3 - Lung Mechanics Flashcards

1
Q

What is ventilation and what is it initiated by?

A
  • Process of inspiration and expiration
  • Neurones in respiratory centre of the brain generate automatic rhythmic impulses that go to inspiratory muscles
  • Normal involuntary
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2
Q

What is the definition of the following terms:

  • Tidal Volume
  • Inspiratory Reserve Volume (IRV)
  • Expiratory Reserve Volume (ERV)
A

TV: volume of air which enters and leaves the lungs on each quiet breath

IRV: Additional amount of air that can be inhaled after a normal inspiration

ERV: Amount of extra air — above anormal breath — exhaled during a forceful breath out

IRV and ERV can be used in exercise

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3
Q

What is residual volume?

A

Can never empty lungs so amount of air left in lungs after forced expiration

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4
Q

What are the different types of lung capacity, as lung capacity is not fixed, it is relative to a point?

A
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5
Q

How do muscles allow inspiration and expiration?

A

Expansion of thoracic cavity through EIM and diaphragm, reduced pressure which pushes air inwards

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6
Q

What is anatomical and alveolar dead space?

A

Anatomical: Volume of the conducting airways from nostils to terminal bronchioles as this air doesn’t participate in gas exchange

Alveolar: Air in alveoli which is not perfused or are damaged so do not take part in gas exchange so ventilating this alveoli is wasted

Physiological Dead Space = Alveolar + Anatomical

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7
Q

What are the equations for pulmonary and alveolar ventilation?

A
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8
Q

What is the resting expiratory level?

A

At the end of quiet expiration just before breathing in the lung is subject to two equal opposing forces, so an equilibrium with no chest wall movement.

Creates negative pressure within intrapleural space as two forces on pleura

Outward: elasticity of chest wall

Inward: elasticity and surface tension of lung

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9
Q

The lungs have a natural elastic recoil, especially with increased stretch, so during inspiration what keeps the lungs open and against the chest wall?

A

Pleural seal

Surface tension between molecules of pleural fluid allows chest wall and lungs to move together

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10
Q

Summarise the volume and pressure changes in the ventilation cycle.

A

Contraction of muscles overcomes the equilibrium of resting expiratory level by overcoming force of the lungs elastic recoil

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11
Q

How does the pleural pressure change throughout respiratory cycle?

A

At rest it is negative, during inpiration it becomes more negative due to expansion of thoracic cavity

The intrapleural pressure is always negative to help maintain proper inflation of the lungs and to help prevent a pneumothorax (i.e. collapsed lung).
The negative pressure of the pleural cavity acts as a suction to keep the lungs from collapsing.

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12
Q

What are the accessory muscles of respiration?

A

- Inspiration: scalene, SCM, serratus anterior, pectoralis major

- Expiration: internal intercostal muscles and abdominal wall muscles

Used in diseases of the lung and during exercise

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13
Q

Why is energy expended in inspiration?

A
  • Needed to overcome the airways resistance and to stretch the lungs
  • Most effort is overcoming elastic recoil not the resistance
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14
Q

What would happen if the pleural seal was broken? e.g pneumothorax from a stabbing

A

Negative pressure in the intrapleural space would draw air in from outside the chest wall and collapse the lung

Atelectasis

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15
Q

What is lung compliance?

A
  • Stretchiness of the lungs
  • Volume change per unit pressure change
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16
Q

What limits the expansion of the lungs and how has the body adapted to overcome this?

A
  • Fluid lining the alveoli, needed for gas exchange, creates surface tension decreasing the compliance

- Surfactant from type II pneumocytes disrupts interation between fluid molecules, decreasing surface tension

  • Without surfactant, wouldn’t overcome inward pull
17
Q

What is the content of surfactant?

A
  • Phospholipids and proteins with detergent properties
  • Hydrophillic ends in alveolar fluid
  • Hydrophobic ends in alveolar gas
  • Surfactant floats on surface of the alveolar fluid disrupting fluid interactions, lowering surface tension
18
Q

Which type of alveoli is surfactant more effective in disrupting surface tension in, and why is this?

A

- Smaller alveoli due to molecules being closer together

  • Surface tension increases as alveoli get larger
  • Reducing surface tension in smaller alveoli prevents pressure rising due to smaller volume so smaller don’t collapse into bigger
19
Q

Why is forced inspiration harder than quiet inspiration?

A

As as the alveoli get larger, the surface tension of the alveoli increases so more energy needed to overcome this

Quiet, or unforced, breathing uses only the Diaphragm and the External Intercostals for inhalation with no accessory muscle contractions.

20
Q

How does surfactant stabilise the lungs and prevent smaller alveoli collapsing into larger alveoli to form bullae?

A

Law of Laplace: Pressure = 2ST/R

As alveolus expands, both ST and R increase due to surfactant. Keeps the pressure the same in any size alveoli

21
Q

What are the two roles of surfactant?

A

Stabilise alveolis especially smaller ones
increase compliance

22
Q

What is respiratory distress syndrome? What is the treatment?

A
  • Surfactant absent from alveoli until fetus is 24 weeks
  • Born less than 28-30 weeks old can get this
  • Apnea, cyanosis, rapid shallow breathing, drawing in of lungs
  • Corticosteroid therapy and ventilator
23
Q

How does resistance of airway tubes vary with diameter?

A

Pouiselle’s Law - smaller radius, increasing resistance sharply

24
Q

If a smaller airway tube confers more resistance then why are the bronchioles so small?

A
  • Tubes are connected in parallel so combined resistance of all these is smaller than one big tube
  • 1/R + 1/R ETC…
25
Q

Where is the biggest resistance to breathing?

A

Upper respiratory tract (trachea and large bronchi) , except when small airways are compressed during forced expiration

26
Q

Why does resistance in the small bronchioles increase during forced expiration?

A
  • Contain no cartilage so airways collapse
  • Tubes get smaller so there is a high resistance to flow making forced expiration hard
  • Harder in asthma to expire as bronchioles even smaller than healthy person