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HUMB3001 > W6 - Altitude > Flashcards

W6 - Altitude Flashcards

1
Q

Describe change to barometric pressure with altitude?

A

Decreases exponentially as altitude increases

Approx halved every 5450m ascent

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2
Q

What is change to PO2 at altitude?

A

Alveolar and arterial PO2 fall
Causing hypoxic hypoxia

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3
Q

Why is decrease in arterial PO2 greater than decrease in ambient PO2?

A

Inspired air is always saturated with water vapour (47 mmHg)

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4
Q

What is PO2 of moist inspired air at 5450m?

A

PO2 = 380-47 x 0.21 = 70 mmHg

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5
Q

What is PO2 at Mt Everest summit?

A

Altitude 8848m, P=253mmHg
PO2 = 43 mmHg

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6
Q

Describe pressure and altitude experienced during air travel.

A

Modern aircraft travel at altitude of 10-11km
Passengers not exposed to this
Cabin is maintained at pressure equivalent to altitude of 1900-2500m

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7
Q

What happens if cabin pressurisation system fails?

A

Rapid decompression
Hypoxia is so severe - causes unconsciousness and death
Useful consciousness lasts for 40s

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8
Q

What is AMS?

A

Acute mountain sickness

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9
Q

When does AMS occur?

A

Rapid exposure to altitudes 3000-6000m

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10
Q

What are symptoms of rapid exposure to 4000m?

A

Hypoxia causes cerebral hypoxia
Deterioration of sensory acuity, judgement, speed of response, manual dexterity

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11
Q

What are the 4 steps of oxygen cascade?

A

Alveolar ventilation
Pulmonary oxygen diffusion
Transport of O2 in blood
Tissue diffusion

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12
Q

Describe change in PO2 during oxygen cascade?

A

Decrease in PO2 at each stage
Total pressure gradient from inspired air to mixed venous blood of 120 mmHg

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13
Q

What is effect of acclimitisation to altitude on O2 cascade?

A

Decrease in slope of oxygen cascade so mixed venous PO2 is little changed

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14
Q

What is LAN?

A

Lower altitude native

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15
Q

What is HAN

A

High altitude native

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16
Q

Is acclimitisation the same in LAN as HAN?

A

Acclimitisation seen in longer term visitors is different from acquired acclimitisation seen in person born and bred at altitude

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17
Q

What causes decrease in slope of O2 cascade niacclimitisation?

A

Reduction in PO2 difference between inspired and alveolar air

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18
Q

What is effect of altitude > 3000m on newly arrived visitor?

A

Hyperventilation
As alveolar PO2 falls to 65 mmHg

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19
Q

What altitude does hyperventilation reach maximum?

A

6000m

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20
Q

What causes hyperventilation at altitude?

A

Stimulation of peripheral chemoreceptors of carotid and aortic bodies by fall in arterial PO2

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21
Q

What is effect of hyperventilation?

A

Increases alveolar ventilation
Reduces fall in PaO2, PalvO2
Increased loss of CO2
Decrease PaCO2 and PalvCO2

Respiratory alkalosis, arterial pH increase

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22
Q

What causes respiratory alkalosis?

A

Hyperventilation

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23
Q

When does arterial pH rise?

A

Hyperventilation causes decrease in PCO2 in alveolar and arterial blood

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24
Q

What is effect of hyperventilation on CSF?

A

PaCO2 causes fall in PCO2 in CSF
Inhibits ventilation

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25
Q

What are the competing influences during initial exposure to hypoxic conditions

A

Fall in PaO2 stimulating ventilation
Fall in PaCO2 (drop in [H+]) inhibiting ventilation

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26
Q

Why is increase in ventilation not seen below 3000m altitude?

A

Competing influences of PaO2 and PaCO2 both dropping

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27
Q

What happens at altitudes between 3000-6000m to ventilation?

A

Drive to ventilation from peripheral chemoreceptors is greater than brake from central chemoreceptors

PaO2 falls to 60mmHg

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28
Q

How long does it take for secondary rise in ventilation to reach maximum increase?

A

1-2 weeks
Stays as long as visitor stays in altitude

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29
Q

What compensates for the decrease in PaCO2?

A

Arterial respiratory alkalosis is compensated for by renal excretion of HCO3-

Too slow to account for rate at which ventilation rises

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30
Q

What happens to sensitivity to CO2 once acclimitisation has occurred?

A

Respiratory system is more sensitive to CO2 so respiratory centres respond to lower PCO2

Respiratory system behaves as through been reset to run at lower PaCO2

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31
Q

Compare ventilation rate between HAN and LAN.

A

HANs have ventilation rate that is 20% less than in acclimatised visitors

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32
Q

Why do HAN have lower ventilation rate?

A

Reduced pulmonary work decreases energy and O2 demands

HAN uses less energy consuming methods to compensate for hypoxic conditions - efficient pulmonary gas exchange

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33
Q

What is effect of increased ventilation on O2?

A

Increases PaO2 and incr driving pressure for oxygen transfer to pulmonary capillary blood

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34
Q

How is pulmonary O2 diffusing capacity increased?

A

Increase alveolar surface area in contact with functioning pulmonary capillaries

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35
Q

Describe pulmonary diffusing capacity in HAN?

A

Capacity in HAN is greater at rest (20-30%)

Much reduced PaO2 - PalvO2 gradient

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36
Q

What are characteristics of HANs?

A

Barrel shaped chest with incr lung volumes (esp residual volumes)

Alveoli are larger and greater in number than LANs of similar stature

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37
Q

Describe pulmonary blood volume in HANs.

A

Increases in pulmonary blood volume
Increased diffusing capacity

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38
Q

Describe pulmonary arterial pressure in HANs.

A

Increase in pulmonary arterial pressure leads to opening of larger number of pulmonary capillaries = recruitment

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39
Q

Describe erythrocyte count in HAN and LAN visitor.

A

Increase in erythrocyte count = polycythaemia

40
Q

What is polycythaemia?

A

Increase in erythrocyte (RBC) count

41
Q

What is impact of altitude on haemoglobin?

A

Concentration in Hb rises due to incr in erythrocyte count

Small proportion of rise is due to small fall in plasma volume

Increases linearly up to 3700m but then increases more rapidly

42
Q

What causes increase in Hb?

A

Increased secretion of EPO resulting from decrease in PaO2 detected by kidneys

43
Q

Describe timing of Hb increase.

A

Lag between EPO and RBC production
RBC does not start to rise till 3-5d of altitude exposure
Takes weeks to develop

44
Q

What is effect of increased Hb on oxygen?

A

Increases oxygen carrying capacity of blood
Ensures arterial oxygen content is maintained at/above value at sea level

If SaO2 falls below 70%, arterial oxygen content declines

45
Q

What is SaO2?

A

Arterial oxygen saturation
Saturation of haemoglobin

46
Q

What happens to CO and circulation in visitors at altitude during first few hours/days?

A

Increase in HR
Variable stroke volume resulting in +- increase in cardiac output

47
Q

Cardiac output formula

A

CO = HR x SV

48
Q

What is effect of cardiac output on visitors at altitude after several days?

A

CO at rest is equal to/slightly above that at seal level

HR remains elevated, SV decreased

49
Q

Describe blood flow distribution in visitors at altitude?

A

Redistribution of blood flow so that vital organs receive larger proportion of CO than at sea level

Distributed away from gut and skin

Coronary blood flow increase on first exposure to altitude (vasodilatory effect of hypoxia)

50
Q

What happens to coronary blood flow after 10 days at altitude by LAN?

A

Coronary blood flow fell by 30%
Oxygen uptake by myocardium maintained by 28% increase in O2 extraction

51
Q

Describe coronary blood flow in HAN?

A

Diminished by 30%
Partly compensated by increased vascularisation of myocardium

52
Q

What is P50 of O2-Hb curve at sea level?

A

50% haemoglobin saturated at PO2 of 26-28 mmHg

53
Q

Describe change in O2-Hb curve at altitude of acclimitised visitor or HAN.

A

Right shift of O2-Hb curve

Rise in P50 (31mmHg after 3 days of altitude)

54
Q

What is impact of right shift in O2-Hb curve?

A

Aids unloading of oxygen from blood in tissues

Attributed to increased concentration of 2,3-BPG in erythrocytes (induced by respiratory alkalosis)

Hinders O2 loading

55
Q

Describe the studies that indicate respiratory alkalosis is not fully compensated for at altitude.

A

Blood remains slightly alkaline

Cause decrease in P50 = left shift of O2-Hb curve

Some studies so no change in P50

56
Q

How does oxygen move from capillary blood to mitochondria?

A

Simple diffusion

Rate is determined by PO2 gradient and distance, SA over which diffusion occurs (Fick’s law)

57
Q

What happens to tissues at altitude?

A

Increased capillarisation of tissues

Aids oxygen diffusion to tissues by decreasing diffusion distance

58
Q

Describe density of functional capillaries when acclimatised at altitude.

A

Increased density of functional capillaries observed in mammalian species acclimatised at altitude especially in cerebral cortex, myocardium, skeletal muscle

59
Q

Describe relationship between capillary density, muscle fibre and body weight.

A

Inverse relationship between capillary density and muscle fibre CSA

Linear relationship between muscle fibre CSA and body weight

Therefore decreased body weight = increased capillary density

60
Q

How do some animals adapt rather than acclimatise?

A

Compensation for hypoxia by increasing extraction of oxygen from blood at tissues

More efficient utilisation of oxygen

Left ward shift of O2-Hb curve

61
Q

What is the main adaptive process which allowed ascent to extreme altitudes?

A

Increase in ventilation

62
Q

Describe relationship between CO and O2 consumption during exercise at altitude.

A

Normal linear relationship between CO and O2 consumption

Maximal cardiac outputs are decreased

VO2max never reaches value obtained at sea level

Diffusion limitation across alveolar capillary membranes

Increasing altitude = progressive fall in SaO2 during exercise

63
Q

Describe lactate paradox in HANs during maximal exercise at altitude.

A

During maximal exercise at altitude, rise in blood lactate concentration is not as great as in maximal exercise at sea level

In HAN, lactate paradox persists for 6 weeks at sea level suggesting developmental/genetic change

Decreased blood lactate due to decreased release of lactate by exercising muscle

64
Q

What does alveolar hypoxia induce?

A

Induces vasoconstriction in small arteries/arterioles of pulmonary circulation

Leads to incr in pulmonary vasc resistance = pulmonary arterial hypertension

65
Q

Which type of people have mild pulmonary hypertension at rest and marked at exercise?

A

Long term visitor at altitude and HANs

66
Q

Describe children born at altitude.

A

Generally low birth weight, reduced in body size and growth rate at all postnatal ages

Due to hypoxia, poor nutritional status, socio-economic conditions

67
Q

Why do children born at altitude and HANs don’t have reduced lung size?

A

Growth of lungs is stimulated by hypoxia

Larger lung volume and vital capacity = advantage of oxygen diffusing capacity

Children of sea level ancestry raised at altitude also have increased lung capacity

68
Q

Describe effect of altitude on foetus.

A

Predicted: foetus at altitude will suffer hypoxia

Maternal hyperventilation & incr Hb concentration found during pregnancy so arterial oxygen content was as high as pregnant women at sea level

69
Q

What changes are visible in placental morphology at altitude?

A

Increased vascularity, shortening of diffusion distances, reduction in oxygen diffusion gradient between mother and foetus

70
Q

What hormones are secreted during hypoxia?

A

Stress hormones; adrenal glucocorticoids, catecholamines

71
Q

Describe thyroid hormone levels of long term visitors and HANs.

A

Increased T4, T3 levels

72
Q

Describe impact of altitude on aldosterone and ADH.

A

Increased RBC and blood volume result in decreased secretion of aldosterone (decr Na+) and vasopressin/ADH (decr H2O)

Increased natriuresis (Na+ secretion) and diuresis (water secretion)

73
Q

List the 4 pathophysiological changes that can happen at altitude.

A

Acute mountain sickness

High altitude pulmonary oedema

High altitude cerebral oedema

Chronic mountain sickness

74
Q

When does AMS occur and what are symptoms?

A

People who ascend to >2500m rapidly

Headache, nausea, vomit, insomnia, poor appetite, muscle weakness

Appears in 8-24h but can be delayed by 4d

75
Q

What is prevalence of AMS?

A

3000m, 30% show symptoms

>4500m, 75% show symptoms

76
Q

When do AMS symptoms decline?

A

3-7 days

77
Q

What is primary stimulus to AMS?

A

Hypoxic conditions

78
Q

Describe role of fluid retention in AMS.

A

On ascent, increased secretion of ADH + adrenal corticoids = fluid retention

Blood shunted from periphery, accumulation of fluid in lungs, GIT, brain

Organs become mildly oedematous

79
Q

How do you prevent AMS?

A

Avoiding too rapid ascent;

300m/day for 3000-4270m

150m/day for 4270m +

Drugs: acetazolamide (carbonic anhydrase inhibitor), dexamethasone (synthetic glucocorticoid)

80
Q

How do glucocorticoids prevent AMS?

A

Correcting respiratory alkalosis which develops on first exposure to altitude allowing acclimatisation to occur more rapidly

81
Q

What is the remedy for AMS?

A

Descent to lower altitude or breathe oxygen

82
Q

What are symptoms of pulmonary oedema?

A

Dyspnoea (difficult breathing), dry cough

Severe: foaming pink sputum is coughed up

Can be fatal

83
Q

What are predisposing factors for HAPO?

A

Rapid ascent

Subjects who exercise in cold

Frequent in younger subjects

84
Q

What causes HAPO?

A

Hypoxic vasoconstriction of pulmonary arteries/arterioles = pulmonary hypertension

Increased filtration of fluid at pulmonary capillaries

Incr in pulmonary capillary permeability and inflammatory response

85
Q

What is treatment for HAPO?

A

Oxygen therapy

Descent to lower altitude

86
Q

What is HACO?

A

High altitude cerebral oedema

87
Q

Describe HACO?

A

Potentially fatal

Develops within hours/days in individuals with AMS

Increased intercranial pressure = coma, death if untreated

88
Q

What are symptoms of HACO?

A

Severe weakness and fatigue, confusion, impaired mental processing, breathlessness, unbalanced walk, possibly loss of consciousness

89
Q

What is incidence of HACO?

A

1% of people exposed to altitudes over 2700m

90
Q

What causes HACO?

A

Movement of fluid and protein from vascular component across BBB due to cerebral vasodilatation and increased capillary pressure

Increased CSF volume distorts brain structures (esp white matter)

91
Q

What is Monge’s disease?

A

Chronic mountain sickness

92
Q

What population gets Monge’s?

A

HAN, middle-aged men particularly

93
Q

What is treatment for Monge’s?

A

None except move to lower altitude

94
Q

Describe difference between AMS and Monge’s.

A

Monge’s is not form of prolonged AMS

Symptoms are associated with changes akin to patient losing acclimatisation to altitude

95
Q

What happens in Monge’s disease?

A

Minute ventilation falls = fall in PaO2

Stimulates erythropoeisis so haematocrit rises to high values (80%) with cyanosis

Pulmonary arterial hypertension becomes exaggerated

96
Q

What is the theory of what causes Monge’s disease?

A

Not fully understood, maybe related to ageing process

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