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phty251 > Respratory system > Flashcards

Respratory system Flashcards

1
Q

how do lungs adhere to chest wall?

A

adhered by intrapleural fluid

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2
Q

what kind of pressure is generated in the intrapleural space because of the difference in elastic recoil between chest wall and lungs?

A

negative pressure is generated relative to atmospheric pressure

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3
Q

what is transpulmonary pressure?

A

the pressure difference between the alveoli and pleural cavity

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4
Q

what is the change in P(ip) during inspiration?

A

P(ip) changes from -4mmHg to -7mmHg

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5
Q

what happens to P(alv) in mid-inspiration?

A

P(alv) changes from 0 to -1mmHg

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6
Q

what is the change in P(tp) during inspiration?

A

P(tp) changes from 4 to 7mmHg

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7
Q

what is P(alv) at the end of inspiration?

A

P(alv) = 0mmHg

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8
Q

what is the primary cause of expiration? and how does this cause air to move out of lungs?

A

expiration is a passive process and occurs via elastic recoil of the lungs, shrinking thorax and thus increasing pressure so air moves out of lungs

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9
Q

what is alveolar volume? (and its value in mL)

A

alveolar volume = tidal volume - anatomic dead space

= 500-150 = 350ml

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10
Q

what is alveolar dead space?

A

part of alveolar volume in alveoli which are inadequately perfused with blood

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11
Q

what is physiological deadspace?

A

physiological dead space = anatomical deadspace + alveolar deadspace

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12
Q

minute ventilation eqauation

A

minute ventilation = tidal volume x frequency of breathing

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13
Q

dead space ventilation equation

A

deadspace ventilation = deadspace x frequency of breathing

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14
Q

alveolar ventilation equation

A

alveolar ventilation= (tidal volume - deadspace) x frequency of breathing

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15
Q

effect of deep slow breathing on alveolar ventilation and dead space

A

deep slow breathing:

  • dead space ventilation decreases
  • alveolar ventilation increases overall
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16
Q

effect of breathing through snorkel on alveolar ventilation and deadspace

A

breathing through snorkel:

  • increase in deadspace, due to volume of snorkel itself
  • minute ventilation increases
  • alveolar ventilation remains the same
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17
Q

effect of fast and shallow breathing on alveolar ventilation and deadspace

A

fast and shallow breathing:

  • minute ventilation decreases
  • deadspace ventilation increases
  • no alveolar ventilation occurs
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18
Q

how is lung compliance measured?

A

measured by the change in volume for a given change in pressure

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19
Q

disadvantages if a highly compliant lung?

A
  • reduced elastic recoil
  • inefficient passive recoil of lungs
  • expiratory muscle activity may be required even in quiet breathing
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20
Q

advantages of a highly compliant lung?

A
  • easy to inflate the lung

- little respiratory muscle activity required

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21
Q

what causes emphysema?

A

destruction of alveoli, alveoli with large air spaces

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22
Q

what characterizes emphysema?

A
  • high compliance of lungs
  • little elastic recoil
  • lungs tend to remain inflated
  • exploratory muscle activity is required to deflate the lungs
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23
Q

disadvantages of low compliant lung

A
  • difficult to inflate the lung

- string inspiratory muscle activity required

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24
Q

advantages of low compliant lung

A
  • elastic recoil of the lung is high and can recoil passively during expiration
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25
Q

how does a patient with a restrictive lung disease tend to breathe?

A
  • a patient with a restrictive lung disease will breathe shallow and rapidly in order to maintain sufficient alveolar ventilation
26
Q

characteristics of pulmonary fibrosis

A
  • low compliance of lung
  • alveolar wall is stiff
  • inspiration is harder, inspiratory muscles have to work harder
  • small lung volumes are achieved
27
Q

2 determinants of lung compliance and elastic recoil

A
  • elastic elements in alveolar interstitium (25%)

- surface tension (75%)

28
Q

how does surface tension increase the risk of alveolar collapse?

A
  • water molecules on the alveolar wall are moe attracted to each other than to the air
  • as alveoli inflate, distance between water molecues and their strength increases
  • thus increasing likelihood of collapse
29
Q

what produces surfactant?

A

type 2 alveolar cells

30
Q

how does surfactant reduce surface tension and increase lung compliance?

A
  • surfactant acts as a detergent

- forms a monolayer between water and air, reduces the interaction between water molecules

31
Q

what is respiratory distress syndrome?

A
  • babies born before 35 weeks can’t synthesize surfactant as their type 2 alveolar cells arent mature enough
  • the work required to overcome alveoli surface tension is too high, and lungs collapse
32
Q

what is airflow dependant on?

A

the pressure gradient divided by airway resistance

33
Q

3 major determinants of airway resistance

A
  • viscosity if air
  • length
  • diameter/radius
34
Q

where is the major site of airway resistance?

A

major site of airway resistance is in medium-sized bronchi - bronchioles

35
Q

what is lateral (radial) traction?

A
  • as the lungs expand, transpulmonary pressure exerts a force on the airways pulling them open
  • elastic tissues outside airways link to surrounding tissue
36
Q

what type of breathing increases the dilating effect of lateral traction?

A

big deep breaths/inspiring large volumes of air (airways resistance is reduced)

37
Q

what type of breathing reduces the dilating effect of lateral traction?

A

during the inspiration of small volumes of air (airway resistance is increased)

38
Q

why is lateral traction greatly reduced during expiration?

A

lateral traction is reduced during expiration as resistance to airflow is higher

39
Q

what 2 chemical factors affect airway resistance (decrease radius)?

A
  • blockage by mucus or infection
  • local inflammatory chemical mediators (histamines, leukotrienes) causing smooth muscle to contract = bronchoconstriction
40
Q

what neural factors affect bronchoconstriction?

A

stimulation of parasympathetic nerves to airways smooth muscle cause bronchoconstriction

41
Q

what is the target/treatment for chronic bronchitis?

A

muscarinic ACh receptor blockers used, by targeting airway smooth muscle parasympathetic innervation

42
Q

what is the concentration of O2 in arterial blood?

A

O2 conc. = 200ml/L of blood

43
Q

what is the respiratory quotient and what does it depend on?

A
  • RQ is the ratio of CO2 produced to 02 consumed

- RQ depends on which macro nutrient fuel source you cells are using

44
Q

at steady state, what is the approximate RQ?

A

approx. 200ml C02 produced for every 250 ml 02 consumed = 0.8

45
Q

what is Boyles law/ what does the magnitude of pressure depend on?

A

P1 V1 = P2 V2

- dependant on concentration of gas and the temperature

46
Q

what is Daltons law?

A

in a mixture of gases, the total pressure exerted is simply the sum of the individual gases partial pressure

47
Q

what is the PO2 of atmospheric air at sea level

A

160 mmHg (0.21 x 760mmHg)

48
Q

what is the alveolar PO2?

A

105mmHg

49
Q

what is the inspired air PO2?

A

150mmHg

50
Q

what is the alveolar PCO2?

A

40mmHg

51
Q

what is inspired air PCO2?

A

approx. 0mmHg

52
Q

3 determinants of alveolar oxygen

A
  • how much air we breathing in from the atmosphere
  • how much fresh air is getting to the alveoli
  • how much O2 is being extracted/used by the body
53
Q

3 determinants of alveolar CO2?

A
  • inspired CO2 (almost always zero)
  • how much fresh air is getting to the alveoli
  • how much CO2 is being produced by the body
54
Q

hypoventilation causes what in alveolar ventilation?

A

hypoventilation causes decreased alveolar ventilation

55
Q

hyperventilation causes what in alveolar ventilation?

A

hyperventilation causes increased alveolar ventilation

56
Q

(Henry’s Law) the number of O2 molecules entering a liquid is proportional to..?

A

the 02 partial pressure in the gas

57
Q

what happens when an equilibrium in the partial pressure of gases is reached

A

when equilibrium is reached, diffusion of gases ceases

58
Q

Ficks law of diffusion

A

(partial P diff. x SA x diffusion coefficient)/thickness of the barrier

59
Q

why does CO2 not diffuse faster between alveoli and capillaries than O2 even though it has a higher diffusion constant?

A

because CO2 has a much lower partial pressure gradient (6mmHg compared to 60mmHg for O2). therefoe not much difference in overall rate of diffusion

60
Q

what is pulmonary oedema and how does it affect diffusion of O2?

A

pulmonary oedema is when fluid leaks out of pulmonary capillaries and into the interstitial space, and reduces the rate if O2 diffusion.

61
Q

what is interstitial fibrosis and how does it affect diffusion of O2?

A

interstitial fibrosis is the thickening of the alveolar wall, thus increasing thickness of the barrier for gas exchange to occur, reducing rate of O2 diffusion

62
Q

what is empysema and how does it affect the diffusion of O2?

A

emphysema is the destruction of alveolar walls which decreases the surface area for gas exchange and the number of pulmonary capillaries, thus reducing O2 diffusion rate

phty251 (6 decks)

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