Mechanics of breathing Flashcards

1
Q

How does air reach gas exchange surfaces?

A

Passing through series of increasingly narrow and numerous airways
So impaired airway function= insufficient ventilation

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2
Q

What is airway resistance?

A

An opposing force that acts to reduce flow of gas through airway
- Occurs when air comes into contact with airway surface

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3
Q

State the 3 major variables that affects airway resistance?

A

Cross-sectional area of the airway lumen
Pattern of airflow
Airway patency (ability of a person to breathe)

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4
Q

State what rate of airflow is dependent on?

A
  • Pressure gradient
  • Level of airway resistance
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5
Q

What is the equation for airflow?

A

Ohm’s law
Airflow (V) = Change in Pressure (P)/ Resistance

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6
Q

Why can increasing the pressure to increase flow be limited?

A

Respiratory system has specific physical limitations

  • Effort/force required to do so may not be able to be generated
  • Or Airway might be completely obstructed.
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7
Q

What is the simplified Hagen-Poiseuille equation?

A

Resistance (R) is proportional to 1/r^4.
r= radius (cross-sectional)

R = 8nl / πr4 (Overall equation) FC

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8
Q

What happens as the airway radius decreases?

A

The resistance increases and airflow decreases dramatically

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9
Q

State events which can reduce size of airway lumen?

A

Contraction of airway smooth muscle
Excessive mucus secretion
Oedema/swelling of the airway tissue
Damage to the integrity of airway structure (loss of patency)

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10
Q

How does pattern of airflow affect resistance?

A

Turbulent flow will lead to higher airway resistance than laminar flow

Healthy airways have laminar flow that has minimal resistance

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11
Q

How is turbulent flow achieved?

A

High velocities of airflow occur due to either

  • Forced breathing manoeuvres
  • Sudden decrease in luminal area e.g. obstructured airways

Generates vibration

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12
Q

What is generated as a result of the vibration from turbulent airflow?

A

Wheezing sound produced in patients with obstructured airways

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13
Q

What is airway patency?

A

“Refers to state of the airway being open or unobstructed
- Loss of patency= closing/obstruction”

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14
Q

Describe airway patency in healthy individuals?

A

“Elastin in surrounding alveoli provides radial traction to splint (support) bronchioles against positive Palv

radial traction as elastic springs that anchor the airway lumen to the lung interstitium (parenchyma) hence helping to keep the airway patent when insp/exp occurs.”

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15
Q

What can reduce airway patency?

A

Pressure differentials between interpleural space and airways during forced expirations

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16
Q

What can occur if COPD occurs to airway patency?

A

Degradation of airway structure
Intrapleural pressure becomes postiive, collapsing force is exerted onto airways
Without radial traction, bronchioles collapse
Airway obstruction occur
Loss of airway patency

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17
Q

What is transpulmonary pressure?

A

Transpulmonary pres. (Ptp) = Alveolar pres. (Palv) – Intrapleural pres. (Pip)
- It determines the level of force acting to expand or compress the lungs

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18
Q

What is lung compliance?

A

The relationship between the level of expansive force (a particular change in transpulmonary pressure) applied to the lung and the resulting change in lung volume
- Essentially describes how easy a lung can expand/distended

More compliance = less force/pressure required to produce volume change

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19
Q

State equation for lung compliance?

A

Compliance (C_L)= ΔVolume/Δ (transpulmonary) Pressure

Transpulmonary pressure = It determines the level of force acting to expand or compress the lungs

20
Q

Describe features of higher lung compliance?

A

Higher lump compliance -> Less elastic recoil -> Less force required to inflate -> Greater volume change per pressure change (greater gradient on volume-pressure curve)
- Looser/easier to inflate lung

21
Q

Describe features of lower lung compliance?

A

Lower lump compliance -> more elastic recoil -> more force required to inflate -> Lower volume change per pressure change (Lower gradient on volume-pressure curve)
- So stiffer/harder to inflate lung

22
Q

What is lung compliance determined by?

A

Structure of the lung tissue

23
Q

On a graph of lung volume vs transpulmonary pressure, what represents
compliance?

A

Gradient of the curve

24
Q

For curve of lung vol. vs transpulmonary pressure, what is used to represent compliance
for static compliance and dynamic compliance

A

Static: Measurements taken when airflow=0
- Steepest part of curve is sued

Dynamic: Measurements taken when airflow is occuring
- Gradient between end tidal inspiratory and end tidal expiratory

25
Q

State factors or diseases that would affect the chest wall mechanics for lung compliance?

A

Scoliosis, Muscular dystrophy, obesity
- All lead to lowered lung compliance

Chest wall naturally recoils outwards so increases compliance as role

26
Q

State factors or diseases that would affect the alveolar surface tension for lung compliance?

A

NRDS (neonatal respiratory distress syndrome)
- Decreases Lung compliance

Alvolar surface tension decreases compliance

27
Q

State factors or diseases that would affect the elastin fibres for lung compliance?

A

Fibrosis- lower lung compliance
COPD (emphysema)- Higher lung compliance

Elastin fibres decrease compliance (resists expansion of lungs)

28
Q

State the effect emphysema and fibrosis have on the lungs?

A

Emphysema (COPD)

  • Degradation of elastin fibres
  • Lungs are less stiff
  • More compliant (but reduced recoil)

Fibrosis:

  • Scarring and deposition of structural fibres e.g. collagen
  • Stiffer lung
  • Less compliant
29
Q

What are alveoli lined with and what is the purpose of this?

A

Lined with fluid to enable gas exchange.
The gas molecules dissolve into water before diffusing.

30
Q

How is surface tension generated within the alveoli?

A
  1. The water-air interface formed by the fluid lining on the wall of an alveolar airspace essentially creates a bubble.
  2. Within the bubble, surface tension arises due to the hydrogen bonds between water molecules.
  3. Combining to exert an overall collapsing force toward the centre of the bubble.
    - A sufficient force must be generated to resist the collpasing pressure,
    Otherwise the bubble will collapse
31
Q

What is the result of the collapsing force of the bubble in an alveoli?

A

The collapsing force produced at the water-fluid interface generates pressure within a bubble

32
Q

How can the amount of pressure in a specific bubble of an alveoli be calculated?

A

Law of Laplace.

33
Q

What does the Law of Laplace for the alveoli describe?

A

Described the relationship between:

  1. Collapsing pressure.
  2. The radius of the bubble.
  3. The surface tension (which varies depending on the nature of the fluid)
34
Q

Equation for the Law of Laplace of the alveoli

A
P = 2T/r
P = Pressure
T = Surface Tension (tendency of liquid surfaces to shrink into the minimum surface area possible)
r = Radius of Bubble
35
Q

What is true if surface tension from the law of laplace remains constant?

A

P ∝1/r
The smaller the alveoli (smaller bubble), the larger the pressure generated.

36
Q

What is the consequence of different sized bubbles of alveoli connected to each other

A

Pressure gradients would be created between different sized alveoli, resulting in smaller alveoli emptying into larger ones.
Occurs due to more collapsing pressure in smaller than larger bubble and pressure gradients move from high to low.
This would make inflation of the lungs extremely difficult.

37
Q

How is alveolar surface tension reduced?

A

Reduced by the presence of pulmonary surfactant.

38
Q

What is pulmonary surfactant secreted from?

A

Secreted by Type II Pneumocytes (alveolar cells)

39
Q

State the two roles of pulmonayr surfactants?

A
  • Reduces alveolar surface tension
  • Equalizes pressure and volume in alveoli of varying size
40
Q

How does pulmonary surfactant prevent smaller alveoli from collapsing?

A

Surfactant molecules are amphipathic
- So naturally position themselves at the air-liquid interface
Presence of surfactants disrupt H-bonds between water molecules
Reduces surface tension and collapsing pressure generated

41
Q

How does pulmonary surfactant equalise pressure and volume in varying alveoli?

A
  1. During inflation of the lungs, as alveoli expand.
  2. The concentration of surfactant molecules decreases.
    - Same number of molecules within an increased surface area
  3. Increasing surface tension.
  4. Overall collapsing pressure increases as alveolar size increases
    - This generates pressure gradients within the lung
    - Now, larger (more inflated) alveoli tend to collapse into smaller ones, helping consistent inflation of the lungs.
42
Q

What does surface tension in alveoli reduce?

A

Surface tension produced at the air-liquid interface reduced hydrostatic pressure in the alveolar tissue
Fluid is pulled out of the surrounding capillaries and into the alveoli and interstital tissue.

43
Q

What does pulmonary surfactant help prevent?

A

Alveolar oedema
- It reduced surface tension so excessive fluid isn’t taken up from the capillary

44
Q

How can alveolar oedema occur when there is insufficient surfactant?

A

High surface tension
Leads to collapsing force produced
Decrease in hydrostatic pressure in tissue surrounding capilalry
Fluid pulled from capillary into alveolus
Alveolar oedema occurs

45
Q

How is neonatal respiratory distress syndrome caused by/

A

insufficient production of pulmonary surfactant

46
Q

Outline the steps of Neonatal Respiratory Distress Syndrome:

A

Premature birth, maternal diabetes, congenital developmental issues. (occurs mostly within infants)

Insufficient surfactant production.

Stiff (low compliance) lungs, alveolar collapse and alveolar oedema

Respiratory failure.

Hypoxia.

Pulmonary vasoconstriction, endothelial damage, acidosis, pulmonary + cerebral haemorrhage.

47
Q

What are the two ways in which insufficient surfactant production is overcome?

A

Maternal glucocorticoid supplementation: stimulate the production of surfactants via maturation of type 2 pneumocytes
Artificial surfactant supplementation of infant.