of Hb

60
Q

how do you calculate VO2?

A

arterial 02 conc x cardiac output - venous 02 conc x cardiac output

61
Q

what are the two main types of airway resistance?

A

lung viscous tissue resistance (10-20%), airway resistance (80-90%)

62
Q

how do you calculate total airway resistance?

A

total airway resistance = PB - PA divided by V (air flow measured by a spirometer)

63
Q

what happens to airway R in the early conducting zones?

A

initially increases due to the decrease in diameter / cross sectional area (resistance increases till generation 7)

64
Q

what happens to resistance in the further conducting and resp zones?

A

it decreases because total cross sectional area is greatly increasing

65
Q

where is airways resistance variable and where is it non variable?

A

upper airways - constant due to cartilage rings causing a constant diameter (first 10 generations)
resistance in lower airways (past generation 10) variable due the smooth muscles control of diameter in the bronchioles

66
Q

what effect does sympathetic innervation have on the bronchioles?

A

vasodilation via B2 adrenoreceptors

67
Q

how do inhalers work?

A

salbutamol - B2 adrenoreceptor agonist promotes vasodilation

68
Q

what factors except for sympathetic stimulation cause vasodilation of the lower airways?

A

cholinergic antagonist e.g. atropine promote vasodilation
hypercapnia

69
Q

what effect does parasympathetic innervation have on the lower airways?

A

acting on cholinergic receptors (M3 muscarinic receptors) caused vasoconstriction,

70
Q

what other factors cause vasoconstriction?

A

hypocapnia and inflammatory mediators such as histamine and leukotrienes, also B2 receptor antagonist

71
Q

why are the terminal bronchioles known as the silent zone when it comes to disease?

A

diseases that effect diameter e.g. cancer can go undetected
this is because the number of tubes is the main determiner of airway resistance

72
Q

what is the mechanism of vasoconstriction in smooth muscle?

A

M3 muscarinic receptors bound by Ach
cause increase in Ca2+

73
Q

explain the mechanism of the vasodilation in the lungs?

A

B2 receptor agonists e.g. adrenaline / salbutamol result in the production of cAMP pathway causing vasodilation

74
Q

how else can drugs promote vasodilation?

A

cAMP is broken down by phosphodiesterase, therefore drugs that inhibit phosphodiesterase increase the cAMP lifetime keeping the second messenger pathway active for longer which allows vasodilation

75
Q

what are the predominant B receptors in the heart?

A

B1

76
Q

what are the predominant B receptors in the lungs?

A

B2

77
Q

how can mucus build up be treated? / what does it cause in the lungs

A

decrease diameter = increase resistance = lower air flow
treated with anti-inflammatory such as the glucocorticoids present in inhalers

78
Q

how does inspiration decrease airways resistance?

A

radial traction as lung volume increases the interconnected tubes are stretched, leading to increased diameter and decrease in pressure and resistance

79
Q

except for HCO3 what else can buffer H+?

A
  • H+ can be buffered by binding to plasma proteins such as albumin
    • H+ can also bind to Hb, deoxy Hb has a high affinity for H+ (deoxyhaemoglobin is a strong base)
      HPO4 2-
80
Q

why is HCO3 work well as a buffer despite physiological PH being very far from its PKa?

A

there is a very high conc of it relative to H+
there is a continuous supply from CO2

Respiratory System (2 decks)

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