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Physio Exam 3 > Jackson 2 > Flashcards

Jackson 2 Flashcards

1
Q

The volume of air in the lungs is determined by the

A

magnitude of the pressure change during inspiration or expiration, and the stretchability of the lung.

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2
Q

Lung compliance describes this

A

stretchability, and is defined as the change in lung volume for a given change in pressure or

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3
Q

Compliance is the inverse of ——, and is indicative of the needed to ventilate the lung.

A

stiffness, amount of muscle

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4
Q

Two factors contribute to compliance

A

lung elasticity

surface tension

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5
Q

Lung elasticity: • if high (green line in figure) –

A

V increases rapidly per unit change in P

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6
Q

Lung elasticity:

• if low (red line in figure) –

A

V increases slowly per unit change in P

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7
Q
  1. surface tension
A
  • measure of the intermolecular attractive forces that stabilize liquid
  • these forces pull molecules together at an air-liquid interface
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8
Q

• for polar molecules like water, surface tension is created by

A

electrostatic force

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9
Q

Forces are strong on the —- side, but weak on the —- side.

A

liquid, air

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10
Q

Consequently, a net force pulls surface molecules toward the

A

water phase which reduces surface area. The remaining surface molecules exert an opposing force called surface tension.

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11
Q

Surface tension (ST) in bubbles cause the liquid lining to be pulled toward the

A

center (note that in a bubble there are two air/liquid interfaces).

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12
Q

inner pressure that is proportional to

A

surface tension and inversely proportional to the radius of the bubble
P = 2 x surface tension / radius

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13
Q

increase ST →

A

increase pressure

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14
Q

decrease radius →

A

increase pressure

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15
Q

If bubbles of difference size (e.g. r1 = 2r2; r1 > r2) are connected, the pressure difference will

A

equilibrate as air flows from bubble 2 into bubble 1.

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16
Q

Surface tension exists at the air-water interface in

A

alveoli, and, as in bubbles, tends to pull the alveolar walls inward. alveoli are connected to each other so the smallest ones are at the greatest risk of collapsing.

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17
Q

Ventilation must produce enough force to counteract the

A

tension.

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18
Q

The amount of force required is minimized by using surfactant from

A

Type II cells to reduce surface tension.

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19
Q

Surfactant reduces surface tension by reducing

A

intermolecular forces between water molecules. Thus, alveoli can be small and numerous, which increases surface area for gas exchange.

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20
Q

Surfactant is an

A

amphipathic phospholipid + protein molecule that forms a monolayer between air and water.

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21
Q

Hydrophilic/hydrophobic interactions concentrate

A

surfactant at the surface.

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22
Q

Reduces surface tension by

decreasing density of

A

H2O molecules

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23
Q

Surfactant does not create

A

additional surface tension and will increase compliance.

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24
Q

surfactant has greater effect in

A

small alveoli than in large

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25
Q

production is regulated by stretch receptors in

A

Type II cells; deep breathing increases surfactant production

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26
Q

Overcoming surface tension is more important than ——- in determining lung compliance

A

lung elasticity

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27
Q

Surfactant deficiency leads to respiratory distress. Acute respiratory distress syndrome is the 2nd leading cause of death in

A

premature infants

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28
Q

Airflow is inversely proportional to

A

airway resistance (re: flow = ΔP/R), and the tube radius is the primary determinant of R with R (resistance) being proportional to 1/r4

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29
Q

Other factors affecting R include: transpulmonary pressure –

A

dilates bronchioles during inspiration

30
Q

Other factors affecting R include: elasticity of tissue between outside of airways and alveolar walls also

A

opens airways during inspiration

31
Q

Other factors affecting R include: neural and chemical

A

control of smooth muscles

32
Q

Abnormalities in compliance and resistance have contrasting effects on

A

breathing

33
Q

increase R leads to

A

breathe more deeply (to increase ΔP)

breathe more slowly because airflow during expiration is limited

34
Q

decrease compliance

A

breathe more rapidly to compensate for reduced ΔV and ΔP

breathe shallowly to minimize muscle effort

35
Q

Asthma causes increased airway resistance because of inappropriate contraction of

A

smooth muscle

36
Q

increase R —->

Can be treated with….

A

à decrease airflow

can be treated with glucocorticoid therapy and/or bronchodilators

37
Q

Chronic obstructive pulmonary disease (COPD) also increases

A

airway resistance; often associated with smoking

38
Q

Emphysema - alveolar tissues

A

damaged or destroyed, perhaps due to overproduction of proteolytic enzymes

results in airway collapse, lack of recoil, and difficulty in expiring

39
Q

Chronic bronchitis - mucus or inflammation impairs

A

airflow

increased resistance –> deeper breathing

40
Q

tidal volume (TV) –

A

V entering lungs per breath; ~500 ml

41
Q

inspiratory reserve volume (IRV) –

A

max V inspired ; ~3000 ml

42
Q

expiratory reserve volume (ERV) –

A

V exhaled beyond TV; ~1500 ml

43
Q

residual volume –

A

V in lungs after maximum exhalation; ~1000 ml

44
Q

vital capacity – IRV + ERV + TV; ~

A

5000 ml

45
Q

total lung capacity – vital capacity + residual volume; ~

A

6000 ml

46
Q

Clinically relevant measures

A

vital capacity

forced expiratory volume in 1 second (FEV1)

47
Q

obstructive lung disease:

A

↓ FEV1; normal VC

48
Q

restrictive lung disease:

A

↓VC, normal FEV1

49
Q

Minute ventilation (ml per min) =

A

tidal V x respiratory rate, e.g. at rest, minute ventilation = 500 ml x 10 breaths/min = 5000 ml/min

50
Q

But not all air reaches

A

alveoli so must consider dead space.

51
Q

Anatomical dead space (~150 ml) reduces the amount of

A

fresh air reaching alveoli.

52
Q

Anatomical dead space reduces

A

alveolar ventilation (AV) which is a more accurate measure of air reaching the alveoli.

53
Q

AV =

A

(tidal V – dead space) x respiratory rate

54
Q

Alveolar dead space exists when there is a mismatch between

A

ventilation and bloodflow

55
Q

Alveolar dead space is always greater than —–, even in normal lungs, due to the effects of

A

zero, gravity on bloodflow

56
Q

Physiologic dead space is the sum of

A

anatomical dead space + alveolar dead space

57
Q

External respiration - gas exchange between

A

air and blood in pulmonary capillaries

58
Q

Internal respiration – gas exchange between

A

blood in systemic capillaries and cells (interstitial fluid)

59
Q

Steps of respiration

A
  1. ventilation (bulk flow) –
  2. external respiration (diffusion) –
  3. gas transport in blood (bulk flow) –
  4. internal respiration (diffusion) –
  5. cellular respiration - consume O2 and produce CO2
60
Q

Dalton’s Law for gases in a mixture of gases states that the total pressure is sum of the

A

individual pressures

61
Q

pressure exerted by gas is independent of

A

pressure exerted by other gases; proportional to temperature & concentration

62
Q

Partial pressures will vary with altitude, but —— does not

A

% composition

63
Q

Henry’s Law states that the amount of gas dissolved in a liquid is proportional to the

A

partial pressure of that gas in equilibrium with the liquid

64
Q

at equilibrium, Pgas is gas phase equals

A

Pgas in liquid phase

65
Q

At a gas mixture/liquid interface, gas will diffuse along a

A

partial pressure gradient

66
Q

Alveolar PO2 (how much O2 is available to the blood) is determined by

A

atmospheric PO2 –

rate of alveolar ventilation –

rate of cellular O2 consumption

67
Q

To summarize, alveolar gas pressures are altered by ratio of

A

ventilation to metabolism

68
Q

Local responses in smooth muscle minimize

A

ventilation –perfusion mismatches due to bronchoconstriction (left side below) or vasoconstriction (right side)

69
Q

Ventilation rates will affect

A

alveolar gas pressure

70
Q

Hypoventilation – ventilation decreased relative to

A

metabolism

71
Q

Ventilation-perfusion inequalities

These will lower

A

blood PO2. Recall there is always a normal mismatch due to gravity making perfusion greater at base of lung.

Physio Exam 3 (19 decks)

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