Mechanics of Breathing Flashcards

1
Q

Q: What is atmospheric pressure?

A

A: Atmospheric pressure is the pressure exerted by the weight of the air in the atmosphere of Earth. At sea level, it is typically measured as 760 mmHg. This pressure acts as the baseline or reference point for the other pressures involved in respiration.

the air around us (carbon + nitrogen)

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2
Q

Q: What is intra-alveolar pressure?

A

in alveoli

Intra-alveolar pressure, also known as intrapulmonary pressure, is the pressure within the alveoli of the lungs. This pressure changes during the breathing cycle:
(70 mm Hg, also more than intrapleural pressure)

During inspiration, intra-alveolar pressure decreases below atmospheric pressure, allowing air to flow into the lungs.
During expiration, intra-alveolar pressure increases above atmospheric pressure, causing air to flow out of the lungs.

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3
Q

Q: What is intrapleural pressure?

A

A: Intrapleural pressure is the pressure within the pleural cavity, the thin fluid-filled space between the two layers of the pleura (the membrane lining the lungs and chest cavity). This pressure is always slightly less than the intra-alveolar pressure and atmospheric pressure:
(if intraalveolar is 760 mm Hg, intrapleural is 756 mm Hg)
if it was higher, it will exert pressure on lungs and cause lungs to collapse

During inspiration, intrapleural pressure becomes more negative, helping to expand the lungs.
During expiration, intrapleural pressure becomes less negative but remains negative, maintaining lung expansion and preventing lung collapse.

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4
Q

Q: What is the main mechanism by which air flows in and out of the lungs?

A

A: Air tends to move from an area of high pressure to lower pressure, driven by alternating reversing pressure gradients between the alveoli and the atmosphere created by breathing.

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5
Q

Q: What are the three important pressures involved in breathing?

A

A:

Atmospheric pressure
Intra-alveolar pressure
Intrapleural pressure

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6
Q

Q: How do the lungs stay in close opposition to the thoracic cavity, which is larger than the lungs?

A

A: The lungs are held in close opposition to the thoracic cavity by a transmural pressure gradient.

lungs attached to thoracid wall due to attraction og H2O water molecules within pleural cavity
==> H-H bond attaches outer membrane of pleural cavity to our ribcay

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7
Q

Q: What is the transmural pressure gradient?

A

transmural gradient. = intra alveolar pressure - intrapleural pressure (e.g. 760 mmHg - 756 mmHg = 4 mmHg)
A: The transmural pressure gradient is the difference between the intra-alveolar pressure (pressure within the alveoli) and the intrapleural pressure (pressure within the pleural cavity). The gradient is always positive because the intra-alveolar pressure is higher than the intrapleural pressure. This positive gradient keeps the lungs inflated and adheres to the inner wall of the thoracic cavity

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8
Q

Q: What happens during muscle contraction in inspiration?

A

A:
inhalation
–> contraction of external intercostal muscle
–> relaxation of internal intercostal muscle
–> pulls sternum upwards + outwards
–> more space so diaphragm flattens, moves downwards

= increasing the volume of the thorax, which decreases intra-alveolar pressure, allowing air to flow into the lungs (high to low

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9
Q

Q: Describe the process of inspiration.

A

A: During inspiration, the intra-alveolar pressure must be less than atmospheric pressure.
high to low pressure, from the air to when it enters the lungs.
This is achieved by increasing the volume within the lungs, following Boyle’s law
volume increase, pressure decrease

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10
Q

Q: How does muscle contraction during expiration affect pressures?
.

A

A: During expiration, the external intercostal muscles relax, relaxation of the diaphragm, contraction of internal intercostal muscles, ==> this flattens the ribs and sternum
decreasing the thoracic volume

increasing intra-alveolar pressure, which pushes air out of the lungs

the contraction of abdominal muscles causes diaphragm to be pushed upward, further reducing the thoracic cavity

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11
Q

pressure changes during inspiration/ expiration

A

a) before inspiration :
- 760 mm Hg in air
- 760 mm Hg in intra alveolar pressure
- 756 mm Hg intrapleural pressure

b) during inspiration
- 760 mm Hg in air
- 759 mm Hg in intra alveolar pressure
- 754 mm Hg intrapleural pressure

entire thoracic cavity expands,due to contraction of inspiratory muscles and lungs stretched to fill the expanded thorax
=volume increase, pressure decreases

c) during expiration
- 760 mm Hg in air
- 761 mm Hg in intra alveolar pressure
- 756 mm Hg intrapleural pressure

entire thoracic cavity shrinks, due to relaxation of inspiratory muscles and lungs recoil

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12
Q

Q: What role does the autonomic nervous system play in airway resistance?

A

A: The autonomic nervous system regulates airway resistance, with parasympathetic innervation causing bronchoconstriction and sympathetic innervation causing bronchodilation.

sympathetic : fight/flight; need O2 to run away

narrow diameter= increase resistance vice versa (vv)

normal bronchiole : no cartilage, only smooth muscles
asthma bronchiole : more mucus, small diameter, less airflow

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13
Q

Q: What are the three key factors that contribute to the physiological properties of the lungs?

A

A:

Compliance: The ability of the lungs to stretch.
Elastic recoil: The ability of the lungs to return to their original shape/ elastic tissue in lung
Surface tension: The force exerted by water molecules lining the alveoli.

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14
Q

Alveolar surface tension

A

The alveoli are lined by water molecules

  • O2 must dissolve in water before it can move across the respiratory membrane
  • Too much water increases surface tension and increases diffusion distance (thick layer of h2O)
  • Tendency for lungs to collapse
  • Impaired gas exchange
  • cells secrete pulmonary surfactant modulates surface tension :: Counteract this by producing pulmonary surfactant

A: Pulmonary surfactant, produced by type II alveolar cells, reduces surface tension at the air-water interface in the alveoli, preventing lung collapse and aiding in gas exchange.

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15
Q

how does pulmonary surfactant

A
  • Lipoprotein produced by type II alveolar cells
  • Reduces surface tension at air-water interface
  • Immunoprotective actions
  1. H2O will join and form water molecules =. collapse lungs
    pulmonary surfactant :
    - lipoprotein makes it spread out
    thin layer around the entire thing
    thinner layer allows gas exchange to occur
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16
Q

Q: How is pulmonary ventilation (minute ventilation) calculated?

A

minute ventilation (how much air moves into the lungs, every minute)

A: Pulmonary ventilation is calculated by multiplying tidal volume by respiratory rate.
- tidal volume (volume after expiration - volume after inspiration)
- respiratory rate (number of breaths per minute)

500 (tidal) x 12 (respiratory rate ) = 6000 (pulmonary)
1200 (deeper breaths) x 5 (take longer to breath again) = 6000
150 (smaller breaths) x 40 (rapidly) = 6000

in healthy individuals, pulmonary ventilation shouldn’t change much
==> if you have same respiratory rate, but tidal volume is low, you can only breathe so much = an issue with lungs
–> can be used to clinically assess lung health

17
Q

Q: Why is alveolar ventilation more important than pulmonary ventilation?

A

A: Alveolar ventilation is more important because it measures the volume of air exchanged between the atmosphere and the alveoli per minute (how much we’re exchanging),

Less than pulmonary ventilation due to anatomic dead space where no gas exchange occurs.

(tidal volume – dead space volume [usually 150mL in adults]) x respiratory rate

18
Q

what is airway dead space volume (150 mL)

A
  1. air from inspiration that was not used in gas exchange
  2. 500 ml of “used air” is expelled out from lung
  3. 150 mL of the 500 mL used air willl get stuck
  4. 150 mL of the air from before leftover + 350/500mL used air is actively expelled out to atmosphere
  5. 500 mL fresh air enter the atmosphere
  6. 350mL contains high O2 conc, but 150mL is used air
  7. the 150 mL fresh air remain in dead space
19
Q

matching airflow to blood flow when its large blood flow, small airflow

A

exmaple : a lot of deoxygenated blood in the lungs

increase in CO2 in alveoli => relaxation of local-airway smooth muscle, causing the bronchioles to dilate, lowering airway resistance for more airflow == remove CO2 to atmosphere

low O2 in alveoli (O2 works on your blood flow) so contraction of local pulmonary arteriorioles smooth muscle, constriction of local blood vessels and increase vascular resistance to lower blood flow
==> constrict blood vessels so less blood to lungs so we don’t have huge elevation to CO2 levels

20
Q

matching airflow to blood flow when its small blood flow, large airflow

A

exmaple : a lot of oxygenated blood in the lungs

low in CO2 in alveoli => contraction of local-airway smooth muscle, the bronchioles to contract, increasing airway resistance for less airflow ==

high O2 in alveoli (O2 works on your blood flow) so relaxation of local pulmonary arterior smooth muscle, dilation of local blood vessels and lower vascular resistance to more blood flow

21
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A