Session 1 - Ventilation and Lung Mechanics Flashcards

1
Q

What is Boyle’s law?

A

This is a gas law that states that in a closed system the pressure exerted by gas inside a container is inversely proportional to the volume of the container.

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2
Q

Comment on the pressures of the following, at the end of quiet inspiration:

  • Intra-alveolar pressure
  • Intrapleural pressure
  • atmospheric pressure
A

This is considered to be an equilibrium position.

The intra-alveolar pressure is equal to the atmospheric pressure.

The intrapleural pressure is strongly negative - this, in addition to the pleural seal, ensures the inflated lung remains adherent to the chest wall

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3
Q

Comment on the pressures of the following, at the end of quiet expiration:

  • Intra-alveolar pressure
  • Intrapleural pressure
  • atmospheric pressure
A

This is considered to be an equilibrium position.

The intra-alveolar pressure is equal to the atmospheric pressure.

The intrapleural pressure is somewhat negative. This ensures the alveoli do not completely collapse during the raised pressures of expiration.

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4
Q

List conditions that would INCREASE lung compliance.

A

Emphysema
Loss of connective tissue with age
Ehlers Danlos syndrome

See this link for more: https://www.physio-pedia.com/Lung_Compliance

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5
Q

List conditions that would DECREASE lung compliance

A
Diffuse Lung fibrosis 
Lung surfactant deficiency (e.g. ARDS of Newborn)
Pulmonary Oedema
Atelectasis
Significant obesity

See this link for more: https://www.physio-pedia.com/Lung_Compliance

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6
Q

List conditions that would DECREASE lung elastic recoil.

A

Emphysema
Loss of connective tissue with age
Ehlers Danlos syndrome

See this link for more: https://www.physio-pedia.com/Lung_Compliance

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7
Q

List conditions that would increase lung elastic recoil.

A
Diffuse Lung fibrosis 
Lung surfactant deficiency (e.g. ARDS of Newborn)
Pulmonary Oedema
Atelectasis
Significant obesity

See this link for more: https://www.physio-pedia.com/Lung_Compliance

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8
Q

What is the role of lung surfactant?

A

Produced by Type II Alveolar cells (Type II pneumocytes)

Lines the alveoli and reduces surface tension. This ensures the alveoli remain inflated at lower pressures, making them generally less likely to collapse.

Laplace’s law tells us that the pressure required to inflate a sphere is directly proportional to the tension in the wall and inversely proportional to the radius of the sphere. This, therefore, applies to the alveoli.

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9
Q

Describe the effects of surfactant deficiency on the ventilation of the lungs.

A

This can be seen in Acute Respiratory Distress of the Newborn.

Lack of surfactant means high surface tension in the alveoli, so higher pressures are needed to inflate the alveoli - the compliance is low.

More difficult to adequately ventilate the lungs causing respiratory distress.

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10
Q

What is Respiratory distress?

A

These are clinical signs which represent an overall difficulty in normal breathing, for whatever reason/from numerous causes

Signs include:
High respiratory rate (tachypnoea)
Use of accessory muscles of respiration
Intercostal and subcostal recessions (usually seen in children rather than adults)
Tracheal tug (usually seen in children rather than adults)
Tripod breathing
Nasal flaring
Grunting

Not to be confused with Acute Respiratory Distress syndrome

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11
Q

Define Dead space.

A

Represents the volume of ventilated air that does not participate in gas exchange.

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12
Q

Define Alveolar dead space.

A

= Anatomical + alveolar dead space

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13
Q

Define Anatomical dead space.

A

Refers to the volume of air in the parts of the respiratory tract responsible for conducting air to the alveoli, but not taking part in gas exchange itself: upper airways, trachea, bronchi and terminal bronchioles.

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14
Q

Define Physiological dead space.

A

= Anatomical + alveolar dead space

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15
Q

Define and calculate pulmonary ventilation rate

A

Also known as minute volume

= Tidal volume x Respiratory rate

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16
Q

Define and calculate the alveolar ventilation rate.

A

= (Tidal volume - Dead space) x Respiratory rate

I hope this makes sense, the part in brackets represents the volume of air involved in gas exchange in quiet breathing

17
Q

Explain the changes in intra-alveolar (IA) and intrapleural (IP) pressure during the respiratory cycle

A

Inspiration:
IP becomes more negative…as the thoracic wall expands

IA becomes more negative… as the diaphragm contracts, air rushes in from the atmosphere until equilibrium is reached.

Expiration:
IP becomes less negative… as it approaches resting expiratory level and the thoracic walls return to resting position.

IA - becomes more positive… air is therefore expelled into the atmosphere until an equilibrium is reached.

18
Q

Describe the mechanism of forced inspiration and accessory muscles

A

SCM contraction –> sternum and clavicles elevation - increasing intrathoracic cavity volume antero-posteriorly

Scalene contraction –> elevate 1 and 2 ribs further increasing intrathoracic cavity volume antero-posteriorly

19
Q

Describe the mechanism of forced expiration and use of accessory muscles.

A

Anterolateral abdominal muscles –>
push diaphragm up, decreasing intrathoracic cavity volume

Internal intercostals and innermost intercostals –> depress ribs, decreasing intrathoracic cavity volume

20
Q

What is the pleura?

A

Serosal membranes of the thorax.

It contains thin layers of serosal tissue which coats the lungs and lines the internal wall of the thoracic cavity.

The pleura in direct contact with the lung is called visceral pleura, and the rest is called parietal pleura.

Between the visceral and the parietal pleura is the pleural cavity - a potential space filled with a small volume of lubricating serosal fluid.

21
Q

What happens to the intrapleural pressure during the respiratory cycle?

A

It is always negative compared to intra-alveolar pressure.

Slightly negative at end of quiet expiration

Strongly negative at the end of quiet inspiration.

Very strongly negative at the end of forced inspiration.

Food for thought:
in forced expiration intrapleural pressure it reaches its least negative/most positive, this can potentially lead to airway collapse if it exceeds the alveolar/airway pressure