Lecture slide material Flashcards

1
Q

Boyle’s law tells us about which phase of respiration?

A

Ventilation.

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2
Q

Fick’s law of diffusion tells us about:

A

Both external diffusion and internal diffusion.

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3
Q

What is external diffusion?

A

Passive movement of gasses between the alveoli and pulmonary circulation.

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4
Q

What is internal diffusion?

A

Passive transport between systemic circulation and tissue cells.

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5
Q

Henry’s law tells us about which phase of respiration?

A

Transportation of gasses in the blood.

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6
Q

Minute ventilation:

A

The total volume of air moved per minute.

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7
Q

Ventilation:

A

The cyclic process where air goes into the alveoli, and an equal volume of pulmonary gas is exhaled.

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8
Q

What is the normal tidal volume?

A

500 mL air exchanged/breath.

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9
Q

Respiratory rate:

A

12-20 breaths/minute.

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10
Q

Inspiration is __________, meaning it requires _________ input going to the muscles of inspiration.

A
  1. Active.
  2. Neural.
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11
Q

True or false: Expiration is active, requiring ATP.

A

FALSE: Expiration is passive, from relaxation of respiratory muscles.

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12
Q

In positive pressure breathing, inspiration is ________ and expiration is _________.

A
  1. Passive.
  2. Active.
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13
Q

Dalton’s law tells us about:

A

Pressure gradient.

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14
Q

Airflow in the upper airways is:

A

Bulk flow (Mass flow) of air from a pressure difference.

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15
Q

Where does the forward velocity of airflow stop in the airways?

A

Where we transition from the conducting zone to the respiratory zone.

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16
Q

Lungs tend to recoil ________.

A

inward.

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17
Q

Chest wall recoils _________.

A

Outward.

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18
Q

At rest, what occurs?

A

The lungs are at functional residual capacity, where inward and outward pulling forces are equal due to the action of intrapleural pressures.

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19
Q

During inspiration, what happens to intrapleural pressure?

A

It becomes more negative.

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20
Q

The interaction between the _____ and the ______ ________ is what holds the alveoli open.

A
  1. Lung.
  2. Chest wall.
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21
Q

During inspiration, what occurs to intrapleural pressure/airflow/alveolar pressure/tidal volume?

A
  1. Tidal volume increases - to 500 mL.
  2. Intrapleural pressure becomes MORE negative.
  3. Airflow becomes negative (air moves into the lungs)
  4. Alevolar pressure becomes negative, making it less than atmospheric pressure.
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22
Q

During expiration, what occurs to intrapleural pressure/airflow/alveolar pressure/tidal volume?

A
  1. Tidal volume decreases back to 0.
  2. Intrapleural pressure becomes less negative.
  3. Airflow is positive - air moves out of the lungs.
  4. Alveolar pressure exceeds atmospheric pressure.
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23
Q

True or false: The volume of fresh air entering and leaving the nose per minute is equal to the volume of fresh air entering and leaving the alveoli per minute.

A

FALSE: they are not equal.

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24
Q

During inspiration, the first air to enter the alveolar space:

A

Air that is already in the conducting airways.

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25
Q

During end inspiration, what occurs to intrapleural pressure/airflow/alveolar pressure/tidal volume?

A
  1. Tidal volume is at maximum - 500 mL.
  2. Intrapleural pressure is the most negative possible.
  3. Airflow = 0.
  4. Alveolar pressure = atmospheric pressure = 0.
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26
Q

In what stage do we have mixing of fresh air, air in the anatomic dead space, and alveolar air?

A

End-inspiration.

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27
Q

Composition of alveolar air - at sea level:

A
  1. PAO2 = 100 mmHg.
  2. PACO2 = 40 mmHg.
  3. PAH2O = 47 mmHg.
  4. PAN2 = 573 mmHg.
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28
Q

Air in the anatomic dead space never participated in:

A

Gas exchange.

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29
Q

Mixed air from the alveoli will participate in:

A

Gas exchange.

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30
Q

What is in the anatomic dead space at end-expiration?

A
  1. Fresh air that never did gas exchange.
  2. Mixed air that did participate in gas exchange.
  3. Mixed air that remained in the dead space.
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31
Q

What is in the anatomic dead space during pre-inspiration?

A

Just mixed air.

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32
Q

What is in the anatomic dead space during inspiration?

A
  1. Fresh air - hasn’t done gas exchange.
  2. Mixed air that did gas exchange.
  3. Mixed air from anatomic dead space.
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33
Q

What happens in the anatomic dead space at end-inspiration?

A

Mixing of the new and old air, while some fresh air remains unmixed.

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34
Q

What is expired out from the anatomic dead space?

A
  1. Fresh air that did not do gas exchange.
  2. Mixed air.
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35
Q

If you want an air sample that most closely represents alveolar air that is participating in gas exchange, what part of expiration do you want?

A

End expiration -

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36
Q

Content of expired air:

A
  1. 13-16% O2
  2. 4-6% CO2
  3. 78% N2.
  4. Others 1%
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37
Q

Does nitrogen diffuse into the tissues?

A

No tissues do not use it.

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38
Q

What do rebreather systems do?

A
  1. Only supply a little extra O2.
  2. Remove CO2.
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39
Q

Work of breathing is influenced by:

A
  1. Respiratory rate.
  2. Respiratory volume.
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40
Q

________ work of breathing: Energy required to overcome elastic forces and inflate the lung.

A

Elastic work.

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41
Q

__________ work of breathing: Energy required to overcome frictional forces of moving air through the system.

A

Resistive work.

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42
Q

What does a high rate of resistive work in breathing tell us?

A

More air is moving through the airways, increasing airway friction.

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43
Q

Why does elastic work decrease at higher respiratory rates?

A

Higher respiratory rate, means smaller changes in alveolar size. Alveoli do not have as much time to decrease in size fully, so elastic forces are less impactful.

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43
Q

An increased respiratory rate is seen in diseases that cause:

A

An increased elastic work - or more elastic forces.

44
Q

A decrease in respiratory rate will be seen in diseases that cause:

A

That has increased airflow resistance, causing an increase in resistive work.

45
Q

Examples of diseases that cause increased elastic resistance:

A
  1. Shallow, rapid breaths.
  2. Fibrosis.
46
Q

Examples of diseases that cause increased airflow resistance:

A
  1. Deeper, slower breaths.
  2. Asthma.
  3. Chronic bronchitis.
  4. Emphysema.
47
Q

Forces to overcome in ventilation:

A
  1. Elastic recoil of the lungs - stored energy from inspiration used in expiration.
  2. Alveolar surface tension.
  3. Resistive work - airway resistance.
48
Q

Elasticity:

A

The tendency to oppose stretch; the ability to return to its original configuration.

49
Q

What is the result of opposing elastic forces between the chest wall and lungs?

A

Negative pressure in the intrapleural space.

50
Q

What would happen if someone was stabbed and air got into the intrapleural space?

A

The pleural membranes will separate causing lungs to recoil in, and chest to recoil out - ultimately causing collapsed lung.

51
Q

What do we call the ease which the lung can be inflated?

A

Pulmonary compliance.

52
Q

Define pulmonary compliance:

A
  1. The change in volume for a given change in pressure.
  2. The ease that the lung can be stretched.
53
Q

Compliance is the inverse to:

A

Elasticity.

54
Q

True or false: Compliance is a component of both the lungs and the chest wall.

A

TRUE!

55
Q

High compliance would indicate:

A
  1. Small distending pressure - causing a large change in volume.
  2. Energy efficient breathing.
56
Q

What is the pressure volume curve for inflation called:

A

Hysteresis loop

57
Q

What determines the shape of the hysteresis loop?

A
  1. Sufactant - variable surface tension.
  2. Elastic recoil.
  3. Alveolar interdependence.
58
Q

What would happen with greater compliance at a lower lung volume:

A
  1. Have the same change in pressure, but a greater increase in volume.
  2. As the lungs expand, compliance decreases - Stretching of elastin fibers and increased alveolar surface tension as we inhale.
59
Q

Emphysema is a disease that causes degeneration of lung tissue, what effects will this have on compliance?

A
  1. Make it easier to inhale but harder to exhale.
  2. Increased compliance, but decreases elasticity.
60
Q

Fibrosis is a disease that will cause scarring and thickening of lung tissue, what effect will this have on compliance?

A
  1. It is harder to inhale or inflate the lungs.
  2. Decreased compliance.
61
Q

______________: Caused by accumulation of air in the intrapleural space, causing equalization of intrapleural pressure with atmospheric pressure.

A

Pneumothorax - collapsed lung.

62
Q

Which forces are acting to collapse the alveoli?

A
  1. Elastic recoil of alveoli.
  2. Surface tension of water.
63
Q

What will reduce surface tension in alveoli, preventing collapse?

A

Surfactant.

64
Q

What property will help keep alveoli open because 1 alveoli wall pulls on other alveoli, and counters elastic recoil?

A

Alveolar interdependence.

65
Q

What does surface tension try to prevent?

A

Alveolar expansion. Acting as a recoil force that is functionally the same as elastic recoil.

66
Q

Surface tension is determined by what law?

A

Laplace’s law.

67
Q

2 Different sized alveoli are connected via a tube. Which way does air move? What would prevent this from occurring.

A

The larger one would fill, and the smaller one would collapse. Surfactant prevents this from happening.

68
Q

What is surfactant?

A

A lipoprotein on the inner surface of the alveoli, made of phospholipids. This acts locally to reduce surface tension by breaking hydrogen bonds - stabilizing the individual alveoli.

69
Q

True or false: As alveoli size increases, the number of surfactant molecules will increase.

A

False: Size in alveoli does not change number of surfactant molecules.

70
Q

_____________ allows for two differently sized alveoli to have equal pressure, and fill fairly.

A

Surfactant.

71
Q

Increase ________ ________ = decreased compliance.

A

surface tension.

72
Q

If the lungs are filled with fluid, what happens to surface tension and compliance?

A
  1. Surface tension is decreased, due to limiting the air-water interface.
  2. Compliance in increased.
73
Q

P-50:

A

The force (pressure) needed to inflate the lung to 50% of total lung capacity.

74
Q

How to find the amount of pressure needed to overcome surface tension alone?

A

P1 - P2

75
Q

In a saline filled lung, what is the only force that you need to overcome?

A

Elastic recoil of the lungs - cause there is no surface tension due to a lack of a air-water interface.

76
Q

In an air-filled lung, what forces do you have to overcome to inflate the lungs?

A

Surface tension and elastic recoil.

77
Q

Without surfact, what would happen to P-50?

A

It would get much larger, and are slope would get less steep.

78
Q

___________ _____________: Is opposing alveolar collapse from alveolar surface tension/elastic recoil, by negative intrapleural pressure holding them open. Causes walls of neighboring alveoli to pull each other open.

A

Alveolar interdepence.

79
Q

_________ pressure breathing: Normal inspiration leads to alveoli being pulled open first, and making an inward change in pressure.

A

Negative pressure breathing.

80
Q

___________ pressure breathing: Centrally located alveoli expand and push open outer alveoli. Air moves between adjacent alveoli via alveolar pores, known as collateral ventilation.

A

Positive pressure breathing.

81
Q

Outer alveoli can potentially become compressed, or collapse, in what kind of ventilation?

A

Positive pressure ventilation.

82
Q

___________ work: Energy required to overcome frictional forces.

A

Resistive work.

83
Q

Airway resistance between gas molecules is increased with:

A
  1. High flow rates.
  2. Turbulent flow.
  3. High respiratory rates.
  4. Upper airway obstructions.
  5. Increased air density.
  6. Decreased airway radius.
84
Q

__________ _______ only occurs in the smallest airways, where flow velocity is low.

A

Laminar flow.

85
Q

___________ ______ - Flow in the large chambers (nose, pharynx, trachea), that may be associated with the vibration of the airways making sound.

A

Turbulent flow.

86
Q

___________ ______ - Airflow is a mixture of laminar and turbulent flow.

A

Transitional flow.

87
Q

30-50% of resistance is in the:

A

Upper conducting airways, maximal around the 3rd generation. Most during nose breathing.

88
Q

Airway resistance is not relevant in what region of the lungs?

A

In the respiratory zone, after the 16th generation.

89
Q

Airway resistance __________, while lung volume ___________.

A
  1. Decreases.
  2. Increases.
90
Q

In normal tissue, how does lung tissue affect resistance?

A
  1. Lung tissue helps hold airways open, reducing resistance
91
Q

Loss of lung tissue would cause an ________ in __________.

A

Increase in resistance.

92
Q

During forced expiration, intrapleural pressure is:

A

positive - leading to dynamic compression.

93
Q

What is dynamic compression?

A

Positive intrapleural pressure during forced expiration, that collapses airways and increases resistance, decreasing airflow.

94
Q

What is the most important control of airway smooth muscle tone?

A

Neural control.

95
Q

True or false: There is both sympathetic and parasympathetic innervation to the airway smooth muscle, parasympathetic just works more effectively.

A

FALSE - There is no direct sympathetic innervation of airway smooth muscle.

96
Q

Airway smooth muscle will respond to sympathetic input via:

A

circulating (hormonal) sympathetic (adrenergic) agents - epinephrine.

97
Q

What is the most important determinant of bronchomotor tone?

A

Parasympathetic - via the vagus nerve.

98
Q

What results from parasympathetic bronchoconstriction:

A

Can completely close the lumen of small airways

99
Q

Increased PANS input to the bronchi will cause what? What about decreased?

A
  1. Increased will cause bronchoconstriction.
  2. Decreased will bronchodilation.
100
Q

What receptor does ach act on in the airway smooth muscle? What result does it cause?

A
  1. M3
  2. Increased inositol triphosphate (IP3), causing increased Ca++, resulting in airway smooth muscle contraction.
101
Q

What happens if Ach binds to receptors on vascular endothelial cells?

A

Vasodilation.

102
Q

How do non-cholinergic parasympathetic nerves work on the lungs?

A
  1. Stimulation of non-cholinergic parasympathetic nerves causes an increase in nitric oxide production.
  2. Leads to increased cGMP.
  3. Subsequent smooth muscle relaxation occurs.
103
Q

____________ ______________: Bind to a large number of B2 adrenergic receptors in the airways, causing bronchodilation.

A

Circulation catecholamines.

104
Q

Why would we use acetylcholine medications in the clinic?

A
  1. Ach will cause bronchodilation, which may be necessary for laryngoscopy, foreign body removal, etc.
105
Q

The majority of local cellular mechanisms cause __________________ to occur.

A

bronchoconstriction.

106
Q

True or false: The lungs receive blood flow from both systemic (bronchial) and pulmonary circulations.

A

True!

107
Q

What does the bronchial circulation provide?

A

Nutrients to pulmonary airways, and parenchyma.

108
Q
A