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physiology of high altitude Flashcards

1
Q

why is blood through the lungs less saturated with O2 at high altitudes?

A

High altitudes = low partial pressures of oxygen – lower driving force to attach O2 to Hb

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2
Q

what causes the physiological effects of altitude?

A

hypoxia

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3
Q

how is increased ventilation stimulated by low PaO2?

A

resulting hypoxaemia stimulates hypoxia detectors in the carotid bodies

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4
Q

what antagonises the hypoxia-driven hyperventilation?

A

antagonised by the more powerful decrease of ventilation
caused by excess blow off CO2 which causes alkalosis at the central chemoreceptors
which then inhibit the increase in respiratory drive

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5
Q

when is the hypoxic drive from carotid bodies significnt?

A

in moderate hypoxia (O2 below 60mmHg) and high pCO2

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6
Q

what is moderate hypoxia

A

O2 below 60mmHg

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7
Q

what type of ascent causes ill effects?

A

rapid ascent

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8
Q

what does rapid ascent to >2000m cause?

A

stimulats SNS to increase resting HR and CO and mildly increased BP

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9
Q

how does rapid ascent lead to mild pulmonary arterial hypertension?

A

low pO2 alveoli
pulmonary circulation reacts to the hypoxia with vasoconstriction
worsens hypoxaemia
pulmonary resistance increases bc the whole pulmonary circulation is increased –> mild pulmonary arterial hypertension

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10
Q

what is acclimatisation?

A

We adapt to high altitudes – initial pulmonary hypertension wears off and hypoxia disappears

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11
Q

how long does acclimatisation to 2000m take?

A

rapid

usually within a day or two

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12
Q

how long does acclimatisation from 2000m-6000m take and in who?

A

will occur in people without respiratory disease - may take a few weeks.

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13
Q

how will fully acclimatised climbers feel at 6000m? what tasks can they carry out?

A

fully acclimatised climbers may expect to feel well, have reasonable appetites, sleep normally and be capable of carrying loads of 20-25 kilos on easy ground

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14
Q

what happens to people at 7000m?

A

significant hypoxia is present. Feel more tired and lethargic. Continuous exercise becomes impossible. Climbing easy slopes becomes difficult

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15
Q

what heights are considered the death zone?

A

above 7500m

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16
Q

what happens to even acclimatised climbers in the death zone?

A

Acclimatised climbers have severe hypoxia and can only remain there for 2-3 days. After that the body’s major systems will show severe physiological damage.

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17
Q

what are the 3 components in the mechanism of acclimatisation?

A

1) Metabolic acidosis caused by acid retention and increased bicarbonate excretion in the kidneys
2) Increase in erythrocyte number (haematocrit)
3) Reduced pulmonary vascular resistance

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18
Q

what causes respiratory alkalosis during acclimatisation?

A
  • Low pO2 in inspired air stimulates increased rate and depth of breathing
  • Blows off excess CO2  respiratory alkalosis
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19
Q

how does metabolic acidosis occur during acclimatisation?

A
  • High pH from resp alkalosis inhibits central chemoreceptors  breathing decreases  hypoxaemia
  • Kidneys response to hypoxaemia by increasing bicarbonate excretion
  • Together w decreased acid excretion  metabolic acidosis
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20
Q

how is normoxia restored in acclimatisation?

A
  • Metabolic acidosis counteracts the respiratory alkalosis  pH restored
  • Drive to central chemoreceptors is restored
  • Now a sustained increase in rate and depth of breathing – restores normoxia
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21
Q

how is haematocrit increased in acclimatisation?

A

• Hypoxaemia also stimulates the interstitial cells in the kidney to raise EPO production  increases haematocrit  increases O2 carrying capacity of the blood

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22
Q

why is there a functional limit to increased haematocrit?

A

bc increased haematocrit increases blood viscosity –> increases PVR  pulmonary arterial hypertension  right heart failure

23
Q

why do athletes train at high altitudes?

A

Bc acclimitisation increases haematocrit, athletes train at high altitudes. Increase lasts for a few weeks  greater aerobic capacity

24
Q

why does PVR fall during acclimatisation?

A

o Reduced hypoxic vasoconstriction response
o Collateral circulations opening up between pulmonary arteries and veins

• Change occurs bc of an increased synthesis of NO in the pulmonary endothelium

25
Q

what happens if the ascent is too high/rapid and there isnt time for acclimatisation?

A

one or more forms of altitude sickness results;

  • acute mountain sickness
  • HACE: high altitude cerebral oedema
  • HAPE: high altitude pulmonary oedema
26
Q

what is the first form of altitude sickness that manifests?

A

acute mountain sickness

27
Q

what are signs and symptoms of AMS?

A 
Headache (essential for diagnosis)
•	Poor sleep
•	Tiredness
Loss of appetite, nausea, vomiting
•	Dizziness 
(similar to hangover symptoms)
28
Q

how do you score and diagnose AMS?

A

All scored 0-3 for severity of symptoms – need score of >3 for AMS diagnosis

29
Q

how do you treat AMS?

A

• If mild, rest (no further ascent)
•If more severe then:
o Immediate Descent
o Oxygen
o Acetazolamide 250mg tds (three times daily)
o Dexamethasone 4mg qds, (four times daily) oral or iv

30
Q

how can you prevent AMS?

A
  • Slow ascent (<300m per day over 3000m)
  • Avoid unnecessary exercise
  • Acetazolamide 250mg bd at start of climb
31
Q

what is acetazolamide?

A

carbonic anhydrase (CA) inhibitor that speeds up the process of acclimatisation

32
Q

why is carbonic anhydrase in the kidneys important?

A

• Carbonic anhydrase in PCT of kidney is vital for renal absorption of bicarbonate

33
Q

what does inhibition of carbonic anhydrase cause?

A

causes increased bicarbonate excretion  metabolic acidosis that compensates for respiratory alkalosis caused by hyperventilation at altitude

34
Q

what part of the body filters bicarbonate? where is it reabsorbed?

A

glomerulus

reabsorbed mainly in the PCT

35
Q

what ion is bicarbonate reabsorption linked to?

A

sodium

36
Q

explain the action of acetazolamide

A
  • Blocks conversion of bicarbonate to CO2 in the lumen so filtered bicarbonate stays in the tubule and is lost in the urine
  • Bc CA is blocked inside the cell, CO2 from the blood can’t be converted to bicarbonate.
  • So no H+ is available for the Na+/H+ ATP-ase – H+ aren’t pumped into the urine  Na+ isn’t reabsorbed
  • Na+ is excreted in the urine instead of protons
37
Q

what is the net effect of acetazolamide?

A

bicarbonate & sodium are lost in urine - not reabsorbed. The urine becomes alkaline and the blood becomes more acidic –> metabolic acidosis

38
Q

what do high doses of acetazolamide cause?

A

inhibit CA in RBCs; blocks transport of CO2 from tissues to lungs - decreases loss of CO2 in lungs,  tends to counteract excessive loss of CO2 from the body by hyperventilation

39
Q

what are symptoms of high altitude cerebral oedema?

A
  • Ataxia – key symptom!
  • Nausea/vomiting
  • Hallucination or disorientation
  • Confusion
  • Reduced conscious level
  • Coma – can lead to unconsciousness and death within 12hrs from onset of symptoms, but normally takes 1-2 days to develop
40
Q

why is a HACE coma so dangerous? how long does it take to develop?

A

can lead to unconsciousness and death within 12hrs from onset of symptoms, but normally takes 1-2 days to develop

41
Q

when should treatment be started for HACE?

A

at first sign of ataxia

42
Q

how should HACE be treated?

A

• Descend immediately - but a PAC (portable altitude chamber) bag will often be used first if available
• Acetazolamide - reduces formation of CSF so reduces intracranial pressure
• Oxygen – 2-4L/min oxygen
• Dexamethasone (Diamox) – corticosteroid widely used as an anti-inflammatory med. Prevents brain swelling.
o 8mg given as first dose
o 4mg then given every 6 hours orally or intravenously (prevents brain swelling)

43
Q

why is acetazolamide used to treat HACE?

A

reduces formation of CSF so reduces intracranial pressure

44
Q

what is dexamethasone?

A

corticosteroid widely used as an anti-inflammatory med. Prevents brain swelling.

45
Q

what does of Diamox should be given to treat HACE?

A

o 8mg given as first dose

o 4mg then given every 6 hours orally or intravenously (prevents brain swelling)

46
Q

why does HACE occur?

A
  • In hypoxaemia ATP supply in nerve cells decreases and Na+ pumps run down
  • Na+ leaks into nerve cells  draws in water  brain cells swell  increased ICP  cerebral veins blocked
  • Cerebral circulation fails  hypoxia gets worse  oxygen-deprived neurons are squashed and start to die
47
Q

what are signs and symptoms of high altitude pulmonary oedema?

A
  • Dyspnoea
  • Reduced exercise tolerance
  • Dry cough
  • Blood stained sputum
  • Crackles on auscultation of chest
48
Q

why does high altitude pulmonary oedema occur?

A
  • Hypoxic pulmonary vasoconstriction that occurs initially on ascent normally decreases with acclimatisation
  • If it doesn’t occur then pulmonary arterial hypertension can develop
  • Raised arterial and capillary pressure leads to fluid leaving the blood and entering the alveoli  pulmonary oedema
  • Worsens already compromised gas exchange
  • Increases hypoxia and increases constriction  vicious cycle occurs
49
Q

what is the treatment for HAPE?

A
  • Descend immediately
  • Sit patient upright
  • Oxygen
  • Nifedipine (calcium channel blocker) 20mg qds orally
  • Hyperbaric chamber
  • Sildenafil* (Viagra) – inhibits altitude-induced hypoxaemia and pulmonary hypertension
50
Q

what is Nifedipine and what is its effect?

A

(calcium channel blocker) helps block pulmonary artery constriction - reduces PAH.qw

51
Q

how does a hyperbaric chamber help?

A

increases PaO2 to improve oxygenation of blood and also reduce hypoxic vasoconstricton

52
Q

what is the effect of Sildenafil?

A

pulmonary hypoxic vasoconstriction bc of lack of NO being released from the pulmonary endothelium
o Slows down the breakdown of cyclic GMP (vasodilator produced by NO)
o Increasing cGMP levels with Viagra relaxes pulmonary arteries, stops PAH and improves blood oxygenation

53
Q

what is the difference between HACE and HAPE in terms of symptoms?

A

HACE is AMS with CNS symptoms

HAPE is AMS with pulmonary symptoms

c2 (37 decks)

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