Resp. Physiology Flashcards

1
Q

What is Boyle’s Law?

A

P = 1/V
- Increase volume = decrease pressure
- Decrease volume = increase pressure

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2
Q

What 2 opposing forces must be overcome in the work of breathing?

A
  1. stiffness of the lungs (related to compliance)
  2. resistance of the airways
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3
Q

What is the formula for compliance?

A

C = ∆V/∆P

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4
Q

What is a clinical example of low lung compliance?

A

Pulmonary fibrosis
◊ Thickening and scarring of alveolar membranes
◊ From chronic inflammation or exposure to chemicals

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5
Q

What chemical phenomena increases the stiffness/elasticity of the lungs? Explain how this works

A

Surface tension from the fluid surrounding the lungs
□ The tendency of a fluid surface to occupy the smallest possible SA
-> Walls of the alveoli very thin - enhances this effect
-> H bonds between water molecules collapse to achieve smallest surface area possible

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6
Q

What is used to reduce surface tension in the alveoli?

A

Surfactant

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7
Q

What cells produce surfactant?

A

type II pneumocytes

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8
Q

How does surfactant work?

A
  • Reduces attractive forces between fluid molecules lining alveoli, making it easier to expand -> increased compliance
  • Surfactant is a detergent/soapy molecule made of mainly phospholipids
    ◊ Inserting phospholipid molecules stops the water molecules from nearing each other and forming H bonds
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9
Q

What is a clinical example of not having enough surfactant?

A

Premature babies don’t produced surfactant, results in respiratory distress syndrome (RDS)

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10
Q

What formula relates radii and resistance?

A

R = 1/r^4

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11
Q

What is the main airway of resistance in the lungs?

A

BRONCHI - because arranged in series
- The small airways contribute very little to resistance b/c high cross sectional area

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12
Q

What is the volume of air moved in and out during normal breathing called?

A

Tidal volume (VT)

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13
Q

What is the extra volume that can be inhaled above tidal volume called?

A

Inspiratory reserve volume (IRV)

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14
Q

What is the extra volume that can be exhaled voluntarily after normal breath out called?

A

Expiratory reserve volume (ERV)

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15
Q

What is the volume remaining after max exhalation called?

A

Residual volume

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16
Q

What is the volume remaining in lungs if they collapsed called?

A

Minimal volume

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17
Q

Define tidal volume

A

Volume of air moved in and out during normal breathing

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18
Q

Define inspiratory reserve volume

A

Extra volume that can be inhaled above tidal volume

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19
Q

Define expiratory reserve volume

A

Extra volume that can be exhaled voluntarily after normal breath out

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20
Q

Define residual volume

A

Volume remaining after max exhalation

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21
Q

Define minimal volume

A

Volume remaining in lungs if they collapsed - can’t get this out

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22
Q

What volumes add to give vital capacity?

A

Inspiratory reserve + Expiratory reserve + Tidal volume

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23
Q

What is vital capacity?

A

Volume of air that can be moved in and out of your lungs

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24
Q

What volumes add to give total lung capacity?

A

Vital capacity + Residual volume

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25
Q

What is total lung capacity?

A

Total volume in lungs when it is filled to max

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26
Q

What volumes add to give inspiratory capacity?

A

Inspiratory reserve + Tidal volume

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27
Q

What is inspiratory capacity?

A

Total volume of air that can be inspired from rest

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28
Q

What volumes add to give functional residual capacity?

A

Expiratory reserve + Residual volume

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29
Q

What is functional residual capacity?

A

Volume remaining in lungs after normal exhalation

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30
Q

What is indicative of a restrictive lung disease?

A

low FEV1

31
Q

What is FEV1?

A

forced expiratory volume in 1 second
a.k.a. how much of forced vital capacity comes out in 1 second

32
Q

What are 2 examples of restrictive lung diseases?

A

fibrosis, insufficient surfactant release (premmie babies)

33
Q

What is indicative of an obstructive lung disease?

A

FEV1/FVC ratio < 0.70

34
Q

What is an example of an obstructive lung disorder?

A

asthma (=bronchial inflammation), COPD

35
Q

What is the formula for alveolar ventilation?

A

VA = (VT - VD) x f

36
Q

What is VD? (subscript D just fyi)

A

Dead space = the inhaled air filling the upper airways that doesn’t reach the alveoli for gas exchange

37
Q

What is alveolar ventialtion?

A

volume of air that gets to the alveoli

38
Q

What is Fick’s Law of Diffusion?
- in words and in formula

A

F = A / T x D (P1 - P2)
Flux (amount flowing) = surface area/thickness x diffusion constant (pressure difference)

39
Q

What factors influence the rate of diffusion?

A
  • SA of membranes
  • Thickness of membranes
  • Pressure difference [MAJOR determinant]
  • Diffusion constant [MINOR determinant]
40
Q

What feature increases the SA of the alveoli?

A

the bulbous structure of the alveoli and high density of capillaries

41
Q

What happens if alveolar SA is reduced?

A

less contact between air and capillaries = O2 exchange reduced

42
Q

What is a clinical example of reduced alveolar SA? What are the effects?

A

Reduction of SA (e.g. emphysema) by dilation of alveolar spaces/destruction of walls = less contact between air and capillaries = O2 exchange reduced

43
Q

What feature contributes to the thick/thinness of the blood air barrier?

A

Blood air barrier is mostly made up of the alveolar and capillary walls = thin = small distance between air and blood

44
Q

What is the driving factor for diffusion of gases across the blood air barrier?

A

Pressure difference

45
Q

What is the pressure difference between?

A

The alveolar and arterial pressures

46
Q

What determines O2 alveolar partial pressure? (3)

A
  • Alveolar ventilation
  • O2 consumption - blood O2
  • Partial pressure of O2 in air (usually constant, so less important)
47
Q

What determines CO2 alveolar partial pressure? (3)

A
  • Alveolar ventilation
  • CO2 production
  • Partial pressure of CO2 in air (negligible)
48
Q

How is O2 transported? (2)

A
  • Dissolved in blood
    • Bound to hemoglobin in RBCs
49
Q

Why is there very little O2 transported dissolved in the blood?

A

O2 has low solubility at physiological partial pressure

50
Q

What reduces O2 binding affinity to hemoglobin? (4)

A
  • Lower pH
  • Higher temp
  • Increased PCO2
  • Increased [BPG]
51
Q

The upper flat part of the sigmoidal curve indicates…

A

moderate changes in PO2 around normal have small effects on % saturation = reserve capacity for exercise etc.

52
Q

The steep part of the sigmoidal binding curve indicates…

A

Steep at low PO2 -> helps with loading in the lungs and unloading in the tissues, small changes in PO2 = large changes to % O2 bound

53
Q

How does exercise influence O2 binding?

A

Increased metabolism = increase CO2 (and .: H+) and temp = shift curve right = reduced affinity for O2

54
Q

How is CO2 transported in the blood? (3)

A
  • Dissolved in plasma (~7%)
  • Combined with proteins as carbamino compounds (23%)
  • As bicarbonate (70%)
55
Q

How is CO2 carried as bicarbonate?

A

○ Carbonic anhydrase enzyme converts CO2 + H20 <==> H2CO3
○ Then dissociates into H+ and HCO3-
- H+ lowers the pH, binds to Hb
- HCO3- into plasma in exchange for Cl- = chloride shift

56
Q

What enzyme is involved in CO2 transport (as bicarbonate)?

A

Carbonic anhydrase enzyme

57
Q

What is an example of CO2 combined with protein as a carbamino compound?

A

Carbaminohemoglobin (HbCO2) - competes with O2

58
Q

What controls respiration? (that we need to know about)

A

Respiratory Rhythmicity Centres

59
Q

What are the functions of the Respiratory Rhythmicity Centres? (3)

A
  1. generate cycles of contraction and relaxation,
  2. establish pace,
  3. modify activity in response to chemical and pressure signals
60
Q

Where is the respiratory rhythmicity centres located?

A

In the medulla (brain)

61
Q

What are the 3 parts that make up the Respiratory Rhythmicity Centres?

A
  1. Inspiratory centers of the dorsal respiratory group (DRG)
  2. Ventral respiratory group (VRG)
  3. Pre-Bötzinger complex
62
Q

What are the inspiratory centers of the dorsal respiratory group (DRG), and what do they control?

A

○ Inspiratory neurons
○ To diaphragm and ext. intercostal muscles

63
Q

When does the ventral respiratory group (VRG) send signals?

A

○ No signals at quiet breathing
○ When required: send signals to…
- Inspiratory centers = to accessory inspiratory muscles
- Expiratory centers = to accessory expiratory muscles

64
Q

What is the role of the Pre-Bötzinger complex?

A

Similar to SA node = rhymical/cyclical respiration

65
Q

What sensors control/influence respiration?

A
  • Central chemoreceptors
    • Peripheral chemoreceptors
    • Inflation/deflation reflexes
    • Protective reflexes
66
Q

Where are the central chemoreceptors located?

A

medulla

67
Q

What are the central chemoreceptors sensitive to?

A

PCO2 of the blood, but not PO2

68
Q

What is the role of the central chemoreceptors?

A

Most important sensors for determining resp activity

69
Q

How do the central chemoreceptors detect changes in pCO2?

A
  1. CO2 diffuses across the blood-brain barrier
  2. Changes pH of cerebrospinal fluid (CSF)
  3. Central chemoreceptors respond to pH change
70
Q

Where are the peripheral chemoreceptors located?

A

carotid and aortic bodies, close to baroreceptors

71
Q

What do the peripheral chemoreceptors respond to?

A

mainly to changes in arterial PO2

72
Q

What is the role of inflation/deflation reflexes? How do they work?

A

○ Input from lungs to stretch receptors
○ Brain then sends efferent output to prevent them stretching too far either way

73
Q

What is the role of protective reflexes?

A

○ Receptors also detect irritation
○ Brain sends efferent signal that triggers sneeze (forceful expiration) or cough (stepwise expiration)

74
Q

What is the process to restore PCO2 homeostasis when arterial PCO2 increases?

A
  1. Change detected by chemoreceptors in the medulla and in arteries, stimulated by increased PCO2 and decreased pH [receptor]
  2. Respiratory muscles stimulated [effector]
  3. This results in increased resp rate and elimination of CO2 at alveoli = decreased arterial PCO2