Pulmonary compliance and elasticity Flashcards

1
Q

Compliance

A

-distension of lung relative to transpulmonary pressure
-in other words, how easy is it for the alveoli to stretch when filled with air

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2
Q

Elasticity

A

-ability of the lung to resist distention/stretch
-in other words, how easy is it for the alveoli to recoil to its original shape

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3
Q

Compliance equation

A

Change in volume divided by change in pressure

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4
Q

What drives compliance?

A

-driven by pressure change

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5
Q

What drives elasticity?

A

-surface tension
-elasticity of lung tissue

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6
Q

Plastic bag vs balloon

A

Plastic bag is highly compliant, but not elastic
Balloon is both compliant and elastic

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7
Q

Compliance high vs. low

A

When high, lung is readily distended (flexible)
When low, lung is not easily distended (stiff)

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8
Q

Elastic components of lung tissue

A
  • Possible due to connective tissue (collagen and elastin)
    o Collagen: provides strength and rigidity
    o Elastin: provides elastic properties
  • Responsible for ~1/3rd of total lung elasticity
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9
Q

Fibrosis (scar tissue) and how it related to elastic force

A

-fibrosis (scar tissue) increases collagen which causes the alveoli to become stiff. Results in increased elastic recoil and therefore low compliance

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10
Q

Cohesive force

A

-molecules of same property exhibit strong intermolecular attractive forces toward each other

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11
Q

Surface tension

A

-alveoli is lined with a fluid surface that creates an air-water interface and allows for the possibility of surface tension
-molecules at the surface have less surrounding neighbours, and the force is enhanced on their nearest neighbours at the surface (compared with cohesive force which is weaker and throughout the solution)

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12
Q

Alveoli surface tension

A

-water that is lining the inner surface of the alveoli exerts attraction to each other and creates a net inward pull known as RECOIL EFFECT
-responsible for 2/3rds of lungs elastic property

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13
Q

Surfactant

A

-complex lipoprotein produced by type II pneumocytes
-have hydrophilic head and hydrophobic tail which prevents it from entering the fluid and means that it stays on the surface

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14
Q

Purpose of surfactant

A

-disrupts surface water attraction (surface tension force)= reduces surface tension of alveoli to prevent atelectasis
-decreases elasticity, improves compliance

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15
Q

Atelectasis

A

-collapsed alveoli

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16
Q

When is surfactant produced?

A

-produced during late gestation
-reason why premature birth often leads to respiratory difficulties (low compliance) in humans and animals

17
Q

Static compliance

A

-linear relationship
- occurs when there is no airflow

18
Q

Dynamic compliance

A

-airflow occurs and air resistance exists
-non-linear relationship

19
Q

Inspiration vs. expiration compliance

A

Differences in compliance because surface tension in alveoli contributes to elasticity and during inspiration greater pressure is needed during the initial phase to overcome the surface tension force
>Ex. initial blowing up of balloon compared to future breaths

In expiration, surface tension aids in shrinking the alveoli, requiring less pressure vs inspiration

20
Q

Hysteresis

A

-differences between required pressure change in inspiration vs expiration
*Non-recoverable work is required during inspiration to overcome the elastic properties

21
Q

Saline-filled lungs

A

Hysteresis is greatly reduced because of the absence of surface tension due to lack of air-fluid interface
*There will always be a small hysteresis present due to elastic properties of lung (elastin, collagen)

-When surface tension is eliminated, it greatly reduced pressure required to change volume
*steeper slope, increase in compliance

22
Q

What does Airway resistance effect?

A

-influences compliance/alveoli distension (how easy/difficult it is for the air to go through tip of nose/mouth)

23
Q

Airway resistance

A
  • The air enters through the nasal/oral passage and encounters air resistance before getting to the alveoli which results in change in pressure generated in the alveoli caused by deviation between static and dynamic compliance.

**increase in air resistance results in decrease in dynamic compliance because less air

24
Q

Where does most airway resistance occur?

A

Most resistance occurs in conducting airways (from bronchi to the terminal bronchioles)
>fast turbulent airflow
>mucous secreting epithelial cells

25
Q

Laminar flow

A

-in respiratory zones
-flow reduces airway resistance

26
Q

Resistance in nasal (turbinate) vs. oral passage

A

-more resistant in nasal (turbinate) passage
-results in reflexive mouth breathing during exercise (naturally occurs because we want to reduce resistance to get more air in for oxygenating alveoli)

27
Q

Factors affecting airway diameter and therefore airway resistance

A

Can be external or internal

-Examples:
1.bronchoconstriction
2.abnormal tissure growth
3. mucous plug (inflammation)
4. pulmonary edema

28
Q

Steps of increased air resistance

A

1.increase air resistance by obstructing airflow in and out of alveoli
2. decrease compliance
3. interfere with gas exchange

29
Q

Pathological disease and compliance

A

different diseases have the ability to increase or decrease compliance and greatly effect animals ability to breath properly

30
Q

Low compliance vs. high compliance

A

Low: hard to inflate the alveoli=hypoxemia
High: hard to deflate the alveoli=hypercapnia

31
Q

Restrictive vs. obstructive

A

-restrictive- difficulty filling lungs with air
-obstructive- difficulty expelling air from lungs

32
Q

Pathological diseases resulting in low compliance

A

-pneumothorax- loss of pleural pressure
-fibrosis-increase elastic recoil
-abdominal/thoracic mass- diaphragm obstruction
-pulmonary edema- fluid in interstitial fluid that pressures the alveoli
-low surfactant- excess surface tension

33
Q

Pathological diseases resulting in high compliance

A

Chronic obstructive pulmonary disease (chronic inflammatory response from something like smoking)
>can lead to Emphysema or chronic bronchitis

34
Q

Emphysema

A

-structural destruction of alveoli wall. Alveolar macrophage produces elastase that degrades elastin fiber and results in loss of elasticity

35
Q

Chronic bronchitis

A

-excess mucous, results in obstructing airway
-obstruction makes it more difficult to get air out than in so air is trapped in lungs (hyperinflation of alveoli)