Applied Physiology Flashcards

1
Q

Where are the areas of main resistance and highest flows in the respiratory system?

A

-Larynx
-Trachea
-Main bronchi
(23 divisions, 5L)

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2
Q

Compare the larynx/trachea with terminal bronchioles

A

Larynx/trachea:

  • Narrow- low cross section
  • High resistance
  • Fast turbulent flow generating sound= bronchial breathing

Terminal bronchioles

  • Numerous- high combined cross section
  • Low resistance
  • Slow silent flow
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3
Q

How is airflow measured in healthy people?

A
  • In healthy people, maximum expiration limited by resistance of large airways
  • Extensive disease of small airways can also limit flow (smoking?)
  • Measured by testing forced expiration
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4
Q

What are the three big questions in respiratory physiology?

A
  1. How narrow (airflow obstruction)
  2. How big? (lung volume)
  3. How blue? (gas exchange)
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5
Q

Why is expiration more important in measuring airflow obstruction compared to inspiration?

A

-Breathing in= negative pressure sucks in air through positive pressure to alveoli
-Breathing out= compress lungs= allow elastic lung to recoil generating positive pressure in alveoli forcing air out. Tube is embedded so airway is narrowed
=cartilage rings and plates to reinforce airway
=No intrinsic stiffness in terminal and respiratory bronchioles so squashed, does not collapse as elastin fibres in alveolar walls

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6
Q

How does airway obstruction effect emphysema (smokers)?

A
  • Normal lung= alveolar walls attached around bronchiole, elastin fibres pull out radially to prevent collapse
  • Emphysema= destruction of alveolar walls, not supported so narrowed (advanced COPD= tube man when expiration collapses)
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7
Q

Airway obstruction in asthma

A
  • Constricted smooth muscle (inflammation)
  • Epithelium oedematous and swollen (damages lumen)
  • Secretion of excess mucous to narrow airway
  • Diurnal variation in peak flow (morning lower)
  • Reversibility (improvement in values) following bronchodilators
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8
Q

Methods of measuring airflow obstruction

A

-Peak flow meter (3 attempts and highest value, morning and evening) GP
=Cheap, simple and widely available
=Effort and technique dependent

-Spirometry (FEV1 and VC)- volume against time/ flow volume loop
=Healthy= FEV1 75% VC/ COPD 50% or lower
=Less effort dependent, comprehensive normal ranges
=More costly equipment, technique and training important

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9
Q

COPD FEV1 and VC measurements

A
  1. Disproportionate reduction in FEV1 compared to VC
  2. Therefore FEV1/VC ratio reduced
  3. Flow volume loop shows very low maximum flows in mid and late expiration due to small airway collapse
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10
Q

How is lung volume affected by disease (COPD)?

A

-In emphysema, small airways collapse trapping air in expiration.
-Also extensive loss of normal lung elastic recoil.
-Result is
chronic airflow obstruction is accompanied by hyperinflation= HIGH LUNG VOLUME (50-100% higher than normal)

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11
Q

How is lung volume affected by disease (pulmonary fibrosis)?

A

-In pulmonary fibrosis, collagen scarring of the lung parenchyma causes stiffening (restricts expansion) and shrinkage of the lungs, with loss of
lung volume.= LOW LUNG VOLUMES
-Honeycomb of fibrous tissue at base of lungs

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12
Q

Why can’t we measure lung volume by measuring exhaled gas?

A

-Some volume can’t be exhaled (residual volume)

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13
Q

Methods of measuring lung volume

A

-Dilution of an inert marker gas
-Plethysmography
=Both measure the volume at start of the measurement (end of tidal breath) and other lung volumes are then deduced from that

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14
Q

Measurement of lung volume by inert gas (helium) dilution

A

-Inert test gas (low concentration helium) mixes evenly with lung volume and is diluted in the process.
-Degree of dilution at
equilibrium (about 10 mins rebreathing) reveals lung volume at the instant patient was connected to circuit.
=Larger lungs dilute more
=Carbon dioxide absorber, oxygen introduced

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15
Q

Measuring lung volume by plethysmography

A

Patient breathing air from box
- No pressure changes seen
- Air just moves between chest
and box

Mouthpiece closed off
- Attempted inspiration “stretches” the trapped lung gas, causing a fall in mouth pressure and expansion of thorax, compressing gas in box.
- A smaller lung volume causes a steeper fall in mouth pressure for same change in chest volume (Like pulling on a syringe with your thumb over the end)
=Change in volume of chest= change in pressure in box

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16
Q

Plethysmography vs inert gas dilution

A

Plethysmography measures all thoracic gas, helium dilution only measures that gas which mixes rapidly with incoming breath – so
misses air cavities and emphysematous bullae

17
Q

Sub divisions of lung volume terminology

A
  1. Total lung capacity (max volume of air lungs can accommodate)
  2. Functional residual capacity (amount of air remaining in lungs at end of NORMAL exhalation)
  3. Residual volume (volume of air remaining after maximum exhalation)
  4. Inspiratory capacity (maximum volume of air inhaled following resting state)
  5. Vital capacity (total amount of air exhaled after maximal inhalation)
18
Q

Lung volumes in obstructive lung disease (COPD)

A
  • More air in chest
  • Inspiratory capacity reduced
  • Vital capacity reduced
  • Exhalation takes longer and more trapped gas (high residual volume)
19
Q

Lung volumes in restrictive lung disease (fibrosis)

A

-Lung volumes proportionally reduced from normal

20
Q

Describe the gas transfer test

A

Use a tracer gas which is avidly taken up in blood: CO – very low concentration (0.01%)
– Breathe in test gas with known CO content
– Wait 10s
– Breathe out and sample late expirate (from alveoli) – how much CO has gone?
– Because uptake is lung size dependent, correct for lung volume by including non-absorbed He in test breath
• Result called “Gas transfer” (Tco)
• When corrected per unit lung volume – called Kco

21
Q

When is gas transfer reduced?

A

-Emphysema, anaemia (haemoglobin) and severe fibrosis

22
Q

When is gas transfer increased?

A

-Pulmonary haemorrhage, exercise

23
Q

Adaptions for gas transfer

A

-Gravity directs both blood flow and inspired air mainly to the bases
-Lobar hypoxia constricts pulmonary arterioles, reducing blood supply to that lobe
-CO2 in airways dilates that airway, so if lobar blood supply fails, airway to that lobe constricts
=ventilation/ perfusion matching

24
Q

How can ventilation/perfusion ratios be disrupted?

A

-Interstitial or airway disease can result in under ventilated or under perfused areas
=Airway narrowing (tumour)
=Embolism (reduced perfusion preserved ventilation)

25
Q

Describe gas transfer in lobar pneumonia

A

-Hypoxic pulmonary veins= constriction to reduce perfusion to lobe
=low pO2
=normal CO2 and H level

26
Q

How is C02 carried in blood?

A
  • CO2 + H2O ↔ HCO3 + H*+ (carbonic anhydrase)
  • Carried mainly as plasma bicarbonate
  • High capacity for transport
  • ↑ ventilation in normal areas can shift more CO2
  • Normal lung can work harder
  • Corrects arterial CO2 to normal
27
Q

How is oxygen carried in blood?

A

Insoluble – a problem!
• Evolution: a transport protein - Hb
• Hb is fully saturated by healthy lung
• So normal lung can’t work harder and take up more O2
• Hypoxic blood emerges from pneumonia lobe
• Normal lung can’t compensate →arterial hypoxia

28
Q

What is Type 1 respiratory failure?

A

-Arterial hypoxia with normal pCO2
-Part of the lung is under ventilated (low V/Q) but other lung regions are normal
=Mild/moderate asthma
=pulmonary oedema
=lobar pneumonia
=pneumothorax

29
Q

What is Type 2 respiratory failure?

A

-Means arterial hypoxia and raised CO2:
=Insufficient lung ventilation overall
=Severely disrupted ventilation/perfusion matching
=Without enough normal lung regions to correct CO2

30
Q

Causes of Type 2 respiratory failure

A
  • Extrapulmonary: Any cause of globally impaired alveolar ventilation (sedative drugs, head injury= central drive to breathe, neuropathy, myopathy=DMD)
  • Pulmonary: Severe generalised airflow obstruction or ventilation perfusion mismatch (With insufficient normal lung tissue to correct CO2)