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Physiology > Lecture 19: Lung anatomy and mechanics > Flashcards

Lecture 19: Lung anatomy and mechanics Flashcards

1
Q

What is the physiological role of the lungs?

A

Make oxygen available for metabolism (“internal respiration”)

Remove CO2 (metabolic byproduct)

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2
Q

Lobes of right and left lung

A

Right: upper, middle and lower lobes

Left: upper, lower and lingula (middle lobe)

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3
Q

What surrounds the lungs and their lobes?

A

Visceral pleura

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4
Q

What demarcates the thoracic cavity?

A

Bone: 12 ribs, sternum, vertebrae

Muscle: chest wall muscles and diaphragm

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5
Q

What do the visceral and parietal pleura form?

A

Pleural sac between lungs and chest wall and diaphragm

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6
Q

Role of the pleural sac

A

Couples the lungs to the chest wall and the diaphragm

Lubricates: allows sliding movement of the lungs relative to the chest wall and diaphragm

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7
Q

What occurs in pneumothorax?

A

Loss of lung-throrax coupling (no transmural pressure gradient)

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8
Q

Types of pneumothorax

A

Primary spontaneous

Secondary spontaneous

Traumatic

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9
Q

Primary spontaneous pneumothorax

A

Cause unknown

Risk factors: males, smoking, family history

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10
Q

Secondary spontaneous pneumothorax

A

With lung disease (COPD, lung infection)

Interstitial lung disease and cancer

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11
Q

Traumatic pneumothorax

A

Blunt or penetrating injury to the chest wall

Penetration of bony points at rib fracture damages lung

Central venous catheter into chest vein

Lung biopsy

Positive pressure ventilation (barotrauma)

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12
Q

Trajectory of air through the upper airway

A

Air enters/exits via the nose & mouth, passing through the pharynx (shared between the digestive and respiratory systems)

Air enters/exits airways via the larynx (contains vocal cords)

Trachea

Airways

Alveolae

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13
Q

Role of epiglottis

A

Air and food have common passageway

Epiglottis prevents food or drink from entering the airways

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14
Q

Role of upper airways

A

Humidification

Protection

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15
Q

Airway branching in the human lung, differences?

A

Bronchi

Bronchioles

Alveolar sacs

See figure

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16
Q

Anatomy of bronchi

A

Cartilage in wall

Airway smooth muscle (controls size of airway)

Ciliated pseudo stratified epithelium

Mucous glands (protective)

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17
Q

Anatomy of bronchioles

A

Terminal bronchioles: no cartilage, reducing smooth muscle, cilia and mucous glands

Respiratory bronchioles: no smooth muscle or cilia, first alveolar bunds

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18
Q

Anatomy of alveolar sacs

A

Type I and II epithelium

Surfactant (surface tension)

Gas exchange

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19
Q

PSNS control of airways - nerve and function

A

Vagal efferents via muscarinic receptors

Mediate bronchoconstriction, pulmonary vasodilation, mucous gland secretion, mucous gland secretion

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20
Q

SNS control of airways

A

Bronchial smooth muscle relaxation, pulmonary vasoconstriction, inhibits mucous gland secretion

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21
Q

Non-adrenergic non cholinergic (NANC)

A

Mixed mediators (ATP, NO, substance P, VIP)

counteracts PSNS

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22
Q

Components of the neural and humeral control of airways

A

PSNS (cholinergic)

Sympathetic (adrenergic)

Non-adrenergic non cholinergic (NANC)

Lung afferents

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23
Q

Lung afferents

A

Vagal sensory fibers

Stretch, irritant receptors, C fibers, reflex responses (cough, bronchoconstriction, mucous release, heart-lung matching)

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24
Q

Where is the greatest resistance in the respiratory system?

A

2nd - 5th generation airways (conducting airways)

Resistance is inversely proportional to cross sectional area

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25
Q

Relationship between resistance and cross sectional area

A

Inversely proportional

Lower resistance in locations with higher cross sectional area

see figure

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26
Q

What effect does bronchoconstriction have on resistance to airflow?

A

Increases resistance

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27
Q

What can induce bronchoconstriction?

A

PSNS induced airway smooth muscle contraction

Allergic - histamine

Physical - mucous, edema, collapse

Physiologic - neural, local decrease in CO2

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28
Q

What effect does bronchodilation have on resistance to airflow?

A

Decreased resistance

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29
Q

What can induce bronchodilation?

A

Sympathetic nerves - airway smooth muscle relaxation

Physiologic - neural stimulation, hormonal, local increase in CO2

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30
Q

How does gas exchange occur between the alveolar and the capillaries?

A

Thin interface between the alveolar and the capillaries

Large surface area

Collateral ventilation

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31
Q

Where does blood come from for gas exchange?

A

Via pulmonary artery (carries deoxygenated blood) and vein (carries oxygenated blood)

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32
Q

What vessels are the airways supported by?

A

Bronchial circulation

Part of systemic circuit

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33
Q

How can we get air to move in and out of lungs?

A

Need to create pressure gradients

Lung cannot expand itself, it can only move passively in response to external pressures

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34
Q

What are the two ways to get air into the lung?

A

Create positive pressure at the airway opening to push air into the lung (in frogs and when a person is manually ventilated with a bag)

Or, create negative pressure within the lung (free breathing in humans)

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35
Q

Anatomy of breathing: respiratory system at equilibrium (end expiration)

A

Lungs are elastic and want to be smaller

Thorax is elastic and wants to be bigger

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36
Q

Anatomy of breathing: inspiration

A

Respiratory muscle contraction increases thoracic volume to stretch the lungs

Creates negative pressure (compared to atmosphere) so air moves in

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37
Q

Anatomy of breathing: exhalation

A

Respiratory muscles relax

Thoracic volume decreases due to pulling forces of the elastic lung

Creates positive pressure so air moves out of lung

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38
Q

What are the two forces that pull the lungs away from the thoracic cage? Opposed by?

A

The lung’s natural tendency to recoil

The surface tension of the alveolar fluid (molecules of fluid lining the alveoli are attracted to each other. This produces surface tension that acts to draw the alveoli together)

Opposed by the natural elasticity of the thorax

Visceral and parietal pleura stay attached by the parietal fluid, so neither the lungs nor the thorax wins

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39
Q

Usual pleural pressure

A

Negative

Due to opposing forces of lungs and thorax

Otherwise, lungs would collapse

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40
Q

What pressures are important in breathing?

A

Atmospheric pressure (Patm)

Intra-alveolar pressure (Palv)

Intra-pleural pressure (Ppl)

Transmural pressure: difference across a boundary

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41
Q

Important transmural pressures in breathing

A

Lung wall = Palv - Ppl

Thoracic wall = Patm - Ppl

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42
Q

How does air move during breathing?

A

Down pressure gradient

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43
Q

Pressure gradients during end expiration

A

Patm = 0

Palv = 0

Ppl = -5

transmural pressure of lung wall = 0 -(-5) = 5

No air flow

See figure

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44
Q

Pressure gradients during inspiration

A

Thorax and lungs increase in size

Patm = 0

Palv = -1

Ppl = -8

Transmural pressure of lung wall = -1 - (-8) = 7

Air flows into lungs

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45
Q

Lung recoil at functional residual capacity

A

lung recoil at FRC = chest wall recoil

See figure

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46
Q

Lung recoil: % vital capacity vs lung pressure

A

Recoil force increases as vital capacity and pressure increase

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47
Q

Recoil pressure at different lung volumes

A

At very negative pressure, the recoil pressure of the lungs is low. The recoil pressure of the thoracic cage is high (wants to expand(

At FRC, the recoil pressure of the lungs is equal to that of the thoracic cage

At tidal volume, the lung recoil pressure is equal to the thoracic recoil pressure

See figure

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48
Q

Respiratory muscles

A

Inspiration: external intercostals, diaphragm

Accessory muscles of inspiration: scaliness, sternocleidomastoid

Muscles of active expiration: abdominal, internal intercostals

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49
Q

Anatomy of inspiration

A

Diaphragm contracts: moves inferiorly and increases the vertical dimension of the thoracic volume

External intercostals: raise ribs to increase anterior-posterior and lateral thoracic volume

Scalenes and sternocleidomastoid: elevate upper ribs and sternum during exertion

50
Q

Anatomy of quiet expiration

A

Passive

Muscles relax, lungs and chest wall return to equilibrium

51
Q

Anatomy of forced expiration

A

Internal intercostals reduce anterior-posterior and lateral thorax volume

Abdominals force diaphragm up

Ppl becomes positive and larger than Palv = dynamic airway compression

52
Q

What is compliance?

A

A measure of the dispensability of a structure

Degree that volume changes in response to change in pressure

delta V / delta P

53
Q

What part of the pressure volume curve represents compliance?

A

Slope

54
Q

Compliance vs elastance

A

Compliance is opposite of elastane

55
Q

What is lung elastic recoil determined by?

A

Elastic fibers in lung interstitial (collagen & elastin)

Surface tension of alveolar lining fluid (surfactant)

56
Q

What determines how much air enters during inspiration?

A

Lung compliance

Pleural pressure

Airflow resistance

57
Q

Pressure-volume relationship in emphysema

A

Increased lung compliance due to tissue destruction

Steeper slope on Volume vs pressure graph

Person breathes at high lung volume (hyperinflation)

See figure

58
Q

Pressure-volume relationship in fibrosis

A

Increased lung stiffness (low compliance) due to lung fibrosis

Breathe at very low lung volume

Rapid, shallow breathing

59
Q

What would happen if the airways and alveoli were lined with water?

A

Water has highly polarized molecules and high surface tension

High surface tension = decreased compliance

Alveoli could collapse

60
Q

What reduces surface tension in the alveoli?

A

Surfactant from alveolar type II cells

Ensures elastic recoil and alveolar stability

61
Q

Composition of surfactant secreted by alveolar type II cells

A

Surfactant complex: phospholipids and proteins

Surfactant proteins: SP-A, B, C, D

Main phospholipid: dipalmitoyl-phosphatidylcholine

62
Q

LaPlace law and elastic recoil

A

P = (2 x surface tension) / radius

Smaller radius = greater pressure

63
Q

Lung compliance vs volume

A

Inversely proportional

Surface forces in alveoli affect lung compliance

64
Q

Pressure volume loop in saline-filled lungs

A

No surface tension

More compliance

Inflation and deflation curves are similar

See figure

65
Q

Pressure volume loop in lungs with surfactant

A

Need higher pressure to distend due to greater surface tension

Inflation and deflation curves ar different

66
Q

What is hysteresis? In lungs?

A

A property of a system such that an output value is not a strict function of the corresponding input

In an air-filled lung, there is a pronounced difference between the inflation and deflation curves

Surfactant is recruited to alveolus during inflation

Surface tension is lower for exhalation

See figure

67
Q

Change in surfactant during breathing

A

Inflation of lungs recruits surfactant

Changes in density with increase and decrease in lung size

68
Q

How is spirometry performed?

A

Using a spirometer

Measures the volume of air moved during inspiration and expiration maneuvers in time (mL air/min = flow)

69
Q

What is tidal volume?

A

TV or Vt

Air inhaled and exhaled with each resting breath

~500 ml in adult

70
Q

What diseases are associated with a surfactant deficiency?

A

RDS and ARDS

Respiratory distress syndrome

71
Q

What is residual volume?

A

RV

Gas remaining in the lungs at the end of maximal exhalation

72
Q

What is inspiratory reserve volume?

A

IRV

Volume (above TV) that can be inhaled by maximum effort

73
Q

What is Expiratory reserve volume?

A

Volume (below TV) that can be exhaled by maximum effort

74
Q

What is Functional residual capacity?

A

FRC

Gas in lungs at the end of a resting tidal breath

75
Q

What is (forced) vital capacity?

A

VC or FVC

total amount of gas that can be exhaled after a maximal inhalation

76
Q

What is total lung capacity?

A

TLC = VC + RV

77
Q

What is inspiratory capacity?

A

IC = IRV + Vt

78
Q

What is used to assess presence of lung disease?

A

Forced vital capacity maneuver

Forced inhalation from FRC to TLC (~1 sec), followed by forceful exhalation from TLC to RV (~5 sec)

79
Q

Two types of lung diseases

A

Obstructive: asthma, emphysema (lungs lose elastic quality), chronic bronchitis (irritation causes increased mucous)

Restrictive: idiopathic pulmonary fibrosis, ILD

80
Q

What can be determined with FVC maneuver

A

FVC: forced vital capacity (maximum amount of air forcibly expired after maximal expiration)

FEV1: volume of gas exhaled during first second

See figure

81
Q

What is a heathy FEV1/FVC? Obstructive? Restrictive?

A

Healthy = 80%

Obstructive = <70%

Restrictive = > 80%

See figure

82
Q

What occurs in obstructive lung disease - resistance, lung volumes, air movement

A

Airway resistance is increased

FEV1 is decreased, FVC is the same

Less easy to blow air out, air gets stuck inside lungs

83
Q

What occurs in restrictive lung disease - compliance, air taken in, lung volumes

A

Lung compliance is reduced

Lung cannot take in as much air

FVC decreases

84
Q

FVC maneuver in airway obstruction

A

FEV1/FVC < 70%

FEV1 decreased

Airway resistance increased

Scooping in flow-volume curve

Can’t move as much air

See figure

85
Q

What occurs in severe obstructive disease - lung volumes

A

i.e. COPD

Hyperinflation of lungs

FVC reduced

Need FEV1 and FVC to rule out restrictive disorders (airway function)

86
Q

What forces does lung inflation need to overcome?

A

1) elastic recoil (including surface forces in alveolae)
2) inertia of respiratory system (negligible)
3) Resistance to airflow

Flow = delta P/resistance

87
Q

Where is the highest resistance in the respiratory system?

A

2nd and 5th generation airways

Small cross sectional area and turbulent flow

88
Q

What happens to airflow as you approach terminal bronchioles

A

Laminar airflow due to increased cross sectional area

Calibre of these airways can determine airflow resistance

89
Q

What are characteristics of asthma

A

obstructive airway disease

Paroxysmal or persistant symptoms (dyspnea, chest tightness, wheeze and cough)

Variable airflow limitation

Airway hyper responsiveness to allergic and non-allergic stimuli

90
Q

Pathophysiology of asthma

A

Chronic airway eosinophil and neutrophil inflammation

Associated with reversible airflow limitation caused by airway constriction, edema, mucous secretion

91
Q

What can happen if asthma is not treated properly?

A

Can be progressive

Develop airway remodelling, which is linked with fixed airway obstruction (permanent mucous plug, thick smooth muscle)

See figure

92
Q

What are common stimuli used in broncho-provocation challenge test

A

Chemical (histamine, methacholine, B-agonists)

Physical (exercise, cold air)

Sensitizers (allergen)

Non-sensitizers (ASA)

93
Q

Bronchoprovocation test - normal vs mild asthma vs moderate asthma

A

Normal: eventually, a dose of constrictor will cause muscle to constrict and a plateau is reached

Mild asthma: less constrictor required to drop FEV1. Plateau is higher

Moderate asthma: More sensitive to constrictor. Cannot et to plateau because airways would close completely

See figure

94
Q

What is PC20?

A

Provocative concentration that drops FEV1 by 20%

See figure

95
Q

PC20 and asthma

A

asthmatics have a PC20 below 8 mg/mL methacholine

See figure

96
Q

How to test for airway hyper responsiveness?

A

Broncho-provocation challenge test

97
Q

How to measure airway function?

A

Response to bronchodilators

98
Q

How to use response to bronchodilators in measurement of airway function

A

1) perform spirometry without bronchodilator
2) inhaled nebulizer or bronchodilator (ex: salbutamol )
3) wait 15+ minutes
4) repeat spirometry

If FEV1 increases greater than 12%, this is a positive result and reversibility is significant

This can be used to guide treatment

See figure

99
Q

What is COPD?

A

Chronic Obstructive Pulmonary Disease

Inflammatory lung disease (neutrophilic) that affects airways (bronchitis) and lung parenchyma (emphysema)

100
Q

What changes occur in the airways and lungs of people with COPD?

A

Airway wall remodelling, pruning of terminal respiratory bronchioles and lung parenchyma destruction (portion of lung involved in gas exchange)

Increased lung compliance = irreversible airway obstruction !!

101
Q

Incidence of COPD

A

~ 5%

4th leading cause of death world wide in next decade

102
Q

Principal cause of COPD

A

Cigarette smoking (90% of cases)

Chronic dust (silica and cotton) or chemical fume exposure are risk factors

103
Q

Airway- lung interdependence

A

Elastic recoil of the lung (alveolar tissue) gives radial traction (parenchyma makes scaffold around alveoli) to tether open airways at larger lung volumes

Airways can collapse during forced expiration

104
Q

What happens to radial contraction in emphysema?

A

Radial traction is lost

Patients breathe at higher lung volume to overcome the obstruction due to loss of radial traction on the airways

105
Q

Lung volume and dynamic airflow resistance (AWR)

A

Increased lung volume: decreased AWR and increased conductance

Decreased lung volume: increased AWR and decreased conductance

106
Q

What does radial traction do to airway calibre?

A

Inspiration: increases calibre

Expiration: decreases calibre

107
Q

What keeps airways open in quiet breathing?

A

Pleural pressure

Usually negative

108
Q

What happens to pleural pressure during forced expiration?

A

Becomes positive

109
Q

What is EPP?

A

Equal pressure point

Airway collapse

Pressure inside airway = pleural pressure (peribronchial)

110
Q

EPP and emphysema

A

EPP is more easily reached in emphysema

Air becomes trapped

111
Q

FVC maneuver in restrictive lung disease

A

ex: idiopathic pulmonary fibrosis (IPF)

FEV1/FVC >80%

FVC is decreased (reduced lung volume due to high stiffness/low compliance)

FEV1 not changed

See figure

112
Q

What is restrictive lung disease?

A

Diffuse parenchymal lung disease

Infiltration of inflammatory cells with scarring of lung parenchyma and widespread lung fibrosis

Decrease in lung compliance

Broad spectrum of physiology depending on etiology

113
Q

Idiopathic pulmonary fibrosis - type of disease, prevalence

A

Restrictive lung disease

Uncommon, unknown etiology

Presents in 5th-7th decade

114
Q

Idiopathic pulmonary fibrosis - onset and symptpms

A

Insidious (gradual) onset: progressive dyspnea; persistent dry hacking cough

Chronic alveolar inflammation causes diffuse, progressive lung fibrosis

Altered ventilation, increased work of breathing

Obliterative vascular injury that impairs pulmonary perfusion and gas exchange

See figure

115
Q

What does flow-volume loop reveal

A

Interplay of lung function determinants

116
Q

Expiration curve in flow-volume loop

A

Rapid rise to peak flow in early forced expiration, then descends slowly for remainder of expiration (descending portion is effort independent due to lung elastic recoil and airway resistance)

See figure

117
Q

What can the shape of the flow-volume loop indicate?

A

Can indicate intrathoracic vs extra thoracic airway obstruction

Inspiratory limb truncation indicates extra thoracic obstruction

118
Q

Flow volume loop: normal

A

Maximal inspiratory airflow (MIF) at 50% of FVC is greater than maximal expiratory airflow (MEF) at 50% due to dynamic compression of airways

See figure

119
Q

Flow volume loop: obstructive

A

Emphysema, asthma

Airflow diminished

Expiratory prolongation with scooping: MEF < MIF

Peak expiratory flow is low, indicates degree of airway obstruction

120
Q

Flow volume loop: restrictive

A

Interstitial lung disease

Loop narrowed because of diminished lung volumes (TLC)

Airflow is greater than normal at comparable lung volumes because the increased stiffness of lungs holds airways open

121
Q

Flow volume loop: tracheal stenosis

A

Top and bottom of loops are flattened

Fixed obstruction limits flow equally during inspiration and expiration

MEF = MIF

Physiology (19 decks)

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