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Cardiorespiratory CC > Physiology of high altitude > Flashcards

Physiology of high altitude Flashcards

1
Q

Partial pressure O2 at high altitudes

A

Less

“driving force” to attach O2 to haemoglobin less

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2
Q

Blood in lungs at high altitudes

A

Less saturated with O2

–> pulmonary hypoxia + hypoxaemia

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3
Q

Ventilation is mainly regulated by

A

PaCO2

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4
Q

PaCO2 at altitude

A

Kept constant by body

BUT body becomes hypoxic because of lower partial pressure of O2

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5
Q

Hypoxic drive

A

Hypoxic drive cannot overcome inhibition by hypercapnic drive

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6
Q

Physiological effects of ascent to altitude are due to

A

Hypoxia

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7
Q

Physiological effects at high altitude

A

Low partial pressure of O2 + resulting hypoxaemia will stimulate increased ventilation via hypoxia detectors in carotid bodies
BUT hypoxia-driven ventilation response partially antagonised by more powerful depression of ventilation caused by excess blow off of CO2
–> alkalosis at central chemoreceptors
–> then inhibit the increase in resp. drive

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8
Q

Ventilatory response at high altitude

A

Inadequate to cope with the low pO2 and a degree of hypoxaemia + hypoxia results

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9
Q

Hypoxic drive from carotid bodies

A

Weak

Normally only becomes significant at PO2 below about 60mmHg

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10
Q

Hypoxic drive significance

A

Only significant in low pO2 together with high pCO2

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11
Q

Rapid ascent to 2000m+

A

Stimulates SNS
Increased resting HR + CO
Mildly increased BP

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12
Q

Rapid ascent 2000m+ after minutes of exposure

A

PO2 in alveoli is low, so pulmonary circulation reacts to hypoxia with vasoconstriction
–> worsens hypoxaemia

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13
Q

Pulmonary resistance rapid ascent 2000m+

A

Increases

–> mild pulmonary arterial hypertension

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14
Q

Acclimatisation

A

Adapting to high altitude

Initial pulmonary arterial hypertension wears off + hypoxia disappears

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15
Q

Acclimatisation from sea level –> 2000m

A

Rapid

Day or two

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16
Q

Acclimatisation from sea level –> 2000-6000m

A

Occur in people without respiratory disease

May take few weeks

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17
Q

Fully acclimatised climbers at 6000m

A

Feel well
Reasonable appetites
Sleep normally
Capable of carrying loads of 20-25kg on easy ground

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18
Q

Above 7000m

A

Significant hypoxia
Tiredness + lethargy increases
Continuous exercise impossible
Climbing easy slopes painstaking + breathless

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19
Q

Above 7500m

A

Death zone
Even acclimatised climbers have severe hypoxia + can only remain 2 or 3 days
–> after that body’s major symptoms will have severe physiological damage

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20
Q

Mechanism of Acclimatisation

A

Metabolic acidosis caused by retention of acid + increased excretion of bicarbonate in kidneys
Increase in erythrocyte number
Reduced pulmonary vascular resistance

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21
Q

Acclimatisation MOA

A

Low pO2 in inspired air increases rate + depth of breathing
BUT blows off excess CO2 + produces respiratory alkalosis
–> high pH inhibits central chemoreceptors
–> decreased breathing
–> hypoxia

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22
Q

Acclimatisation MOA Pt 2 (kidneys)

A

Kidneys respond to hypoxaemia by increasing bicarbonate excretion
Decreased excretion of acid
–> metabolic acidosis
Metabolic acidosis counteracts the respiratory alkalosis
–> restores pH to normal
Drive to central chemoreceptors restored –> sustained increase in rate and depth of breathing to restore normoxia

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23
Q

Hypoxia during acclimatisation

A

Stimulates interstitial cells in kidney to raise EPO

–> increases haematocrit –> increases O2 carrying capacity of blood

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24
Q

Haematocrit maximum

A

Functional limit to max haematocrit
Increased haematocrit = increased blood viscosity
Higher viscosity –> higher pulmonary vascular resistance –> pulmonary arterial hypertension + right sided heart failure

25
Q

Pulmonary vascular resistance during acclimatisation

A

Pulmonary vascular resistance falls
Partially due to reduced hypoxic vasoconstriction response
Partly due to collateral circulations opening up between pulmonary arteries + veins

26
Q

Increased synthesis of NO in pulmonary endothelium

A

Causes collateral circulations to open up between pulmonary arteries + veins

27
Q

Acute Mountain Sickness

A

First sign that something is wrong

28
Q

High Altitude Cerebral oedema

A

Can follow is AMS untreated
Serious neurological condition
Fatal if not treated

29
Q

High Altitude Pulmonary Oedema

A

Equally serious to HACE

Can follow on from AMS

30
Q

AMS signs + symptoms

A 
Headache
Poor sleep
Tiredness
Loss of appetite, nausea, vomiting
Dizziness

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

Like symptoms of hangover

31
Q

1500-2000m rapid ascent from sea level AMS

A

Unlikely in most individuals

Mild illness

32
Q

2500m rapid ascent from sea level AMS

A

1 in 5 people have symptoms if ascend within a day

Most ppl will acclimatise within a day or so

33
Q

5000m rapid ascent from sea level AMS

A

Everyone temporarily ill if ascend within few hours to 5000m (e.g. plane)
Acclimatisation can take several days or more

34
Q

AMS Treatment Mild

A

Rest

No further ascent

35
Q

AMS Treatment Severe

A

Immediate descent
O2
Acetazolamide 250mg (3x day)
Dexamethasone 4mg (4x daily) oral or IV

36
Q

AMS Prevention

A

Slow ascent- <300m per day over 3000m
Avoid unnecessary exercise
Acetazolamide 250mg 2x day at start of climb

37
Q

Acetazolamide (Diamox)

A

Carbonic anhydrase inhibitor

38
Q

Carbonic anhydrase

A

In proximal tubule of kidney

Vital for renal reabsorption of bicarbonate

39
Q

Acetazolamide MOA

A

Inhibits CA activity
Increases bicarbonate excretion –> metabolic acidosis
Compensates for the respiratory alkalosis caused by the hyperventilation at altitude

40
Q

Acetazolamide MOA compared to normal

A

Kidneys produce metabolic acidosis anyway as part of acclimatisation
–> Diamox speeds up process

41
Q

Bicarbonate reabsorption Pt 1

A

CO2 diffuses from blood into proximal tubule cells
Converted into carbonic acid (H2CO3) by Carbonic Anhydrase A inside the cells
H2CO3 –> H+ and HCO3-
Protons formed are ejected into tubular lumen by a Na+/H+ exchange ATPase
–> sodium reabsorbed from tubular fluid + protons ejected into it
–> bicarbonate collects in cell

42
Q

Bicarbonate reabsorption Pt 2

A

Excreted protons react with bicarbonate which has been filtered by glomerulus
The two ions are converted to CO2 + water by CA lining the tubule
CO2 diffuses back into tubule cell where converted back into carbonic acid (H2CO3)
–> bicarbonate is reabsorbed from tubule into tubular cells

43
Q

Bicarbonate reabsorption part 3

A

CO2 that has diffused back into cell then converted back to H2CO3 by CA inside tubular cells
H2CO3 –> H+ and HCO3-
Protons pumped out to continue the reabsorption cycle
HCO3- transferred from tubular cells back into blood

44
Q

Acetazolamide

A

Conversion of HCO3- to CO2 in lumen is blocked

–> filtered bicarbonate is lost in urine

45
Q

CA blocked inside cell

A

CO2 from blood can’t be converted to HCO3-

  • -> no H+ available for the Na+/H+ ATP-ase
  • -> protons not pumped into urine + Na+ not reabsorbed
  • -> Na+ excreted in urine instead of H+
46
Q

Acetazolamide net effect

A

Bicarbonate + Na+ lost in urine
Urine becomes alkaline
Blood becomes more acid

47
Q

High levels of acetazolamide

A

Also inhibit CA in erythrocytes
Blocks transport of CO2 from tissues –> lungs
–> decreases loss of CO2 in lungs
–> counteracts excessive loss of CO2 from body by hyperventilation

48
Q

High altitude cerebral oedma (HACE) Symptoms

A 
Can follow AMS if AMS left untreated
Ataxia
Nausea/vomiting
Hallucination or disorientation
Confusion
Reduced conscious level
Coma
49
Q

HACE MOA

A

In hypoxaemia, supply of ATP in nerve cells decreases + sodium pumps run down
Sodium leaks into nerve cell –> pulls water with it + brain swells
Raises ICP + blocks cerebral veins
Cerebral circulation fails, hypoxia gets worse + neurones die (starved of O2 + squished)

50
Q

HACE treatment

A

Descend immediately
Acetazolamide (reduces formation of CSF so decreases ICP)
O2
Dexamethasone 8mg then 4mg 4x day orally or IV (prevents brain swelling)
Hyperbaric chamber

51
Q

High altitude pulmonary oedema (HAPE) sings + symptoms

A 
Dyspnoea
Reduced exercise tolerance
Dry cough
Blood stained sputum
Crackles on chest ausculation
52
Q

HAPE MOA

A

Hypoxic pulmonary vasoconstriction normally decreases with acclimatization
–> if doesn’t occur, pulmonary arterial hypertension can develop
Raised arterial + capillary pressure –> fluid leaving blood + entering alveoli
–> worsens already compromised gas exchange
–> increases hypoxia + constriction
–> VISCIOUS CYCLE

53
Q

HAPE treatment

A

Descend immediately
Sit patient upright
O2
Nifedipine (Ca channel blocker) 20mg 4x day
Hyperbaric chamber
Viagra (inhibits altitude-induced hypoxaemia + pulmonary hypertension)

54
Q

Nifedipine

A

Blocks constriction of pulmonary arteries

–> reduces PAH

55
Q

Hyperbaric chamber

A

Increases partial pressure of O2 to improve oxygenation of blood
Reduces hypoxic vasoconstriction

56
Q

Viagra

A

Slows down breakdown of cyclic GMP, which is the vasodilator produced by NO
Increases cGMP levels relaxes pulmonary arteries, stops PAH + improves O2 oxygenation

57
Q

Pulmonary hypoxic vasoconstriction

A

Due to lack of NO being released from pulmonary endothelium

58
Q

HACE + HAPE symptoms

A 
HACE= AMS with CNS symptoms
HAPE= AMS with pulmonary symptoms

Cardiorespiratory CC (34 decks)

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