Lung mechanics Flashcards

1
Q

What is internal respiration?

A

The exchange of gases (oxygen and carbon dioxide) between blood, interstitial fluid, and cells.

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2
Q

What is external respiration?

A

The exchange of gases (oxygen and carbon dioxide) between blood and the external environment.

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3
Q

What 3 processes are involved in external respiration?

A

Pulmonary ventilation
Gaseous diffusion.
Transport of oxygen and carbon dioxide.

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4
Q

what is pulmonary ventilation

A

The physical movement of air into and out of the lungs

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5
Q

What drives the movement of air through the airways?

A

Airflow is driven by the pressure gradient between the mouth and alveoli, expressed as:
Flow = ΔP / R, where ΔP = pressure difference and R = resistance.

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6
Q

What are the two main pressure gradients in breathing?

A

Pressure gradient driving air: From the mouth to alveoli (mouth - alveolar).

Pressure gradient distending the lung: Transmural pressure (alveolar - intrapleural).

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7
Q

What is transmural pressure?

A

The pressure difference between the alveolar pressure and the intrapleural pressure that distends the lung.

transmural = alveolar - intrapleural

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8
Q

What is required for the bulk flow of air along the airways?

A

A pressure gradient must be generated between atmospheric pressure (PB) and airway pressure (Paw).

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9
Q

when does air flow into the lungs?

A
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10
Q

What happens to airway pressure during inspiration?

A

During inspiration, Paw decreases, creating a pressure gradient that allows air to flow into the lungs.

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11
Q

What is the equation for airflow through the airways?

A

Flow (Q) = ΔPressure (P1 - P2) / Resistance (R),
where P1 is atmospheric pressure and P2 is airway pressure.

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12
Q

What creates the flow of air during expiration?

A

Air flows out when Paw (airway pressure) > PB (atmospheric pressure), generating a pressure gradient.

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13
Q

What is the equation for airflow during expiration?

A

Flow (Q) = ΔPressure (P1 - P2) / Resistance (R),
where P1 is airway pressure and P2 is atmospheric pressure.

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14
Q

What does Boyle’s Law state?

A

The pressure of a fixed number of gas molecules at constant temperature is inversely related to the volume of the container. (PV = constant)

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15
Q

What happens to pressure when the volume of a gas is decreased?

A

When volume decreases, pressure increases due to the gas molecules being compressed into a smaller space.

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16
Q

What happens to pressure when the volume of a gas is increased?

A

When volume increases, pressure decreases as gas molecules are distributed over a larger space.

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17
Q

What is the mathematical representation of Boyle’s Law?

A

P1 × V1 = P2 × V2

where P and V are initial and final pressure and volume, respectively.

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18
Q

How is Boyle’s Law applied in respiration?

A

During inhalation, lung volume increases, leading to a decrease in pressure and air inflow. During exhalation, lung volume decreases, increasing pressure and pushing air out.

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19
Q

How are the lungs mechanically coupled to the chest wall?

A

by the pleural fluid, which prevents lung collapse by balancing the inward recoil of the lungs with the outward recoil of the chest wall.

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20
Q

What is the value of intrapleural pressure at resting end-expiration?

A

Intrapleural pressure is negative, approximately -5 cm H₂O at resting end-expiration.

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21
Q

What happens to intrapleural pressure during inspiration?

A

The expansion of the thoracic cage during inspiration further reduces intrapleural pressure, which allows the lungs to expand.

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22
Q

How does increased lung volume affect airway pressure?

A

Increased lung volume leads to a decrease in airway pressure, which drives air into the lungs.

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23
Q

What is the relationship between alveolar pressure (Pₐ) and atmospheric pressure (Pᵦ) during inspiration?

A

During inspiration, alveolar pressure (Pₐ) becomes less than atmospheric pressure (Pᵦ), allowing air to flow into the lungs.

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24
Q

How are respiratory pressures generally expressed?

A

Respiratory pressures are expressed relative to atmospheric pressure (Pᵦ).

unless stated otherwise

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25
Q

How does the ribcage contribute to ventilation?

A

How does the ribcage contribute to ventilation?

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26
Q

What 4 things makes up the thoracic cage?

A

The thoracic cage consists of 12 pairs of ribs, a sternum, and internal and external intercostal muscles.

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27
Q

What occurs during the pre-inspiration state?

A

At pre-inspiration (end-expiration), the pressures inside and outside the lungs are equal, so there is no air movement.

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28
Q

Is inspiration active or passive, and how is it achieved?

A

Inspiration is always active and involves the contraction of inspiratory muscles, including the diaphragm.

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29
Q

Is expiration at rest active or passive?

A

Expiration at rest is passive, as it involves the relaxation of inspiratory muscles.

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30
Q

What happens during expiration when ventilatory demands increase?

A

Expiration becomes active, requiring the recruitment of expiratory muscles to increase airflow.

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31
Q

What are the 4 obligate inspiratory muscles

A
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32
Q

what is an example of an accesssory inspiratory muscle

A

Sternocleidomastoid muscles (neck muscles).

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33
Q
A
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34
Q

What is transmural pressure?

A

Transmural pressure is the pressure differential between the inside compartment and the outside compartment.

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35
Q

What are the different types of transmural pressures in the respiratory system?

A
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36
Q

Why is transpulmonary pressure (P_L) important?

A

P_L acts as the distending pressure that inflates the lungs. It must become more positive to expand the lungs during inspiration.

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37
Q

What is the transpulmonary pressure (P_L) at the end of expiration?

A

Transpulmonary pressure (P_L) is +5 cm H₂O, calculated as alveolar pressure (0 cm H₂O) minus intrapleural pressure (-5 cm H₂O).

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38
Q

How does the transpulmonary pressure (P_L) change during inspiration?

A

Transpulmonary pressure (P_L) increases to +7 cm H₂O, as alveolar pressure becomes -1 cm H₂O and intrapleural pressure decreases to -8 cm H₂O.

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39
Q

Is expiration at rest active or passive?

A

Expiration at rest is passive, relying on the relaxation of inspiratory muscles.

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40
Q

What happens to intrapleural pressure during expiration

A

Intrapleural pressure becomes less negative so transpulmonary pressure (PL) decreases

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41
Q

What causes air to flow out of the lungs during expiration?

A

Alveolar pressure (P_A) becomes greater than atmospheric pressure (P_B), driving air out until P_A equals P_B.

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42
Q

what happens during force expiration

A

During forced expiration, expiratory muscles are additionally activated
Intrapleural pressure may be positive in these circumstances
Lung elastic recoil acts in series with positive Ppl to further increase PA&raquo_space;> PB

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43
Q

How does pleural pressure change during inspiration and expiration?

A

During inspiration, pleural pressure becomes more negative (e.g., -5 to -7 cm H₂O). During expiration, it becomes less negative.

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44
Q

What happens to alveolar pressure during inspiration and expiration?

A

During inspiration, alveolar pressure decreases below atmospheric pressure to allow airflow into the lungs. During expiration, it increases above atmospheric pressure to drive airflow out.

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45
Q

What determines the direction of airflow during the respiratory cycle?

A

Airflow is driven by pressure gradients:

Inspiration: Alveolar pressure < Atmospheric pressure (air flows in).
Expiration: Alveolar pressure > Atmospheric pressure (air flows out).

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46
Q

What happens to tidal volume during inspiration and expiration?

A

Tidal volume increases during inspiration as air enters the lungs and decreases during expiration as air exits.

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47
Q

What is Functional Residual Capacity (FRC)?

A

FRC is the volume of air remaining in the lungs at the end of a normal, unforced expiration.

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48
Q

what is tidal volume

A

Amount of air moved in one cycle = tidal volume (VT)

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49
Q

what is the value of tidal volume

A

approximately 500ml

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50
Q

what is dead space

A

airway volume with no gas exchange


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51
Q

What is anatomic dead space, and what is its typical volume?

A

Anatomic dead space includes all airways except alveoli and respiratory bronchioles, with a typical volume of 150 ml.

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52
Q

How is physiologic dead space different from anatomic dead space?

A

Physiologic dead space includes anatomic dead space plus areas where gas exchange is dysfunctional.

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53
Q

How are anatomic and physiologic dead spaces related in healthy individuals?

A

In healthy individuals, physiologic dead space is approximately equal to anatomic dead space.

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54
Q

What is the formula for physiologic dead space?

A
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55
Q
A
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56
Q

What is the typical tidal volume in a healthy adult?

A

500 ml.

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57
Q

What is the typical volume of anatomic dead space?

A

150 ml.

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58
Q

What is the total ventilation per minute?

A

7500 ml/min.

59
Q

What is the normal breathing frequency?

A

15 breaths per minute.

60
Q

How is alveolar ventilation calculated?

A

Alveolar ventilation = Minute ventilation - Dead space ventilation.

61
Q

If total ventilation is 7500 ml/min and dead space ventilation is
150 × 15
what is the alveolar ventilation?

A

7500−2250=5250ml/min.

62
Q

What is the volume of pulmonary capillary blood?

A

70 ml.

63
Q

What is the typical pulmonary blood flow per minute?

A

5000 ml/min.

64
Q

What is the typical volume of alveolar gas?

A

3000 ml.

65
Q

What are the two main sources of resistance the respiratory muscles must overcome during inspiration?

A
  1. Elastic resistance of the lung
  2. Airway resistance to airflow
66
Q

How do lung diseases affect breathing resistance?

A

In many lung diseases, one or both sources of resistance (elastic resistance and airway resistance) increase, leading to an increased work of breathing and symptoms such as dyspnoea (breathlessness).

67
Q

What is elastic resistance in the lungs?

A

Resistance to the stretch of lung tissues and the air-liquid interface lining the alveoli.

68
Q

What causes airway resistance?

A

Airway resistance is caused by friction between layers of flowing air and between the air and the airway walls.

69
Q

How is airway resistance (RAW) calculated?

A
70
Q

What are the two types of airflow patterns that determine airway resistance?

A

Laminar flow (smooth) and turbulent flow (disorganized).

71
Q

What happens to airflow when there is high velocity or sharp edges in the airways?

A

It disrupts laminar flow, leading to turbulence, which increases resistance and causes vibrations.

72
Q

Why do narrowed airways produce lung sounds?

A

High-velocity airflow through narrowed airways causes turbulence, which generates audible lung sounds.

73
Q

How are wheezes generated in the airways?

A

Wheezes are caused by oscillations in the walls of airways near the point of closure.

74
Q

Why might wheezes disappear in severe airway obstruction?

A

In severe obstruction, airflow is so limited that oscillations (and wheezes) can no longer occur - Hence the ominous silent chest in very severe asthma

75
Q

What does a “silent chest” indicate in very severe asthma?

A

It suggests critically severe obstruction with minimal or no airflow, requiring urgent intervention.

76
Q

What 3 factors affect airway resistance?

A

Length of the airway (L)
Radius of the airway (𝑟)
Viscosity of the fluid (𝑉)

77
Q

How does Poiseuille’s law describe airway resistance?

A
78
Q

What happens to resistance if the radius of the airway is halved?

A

If the radius is halved, resistance increases 16-fold.

79
Q

What happens to flow if airway resistance increases due to halved radius?

A

With the same pressure gradient, flow is reduced to 1/16th of the original value.

80
Q

What is the equation for flow in relation to pressure and resistance?

A
81
Q

How is flow expressed in Poiseuille’s Law?

A

the red part

82
Q

Flow is proportional to the

A

fourth power of the radius (yellow box)

83
Q

which 3 places is airway resistance highest in the whole respiratory system?

A

In the nose, pharynx, and larynx.

84
Q

Which part of the lungs contributes most to airway resistance?

A

The medium-sized bronchi.

85
Q

Why is the net resistance in smaller distal airways low despite high individual resistance?

A

Because their large numbers in parallel reduce the net resistance.

86
Q

Which bronchial generations contribute most to resistance?

A

Medium-sized bronchi around generations 3–5.

87
Q

What are the two main factors causing variations in airway resistance (RAW)?

A
88
Q

How does negative intrapleural pressure during normal breathing affect airways?

A

It holds the airways open.

89
Q

How does positive intrapleural pressure during forced expiration affect airways?

A

It creates a collapsing force on the airways.

90
Q

Which factors promote bronchodilation in airway smooth muscle?

A
  1. β2-Adrenergic agonists (e.g., adrenaline, salbutamol).
  2. NANC (Non-Adrenergic, Non-Cholinergic) inhibitory nerves releasing NO (Nitric Oxide) and VIP (Vasoactive Intestinal Peptide).
  3. Increased CO2 levels
91
Q

Which factors promote bronchoconstriction in airway smooth muscle?

A
  1. Histamine, prostaglandins, leukotrienes (released from mast cells and eosinophils).
  2. Vagal efferents acting via Ach (Acetylcholine) on M3 receptors.
  3. Substance P (SP) and neurokinins from NANC excitatory nerves.
92
Q

What is dynamic compression of airways?

A

It is the collapse of airways during forced expiration when pressure within the airways falls below pleural pressure (Ppl).

93
Q

Where in the respiratory system is dynamic compression most likely to occur?

A

Airways around generation 3 or 4, which have the maximum airway resistance.

94
Q

Does dynamic compression occur in healthy individuals?

A

Yes, it occurs in normal people but is more pronounced if airway resistance is high.

95
Q

why is expiration airflow limited in normal people

A

Because of “dynamic compression of airways”, even in normal people expiratory airflow is limited and at low lung volume does not increase if you try harder (it is “effort independent”)

96
Q

What causes dynamic compression of airways during forced expiration?

A

High intrathoracic (intrapleural) pressure compresses airways, limiting expiratory airflow.

97
Q

How does dynamic compression affect lungs with high RAW?

A

Slow expiration
Low peak expiratory flow rate
Air trapping
Expiratory wheezes

98
Q

What is lung compliance?

A

Lung compliance is the measure of the stretchiness of the lung, calculated as:

99
Q

Where is lung compliance maximized on the pressure-volume curve?

A

Compliance is maximum around the normal tidal volume range.

100
Q

When is lung compliance minimized?

A

Compliance is lowest at very high and low lung volumes, near total lung capacity (TLC) and residual volume (RV).

101
Q

What is the typical value of lung compliance in an adult male?

A

1.5 L·kPa⁻¹

102
Q

What happens to lung compliance when the lungs are stiff?

A

Stiff lungs have low compliance due to high elastic resistance.

103
Q

How does lung fibrosis affect lung compliance?

A

Lung fibrosis causes scarring and stiffness, resulting in low compliance.

104
Q

How does emphysema affect lung compliance

A

In emphysema, tissue destruction and loss of elasticity make the lungs floppy, leading to high compliance.

105
Q

What are the main components contributing to the elastic resistance of the lungs?

A

elastin and collagen, and the air-fluid interface in alveoli.

106
Q

How does the air-fluid interface in alveoli contribute to elastic resistance?

A

The air-fluid interface contributes to elastic resistance because stretching it requires overcoming its surface tension.

107
Q

What is the LaPlace equation, and what does it describe?

A

It describes the relationship between pressure and the radius of a bubble or alveolus, showing that smaller radii require higher pressure to balance surface tension.

108
Q

What happens to pressure when the radius of a bubble decreases?

A

When the radius decreases, the pressure increases,

109
Q

Why does a small bubble collapse into a larger one?

A

A small bubble has a higher internal pressure (P1) than a larger bubble (P2) due to its smaller radius. This pressure difference causes air to flow from the small bubble to the larger bubble, leading to the collapse of the smaller bubble.

110
Q

How does surface tension (𝑇) contribute to bubble collapse?

A

Surface tension creates an inward force that increases the internal pressure of smaller bubbles, contributing to their collapse into larger bubbles where the tension is balanced across a larger radius.

111
Q

which cells produce surfactant in the lungs?

A

Type II alveolar cells.

112
Q

What is surfactant composed of?

A

A mixture of phospholipids (e.g., phosphatidylcholine) and surfactant proteins (SP-A, SP-B, SP-C, SP-D).

113
Q

What is the main function of surfactant in the lungs?

A

To lower the surface tension of the alveolar lining fluid.

114
Q

How do the phospholipids in surfactant function?

A

They have an insoluble fatty acid end and a hydrophilic end, allowing them to float on the surface of the alveolar lining fluid.

115
Q

How does surfactant reduce surface tension?

A

It reduces surface tension in proportion to its surface concentration.

116
Q

How does surfactant affect lung compliance?

A

Surfactant increases lung compliance.

117
Q

How does surfactant prevent alveoli from collapsing?

A

It reduces the tendency of alveoli to collapse, especially in small alveoli where surface concentration is high.

118
Q

What is the role of surfactant in preventing fluid accumulation in alveoli?

A

It reduces the tendency to suck fluid into alveoli (transudation).

119
Q

What is Neonatal Respiratory Distress Syndrome,

A

NRDS occurs in premature babies due to inadequate surfactant production, leading to reduced compliance and alveolar collapse.

120
Q

What problems arise in Neonatal Respiratory Distress Syndrome?

A

Increased work of breathing due to reduced compliance and alveolar collapse.

121
Q

what is alveolar dependency

A

Joining of alveoli to each other also helps alveoli resist collapse

122
Q

what abnormalities occur as a result of low lung compliance and high lung compliance

A
123
Q

What are the two main categories of lung diseases evaluated by lung function tests?

A

Obstructive lung disease and restrictive lung disease.

124
Q

What characterizes obstructive lung disease?

A

Narrow airways reduce airflow.

Eg asthma, chronic obstructive pulmonary disease (COPD) (NB: COPD pathology - small airway inflammation & emphysema)

125
Q

What are the key pathologies in COPD?

A

Small airway inflammation and emphysema.

Eg lung fibrosis, respiratory muscle weakness, phrenic nerve damage

126
Q

how can airway resistance (RAW) be measured directly?

A

plethysmograph

127
Q

What are simpler tests used to assess high airway resistance indirectly?

A

Forced expiratory maneuvers, such as peak flow and FEV₁/FVC measurements.

128
Q

What is the procedure for peak flow and FEV₁/FVC tests?

A

The subject breathes in to total lung capacity and breathes out as hard and fast as possible.

129
Q

What do forced expiratory spirograms measure?

A

Volume versus time during forced expiration to assess lung function.

130
Q

What is FEV₁?

A

Forced expiratory volume in 1 second.

131
Q

What is FVC?

A

Forced vital capacity, the total volume of air exhaled during a forced expiration.

132
Q

What is the normal FEV₁/FVC ratio?

A

Greater than 70%, though this is age-dependent.

133
Q

How can FEV₁ and FVC patterns distinguish between obstructive and restrictive lung diseases?

A

Obstructive diseases reduce FEV₁/FVC ratio, while restrictive diseases maintain the ratio but with reduced absolute volumes.

134
Q

What does BTPS stand for in spirometry?

A

Body Temperature and Pressure Saturated, standard conditions for volume measurements.

135
Q

What are the spirometry characteristics of healthy lungs?

A

FEV₁, FVC, and FEV₁/FVC ratio are all normal.

A on the graph

136
Q

How does obstructive lung disease affect spirometry?

A

Obstructive disease:
FEV1 ↓↓
FVC ↓ or normal
FEV1/FVC ↓

B on the graph

137
Q

How does restrictive lung disease affect spirometry?

A

Restrictive disease:
FEV1 ↓
FVC ↓
FEV1/FVC normal or ↑

C on graph

138
Q

What does a normal maximum flow-volume loop look like?

A

It has a smooth curve with high peak expiratory flow and symmetrical inspiratory and expiratory phases.

139
Q

What are the characteristics of the flow-volume loop in obstructive airway disease (e.g., COPD)?

A

Concave appearance of the forced expiratory curve.

Forced inspiratory flow is less affected than expiratory flow.

140
Q

What are the characteristics of the flow-volume loop in restrictive lung disease?

A

Low peak flow rates.

The loop is narrower and related to low lung volume.

141
Q

How does lung fibrosis affect FRC?

A

Lung fibrosis increases lung stiffness, leading to increased lung recoil and a reduced FRC.

142
Q

How does emphysema affect FRC?

A

Emphysema involves tissue loss, reducing lung recoil and leading to an increased FRC (barrel chest appearance).

143
Q

How does respiratory muscle weakness affect FRC?

A

In respiratory muscle weakness, the balance between lung and chest wall recoil remains normal, so FRC is unaffected.