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Pulmonary system > Mechanics of ventilation lecture > Flashcards

Mechanics of ventilation lecture Flashcards

1
Q

Importance of Static lung volumes

A
  • air flow because of pressure changes set up by chest/lung volumes
  • measurement of lung volumes important for diagnosis/treatment of respiratory diseases
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2
Q

Spirometry - how it works

A

-expiration/inspiration move drum up and down
-movements recorded on a rotating drum
(now have solid state sensors)
-in both cases get a plot of volume of air inspired or expired against time

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3
Q

Resting tidal volume

A

-volume of air inspired or expired during normal quiet breathing at rest

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4
Q

Inspiratory reserve volume

A
  • additional volume of air with maximum breath in

- max vol that can be inspired from normal end inspiratory position

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5
Q

Expiratory reserve volume

A
  • additional volume of air with maximum breath out

- max vol that can be expired from normal end expiratory position

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6
Q

Residual volume

A

Volume of air remaining in the lungs at the end of max. expiration

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7
Q

Capacities

A
  • a combination of 2+ volumes defined
  • while volumes determined by inspiratory and expiratory effort the capacities are largely determined by the size of the chest
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8
Q

Total lung capacity (TLC)

A

-the sum of the tidal volume and the inspiratory reserve volume, expiatory reserve volume and the residual volume

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9
Q

Functional residual capacity (FRC)

A
  • ERV + RV

- volume of gas in lungs at end of normal expiration

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10
Q

Measuring Volume of air left in the lungs after expiration via spirometry

A

Cant be measured by spirometry

  • i.e. can’t measure RV, FRC, & TLC by spirometry
  • is a limitation of spirometry (especially as these are important measures of disease)
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11
Q

Mechanical properties of lungs and chest wall at rest (when lungs at functional residual capacity - at end of normal expiration) - balance at this point

A
  • no air is moving into or out of the lungs at this point so lung volume is constant (static condition)
  • corresponds to the lung volume at which the inward recoil forces of the lung are perfectly balanced by the outward recoil forces of the chest wall
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12
Q

Cause of inward recoil of lungs

A

1) Elasticity of cells & extracellular matrix in lung tissue

2) Surface tension forces in alveoli

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13
Q

Causes of outward recoil of the chest

A

1) Tendency of ribs to spring outwards

2) Resting tension in muscles of respiration

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14
Q

What happens when inward or outward recoil forces change (as they do in many disease processes)

A

-if balance between two forces changes then functional residual capacity will change
ie if inward recoil force increases then the collapsing effect of lungs will override the outward recoil of the chest wall and FRC will decrease

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15
Q

Intrapleural pressure at FRC (averaged over the whole of the intrapleural space)

A

5 cm of H2O less than atm pressure

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16
Q

Importance of intrapleural pressure

A

-critical determinant of the pressure gradients that drive the flow of air into or out of the lungs

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17
Q

What structures “ feel” intrapleural pressure

A

All intra thoracic structures are subject to intrapleural pressure
ex: As breathe in intrapleural pressure decline and that draws venous blood back up into the chest
venous return to right side of heart varies according to respiratory cycle

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18
Q

Alveolar pressure at FRC

A
  • at FRC no pressure gradient (no air moving into or out of the lungs)
  • so pressure in the alveoli at this point must be equal to atmospheric pressure (PA = 0)
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19
Q

Transpulmonary pressure

A

-alveolar pressure is 0
-Intrapleural ressure is -5 (always??)
-therefore is pressure gradient between the alveoli and intrapleural space (= transpulmonary pressure)
-at rest is eqaul to the opposite of pleural pressure
Ptp = Pa-Ppl

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20
Q

Relationship transpulmonary pressure and alveoli

A
  • the pressure that determines the size of the alveoli (the descending force that determines alveolar size and therefore lung volume)
  • If increases than alveoli will increase in size = descending force that determines the size of the alveoli (this pressure will therefore vary during normal breathing as the alveoli enlarge and deflate)
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21
Q

What happens to intrapleural pressure in pneumothorax

A

-air enters intrapleural space and intrapleural pressure will become less negative (closer to atmospheric pressure)

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22
Q

Transpulmonary pressure at rest in pneumothorax

A
  • intrapleural pressure decreased
  • alveolar pressure still 0 as is no air moving into or out of the lungs at rest
  • transpulmonary pressure declines
  • i.e. the pressure normally keeping the alveoli inflated decreases and the lung starts to collapse
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23
Q

How to reinflate the alveoli after pneumothorax

A
  • need to increase transpulmonary pressure up to or greater than +5 cm H2O
  • looking at equation Ptp = Pa -Ppl need to either
    1) Apply pressure to airways to increase alveolar pressure (bag with mouthpiece)
    2) Insert a underwater seal drain so air can escape from the pleural cavity and restore intrapleural pressure to more negative value (with each expiration more air is pushed out f intrapleural space)
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24
Q

Respiratory pressure changes during quiet inspiration

A
  • for air to flow into alveoli during inspiration the pressure within the alveoli must be reduced below atm (for air to flow from the atm into the alveoli)
    1) Inspiratory muscles contract – causes intrapleural pressure to become more negative
    2) More neg intrapleural pressure increases transpulmonary pressure (right before start of inspiration) This causes the alveoli to expand.
    3) Boyles law - the pressure exerted by a gas in a confined space is inverselyproportional to the volume of the gas in that confined space –> means that as the alveoli expand the pressure of the air within the alveoli decreases
    4) Alveolar pressure falls from 0 to some negative value (in ex was -1).
    5) Pressure in alveoli is now less than atm pressure and air will flow into the alveoli (established a pressure gradient)
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25
Q

Respiratory pressure changes during quiet expiration

A
  1. Inspiratory muscles stop contracting and relax
  2. Ppl becomes less negative
  3. P tp distending the alveoli decreases
  4. As alveoli decreases in size PA initially increases to above atmosphreic pressure (Boyl’e’s law)
  5. Air flows down new pressure gradient from alveoli to atmosphere
  6. As air flows out of the alveoli Pa returns to 0 cm H2O. Airflow out of lung ceases when Pa = P atm
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26
Q

2 main ways of replacing spontaneous respiration

A
  1. Positive pressure ventilation (manually or mechanical ventilators)
    - positive pressure applied to airway and air pushed into alveoli
    - when positive pressure ceases passive expiration takes places (lungs go back to normal resting state)
  2. Negative pressure ventilation
    - closer to physiological breathing - sucks air into lungs like respiratory muscles
    - a patient is placed into a chamber (iron lung). Air tight seal around the patieents neck, vacuum pump sucks air out of chamber to give artial vaccuum in the chamber - acts to expand the patients chest
    - intrapleural pressure increases
    - alveolar pressure falls
    - air flows from atmosphere into the aveoli
    - when vaccuum in chamber terminated -lung recoil leads to passive expiration
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27
Q

Factors that influence ventilation during normal quiet breathing

A
  1. Distensibility (stretchiness of lungs and chest wall), determined by :
    a) elasticity of lung tissue (and chest wall)
    b) surface tension at the liquid-gas interface within the alveoli
  2. Frictional resistance due to:
    - movement/deformation of lungs and chest wall (tissue resistance)
    - airflow through the airways (airway resistance)
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28
Q

What contributes to elasticity of lung tissue

A
  • cells and connective tissue surrounding the airways possess elastic properties
  • ECM contains elastin fibers that are distendable and collagen fibers that are not easily stretched
  • relative amounts of elastin vs. collagen in ECM influence lung elasticity (if balance changes will cause changes in respiratory function)
29
Q

2 disease processes that can change balance between elastin and collagen

A
  1. Emphysema

2. Pulmonary fibrosis

30
Q

Emphysema pathophysiology

1) Overall how does emphysema result in reduced elastic recoil of the lungs
2) 3 consequences of reduced elastic recoil of the lungs

A

-disease process results in destruction of alveolar wall –> this leads to less elastin in the lung tissue –> leading to reduced elastic recoil of the lungs
3 consequences:
1) lungs are easier to distend (no elastic recoil opposing lung expansion) = easier to breath in (less muscular effort)
2) Much more difficult to breath out :
-normally elastin fibers are attached to walls of airways keeping them open=when elastin lost not holding the small airways open= airways become narrower
-narrowing = increase in resistance to flow of air through them creating resistance to exhale air through small airways
3) Reduction in inward elastic recoil - lungs become more subject to outward recoil of the chest wall

Overall effect of 1+2+3 = resting lung volume increases and develop a broad chest over time because breathing at high lung volumes (barrel chest)

**pull on airways from remaining elastin fibers increases at higher lung volumes = increases the diameter of narrow small airways = slighlty offsets the resistance sees in emphysema - does not overide if but helps to breath out

31
Q

Pathophysiology of pulmonary fibrosis

A

-deposition of collagen fibers
-not easily stretched so increase the inward recoil force of the lungs
Consequences:
1) more difficult to inflate the lungs (need a lot of muscular effort)- hard to breathe in
2) collagen fibers pull on the walls of the small airways and increase their diameter - so resistance of flow of air in the airways declines (so patients don’t have any problem exhaling)

32
Q

Surface tension at liquid-gas interface within each alveoli - importance

A

-accounts for 2/3 of total inward recoil force of lungs

33
Q

Explanation of surface tension - what causes it

A

Molecules of water covering the alveolar surface attract each other
Attraction leads to generation of cohesive force between water molecules
Cohesive force between H20 molecules=surface tension (inward collapsing force)

34
Q

Result of surface tension (2 consequences)

A

1) Make it harder to inflate the lungs (by contributing to inward elastic recoil)
-because cohesive force between each of H2O molecules will tend to come together and therefore decrease the size of an alveolus (decreased size = gas occupying more space = increased pressure i.e. Boyles law)
-surface tension forces are tiny within an individual alveolus - but there are so many alveoli so forces add up - at level of lungs surface tension forces increase the inward elastic recoil of the lungs (always trying to collapse the lungs)
2) Promote instability of different sizes of alveoli
The pressure of gas in a spherical structure is directly proportional to the tension and inversely proportional to the radius (Laplace’s equation)
-means that pressure of air in small diameter alveolus is slightly higher than the pressure of air in larger diameter alveolus (Boyles law again)
-functionally means that if two alveoli of different sizes are connected to a common airway, air will flow from the small alveolus into the larger one
-therefore the small alveolus will tend to collapse into the large one (collapse = atelectesis)

35
Q

Role of pulmonary surfactant

A
  • secreted into the alveoli

- acts to decrease surface tension forces

36
Q

When does production of surfactant begin

A

-only around 25 weeks gestation

37
Q

Consequence prematurely born infants -pulmonary surfactant

A

-can lack pulmonary surfactant
= increased surface tension forces
=increased elastic recoil and alveolar instability
=harder to inflate lungs and areas of collapse and hyper-inflation
=neonatal respiratory distress syndrome (treatment with synthetic surfactant and mechanical ventilation)

38
Q

Mechanical ventilation on pulmonary surfactant

A

-can decrease the production of pulmonary surfactant (why it may be hard to get these infants off of the ventilators)

39
Q

Measuring the amount of elastic recoil in the lungs (what do measure)

A

-measure the compliance = how easy is for the patient to expand their lungs (the amount of distensibility of an elastic structure = 1 /elastic recoil)

40
Q

Definition of compliance

A

-the change in lung volume produced by change in transpulmonary pressure (aka the force that distends the alveoli)

41
Q

How to measure lung compliance

A
  • take a big deep breath in to total lung capacity
  • ask the patient to take small breaths out (breath out in steps all the way down to residual volume)
  • at each of these steps by definition alveolar pressure must equal atm presure i.e. 0 (because no movement of air going in and out) -therefore can measure intrapleural pressure to get transpulmonary pressure (the destending force)

Get plot of change in lung volume vs. transpulmonary pressure
Compliance = Change in volume/ Change in transpulmonary pressure -take two points on the graph to determine

42
Q

Relationship lung volume and transpulmonary pressure

A
  • as increase transpulmonary pressure, lung volume increases
  • but slope of relationship declines at high lung volumes - because lungs start to become less distensible (less compliance) - reaching limit of distensibility
43
Q

Transpulmonary pressure vs. lung volume in emphysema

A
  • lung elastic recoil reduced - so increase distensibility = smaller increase in transpulmonary pressure = greater increase in lung volume
  • i.e. lung compliance increased
44
Q

Transpulmonary pressure vs. lung volume in fibrosis

A
  • need very large increase in transpulmonary pressure to produce same increase in lung volume
  • due to decreased distensibility of lungs (more collagen)
45
Q

Restrictive lung disease

A
  • conditions that decrease lung (or chest wall) compliance leading to decrease in lung volume and making it harder to inflate lungs
  • i.e. pulmonary fibrosis, obesity..
  • diseases that restrict flow of air into the lungs during inspiration
46
Q

Airway resistance

A

-opposition to flow of air caused by friction

47
Q

What determines airway resistance

A
  1. Pattern of airflow

2. Airway dimension

48
Q

Types of airflow that require only a small driving pressure to cause the flow of air

A
  • slow, smooth flow

i. e. laminar flow (low resistance to flow)

49
Q

Type of airflow that requires a large driving pressure to cause flow of air

A
  • fast, disordered

- i.e. turbulent flow (high resistance to flow)

50
Q

Airway dimensions causing low and high resistance to flow

A
  • large radius = low resistance to flow

- small radius = high resistance to flow

51
Q

Importance of cross-sectional area to airway dimension

A

-many more smaller airways then larger airways
-need to add up their cross-sectional area to determine their airway resistance
-i.e. much larger total cross-sectional area for smaller airways
-i.e. not much resistance to flow of air in entire aveoli system (most of resistance to flow of air in respiratory system actually happens in larger airways)
Flow of air in large airways = fast and turbulent, flow of air in small airways = slow and laminar

52
Q

Obstructive airway disease

A
  • Any condition that causes narrowing of airways causes increased airway resistance
    a) bronchoconstriction
    b) inflammation
    c) excess mucous production
  • all lead to reduced elastic recoil

all of these = obstructive lung diseases (obstruct flow of air during EXPIRATION)
-i.e. expiratory flow rates at any given lung volume are reduced compared to normal values (while inspiratory flow rates are not affected)

53
Q

Respiratory conditions causing bronchoconstriction

A

1) asthma/chronic pulmonary obstructive disease (COPD)

2) Inflammation (asthma, chronic bronchitis, COPD, bronchiolitis)

54
Q

Respiratory conditions causing inflammation

A
  • asthma
  • chronic bronchitis
  • COPD
  • bronchiolitis
55
Q

Respiratory conditions causing excess mucous production

A
  • asthma
  • chronic bronchitis
  • cystic fibrosis
56
Q

Why airflow during inspiration is not affected in patients with obstructive lung diseases

A

-inspiration tends to increase small airway diameter (offsetting the disease effect)

57
Q

Consequence of decreased expiratory flow rate in obstructive lung disease

A
  • expiration is no longer passive
  • now need to use muscles of expiration to increase pressure of air in the alveoli forcing through narrow airways
  • large amount of muscular effort can lead to the collapse of airways (generate so much pressure that small airways collapse)
58
Q

Explanation small airway collapse in obstructive lung disease

A
  1. Contraction of expiratory muscles raises intrapleural pressure above atmospheric pressure
  2. Alveolar pressure increases
  3. Air flows from alveolus to atmosphre
  4. Resistance to airflow means that pressure in airway falls rapidly from alveolus to atmosphere
  5. When intrapleural pressure increases passed the equal pressure point (EPP = pressure in airway = pressure surrounding it or Ppl) then the airways are compressed
  6. When airway collapses air is trapped in lungs
59
Q

Measure airway resistance - what measuing

A

-interested in the practical effects of increased airway resistance - degree to which expiratory airflow is obstructed

60
Q

Measuring degree to which expiratory airflow is obstructed

A
  • breath into peak flow meter

- will measure the maximum flow rate during a forced expiration from full lung volume

61
Q

Advantage of peak expiratory flow rate

A
  • easy to teach even to young children
  • quick
  • inexpensive
  • useful for assessment of therapy in asthmatic
62
Q

Disadvantage of peak expiratory flow rate

A
  • normal ranges are wide
  • PEFR depends on voluntary effort, muscular strength of patient and technique
  • primarily reflects air flow in large airways (normal results do not exclude diagnosis of small airway disease i.e asthma)
  • various causes of PEFR and restrictive deficits cannot be detected reliably (obstructive and respiratory disease share the same main symptom -shortness of breath)
63
Q

Advantage of spirometry

A

1) Able to detect and differentiate between obstructive, restrictive & mixed problems
2) Provides estimates of severity of expiratory airway obstruction and lung restriction
3) Accurately monitors disease progression + response to treatment

64
Q

Standard measurements from a spirometer

A

1) Forced vital capacity (forced expiration from total lung capacity to residual volume)
2) Forced expiratory volume in one second (FEV1 = volume of air expired in the first second of forced vital capacity maneuver)
3) Ratio of FEV1/FVC expressed as a percentage of total FVC expelled from lungs during 1st sec of forced expiration

65
Q

FVC, FEV1 in normal person

A
  • FVC around 5 L
  • FEV1 - 4L
  • FEV1 /FVC % = 80% (norm 70-80%)
66
Q

FVC, FEV1 in obstructive lung disease

A
  • harder to expired
  • FVC is reduced because get airway collapse and some air is trapped in the lungs -so can’t get down to RV
  • FEV1 is reduced because of narrow airways (increased resistance)
  • amount of air out of lungs in first sec is reduced proportionately more than the total amount of air that you can get out - therefore FEV1/FVC percent declines
67
Q

How to tell if patient with obstructive lung disease has asthma

A
  • disease process is reversible

- i.e. if gave a beta agonist and retested in 15-20 the FEV1/FVC % should increase back towards normal levels

68
Q

FVC, FEV1 in restrictive lung diseases

A
  • decreased distensiblity
  • reduction in FVC (because lung is shrunk/stiff-reduced vital capacity
  • collapgen fibers pulling on walls of airways so airway resistance is quite low -so can exhale reduced volume quite quickly
  • so FEV1/FVC % is increased or normal (typically normal)

Pulmonary system (19 decks)

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