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Block 2 Week 6 > Pulmonary Mechanics > Flashcards

Pulmonary Mechanics Flashcards

1
Q

From the trachea to the alveolar sacs, what happens to Cross Sectional Area? What about velocity?

A

it increases

velocity decreases

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2
Q

What is the flow of blood through the respiratory system driven by?

A

pressure gradients

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3
Q

Where do you have gas exchange?

A

in the respiratory zone, THERE IS NO gas exchange in the conducting zone

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4
Q

For inspired air to reach the alveoli, where exchange actually occurs, it must first pass through a network of (blank) .

A

branching airways

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5
Q

Each airway divides into (blank) daughter airways at each branching point. Each division is referred to as a generation. There are approximately (blank) generations of airways in the lung. The result is a “pulmonary tree”.

A

two

23

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6
Q

Airways within the lung can be divided into two functional domains, what are they?

A

conducting zone, and respiratory zone

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7
Q

What are the components of the conducting zone and what volume does it contain, does gas exchange occur here?
Is this the first 16 generations or the last 7?

A

trachea, bronchi, bronchioles, and terminal bronchioles
150 ml
No gas exchange (anatomical dead space)
First 16

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8
Q

What are the components of the respiratory zone? What is the functional unit of the respiratory zone?
What volume does it contain?

A

respiratory bronchioles, alveolar ducts, alveolar sacs
acinus
3,000 ml

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9
Q

The distance from terminal bronchiole to distal alveolus is only a few (blank)

A

mm

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10
Q

Lung volumes and how they are defined can be illustrated by the results obtained from the use of a (blank).

A

spirometer

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11
Q

Normal/relaxed breathing is referred to as (blank)

A

tidal volume

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12
Q

You still have volume in your lungs even after expiration, this left over is called (blank)

A

functional residual capacity

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13
Q

The difference between max inspiration and max expiration is called the (Blank)

A

vital capacity

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14
Q

(blank) is the volume following maximal inspiration

A

total lung capacity (TLC)

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15
Q

(blank) is the volume left after maximal expiration.

A

residual volume (RV)

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16
Q

(blank) is TLC-RV

A

vital capacity (VC=TLC-RV)

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17
Q

(blank) is the volume inspired under normal resting conditions

A

Tidal Volume (Vt)

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18
Q

(blank) is the volume remaining at end of normal tidal expiration

A

Functional Residual Capacity (FRC)

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19
Q

(blank) is the volume expelled during maximal forced expiration starting at the end of normal tidal expiration.

A

Expiratory Reserve Volume (ERV)

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20
Q

(blank) is the volume inspired during maximal inspiratory effort starting at the end of normal tidal inspiration.

A

Inspiratory Reserve volume (IRV)

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21
Q

(blank) is the volume inspired during maximal inspiration starting after at the end of normal tidal expiration.

A

Inspiratory Capacity (IC)

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22
Q

When you lay down, the contents of your abdomen push down on your diaphragm which reduces (blank)

A

functional residual capacity

ERV decreases as well and IRV increases

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23
Q

Which lung volumes cannot be measured with a spirometery? Why?

A

FRC, TLC, RV

no real zero

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24
Q

What are the three ways to measure FRC?

A

nitrogen dilution, helium dilution, plethysmography

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25
Q

How does nitrogen dilution work?

A

breath in 100% oxygen, all nitrogen gets out of your lungs which then can be measured to figure out FRC

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26
Q

How does helium dilution work?

A

put helium in and wait for equilibrium and solve for amount in lungs

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27
Q

How does plethysmography work?

A

Use boyles law and measure change in pressure while an individual is in a box

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28
Q

How does positive breathing work?

A

create gradient by blowing air into your lungs

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29
Q

How does negative pressure breathing work?

A

create pressure gradient by making inside more negative via boyle’s law. (make intrapleural space negative by increasing volume) This negative pressure will allow the outside air to be more positive so air will go into your lungs

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30
Q

What is the most important muscle for negative breathing?

A

diaphragm

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31
Q

When the (blank) contracts, the volume of the chest cavity increases, while the abdominal contents are forced down and forward.

A

diaphram

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32
Q

Beside the diaphragm, the (blank) muscles also contribute to inspiration by pulling the ribs upward, which expands the chest cavity.

A

external intercostal

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33
Q

(blank) muscles play a role in inspiration during conditions such as exercise or in patients with chronic obstructive pulmonary disease.

A

accessory

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34
Q

What are the two helpful accessory muscles for inspiration?

A 
scalene muscles (which lift the first 2 ribs)
Sternomastoid muscles (which raise the sternum)
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35
Q

Which is an active process and which is a passive process inspiration or expiration?

A

inspiration is active and expiration is passive

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36
Q

(blank) is normally a passive process during quiet breathing. The lung and chest wall are (blank) and tend to return to their equilibrium positions upon relaxation of the inspiratory mus

A

expiration

elastic

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37
Q

During conditions such as exercise, expiration can become (blank). The most important muscles for expiration are what?

A 
active
Abdominal (rectus abdominus, internal and external obliques, transversus abdominis)
Internal intercostals pull their rib cage down
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38
Q

How do you find transpulmonary pressure?

A

transpulmonary pressure= alveolar pressure- intrapleural pressure

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39
Q

Is there a pressure gradient between alveolar pressure and atmospheric pressure? How is there a negative pressure in intrapleural space then?

A

no

Due to elastic recoil pressure which will allow for pressure gradient (transpulmonary pressure gradient)

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40
Q

At FRC alveolar pressure (PA) or the pressure inside the lungs is (blank) to the,atmospheric or barometric pressure (Pa)

A

equal

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41
Q

the intrapleural pressure (PIP) or the pressure in the space between the lungs and the chest wall is (blank) relative to the atmospheric pressure (PB).
As a results there is a (blank) (PL) gradient, which is the difference between the alveolar pressure (PA) and the intrapleural pressure (PIP).

A

negative

transpulmonary pressure

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42
Q

The (blank) reflects the elastic recoil properties of the lung and is sometimes referred to as the elastic recoil pressure.

A

transpulmonary pressure (PL)

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43
Q

Changes in lung volume are due to changes in the (blank)

A

transpulmonary pressure

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44
Q

Increase (blank) of chest cavity, reduce pressure, cause lung to expand due to elastic properties of chest wall and lungs, then that will decrease pressure in lungs which will then allow for a pressure gradient between atmosphere and lungs which will drive inspiration.

A

volume

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45
Q

changes in lung volume are due to changes in the (blank)

A

transpulmonary pressure

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46
Q

Changes in transpulmonary pressure are also associated with changes in the what?

A

transrespiratory pressure (Prs) and transthoracic pressure (Pcw)

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47
Q

What is the equation for transpulmonary pressure?

A

transpulmonary pressure (Pl)= alveolar pressure (PA)-intrapleural pressure (Pip)

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48
Q

What is the equation for transrespiratory pressure?

A

Prs=Alveolar pressure (PA)-atmospheric pressure (Pb)

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49
Q

What is the equation for transthoracic pressure (Pcw)?

A

Transthoracic pressure (Pcw)= intrapleural pressure (Pip)-atmospheric pressure (Pb)

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50
Q

Upon inspiration as you increase volume what happens to your intrapleural pressure? What happens to your flow? what happens to alveolar pressure?

A

becomes more negative
flow increases, reaches a peak and then decreases
Becomes more negative, peaks, then increases

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51
Q

As you decrease pressure you will increase (blank)

A

volume

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52
Q

The slope of a line on a pressure volume graph denotes what ?

A

compliance

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53
Q

Why don’t you want high compliance in the lung?

A

You don’t want high compliance because you want a change in pressure so that you can get exhalation and inhalation. In emphysema the compliance is increased and elastance is decreased.

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54
Q

Compliance is the inverse of (blank)

A

elastance (ΔP/ΔV)

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55
Q

The slope of the pressure-volume (ΔV/ΔP) curve is known as the (blank) .

A

compliance

56
Q

The compliance of the lung varies at different lung volumes. For example, the lung is much less compliant at (blank) lung volumes. This is normal.

A

high

57
Q

(blank) can also vary in different diseases states. For example, compliance decreases with pulmonary fibrosis, while compliance increases in conditions such as emphysema.

A

Compliance

58
Q

The pressure in the intrapleural space is less than atmospheric because of the (blank) of the lung.

A

elastic recoil properties

59
Q

The elastic properties of the lung are due to the (blank) that surround the bronchi and alveoli.

A

elastin and collagen fibers

60
Q

The relationship between lung volume and intrapleural pressure differ between inspiration and expiration. This is called (blank).

A

hysteresis

61
Q

The lung volume at any given intrapleural pressure is greater during (blank) than it is during (blank).

A

deflation (expiration)

inflation (inspiration).

62
Q

Even when there is no transpulmonary pressure gradient, there is still (blank) in the lung (the volume is not zero).

A

some air

63
Q

Inflating the lung with saline (instead of air) increases (blank) and eliminates (blank).

A 
compliance
hysteresis (eliminated due to lack of surface tension since there is no air water interface)
64
Q

What is responsible for hysteresis?

A

SURFACE TENSION
an air water interface which allows for surface tension (attractive forces between fluid molecules) which contributes to the process.

65
Q

What are the effects of surface tension on elasticity?

A

compliance decreases and elasticity increases

66
Q

(blank) is due to the liquid film lining the alveoli.

A

Surface tension

67
Q

Surface tension reflects the attractive forces that exist between adjacent molecules of liquid. Those forces are much (blank) than the forces that exist between liquid and gas molecules.

A

greater

68
Q

(blank) due to the liquid lining the alveoli creates a force that contributes to the elastic recoil pressure of the lung.

A

Surface tension

69
Q

The pressure created by surface tension is described by Leplace’s Law, what is the equation for this?

A

Pressure is proportional to Surface tension/ radius of the sphere

70
Q

Why do you get spheres with bubbles?

A

creates the least possible surface area via the forces of surface tension

71
Q

Leplace’s law indicates that the pressure created by surface tension is greater the smaller the (blank).

A

radius

72
Q

This would suggest that small alveoli would tend to collapse causing larger alveoli to get bigger and bigger until they burst. But this doesn’t happen. Why?

A

surfactant

73
Q

Surfactant is a complex secreted by (blank)

A

type II alveolar cells

74
Q

Surfactant consists of lipids (85-90%) and proteins (10-15%). The main component is the (blank). DPPC is (blank): it is hydrophobic on one end and hydrophilic on the other.

A

phospholipid dipalmitoyl phosphatidylcholine (DPPC).

amphipathic

75
Q

When surfactant molecules align themselves along the surface of the lung, their intramolecular repulsive forces (blank) the attractive forces of the liquid responsible for creating surface tension

A

oppose

76
Q

These repulsive forces of the surfactant are greater when the molecules are (blank) together. Thus surfactant tends to reduce the pressure created by surface tension more in smaller alveoli.

A

compressed

77
Q

These repulsive forces of the surfactant are greater when the molecules are compressed together. Thus surfactant tends to (blank) the pressure created by surface tension more in smaller alveoli.

A

reduce

78
Q

Hysteresis is due to (blank) not surfactant

A

surface tension

79
Q

By reducing surface tension, (blank) actually reduces hysteresis

A

surfactant

80
Q

Surfactant also increases (blank)

A

compliance

81
Q

(blank) counteracts the forces of surface tension, also increase compliance, also allows you to expand, contract alveoli.

A

surfactant

82
Q

What is this, surfactant is not produced by the lung until the 4th month of gestation and may not be fully functional until the 7th month.

A

infant respiratory distress syndrome

83
Q

What is this, hypoxia/hypoxemia leads to a decrease in surfactant

A

acute respiratory distress syndrome

84
Q

What is this:
increases effort required to inflate lungs because of decreased compliance
increases tendency for alveoli to collapse

A

Absence/loss of surfactant

85
Q

The elastic recoil properties of the lung that tend to collapse lung volume are offset by the (blank) that tend to expand the chest cavity. These opposing forces are what contributes to the negative intrapleural pressure at rest (functional residual capacity).

A

elastic recoil properties of the chest wall

86
Q

(blank) is determined by the balance between the outward elastic recoil properties of the chest wall and the inward elastic recoil properties of the lung.

A

Functional residual capacity

87
Q

Functional residual capacity is determined by the balance between the (blank) elastic recoil properties of the chest wall and the (blank) elastic recoil properties of the lung. There is a balance between these 2 effects.

A

outward

inward

88
Q

Empheysema has increased (blank)

A

TLC and lung volume and FRC

89
Q

Fibrosis has decreased (blank)

A

TLC and lung volume and FRC

90
Q

(blank) is determined by the balance between the outward elastic recoil properties of the chest wall and the inward elastic recoil properties of the lung.

A

Functional residual capacity

91
Q

The effect of (blank) on the lung itself contributes to a gradient of intrapleural pressure.

A

gravity

92
Q

The effect of gravity on the lung itself contributes to a gradient of intrapleural pressure.
At the base of the lung, where the effect of the weight of the lung is greatest, the intrapleural pressure is less (blank) than it is at the apex of the lung.

A

negative

93
Q

the alveoli in the base of the lung are more (blank) than those at the apex.

A

compressed

94
Q

Compliance at the base is (blank) than compliance at the apex.

A

greater

95
Q

Transpulmonary pressure is going to be greater at the (blank)

A

apex than at the base

96
Q

At normal resting lung volumes the Alveoli in the base of the lung are operating at a low volume, where according to the pressure-volume relationship the lung is very (blank). As such, small changes in transmural pressure tend to cause a greater change in (blank).

A

compliant

volume

97
Q

At normal resting lung volumes the Alveoli in the apex of the lung are operating at a higher volume, where the compliance is (blank). As such, small changes in transmural pressure tend to cause less of a change in volume.

A

lower

98
Q

At normal resting lung volumes the Alveoli in the base of the lung are operating at a (blank) volume. Alveoil in the apex of the lung are operating at a (blank) volume.

A

low

high

99
Q

At normal resting lung volumes the alveoli at the base of the lung tend to be better (blank) than those in the apex.

A

ventilated

100
Q

At low resting lung volumes
If the intrapleural pressure at the base of the lung exceeds atmospheric pressure, these alveoli can (blank), in which case small changes in transpulmonary pressure may not be sufficient to inflate them.

A

collapse

101
Q

At low resting lung volumes, alveoli in the apex of the lung may be operating at a volume where compliance is relatively (blank), so that small changes in transpulmonary pressure cause significant changes in volume and therefore ventilation.

A

high

102
Q

There is some interaction between lung, chest wall and pleural space which creates friction which contributes to (blank).

A

non elastic resistance

103
Q

What are the two resistances that must be overcome for breathing?

A 
elastic resistance (elastic properties of lung) 
non-elastic resistance
104
Q

Air flows through tubes when there is a pressure gradient and it produces either (blank) or (blank).
What has greater resistance?

A 
laminar airflow (at low flow rates)
turbulent airflow (at high flow rates)
Turbulent flow has greater resistance
105
Q

The pressure-flow relationship for lamina airflow is described by poiseuille’s law, which states what?

A

that flow of air is directly related to pressure gradient and radius to the fourth power. I.e change radius, huge difference in air flow

106
Q

changing the (blank) is one of the most important ways you can affect airflow

A

radius (16 fold)

107
Q

For turbulent flow, it is proportional to what?

A

the square root of the change of pressure

108
Q

How can you determine if flow will be laminar or turbulent?

A

Reynolds number, the higher the reynolds number the more likely flow will be turbulent

109
Q

What is the equation for reynolds number

A

Re= 2rvd/ viscosity

110
Q

Turbulent flow is most likely to occur under what conditions?

A

velocity is high, radius is large and gas is dense

111
Q

turbulent flow tends to occur in the (blank) at high flow rates (i.e., during exercise)

A

trachea

112
Q

laminar flow is most likely to occur in (blank)

A

smaller airways (i.e., terminal bronchioles)

113
Q

As airways branch on their way to the alveolar sacs, they become smaller. According to Poiseuille’s law, one might think that the resistance to airflow continues to increase as you move further out into the bronchial tree. However, the resistance peaks at the (blank) (~7th generation), and then it actually decreases the further out you go. This is because the total cross sectional area actually increases because of the large number of airways

A

medium sized bronchioles

114
Q

Increase CSA you get decrease in (blank).

A

resistance

115
Q

Airway (blank) is the principal factor affecting airway resistance, however lung volume affects airway radius.

A

radius

116
Q

(blank) are supported by the radial traction of the surrounding lung tissue, and their caliber increases as the lung expands.

A

Bronchi

117
Q

At low lung volumes, (blank) airways can completely close especially at the base of the lung.

A

small

118
Q

Patients with increased airway resistance often breathe at (blank) lung volumes in an attempt to reduce that resistance.

A

high

119
Q

The connective tissue that surrounds the airways of the lungs are called the parenchyma. This forms a sort of scaffold around the airways, keeping them open with a force known as (blank) .

As inspiration takes place, the traction increases as the fibers that make the parenchyma are stretched.

A

radial traction

120
Q

(blank) contraction regulates airway radius, and thus resistance.

A

Bronchial smooth muscle

121
Q

(blank) stimulation primarily involving circulating epinephrine activates (blank) relaxing airway smooth muscle and decreasing resistance.

A

sympathetic

beta-2 adrenergic receptors

122
Q

(blank) stimulation involving direct activation of (blank) receptors by acetylcholine contracts airway smooth muscle and increases resistance.

A

parasympathetic

muscarinic

123
Q

(blank) such as leukotrienes and histamine released during asthma attacks or allergic responses cause bronchial smooth muscle constriction increasing airway resistance

A

Inflammatory mediators

124
Q

Airway resistance can also be affected by the degree of (blank). This can be illustrated by plotting the relationship between flow and volume during expiration.

A

respiratory effort

125
Q

Flow rises rapidly to a (blank) value but then it declines over the remainder of expiration.The degree of expiratory effort does not affect the (blank) in the declining phase. Something limits expiratory flow over most lung volumes.

A

high

flow rate

126
Q

As you get more and more effort upon inspiration you get greater (blank). Because of the effect this can have on airway, pressure causes the airways to expand.. However during (blank) this does not hold true. No matter what effort we give we cannot increase our rate of flow past a certain point upon expiration.

A

flow

expiration

127
Q

During preinspiration what is happening to your intrapleural pressure, alveolar pressure, transpulmonary pressure, and transpulmonary pressure gradient?

A

intrapleural pressure is negative
alveolar pressure is at equilibrium
transpulmonary pressure is positive
transpulmonary pressure gradient is uniform

128
Q

For the dynamic compression of airways, the limiting factor is the effect that the increase in intrapleural pressure has on the (blank) pressure along the airway

A

transpulmonary

129
Q

During inspiration, what is happening to your intrapleural pressure, alveolar pressure, transpulmonary pressure?

A

intrapleural pressure becomes neegative
alveolar pressure isn’t at equilibrium w/ atmospherc pressure
The transpulmonary pressure gradient isn’t uniform
as you move closer to the mouth, it becomes more positive, increasing airway diameter and reducing resistance

130
Q

During end inspiration, what is happening to your intrapleural pressure, alveolar pressure, transpulmonary pressure?

A

intrapleural pressure is more negative than preinspiration
alveolar pressure is at equilibrium w/ atmospheric pressure
transpulmonary pressure gradient is uniform again

131
Q

During forced expiration, what is happening to your intrapleural pressure, alveolar pressure, transpulmonary pressure?

A

intrapleural pressure increases dramatically
alveolar pressure is not at equilibrium w/ atmospheric pressure
transpulmonary pressure gradient is no longer uniform
As you move closer to the mouth it can exceed the airway pressure, decreasing airway diameter and increasing resistance

132
Q

As you move closer to the mouth what happens to your airway diameter and resistance?

A

airway diameter gets smaller and your resistance increases

133
Q

You can cause airways to collapse if you give what?

A

very hard forced expiration

134
Q

Expiration is normally a passive process. If you have elastic problem (like in empheysema) you will have increase FRC becuase they have problems breathing out. Now your expiration is no longer (blank) but is now (blank).

A

passive, it is now active

135
Q

During (blank), transpulomary pressure is reduced and now you are more likely to collapse airways and increase resistance

A

forced expiration

Block 2 Week 6 (6 decks)

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