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
production is regulated by stretch receptors in
Type II cells; deep breathing increases surfactant production
26
Overcoming surface tension is more important than ------- in determining lung compliance
lung elasticity
27
Surfactant deficiency leads to respiratory distress. Acute respiratory distress syndrome is the 2nd leading cause of death in
premature infants
28
Airflow is inversely proportional to
airway resistance (re: flow = ΔP/R), and the tube radius is the primary determinant of R with R (resistance) being proportional to 1/r4
29
Other factors affecting R include: transpulmonary pressure –
dilates bronchioles during inspiration
30
Other factors affecting R include: elasticity of tissue between outside of airways and alveolar walls also
opens airways during inspiration
31
Other factors affecting R include: neural and chemical
control of smooth muscles
32
Abnormalities in compliance and resistance have contrasting effects on
breathing
33
increase R leads to
breathe more deeply (to increase ΔP) breathe more slowly because airflow during expiration is limited
34
decrease compliance
breathe more rapidly to compensate for reduced ΔV and ΔP | breathe shallowly to minimize muscle effort
35
Asthma causes increased airway resistance because of inappropriate contraction of
smooth muscle
36
increase R ----> Can be treated with....
à decrease airflow can be treated with glucocorticoid therapy and/or bronchodilators
37
Chronic obstructive pulmonary disease (COPD) also increases
airway resistance; often associated with smoking
38
Emphysema - alveolar tissues
damaged or destroyed, perhaps due to overproduction of proteolytic enzymes results in airway collapse, lack of recoil, and difficulty in expiring
39
Chronic bronchitis - mucus or inflammation impairs
airflow increased resistance --> deeper breathing
40
tidal volume (TV) –
V entering lungs per breath; ~500 ml
41
inspiratory reserve volume (IRV) –
max V inspired ; ~3000 ml
42
expiratory reserve volume (ERV) –
V exhaled beyond TV; ~1500 ml
43
residual volume –
V in lungs after maximum exhalation; ~1000 ml
44
vital capacity – IRV + ERV + TV; ~
5000 ml
45
total lung capacity – vital capacity + residual volume; ~
6000 ml
46
Clinically relevant measures
vital capacity forced expiratory volume in 1 second (FEV1)
47
obstructive lung disease:
↓ FEV1; normal VC
48
restrictive lung disease:
↓VC, normal FEV1
49
Minute ventilation (ml per min) =
tidal V x respiratory rate, e.g. at rest, minute ventilation = 500 ml x 10 breaths/min = 5000 ml/min
50
But not all air reaches
alveoli so must consider dead space.
51
Anatomical dead space (~150 ml) reduces the amount of
fresh air reaching alveoli.
52
Anatomical dead space reduces
alveolar ventilation (AV) which is a more accurate measure of air reaching the alveoli.
53
AV =
(tidal V – dead space) x respiratory rate
54
Alveolar dead space exists when there is a mismatch between
ventilation and bloodflow
55
Alveolar dead space is always greater than -----, even in normal lungs, due to the effects of
zero, gravity on bloodflow
56
Physiologic dead space is the sum of
anatomical dead space + alveolar dead space
57
External respiration - gas exchange between
air and blood in pulmonary capillaries
58
Internal respiration – gas exchange between
blood in systemic capillaries and cells (interstitial fluid)
59
Steps of respiration
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
Dalton’s Law for gases in a mixture of gases states that the total pressure is sum of the
individual pressures
61
pressure exerted by gas is independent of
pressure exerted by other gases; proportional to temperature & concentration
62
Partial pressures will vary with altitude, but ------ does not
% composition
63
Henry’s Law states that the amount of gas dissolved in a liquid is proportional to the
partial pressure of that gas in equilibrium with the liquid
64
at equilibrium, Pgas is gas phase equals
Pgas in liquid phase
65
At a gas mixture/liquid interface, gas will diffuse along a
partial pressure gradient
66
Alveolar PO2 (how much O2 is available to the blood) is determined by
atmospheric PO2 – rate of alveolar ventilation – rate of cellular O2 consumption
67
To summarize, alveolar gas pressures are altered by ratio of
ventilation to metabolism
68
Local responses in smooth muscle minimize
ventilation –perfusion mismatches due to bronchoconstriction (left side below) or vasoconstriction (right side)
69
Ventilation rates will affect
alveolar gas pressure
70
Hypoventilation – ventilation decreased relative to
metabolism
71
Ventilation-perfusion inequalities | These will lower
blood PO2. Recall there is always a normal mismatch due to gravity making perfusion greater at base of lung.