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Semester 3 - respiratory > 3. Disorders of Ventilation and Lung Mechanics > Flashcards

3. Disorders of Ventilation and Lung Mechanics Flashcards

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1
Q

what is the conducting portion of the respiratory tract?

A 
Nasal cavity
Pharynx
Larynx
Trachea
Primary bronchi
Secondary bronchi
Bronchioles
Terminal bronchioles
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2
Q

what is the respiratory portion of the respiratory tract?

A

Respiratory bronchioles
Alveolar ducts
Alveoli

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3
Q

what do lungs need to overcome to expand?

A
  • Elastic properties of alveolar walls

* Surface tension of alveolar fluid

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4
Q

what does expiration need to overcome?

A

– Need to overcome airways resistance

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5
Q

define elastance

A

Elastance is a measure of elastic recoil = the tendency of something that has been distended to return to its original size

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6
Q

defien complliance

A

Ease at which an elastic structure can be stretched

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7
Q

What is the relationship between compliance and elastic recoil (measured in elastance)?

A

Inversely proportional

In tissues with a high compliance (easier to stretch), the elastic recoil is less
In tissues with a low compliance, elastic recoil (tendency to return to original size) is high

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8
Q

define lung elasticity

A

Lung Elasticity represents mechanical properties of the lungs to be expanded (distended) by pressures surrounding or inflating the lungs, and to collapse as soon as pressures disappear

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9
Q

Which factors affect lung compliance? State their relationship to compliance/how they affect compliance

A

Connective tissue surrounding alveoli - inversely prop (bcs the more elastic fibres –> increase in elastic recoil, meaning decrease in compliance).

Alveolar fluid surface tension - inversely prop (bcs increase in surface tension, meaning decrease in compliance).

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10
Q

If there is an increase in surfactant, what effect would this have on compliance? Why?

A

Increase in compliance bcs decrease in surface tension

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11
Q

How does “connective tissue surrounding alveoli tissue” and “alveolar fluid surface tension” affect elastic recoil?

A

•Directly related to connective tissue surrounding
alveoli - elastic fibers including elastin & collagen
and other matrix elements within the lung
parenchyma
•Directly related to alveolar fluid surface tension

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12
Q

what does ventilation depend on?

A

balance between compliance and elastic recoil

airway resistance

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13
Q

what does airway resistance depend on?

A 
– Surface tension within airways
– Diameter airways
• Mucous in airways
• Pulmonary pressure gradients
• Radial Traction
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14
Q

How does the structure of a bronchus compare to the structure of a bronchiole?

A

How does the structure of a bronchus compare to the structure of a bronchiole?

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15
Q

Bronchioles have no cartilage.

How do they stay open in expiration?

A

• Due to Radial traction (outward tugging
action) of the surrounding alveolar walls
on bronchioles
• Prevents collapse of bronchioles during
expiration

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16
Q

Why would bronchioles collapse during expiration?

A

intra pulmonary pressure high pushing on bronchioles

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17
Q

Why is airway obstruction worse in expiration than inspiration?

A

Negative pressure in pleural space during inspiration helps to keep lower airways open whereas in expiration the pressure is positive which exacerbated narrowing of intra-thoracic airways.

Bronchioles don’t have rigid cartilage islands to oppose those (positive) pressures.

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18
Q

What is Atelectasis?

A

Lung collapse - Inadequate expansion of air spaces

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19
Q

Is atelectasis reversible?

A

-Yes, except for CONTRACTION ATELECTASIS

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20
Q

Give 3 causes of atelectasis?

A

Impaired pulmonary surfactant production
Compression (causing collapse)
Obstruction (causing collapse)

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21
Q

Explain how impaired pulmonary surfactant production leads to atelectasis (lung collapse)?

A

Alveoli collapse due to increased surface tension so can’t expand to ventilate lungs. Decreases compliance so lungs can’t expand and so collapse.

alveoli never expand in the first place or only partially expand

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22
Q

Explain how compression can lead to atelectasis (lung collapse)? Give 3 examples of things that can cause this compression?

A

Air in pleural cavity (pneumothorax)
Fluid in pleural cavity (pleural effusion)
Tumour

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23
Q

Explain how obstruction of airways leads to atelectasis (lung collapse). what is the name of this type of atelectasis?

A

Resorption collapse: due to obstruction of a large airway (e.g. Lung cancer, mucous plugs)
– Airway obstructed; air downstream of
blockage slowly absorbed into blood stream
– Alveoli collapse

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24
Q

How does atelectasis cause impaired respiratory function?

A

• Alveoli not ventilated

– So can’t participate in gas exchange –> impaired oxygenation and CO excretion.

• Collapsed alveoli more suggestible to lung infection

including pneumonia

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25
What is interstitial lung disease?
an umbrella term used for a large group of diseases characterized by Thickening of pulmonary interstitium, fibroblast proliferation, collagen deposition, and, if the processremains unchecked, pulmonary fibrosis
26
is the thickening of pulmonary interstitium reversible?
sometimes reversible – sometimes not - depends - scarring due to increased collagen and pulmonary fibrosis
27
what is the common final pathway for interstitial lung disease if not reversible, or if reversible but cause not diagnosed,?
lung fibrosis –Early detection/treatment key to preventing irreversible progression
28
what does the interstitium contain?
* elastin fibres * collagen fibres * Fibroblasts * Matrix substance
29
What is the interstitial space (in the lungs) and when is this space apparent?
Potential space between alveolar cells and the capillary basement membrane. Only apparent in disease states when it may contain fibrous tissue, cells or fluid
30
How does interstitial lung disease/pulmonary fibrosis impair GE?
Affects both movement of air in airway (stiffer) and diffusion of gases : Fewer alveoli and caps bcs replaced by scar tissue. Increased space btwn cap and alveoli . Thickened alveolar capillary membrane means diffusion distance increases.
31
interstitial lung disease can follow?
• Specific exposure - e.g., asbestos, drugs, mouldy hay etc OR • Autoimmune-mediated inflammation OR • Unknown injury (e.g., idiopathic pulmonary fibrosis)
32
Give causes of interstitial lung disease, including - occupational, treatment related (iatrogenic), autoimmune, immunological causes.
``` • Idiopathic - IPF • Occupational - coal miners lung (pneumoconiosis), - farmers lung (mouldy hay), - asbestos • Treatment related - radiation/chemo, methotrexate, nitrofurantoin • Autoimmune - SLE, RA • Immunological - sarcoidosis ```
33
How is compliance affected in interstitial lung disease?
Reduced - lungs are stiff so harder to expand
34
How is elastic recoil of lungs affected in interstitial lung disease? What effect does interstitial lung disease have on the size of the lungs?
Elastic recoil of the lungs is increased - the resting lung volume is smaller than normal – but RATE of airflow not impaired
35
what type of defect will be seen on spirometry for interstitial lung disease
‘Restrictive' type of ventilatory defect on spirometry
36
What effect does interstitial lung disease have vital and inspiratory capacity?
Reduced.
37
Why are the airways not narrowed in interstitial lung disease?
Fibrous tissue exerts an outward 'pull' (known as | radial traction) on the small bronchioles keeping airways open
38
What effect does interstitial lung disease have on diffusion distance?
Increases diffusion distance, effect is greater on oxygen than CO2 which is more soluble
39
What are the symptoms of interstitial lung disease?
– Dry cough – Dyspnoea on exertion progressing to at rest – Fatigue – Typically gradual, insidious progression
40
What are the signs of interstitial lung disease?
* decreased lung excursion on palpation * bi-basal end inspiratory lung crackles * Finger clubbing * Small pleural effusions * tachypnoea (increased respiratory rate), * tachycardia * reduced chest movement (bilaterally),
41
What is Functional residual capacity?
the volume of air in the lungs at the end of a quiet expiration
42
summarise the effect of fibrous lung tissue
``` With fibrous tissue in the lung interstitium • Lungs are stiff and hard to expand • Lung elastic recoil is increased • and the lung volume is smaller • Compared with normal lungs ```
43
in interstitial lung disease explain why lungs are harder to expand but can still be recoiled
• The lungs are stiffer and harder to expand, since collagen fibres are less stretchy than elastin fibres. • Therefore, lung compliance is reduced. • The elastic recoil of the lungs is increased. The term elastic recoil is not limited to the recoil of elastin fibres, but by the tendency of BOTH elastin and collagen fibres to return to their original size when stretched)
44
what is asbestosis
form of interstitial lung disease caused by asbestos exposure
45
WHat is hypersensitivity pneumonitis
Another cause of interstitial lung disease is untreated - an immunologically mediated lung disease caused by repetitive inhalation of antigens; most new cases arise from residential exposures, notably to birds – “bird fancier’s lung.”
46
What is neonatal respiratory distress syndrome?
Caused by deficiency of surfactant in premature babies, particularly those less than 30 weeks old
47
when does the fetus begin producing surfactant?
starts at 24 – 28 weeks gestation; | • increasing amounts by 32 weeks
48
What happens in RDS due to lack of surfactant?
* Insufficient surfactant à high surface tension * This makes the lungs harder to expand at birth; lung expansion at birth is incomplete; * some alveoli remain collapsed (airless); no gas exchange occurs in these alveoli * The lung is stiff - lung compliance is low * Increased effort is required to breathe – respiratory difficulty * Results in impaired ventilation
49
What are the sign of RDS?
``` Ø Grunting, Ø Nasal flaring, Ø Intercostal and subcostal retractions Ø Rapid respiratory rate (tachypnoea) Ø Cyanosis ```
50
What is the treatment for RDS?
Surfactant replacement via an endotracheal | tube, and supportive treatment with oxygen and assisted ventilation
51
Why do intercostal recessions occur in RDS?
Increases surface tension in alveoli make them hard to expand, they also have increased elastic recoil so interpleural pressure becomes more negative, especially during end of inspiration. This causes a pull on the intercostal and subcostal spaces pulling them inwards.
52
compare RDS and diffuse pulmonary fibrosis
Both have stiff lungs Both decreased compliance and increased elastic recoil Different underling mechanisms - First due to insufficient surfactant production whereas second due to increase in elastin fibres and collagen leading to fibrosis of lungs and smaller resting volume.
53
what is COPD
• Clinical syndrome characterised by chronic respiratory symptoms with associated pulmonary abnormalities – all conditions share impaired airflow that is not fully reversible – classic definition encompasses two medical conditions – Chronic bronchitis – Emphysema – Above two conditions actually co-exist
54
What is pre-COPD?
Airflow impaired but no clinical symptoms yet and "normal spirometry" - but at very high risk for developing COPD in the next 5 years.
55
What is chronic bronchitis?
inflammation of the bronchi and bronchioles due to chronic exposure to irritants
56
What happens to level of mucus in chronic bronchitis and what does this cause?
Hypersecretion from goblet cells and submucosal glands, causes narrowing of the airways
57
What happens to cilica in chronic bronchitis?
Reduced, therefore mucus not cleared properly.
58
what does hypersecretion of mucus and reduction of cilia cells in chronic bronchitis result?
– airflow limitation/obstruction by luminal obstruction of small airways – worse on expiration – epithelial remodelling, – alteration of airway surface tension predisposing to collapse
59
What criteria need to be met to diagnosis chronic bronchitis?
cough productive sputum > three months of the | year for > one year
60
What is emphysema?
Loss of elastin and breakdown of alveolar walls causing increased lung compliance, decreased elastic recoil, narrowing of small airways (non-reversible) and loss of alveolar surface area
61
Describe the pathophysiology of emphysema
(Smoking) —-> inflammatory cells accumulate—-> release elastase and oxidants——> destroy alveolar walls and elastin --> decrease elastic recoil (therefore increase compliance).
62
What is the effect of destruction of alveolar walls and reduced elastic recoil in emphysema?
Destruction : 1 big alveolus instead one lots of little ones. Leads to large air spaces and reduced SA for GE. Reduces RADIAL TRACTION so bronchioles collapse during expiration (positive pressures). Reduced recoil : air enters bronchiole but it collapses during expiation so trapped air —> stale air.
63
What causes barrel chest in emphysema?
• At rest the lungs are hyper-inflated, (i.e. more expanded than normal), due to the loss of elastic recoil Air trapping Imbalance of chest wall recoil (same) vs lung recoil (decreased).
64
What effect does emphysema have on the level of the diaphragm?
Diaphragm normally at the level of 5th rib anteriorly, will be below that in emphysema
65
What happens to the diameter of small airways in emphysema?
Narrowed, loss of elastic fibres so reduced radial traction
66
summarise effects on lung elastic recoil and compliance in emphysematous COPD
Lungs have increased compliance and are easier to expand | Lung elastic recoil is decreased and the lung volume is increased compared with normal lungs - stale air not fresh
67
what type of ventilatory defect is seen on Spirometry in emphysema?
onstructive
68
Emphysema vs pulmonary fibrosis
Emphysematous Dominant COPD • Loss of elastic tissue • Increased compliance & reduced elastic recoil • Hyper inflated: Barrel chest • Small airways collapse in expiration (loss of radial traction) • Air trapping (because of obstruction and ↓recoil) • Obstructive pattern on spirometry testing Pulmonary Fibrosis • Increase of fibrous tissue • Less compliant - Stiff - harder to expand • Smaller lungs • Decreased functional residual capacity and other lung volumes • No airway obstruction • Restrictive disease on Spirometry testing
69
What is asthma?
Chronic inflammatory process, causes airway narrowing
70
How is the airways narrowed in asthma?
Due to bronchial smooth muscle contraction, thickening of airway walls by mucosal oedema and excess mucus production which can partially block the lumen
71
What is pneumothorax?
A disorder where air enters the pleural space, with loss of pleural seal and lung collapse * If the chest wall or the lung is breached, * A communication is created between pleural space and atmosphere * Air flows from atmosphere (higher pressure) à into the pleural cavity (lower pressure) * Until the pleural pressure = atmospheric pressure
72
Why does the lung collapse in pneumothorax?
Pleural seal is broken, and the elastic recoil of the lung causes it to collapse towards the hilum, as the negative pleural pressure and outward recoil of the chest wall can no longer counteract it.
73
What are the symptoms of emphysema?
Shortness of breath, reduced exercise tolerance, cough
74
What initiates the cough reflex?
irritation of mechano- and/or chemoreceptors in the respiratory epithelium.
75
Outline coughing reflex
Initiated by irritation of mechano- and/or chemoreceptors in the respiratory epithelium. * Deep inspiration * The glottis is closed by vocal cord adduction * Strong contraction of the expiratory muscles (abdominal muscles, internal intercostal muscles) which builds up intrapulmonary pressure * Sudden opening of the glottis causes an explosive discharge of air.
76
Define a cough
Cough is an explosive expiration of air from the lungs
77
Where is the cough reflex coordinated from in brain?
Cough centre in Medulla oblongata
78
define Anatomical dead space
The volume of air in the conducting airways
79
define Alveolar dead space
air in alveoli which do not take part in gas exchange | These are alveoli which are not perfused or are damaged
80
define Physiological dead space
Anatomical dead space + Alveolar dead space

Semester 3 - respiratory (20 decks)

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