Respiratory Physiology Flashcards

1
Q

What are 6 functions of the Respiratory System?

A
  1. Provide O2 and eliminate CO2 (homeostatic regulation of blood gases)
  2. Protect against microbial infection (filter)
  3. Regulate blood pH (with kidney)
  4. Contribute to phonoation (passage of air through vocal cords = speech)
  5. Contributes to olfaction
  6. Reservoir for blood
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2
Q

What is the fundamental unit of the respiratory system?

A

Alveoli

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3
Q

The alveoli are embedded in a dense network and tissue characterized by: _______, ________, and ________ with a large number of _______

A

The alveoli are embedded in a dense network and tissue characterized by: smooth muscle tissue, smooth muscle cells and connectie tissue with a large number of capillaries

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4
Q

What is the passage of air in the upper respiratory tract?

A

Larynx -> trachea -> two primary bronchi -> lungs

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5
Q

How are the trachea and primary bronchi structurally similar?

A

Both are semi-cartilaginous

  • C-shaped ring (made of cartilage) in front and smooth muscle in the back
  • Provides protection for the airway and gives elasticity
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6
Q

How is the structure of the bronchi different from the trachea and primary bronchi?

A
  • Still have cartilaginoous structures but the air pathways are no longer C-shaped
    • C-shaped rings of cartilage are replaced by plates of cartliage and smooth muscle
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7
Q

What provides the structure for bronchioles (prevents collapse)?

A

Smooth muscle (No cartlage)

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8
Q

What are the two regions of the tracheobronchial tree?

A
  1. Conducting zone
    • no alveoli = no gas exchange
    • “anatomical dead space”
  2. Respiratory zone
    • contains alveoli = gas exchange
    • Respiratory bronchioles, alveolar ducts and alveolar sacs
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9
Q

Why is the conducting zone of the tracheobronchial tree called “anatomical dead space”?

What structures are included in this region?

A

Because there are no alveoli therefore no gas exchange occurs.

  • trachea, primary bronchi, bronchioles and terminal bronchioles
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10
Q

What structures are included in the respiratory zone?

A

Respiratory bronchioles, alveolar ducts, and alveolar sacs

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11
Q

What are the smallest airways without alveoli?

A

Terminal bronchioles

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12
Q

What airway structure has sparse, occasional alveoli?

A

Respiratory bronchioles

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13
Q

What are alveoli? How does the amount of blood in contact with alveoli change?

A
  • Tiny sacs with a very thin wall
  • Highly vascularised - many capillaries that contact the alveolar surface
  • Amount of blood in capillaries is variable and changes with metabolic demand
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14
Q

What are type 1 alveolar cells?

A
  • Flat epithelial cells
  • Internal surface of the alveoli is lined with liquid that contains a surfactant
  • Do not divide - susceptible to inhaled or aspirated toxins
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15
Q

Why is surfactant important?

A

For stabalization of the alveolar sac

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16
Q

What are two functions of Type II Alveolar cells?

A
  • Not as common as type one
  • Functions:
    1. Produce the surfactant
    2. Act as a progenitor - have the ability to replicate and differentiate into Type I Alveolar cells
      • potential for fixing damaged alveoli
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17
Q

Oxygen and carbon dioxide diffuse through the _________ in less than _____second(s)

A

Respiratory membrane in less than 1 second

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18
Q

What is the respiratory membrane?

A

Very thin respiratory surface composed of the alveolar epithelial cell (Type I) and the pulmonary capillary endothelial cell

  • Alveolar fluid (w/ surfactant)
  • Alveolar epithelium
  • Basement membrane of alveolar epithelium
  • Interstitial space
  • Basement membrane of capillary endothelium
  • capillary endothelium
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19
Q

What are the five steps of respiration?

A
  1. Ventilation
  2. Exchange of CO2 and O2 btwn alveoli and blood
  3. Transport of O2 and CO2 through pulmonary and systemic circulation by bulk flow
  4. Exchange of O2 and CO2 between blood in tissue capillaries and cells in tissues via diffusion
  5. Cellular utilization of O2 and production of CO2
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20
Q

What is ventilation?

A

First step of repiration:

  • Consists of movement of the gas from the atmosphere to the alveoli by bulk flow, independent of the gas composition
    • movement is generated due to changes in volume and pressure that will promote movement from areas of high pressure to areas of low pressure
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21
Q

Where does step two of respiration occur:

“Exchange of O2 and CO2 between the alveoli and the blood system via diffusion”

A
  • Occurs at the level of the respiratory membrane due to changes in pressure of O2 and CO2 between the alveoli and the blood
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22
Q

How is O2 driven into the tissue cells and CO2 out?

A
  • Differential pressure between the blood and the peripheral tissue will drive oxygen from the blood to the peripheral tissue and CO2 will move from the peripheral tissue to the blood to be eliminated
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23
Q

How is Ventilation produced?

A
  • CNS sends an excitatory drive to respiratory motor neurons that innervate the respiratory muscles
  • Respiratory muscles contract
  • Changes the thoracic volume, the thoracic pressure and intrapulmonary pressures
    • These changes involving pressure allow for gas movement
  • Air flows in and out with the different muscle contraction and relaxations
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24
Q

What are the three categories of muscles involved in respiration?

A
  1. Pump muscles
    • inspiratory and expiratory
    • change pressure and volume and level of lungs
  2. Airway muscles
    • keep airways open
  3. Acessory muscles
    • facilitate respiration during forced breathing
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25
What is the most important muscle for respiration?
The diaphragm
26
How does the diaphragm participate in respiration?
* Active during **inspiration**: dome-shaped structure separating lungs from abdominal contents * When the diaphragm **contracts** it moves down, allowing the abdominal content to be pushed down and the *rib cage to be pushed outward* * OVERALL EFFECT: * Increase in thoracic volume when it contracts
27
How do the external intercostals participate in breathing? To which of the three respiratory muscle groups do they belong?
* inspiratory pump muscle * Contract and lift the rib cage, promotes a lateral increase in the thoracic volume * Contract and lift the rib cage to promote lateral increase in the thoracic volume * expansion of thorax * Motion similar to lifting a bucket handle = bucket handle motion
28
How do the **parasternal intercostals** contribute to breathing? To which of the three respiratory muscle categories do these muscles belong?
* Inspiratory Pump muscle * Contract and pull sternum forward - increases anterior posterior dimension of the rib cage * Pump handle motion
29
How do the abdominals contribute to breathing? To which category of respiratory muscle do they belong?
* Expiratory pump muscles * Contraction forces lung to return to resting position
30
How do the internal intercostals contribute to breathing? To which category of respiratory muscles do they belong?
* Expiratory pump muscles * Relaxed at rest and recruited during forced expiration * Push the rib cage down to reduce the amount of air or reduce the volume of the thoracic cage
31
How do the accessory muscles contribute to breathing?
* Scalenes, sternocleidomastoid, and pectoralis minor * Not commonly active during resting breathing; active during exercise and forced respiration
32
What are the inspiratory pump muscles?
1. Diaphragm 2. External intercostals 3. Parasternal intercostals
33
What are the expiratory pump muscles?
1. Abdominals 2. Internal intercostals
34
Describe what happens during inspiration at rest (ie quiet breathing)
1. Diaphragm contracts * pushing the abdominal content down and expanding the thorax as air comes in 2. External intercostals and parasternal intercostals contract (bucket handle and pump motion) increasing volume of the thorax
35
How does inspiration change during forced breathing?
Stronger contaction of the diaphragm, and recruitment of the accessory muscles - further expanding the thoracic cavity
36
What happens during quiet expiration?
* No active contraction * Relaxation of the inspiratory muscles (diaphragm, external and parasternal intercostals) * Air moves out because of lung recoil
37
How does expiration change during forced breathing?
* Abdominal muscles contract intensely * pushes abdominal content upward forcing the diaphragm higher than its resting level * Internal intercostals contract and push the rib cage down
38
What is obstructive sleep apnea?
* reduction in upper airway latency during sleep = reduction in openness of airway * Depressed tone of upper respiratory muscles is depressed and they become a floppy muscle * Air cannot go in and out = daytime sleepiness, low o2 saturation in blood and cardiovascular risks
39
What causes obstructive sleep apnea?
* result of a problem with the neural control of breathing * Lack of excitatory drive = needed to maintain tone of resp. muscles as well as anatomical defect
40
What regions of the respiratory tract are involved in filtering?
* respiratory zone and at the level of the alveoli * At conducting zone = muco-ciliary escalator
41
The filtering action that occurs in the conducting zone of the Respiratory tract is called the \_\_\_\_\_\_\_
**Muco-ciliary escalator:** * Two types of cells lining the surface of the trachea: * Goblet Cells - produce mucus * Ciliated Cells - have cilia on apical surface
42
What are the components of the muco-ciliary escalator in the conducting airway?
There are two cell types lining the trachea that make up the muco-ciliary escalator: 1. Goblet Cell - produce mucus 2. Ciliated Cell - have cilia on the apical surface; movement has preferential direction * produce periciliary fluid Both cell types function in a coordinated manner to entrap inhaled biological and inert particulates and remove them from the airways
43
What fluid is produced by ciliated cells in the conducting zone and why is it important?
* Periciliary fluid * Quite liquid (low density) * Sits on top of the ciliated cells = **sol layer** * Allows cilia to move freely because of low density
44
What do the goblet cells in the conducting zone produce?
Thick, dense mucus = **Gel layer** * Sparse * trap particulates that enter the resp system during inhalation
45
What cells produce the SOL layer and what cells produce the gel layer?
SOL Layer = periciliary fluid from ciliated cells Gel Layer = mucus from goblet cell
46
Once particulates are trapped in the mucus, how are they removed from the resp tract?
Through cilia movements: * cilia move in the SOL layer and the tip of the cilia touches the mucus and pushes it continuously in one direction * Cilia movement is **downward** in the **nasopharynx** and **upward** at the level of the **trachea** to eliminate mucus through the esophagus
47
What is responsible for the filtering that occurs at the level of the alveoli?
Macrophages in the alveoli -phagocytose particulates and digest them
48
What is the result of inhaling silica dust or asbestos?
* Macrophahes phagocytose the silica dust/asbestos but cannot digest them * the silica dust/asbestos break/kill the macrophages which then disintigrate * releases chemotactic factors * promotes recruitment of fibroblasts into the alveoli * increases the introduction of collagen = stiffens the lungs * Results in **pulmonary fibrosis**
49
What is spirometry?
A pulmonary function test that determines the amount and the rate of inspired and expired at each breath
50
Define **tidal volume**
The volume of air moved IN OR OUT of the respiratory tract during each ventilatory cycle
51
# Define **expiratory reserve volume** How is it assessed?
The additional volume air that can be forcibly exhaled following a normal expiration * Can be assessed simply by expiring maximally to the Maximum Voluntary Expiration
52
Define **Inspiratory Reserve Volume**
The additional volume of air that can be forcibly inhaled following a normal inspiration; it can be accessed simply by inspiring maximally to the *Maximum Possible Inspiration*
53
What is **residual volume?** Can it be measured with spirometry?
The volume of air remaining in the lungs after a maximal expiration; it cannot be expired no matter how vigorous or long the effort ## Footnote **RV cannot be measured with a spirometry test** **RV= FRC-ERV** **(FRC: functional residual capacity** **ERV: expiratory reserve volume**
54
How do you calculate Residual Volume (RV)?
RV = (FRC-ERV) FRC: functional residual capacity ERV: Expiratory reserve volume
55
Why is in important that there is always a small volume of air in the lungs (eg the residual volume)
Prevents collapse of the alveoli (Atelectasis)
56
Capacities are measurements of lung ________ and correspond to the sum of:
Capacities are measurements of lung _volumes_ and correspond to the sum of: 2 or more lung volumes
57
What is Vital Capacity? How is it calculated?
Maximal volume of air that can be forcible exhaled after a Maximal inspiration **VC = TV + IRV + ERV** TV: tidal volume IRV: Inspiratory reserve volume ERV: expiratory reserve volume
58
What is **inspiratory capacity**? How is it calculated?
* Inspiratory capacity is the maximal volume of air that can be forcibly inhaled * **IC = TV + IRV** TV= Tidal Volume IRV = Inspiratory Reserve Volume
59
What is the **Functional Residual Capacity (FRC)**? How is it calculated?
* The volume of air remaining in the lungs at the end of a normal expiration * **FRC = RV + ERV** Functional residual capacity RV" Residiual Volume ERV: Expiratory reserve volume
60
What is the **Total Lung Capacity (TLC)**? How is it calculated?
* Volume of air in the lungs at the end of a Maximal Inspiration * **TLC = FRC + TV + IRV = VC +RV**
61
What measurements cannot be determined using spirometry?
Residual volume and any capacity that relies on RV in it's formula. Therefore, we cannot measure: Residual Volume Functional Residual Capacity (FRC) Total lung capacity (TLC) TLC = FRC +TV + IRV FRC = RV + ERV
62
What is the tidal volume in a healthy adult?
500mL (Tidal Volume = air moved in or out of the respiratory tract during each ventilatory period)
63
What is total or minute ventilation? How is it calculated?
The amount of air that is exchanged within a rate time, or within a minute **Total/minute ventilation = (tidal volume)(resp. freq)** **= (0.5L)(15/min)** **=7.5 L/min \*** **\***Not all of this will be available for gas exchange (have to take into account the anatomical dead space)
64
What is **alveolar ventilation**? How is it calculated? How will it compare to minute ventilation?
**Alveolar Ventilation**: The amount of air moved into the alveoli per minute * Will be LESS than Minute Ventilation as it depends on the anatomical dead space * Calculated by subtracting the anatomical dead space volume from the tidal volume and multiplying by the respiratory frequency: * **VA= (TV - VADS) (Resp. Freq)**
65
Tidal volume (air that enters the resp system) is \_\_\_\_\_\_mL and conducting airways have a volume of about \_\_\_\_\_mL (volume of air that is leftover from previous breath; no gas exchange). What does this mean?
Tidal volume (air that enters the resp system) is **_500_**mL and conducting airways have a volume of about **_150_**mL (volume of air that is leftover from previous breath; no gas exchange) Which means, ~1/3 of a normal breath is not available for gas exchange
66
How do we improve alveoli ventilation?
Divers inhale slowly and very deeply; this improves ventilation of the lung - majority of minute ventilation is dedicated to or available for gas exchange _Deep breathing is more effective at increasing alveolar ventilation than is fast, shallow breathing_
67
Spirometry is used to determine the ________ in ____ second(s) and the forced \_\_\_\_\_\_\_\_\_\_
Spirometry is used to determine the _forced expiratory volume_ in _1_ second(s) and the forced _vital capacity_
68
What two volumes can be determined from Spirometry?
1. Forced expiratory volume in 1 second (FEV-1) 2. Forced vital capacity (FVC)
69
What is FEV-1
Forced Expiratory Volume in 1 second: * forced expiratory volume is how much of the vital capacity volume that can be expelled in one second
70
Forced vital capacity is about _______ in a healthy person
Forced vital capacity is about _5 Litres_ in a healthy person
71
What can a spirometry test diagnose?
Obstructive disease or restrictive disease
72
Patients affected by obstructive lung disease have shortness of breath due to difficulty in ______ because of \_\_\_\_\_\_\_\_
Patients affected by obstructive lung disease have shortness of breath due to difficulty in *_exhaling_* _all the air from their lungs_ because of _damage to the lungs or narrowing of the airways inside the lungs - exhaled airs comes out more slowly_
73
What would a spirometry test show in a patient with Obstructive Lung Disease?
* FEV-1 is significantly reduced * Process of expiration is also much slower (shown by a lower slope) * FVC can be normal or slightly reduced * Ratio between FEV-1/FVC is also reduced (\<0.7)
74
What is restrictive lung disease?
* Patients cannot fully fill their lungs with air - restricted from expanding * Most often results from a condition causing stiffness in the lungs * Can also be caused by stiffness of the chest wall, weak muscles or damaged nerves
75
What would a spirometry show that would indicate restrictive lung disease?
* FVC is reduced * FVC is reduced in patients compared to normal because less air enters therefore the IRV is much smaller than in a normal patient even though he has the full ability to expel * FEV-1 is reduced in comparison to a normal calculation * Ratio between FEV-1/FVC will be similar to a normal healthy person BUT the volume measured with FEV-1 and FVC will be reduced
76
What method can be used to measure the functional residual capacity?
Recall: FRC = is the volume remaining in the lungs after a normal, passive exhalation Can be measured with Helium dilution method
77
What are the static properties of the lung? Why are they necessary?
* Mechanical properties that are present in the lungs when no air is flowing * Necessary to maintain lung and chest wall at a certain volume * Include: * intrapleural pressure (PIP), * transpulmonary pressure (PPT), * static compliance of the lung and * surface tension of the lung
78
What are the dynamic properties of the lung?
* Mechanical properties when the lungs are changing volume and air is flowing in and out (*necessary to permit airflow*) * Alveolar pressure * Dynamic lung compliance * airway and tissue resistance
79
The exchange of air between the atmosphere and the alveoli is:
Ventilation
80
What causes ventilation to occur?
Change in pressure, or the generation of a pressure difference, between the atmosphere and the alveoli that will move air into and out of the lungs
81
In ventilation, air flows by _____ from a region of higher pressure to a region of lower pressure
In ventilation, air flows by _bulk flow_ from a region of higher pressure to a region of lower pressure
82
What is Boyle's law?
For a fixed amount of an ideal gas that is kept at constant temperature the **pressure and the volume are inversely proportion** * The product of pressure and volume will be a constant * With an increase in volume, there will be a corresponding decrease in presure **P1V1=P2V2**
83
During the expiratory phase of the lungs, a reduction in volume will generate an increase in \_\_\_\_\_\_\_\_
During the expiratory phase of the lungs, a reduction in volume will generate an increase in _alveolar pressure_
84
What is the equation for flow?
**Flow =** ΔP/R ΔP = Change in pressure (difference in pressure between the alveolar pressure and atmospheric pressure) R = Resistance
85
Lungs have a tendency to collapse due to \_\_\_\_\_
Lungs have a tendency to collapse due to _elastic recoil_
86
During inspiration and expiration air moves in and out of the lungs due to variation of the:
* Intrapleural pressure - Pressure that is inside the pleura * acts like a vacuum * Alveolar pressure (PALV) * Transpulmonary pressure (PTP) - derived from the difference of the alveolar pressure minus the intrapleural pressure
87
Because the intrapleural space acts as a relative vacuum, the intrapleural pressure is _\_\_\_\_\_\_\_\_\_\__
Because the intrapleural space acts as a relative vacuum, the intrapleural pressure is _älways negative_
88
* Intrapleural pressure fluctuates with breathing but it is always _______ due to: * What would result if the PIP = PALV
* Intrapleural pressure fluctuates with breathing but it is always _subatmospheric_ due to: _opposing directions of the elastic recoil of lungs and thoracic cage_ * What would result if the PIP = PALV * The lungs would collapse
89
\_\_\_\_\_\_\_\_\_\_ is the force responsible for keeping the alveoli open, expressed as the pressure gradient across the alveolar wall
_Transpulmonary Pressure (PTP)_ is the force responsible for keeping the alveoli open, expressed as the pressure gradient across the alveolar wall
90
P\_\_ should always be \> than P\_\_\_ in order to maintain the lungs expanded in the thorax
P_alv _should always be \> than PIP in order to maintain the lungs expanded in the thorax
91
P\_\_ is a static parameter which does **not** cause airflow, but determines lung volume (VL)
PTP is a static parameter which does **not** cause airflow, but determines lung volume (VL)
92
P\_\_ is a dynamic component that determines air flow
PALV is a dynamic component that determines air flow
93
During an inspiratory effort: * CNS sends an _______ to the muscles of inspiration (\_\_\_\_\_, ______ and \_\_\_\_\_\_\_\_) * Muscles contract and generate an ______ in thoracic volume * Intraplueral pressure \_\_\_\_\_\_\_ * Transpulmonary pressure \_\_\_\_\_\_\_\_ * Lung volume \_\_\_\_\_\_\_ * Alveoli pressure \_\_\_\_\_\_\_ * generates movement of _____ from low _____ to high \_\_\_\_\_
During an inspiratory effort: * CNS sends an _excitatory drive_ to the muscles of inspiration (_diaphragm_, _intercostals_ and _parasternals_) * Muscles contract and generate an _increase_ in thoracic volume * Intrapleural pressure _decreases (becomes more subatmospheric ie more negative)_ * Transpulmonary pressure _increases_ * Lung volume _increases_ * Alveoli pressure _decreases (below atmospheric)_ * generates movement of _gas_ from low _pressure_ to high _pressure_
94
Expiration: * Relaxation of the _\_\_\_\_\_\_\__ muscles → * chest wall _\_\_\_\_\_\_\__ (goes back to its resting state) → * _\_\_\_\_\_\_\__ moves back to a pre-inspiratory value→ * as transpulmonary pressure is equal to the alveolar pressure minus the intrapleural pressure, the transpulmonary pressure will also will be _\_\_\_\_\_\_\__ as the intrapleural pressure returns to pre-inspiratory values → * as transpulmonary pressure is also linked to lung volume, _\_\_\_\_\_\_\__and a reduce _\_\_\_\_\_\_\__, generating _\_\_\_\_\_\_\__ of the gas molecules inside the alveoli → * increase in _\_\_\_\_\_\_\__ so it is greater than the atmospheric pressure → * air will move from a region of high _\_\_\_\_\_\_\__to a region of low _\_\_\_\_\_\_\__, flowing out of the lungs to the environment
Expiration: * Relaxation of the _inspiratory_ muscles → * chest wall _recoils_ (goes back to its resting state) → * _intrapleural pressure_ moves back to a pre-inspiratory value→ * as transpulmonary pressure is equal to the alveolar pressure minus the intrapleural pressure, the transpulmonary pressure will also will be _reduced_ as the intrapleural pressure returns to pre-inspiratory values → * as transpulmonary pressure is also linked to lung volume, _lungs recoi_l and a reduce _volume_, generating _compression_ of the gas molecules inside the alveoli → * increase in _alveolar pressure_ so it is greater than the atmospheric pressure → * air will move from a region of high _pressure_ to a region of low _pressure_, flowing out of the lungs to the environment
95
Lungs are embedded inside the pleural tissue called: \_\_\_\_\_\_\_ The inside of the chest wall is lined by another pleural tissue called the \_\_\_\_\_\_\_\_
Lungs are embedded inside the pleural tissue called: _visceral pleura_ The inside of the chest wall is lined by another pleural tissue called the _parietal pleura_
96
What forces can affect resistance to air flow?
* Intertia of the respiratory system * Friction forces 1. friction between the different alveolar sacs 2. friction between the lung and the chest wall 3. Resistance that the airflow incurs when it enters the airway * accounts for 80% of total airway resistance
97
Airflow resistance is most sensitive to changes in radius when flow is \_\_\_\_\_\_
Airflow resistance is most sensitive to changes in radius when flow is _NOT laminar (turbulent)_
98
What is transitional airflow and where would you likely see it?
Mixture of laminar (linear) and turbulent (not smooth) * It takes extra energy to produce vortices = increases resistance * Airflow is transitional throughout most of the bronchial tree, at the ramifications or branches of the bronchial tree
99
Where would you find turbulent flow?
In larger airways, such as the trachea, the larynx and the pharynx * larger diameter = velocity of gas molecules is higher resulting in turbulent flow
100
What law is used to determine airflow resistance?
Poiseuille's Law R=(8ηL)/(πr4) n=viscosity L = length \*Based on this formula, as the radius is reduced, the resistance will dramatically increase\*
101
How do you determine the resistance for branched airways arranged in **series** vs in **parallel**?
* **In Series** * Resistance is simply the sum of the individual resistances * **In Parallel** * The resistance at each specific generation, when there is respiratory airflow, will be given by the inverse of each specific resistance; * as a consequence, the respiratory resistance at the level of the small airways at the level of the respiratory zone is minimal
102
Why are small airways the most important in pathological conditions?
Because their overall resistance can change significantly in pathological conditions * small airways can easily be occluded: * as they are surrounded by smooth muscle, contraction of smooth mm will increase resistance
103
What are three ways that small airways can be occluded?
1. Small airways are surrounded by smooth muscle, contraction of which will increase resistance 2. **Edema**: presence of fluid in the small airways can reduce the space available for airflow to move in or for the air to flow into alveolar sacs 3. **Mucus** accumulation can reduce the alveolar space at the level of the bronchioles
104
Why can lung compliance be determined both as a dynamic property and a static property?
Because lung compliance can be measured both in the presence or absence of airflow
105
What is lung compliance?
Measure of the elastic properties of the lungs and a measure of how easily the lungs can expand * given by the magnitude of the change in lung volume produced by a given change in transpulmonary pressure * Determined from a plot of transpulmonary pressure (x-axis) and lung volume (y-axis) *compliance is the slope*
106
What is static compliance of the lung? How is it measured?
* Represents the lung compliance (elastic properties of the lungs) when no air is flowing through * To measure: * Pt is asked to make a maximal inspiration and then release a small amount of air, at which time lung volume and transpulmonary pressure are measured * this continues in intervals (where pt exhales small amount of air and then stops) * the curves illustrate the ability of the lungs to expand and how much effort is put into inhaling or increasing lung volume at each respiratory breath
107
What effect on lung compliance does pulmonary fibrosis have?
* Lung compliance is low * Overproduction of collagen makes the lungs stiff which means that the patient has to make a big effort to expand the chest wall in order to increase the transpulmonary pressure that is responsible for changing the lung volume * A large change in transpulmonary pressure will result in a small change in lung volume (slope is reduced)
108
How does emphysema affect lung compliance?
* Lung compliance is high * Gradual reduction in lung elastic components * Small change in transpulmonary pressure will result in a large change in lung volume * Slope increases * "floppy lungs" - lost alveolar tissue resulting in less surface respiratory membranes available for gas exchange
109
What is dynamic compliance of the lung?
* Measured during periods of gas flow (either during inspiration or expiration) * Takes into consideration not only the **elastic properties** of the lungs, or the **stiffness**, but also the **airway resistance** that the air encounters during breathing that could potentially reduce the expansion of the lungs
110
Compare dynamic compliance and static compliance
Dynamic: * measured when air is flowing * elastic properties AND airway resistance * Usually less than or equal to static compliance (b/c of airway resistance) Static: * elastic properties when no air is flowing
111
At functional residual capacity (FRC) what will the compliance graphs look like?
At FRC, the slope of the curve will be **reduced** in the case of Dynamic compliance and it will be **increased** in the case of Static compliance
112
In the image we see that the curve for Deflation is different from the curve for inflation, what is this difference defined by?
Hysteresis
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What events do the numbers on the graph represent? 1. \_\_\_\_\_\_\_ * at low lung volumes it's difficult to __________ therefore rising ____ has little effect on \_\_\_\_\_ 2. \_\_\_\_\_\_\_\_ * First increases in ____ reflect the popping open of the ______ followed by their expansion and recruitment of others as air flows into the _______ which progressively increases the \_\_\_\_\_\_ 3. \_\_\_\_\_\_\_\_ * When all airways are open, making ____ more negative by chest wall expansion inflates the lungs and increases _____ in a linear fashion * ______ will expand until basically the _____ properties of the lungs do not allow further expansion 4. \_\_\_\_\_\_\_\_\_ * Curve reaches a plateau as it reaches the ______ of \_\_\_\_\_\_\_\_\_ * At high _____ lung compliance \_\_\_\_\_\_
What events do the numbers on the graph represent? 1. _Stable VL_ * Collapsed lung - medium and small airways will be collapsed = little gas exchange * at low lung volumes, it's difficult to _pop open an almost completely collapsed airway_ therefore rising _PTP_ has little effect on _VL_ 2. _Opening of airways_ * First increases in _VL_ reflect the popping open of the _proximal airways_ followed by their expansion and recruitment of others as air flows into the _alveolar sacs_ which progressively increases the _PTP_ 3. _Linear expansion of open airways_ * When all airways are open, making _PIP_ more negative by chest wall expansion inflates the lungs and increases _VL_ in a linear fashion * _alveoli_ will expand until basically the _elastic_ properties of the lungs do not allow further expansion 4. _Limit of airway inflation_ * Curve reaches a plateau as it reaches the _limit_ of _airway inflation_ * At high _VL_ lung compliance _decreases_
114
What is hysteresis?
Difference between the inflation and deflation compliance pathway (Where compliance is measured as the slope of transpulmonary pressure (x)/Lung volume graph (y)) C= ∆VL / ∆PTP
115
Why does hysteresis exist?
Because a greater pressure difference is required to open a previously closed (or narrowed) airway than to keep an airway from closing; * Related to the elastic properties of the lungs
116
What are two factors that determine lung compliance?
* Elastic components of lungs and airway tissue * anatomic structures of the lungs and tissues * **elastin and collagen** * Surface Tension at the air-water interface within the alveoli
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Elastin and collagen are localized in \_\_\_\_\_\_\_\_, around ______ and \_\_\_\_\_\_ * Influence: * *Dynamic*:
Elastin and collagen are localized in _alveolar walls_, around _blood vessels_ and _bronchi_ * Influence: * how elastic or stiff the lung is * *Dynamic*​: * the amount of these proteins varies considerably with changes in life
118
What is it about Elastin and Collagen that affects lung compliance (elasticity)? What does each protein influence?
* Geometric arrangement of the molecules * **Elastin**: * Gives lung *high extensible properties* b/c of it's SPRING SHAPE * Improve the ability of lungs to *stretch* * **Collagen** * gives stiffness (like a strong twine = high tensile strength/inextensible) * increase in collagen causes fibrosis = low compliance = require higher PTP to inflate lung at low volumes
119
What does the image show?†
* Healthy lung tissue * well organized with very regularly shaped alveoli and a dense network of alveoli within the lung tissue * Emphysema * still see some alveoli that are similarly shaped to healthy lung * many large alveolar spaces = ↓surface area available for gas exchange * ↑Compliance = small ∆pressure → large ∆volume * Floppy lungs = less elastic recoil (high compliance)
120
What is surface tension and how does it contribute to lung compliance?
Surface tension: property or phenomenon that occurs at the level of the interface between the surface and the air * Makes lungs collapse or gives the lungs elastic recoil * Surface tension decreases lung compliance
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Surface tension is a property of:
The molecules of the fluid that are in contact with the air/fluid interface * molecules in the bulk of the fluid will tend to interact with each other (esp if they are polar) * water molecule deeply embedded in the liquid will interact with molecules in all directions forming strong bonds * Water molecules at the surface are interacting with water molecules but will have little interaction with gas = creates a strong attractive force at the level of the air interface **Surface tension =** measure of the attracting forces acting to pull a liquid's surface molecules together at an air liquid interface
122
Surface tension is seen at all air-fluid boundaries and arises as a result of:
Surface tension is seen at all air-fluid boundaries and arises as a result of: Hydrogen bonding of water molecules
123
The image shows the importance of surface tension using a P-V curve in which surface tension is eliminated with saline-filled lung. Explain.
If you fill an isolated deflated lung with liquid (saline in this case) so that there is NO air in the lung, the pathway of lung compliance is much steeper because surface tension is not involved - therefore, the effect of surface tension is to "cause" the surface to maintain as small an area as possible - influences mvmt to the right of the lung compliance curve
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What is the relationship between type I alveolar cells and surface tension?
* Type I alveolar cells line the surface of the alveolar walls * They are in contact with fluid that contains surfactant * the internal surface of the alveoli is lined with a thin layer of fluid and air continuously comes in and out of the alveoli
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As air enters the lungs it is humidified and saturated with water vapour at body temperature so that when it reaches the alveoli, it means that \_\_\_\_\_\_\_\_\_
Water molecules cover the alveolar surface creating substantial surface tension = reduces the volume of the ideal sphere (or alveoli)
126
What is Laplace's equation?
Describes the equilibrium that balances the pressure necessary to keep the alveoli open and the tendency for alveoli to collapse P = 2T/r T = Surface tension r = radius * the smaller a bubble's radius = the greater the pressure needed to keep it inflated
127
Does a large alveoli or small alveoli require more pressure to stay open?
According to Laplaces eqn, a large alveoli requires less pressure to remain open than does a small alveoli =means that there is a region of higher pressure in small alveoli and a region of lower pressure in larger alveoli
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Because of surface tension and Laplaces eqn, logic states that smaller alveoli would collapse into larger alveoli. Why does this not occur in physiology?
Because of surfactant - reduces surface tension at alveoli - makes alveoli stable against collapse
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What produces surfactant?
type ii alveolar cells (ie type ii pneumocytes)
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What are 4 functions of surfactant?
1. Reduce the surface tension at the level of the alveoli 2. Improve lung compliance = less work needed to breath 3. stabalize alveoli against collapse 4. allows alveolar communication between dif sized alveoli without collapsing
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Surfactant is a mixture of \_\_\_\_\_\_\_\_
Surfactant is a mixture of _phospholipids_ * for interest: dipalmitoyl-phosphatidylcholine (DDPC), Phosphatidyl-choline, surfactant apoproteins and Ca2+ * Recall: phospholipids are AMPHIPATHIC * hydrophobic and hydrophilic properties * **interferes with water-water interactions \***
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How are alveoli stabilized by surfactant? What is the importance of the T/r between large and small alveoli (Surface tension/radius ratio)?
* Surfactant, which is always present on the surface of the air/water interface in alveoli, will be closer together or further apart depending on the phase of the respiratory cycle * T/r ratio is constant across dif sizes of alveoli * because alveoli have equal concentration of surfactant, it must be organized differently based on size * small alveoli = surfactant is closer together * larger alveoli = surfactant is farther apart * surface tension is increased in large alveoli and decreased in small alveoli
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What happens when surfactant is more concentrated on the surface of the alveoli? Where would we see this situation?
you will have lower surface tension as seen in smaller alveoli
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Why is it important that surfactant is dynamic?
Allows the alveolar tension to change with inflation and deflation - thickness of the surfactant layer varies inversely with the surface area
135
Why do premature babies have difficulty with breathing?
They do not have enough surfactant in their lungs = have to make a large inspiratory effor to increase lung volume **infant respiratory distress syndrom** *dr administers surfactant to the airways*
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Surfactant improves _______ and stabalizes \_\_\_\_\_\_\_
Surfactant improves _compliance_ and stabalizes _alveolar size_
137
What did the inhalation test with radioactive xenon show? What conclusion can be drawn from this?
That ventilation is not equal throughout the lung: * ventilation was higher in the lower zone of the lung (bottom) and lower in the upper zone * If patient was laying flat, the highest ventilation was towards his back * Shows that *regional ventilation changes have to do with gravity and posture*
138
How do we explain the difference in ventilation between different regions of the lungs?
* There is *negative pressure* in the *intrapleural space* (**subatmospheric**) which changes between the top and bottom of the lung * PIP is much *more negative* at the top of the lung than the bottom * PIP is generated by the balance between the elastic recoil of the lung and the elastic chest wall * The lungs have weight and are affected by gravity * weight increases pressure = PIP less negative (increase) at the bottom and decrease (more negative) at the top
139
Why do alveoli at the bottom of the lung have an advantage during inhalation?
* more deflated = can expand more = receive larger portion of inspired air At the beginning of an inspiration, the alveoli that are at the bottom of the lungs start being *more deflated* because the transpulmonary pressure that generates the lung volume is influenced by the values of intrapleural pressure; when inflation occurs, small changes in PIP will generate large changes in VL
140
What is Dalton's Law?
States that in a mixture of gas, such as air, each gas has its specific pressure and the total pressure of this mixtures is given by the **sum of the individual pressures**
141
Gas exchange occurs at the level of the ____________ (very thin layer of tissue)
Gas exchange occurs at the level of the _Respiratory membrane_ (very thin layer of tissue) * contains the fluid, epithelial cells in the alveoli, interstitial space, basement membrane of the capillary epithelium, and the epithelium * Thinness is an advantage
142
What is Fick's Law?
Explains diffusion through the respiratory membrane: * States that the rate of transfer of a gas (V; L/min) through a sheet of tissue per unit time is proportional to the Surface area of the membrane (A) and depends on the difference in partial pressures between the two environments, (P1-P2) and inversely proportional to the thickness (T) of the membrane. * D= diffusion constant **Vgas =** (A÷T) • D • (P1-P2)
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The diffusion constant (in ______ law) is proportional to the _________ and inversely proportional to \_\_\_\_\_\_\_\_ Conclusion?
The diffusion constant (in _FICK's_ law) is proportional to the _solubility of the gas_ and inversely proportional to _square root of the molecular weight_ Conclusion? * Solubility of the gas in the fluid will influence the diffusion process * CO2 is much more soluble than oxygen * CO2 will have a faster diffusion process compared to O2
144
Which gas diffuses faster between CO2 and O2? Why?
CO2 diffuses faster because it has a much higher solubility than O2
145
What is Henry's Law?
The amount of gas dissolved in a liquid is directly proportional to the partial pressure of gas in with the liquid is in equilibrium
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The concentration of gas in a liquid is determined by:
Partial pressure and solubility [gas] in liquid = (P • Sol) Therefore, if two gases are at the same PP but differ in sol, their content within sol'n will differ \*ONLY GAS DISSOLVED IN SOL'N CONTRIBUTES TO PP (O2 bound to Hb = no longer dissolved)
147
PP of water is variable and depends on \_\_\_\_\_\_\_\_\_\_
PP of water is variable and depends on _how saturated the air is_
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At the level of the alveoli: * PPO2 is \_\_\_\_\_\_ * PPCO2 is \_\_\_\_\_
At the level of the alveoli: * PPO2 is _reduced_ * PPCO2 is _increased_
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Venous blood returns to the heart from the systemic circulation, and then travels by the pulmonary arteries to the lung capillaries. * Mixed venous blood containing _\_\_\_\__and _\_\_\_\__ returns to the lung capillaries available for the gas exchange * PO2 in the atmosphere is _\_\_\_\_ mmHg_; PO2 at the level of the alveoli is _\_\_\_\__ mmHg * When the mixed venous blood enters the pulmonary circulation, PO2 is _\_\_\_\__ mmHg _(\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_)_ * The diffusion process from the alveoli to the lung capillaries is very fast and _\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\__ * Blood exiting the lung is equivalent to the gas that is present at the level of the _\_\_\_\__ * PO2 in blood exiting the pulmonary capillaries is 100 mmHg (similar to 105 mmHg seen in the alveoli)
Venous blood returns to the heart from the systemic circulation, and then travels by the pulmonary arteries to the lung capillaries. * Mixed venous blood containing _oxygen_ and _carbon dioxide_ returns to the lung capillaries available for the gas exchange * PO2 in the atmosphere is _160 mmHg_; PO2 at the level of the alveoli is _105_ mmHg * When the mixed venous blood enters the pulmonary circulation, PO2 is _40_ mmHg _(lower in blood than in atmosphere)_ * The diffusion process from the alveoli to the lung capillaries is very fast and _oxygen will move from the alveoli to the lung capillaries as soon as air enters the alveoli_ * Blood exiting the lung is equivalent to the gas that is present at the level of the _alveoli_ * PO2 in blood exiting the pulmonary capillaries is 100 mmHg (similar to 105 mmHg seen in the alveoli)
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Why is PO2 in the alveoli (105 mmHg) not the same as PO2 in the atmosphere (160 mmHg)? (3)
* Air enters the respiratory system and reaches the alveoli where it is warmed up and humidified; partial pressure of water will increase and the partial pressure of O2 will decrease * As soon as air enters the alveoli = lots of blood available for diffusion = reduce Po2 * Once air enters the alveolar network, it mixes with air that makes up the functional residual capacity = decrease PO2
151
What 4 factors determine the alveolar PO2?
1. PO2 in the atmosphere * higher altitudes = reduced atm pressure = decrease PO2 proportionally 2. Alveolar ventilation * how much air is exchanged per unit time * ↑ alveolar ventilation = more air will be continuously exchange * Air at level of alveoli will be more similar to the air at the level of the atmosphere 3. Metabolic rate (eg exercise) 4. Lung perfusion * change in cardiac output = change in amount of blood passing through resp. system
152
What are four determinants of alveolar PCO2?
1. Atmospheric PCO2 (essentially zero) * CO2 moves out of blood into alveoli = increases alveolar PCO2 2. Alveolar ventilation * decrease in alveolar ventilation will lead to less exhalation of CO2 from alveoli to atm and therefore PCO2 will be increased in the alveoli 3. Metabolic rate = increases PCO2 4. Lung perfusion
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Increasing **alveolar ventilation (VA)** will increase alveolar P_**\_\_**_ and decrease alveolar P\_\_ * Why?
Increasing **alveolar ventilation (VA)** will increase alveolar P**_O2_** and decrease alveolar PC**_O2_** * Due to increased ventilation, there will be an increase in PO2 because the alveolar air will be more similar to the air that is present in the atmosphere * When the ventilation is increased, more CO2 is eliminated
154
What will happen if alveolar ventilation is reduced?
Reduce the amount of gas exchange between the alveoli and the atmosphere = increase in alveolar PCO2 and decrease in alveolar PO2
155
What determines arterial levels of PP gas
PP of gas in alveoli determines arterial levels
156
Why do we need pulmonary circulation to be low pressure?
The respiratory membrane is extremely fragile High bp can damage the respiratory membrane and edema and influx of plasma or RBC could move into the lungs and affect resp function
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Why is pulmonary circulation a low resistance system? What law defines this resistance?
Resistance defined by Poiseuille's law * length of vessels and the fourth power of the radius affects resistance * short wide vessels consistently reduce the resistance of the pulmonary circulation
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What does it mean when we say that the pulmonary circulation system is high compliance?
* Thin walled vessels * Vessels have very little smooth mm and small changes in pressure = large expansion * vessels will dilate in response to modest increase in arterial pressure
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The pulmonary system is _____ pressure, ____ resistance, and ______ compliance
The pulmonary system is _low_ pressure, _low_ resistance, and _high_ compliance
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Is the flow in the pulmonary circulatory system more or less than the flow in the systemic circulatory system?
They are equal
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Alveolar capillaries are collapsible, what does this mean?
If the capillary pressure falls below alveolar pressure, the capillaries close off, diverting blood to other pulmonary capillary beds with higher pressures
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What is the ventilation-perfusion relationship for respiration/circulation?
Ventilation/perfusion ration is the balance between the ventilation (bringing O2 into/removing CO2 from the alveoli *atm-alveoli*) and the perfusion (removing O2 from the alveoli and adding CO2 *alveoli-blood*)
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The ratio between ventilation and perfusion is one of the major factors affecting:
Alveolar (and therefore arterial) levels of O2 and CO2
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The greater the ventilation:
The greater the ventilation, the more closely alveolar PO2 and PCO2 approach their respective values in inspired air (ie closer to atm values)
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The greater the perfusion:
The more closely the composition of local alveolar air approaches that of mixed venous blood (reduced PO2 and increased PCO2)
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Under what conditions would we see a high ventilation/perfusion ratio? What is the result in terms of alveolar PO2 and PCO2
* Seen when there is a collapsing of the lung capillaries, *pleurisy* or other diseases that affect the vasculatory system * Blood flow is obstructed or occluded * No blood available for gas exchange * ↑PO2 at alveoli (no O2 passing from lungs to caps) * ↓PCO2 at alveoli (no CO2 entering lungs from blood) * Region is **under-perfused** or **under-ventilated** * Anatomical dead volume
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Under what conditions might you see a low Ventilation/perfusion (V/Q) ratio? How would this affect alveolar PCO2 and PO2
* Obstruction: collapsed bronchi or bronchioles * no gas exchange between the alveolar air or alveolar space and the atmosphere * Blood still moves through alveolar space and contacts alveolar spce through the resp membrane * Decrease in **alveolar** **PO2** and increase in **PCO2** * Amount of blood passing through this system is called a **shunt**
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What is a pulmonary shunt?
refers to the passage of deoxygenated blood from the right side of the heart to the left without participation in gas exchange in the pulmonary capillaries * alveolar occlusion =\> V/Q (ventilation/perfusion) ratio is low
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Both _\_\_\_\_\_\_\_\_\__and _\_\_\_\_\_\_\__ decrease from the bottom of the lungs to the top of the lungs * The ______ of the two lines representing perfusion and ventilation is different * This leads to the ventilation/perfusion ratio being _\_\_\_\_\__at the bottom of the lungs and _\_\_\_\_\_\__ at the top of the lungs
Both _blood flow (perfusion)_ and _ventilation_ decrease from the bottom of the lungs to the top of the lungs * The slope of the two lines representing perfusion and ventilation is different * This leads to the ventilation/perfusion ratio being _lower_ at the bottom of the lungs and _higher_ at the top of the lungs
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Homeostatic mechanisms exist to limit ______ between ventilation and perfusion
Homeostatic mechanisms exist to limit _mismatch_ between ventilation and perfusion
171
How do pulmonary capillaries respond to low O2?
* **Pulmonary hypoxic vasoconstriction** * a homeostatic mechanism that is intrinsic to the pulmonary vasculature. Intrapulmonary arteries **constrict** in response to alveolar hypoxia (↓O2), diverting blood to better-oxygenated lung segments, thereby **optimizing ventilation/perfusion matching** and systemic oxygen delivery
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What is Pulmonary hypoxic vasoconstriction?
a homeostatic mechanism that is intrinsic to the pulmonary vasculature. Intrapulmonary arteries **constrict** in response to alveolar hypoxia (↓O2), diverting blood to better-oxygenated lung segments, thereby **optimizing** **ventilation/perfusion matching** and systemic oxygen delivery
173
What is the homeostatic response to low blood flow (decreased perfusion) and low airflow (decreased ventilation)?
174
In what two forms is O2 carried in the blood?
1. Dissolved in plasma (~2% - O2 has low solubility) 2. Combined with hemoglobin (~98%)
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Dissolved O2 follows ________ Law
Dissolved O2 follows _Henry's_ Law * Henry's law is one of the gas laws states that: at a constant temperature, the amount of a given gas that dissolves in a given type and volume of liquid is **directly proportional** to the **partial pressure** of that gas in equilibrium with that liquid. * O2 content ∝ PO2 and solubility
176
What is the composition of hemoglobin ?
Protein composed of 4 aa subunits called Globin (2 alpha and 2 beta) and 4 Heme groups
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What is a heme group? What is it called when it's bound to oxygen? Unbound?
* What is a heme group? * porphyrin ring structure in which an iron atom binds to oxygen * each heme binds a molecule of oxygen = 4O2 molecules/Hb * What is it called when it's bound to oxygen? Unbound? * Bound * Oxyhemoglobin * No O2 bound * deoxyhemoglobin * Interaction between O2 and hemoglobin is reversible and is strongly influenced by the arterial partial pressure of O2
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What does an oxygen dissociation curve show?
The interaction between hemoglobin and the arterial PO2
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When bood exits the pulmonary capillaries, the percentage of hemoglobin saturation is \_\_\_\_\_\_\_
When bood exits the pulmonary capillaries, the percentage of hemoglobin saturation is _100%_
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At rest, when blood moves back in the venous system it has \_\_\_\_% O2 attached to Hb. What does this indicate?
At rest, when blood moves back in the venous system it has _70_% O2 attached to Hb. What does this indicate? * The amount of O2 unloaded in the tissue capillary is minimal at rest
181
What is oxygen capacity?
The amount of O2 that can be combined with Hb
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What does O2 Capacity depend on?
How much Hb is present in the blood •change in amount of Hb will change O2 capacity
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What is Hemoglobin Saturation? What does it tell us about O2 capacity?
The percentage of available hemoglobin binding sites that have O2 attached * tells us very little about the O2 capacity
184
What four factors can influence the interaction between Hemoglobin and oxygen (Hb saturation)?
1. Arterial PO2 * MOST important * As PO2 changes, the percentage of Hb saturation changes 2. pH in blood 3. PCO2 4. Temperature
185
Why is the Hb-O2 dissociation cure not linear?
* Hb-O2 dissociation curve is *sigmoidal* * because of cooperative binding
186
What is cooperative binding and why does it occur?
Cooperative binding occurs due to the fact that we have deoxyhemoglobin * First molecule of O2 interacts with heme group and changes the conformation of the heme group and the globin chains * globin chains change conformation from tens to relaxed * Next o2 will attach much easier * causes sigmoidal shape of Hb-O2 binding curve
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Why is it important that PO2 remains relatively high in capillary of peripheral tissue?
Because PO2 is necessary to drive diffusion of O2 from RBC to blood to cells and mitochondria
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In what situation would PO2 go below 40 mmHg?
During a high metabolic rate when peripheral tissue is using a lot of O2
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Changes in Hb concentration can change oxygen concentration or oxygen capacity without affecting the \_\_\_\_\_\_
Changes in Hb concentration can change oxygen concentration or oxygen capacity without affecting the _Hb saturation_
190
What is the difference between the Sigmoidal curves?
1. Hb at 10gm/100ml - **low Hb (anemia)** 2. Hb at 15 gm/100ml of blood - Normal 3. Hb at 20gm/100ml of blood - High Hb **polycythemia** * If the hemoglobin is fully functional it will still be able to bind to O2 and therefore the sigmoidal curve will not be affected * At a high PO2 level (120mmHg) 100% of Hb saturation is seen with 10, 15 or 20 * y axis shows how much O2 can be transported * very different with differing [Hb] * Curve showing Hb at 10 has a lower [O2] in the blood compared to the curves with higher [Hb].
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What is the effect of CO in the respiratory tract?
CO (carbon monoxide) has 200x the binding affinity for Hb compared to o2 * Reduce O2-Hb binding * Confomational change * Less O2 delivered to peripheral tissue * Harder to unload O2
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Describe the diffusion of O2 between the lung and the blood capillary and the pressure gradients that drive it:
* Alveolar space has a high PO2 just before the diffusion process (higher than the PO2 in the plasma) * Pressure gradient between plasma and alveoli pulls O2 across the respiratory membrane and into the plasma * Another pressure gradient between the plasma and the inside of the RBC * O2 will move from plasma into RBC where they will bind with Hb according to the **Hb oxygen dissociation curve**
193
Describe the diffusion of O2 between the Blood and the peripheral tissue and the pressure gradients that drive it:
* Capillary is next to a peripheral tissue * Peripheral tissue is composed of tissue cells surrounded by interstitial fluid (IF) * Peripheral tissue cells consume O2 for metabolism * O2 moves from RBC → plasma → IF →space between cells → intracellular space → MIT * oxygen use by MIT creates pressure gradients * Low PO2 in plasma will recall o2 from inside RBC
194
What is the major factor influencing the binding between Hb and O2? What are 3 other factors that affect the O2 dissociation curve?
Major factor: arterial PO2 Other factors: 1. Temperature * ↑ temp → ↑ O2 unloading 2. pH * ↓pH → ↑ O2 unloading 3. pCO2 * ↑PCO2 → ↑ O2 unloading
195
In what 3 forms is CO2 carried in the blood?
* Dissolved (5%) * Bicarbonate (HCO3: 60-65%) * Carbamino compounds (25-30%)
196
How is Carbonic Anhydrase formed in the RBC?
In RBC: 1. CO2 + H2O → H2CO3 * Extremely fast reaction 2. Carbonic acid dissociates into H+ and bicarbonate: * H2CO3 → H+ + HCO3
197
RBC's exchange bicarbonate for ____ using:
RBC's exchange bicarbonate for _Cl-_ using: the anion exchange protein * Chloride shift * Bicarbonate exits the RBC into the plasma; Cl- moves into RBC to maintain electrical neutrality
198
What is the function of chloride shift?
Maintain electrical neutrality in the RBC's as bicarbonate leaves the RBC
199
What change allows for HCO3- to exit the cells?
H+ will increase in venous blood = decrease pH but maintains electrical neutrality
200
CO2 interacts with the globin chain of hemoglobin to form a carbamino compound called \_\_\_\_\_\_\_
CO2 interacts with the globin chain of hemoglobin to form a carbamino compound called _carbaminohemoglobin_ Hb + CO2 ⇔ HbCO2 No enzyme required
201
Co2 has a higher affinity for (deoxyhemoglobin or oxyhemoglobin)
deoxyhemoglobin * CO2 will bind deoxyhemoglobin and shift equilibrium towards a more dissociated hemoglobin-o2 molecule * If PCO2 increases, the O2 dissociation curve shifts to the right = lower %O2 bound to Hb * increased O2 unloading because CO2 will bind preferentially to deoxyhemoglobin
202
What are two effects from the interaction between hemoglobin and H+?
1. Unloading of O2 * lower pH = reduced % Hb saturation = increased O2 unloading 2. Hemoglobin buffers the change in pH at the level of venous blood
203
What is Respiratory acidosis?
**hypoventilation** (CO2 production \> CO2 elimination): Increase PCO2 and Increase H+ concentration
204
What is Respiratory alkalosis?
Hyperventilation ( CO2 Production \< CO2 elimination): ↓PCO2 and ↓H+ (increase pH)
205
What causes Metabolic acidosis?
↑ in blood H+ concentration independent from changes in PCO2
206
What causes Metabolic Alkalosis?
↓ in blood H+ concentration independent from changes in PCO2
207
neural control of breathing is established in the \_\_\_\_\_\_\_\_
neural control of breathing is established in the _central nervous system_ * Drives inspiratory and expiratory muscles
208
What are three important regions in the brainstem that control breathing?
1. pontine respiratory group 2. dorsal respiratory group 3. ventral respiratory group
209
Which part of the brainstem generates respiratory rates?
Ventral respiratory group Contains both the inspiratory rhythm generator and the expiratory rhythm generator
210
Breathing is * initiated in the ______ by \_\_\_\_\_\_ * Modified by \_\_\_\_\_\_\_\_
Breathing is * initiated in the _medulla_ by _specialized neurons_ * Modified by _higher structures of the CNS and inputs from central and peripheral **chemoreceptors** and **mechanoreceptors** in the lung and chest wall_
211
\_\_\_\_\_\_ and _____ neurons drive activity in premotor neurons which excite motorneurons that activate rhythmically respiratory muscles
_PreBötC_ and _pFRG_ neurons drive activity in premotor neurons which excite motorneurons that activate rhythmically respiratory muscles
212
What are pre-Bötzinger and parafacial respiratory groups important for?
* Fundamental for generating rhythm which is produced by several factors * Neuromodulatory factors (NT's) * Suprapontine influences that are volitional or emotional * Sensory inputs can also influence the rhythm of breathing
213
What excites inspiratory pre-motor neurons in ventral respiratory group which then excite motor neurons and activate the diaphragm and external intercostals
Pre-Bötzinger complex
214
Rhythm is generated by the \_\_\_\_\_
pFRG
215
What senses changes in PCO2, PO2 and pH?
Peripheral and central chemoreceptors - provide an exctiatory drive to brain centres that control the respiratory group (Dorsal and Ventral respiratory group in medulla)
216
Hypoxia, Hypercapnia and acidosis all cause an ______ in \_\_\_\_\_\_\_
Hypoxia (low PO2), Hypercapnia (high PCO2) and acidosis all cause an _increase_ in _ventilation_
217
What are two peripheral chemoreceptors mentioned in lecture\>
Carotid and aortic bodies
218
Carotid and aortic chemoreceptors sense:
mainly changes in arterial PO2 and will be activated by changes in pH Sense primarily hypoxia (low arterial PO2)
219
What are the 2 cell populations in the carotid bodies?
Type 1 glomus cell: chemosensitive - drive response to change in arterial PO2 Type II sustentacular cells: supporting cells
220
glomus cells (in carotid bodies) have characteristics similar to:
neurons * -voltage gated ion channels * generate AP's following depolarization * Vesicles with NT's * excite the terminals of the glossopharyngeal afferents * Increase respiratory drive = increase ventilation
221
what are central chemoreceptors?
specialized neurons located close to the ventral surface of the medulla (close contact with blood vessels and CSF)
222
Which chemoreceptor pathway is the principle pathway that responds to PCO2 levels
Central chemoreceptor pathway - responsible for 70% of the response to hypercapnia - mediated by effects at the level of the dorsal and ventral respiratory groups that change ventilation