Ventilation Flashcards

1
Q

What are the 3 phases of respiration?

A

External - ventilation (breathing)
Internal - pulmonary gas exchange, gas transport, systemic gas exchange
Cellular - metabolism

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2
Q

What different types of cell are the alveolar membranes composed of?

A

Type I cells - simple flat epithelial cells where gas exchange happens

Type II cells - septal cells, specialised surfactant secreting cells, free surface has microvilli

Alveolar dust cells - wandering macrophages removing debris - defence

Pores of Kohn - permit collateral airflow between alveoli. Number varies - more in well ventilated areas

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3
Q

What is alveolar gas exchange dependent on?

A

Fick’s law

Q (net diffusion rate) proportional to:

conc gradient x surface area of membrane x diffusion coefficient
\
thickness of membrane

The diffusion coefficient = membrane permeability / square root of MW of diffusing substance

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4
Q

What are the two components associated with the stretchy behaviour of the lungs?

A

Compliance - ease with which lungs are stretched. A lung with normal compliance can be stretched easily with a small transmural pressure gradient. A poorly compliant (stiff) lung is not very stretchy - emphysema - destruction of elastic tissue

Elastic recoil - how readily the lungs recoil after stretching (responsible for quiet expiration) - a lung with normal elastic recoil will allow passive expiration - pulmonary fibrosis

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5
Q

What do elastic recoil and compliance depend on?

A
  • Alveolar surface tension created by the thin film of liquid lining each alveolus
  • Surface tension pulls alveolus inwards because water molecules are involved in H-bonding strongly attached to each other
  • Mesh of elastin fibres (connective tissue) also has role in recoil and compliance
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6
Q

Describe alveolar surface tension

A
  • Surface tension induced by H-bonding and strongly elastic fibres is very strong
  • Unchecked these forces would collapse
  • Surface tension decreased by pulmonary surfactant - secreted by T2 alveolar cells so decreased work required to inflate lungs (dec tendency to recoil, prevent collapse)
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7
Q

What is La Place’s Law?

A

P=2T/r

P=inward directed collapsing pressure
T=surface tension
r=radius of alveoli (strictly a bubble)

i.e. the smaller the alveolus, the smaller the radius, the greater the tendency to collapse

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8
Q

What are collapse forces overcome by?

A

Surfactant - reduces surface tension more in smaller alveoli

Surrounding alveoli - if one alveolus starts to collapse, the surrounding alveoli, joined by connective tissue, resist the collapse due to their own elasticity

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9
Q

Surfactant and the new-born

A
  • Premature babies (< 7 months) not able to produce surfactant so can’t overcome alveolar surface tension easily
  • Lungs tend to collapse after exhalation
  • Lots of effort required to inflate lungs - not compliant and baby has underdeveloped muscles
  • May die due to exhaustion/lack of oxygen
  • Thought that surfactant production has tole in triggering labour
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10
Q

What are the 3 pressures involved in mechanics of breathing?

A

Atmospheric pressure
Intra-alveolar pressure (pressure within alveoli)
Intrapleural pressure (pressure in pleural sac - lower than other two)

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11
Q

What are the different muscles involved in inspiration and expiration?

A

Accessory muscles of inspiration - contract only during forceful inspiration

Major muscles of inspiration - contract every inspiration - relaxation causes passive expiration

Muscles of active expiration - contract during active expiration

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12
Q

Define Boyle’s law

A

At constant temp the volume of a given mass is inversely proportional to the pressure

V proportional to 1/P

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13
Q

Talk through inspiration

A

Active process brought about by contraction of inspiratory muscles, the chest wall and lungs stretched, the increase in size of the lungs make the intra-alveolar pressure to fall,

This is because air molecules become contained in a larger volume - Boyle’s law

The air then enters down the pressure gradient into the lungs until the intra-alveolar pressure becomes equal to the atmospheric pressure

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14
Q

Describe expiration

A

Passive process brought about by relaxation of inspiratory muscles. The chest wall and stretched lungs recoil to their preinspiratory size because of their elastic properties. The recoil makes the intra-alveolar pressure rise. This is because air molecules become contained in a smaller volume. Air leaves lungs down pressure gradient until intra-alveolar pressure equals atmospheric pressure

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15
Q

What condition abolishes the transmural pressure gradient?

A

Pneumothorax

Air in pleural space

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16
Q

Discuss spirometry

A

Look at lecture slides for graph

17
Q

What changes in obstructive lung disease?

A

Difficult to empty lungs

So…RV increases, FRC increases

18
Q

What changes in restrictive lung disease?

A

Lungs have reduced volume

VC and TLC are lower

19
Q

What is dead space and what are the two types?

A

Not all inspired gas gets to the site of gas exchange - some remains in the trachea - anatomical or airway dead space

We can measure the volume of lungs which do not eliminate Co2 - this is physiological dead space

If healthy both physio and anatom dead spaces similar. In lung disease patients the physio dead space likely to be higher

20
Q

What are pulmonary and alveolar ventilation?

A

PV is air breathed in/out in 1 min
Tidal vol x resp rate

AV is volume of air exchanged between atmosphere and alveoli per minute
(TV-dead space)x resp rate