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CR2 > Physiology Of High Altitude > Flashcards

Physiology Of High Altitude Flashcards

1
Q

Partial pressure driving o2 uptake at sea level

A

9.5 kPa

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2
Q

Why is a difference in partial pressure of oxygen needed between alveoli and pulmonary capillaries

A

Allow o2 to diffuse on capillary blood

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3
Q

Why does partial pressure of o2 decrease between inhalation and reaching alveoli

A

Addition of water vapour
Mixing w ‘old’ alveolar gas

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4
Q

How does atmospheric partial pressure change as altitude increases

A

Decreases

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5
Q

Why does oxygen partial pressure decrease with altitude

A

Decreased atmospheric pressure

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6
Q

What causes gas pressure

A

Collisions of gas particles + container walls

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7
Q

How does increasing CO2 effect response to hypoxaemia

A

Increases response

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8
Q

Is PaCO2 high or low at high altitude

A

Low

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9
Q

Where are receptors detecting hypoxaemia

A

Carotid bodies

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10
Q

What is the first adaptation to hypoxaemia

A

Hyperventilation

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11
Q

Is hypoxaemia detected by peripheral or central receptors

A

Peripheral - carotid bodies

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12
Q

Why do central nervous chemoreceptors depress hypoxaemia driven hyperventilation

A

Hyperventilation -> excess blow off CO2 -> alkalosis at central chemoreceptors -> depress respiratory drive

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13
Q

How does adaptation to altitude effect central chemoreceptors

A

Receptors reset to decr depression of hyperventilation

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14
Q

Which nervous system is stimulated by hypoxaemia

A

Sympathetic

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15
Q

Which response to hypoxaemia is maladaptive

A

Pulmonary vasoconstriction

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16
Q

Why does pulmonary vasoconstriction occur in hypoxaemia

A

Ventilation-perfusion matching mechanism due to low alveolar ppO2

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17
Q

Why is pulmonary vasocontriction in response to hypoxaemia maladaptive, and when is it effective

A

All of lung effected
Effective when only part of lung damaged so perfusion decreases in badly ventilated area

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18
Q

What happens first in high altitude - acclimatisation or adaptation

A

Adaptation

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19
Q

What is the first step in acclimatisation to hypoxia

A

Plasma volume gradually decreases 10-25%

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20
Q

Why does plasma volume decrease in acclimatisation to hypoxaemia

A

Temporarily increases haematocrit

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21
Q

How is RBC production increased in acclimatisation to hypoxaemia

A

Erythropoietin released from kidney interstitial cells

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22
Q

Why is there a functional limit to haematocrit

A

Increased haematocrit increases blood viscosity, increasing pulmonary vascular resistance

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23
Q

What does oxygen dissociation curve show

A

How easily Hb takes up or releases O2

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24
Q

How does acute hyperventilation and respiratory alkalosis shift the oxygen dissociation curve

A

Left

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25
Q

What molecule is increased when adapting to hypoxaemia to shift oxygen dissociation curve to the right

A

2,3DPG

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26
Q

Main pH buffer system of the body

A

Bicarbonate buffer system

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27
Q

Bicarbonate buffer system equation

A

CO2 + H2O <—> H2CO203 <—> h+ + HCO3-

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28
Q

Where is carbonic anhydrase present

A

All cells

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29
Q

Is carbonic anhydrase found in plasma

A

No

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30
Q

What does carbonic anhydrase catalyse

A

Bidirectional conversion of CO2 + H2O into HCO3 + H+

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31
Q

What ion is plasma pH directly proportional to

A

HCO3-

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32
Q

What is plasma pH inversely proportional to

A

pCO2

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33
Q

What pH disturbance does hyperventilation cause

A

Respiratory alkalosis

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34
Q

How do kidneys respond to respiratory alkalosis

A

Decrease excretion of protons
Decrease reabsorption of bicarbonate
Increase excretion of bicarbonate

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35
Q

What does renal bicarbonate reabsorption do

A

Removes filtered bicarbonate from the tubular fluid and reabsorbed it

36
Q

What happens to protons pumped into kidney tubules in renal bicarbonate reabsorption

A

React with bicarbonate filtered from blood forming CO2 and water

37
Q

What happens to CO2 produced in kidney tubules in renal bicarbonate reabsorption

A

Diffuses back to tubule cell and converted back to bicarbonate

38
Q

How is proton excretion from the kidneys effected by respiratory alkalosis

A

Decreased

39
Q

Where are carbonic anhydrase levels down regulated in response to respiratory alkalosis

A

Kidney Tubular cells
Kidney tubule lumen

40
Q

Why is carbonic anhydrase down regulated in kidney tubular cells in response to respiratory alkalosis

A

Less CO2 converted to bicarbonate and protons -> less protons in tubular cell -> less protons excreted into urine

41
Q

How are protons excreted from kidney tubular cells to urine

A

Sodium proton exchange ATPase in luminal wall

42
Q

How does bicarbonate reabsorption change in response to respiratory alkalosis

A

Decrease

43
Q

Where is carbonic anhydrase down regulated to decrease bicarbonate reabsorption
Kidney tubular cells

A

Kidney Tubular lumen

44
Q

Why is carbonate anhydrase decreased in kidney tubular lumen in response to respiratory alkalosis

A

Less bicarbonate converted to CO2 in tubule

45
Q

What causes decreased pulmonary vascular resistance in acclimatisation to hypoxia

A

Reduced initial hypoxic vasoconstriction response
Collateral circulations open between pulmonary arteries and veins

46
Q

How does pulmonary resistance change in hypoxia at high altitude

A

Initially - increase
Once acclimatised - decrease

47
Q

What genetic aspects impact hypoxia acclimatisation

A

Activity of carbonic anhydrase
Ability to make NO
Ability to make 2,3-DPG

48
Q

What causes AMS, HACE, and HAPE

A

Too rapid or high ascent without time for acclimatisation

49
Q

Acute mountain sickness AMS

A

First sign of illness due to hypoxia

50
Q

What conditions can follow on from acute mountain sickness

A

HACE high altitude cerebral oedema
HAPE Hugh altitude pulmonary oedema

51
Q

Acute mountain sickness symptoms

A

Headache
Insomnia
Fatigue
Anorexia
Nausea
Vomiting
Dizziness
Lightheadedness

52
Q

Which symptom is required for an acute mountain sickness diagnosis

A

Headache

53
Q

What signs are found in a physical exam of a patient with acute mountain sickness

A

Usually none

54
Q

What is needed for a diagnosis of acute mountain sickness

A

Headache
Symptoms score >3

55
Q

How likely is AMS after a rapid ascent to 1500-2000m above sea level

A

Unlikely

56
Q

How likely is ams after a rapid ascent to 2500m above sea level

A

Fairly likely - 1 in 5 people

57
Q

How likely is AMS after a rapid descent to 5000m above sea level

A

Extremely likely

58
Q

Mild AMS treatment

A

Rest
stop ascending

59
Q

Severe AMS treatment

A

Immediate descent
Oxygen
Acetazolamide
Dexamethasone

60
Q

AMS prevention

A

Slow ascent
Avoid unnecessary exercise
Acetazolamide prophylaxis

61
Q

What is Acetazolamide

A

Carbonic anhydrase inhibitor

62
Q

How does Acetazolamide treat AMS

A

Speeds up carbonic anhydrase activity decrease occurring in acclimatisation

63
Q

How does high doses of Acetazolamide decrease loss of CO2 from hyperventilation

A

Inhibits carbonic anhydrase in RBCs decreasing transport of CO2 to lungs

64
Q

Dexamethasone

A

Corticosteroid to prevent brain swelling and inflammation

65
Q

How can Dexamethasone be administered

A

Orally
Intramuscular
Intravenous

66
Q

High altitude cerebral oedema symptoms

A

Worsening headache
Photophobia
Hallucinations
Vomiting
Difficulty speaking
Confusion

67
Q

Signs of high altitude cerebral oedema

A

Truncus ataxia
Altered consciousness
Seizures
Coma

68
Q

How does HACE happen

A

ATP supply decreases -> sodium pumps run down -> Na leaks into nerve cells -> water follows causing swelling + intracranial pressure incr -> cerebral veins blocked -> neurons die -> dead neurons release ions and fluids worsening oedema

69
Q

What raises intracranial pressure in HACE

A

Sodium leaks into brain cells bring water with it

70
Q

HACE treatment

A

Descend immediately
Dexamethasone
Acetazolamide
Oxygen
Hyperbaric oxygen treatment

71
Q

How does Acetazolamide treat HACE

A

Reduces cerebrospinal fluid volume decreasing intracranial pressure

72
Q

HAPE symptoms

A

Dyspnoea
Decr exercise tolerance
Dry cough
Haemoptysis
Orthopnoea

73
Q

Dyspnoea

A

Breathlessness

74
Q

Haemoptysis

A

Coughing up blood

75
Q

Orthopnoea

A

Dyspnoea when lying flat

76
Q

HAPE signs

A

Tachypnoea
Tachycardia
Fever
Rales on chest auscultation
Mental status changes

77
Q

Rales

A

Diffuse crackles in chest on auscultation

78
Q

What causes HAPE

A

Initial hypoxic pulmonary vasoconstriction doesn’t decrease -> pulmonary arterial hypertension -> fluid moves from blood to alveoli -> pulmonary oedema -> worsens hypoxia and vasoconstriction

79
Q

How does HAPE form a vicious cycle

A

Pulmonary oedema further worsens gas exchange causing more hypoxia which causes more vasoconstriction and more hypoxia

80
Q

HAPE treatment

A

Descend immediately
Sit patient upright
Oxygen
Acetazolamide
Dexamethasone
Nifedipine
Hyperbaric o2 chamber
Sildenafil

81
Q

Nifedipine

A

Calcium channel blocker

82
Q

How do nifedipine and Sildenafil help HAPE

A

Relax smooth muscle decreasing vascular resistance

83
Q

Sildenafil

A

Increases cGMP levels and decreases intracellular calcium -> relax smooth muscle
VIAGRA

84
Q

Long term adaptations to hypoxia

A

Incr erythropoietin
Incr Hb
Incr capillary density

85
Q

Adaptations to hypoxia

A

Incr 2,3-DPG
hyperventilation
Decr renal bicarbonate reabsorption
Decr renal proton excretion

CR2 (33 decks)

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