31-10-22 - Ventilation - the Physics of Breathing Flashcards

1
Q

Learning outcomes

A
  • Define the terms intrapleural pressure and intrapulmonary pressure
  • Explain what causes intrapleural pressure
  • Describe the processes involved in quiet inspiration and expiration
  • Describe the processes involved in forced inspiration and expiration
  • Define the term: work of breathing, and list what the work of breathing involves
  • Define airway resistance and explain what determines it
  • Define compliance and describe how it changes in different disease states
  • Explain how alveolar surface tension is reduced in health and be able to describe conditions when it would be raised
  • Describe the respiratory volumes measured by a spirometer
  • Describe how pulmonary function tests can be used
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2
Q

What is ventilation?

What is perfusion?

How do these vary in lungs?

What is the function of ventilation?

What are 5 ways function of ventilation is achieved?

What are 2 non-respiratory functions of ventilation?

A
  • Ventilation (V) refers to the flow of air into and out of the alveoli
  • Perfusion (Q) refers to the flow of blood to alveolar capillaries.
  • Individual alveoli have variable degrees of ventilation and perfusion in different regions of the lungs.
  • Function of ventilation is to provide O2 to the tissues and remove CO2
  • 5 ways function of ventilation is achieved:

1) Pulmonary ventilation (movement of air from atmosphere to alveoli)

2) Regulation of ventilation

3) Matching of pulmonary blood flow to alveolar ventilation

4) Movement of O2 and CO2 between alveoli and blood

5) Transport of O2 and CO2 in blood and body fluids

  • 2 non-respiratory functions of ventilation:

1) Expulsion of foreign bodies

2) Defence against infection/disease

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3
Q

What is pulmonary ventilation?

What is alveolar ventilation?

What is anatomic dead space air?

How much anatomic dead space air do we breathe per breath?

What is the formula for Minute total ventilation rate?

What is the formula for alveolar ventilation rate?

What is alveolar ventilation a major factor for?

A
  • Pulmonary ventilation is the process of air flowing into the lungs during inspiration (inhalation) and out of the lungs during expiration (exhalation)
  • Alveolar ventilation is the exchange of gas between the alveoli and the external environment.
  • Anatomic dead space air refers to air that is breathed in and never reaches gas exchange areas (alveoli and its capillaries), but fills respiratory passages (e.g. nose, pharynx, trachea)
  • We breath in about 150ml of anatomic dead space air per breath
  • Alveolar ventilation is one of major factors determining O2 and CO2 concentrations in alveoli
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4
Q

What are the 3 ways the lungs/thorax can be expanded and contracted?

Which mechanism is used in quiet breathing?

What needs to occur during heavy breathing?

A
  • 3 ways the lungs/thorax can be expanded and contracted:

1) Movement of the diaphragm up and down to lengthen/shorten the chest cavity
* Lengthening of chest cavity on inspiration
* Contraction of diaphragm during inspiration flattens the domes
* Abdominal wall relaxes to allow abdominal contents to move downwards

2) Movement of the ribs/sternum forwards and back
* Pump handle movement
* Increases anteroposterior dimensions of chest cavity

3) Movement of ribs upwards and laterally
* Bucket handle movement
* Increases lateral dimensions of chest cavity

  • Normal quiet breathing is accomplished entirely by the movement of the diaphragm
  • During heavy breathing, normal elastic recoil is not quick enough, so need contraction of abdominal muscles too
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5
Q

What are the 5 most important type of muscles that raise the rib cage during forced inspiration?

What are the 2 most important type of muscles that lower the rib cage during forced expiration?

A
  • 5 most important type of muscles that raise the rib cage during forced inspiration:

1) External intercostals
* With first rib fixed, two movements:
* Forward movement of lower end of sternum
* Upward and outward movement of ribs

2) Sternocleidomastoid (lift upward on sternum)

3) Anterior serrati (lift many ribs)

4) Scaleni (lift first two ribs)

5) Trapezius

  • 2 most important type of muscles that lower the rib cage during forced expiration:

1) Rectus abdominis (top layer of Ab muscles – 6 pack – made of 2 paired parallel muscles)

2) Internal intercostals

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6
Q

What is the structure of the lung like?

Where is the pleural cavity?

How do lungs sit in the thoracic cavity?

What is the structure of the chest wall like?

What structures always want to collapse/expand?

How are the lungs kept inflated?

What does this mechanism also prevent?

What does this equilibrium dictate?

What can happen to our lungs and the shape of our chest during a pneumothorax?

How does lymphatic drainage aid in the generation of the suction between the lungs and the thoracic wall?

A
  • Lung is an elastic structure that collapses like a balloon when no force Is applied to keep it inflated, which is due to the elastic recoil of the lungs
  • The pleural cavity is the area between the visceral pleura lining the lungs and the parietal pleura lining the chest wall
  • Lungs are not attached to the chest wall, and float in the thoracic cavity surrounded by a thin layer of pleural fluid that acts as a lubricant
  • The chest wall also has an elastic recoil nature like the like lungs
  • The lungs are always trying to contract and collapse due to their elastic recoil nature, while the thoracic wall is always trying to expand due to its elastic recoil nature
  • The fluid in the pleural cavity generates suction, so the tension between the pleura of the thoracic wall and the lungs keeps the lungs from collapsing as they are pushed against the thoracic wall, and move with the movement of the thoracic wall
  • This also prevents the thoracic wall from over-expanding
  • The equilibrium between the elastic recoil of the lungs and the elastic recoil of the chest wall is what dictates the shape of our chest
  • During a pneumothorax, the lung collapses, leading to the loss of this equilibrium
  • This will result in the chest sticking out more on the side of the pneumothorax, as the thoracic wall over expands due to the lack of elastic recoil from the lung to prevent it
  • Lymphatic drainage of excess fluid between lung pleural membrane and pleural surface of thoracic wall leads to the suction effect – lungs held against thoracic wall
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7
Q

What is intra-pleural pressure?

How does pleural pressure differ over the lung?

How does IP vary at the start of respiration and during respiration?

How is this different during expiration?

What does the negative intra-pleural pressure also help stay open?

A
  • Intrapleural (Pleural) pressure (IP) is the pressure of the fluid in thin the pleural cavity - usually slight negative pressure
  • IP pressure varies over the length of the lungs
  • At start of respiration, pleural pressure is about -5 cm H2O
  • During inspiration, expansion of the chest wall pulls lungs outward, so negative pressure decreases to about -7.5 cm H2O, which sucks air into lungs
  • During expiration, this process is reversed (-7.5 to -5.0 cmH2O)
  • The negativity of the intrapleural pressure stops the lungs from collapsing
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8
Q

What is alveolar pressure?

What is this also called?

What is the respiratory tree pressure when no air is flowing?

How does alveolar pressure change with inspiration? What is tidal volume?

What is a normal value for tidal volume?

How does alveolar pressure change in expiration?

What is transpulmonary pressure?

What is it a measure of?

A
  • Alveolar pressure (aka intrapulmonary pressure) is the pressure of air inside the lung alveoli
  • When the glottis is open and no air is flowing, pressure in all parts of respiratory tree is equal to atmospheric pressure (0 cm H2O)
  • During inspiration and chest wall expansion, alveolar pressure decreases to about -1 cm H2O
  • Tidal volume is the amount of air that moves in or out of the lungs with each respiratory cycle
  • A normal tidal volume is 0.5L, so 0.5L moves in on inspiration, and 0.5L moves out on expiration
  • During expiration, the alveolar pressure increases from -1cm H2O to a bit more than 0cm H2O (as diaphragm is pushing air out of the lungs) then back down to 0cm H2O
  • Transpulmonary pressure is the pressure difference between that in the alveoli and that on the outer surfaces of the lungs (difference between pleural and alveolar pressures aka difference between intrapleural pressure and intrapulmonary pressure)
  • It is a measure of the elastic forces that tend to collapse the lungs (recoil pressure)
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9
Q

Is quiet expiration active or passive?

How does it occur?

What 3 things pushes air out of the lungs during quiet expiration?

How much does the thoracic volume decrease by on expiration?

What 2 muscle contractions occur during forced expiration?

A
  • Quiet expiration is passive – no direct muscle action normally
  • Quiet expiration occurs via cessation (relaxation) of muscle contraction
  • 3 things that push air out of the lungs during quiet expiration:

1) Intrapulmonary (alveolar) and intrapleural pressure increase and transpulmonary pressure decrease

2) Elastic recoil of the lungs (lungs contract and force air out)
* When the lungs exhale, the diaphragm relaxes, and the volume of the thoracic cavity decreases, while the intrapulmonary and intrapleural pressure within it increases.
* As a result, the lungs contract and air is forced out

3) Air moving down a pressure gradient

  • Thoracic volume decreases by 500 ml on expiration (normal tidal volume)
  • Muscle contractions during forced expiration:

1) Rectus abdominis (top layer of Ab muscles – 6 pack – made of 2 paired parallel muscles)
* Forced abdominal contents up against diaphragm

2) Internal intercostals
* Pulls ribs downwards

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10
Q

What is the equation for flow of air ((F) - on picture)?

What does this formula tell us?

What is the Poiseuille’s Law equation (on picture)?

What factor has the biggest effect on airway resistance according to this equation?

A
  • This equation for flow of air (F) tells us the amount of air that flows is determined by change of pressure divided by resistance
  • The Poiseuille’s law equation tells us that airway radius has greatest effect on airway resistance, as radius is to the power of 4, meaning small changes in radius will drastically alter airway resistance
  • Smaller radius = more resistance to flow
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11
Q

How does radius affect resistance to flow?

When is turbulent flow likely to occur?

What is the formula for cross-sectional area?

Where in the respiratory tree is there the greatest resistance to flow?

Why is this?

Where in the respiratory tree is the lowest resistance to flow?

Why is this?

A
  • Smaller radius = more resistance to flow
  • Cross sectional area = πr^2 (r = radius)
  • Turbulent flow is likely to occur with high velocities and large diameter airways
  • Greatest resistance to airflow is found in the segmental bronchi, as the cross-sectional area is relatively low and the airflow is high and turbulent
  • At the smallest airways (e.g bronchioles) the resistance is small, and there is low velocity flow, which allows for laminar flow
  • There is a large total cross-sectional area in smaller airways due to the large number of small airways arranged in parallel, which allows for low resistance, even though each individual airway has a small cross-sectional area
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12
Q

What is static compliance (C)?

What does a high static compliance mean?

What is the formula for static compliance (in picture)?

What is elastance (E) the measure of?

What is the formula for elastance?

How does this link together compliance and elastic recoil?

What are the 2 elastic forces that determine compliance?

A
  • Static Compliance (C) is the extent to which the lungs will expand for each unit increase in transpulmonary pressure (given time to reach equilibrium) i.e 0.5 litres of expansion for every +2.5cm H2O in transpulmonary pressure
  • A high static compliance means the lungs will expand easier
  • Elastance (E) of the lungs is the measure of elastic recoil of the lungs
  • Elastance is the reciprocal of compliance (E=1/C), so high compliance means lungs will expand easier, but there is lower elastic recoil
  • 2 elastic forces that determine compliance:

1) Elastic forces of the lung tissue itself
* Determined mainly by elastin and collagen fibres among lung parenchyma, which give the lung its elastic properties
* Deflated lungs, fibres are contracted and kinked – more difficult to expand
* Expanded lungs, fibres become stretched and unkinked – this stretch gives the elastic recoil that the lungs need to deflate

2) Elastic forces caused by surface tension of fluid that lines alveoli

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13
Q

What are 3 lung conditions that affect lung compliance?

What is COPD?

A
  • 3 lung conditions that affect lung compliance:
    1) Pulmonary fibrosis – restrictive lung disease
    2) Emphysema (COPD)
    3) Chronic Bronchitis (COPD)
  • Chronic obstructive pulmonary disease (COPD) is the name for a group of lung conditions that cause breathing difficulties.
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14
Q

What is spirometry?

What is:
* Tidal volume (TV)
* Inspiratory reserve volume (IRV)
* Expiratory reserve volume (ERV)
* Residual volume (RV)
* Inspiratory capacity (IC)
* Functional Residual Capacity (FRC)
* Vital capacity (VC)
* Total lung capacity (TLC)?

What are normal values for each?

A
  • Spirometry is a method for studying pulmonary ventilation
  • Definitions of and typical values of:

1) Tidal volume (TV)
* Volume of air inspired or expired with each normal breath (500ml)
* 0.4 - 0.5L (litres)

2) Inspiratory reserve volume (IRV)
* Extra volume of air that can be inspired over and above normal tidal volume (2500ml)
* 1.9 - 2.5L

3) Expiratory reserve volume (ERV)
* Max extra volume of air that can be expired by forceful expiration after end of normal tidal expiration (1100ml)
* 1.1 - 1.5L

4) Residual volume (RV)
* Volume of air remaining in lungs after most forceful expiration (1200ml)
* 1.5 - 1.9L

5) Inspiratory capacity (IC)
* TV + IRV
* Volume or air breathed in by max inspiration at the end of a normal expiration
* 2.3 - 3.0L

6) Functional Residual Capacity (FRC)
* ERV + RV
* Volume of air left in lungs at end of normal expiration.
* Buffer against extreme changes in alveolar gas levels in each breath
* 2.6 - 3.4

7) Vital capacity (VC)
* IRV + TV+ ERV
* Volume of air that can be breathed by max inspiration following a max expiration
* 3.4 - 4.5L

8) Total lung capacity (TLC)
* VC + RV
* Key point - only a fraction of TLC used in normal breathing
* 4.9 – 6.4L

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15
Q

What is pulmonary fibrosis?

How does this affect lung compliance?

How does pulmonary fibrosis affect patients breathing?

What 3 things does pulmonary fibrosis show decreases in?

A
  • Pulmonary fibrosis is a disease that causes deposition of fibrous tissue, so lungs become stiff, making it harder to expand the lungs
  • Lung compliance is decreased, resulting in smaller than normal changes in lung volume for changes in transpulmonary pressure
  • Patients breath more shallowly and rapidly
  • 3 things pulmonary fibrosis shows decrease in:
    1) RV – residual volume
    2) FRC – Functional residual capacity
    3) TLC – Total lung capacity
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16
Q

What is emphysema considered part of?

What is emphysema a consequence of?

What is damaged in emphysema?

How does this alter compliance and airway resistance?

How does emphysema affect breathing?

What 3 does emphysema show increases in?

A
  • Emphysema is considered part of COPD
  • Emphysema is a common consequence of cigarette smoking
  • In emphysema, alveolar and capillary walls progressively destroyed, particularly elastic tissue
  • Lung compliance is increased, resulting in larger than normal changes in lung volume for small changes in transpulmonary pressure – it is easier to expand lungs, but difficult to close lungs down now due to elastic tissue damage affecting elastic recoil
  • However, as airways tend to collapse on expiration, airway resistance is also increased
  • Patients with emphysema breath more slowly and deeply, as they have to actively push air out of their lungs through contraction of accessory muscles due to lack of elastic recoil,
  • 3 things emphysema shows increases in:
    1) RV – residual volume
    2) FRC – Functional residual capacity
    3) TLC – Total lung capacity
17
Q

What is chronic bronchitis part of?

What is chronic bronchitis?

How does it affect compliance?

What 3 things does chronic bronchitis show increases in?

A
  • Chronic bronchitis is part of COPD
  • Chronic bronchitis is when mucus and airway inflammation produces an increase in airway resistance
  • Compliance is not affected?
  • 3 things Chronic Bronchitis shows increases in:
    1) RV – residual volume
    2) FRC – Functional residual capacity
    3) TLC – Total lung capacity
18
Q

Why do we need water on the surface of alveoli?

What is surface tension a measure of?

What is surface tension always trying to do in alveoli?

What does the Law of LaPlace state in terms of alveoli?

What formula does this make?

How does this apply to 2 alveoli of different diameter being connected?

Why can this system not be used?

What needs to be included to correct this system?

A
  • We need water on the surface of alveoli so that we have an air-liquid interface to allow for oxygen and CO2 exchange through the alveolar wall
  • Surface tension is a measure of the force acting to pull a liquid’s surface molecules together at an air-liquid interface
  • Surface tension is always trying to collapse the alveoli by moving water molecules together and pushing air out of the alveoli
  • Law of Laplace states that the pressure (P) within a fluid-lined alveolus is dependent on the surface tension of the fluid (T) and the radius of the alveolus (r), which makes the formula - P = (2 X T) / r
  • If 2 alveoli are connected together but have different diameters, air will flow from smaller alveoli to larger alveoli because of a greater pressure in the smaller alveoli pushing air into larger alveoli
  • This system is ineffective, inefficient, and will eventually lead to the collapse of the alveoli
  • Surfactant lines that alveoli and helps to reduce surface tension at the air-liquid interface to prevent this from occurring
19
Q

What is the main role of surfactant?

How does surfactant decrease surface tension?

How does this affect compliance of alveoli?

How does this affect fluid accumulation?

How does surfactant alter alveolar size?

What does this improve?

What does this help to reduce?

How can surfactant allow for more uniform size of alveoli?

A
  • Surfactant greatly reduces the surface tension of H2O
  • Surfactant reduces surface tension by reducing pressure (by about 4.5 times) as P = (2 X T) / r
  • This increases compliance of each alveoli, which makes it easier to inflate the lungs
  • This decrease in surface tension also minimises fluid accumulation in alveolus i.e fluid moving from smaller to larger alveoli
  • Surfactant helps keep alveolus size relatively uniform during respiratory cycle, as it allows for a better distribution of air in the alveoli
  • This allows for more similar sized alveoli, which improves gaseous exchange
  • This also helps to reduce atelectasis – alveolar collapse
  • Surfactant can allow for a more uniform size of alveoli by preventing the expansion of larger alveoli, while allowing for the expansion of smaller alveoli during inspiration
  • A larger alveolus will have a lower surface density of surfactant, causing increased surface tension and elastic recoil, leading to a brake on expansion
  • A smaller alveolus will have a higher surface density of surfactant, which will keep surface tension and elastic recoil lower, leading to less of a break on expansion, and allowing the small alveolus to get bigger
20
Q

What are the 2 types of alveolar cell?

How is surfactant produced?

What 3 things does surfactant consist of?

How do these components interact with fluid?

How is surfactant degraded/recycled?

A
  • 2 types of alveolar cell:
    1) Type I alveolar cell: permit diffusion
    2) Type II alveolar cell: produce surfactant that reduces the tendency for pulmonary alveoli to collapse
  • Surfactant is produced when lipid components enter type II alveolar cells
  • These Type II alveolar epithelial cells then secrete surfactant
  • Surfactant is a complex mixture of phospholipids:
    1) Dipalmitoylphosphatidylcholine (DPPC)
    2) Proteins (surfactant apoproteins, SP- A, SP-B, SP-C & SP-D)
    3) Ions (calcium)
  • Part of DPPC molecule dissolves in fluid while rest spreads over surface of fluid
  • Alveolar macrophages help in degrading surfactant, Type II cells take up rest and recycle or destroy it