Lung Mechanisms And Ventilation Of The Lungs session2 Flashcards

1
Q

Tidal volume

A

The volume of air being inhaled or exhaled at rest

Anatomical dead space + alveolar ventilation

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2
Q

How is air drawn in in quiet inspiration?

A

ACtIVE expansion of the thoracic cavity which in turn expands the lungs (pleural seal)

Ribs are drawn up laterally and superiorly by external ICM contracting

Diaphragm contracts (80% of volume increase)

Air is drawn in from high atmospheric to low intra-thoracic pressure

Muscles/ diaphragm contractions overcome the inward pull of the lung recoil

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3
Q

How is air expelled in quiet expiration?

A

PASSIVELY muscles of inspiration relax -> reduces volume of thoracic cavity & lungs

Air leaves from higher intra-thoracic pressure to lower atmospheric

Chest wall and diaphragm no longer overcome the inward pull of lung recoil

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4
Q

What keeps the lungs against the chest wall on inspiration and expiration

A

Lungs have elastic recoil so a tendency to want to collapse in

but pleural fluid between visceral and parietal pleura in intrapleural space forms a seal between the lung and thoracic wall (surface tension between the pleural surfaces)

so lungs expand with the thoracic cavity

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5
Q

When does the state of equilibrium occur and what is involved?

A

the resting expiration level- between quiet inspiration and quiet expiration

Lungs pull in and up (lung elasticity)

Chest wall pulls out (elastic recoil)

Diaphragm pulls down (passive stretch)

Forces are equal and opposite - tendency to want to return to this resting state

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6
Q

Definition of elasticity , what creates lung elasticity?

A

The ability of an object/ material to resume its normal shape after being stretched or compressed

In lungs: Primarily determined by elastin in the elastic fibres in Ct of lungs and surface tension of alveoli

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7
Q

Definition of compliance. What creates lung compliance?

A

Compliance - the ease with which an elastic structure can be stretched - distensibility

Lung compliance: also related to lung elastic fibres and alveoli surface tension

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8
Q

3 factors involved in ventilation

A

Lung elasticity

Lung compliance

Airways resistance (airway diameter and surface tension determine)

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9
Q

How do compliance and elastic recoil relate to one another?

A

Elastance= measure of elastic recoil

Compliance is inversely proportional to elastance e.g. compliance directly proportional to 1/elastance

Tissues with a high compliance have less elastic recoil

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10
Q

What is functional residual capacity? What does it depend on?

A

The volume of air in the lungs at the end of a quiet expiration

Depends on balance between lung elastic recoil inwards and chest wall elastic recoil outwards ( compliance )

So if lung elastic recoil is high (fibrosis) lower lung volume at rest

If lung elastic recoil is low (emphysema) greater lung volume at rest (hyper inflated)

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11
Q

What’s the main differences between a small bronchus and a bronchiole?

A

Small bronchus: small islands of cartilage and glands in submucosa

Bronchiole: no cartilage or glands, surrounding alveoli keep lumen open
Diameter 1mm or less

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12
Q

How do bronchioles stay open in expiration?

A

No cartilage

Radial traction (outward tugging force) from surrounding alveolar walls

Prevents collapse of bronchioles during expiration

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13
Q

What is surfactant, what is it made from and what is it’s function?

A

Lines alveoli

Mix of phospholipids and lipoproteins

Diminishes the surface tension of the water film that lines alveoli

Thereby decreasing the tendency of alveoli to collapse and the work required to inflate them

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14
Q

What is hypoventilation and what are some Causes?

A

Inability to expand chest

Sleep apnoea
Duchenne muscular dystrophy 
COPD
Opiates
Head injury 
Myasthenia gravis 
Pneumothorax
Respiratory distress
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15
Q

What is a pneumothorax? How do you treat it?

A

Air in the pleural space with a loss of pleural seal -> lung collapses

Chest injury
Lung disease

✅ drain air from pleural space, chest drain inserted, using an underwater seal (prevents fluid or air end Teri get pleural cavity)

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16
Q

What is interstitial lung disease? What are some causes? What are some clinical symptoms and signs?

A

Increased collagen in alveolar walls, lungs stiff makes lung expansion difficult -> reduced lung compliance, elastic recoil of lungs is increased
Increased diffusion distance

200 different types

Thickening of pulmonary interstitium (microscopic space between alveolar epithelium and capillary endothelium made from elastin fibres, collagen fibres, fibroblasts, matrix substance)-> common final pathway is lung fibrosis (sometimes irreversible)

Can follow specific exposure e.g. asbestos, drugs (methotrexate), radiation, mouldy hay or autoimmune (sarcoidosis) or idiopathic 20% (Cryptogenic alveolitis)

Clinical symptoms: dry cough, dyspnoea, fatigue, gradual progression

Signs: decreased lung excursion, bi-basal end inspiratory lung crepitations, finger clubbing, pleural effusions

17
Q

What is respiratory distress in the newborn? Symptoms? Treatments? At what age will this no longer be a problem?

A

Often in premature babies when they can’t produce sufficient surfactant so increased surface tension of alveoli making lung expansion difficult, some alveoli remain collapsed

Symptoms: grunting, nasal flaring, intercostal and subcostal retractions, rapid respiratory rate (tachyonea), cyanosis

Surfactant made 24-28 weeks, sufficient amounts by 25-36 weeks

✅steroids encourage production or put on surfactant ventilator

18
Q

When might quiet expiration be difficult? Why are problems with airflow typically worse in expiration compared with inspiration?

A

When airways resistance is high and elastic recoil is low e.g asthma, COPD (chronic bronchitis and emphysema) also have decreased elastic recoil of lungs

Intra pulmonary pressure is positive in expiration so exacerbates narrowing of intra thoracic airways

19
Q

What is COPD? What’s the new term for someone likely to get COPD and what are the criteria?

A

Third leading cause of death
Smoking/ inhaled pollutants interact with genetic vulnerability

Chronic respiratory symptoms with associated pulmonary abnormalities - impaired airflow not fully reversible (chronic bronchitis and emphysema)

‘PRE-COPD’ no clinical symptoms but airflow impaired and normal spirometry, high risk developing in next 5yrs

20
Q

What is chronic bronchitis? Possible causes? Diagnosis criteria

A

Bronchi-> bronchioles

Inflammatory cells/ oxidative stress/ infection -> Mucus hypersecretion, reduced cilia -> blocked lumen airways, epithelial remodelling, increased surface tension predisposing to collapse

Diagnosis: cough productive sputum >3months for > one year

21
Q

What is emphysema? What is the disease pathology? What can develop in the anatomical chest with chronic emphysema?

A

Permanently enlarged air sacs distal to terminal bronchioles with destruction of alveolar walls

Inflammatory cells accumulate -> elastases + oxidants -> destroy alveolar walls and elastin (protease mediated)

Reduced elasticity (airway trapping) and reduced surface area for gas exchange

Bc the lungs are chronically overinflated the rib cage stays partially expanded all the time -> barrel chest (ratio of anteroposterior to transverse/ lateral diameter is 1:2 normally, becomes 1:1 as AP enlarges and diaphragm crosses 8th rib bc flattened rather than 5th)

22
Q

what is atelectasis? Several causes and the main complication.

A

Lung collapse

Inadequate expansion of air spaces

  • Neonatal- respiratory distress due to lack of surfactant
  • compression collapse due to pneumothorax or pleural effusion
  • compression from abdominal distension (compresses alveoli)
  • resorption collapse due to obstruction (airway obstructed, air downstream of blockage slowly absorbed into blood stream & not replaced, alveoli collapse)

Can lead to pneumonia if not restored
Clinical sign: Crackles at base of lung

23
Q

What is cough reflex? Where is it mediated? What occurs in order to cough?

A

Co-ordinated by cough centre in medulla oblongata
Initiated by irritation of me and and/or chemoreceptors in the respiratory epithelium

  1. deep inspiration
  2. Glottis closed by vocal cord adduction
  3. Strong contraction of expiration muscles (abdo, internal intercostal) builds up intrapulmonary pressure
  4. Sudden opening of glottis -> explosive discharge of air
24
Q

What is anatomical dead space?

A

The volume of air in the conducting airways

25
Q

What is alveolar dead space?

A

Air in alveoli which do not take part in gas exchange

26
Q

What is physiological dead space

A

Anatomical dead space + alveolar dead space

27
Q

How to calculate total pulmonary ventilation and alveolar ventilation

A

trv: Tidal volume X respiratory rate

Alveolar ventilation: (tidal volume - dead space) X respiratory rate

28
Q

What is inspiratory reserve volume?

A

The extra volume of air that can be inspired after a normal inspiration (tidal volume)

29
Q

What is expiratory reserve volume?

A

The extra volume of air that can be expired after a normal expiration (tidal volume)

30
Q

What are the accessory muscles of inspiration required for forced inspiration?

A

PSSS

Pectoralis major
Serratus anterior
Scalene muscles
Sternocleidomastoid

31
Q

Which accessory muscles of expiration are required for forced expiration? Is this a passive or active process?

A

Internal intercostal

Abdominal wall muscles

No longer passive

32
Q

When are accessory muscles used?

A

Exercise and when diseases affect the lungs

33
Q

How does surfactant prevent small alveoli collapsing into bigger ones?

A

Smaller alveoli would normally have higher pressure so more likely to collapse and harder to inflate BUT

Bc surfactant is more effective when its molecules are closer together e.g. smaller alveoli has more of an effect

Reduces surface tensions more in smaller alveoli -> reduces pressure so both small and big equal

34
Q

As air moved through airways to alveoli it needs to overcome resistance to flow. Small diameter tubes have higher resistance to flow, how is this overcome in the body? Where is resistance to flow highest?

A

Individual resistance of tubes is high but there is

Parallel arrangement of small airways which compensates

So combined resistance is low

Highest resistance is in upper respiratory tree (trachea and large bronchi) and lowest in smaller airways

35
Q

What takes the most effort in respiration?

A

Overcoming elastic recoil of lungs