Session 1- Clinical Application in Ventilation and Lung Mechanics Flashcards

1
Q

Atelactasis

A

Complete or partial lung collapse

Impaired pulmonary surfactant production

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2
Q

Interstitial lung disease

A

Lung expansion difficult secondary to stiff lungs from increased collagen in alveolar walls – decreased compliance/increased elastic recoil

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3
Q

hypoventilation

A

Inability to expand chest and ventilate

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4
Q

Pneumothorax

A

Air in the intrapleural space with loss of pleural seal

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5
Q

Obstructive lung disease- COPD and asthma

A

Increase in airways resistance and, in emphysema decreased elastance/elastic recoil secondary to loss elastic fibres – compliance increased but elastic recoil decreased

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6
Q

Respiratory distress syndrome new born

A

Decrease in surfactant leads to increased surface tension and decreased compliance

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7
Q

What is COPD

A

Clinical syndrome characterised by chronic respiratory symptoms with associated pulmonary abnormalities- all conditions share impaired airflow that is not fully reversible

  • chronic bronchitis
  • emphysema
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8
Q

Chronic bronchitis

A

A disease of the small airways- inflammation in the smaller bronchi and bronchioles- airways chronically inflamed

– Increased air flow resistance– worse on expiration
– Alteration of airway surface tension(increased) predisposing to small airway
collapse - worse on expiration

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9
Q

Pathology of chronic bronchitis

A
  • Mucous hypersecretion
  • Reduced cilia and impaired function – mucous is not cleared effectively - narrows airways
  • Epithelial remodelling - also narrows airways
  • Loss of small airways
  • Increased airway surface tension - fewer clara cells (less surfactant-like material in airways)
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10
Q

What is COPD emphysema

A

Abnormal permanent enlargement of the air spaces distal to the terminal bronchiole with destruction of alveolar walls

Inflammatory cells accumulate
-release elastases and oxidants which destroy alveolar walls

Reduced elastic recoil

  • harder to exhale
  • small airways collapse
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11
Q

Difference between structure of bronchus and bronchiole

A

Bronchus has small islands of cartilage and glands in submucosa

Bronchiole has no cartilage or glands

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12
Q

How do bronchioles stay open

A

Radial traction

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13
Q

What is radial traction

A

Outward tugging action Prevents collapse of bronchioles during expiration

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14
Q

What is Barrel chest

A

Increased air flattens diaphragm- cant contract as effectively- impaired inspiration

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15
Q

Airway obstruction in COPD

A

Small airways narrowed through thickened bronchioles periphery wall causes by inflammation and field narrowing asa result of fibrosis

Luminal occlusion by mucus and inflammatory exudate

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16
Q

Compression alectasis aetiology

A

Pressure on alveoli

  • air in pleural cavity
  • Fluid in pleural cavity
  • abdominal obesity
  • GI surgery post-opp distension pushing up and compressing alveoli
17
Q

Resorption collapse

A

is a form of lung collapse that is due to obstruction of the airways supplying a lung segment or lobe
Alveoli collapse

18
Q

What is contained within the interstitium between the alveolus and capillary

A

Elastin fibres

Collagen

Fibroblasts

Matrix substance

BASEMENT MEMBRANE

19
Q

What is the state of the pulmonary interstitium in pulmonary fibrosis

A

Thickened which increases diffusion distance for 02 and c02

Impairs gas exchanges

20
Q

Interstitial lung disease lung mechanics

A

Lung compliance is reduced- lungs re stiff and harder to expand

Elastic recoil of the lungs is increased - he resting lung volume is smaller than normal

Restrictive type of ventilators defect

21
Q

Interstitial lung disease symptoms

A

– Dry cough
– Dyspnoea on exertion progressing
to at rest
– Fatigue

22
Q

Signs of interstitial lung disease

A
  • decreased lung excursion on palpation
  • bi-basal end inspiratory lung crackles

-Finger clubbing - Small pleural effusions

23
Q

In diffuse pulmonary fibrosis will functional residual capacity be reduced or increased

A

Decreased

24
Q

Functional residual capacity

A

Volume of air in the lungs at the end of quiet expiration

25
Q

What produces surfactant

A

Type 2 pneumocytes

26
Q

When is the amount of surfactant surffienct

A

35-36 weeks

27
Q

Neonatal respiratory distress syndrome

A

Lac of surfactant in pre term babies

Lung expansion is incomplete
Some alveoli remain collapsed
Lung is stiff
Increased effort is required to breathe

28
Q

Neonatal respiratory distress syndrome signs

A
Ø Grunting,
Ø Nasal flaring,
Ø Intercostal and subcostal retractions
Ø Rapid respiratory rate (tachypnoea)
Ø Cyanosis
29
Q

In COPD emphysema will FRC at the end of quiet expiration be reduced or increased

A

Increased

Increased compliance due to low of elastic tissue which means decreased elastic recoil

30
Q

Problem with airflow in emphysematous dominant COPD

A
  • loss of elastic tissue
  • increased compliance and reduced elastic recoil
  • hyper inflated
  • small airways collapse in expiration
  • air trapping
  • increased FRC
31
Q

Problem with airflow in pulmonary fibrosis

A
  • increase of fibrous tissue
  • less compliant
  • smaller lungs
  • decreased FRC
  • no airway obstruction
32
Q

What would h happen if the pleural seal was broken

A

Collapse

33
Q

What happen s in pneumothorax

A
• Chest wall or the lung is
breached - tear in parietal or
visceral pleura
• 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
• The pleural seal is lost
• Lung elastic recoil not
counter-balanced by negative
pleural pressure/chest wall • Lung collapses to unstretched
size
`
34
Q

What is hypoventilation

A

Failure to breathe rapidly enough or deeply enough