Case 6 - physiology part 2 Flashcards

1
Q

How does compliance change in pneumothorax

A

A puncture in the thoracic case will cause the lungs to collapse as air enters. The thoracic cage then expands outwards as it undergoes elastic recoil

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2
Q

What is surfactant

A

It is secreted by type 2 alveolar cells, it is a mixture of phospholipids and proteins.

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3
Q

Role of surfactant

A

It reduces the surface tension forces in the alveoli:
• This reduces the work of breathing.
• Helps prevent fluid accumulation in the alveoli.
• Helps keep alveoli uniformly ventilated.

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4
Q

Amount of surfactant in the alveoli

A

There is a higher concentration of surfactant in the smaller alveolus so it has a lower surface tension. The surface tension of water and surfactant is proportional to the surface area. This will improve ventilation making it more uniform between the different alveolus as its normally more difficult to inflate a smaller alveolus

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5
Q

What is responsible for elastic recoil?

A
  • Elastic fibres in the lungs= elastin and collagen fibres in the alveolar walls and around vessels and bronchi. These are affected by emphysema and change with age.
  • Surface tension= there is a liquid film lining the alveoli, the attractive forces between adjacent liquid molecules are much stronger than those between liquid and gas. This keeps the lungs and chest wall together.
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6
Q

What is surface tension

A

A measure of the forces acting to pull a liquid’s surface molecules together at an air-liquid interface, The surface tension in the alveolus has to be overcome in inspiration

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7
Q

What forces do the respiratory muscles have to overcome in inspiration?

A
  • Elastic recoil and thorax, 80% of the work of breathing.
  • Resistance to airflow in airways.
  • Resistance due to deformation of tissue in the lungs and thorax (tissue resistance).
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8
Q

Importance of the intrapleural pressure

A

This pressure keeps the lungs and chest wall stuck together, the fluid molecules in the intrapleural space are attracted to each other keeping the lungs and chest together.

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9
Q

What does the intrapleural pressure vary with:

A
  • Stage in respiration (inspiration vs expiration).
  • Position in the lung (apex vs base) when they are standing up.
  • Pattern of breathing (rest vs forced breathing), forced inhalation will cause a more negative pressure
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10
Q

Intrapleural pressure in the base

A

End of expiration= -0.4kPa

End of inspiration= -0.8kPa

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11
Q

Intrapleural pressure in the apex

A

End of expiration= -1.0kPa

End of inspiration= -1.4kPa

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12
Q

Intrapleural pressure during forced breathing

A

End of expiration= +3kPa

End of inspiration= -4kPa

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13
Q

What is lung compliance

A

The ease in which a lung can be inflated. A measure of the change in lung volume which occurs with a specific change in pressure

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14
Q

Lung compliance equation

A

Compliance= Change in lung volume / Change in intrapleural pressure

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15
Q

Compliance in inspiration and expiration

A

High pressure causes a higher volume, it then plateaus out. In expiration you will have a higher volume for a given pressure. The lung never fully empties so the volume cant be 0.

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16
Q

Specific compliance equation

A

Specific compliance= Compliance / lung volume (one lung)
As compliance is affected by lung volume, it is difficult to use references as people have different lung volumes. This is why you use specific compliance

17
Q

Compliance in a healthy person

A

2L/kPa

18
Q

Response to CO2 in hypoxia

A

The effect of hypoxia and Hypercapnia is more then the sum of hypoxia alone and Hypercapnia alone

19
Q

What part of the lungs offer the most and least resistance

A

The bronchi have the most resistance as the cross sectional area is the lowest, the resistance is lowest in the bronchioles because they have the highest cross-sectional area

20
Q

Equation for airway resistance

A

Airway resistance= Driving pressure / gas flow

21
Q

What is driving pressure (resistance)

A

The difference between the atmospheric pressure (mouth) and the average pressure across all alveoli in the lungs

22
Q

Factors affecting airway resistance- tethering

A

A normal airway will be held open by the tethering effect of the alveolar wall whilst a ‘floppy’ airway in patients with emphysema will no longer be supported by alveolar tissue. A floppy airway will have increased resistance as the airway collapses when you breathe out, and becomes constricted. The tethering tissue is lost in emphysema

23
Q

Other factors that affect airway resistance

A

1) A high lung volume causes decreased resistance
2) A foreign body in the airways reduces diameter
3) Contraction of smooth muscle, controlled by ANS reduces diameter
4) Breathing out creates a more positive intrapleural pressure which compresses the airway and increases resistance, this occurs in emphysema. As less air can be removed there will be a bigger starting volume and reduced compliance

24
Q

Local control of airway diameter (produced in the airways)

A
  • Histamine- increases smooth muscle contraction, increases vascular permeability causing airway odema, increases mucus secretion.
  • Prostaglandins and thromboxanes- contraction or relaxation of smooth muscle
  • Leukotrienes- contraction of smooth muscle, antagonists are used in cancer treatment.
25
Q

What causes Bronchoconstriction

A

Histamines, leukotrienes, prostaglandin, pulmonary stretch receptors and irritant receptors.

26
Q

What causes Bronchodilation

A

Sympathetic Beta2 stimulation, adrenaline and increased CO2 tension.

27
Q

What activates the irritant fibres

A

Mechanical and chemical stimulation

28
Q

What activates the C-fibre receptor

A

Chemical stimulation

29
Q

Parasympathetic innervation of airways

A

The afferent branch of the Vagus nerve is a parasympathetic nerve activated by the irritant receptor. It sends signals to the CNS. C-fibre receptors also send signals to the CNS. The CNS sends an efferent nerve to the mucus gland and smooth muscle. They release Ach which binds to Muscarinic Receptors, there is an increase in Ca+2 concentration which causes bronchoconstriction. There is also mucus secretion from goblet cell which decrease luminal diameter and increase resistance

30
Q

Sympathetic innervation of the airways

A

By adrenaline which binds to Beta2 adrenergic receptors which cause vasodilation by increasing Cyclic AMP. The Alpha-1 adrenergic receptor inhibits. Has little effect

31
Q

What drugs can reduce bronchial muscle tone and airway resistance

A
Beta 2 agonist
Antihistamines
Muscarinic antagonists
Leucocyte anatgaonists
Steroids
Adrenaline