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Respiratory Unit > 2.2 clinical application in ventilation and lung mechanics > Flashcards

2.2 clinical application in ventilation and lung mechanics Flashcards

1
Q

what structures are in the conducting portion of the respiratory system?

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

what is the indentation on the left lung where the heart sits called?

A

the cardiac notch

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3
Q

what structures are in the respiratory portion of the respiratory tract?

A

respiratory bronchioles
alveolar ducts
alveoli

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4
Q

to expand lungs, what forces need to be overcome?

A
  • Elastic properties of alveolar walls

* Surface tension of alveolar fluid

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5
Q

why is intrapleural pressure more negative on inspiration?

A

as there is greater pull of inward forces - greater pull of parenchyma elastic recoil and increased surface tension

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6
Q

what is compliance?

A

Compliance is a measure of distensibility – change in volume relative to change in pressure

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7
Q

what is 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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8
Q

what is the relationship between compliance and elastance?

A

compliance is inversely proportional to elastance

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9
Q

what is lung compliance inversely related to?

A

connective tissues surrounding alveoli - elastic fibres including collagen and matrix elements within the lung parenchyma
alveolar fluid tension

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10
Q

what is airway resistance dependent on?

A

the surface tension within the airways

diameter of airways - mucus in airways, pulmonary pressure gradients, radial traction

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11
Q

compare the structure of a bronchus to a bronchiole

A

small bronchus: small islands of cartilage and glands in the submucosa
bronchiole: no cartilage and no glands

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12
Q

what keeps small bronchi from collapsing?

A

small islands of cartilage in its wall. Keeps the small bronchus semi rigid

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13
Q

what stops bronchioles from collapsing during expiration?

A

no cartilage and thin walled. the only thing that stops bronchioles from collapsing is is radial traction

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14
Q

what is radial traction?

A

the outward tugging action of the surrounding alveolar walls on the bronchioles. Keeps the bronchioles from collapsing on expiration

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15
Q

why is airway obstruction worse in expiration than inspiration?

A

during inspiration the negative pressure in the pleural space is greater and this helps keep the lower airways open.
in expiration the positive intrapulmonary pressure during expiration exacerbates narrowing of the intra thoracic airways

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16
Q

what is atelectasis?

A

lung collapse

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17
Q

what is interstitial lung disease?

A

lung expansion is difficult. Occurs secondary to stiff lungs from increased collagen in alveolar walls - decreased compliance

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18
Q

what is hypoventilation?

A

the inability to expand chest

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19
Q

what is pneumothorax?

A

air in the pleural space with loss of pleural seal

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20
Q

what is obstructive lung disease?

A

COPD and asthma
increased airway resistance and in emphysema decreased elastance secondary to loss of elastin - compliance actually increased.

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21
Q

what is respiratory distress syndrome in the newborn?

A

decreased surfactant leads to increased surface tension and decreased compliance

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22
Q

what are the different things that might cause atelectasis?

A
  • Function collapse - impaired pulmonary surfactant production. increased surface tension leads to collapse of the alveoli
  • compression collapse - due to air in the pleural cavity, fluid in the pleural cavity or a tumour
  • resorption collapse - due to obstruction of the airway causing the air downstream of the blockage slowly absorbed into blood stream. This causes alveolar collapse. May be caused by aspiration, lung cancer or mucous plugs.
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23
Q

how does atelectasis cause impaired respiratory function?

A

Alveoli not ventilated – So can’t participate in gas exchange – impaired oxygenation and CO2 elimination
Also, collapsed alveoli more susceptible to lung infection
including pneumonia

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24
Q

how does interstitial lung disease cause impaired respiratory function?

A
  • thickening of the pulmonary interstitial impairs gas exchange. Alveolar capillary membrane is thickened which increased the diffuse distance.
  • diffuse pulmonary fibrosis leads to decreased lung compliance
25
Q

why is key detection and treatment essential in interstitial lung disease?

A

as interstitial lung disease is sometimes reversible in its early stages. But interstitial Lung disease almost always progresses to lung fibrosis which is irreversible

26
Q

what is contained within the interstitium of the lung?

A

elastin fibres
collagen fibres
fibroblasts
matrix substance

27
Q

what causes interstitial lung disease?

A

can occur following:
occupational - occupation resulting in specific exposure to irritant - e.g., asbestosis, coal workers pneumoconiosis, mouldy hay etc
Connective tissue disease -Autoimmune-mediated inflammation (RA, SLE, Polymyositis, scleroderma, sjogrens)
Idiopathic - idiopathic pulmonary fibrosis
Immunological - sarcoidosis, extrinsic allergic alveolitis
treatment related - radiation, methotrexate, nitrofurantoin, amiodarone, chemotherapy.

28
Q

describe how interstitial lung disease appears on spirometry?

A

restrictive type of ventilatory defect on spirometry the resting lung volume is smaller than normal
rate of airflow is not impaired

29
Q

what are the clinical symptoms of interstitial lung disease?

A

dry cough
dyspnoea on exertion progressing to at rest
fatigue
typically gradual and insidious progression of symptoms

30
Q

what are the signs of interstitial lung disease?

A

decreased lung movement on palpation
Bi-basal end inspiratory lung crackles
finger clubbing
small pleural effusions

31
Q

at what age does the foetus usually have sufficient amounts of surfactant?

A

35-36 weeks

32
Q

when is a baby described as pre term?

A

at below 37 weeks

33
Q

describe the pathophysiology of neonatal respiratory distress syndrome?

A
  • Insufficient surfactant resulting in high surface tension
  • lung expansion at birth is incomplete
  • some alveoli remain collapsed (airless); no gas exchange occurs in these alveoli
  • The lung is stiff
  • Increased effort is required to breathe – respiratory difficulty
34
Q

what babies are most susceptible to experience neonatal respiratory distress syndrome?

A

Severly pre term babies ( below 30 weeks)

35
Q

what are the symptoms of neonatal respiratory distress syndrome?

A 
Grunting,
Nasal flaring,
Intercostal and subcostal retractions
Rapid respiratory rate (tachypnoea)
Cyanosis
36
Q

what is the similarity in the pathophysiology of neonatal respiratory distress syndrome?

A

Both have stiff lungs

Both decreased compliance and increased elastic recoil

37
Q

what is the primary cause of COPD?

A

Primarily caused by smoking and/or inhaled pollutants interacting with genetic vulnerability

38
Q

what are the 2 medical conditions encompassed in COPD?

A

chronic bronchitis

emphysema

39
Q

what is pre- COPD?

A

where airflow impaired but no clinical symptoms yet and “normal spirometry” – but at very high risk for developing COPD in the next 5 years

40
Q

what is chronic bronchitis?

A

An airways disease that occurs from bronchi to
bronchioles
Mucous hypersecretion (from goblet cells & sub mucus glands)
Reduced cilia – mucus is not cleared effectively
Effects of above lead to:
– airflow limitation/obstruction by luminal obstruction of small
airways – worse on expiration
- epithelial remodelling
- alteration of airway surface tension predisposing to collapse

41
Q

how is chronic bronchitis diagnosed?

A

• Clinical diagnosis – cough productive of sputum > three months of the year for > one year

42
Q

what is emphysema?

A

A disease of the air sacs of the lungs.
Abnormal, permanent enlargement of the air spaces distal to the terminal bronchiole
With destruction of alveolar walls ( No fibrosis)
Inflammatory cells accumulate; which release elastases and oxidants which destroy alveolar walls and elastin
Protease mediated destruction of elastin is an
important feature
Reduced elastic recoil is a key problem resulting in airway trapping
Also, reduced large air spaces leads to reduced surface area

43
Q

why is air trapping seen in emphysema?

A

due to the loss of radial traction as there are less surrounding alveolar walls due to destruction to produce the outward tugging action. Therefore the bronchioles collapse, trapping air in the enlarged compliant air spaces distal to the terminal bronchioles.

44
Q

what is the clinical sign of emphysema?

A

barrel chest

- increased anteroposterior diameter of the chest due to increase lung volume and air trapping

45
Q

what diseases cause an obstructive pattern of spirometry testing?

A

asthma (during attack)

emphysematous dominant COPD

46
Q

what disease causes a restrictive pattern on spirometry testing?

A

pulmonary fibrosis

47
Q

what is a pneumothorax?

A

accumulation of air within the pleural cavity/ intrapleural space, which destroys the pleural seal. Causes atelectasis of the lung.

48
Q

describe the pathophysiology of a pneumothorax?

A
  • Chest wall or the lung is breached
  • A communication is created between pleural space and atmosphere
  • Air flows from atmosphere (higher pressure) into the pleural cavity (lower pressure) • Until the pleural pressure = atmospheric pressure
    • The pleural seal is lost
    • Lung elastic recoil not counter-balanced by negative pleural pressure
    • Lung collapses to unstretched size
49
Q

what might cause hypoventilation?

A

brain stem - opioids and head injury
spinal cord - trauma
phrenic and intercostal nerves - Guillian- barre syndrome
neuromuscular junction - myasthenia gravis
muscles of respiration - Duchenne muscular dystrophy
chest wall - severe obesity, hyphoscoliosis, flail segment
pleural cavity - pneumothorax, large pleural effusions
poor lung compliance - lung fibrosis, respiratory distress of the newborn
upper airway obstruction - laryngeal oedema, foreign body
high airway resistance - severe acute asthma, late stages of COPD

50
Q

what is a cough?

A

an explosive expiration of air. from the lungs

51
Q

how is a cough initiated?

A

initiated by irritation of mechano- and/or chemoreceptors in the respiratory epithelium.
Cough reflex is co-ordinated by cough centre in the medulla oblongata

52
Q

what are the normal steps that occur in order to cough?

A
  • 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.
53
Q

what is meant by anatomical dead space?

A

the volume of air within the conducting airways that cannot participate in gas exchange

54
Q

what is the alveolar dead space?

A

air in alveoli which do not take part in gas exchange (These are alveoli which are not perfused or are damaged)

55
Q

what is physiological dead space?

A

Anatomical dead space + Alveolar dead space.

56
Q

what is the calculation for tidal volume?

A

Anatomical Dead space + alveolar ventilation

57
Q

what is the calculation for total pulmonary ventilation (minute volume)?

A

tidal volume x respiratory rate

58
Q

what is the calculation for alveolar ventilation?

A

(tidal volume - anatomical dead space) x respiratory rate

Respiratory Unit (12 decks)

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