Mechanical Properties of the Lung (B2: W6) Flashcards

1
Q

Describe the pulmonary tree

A

A series of airways, and each divides into two daugher airways

  • Approximately 23 generations total
  • Conducting airways - first 16 generations or so
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2
Q

When does the respiratory zone begin in the pulmonary tree?

A

At generation 17 and above

  • Gas exchange occurs here
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3
Q

The diameter of the bronchioles decreases as they branch; what happens to the total cross sectional area?

A

Total cross sectional area increases dramatically

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4
Q

What is the volume of the conducting zone?

A

150 mL

  • Anatomical dead space - no gas exchange
  • Trachea, bronchi, bronchioles, and terminal bronchioles
  • First 16 generations
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5
Q

What is the volume of the respiratory zone?

A

3 Liters (3,000 mL)

  • Respiratory bronchioles, alveolar ducts, alveolar sacs
  • Functional unit is called an acinus
  • DIstance from terminal bronchiole to distal alveolus is only a few mm
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6
Q

What is the total lung capacity?

A

TLC = volume following maximal inspiration

  • Vital capacity + Residual volume
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7
Q

What is residual volume?

A

RV = volume left after maximal expiration

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8
Q

What is vital capacity?

A

VC = Total lung capacity - Residual volume

  • Inspiring as much as possible and expiring as much as possible
    • Beyond peaks of tidal volume
    • Upper limit for total capacity
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9
Q

What is the tidal volume?

A

VT = volume inspired under normal resting conditions

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10
Q

What is the functional residual capacity?

A

FRC = volume remaining at the end of normal tidal expiration

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11
Q

What is the expiratory reserve volume?

A

EVR = volume expelled during maximal forced expiration starting at the end of normal tidal inspiration

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12
Q

What is the inspiratory reserve volume?

A

IRV = volume inspired during maximal inspiratory effort starting at the end of normal tidal inspiration

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13
Q

What is the inspiratory capacity?

A

IC = volume inspired duing maximal inspiration starting at the end of normal tidal expiration

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14
Q

What comprises the total lung capacity in a person standing upright?

A

Half is inpiratory capacity (3.0 L) and half is functional residual capacity (3.0 L)

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15
Q

What happens to the distribution of the total lung capacity when a person lies down supine?

A

Functional residual capacity decreases

  • Inspiratory capacity increases
  • Inspiratory reserve volume: larger
  • Expiratory reserve volume: smaller
  • Tidal volume doesn’t really change
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16
Q

What is the reason for the changes in lung volumes while lying supine?

A

Abdominal contents push up more on the diaphragm → change in distribution

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17
Q

Which lung volumes cannot be measured using spirometry?

A

We can’t define zero, so can’t measure

  • Functional residual capacity
    • Once you calculate FRC via another method, you can calculate others
  • Residual volume
  • Total lung capacity
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18
Q

How is functional residual capacity calculated?

A
  • Nitrogen washout (nitrogen dilution method)
    • Start with air in the lungs and goes to the compartment
  • Helium dilution
    • Start with air in the container and go to the lungs
  • Plethymography
    • Uses Boyle’s law
    • During inspiration in a closed box: ∆Vbox = ∆Vlungs
    • ∆Vlungs = FRC
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19
Q

What are the basics of pulmonary mechanics?

A

To understand the mechanics of breathing, one must understand

  • The forces that affect the movement of air into and out of the lungs
  • The resistances that must be overcome
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20
Q

What are the forces that move air in and out of the lungs?

A
  • Positive pressure breathing
  • Negative pressure breathing

Boyle’s law: Pressure (P) x Volume (V) = a constant (k)

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21
Q

How does positive pressure breathing work?

A
  • Create a gradient: pressure outside is greater than pressure inside
  • Ex: ventilator
  • Not what we use normally
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22
Q

How does negative pressure breathing work?

A
  • Pressure gradient: greater outside than inside
  • Create negative pressure in the alveolar space
  • Intrapleural space needs to be more negative than the alveolar space (< -10 cm H2O)
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23
Q

What is the most important muscle involved in respiration?

A

Diaphragm

  • When it contracts, volume of the chest cavity increases
  • Abdominal contents are forced down and forward
  • Decrease in intrapleural pressure
  • Inspiration is active, expiration is passive
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24
Q

How are the external intercostal muscles involved in inspiration?

A

They pull the ribs upward, which expands the chest cavity

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25
Q

What are the most important muscles for expiration?

A

Expiration is passive through relaxation

Can become active during exercise

  • Abdominal
    • Rectus abdominus
    • Internal and external obliques
    • Transversus abdominus
  • Internal intercostals - pull the ribcage down
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26
Q

What two components are essential for creating the pressure gradient for breathing?

A

Atmosphere and alveolar space (driving pressure)

  • Intrapleural space has to be negative
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27
Q

Describe the elastic properties to lung and to chest wall

A
  • Lungs tend to recoil inwards
  • Chest wall is typically going the opposite direction - springs outward with elastic recoil
  • These properties create negative intrapleural pressure
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28
Q

How is transpulmonary pressure calculated?

A

Transpulmonary pressure = alveolar pressure - intrapleural pressure

  • Positive transpleural pressure
  • Due to elastic recoil - referred to as the elastic recoil pressure
  • Changes in lung volume are due to changes in the transpulmonary pressure
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29
Q

When is the alveolar pressure (PA - pressue inside the lungs) is equal to the atomospheric or barometric pressure (PB)

A

At functional residual capacity (FRC)

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30
Q

What is the intrapleural pressure?

A

PIP - the pressure in the space between the lungs and the chest wall

  • Intrapleural pressure is negative relative to the atmospheric pressure (PB)
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31
Q

What additional factors are associated with changes in the transpulmonary pressure?

A

Transrespiratory pressure (PRS) and transthoracic pressure (PCW)

  • Transrespiratory pressure = alveolar pressure (PA) - atmospheric pressure (PB)
  • Transthoracic pressure = intrapleural pressure (PIP) - atmospheric pressure (PB)
32
Q

What happens to the intrapleural pressure during inspiration and expiration

A
  • Inspiration
    • Intrapleural pressure gets more negative
  • Expiration
    • Intrapleural pressure increases
33
Q

What happens to the alveolar pressure during inspiration and expiration?

A

Alveolar pressure gets more negative

  • As air moves into the lung, the pressure gradient becomes equilibrated
34
Q

What does the slope of the pressure-volume relationship reflect?

A

Slope reflects compliance

  • Change in volume for a given change in pressue
  • Starting from residual volume and going to total lung capacity
35
Q

How is compliance related to elastance?

A

Compliance is the inverse of elastance

  • Properties of lung due to connective tissue and elastic fibers
  • Compliance: ∆V/∆P
  • Elastance: ∆P/∆V
36
Q

What happens to compliance at higher lung volumes?

A

Slope/compliance becomes less at higher lung volumes

  • As you inflate lungs, the fibers get more stretched
  • Relationship gets flatter
37
Q

What happens to the compliance of the lungs in the event of emphysema?

A

There is a breakdown of connective tissue of the lungs

  • Compliance increases
  • Lungs become more distensible - slope becomes steeper
38
Q

What happens to the compliance of the lungs in the event of pulmonary fibrosis?

A

Compliance decreases with pulmonary fibrosis

  • Compliance can vary in different disease states
39
Q

What components are responsible for the elastic properties of the lungs?

A

Elastin and collagen fibers that surround the bronchi and alveoli

  • The pressure in the intrapleural space is less than atmospheric because of the elastic recoil properties of the lungs
40
Q

Explain the phenomenon of hysteresis

A
  • The relationship between lung volume and intraplerual pressure differs between inspiration and expiration - known as hysteresis
  • The lung volume at any given intrapleural pressure is greater during deflation (expiration) than it is during inlation (insparation)
    • Compliance is greater during expiration
  • Even when there is no trasnpulmonary pressure gradient, there is still some air in the lung (the volume is not zero)
41
Q

How does inflating the lung with saline rather than air increase compliance and eliminate hysteresis?

A

Surface tension!

  • Surface tension is due to the liqud film lining the alveoli
  • Reflects the attractive forces that exist between adjacent molecules of liquid
    • Greater than the forces that exist between liquid and gas molecules
  • Creates a force that contributes tot the elastic recoil pressure of the lung
42
Q

What defines the relationship between pressure, surface tension, and radius?

A

Laplace’s Law

  • Pressure generated by surface tension is directly proportional to surface tension
  • Pressure is indirectly proportional to the radius of the alveolus
43
Q

What does Leplace’s law indicate about pressure and radius as alveoli get smaller?

A

Pressure created by surface tension is greater the smaller the radius

  • Surface tension is greater in small alveoli
    • Greater elastic recoil
44
Q

Why do small alveoli not collapse, causing larger alveoli to get bigger until they burst?

A

Surfactant lines the alveoli

  • Main component: dipalitoyl phosphatidylcholine (DPPC)
    • Amphipathic: hydrophobic and hydrophillic
    • These interactions create opposing forces that counteract the attractive forces of surface tension
  • In small alveoli, the molecules are closer together and thus the repulsive forces are greater
    • Surfactant tends to reduce the pressure created by surface tension
45
Q

Which cells secrete surfactant?

A

Type II alveolar cells

  • Consists of lipids (85-90%) and proteins (10-15%)
  • Amphipathic
46
Q

What is the relationship between surfactant and hysteresis?

A

Hysteresis is due to surface tension, NOT surfactant

  • By reducing surface tesion, surfactant actually reduces hysteresis
  • Surfactant also increases compliance
47
Q

What is the significance of surfactant in premature infants?

A

Don’t produce enough surfactant

  • Infant respiratory distress syndrome (RDS)
    • Common in infants born more than 6 weeks prematurely
    • Affects nearly all infants born more than 12 weeks prematurely
  • Alveoli can collapse
  • Decrease in compliance so it is harder to get air in
48
Q

What is the cause of acute respiratory distress syndrome?

A

Hypoxia/hypoxemia leads to a decrease in surfactant

  • Increases effort requried to inflate lungs because of decreased compliance
  • Increases tendency for alveoli to collapse
49
Q

What happens in the event of a pneumothorax?

A

There is a hole in the chest wall

  • Lung tends to contract inward, so it shrinks
  • Chest tends to contract outward, so the volume of the chest cavity will tend to increase and expand
  • Equalizes the atmospheric and intrapleural pressures
50
Q

How is functional residual capacity determined?

A

FRC is determined by the balance between outward elastic recoil properties of the chest wall and the inward elastic recoil properties of the lung

  • An increase in airway pressure expands the lung
    • It’s natural state is to collapse
  • Chest wall is the opposite
    • At equillibrium, it expands and volume is high
51
Q

How do emphysema and fibrosis affect the compliance of the lung?

A
  • Emphysema can increase compliance
  • Fibrosis can decrease compliance
    • More pressure required for a change in volume
52
Q

What happens to the functional residual capacity with emphysema?

A
  • Lung can’t compete with the elastic properties of the chest wall, and the chest wall will win out
    • Upward shift in curve
  • Functional residual capacity increases dramatically
  • Vital capacity will be reduced

Too inflated

53
Q

What happens to the functional residual capacity with fibrosis?

A
  • The lung becomes less compliant
    • Equilibrium point shifted down
  • Functional residual capacity is decreased
  • Vital capacity is reduced

Cannot fully inflate

54
Q

What is the cause of regional differences in ventillation of the lungs?

A

The effect of gravity contributes to a gradient of intrapleural pressure

  • At the base, where the effect of the weight is the greatest, the intrapleural pressure is less negative than it is at the apex
  • As a consequence, the alveoli in the base of the lung are more compressed
55
Q

Why are alveoli at the base of the lung ventilated better than those in the apex?

A
  • Alveoli at base are operating at a low volume where the lung is very compliant
    • Small changes in transmural pressure tend to cause a greater change in volume
  • Alveoli at the apex are operating at a higher volume where compliance is lower
    • Small changes in transmural pressure tend to cause less of a change in volume
56
Q

What happens to regional ventilation at lower than normal lung volumes

A
  • Intrapleural pressures are different
    • Gradient of pressure is different
  • Intrapleural pressure at the base can exceed atmospheric pressure
    • Alveoli can collapse
    • Transpulmonary pressure may not be sufficient to inflate them
  • Alveoli in the apex may be operating at a volume where compliance is high, so small changes in pressure cause significant changes in volume
    • Ventilation is better at the apex at low pressure!
57
Q

What determines regional ventilation?

A

Regional ventilation epends on conditions that you are breathing under, and the volume of the lung to begin with

  • Has to do with graidents of interapleural pressure and the compliance
  • When things are collapsed, there is no exchange
58
Q

What factors are involved in the mechanics of breathing?

A
  • The forces that affect the movement of air into and out of the lungs
  • The resistances tha must be overcome
    • Elastic resistance (65%)
    • Non-elastic resistance (35%)
      • Airflow (30%)
      • Viscous (5%)
59
Q

Describe airflow through the lungs during normal circumstances

A
  • Airflow is typically laminar, especially at lower flow rates
  • Turbulent flow can occur at higher flow rates
    • Harder to move air in and out when air is turbulent
60
Q

What is one of the most important ways of affecting airflow?

A

Changing the radius

  • Pressure-flow relationship for laminar airflow is described by Poiseuille’s law:

V = ∆Pπr4 / 8nl

  • Ex: doubling the radius increases airflow 16 fold
61
Q

What is the most important factor for altering turbulent airflow?

A

Pressure gradient

  • Flow is proportional to the square root of the change in pressure (∆P)
62
Q

WHat determines if airflow is laminar or turbulent?

A

Calculate Reynold’s number (Re):

Re = 2rvd / n

d = density

r = radius

v = velocity (major player)

n = viscosity

63
Q

Where and when is turbulent flow more likely to occur?

A
  • Turbulent flow is most likely to occur when
    • Velocity is high
    • Radius is large
    • Gas is dense
  • Turbulent flow tends to occur in the trachea at high flow rates
    • Radius is large
    • Ex: during exercise
  • Laminar flow is most likely to occur in smaller airways, like terminal bronchioles
64
Q

Why does airway resistance not increase along the bronchial tree as airways become smaller?

A
  • Greatest resistance to airflow is not just determined by radius
  • Total cross sectional area increases with continued branching
    • Large number of airways
65
Q

Where is the point of greatest airway resistance?

A

Resistance peaks at the medium sized bronchioles (5-7th generation)

  • Decreases with further branching
  • Cross sectional area increasing
66
Q

Dow does lung volume affect airway resistance?

A
  • Bronchi are supported by the radial traction of the surrounding lung tissue, and their diameter increases as the lung expands
  • At low lung volues, small airways can completely close
    • Especially at the base of the lung
    • Patients with increased airway resistance often breathe at high lung volumes in an attempt to reduce that resistance
67
Q

How do nerve innervation and inflammation affect airway resistance?

A

Bronchial smooth muscle contraction regulates airway radius and thus resistance

  • Sympathetic ß2 adrenergic stimulation (Epi) - causes relaxation of smooth muscle and increases airway diameter
    • Decreases resistance to airflow
  • Parasympathetic muscarinic stimulation (ACh) - causes contraction of the smooth muscle and decreases diameter
    • Increases resistance to airflow
  • Inflammatory mediators (leukotrienes and histamine) - released during asthma attacks or allergic responses and cause bronchial smooth muscle constriction
    • Increases resistance to airflow
68
Q

How does the respiratory effort affect airway resistance?

A
  • Increased amount of expiratory effort causes changes in rate of flow out of lungs
    • Effort dependence happens early on
    • There can be a decrease in airway diameter and an increase in airway resistance
    • Due to dynamic compression of airways
  • There is a return to a point of effort independence
69
Q

What is the limiting factor for dynamic compression of the airways?

A

The limiting factor is the effect that the increase in intrapleural pressure has on the transpulmonary pressure along the way

70
Q

What are the conditions pre-inspiration regarding dynamic airway compression?

A
  • Intrapleural pressure is negative (-5)
  • Alveolar pressure is at equilibrium with atmospheric pressure (0)
  • Transpulmonary pressure is positive (+5)
  • Transpulmonary pressure gradient is uniform (0-0)
71
Q

What are the conditions during inspiration in regards to dynamic airway compression?

A
  • Intrapleural pressure becomes more negative (-7)
  • Alveolar pressure is not at equilibrium with atmospheric pressure
  • Transpulmonary pressure gradient is no longer uniform
  • More positive towards the mouth, increasing airway diamter and reducing resistance
    • This is why the effor dependence of inspiration always increases with the amount of effort you apply
72
Q

What are the conditions at the end of inspiration in regards to dynamic compression of airways?

A
  • Intrapleural pressure is still more negative that preinspiration
  • Alveolar pressure is again at equilibrium with atmospheric pressure
  • Transpulmonary pressure gradient is uniform once again
73
Q

What happens during forced expiration due to dynamic compression of the airways?

A
  • Intrapleural pressure increases dramatically
  • Alveolar pressure is not at equilibrium with atmospheric pressure
  • Transpulmonary pressure gradient is no longer uniform
  • Moving closer to the mouth, the transpulmonary pressure drops
    • Differences in pressure causes airways to collapse
    • Increase in resistance to airflow
    • This is the reason for the effort independent component of the forced expiration curve
74
Q

What does the effort independent component of the forced expiration curve signify?

A

No matter how hard you try, you cannot increase airflow because you are starting to collapse the airways

75
Q

What happens during forced expiration in the case of chronic obstructive pulmonary disease and emphysema?

A
  • Elastic recoil is reduced and compliance is increased
  • Pressures inside airways are different, even with the same intrapleural pressures, because the lungs are more compliant and less elastic
  • Transpulmonary gradient (from alveolus to mouth) may become negative and obstruct airflow
  • Can’t get all of the air out of the lungs