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Enviro > Hypobaric Environment > Flashcards

Hypobaric Environment Flashcards

1
Q

Barometric pressure ____ ___ as altitude increase

A

Decreases exponentially

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2
Q

What happens to arterial and alveolar PO2 at high altitude?

A

Decreases resulting in hypoxic hypoxia

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3
Q

How high is Mt Everest?

A

8848m

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4
Q

What is the overall pressure and PO2 @ Mt Everest?

A

100mmHg barometric, 20mmHg O2

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5
Q

Why is the decrease in alveolar and arterial PO2 grater than the decrease in ambient PO2 at altitude?

A

Because inspired air is always saturated with water

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6
Q

At what altitude is the highest permanent resident population?

A

5400m

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7
Q

What is the altitude of pressure inside of an airplane?

A

1900-2500m

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8
Q

Why aren’t planes pressurised to sea level?

A

Reduces pressure on fuselage, and reduces weight of the plane.

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9
Q

What sickness is associated with rapid ascension to >3000m?

A

Acute Mountain Sickness

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10
Q

What are the symptoms associated with acute mountain sickness?

A

Bad sleep, dizziness, fatigue, headache, nausea, rapid HR, shortness of breath

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11
Q

At what altitude do you lose consciousness?

A

> 6000m

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12
Q

Who are Reinhold Messner and Peter Habeler?

A

Reinhold: First to complete solo ascent of Everest. First climber to climb all peaks >8000m
Peter: First w/ Reinhold to complete climb of Everest w/out supplemental oxygen

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13
Q

Who is Lincoln Hall?

A

Veteran Aus Mountaineer who was part of first Australian expedition to climb Everest. Survived night at 8700m

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14
Q

Why was Lincoln Hall ‘Dead Lucky’?

A

During 2006 descent from peak he was struck by cerebral oedema = collapse in snow. Sherpas tried reviving him but had to leave him at night. Next day he was fount by guides.

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15
Q

What are the 4 steps in O2 transfer?

A
  1. Alveolar ventilation
  2. Pulmonary oxygen diffusion
  3. Transport of Oxygen in blood
  4. Tissue diffusion
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16
Q

What is the PO2 range in the body? Where is the body is the max and min?

A 
Max = 160mmHg = Alveoli
Min = 40mmHg = Venous blood
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17
Q

Is there a difference in the mode of pulmonary ventilation alteration in higher climates between LAN and HAN individuals?

A

No

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18
Q

What is the difference in mode of pulmonary ventilation for LAN and HAN individuals at high altitudes?

A

Hyperventilation

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19
Q

What causes hyperventilation due to altitude?

A

The decrease in air pressure at higher altitude; each breath brings in a smaller pp. of oxygen, thus to obtain the same amount of O2 a person much breathe more frequently.

P1V1 = P2V2 principle.

peripheral chemoreceptors respond to decrease in Po2, thus at about 3000m the decrease in O2 is substantial enough to illicit a response from these receptors; called hypoxic drive.

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20
Q

Disadvantages of hyperventilation

A

Hypocapnea + Respiratory alkalosis.

  • With time this alkalosis is accounted for by increased renal excretion of HCO3-
    • But this is too slow, thus other mechanisms must be involved
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21
Q

Why does hyperventilation significantly increase above 3000M?

A
  • The drive to ventilate from peripheral chemoreceptors (hypoxia) overcomes the central chemoreceptor inhibition (hypocapnea in CSF)
  • Hypoxic drive
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22
Q

At what alt. does LAN individuals reach secondary rise in ventilation and how long does this take to reach maximum increase?

A

3000-4000m, 1-2 weeks

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23
Q

How is arterial respiratory alkalosis compensated for?

A

Increased renal excretion of HCO3-

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24
Q

Due to renal excretion being a slow process and not enough to fully compensate for respiratory alkalosis at altitude, what other mechanisms are at work?

A

Respiratory system resets to work at a lower PaCO2

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25
Q

What races are HAN?

A

Tibetans, Ethiopians, Andeans

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26
Q

Why do HAN have 20% smaller respiratory rate at altitude than LAN?

A

Increased lung volume, increased RBC, increased Hb, higher capillary density, shorter average height, increased nitric oxide concentrations, barrel chested (due to larger lungs)

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27
Q

By how much is HAN pulmonary diffusion capacity increased in compared to LAN?

A

20-30%

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28
Q

What is polycythaemia?

A

Increase in erythrocyte count

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29
Q

Do HAN or LAN experience polycythaemia at altitude?

A

Both

30
Q

What is the result of polycythaemia?

A

[Hb] increase

31
Q

What is the outcome of decreased plasma and increased [Hb]

A

haemoconcentration

32
Q

What is the physiological stimulus behind polycythaemia? Is it time dependant?

A

Increase Erythropoetin from kidneys. Yes, as a person is exposed to a certain PO2 for longer their body has longer to respond. Seeing as it is a hormonal mechanism (and not a neural one) it will take time to fully enact.

33
Q

How does altitude affect CO?

A

May increase or decrease = mixed studies

34
Q

How does altitude affect HR?

A

Increases

35
Q

How does altitude affect SV?

A

variable then after several days, decreases

36
Q

How does altitude affect blood distribution in LAN?

A

Increase perfusion to vital organs. Decreased perfusion to less vital (Skin, gut). Hypoxia = vasodilation of coronary BVs as heart takes 60% O2 from Hb thus isnt O2 reserve for those with hypoxia

37
Q

How does blood supply to the heart differ between LAN and HAN?

A

LAN: blood flow decreases but oxygen uptakke by myocardium increase. HAN: Blood flow decreased but vascularisation of heart increased

38
Q

WHAT HAPPENS TO THE HB-O2 DISSOCIATION CURVE IN ACCLIMATISED HANs & LANs?

A
  • The decrease in the affinity of haemoglobin and oxygen caused by
    • increased 2,3BPG caused by a respiratory alkalosis in HAN
39
Q

What is happening to the HB-O dissociation curve to those in high altitude?

A

Alkalosis shifts curve to left, 23BPG shifts curve to the right pretty much evens out

40
Q

What happens to mammals at high alt?

A

Rely on loading up w/ O2 rather than humans who rely on greater efficiency of delivery

41
Q

How do birds cope at higher altitudes?

A
  • Large lungs
  • Deep inhalations
  • Parabronchus: one-way countercurrent system, blood in one direction air flows in other allows optimised air extraction. Air sacs
42
Q

Where do the highest livin people be?

A

5400 chilean miners

43
Q

What determines rate of diffusion to tissues?

A

PO2 gradient and by distance and SA which diffusion occurs = Ficks Law

44
Q

How can increased capillarisation increase diffusion rate?

A

Increases SA available, may decrease distance of diffusion.

45
Q

How is PAO2 maintained when climbing Everest in 42mmHG O2 conditions?

A

4x increase in alveolar ventillation = hyperventillation

46
Q

What is the mean PaO2 and PaCO2 at everest? compared to sea level?

A

30mmHg and 12mmHg. SL: 95, 35 mmHg respectively

47
Q

What limits Vo2max at sea level?

A

Blood moves through lungs too quick to fully equilibrate. CO increases, thus blood doesnt stay in the lungs long enough to pick up O2.

48
Q

What us the lactate paradox?

A

basically that in maximal exercise at an increased altitude lactate production is decreased compared to that of lower altitude. it would make more sense that lactate production would be greater due to less oxygen

only evidence is that it appears that skeletal muscle reduces the release of lactate into the blood

49
Q

What are the advantages of altitude training?

A
  • Increased RBC production due to EPO
  • Increased mitochondria
  • Increased vascularization of tissues.
  • Increased Hb, increased 2,3 BPG (left shift of oxygen dissociation curve)
50
Q

What are the disadvantages to altitude training?

A
  • Athletes have a slower rate of recovery
  • Increase in cortisol
  • Decrease of REM sleep
  • Decreased immunity
51
Q

What are ‘other effects’ of chronic hypoxia?

A
  1. Pulmonary hypertension
  2. Growth in the high altitude native
  3. Maternal & foetal physiology
  4. Endocrine changes
52
Q

Pulmonary hypotension as a result of chronic hypoxia. WHy?

A

Alveolar hypoxia induces vasoconstriction in the small arteries & arterioles of the pulmonary circulation, leading to an increase in pulmonary vascular resistance and to pulmonary arterial hypertension. This is a minor effect in the short-term visitor since the respiratory alkalosis which develops slows the response of the pulmonary arterioles to hypoxia.

53
Q

Why are baby HANs smol?

A

Shorter/smaller and barrel chester - big lungs doe

children generally born at LBW (as a result of hypoxia) (plus in a lot of these areas it is low socioeconomic anyways, which isnt helpful) -

54
Q

What hormones are affected by altitude?

A

TSH. GnRH, Aldosterone, ADH - mainly in 1st wk, then back to normal

55
Q

How are T3,T4 lvls different between HANs at altitude,

A

higher

56
Q

How are adh and aldosterone affected by altitude?

A

Increase RBC and plasma = decrease in ADH and aldosterone secretion = increase pee.

57
Q

Who would be expected to have high ANP at altitude?

A

Those with pulmonary oedema as wel

58
Q

What are 4 pathophysiological differences at altitude?

A
  1. Acute mountain sickness (AMS) 2. High altitude pulmonary oedema 3. High altitude cerebral oedema 4. Chronic mountain sickness.
59
Q

What tends to be the main cause of AMS?

A

hypoxia, disturbances in fluid distribution and volume retention.

60
Q

What are the steps in developing AMS?

A

Ascent = increase ADH and adrenal corticoids = fluid retention.
Hypoxia = peripheral constriction
Thus fluid directed to lungs, gut and brain.
Thus thus = oedema

61
Q

What is recommended rate of ascent to prevent AMS?

A

300m/day between 3000-4270, 150m/day afer that

62
Q

What drugs treat AMS and how?

A
  • Acetazolamide
  • Dexamethasone
  • Nifedipine.
    They are all carbonic anhydrase inhibitors = counteracts resp alkalosis, facilitates excretion of bicarbonate by urine.
63
Q

What is HAPE?

A

High altitude pulmonary oedema

64
Q

Symptoms of HAPE. Why can HAPE be fatal?

A

Cough w/out phlegm, interrupted breathing cycle, foaming pink fluid cough. Fatal: build up of fluid in lungs that prevent perfusion of air.

65
Q

Physiological consequences of HAPE?

A

Hypoxic vasoconstriction = increase pulm. art pressure = may burst thus blood enters lungs
pp rises in pulm capillary bed = push fluid into alveoli
inflammatory response

66
Q

What is HACE?

A

high altitude cerebral oedema

67
Q

Symptoms of HACE?

A

Confusion, loss of consciousness, rapid HR, breathlessness, Brain swelling -> coma -> Death

68
Q

Physiological consequences of HACE

A

Compromised BBB = large molecular movement into brain. Fluid + prot. acros BBB. CSF accumulation distorts brain structure.

69
Q

What is CMS?

A

Chronic mountain sickness

70
Q

Symptoms of CMS?

A

Loss of ability to survive at altitudes. Tinnitus,
palpitations
fatigue

71
Q

Who is most susceptible to CMS?

A

Middle aged men, long term residents of altitude (potentially to do with aging process)

Enviro (9 decks)

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