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Exercise & Environment > Integrated human response to hypoxia > Flashcards

Integrated human response to hypoxia Flashcards

1
Q

percentage of nitrogen in the air

A

78.08%

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2
Q

percentage of oxygen in the air

A

20.95%

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3
Q

percentage of co2 in the air

A

0.04%

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4
Q

percentage of argon in the air

A

0.93%

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5
Q

barometric pressure

A

total pressure of air, from mixture of the different gases

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6
Q

partial pressure

A

partial pressure of a gas in a mixture is the pressure that gas would exert if it occupied that volume alone

fractions concentration x barometric pressure = partial pressure

Dalton’s law

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7
Q

total pressure of a gas mix

A

sum of all their partial pressures

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8
Q

PO2 cascade at sea level

A

PO2 decreases from atmospheric air to alveoli because
- addition of water vapour
- gas exchange with CO2
PO2 decreases further in capillary blood because
- gas exchange with tissues

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9
Q

change in PO2 from ambient air -> inspired air -> alveolar gas

A

dry ambient air quickly becomes saturated with water as it passes through airways

  • water has its own partial pressure which must be accounted for
  • PH2O changes with temp, at body temp is 6.35kPa/47mmHg
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10
Q

PH2O at body temp

A

6.35kPa // 47mmHg

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11
Q

PAO2 can be calculated with what equation

A

alveolar gas equation

PAO2= {fractional [O2] x (barometric pressure - PH2O)} - (PaCO2/R)

aka PO2 entering alveoli - PO2 leaping alveoli

R = respiratory quotient =VCO2/VO2

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12
Q

R

A

respiratory quotient =VCO2/VO2

normally 0.8 at rest with normal diet

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13
Q

V

A

flow of gas across a diffusion barrier

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14
Q

flow of gas cross a diffusion barrier is proportional to

A
  • diffusabilty of gas (d)
  • area (A)
  • thickness (1/T)
  • partial pressure gradient (P1-P2)

= Fick’s law
V=d x A/T x (P1-P2)

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15
Q

Fick’s law

A

V=d x A/T x (P1-P2)

  • diffusabilty of gas (d)
  • area (A)
  • thickness (1/T)
  • partial pressure gradient (P1-P2)
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16
Q

what must respiratory gases diffuse through

A

gaseous and liquid phase

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17
Q

uptake of oxygen in pulmonary capillaries and extraction of oxygen at tissues is influenced by

A
  • partial pressure gradient
  • properties of diffusion barrier
  • relationship between PO2 and Hb saturation
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18
Q

when is it important to consider the partial pressure gradient for oxygen uptake and extraction

A

high altitudes

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19
Q

when do the properites of diffusion barrier to oxygen change

A

they are fixed in health but change in disease

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20
Q

relationship between amount of oxygen in blood and Hb saturation

A

sigmoidal

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21
Q

functional significance of flat part of sigmoidal curve

A

association region

  • even if oxygen levels reduce in the lungs, we still get almost complete loading of Hb
  • we are not impaired by blood oxygen content
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22
Q

functional significance of steep part of sigmoidal curve

A

dissociation region

  • ensures adequate delivery of oxygen to tissues whilst maintaining arterial PO2
  • if PO2 in tissues reduces, Hb will release lots of oxygen
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23
Q

what is a key fact about the relationship between amount of oxygen in the blood and Hb saturation

A

it is not a fixed relationships. oxygen binding affinity for Hb varies

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24
Q

what causes a shift to the right for the Hb dissociation curve

A
  • increase in PCO2
  • decrease in pH
    = Bohr effect
  • increase in temperature
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25
Q

what causes a shift to the left for the Hb dissociation curve

A
  • decrease in PCO2
  • increase in pH
  • Decrease in temperature
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26
Q

Lung PO2

A

~13 kPa (far right of curve)

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27
Q

tissue PO2

A

~4 kPa (Left of curve)

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28
Q

auto regulated oxygen delivery to tissues

A
  • increased tissue metabolism
    = shift to the right due to PCO2, pH and temperature change
    = increased oxygen delivery to the site of increased metabolism
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29
Q

why is oxygen needed at tissues

A

final electron acceptor in ETC
helps creation of proton gradient either side of inner mitochondrial embrace to drive oxidative phosphorylation in the production of ATP

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30
Q

why does PO2 change at high altitude

A

bariatric pressure reduces and so inspired PO2 will also be reduced

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31
Q

PO2 cascade at altitude

A

low PO2 is transfered all the way along oxygen cascade

- if low enough = hypoxia and cellular function may be compromised

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32
Q

is acute exposure to low atmospheric PO2 compatible with life

A

no

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33
Q

how can we survive summiting without oxygen supplementation of acute exposure to low atmospheric PO2 isn’t compatible with life

A

acclimatisation

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34
Q

what kind of response is acclimatisation

A

integrated, slow developing response which requires adjustments from three systems

  • cardiac, hours
  • respiratory, days
  • haematological, weeks/months
35
Q

what systems must adjust for acclimatisation

A
  • cardiac, hours
  • respiratory, days
  • haematological, weeks/months
36
Q

systemic oxygen delivery

A

DO2 = CO X CaO2

Systemic O2 delivery = cardiac output x O2 content of arterial blood

37
Q

CaO2

A

O2 content of arterial blood

38
Q

DO2

A

Systemic O2 delivery

39
Q

when partial pressure of inspired oxygen decreases:

A

CaO2 and therefore DO2 will reduce

40
Q

first line of defence against reduced PO2

A

increase CO to maintain DO2

  • immediate increase in HR upon hypoxic exposure
  • SV remains constant
41
Q

change in HR at 4500m

A

10-15% higher

42
Q

change in HR at 7600m

A

100% higher

43
Q

methods of restoring CaCO2

A
  • ventilatory adjustments

- haematological adjustments

44
Q

what is hyperventilation

A

where CO2 is eliminated in expired rate at a faster rate than it is produced, causing a reduction in PaCO2

NOT exercise hyperpnoea

45
Q

does hyperventilation occur in exercise

A

not commonly, that is hyperpnoea.

But, above anaerobic threshold hyperventilation can occur

46
Q

why does hyperventilation occur

A

hypoxic stimulation of arterial chemoreceptors

= most important feature of acclimatisation to high altitudes

47
Q

what is the most important feature of acclimatisation to high altitudes

A

hyperventilation

48
Q

why does hyperventilation cause CO2 blow off

A

increase in ventilation = decrease in alveolar CO2

  • PO2 is proportionate to CO2 production
  • PO2 is inversely proportionate to alveolar ventilation
49
Q

how is hyperventilation beneficial

A
  • increase in CO2 blow off leads to increased alveolar PO2
    = counteracts the lower barometric pressure
  • alveolar PO2 and PCO2 are inversely related
50
Q

relationship between PO2 and PCO2

A

inverse

51
Q

development of hyperventilation during climb

A
  • as altitude increases, PO2 decreases and so hypoxic ventilatory drive increases
    = reduction in PCO2 for more PO2
  • at certain altitudes, response aims to keep PO2 above certain threshold e.g 35mmHg
  • this causes extreme hyperventilation
    = PCO2 reduced to as low os <10mmHg
52
Q

hyperventilation in numbers

A
  • at pikes peak, PaO2 has halved
  • but, hyperventilation can cause ventilation to double
  • therefore PCO2 has doubled
  • now PaO2 has only reduced by 25%

a double in ventilation caused only half the reduction in PAO2
- inverse relationship

53
Q

respiratory alkalosis with altitude

A

likely how summiting Everst is possible
- hyperventilation causes PC2 to drop and alkalosis
- alkalosis reduces stimulation of central chemoreceptors
- this has negative feedback on ventilatory drive
= hyperventilation inhibited

54
Q

what inhibits hyperventilation

A

respiratory alkalosis

55
Q

how is negative feedback of hyperventilation reduced

A

metabolic compensation
- body removes bicarbonate ions which returns pH to normal
- once pH returns to normal, inhibitor is reduced
= hyperventilation

56
Q

metabolic compensation

A

removes negative feedback on hyperventilation

  • hyperventilation produces H+
  • H+ buffered by HCO3
  • after days, HCO3 transported out of CFS
  • pH returns to normal
  • inhibition of hyperventilation is removed
  • simultaneously HCO3 reabsorption in kidneys is reduced so excreted in urine
  • Urine pH increases, blood pH returns to normal
57
Q

is metabolic compensation beneficial

A

yes because it supports hyperventilation

BUT it may hinder ascent at extreme altitudes because alkalosis may be beneficial, because it causes a left shift

58
Q

is alkalosis beneficial

A

no, because it inhibits hyperventilation

BUT at extreme altitudes it may be useful because it causes a left shift

59
Q

how is alkalosis beneficial at extreme altitudes

A

left shift enhances the landing of oxygen in the pulmonary capillaries

60
Q

what would happen after days at extreme altitudes

A

after several days, renal HCO3 removal will cause pH to return to normal and loss of advantageous left shift

61
Q

strategy to summit Everest

A
  • acclimatise at lower camps
  • ensure final summit is as rapid as possible
    = ensures acclimatisation ot high altitude, but also takes advantage of an uncompensated alkalosis by summiting quickly (left shift)
62
Q

which method of CaO2 restoration takes longest

A

haematological adjustment

63
Q

[Hb] =

A

total Hb (g) / total plasma (L)

64
Q

how can [Hb] be increased

A
  • decrease plasma volume

- increase total Hb

65
Q

when is plasma volume decreased to increase [Hb]

A

acute response to altitude over hours-days

66
Q

how is total Hb increased

A

erythropoiesis - slow response that takes weeks

67
Q

How does erythropoiesis work

A
  • cells in kidney and liver sense reduced PO2 via HIF
  • respond to HIF by releasing EPO
  • EPO stimulates bone marrow to produce more RBC
    = more Hb
68
Q

what is HIF

A

hypoxia-inducible factor

it is an oxygen-sensing transcription factor

69
Q

oxygen-sensing transcription factor

A

HIF

70
Q

where is HIF

A

Liver and kidneys

71
Q

what happens to HIF in normoxia

A

-HIF alpha submits are hydroxylated by PH
- tagged with ubiquitin by VHL
= labelled for degradation

72
Q

what happens to HIF in hypoxia

A
  • HIF alpha subunits are stabilised
  • translocated into nucleus
  • # this increases transcription of several genesEPO
    VEGF
    glycolytic & gluconeogenic enzymes
    glucose transporters
73
Q

what does HIF increase transcription of in hypoxia

A

EPO
VEGF
glycolytic & gluconeogenic enzymes
glucose transporters

74
Q

what increases transcription of these & when

EPO
VEGF
glycolytic & gluconeogenic enzymes
glucose transporters

A

HIF in hypoxia

75
Q

Summary of acclimatisation

A

3 pathways

  • alternations in ANS to increase HR and CO
  • stimulation of arterial chemoreceptors to increase ventilation which is maintained by metabolic compensation when alkalosis occurs
  • HIF signalling in kidney and liver cells to produce more EPO for Hb production

all work to maintain DO2

76
Q

what decreases the most during ascent to everest, after acclimatisation

A

PaO2, becuase of gradient from atmosphere to blood

77
Q

what happens to levels in [Hb} durng ascent to Everest in acclimatised person

A

increase

78
Q

what is universally accepted bout acclimatisation

A

the ability to acclimatise to high altitude is achieved by increasing CaCO2 to sea level values or above

79
Q

what is still not completely understood about altitude

A
  • exercise performance at altitude

- susceptibility of high altitude illness

80
Q

what happens to exercise capacity at high altitude

A

severely reduced
- at 500m, VO2 max is 60% os sea level
at everest, VO2 max is 35%

81
Q

how does changing CaO2 at altitude effect physical performacne

A

they don’t
exercise capacity is still significantly reduced despite relatively normal DO2
- not understood

82
Q

other possible factors related to cellular VO2 or alterations of oxygen movement at tissue cell level for further research

A
  • changes in mitochondrial enzymes
  • o2 diffusion from capillaries to mitochondria
  • local distribution of blood flow to exercising muscle
83
Q

does sea level performance predict high altitude performance

A

nope, confused.com

Exercise & Environment (14 decks)

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