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BMS: Physiology in the extreme > Hypobaric > Flashcards

Hypobaric Flashcards

1
Q

as you go up atmospheric pressure

A

decreases. (pp of oxygen also drops)

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2
Q

every 5500m the barometric (atmospheric pressure) falls by

A

half

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3
Q

big issue with altitude

A

reduction in oxygen availability

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4
Q

when you breath in you hudifiy the air the effect this has on oxygen partial pressure

A

reduces it (160-150mmHg)

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5
Q

inspired oxygen levels and alveoli oxygen levels

A

alveoli levels less as air already in lungs so fresh air is diluted

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6
Q

at higher altitudes you increase your

A

ventilation rate =
-so difference between alveoli and fresh air is lower
-

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7
Q

hypoxic

A

deficiency in amount of oxygen reaching tissues

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8
Q

pp of oxygen change around the body is around at sea level

A

60mmHg

100–>40 when it comes back to be reoxygenised at the lungs

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9
Q

at sea level at rest: Hb is ___ saturated with oxygen, when venous blood returns to the heart and enters pulmonary circulation Hb is __ saturated

A

97.5% –> 75%

So at rest body consumes 22.5% of the oxygen carried by Hb

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10
Q

At sea level: So at rest body consumes__% of the oxygen carried by Hb

A

22.5%

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11
Q

at 3000m at rest: alveolar pp of oxygen is ~60-65mmHg, Hb is __% saturated with Oxygen.
when venous blood returns to the heart and enters pulmonary circulation Hb is __ saturated

A

88% –> 65.5%

this equates to change of pp of oxygen of 60-33mmHg =27 mmHg

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12
Q

pp of oxygen change around the body is around at 3000m

A

60 -> 33 = 27 mmHg

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13
Q

the shape of oxygen-Hb curve helps _____ cals in arteriole Po2 at high altitude

A

minimise

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14
Q

early compensation and acclimatisation at high altitudes:

A

reduction in arteriol PO2–> stimulates peripheral chemoreceptors –> stimulates ventilation THIS HAS 3 IMMEDIATE EFFECTS
-over a few days -weeks acclimatisation takes places

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15
Q

stimulation of peripheral chemoreceptors –> stimulates ventilation;; 3 immediate effects:

A
  • minimises difference in alveolar PO2 and atmospheric PO2
  • hyperventilation leads to respiratory alkalosis (reduces effect on ventilation)
  • increase in cardiac output
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16
Q

short term acclimatisation takes places at high altitudes =

A
  • sustained higher ventilation rate (further reduction between alveolar and atmospheric PO2 and fall in PCO2)
  • linked to decrease in pH (plasma back to 7.4) of cerebrospinal fluid & changes in sensitivity of peripheral chemoreceptors to hypoxia
  • renal (kidney) compensations - reduced acid secretion, compensation for alkalosis
17
Q

what does the renal compensation of early acclimatisation lead to

A

bicarbonate loss in the urine and diuresis. Correction of the alkalosis further stimulates ventilation

18
Q

long term changes (acclimatisation)

A
  • INCREASE IN HAEMATOCRIT
  • -long term hypoxia leads to increase in the release of erythropoietin
  • -stimulation of RBC production in bone marrow
  • PULMONARY DIFFUSION CAPACITY
    • increased capillary blood volume (increase SA of capillaries in lungs)
  • -increase perfusion to upper regions of the lungs
  • INCREASE IN TISSUE CAPILLARY DENSITY
  • -angiogenesis in tissues, increasing SA for diffusion
  • OXIDATIVE ENZYMES
  • -stimualtion oxidative enzymes in mitochondria
19
Q

problems with increasing haematocrit

A

increase viscosity of blood, its thicker

20
Q

molecular basis of acclimatisation changes:

A

linked to stimulation of Hypoxia Induced Factors

  • HIF-1alpha
  • HIF-1beta
21
Q

Acute mountain sickness linked to

A

-linked to rapid ascent in altitude

22
Q

Acute mountain sickness: symptoms

A
  • headache, nausea, anorexia, malaise, lack of energy, disturbed sleep, occasionally vomiting
  • symptoms usually subside after 2-3 days
23
Q

Acute mountain sickness: CAUSES

A
  • increases in intracranial pressure
  • -opposing effect–> hypoxia will increase cerebral blood flow, hypocapnia (lack of CO2) will reduce cerebral flow (balance)
  • increase microvascular permeability linked to elevated plasma eicosanoids
24
Q

Acute mountain sickness: Prevention

A

slow ascent to high altitude

  • if altitude above 3000m u ascend 300m/day with rest days every 2/3 days
  • use of acetazolamide (inhibit/reduce bicarbonate reabsorpment by the kidney)
25
Q

Acute mountain sickness: TREATMENT

A
  • descend from altitude
  • take oxygen
  • many remain at altitude for 2/3 days to see if symptoms subside
26
Q

High altitude pulmonary oedema

A
  • increase in blood pressure in the lungs due to excess water
  • potentially lethal
27
Q

High altitude pulmonary oedema: symptoms

A

someone who has had AMS symptoms for a few days 1 in 200 people

  • -become breathless
  • cough - dry then ‘frothy’ contains blood (damage of alveoli)

-tachycardia (abnormal HR)

28
Q

High altitude pulmonary oedema causes:

A

increase in pulmonary arterial pressures, linked to pulmonary vasoconstriction

29
Q

High altitude pulmonary oedema treatment

A

rapid descent from altitude

  • adminitset oxygen
  • possibly use nidefipine or phosphodiesterase inhibitors
30
Q

High altitude cerebral oedema

A

-potentally lethal
-begins as severe AMS
-develops headaches and malaise progressing to ataxia, confusion, alters consciousness, coma
Cause: cerebral oedema (swelling in brain)
-treatment rapid descent
administer Oxygen

31
Q

Genetic changes: Tibetans

A

mutations help prevent CMS and help adapt to high altitudes

32
Q

Genetic changes: Tibetans 2 genes involved

A
  • EPAS1 encodes HIF2𝛂 - Stimulates erythropoiesis alters iron homeostasis, metabolism and vascular permeability
  • EGLN1 encodes prolyl hydroxylase domain-containing protein 2 (PHD2) – activity is dependent on oxygen levels.
33
Q

Genetic changes: Tibetans genes at normal oxygen

A

PHD2 acts to breakdown HIF2𝛂 and prevents overproduction of haemoglobin

34
Q

Genetic changes: Tibetans genes at hypoxia

A

PHD2 is inhibited, and then HIF2𝛂 levels rise and activates downstream responses.

BMS: Physiology in the extreme (9 decks)

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