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Physiology Of High Altitude Flashcards

(85 cards)

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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
What molecule is increased when adapting to hypoxaemia to shift oxygen dissociation curve to the right
2,3DPG
26
Main pH buffer system of the body
Bicarbonate buffer system
27
Bicarbonate buffer system equation
CO2 + H2O <—> H2CO203 <—> h+ + HCO3-
28
Where is carbonic anhydrase present
All cells
29
Is carbonic anhydrase found in plasma
No
30
What does carbonic anhydrase catalyse
Bidirectional conversion of CO2 + H2O into HCO3 + H+
31
What ion is plasma pH directly proportional to
HCO3-
32
What is plasma pH inversely proportional to
pCO2
33
What pH disturbance does hyperventilation cause
Respiratory alkalosis
34
How do kidneys respond to respiratory alkalosis
Decrease excretion of protons Decrease reabsorption of bicarbonate Increase excretion of bicarbonate
35
What does renal bicarbonate reabsorption do
Removes filtered bicarbonate from the tubular fluid and reabsorbed it
36
What happens to protons pumped into kidney tubules in renal bicarbonate reabsorption
React with bicarbonate filtered from blood forming CO2 and water
37
What happens to CO2 produced in kidney tubules in renal bicarbonate reabsorption
Diffuses back to tubule cell and converted back to bicarbonate
38
How is proton excretion from the kidneys effected by respiratory alkalosis
Decreased
39
Where are carbonic anhydrase levels down regulated in response to respiratory alkalosis
Kidney Tubular cells Kidney tubule lumen
40
Why is carbonic anhydrase down regulated in kidney tubular cells in response to respiratory alkalosis
Less CO2 converted to bicarbonate and protons -> less protons in tubular cell -> less protons excreted into urine
41
How are protons excreted from kidney tubular cells to urine
Sodium proton exchange ATPase in luminal wall
42
How does bicarbonate reabsorption change in response to respiratory alkalosis
Decrease
43
Where is carbonic anhydrase down regulated to decrease bicarbonate reabsorption Kidney tubular cells
Kidney Tubular lumen
44
Why is carbonate anhydrase decreased in kidney tubular lumen in response to respiratory alkalosis
Less bicarbonate converted to CO2 in tubule
45
What causes decreased pulmonary vascular resistance in acclimatisation to hypoxia
Reduced initial hypoxic vasoconstriction response Collateral circulations open between pulmonary arteries and veins
46
How does pulmonary resistance change in hypoxia at high altitude
Initially - increase Once acclimatised - decrease
47
What genetic aspects impact hypoxia acclimatisation
Activity of carbonic anhydrase Ability to make NO Ability to make 2,3-DPG
48
What causes AMS, HACE, and HAPE
Too rapid or high ascent without time for acclimatisation
49
Acute mountain sickness AMS
First sign of illness due to hypoxia
50
What conditions can follow on from acute mountain sickness
HACE high altitude cerebral oedema HAPE Hugh altitude pulmonary oedema
51
Acute mountain sickness symptoms
Headache Insomnia Fatigue Anorexia Nausea Vomiting Dizziness Lightheadedness
52
Which symptom is required for an acute mountain sickness diagnosis
Headache
53
What signs are found in a physical exam of a patient with acute mountain sickness
Usually none
54
What is needed for a diagnosis of acute mountain sickness
Headache Symptoms score >3
55
How likely is AMS after a rapid ascent to 1500-2000m above sea level
Unlikely
56
How likely is ams after a rapid ascent to 2500m above sea level
Fairly likely - 1 in 5 people
57
How likely is AMS after a rapid descent to 5000m above sea level
Extremely likely
58
Mild AMS treatment
Rest stop ascending
59
Severe AMS treatment
Immediate descent Oxygen Acetazolamide Dexamethasone
60
AMS prevention
Slow ascent Avoid unnecessary exercise Acetazolamide prophylaxis
61
What is Acetazolamide
Carbonic anhydrase inhibitor
62
How does Acetazolamide treat AMS
Speeds up carbonic anhydrase activity decrease occurring in acclimatisation
63
How does high doses of Acetazolamide decrease loss of CO2 from hyperventilation
Inhibits carbonic anhydrase in RBCs decreasing transport of CO2 to lungs
64
Dexamethasone
Corticosteroid to prevent brain swelling and inflammation
65
How can Dexamethasone be administered
Orally Intramuscular Intravenous
66
High altitude cerebral oedema symptoms
Worsening headache Photophobia Hallucinations Vomiting Difficulty speaking Confusion
67
Signs of high altitude cerebral oedema
Truncus ataxia Altered consciousness Seizures Coma
68
How does HACE happen
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
What raises intracranial pressure in HACE
Sodium leaks into brain cells bring water with it
70
HACE treatment
Descend immediately Dexamethasone Acetazolamide Oxygen Hyperbaric oxygen treatment
71
How does Acetazolamide treat HACE
Reduces cerebrospinal fluid volume decreasing intracranial pressure
72
HAPE symptoms
Dyspnoea Decr exercise tolerance Dry cough Haemoptysis Orthopnoea
73
Dyspnoea
Breathlessness
74
Haemoptysis
Coughing up blood
75
Orthopnoea
Dyspnoea when lying flat
76
HAPE signs
Tachypnoea Tachycardia Fever Rales on chest auscultation Mental status changes
77
Rales
Diffuse crackles in chest on auscultation
78
What causes HAPE
Initial hypoxic pulmonary vasoconstriction doesn’t decrease -> pulmonary arterial hypertension -> fluid moves from blood to alveoli -> pulmonary oedema -> worsens hypoxia and vasoconstriction
79
How does HAPE form a vicious cycle
Pulmonary oedema further worsens gas exchange causing more hypoxia which causes more vasoconstriction and more hypoxia
80
HAPE treatment
Descend immediately Sit patient upright Oxygen Acetazolamide Dexamethasone Nifedipine Hyperbaric o2 chamber Sildenafil
81
Nifedipine
Calcium channel blocker
82
How do nifedipine and Sildenafil help HAPE
Relax smooth muscle decreasing vascular resistance
83
Sildenafil
Increases cGMP levels and decreases intracellular calcium -> relax smooth muscle VIAGRA
84
Long term adaptations to hypoxia
Incr erythropoietin Incr Hb Incr capillary density
85
Adaptations to hypoxia
Incr 2,3-DPG hyperventilation Decr renal bicarbonate reabsorption Decr renal proton excretion

CR2 (33 decks)

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