work of Breathing Flashcards

1
Q

Lung Compliance is a fancy way of saying what?

A

‘lung stretchiness’

or more formally, the effort required to stretch the lungs during inspiration

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2
Q

degradation of elastin fibers leads to what?

A

degredation of elastin fibers (alpha1 anitrypsin deficiency) = lungs are TOO compliant

fibrosis of lung = lungs are not stretchy enough

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3
Q

what kind of curves are the expiration and inspiration curve in a ‘hysteresis’ (compliance curve)

A

Inspiration = sigmoidal

expiration = opposite of exponential?

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4
Q

how do you compute the ‘work’ of the compliance curve?

A

by finding the area of the compliance curve - a small amount of work is normal - indicates that it doesn’t require much work to inflate the lung, however a large amount of work indicates a diseased lung

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5
Q

during normal ‘quiet breathing’ what sort of work is being done?

A

in normal quiet breathing, inspiratory muscles do all the work as expiration is passive

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6
Q

what does the restrictive vs. obstructive lung disease look like on a Hysteresis graph?

A

in obstructive disease, while compliance may be unchanged, the work of breathing is increased by the elevated airway resistance

in restrictive disease, lung compliance is low and the elastic work of breathing is increased

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7
Q

what is the ‘elastic work’?

What is ‘non-elastic’ work?

A

elastic work = force to expand lugn against its elastic properties

non-elastic= airway resistance work = force to move air through airways

(elastic forces representing 70% of the total work)

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8
Q

how much of our total oxygen consumption is consumed by the lungs themselves?

A

2-5% - it’s very low and efficient - though it increases with exercise

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9
Q

the higher the tidal volume, the greater the… ?

A

the higher the tidal volume, the greater the elastic work

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10
Q

the higher the respiratory rate, the higher the… ?

A

the higher the flow and resistive (non-elastic work)

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11
Q

what is the optimum combination of tidal volume and rate to minimise work of the lungs?

A

rate 15/min

tidal volume 500ml

the higher the tidal volume the greater the elastic work

the higher the respiratory rate, the higher the flow and resistive (non-elastic) work

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12
Q

what makes up the elastic work?

A

tissue elastic forces = elastin fibers present in the airways and alveoli contribute to the behaviour of the lungs as an elastic body

surface tension force = develops at air-liquid interfaces and pressure inside alveoli is dtermined by surface tension and alveolar radius (Laplace’s law)

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13
Q

what is the alveolar surface tension?

A
  • Thin liquid film lines each alveolus
  • Air-water interface
  • Water molecules more attracted to each other than air (surface tension)

–Resists expansion (water molecules oppose being pulled apart)

Reduces alveolar size

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14
Q

what would happen if alveoli are lined with water alone?

A
  • If alveoli were lined with water alone, the surface tension would cause lungs to collapse. (becuase as we exhale the alveoli shrink and if there was also a tension force helping them collapse, it would be very difficult to reexpand them)
  • Coupled with recoil force of elastin fibres.
  • Would exceed opposing stretching force of transmural pressure.
  • Would require exhaustive muscular pressure to breath.
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15
Q

what are the two factors that oppose the surface tension of water in the lungs?

A

1) pulmonary surfactant (secreted by type 2 alveolar cells) 90% lipids, 10% proteins - lowers surface tension, mixture of lipids and proteins, increases compliance, reduces lung tendency to recoil and collapse - note that surfactant is produced when you’re still a fetus
2) alveoli interdependence - when alveolus in a group of interconnected alveoli begin to collapse, the surrounding alveoli are stretched/recoil in response

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16
Q

if you have a smaller volume of alveoli- what is the pressure like?

A

small volume = high pressure

large volume = low pressure

therefore in the absense of any other factors, air would move from small alveoli into larger alveoli and we would be left with less and less alveoli

*this is also why surfactant is important = it stabilizes the small alveoli

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17
Q

what is Laplace’s Law?

A

small radius = high pressure

P= 2T/r

18
Q

what does surfactant do to the surface tension ? How does it impact Laplace’s law?

A

surace tension is no longer a constant with surfactant = the surface tension becomes smaller as the alveoli get smaller because there is a larger concentration of surfactant = therefore the small and large alveoli equal out in pressure so there is no net movement of air between the two

19
Q

how does the surfactant reduce the surface tension of the surfactant?

A

the lipid content of it avoids the water molecules - therefore it prevents the water molecules from collapsing due to surface tension - it’s like a wall between two magnets

20
Q

what is respiratory distress syndrome of newborn?

A
  • Developing foetal lungs do not normally synthesise surfactant until late in pregnacy.
  • Therefore, premature infants may not have enough pulmonary surfactant and struggle to breathe.
  • Treatment:
  • Stimulated by corticosteroids given to mother prior to delivery of premature infant
  • Oxygen through continuous positive airway pressure
  • Survanta (surfactant)
  • Acute cases may require mechanical ventilator
21
Q

what is alveoli interdependence?

A
  • When an alveolus in a group of interconnected alveoli begin to collapse, the surrounding alveoli are stretched.
  • Neighbouring alveoli recoil in response to being stretched, pulling outwards on the collapsing alveoli and keeping it open.
22
Q

what are the functions of surfactant?

A
  • Lowers surface tension of fluid lining alveoli
  • Increasing compliance and reducing work of breathing
  • Preventing collapse at low lung volumes (atelectasis)
  • Allows small and large alveoli to co-exist
  • Influencing regional distribution of ventilation and relationship of ventilation to perfusion
  • Contributes to defence mechanisms in the lung

Enhancing immune system activity (SPA & SPD)

23
Q

what is the ‘resistance to air-flow’?

A

•Airway resistance is the impedance of air flow through the tracheobronchial tree as a result of friction of gas molecules

24
Q

how does radius effect airway resistance?

A
  • Hagen-Poiseuille Law
  • Relates flow rate (volume transported per time unit) to airway radius and to distance the air is transported
  • Applies to a scenario of laminar flow in a straight circular tube.
  • Note the strong influence of the airway radius!!!

*the equation condition is that the trachea is a perfect cylindrical tube*

25
Q

How can we use the Hagen-Poiseuille law to express airway resistace?

A

Resistance is low when a given driving pressure results in a high flow rate

  • Again, note the influence of the airway radius!
  • If airway radius reduced to 50%, resistance increases 16-fold!
26
Q

we have determined that a large radius = a smaller resistance value… •Would this not suggest a high resistance in the brionchioles when compared to the trachea?

A

no-

An individual bronchiole obviously has a far smaller radius than the trachea.

However, the large number of bronchioles means that overall the airway widens

Therefore, resistance in trachea is higher than in the bronchioles

27
Q

How is airway resistance affected by lung volume?

A

there is an inverse relationship between airway resistance and lung volume

28
Q

what is laminar flow? What is turbulent flow?

A
  • Laminar flow is a streamline flow (smooth)
  • Well ordered (not chaotic)
  • Turbulent flow is chaotic, not streamline/smooth
  • Turbulent flow is very inefficient and consumes energy
  • à Turbulences increase air flow resistance
29
Q

how do we determine if the flow of air is turbulent or laminar?

A

we use reynolds number which determines if the flow is turbulent or laminar

30
Q

Turbulent flow is more likely to occur in what state?

A

during exercise

31
Q

what factors determine airway resistance?

A
  • Airway diameter- trachea and main bronchi are wide =
  • bronchial smooth muscle tone
  • thickness of mucous lining and submucosa
32
Q

what are the determinants of lower airway diameter?

A

outside of trachea = radial traction of elastic tissue (instead of cartilage- so opens up during inhalation)

in the wall = smooth muscle tone (thickness of mucosa)

in the lumen = mucus (increased infection)

33
Q

what hormones can influence smooth muscle tone in the lower airways?

A
  • Circulating epinephrine (adrenaline)
  • causes bronchodilation
  • bronchiolar smooth muscle relaxation
  • Bronchoconstriction (decrease in radius of bronchioles)
  • via Acetylcholine
  • Contraction of bronchiolar smooth muscles

  • Need for O2 is high?
  • Bronchodilation
  • Maximum airflow rate: Minimum resistance
  • Ephedrine used clinically to treat bronchial spasms

Asthma etc.; contraction of bronchial muscles

34
Q

what are some intrinsic factors which control the smooth muscle tone by chemical mediators?

A
  • Mast cell degranulation = causes bronchoconstriction
  • CO2 levels effect smooth muscle directly - when raised, bronchodilation increase flow and ventilation. When lowered, bronchoconstriction leads to decreased flow and ventilation
35
Q

what factors influence the secretions of the goblet cells (mucocilliary system) that line the respiratory system?

A
  • Increased in infections & allergies
  • Increased in chronic bronchitis
36
Q

what is Chronic Bronchitis ?

A
  • Long term inflammatory condition
  • Lower respiratory airways
  • Triggered by frequent exposure to smoke, pollutants or allergens
  • Chronic irritation leads to mucus secretion & swelling
  • Narrowing of airways
  • Irritants cause cillia to be immobilized; reduced clearing of mucus
  • Infections frequently occur.
37
Q

**** THIS ONE ON QUIZ*** why is chronic bronchitis and obstructive respiratory disease?

A
  • Obstructive respiratory diseases (COPD, Asthma)
  • Interfere with the movement of air through airways
  • Increases flow-resistive work
  • No effect on elastic work
  • Decreases FEV1 but not FVC (or only slightly) (-> ratio decreased) -
38
Q

*** on quiz*** How do we define Restrictive respiratory disease?

A
  • Restrictive respiratory diseases (Pulmonary Fibrosis)
  • Interfere with ability to expand the lungs (-> compliance is decreased)
  • Increases elastic work
  • No effect on flow-resistive work

Decreases FEV1 and FVC (-> ratio remains normal)

39
Q

is turbulent flow linked to a high diameter or low diameter?

A

turbulent flow is linked to a high diameter of airway

40
Q

a non-compliant lung requires more or less transmural pressure gradient on inspiration to produce the lung expansion of a healthy person?

A

a non-compliant lung = less stretchy, therefore it requires a greater transmural pressure gradient to produce the same expansion