Ventilation Flashcards

1
Q

What are the primary functions of the respiratory system?

A
  • To obtain O2 from external environment for metabolism in body cells.
  • To eliminate CO2 from cells and remove to the external environment.
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2
Q

What are the 3 phases of respiration?

A
  1. External
    • Ventilation (breathing)
  2. Internal
    • Pulmonary gas exchange
    • Gas transport
    • Systemic gas exchange
  3. Cellular
    • Metabolism
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3
Q

Describe phase 1 of respiration (external).

A
  • Ventilation (breathing)
    • Air is moved into / out of the lungs to facilitate gas exchange between the atmosphere and alveoli (air sacs) in lungs.
      • Rate is regulated according to necessity to remove waste CO2 and metabolic demand for O2.
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4
Q

Describe phase 2 of respiration (internal).

A
  • Pulmonary gas exchange
    • Diffusion of O2 / CO2 between alveoli and blood, via pulmonary capillaries.
  • Gas transport
    • O2 / CO2 transported in blood between lungs and tissues.
      • Facilitated by the circulatory system.
  • Systemic gas exchange
    • Diffusion of O2 / CO2 between blood and tissues via systemic (tissue) capillaries.
      • Facilitated by the circulatory system
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5
Q

Describe phase 3 of respiration (cellular).

A
  • Cellular metabolism
    • Intracellular metabolic processes carried out in mitochondria.
      • O2 and nutrients are converted to ATP, H2O and CO2.
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6
Q

Label all the components of the respiratory system.

A
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7
Q

Describe the structure of the lung.

A
  • 2 lungs, each supplied by one bronchus.
  • Lungs divided into lobes.
  • Lung tissue comprises highly branched airways, alveoli, pulmonary vessels and elastic connective tissue.
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8
Q

Describe the conducting and non-conducting zones of the respiratory tree.

A
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9
Q

Describe the structure of alveoli?

A
  • Sites of gas exchange between air and blood.
  • 150-300 million per lung.
  • 250-300µm diameter.
  • Thin-walled (single cell thickness) - huge surface area.
  • Surrounded by pulmonary capillaries, separated by a very small gap (0.2-0.5µm).
  • Thickness very small, surface area very large (50-100m2) so excellent diffusion.
  • Walls not muscular - inflation / deflation occurs by altering thoracic capacity.
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10
Q

Describe the structure of alveolar membranes.

A

Composed of:

  • Type 1 cells
    • ​​​Simple, flat epithelial cells where gas exchange occurs.
  • Type 2 cells
    • Septal cells
    • Specialised surfactant secreting cells
    • Free surface has microvilli
  • Alveolar dust cells
    • Wandering macrophages removing debris - defence
  • Pores of Kohn
    • Permit collateral airflow between alveoli
    • Number varies - more in well ventilated areas (not well understood)
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11
Q

Describe alveolar gas exchange using Fick’s Law.

A
  • Q (net rate of diffusion is dependent on Fick’s Law.
  • Where:
    • ΔC = concentration gradient
    • A - surface area of membrane
    • ΔX = thickness of membrane
    • D = diffusion coefficient, where D = P/√MW
    • P = permeability of membrane
    • MW = molecular weight of diffusing substance
  • All of these are constant, except concentration gradient.
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12
Q

Describe lung compliance.

A
  • Compliance = ease with which the lungs are stretched.
    • A lung with ‘normal’ compliance can be stretched easily with a small transmural pressure gradient.
    • Poorly compliant lung = ‘stiff lung’ - not very stretchy.
      • Emphysema - destruction of elastic tissue.
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13
Q

What factors do elastic recoil and compliance depend upon?

A
  • Alveolar surface tension created by the thin film of liquid lining each alveolus.
  • Surface tension pulls alveolus inwards because water molecules are involved in H- bonding strongly attracted to each other.
  • Mesh of elastin fibres (connective tissue) also has a role in recoil and compliance.
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14
Q

Describe alveolar surface tension and how it is controlled.

A
  • Surface tension induced by H-bonding and strongly elastic fibres is very strong.
  • Unchecked, these forces would collapse alveoli completely, making inspiration very difficult.
    • Think of a balloon - you stretch it before you blow it up. The work of the alveoli would be too much to start from completely deflated and unstretched every time.
  • Surface tension is decreased by pulmonary surfactant.
    • (Secreted by type 2 alveolar cells)
    • So, decreased work is required to inflate the lungs.
      • Decreased tendency to recoil.
      • Prevents collapse.
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15
Q

Describe LaPlace’s Law.

A

Where

  • P = inward directed collapsing pressure.
  • T = surface tension.
  • r = radius of alveoli.
  • I.e. The smaller the alveolus, the smaller the radius, the greater the tendency to collapse.
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16
Q

What would happen if two alveoli of unequal size were connected by an airway?

A
  • REMEMBER P = {2T / r}
  • Left ‘unchecked’ the smaller one will tend to collapse and the air will be expelled into the larger one.
  • This doesn’t happen in health. Why?
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17
Q

What are the components which overcome collapse forces?

A
  • Surfactant - reduces surface tension more in smaller alveoli.
  • Surrounding alveoli - if one alveolus starts to collapse, the surrounding alveoli, joined by connective tissue, resist the collapse due to their own elasticity.
  • This is interdependence.
18
Q

Describe the role of surfactant in the new-born.

A
  • Prematue babies (under 7 months) are not able to produce surfactant so cannot overcome alveolar surface tension.
  • Lings tend to collapse after exhalation.
  • Lots of effort is required to inflate the lungs - they are not compliant and baby has underdeveloped muscles.
  • May die due to exhaustion / lack of O2.
  • It is thought that surfactant production has a role in triggering labour.
19
Q

Which three pressures are critical in ventilation?

A
  • Atmospheric pressure - the pressure exerted by the weight of the gas in the atmosphere on objects on the earth surface - 760mmHg at sea level.
  • Intra-alveolar pressure - the pressure within the alveoli - 760mmHg when equilibrated with atmospheric pressure.
  • Intrapleural pressure - the pressure within the pleural sac; the pressure exerted outside the lungs within the thoracic cavity, usually less than atmospheric pressure at 756mmHg.
20
Q

What is the transmural pressure gradient across the lung wall?

A

Transmural pressure gradient across the lung wall = intra-alveolar pressure minus intrapleural pressure.

21
Q

What is the transmural pressure gradient across the thoracic wall?

A

Transmural pressure gradient across the thoracic wall = atmospheric pressure minus intrapleural pressure.

22
Q

What are the major muscles of inspiration?

A
  • Major muscles of inspiration contract every inspiration; relaxation of these muscles causes passive expiration.
  • Diaphragm
  • External intercostals
23
Q

What are the accessory muscles of inspiration?

A
  • Accessory muscles of inspiration contract only during forceful inspiration.
  • Sternocleidomastoid
  • Scalenus
24
Q

What are the muscles of active expiration?

A
  • Muscles of active expiration contract only during forced expiration.
  • Internal intercostals.
  • Abdominal muscles.
25
Q

Describe the action of the muscles of inspiration.

A
  • Contraction of external intercostal muscles causes elevation of the ribs, which increases the lateral dimension of the thoracic cavity.
    • Elevation of the ribs causes the sternum to move upward and outward, which increases anterior-posterior dimension of the thoracic cavity.
  • Lowering of the diaphragm on contraction increases vertical dimension of the thoracic cavity.
26
Q

Describe Boyle’s Law.

A
  • At constant temperature the volume (V) of a given mass of gas is inversely proportional to the pressure (P).
  • The higher the pressure, the smaller the volume.
27
Q

Describe inspiration.

A
  • Inspiration is an active process brought about by contraction of inspiratory muscles.
  • The chest wall and lungs are stretched.
  • The increase in the size of the lungs make the intra-alveolar pressure to fall.
  • This is because air molecules become contained in a larger volume (Boyle’s Law).
  • The air then enters the lungs down its pressure gradient until the intra-alveolar pressure becomes equal to the atmospheric pressure.
28
Q

Describe expiration.

A
  • Normal expiration is a passive process brought about by relaxation of inspiratory muscles.
  • The chest wall and stretched lungs recoil to their preinspiratory size because of their elastic properties.
  • The recoil makes the intra-alveolar pressure rise.
  • This is because air molecules become contained in a smaller volume (Boyle’s Law).
  • Air leaves the lungs down the pressure gradient until intra-alveolar pressure equals atmospheric pressure.
29
Q

Describe the changes in intra-alveolar and intra-pleural pressures during the respiratory cycle.

A
30
Q

What is a pneumothorax?

A

Air in the plural space.

31
Q

What is the effect of a pneumothorax on the transmural pressure gradient?

A

Pneumothorax abolishes the transmural pressure gradient. $

32
Q

Describe a spirogram produced by a ‘normal’ healthy individual and list the expected volumes.

A
  • TV = tidal volume (500ml)
  • IRV = inspiratory reserve volume (3,000ml)
  • IC = inspiratory capacity (3,500ml)
  • ERV = expiratory reserve volume (1,000ml)
  • RV = residual volume (1,200ml)
  • FRC = functional residual capacity (2,200ml)
  • VC = vital capacity (4,500ml)
  • TLC = total lung capacity (5,700ml)
33
Q

Describe the spirogram produced by a patient with obstructive lung disease.

A
  • Normal total lung capacity.
  • High functional residual capacity.
  • High residual volume.
34
Q

Describe the spirogram produced by a patient with restrictive lung disease.

A
  • Low vital capacity.
  • Low total lung capacity.
  • In restricetive lung disease the lungs have a reduced volume.
35
Q

What is dead space?

A
  • There are 2 kinds - anatomical and physiological. In disease states physiological dead space increases greatly. It is a measure of the amount of lung tissue which is not actively involved in gas exchange.
  • Not all inspired gas gets to the site of gas exchange (alveoli). Part remains in the conducting airways (e.g. the trachea) where there is no gas exchange.
  • This is called the anatomical dead space (AKA airway dead space).
    • Average healthy young adult - the volume of the conducting airways is approximately 150ml.
  • For every 500ml we breathe in, only 350ml reaches the site of gas exchange.
  • In ‘normal’ breathing, the breaths we take dilute the old air in the lungs with fresh air.
36
Q

Describe the state of dead space after inspiration, before expiration.

A
37
Q

Describe the state of dead space during expiration.

A
38
Q

Describe the state of dead space during inspiration.

A
39
Q

What is physiological dead space?

A
  • The volume of the lungs which do not eliminate CO2.
  • In healthy individuals the volume of anatomical dead space will be very nearly the same as the physiological dead space.
  • The volume of physiological dead space is likely to be much higher in subjects with lung disease.
40
Q

How do you calculate the pulmonary (minute) ventilation?

A
  • Air breathed in / out in 1 minute.
  • Pulmonary ventilation (PV) = air breathed in / out in 1 minute.
  • PV = Tidal volume (TV) x Respiratory rate (RF)
41
Q

How do you calculate alveolar ventilation (AV)?

A
  • Alveolar ventilation (AV) is the volume of air exchanged between atmosphere and alveoli per minute.
  • AV = (TV - Dead Space (DS)) x RF
42
Q

How is air and blood flow to individual alveoli controlled?

A
  • Both air flow (ventilation) and blood flow (perfusion) can be controlled.
  • Individual airways supplying individual alveoli can be adjusted in response to change in local conditions, allowing efficient exchange of CO2 and O2.
  • For most efficient ventilation; ventilation and perfusion are matched.