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PHGY 502 > Airway response to hyperpnea > Flashcards

Airway response to hyperpnea Flashcards

1
Q

What is the typical heart rate response to progressive exercise?

A

HR increases linearly in normal subjects
o HR is expected to reach a maximum at the horizontal line (220-age)
o Along with an increase in HR there is an increase in stroke volume allowing for good cardiac output

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2
Q

What is the typical ventilatory response to progressive exercise?

A

Minute ventilation increases

o Interpreted as 2 linear lines, at one point the slope increases (ventilation increases more steeply)

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3
Q

What is PetCO2 and what does it represent?

A

PETCO2 (end tidal partial pressure of CO2) = Level of CO2 released at the end of exhalation. Estimates alveolar gas composition.

Alveolar CO2 in equilibrium with arterial CO2 –> gives good idea of arterial blood

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4
Q

How does minute ventilation change with increasing work rate?

A

• VE = minute ventilation; curvilinear; increases with increased work. The point at which the slope changes –> “anaerobic” threshold

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5
Q

How does VCO2 (CO2 production) change with increasing work rate?

A

• CO2 production increases (tightly coupled with ventilation)

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6
Q

How does VO2 change with increasing work rate?

A

• VO2 (O2 consumption) increases linearly, while VCO2 increases disproportionately

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7
Q

How does pH change with increasing work rate?

A

• Lactate and hydrogen ions are produced –> H+ binds to bicarbonate (–>Carbonic acid–> (carbonic anhydrase)–> CO2+water), then released as CO2), so bicarbonate levels decrease, and pH decreases.

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8
Q

What is the respiratory exchange ratio and which values can it reach?

A

VCO2:VO2 ratio = respiratory exchange ratio.

At rest, max value is 1 based on CHO metabolism. In exercise, can go > 1 because it isn’t about the metabolic production of CO2 but the displacement of CO2.

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9
Q

What is the total lung capacity?

A

The total capacity (volume) of the lungs, including residual volume (RV).

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10
Q

What is the total lung capacity minus the residual volume?

A

Vital capacity

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11
Q

Which volumes are included in the inspiratory capacity?

A

Tidal volume + Inspiratory reserve volume

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12
Q

With exercise, how is FRC affected?

A

It decreases (more of the expiratory reserve volume used)

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13
Q

With exercise, how are inspiratory and expiratory flows affected?

A

They increase. (Think of flow-volume loops)

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14
Q

How is airway temperature affected by an increase in ventilation?

A

• As ventilation increases, temperature of air decreases (+ cold)
In both carina (further up) and AS (further down) respiratory track, as ventilation increases, temperature in those airways decreases

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15
Q

What is the respiratory heat exchange formula?

A

RHE = VE [HC (Ti-Te) + HV (WCi-WCe)]

VE = minute ventilation 
HC = specific heat capacity of air
HV = heat of vaporisation of water 
WC = water content (internal and external)
T = temperature
--> Heat is lost from the airway surface
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16
Q

How do upper airways contribute to heat conservation when breathing?

A
  • Heat loss if maximized when the air is expired through warm upper airways
  • Heat is conserved by expiring through cool upper airways
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17
Q

Explain the heat conserving countercurrent mechanism of the airways

A

Air coming in gets progressively warmer as it gets to lower alveolar compartments, and gets progressively cooler when coming out

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18
Q

How is the nose useful to retain water? How much of the exhaled water is retained in humans?

A
  • Water is lost and strategies designed to conserve water are favourable adaptive features
  • Water is deposited on cold surfaces so that extension of surfaces such as the nose is useful
  • The seal has a nasal turbinate mucosal area that exceeds its total body surface area
  • Seal and desert rat recover 80-90% and man 30-40% of the exhaled water
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19
Q

How does water loss change with airway generations?

A

In proximal airways, there is a significant fluid loss. As you go peripherally, fluid loss is negligible because there is no need for evaporation of airway fluid.

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20
Q

How is airway hydration maintained during periods of increased ventilation?

A

• Water is provided by the bronchial circulation
• Bronchial blood flow increases as the airways cool
o Peripherally, it decreases (vasoconstrictions) with cooling

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21
Q

How does bronchial blood flow react to dry air?

A

o Hyperventilation with humid air vs dry air
o Blood flow was higher in hyperventilation in dry air
o Dry air caused cooling of airways

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22
Q

How does upper airway blood flow change in humid and dry air?

A
  • Blood flow in tracheal mucosa was virtually unchanged in humid and dry air
  • With endotracheal tube (bypass upper airways), dry air caused an increase in blood flow to tracheal mucosa. Humid air did not show as much of an increase.

–> Intact upper airways minimized changes in temperature in humidity that trigger changes in blood flow.

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23
Q

What are the two opposing theories of exercise induced bronchoconstriction?

A

Thermal theory

Osmotic theory

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24
Q

How is the fall in FEV1 after exercise related to environment humidity?

A

EIA is related to inspired water concentration

The more water in the inspired air, the less the fall in FEV1.

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25
Q

How is the airway blood flow different in asthmatic vs healthy subjects?

A

In normal people, the expired air temperature is cooler than in asthmatic patients (expire warmer air).
In asthmatic subjects, there is an increased number of blood vessels within the airway wall (leads to more heat loss).
Following exercise challenge (which leads to cooling of the airways), recovery of airstream temperature is faster in asthmatic subjects vs non-asthmatics. They have a capacity to heat the air more rapidly, but this could also contribute to airway narrowing.

26
Q

Do the conditions of the inspired air post-exercise change the response to hyperpnea challenge?

A

No: The conditions of the inspired air postexercise do not change the response to hyperpnea challenge.

If participants do exercise (fall in FEV1), whether they breathe cold or warm air after exercise does not change the bronchoconstriction response
This is likely due to the fact that the body has already reacted (mediators released) – cannot be modified by changing temperature and humidity of the air post-exercise

27
Q

How does air temperature affect the fall in FEV1 post-exercise (for a given humidity level)?

A

Fall in FEV1 quite similar among large range of temperatures
–> Suggests that dryness of air is important, maybe > temperature.

28
Q

How is mucociliary clearance affected with dry air hyperpnea in asthmatic patients? In healthy patients?

A

Mucous clearance is reduced in dry air in asthmatic patients, less so in healthy patients
Drying of the airways is an important phenomenon in triggering mucus clearance (as an index of disturbed lining layer of the airways)

29
Q

How is airway fluid osmolality affected by hyperpnea in cold and dry air?

A

Using a bronchoscope, catheter and filter paper, fluid was collected from the airway surface.
• There was no discernable effect of hyperpnea on ASL osmolarity.
• Is there a real effect on airway osmolarity??? Remains to be documented…

30
Q

Which pathway is involved in the conversion of arachidonic acid into leukotrienes?

A

5-Lipoxygenase (5-LO) pathway

31
Q

Which two leukotrienes are potent bronchoconstrictors?

A

LTD4 and LTC4 are potent bronchoconstrictors, involved in airway reactions to hyperpnea challenges

32
Q

What does LTB4 do?

A

chemoattractant for neutrophils

33
Q

How is LTC4 made?

A

Glutathione can be bound to LTA4 by LTC4 synthase –> LTC4

34
Q

How is LTD4 made?

A

Glutathione can be bound to LTA4 by LTC4 synthase –> LTC4 –> (cleaving of glu amino acid) –> LTD4

35
Q

Which cells release LTC4?

A

Tracheal epithelial cells, alveolar macrophages, mast cells, basophils, eosinophils…

36
Q

What does LTD2 do? Which cells produce it?

A

constrictor (produced by tracheal epithelial cells and mast cells)

37
Q

How are cysteinyl leukotrienes compared to histamine for bronchoconstriction?

A

Histamine and methacholine give similar bronchoconstriction based on similar inhaled amounts.
PGF2-alpha is a constrictive prostaglandin; PGD2 is another constrictive prostaglandin.
LTD4 is a lot further right on the graph, meaning that a much lesser concentration is required to cause a decrease in FEV1 –> very potent bronchoconstrictor

38
Q

How are CysLTs and PGE2’s concentrations in asthmatics compared to healthy people?

A

EIB patients had more leukotrienes in their sputum (CytLT) than those without EIB

PGE2 is a bronchodilating prostaglandin, is also increased in EIB+ patients

CytLT/PGE2 ratio was higher in patients with EIB

39
Q

Which drug can prevent dip in FEV1 following exercise?

A

Anti-leukotriene (cys-LT1R antagonist) prevents EIB –> Montelukast (leukotriene receptor antagonist)

40
Q

Which dietary factor can influence EIB? What is the mechanism behind this?

A

Diet rich in fish oil reduces EIB
CysLT produced changes (LTC5 is produced instead of LTC4) –> reduces exercise-induced bronchospasm
Very large doses of fish oil needed for this…

41
Q

Do EIB patients shed epithelial cells?

A

Yes. In addition to producing leukotrienes, EIB patients also shed epithelial cells
Strong correlation between concentration of leukotrienes in the sputum and the epithelial cells that are shed

42
Q

Which sports are more responsive to methacholine challenge?

A
  • Elite swimmers meet criteria for asthma more frequently than healthy controls
  • Cold-air athletes (e.g. Skiers) also have many individuals who are hyperresponsive to methalcholine
43
Q

Which sports shed more epithelial cells?

A
  • Swimmers shed more airway epithelial cells than both asthmatics and healthy controls
  • Not an issue in cross-country skiers
44
Q

Which compounds increase in the sputum after an exercise challenge in swimmers?

A

After voluntary hyperventilation challenge, there is an increase in some inflammatory mediators (like IL-6, IL-1B, TNF)

45
Q

What is the main nerve innervating the lungs?

A

Vagus nerve

46
Q

Where do nerve fibers enter the lungs? What do they innervate?

A

Enter at the hilum (same as blood vessels)

• Then distribute on the airways to innervate the airway smooth muscles, mucus glands

47
Q

How do afferent nerve fibers affect bronchoconstrictions?

A

• Afferent fibers act as irritant receptors – can sense chemicals in the airways, send messages up to CNS and reflex bronchoconstriction via the vagus nerve.

48
Q

How do afferent nerves react to chemicals? How do they sense them?

A
  • Nerves react to chemicals through transient receptor potential channels
  • Large family of channels
  • Each channel has some degree of specificity to the things they will react to.
49
Q

What does the TRPA1 channel react to?

A 
Cold temperatures
Mustard oil
Garlic
Cannabis
Mint
50
Q

What do the TRPV2 and TRPV1 channel react to?

A

Heat

51
Q

Why does pepper spray trigger bronchoconstriction?

A

Because chilli peppers (capsaicin) are sensed by afferent neurons through the TRPV1 channel and trigger bronchoconstriction of the airways

52
Q

Are TRP channels reacting only to temperature?

A

No - they react to different compounds and to changes in osmolality.

53
Q

What does the TRPM8 channel react to?

A 
Cold temperatures
Mint
Eucalyptus 
Cinnamon
Geranium
54
Q

Which TRP channels react to cold temperature, and how do they trigger a response?

A

• TRPM8, TRPA1

react to cold temperature allowing for calcium influx –> release of neuropeptides.

55
Q

Which TRP channels react to hot temperature, and how do they trigger a response?

A

• TRPV1, TRPV2, TRPV4…, for e.g., reacts to warm temperature, allows for the influx of calcium –> release of neuropeptides –> neurogenic inflammation

56
Q

What are TRPV1 channels sensitive to?

A

• Sensitive to vanilloids like capsaicin (hot pepper), heat, fall in pH
Then, they release neurokinins

57
Q

Why was capsaicin given in an experiment about hyperventilation challenge?

A

To stimulate sensory nerves through TRPV channels. Treatment was given for a week before the experiment to deplete airway C fiber neurokinins

58
Q

What did neurokinin depletion show in guinea pigs?

A

Both neurokinin receptor antagonists, neurokinin depletion and cysLT RI antaginists blocked bronchoconstriction: Thus, both the sensory nerves releasing neurokinins and the leukotrienes are important for bronchoconstriction, both leukotrienes and neurokinins must be working together (interacting) in some way…

59
Q

How does neurokinin inhibition affect CysLT levels?

A

Inhibition of neurokinins or depletion of sensory nerves of neurokinins prevents cysLT synthesis.
Note the increase in cys-LTs after dry gas challenge (test) but not warm air challenge (control). Capsaicin (a neurotoxin that damages sensory C fibers and depletes them of neurokinins) and NK antagonists blocked the increase in cys-LTs. The cys-LTs are assayed in the bile since they are taken up from the blood stream by the liver and excreted in the bile.

60
Q

What happens first - nerve activation or CysLT synthesis?

A

First thing occurring is activation of the nerves; they sense the change in environment based on the hyperpnea, this releases neuropeptides, which then trigger the synthesis of leukotriene to cause bronchoconstriction. (in animals)
• In humans, we are not sure yet.

PHGY 502 (6 decks)

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